PROVIDER MANUAL

© 2016 American Heart Association

ISBN 978-1-61669-400-5
Printed in the United States of America
First American Heart Association Printing March 2016
eBook edition © 2016 American Heart Association.

Acknowledgments
The American Heart Association thanks the following people for their contributions to the development of this manual:
Michael W. Donnino, MD; Kenneth Navarro, MEd, LP; Katherine Berg, MD; Steven C. Brooks, MD, MHSc; Julie
Crider, PhD; Mary Fran Hazinski, RN, MSN; Theresa A. Hoadley, RN, PhD, TNS; Sallie Johnson, PharmD, BCPS;
Venu Menon, MD; Susan Morris, RN; Peter D. Panagos, MD; Michael Shuster, MD; David Slattery, MD; and the AHA
ACLS Project Team.
To find out about any updates or corrections to this text, visit www.heart.org/cpr, navigate to the
page for this course, and click on “Updates.”

To access the Student Website for this course, go to www.heart.org/eccstudent and enter this code:
acls15
Part 1
Introduction

Course Description and Goal

Course Objectives
Course Design
Course Prerequisites and Preparation
BLS Skills
ECG Rhythm Interpretation for Core ACLS
Rhythms
Basic ACLS Drug and Pharmacology
Knowledge
Course Materials
ACLS Provider Manual
Student Website
Pocket Reference Cards
Precourse Preparation Checklist
Requirements for Successful Course Completion
ACLS Provider Manual Abbreviations
Advanced Cardiovascular Life Support
Closing the Gaps
Quality Assessment, Review, and Translational
Science
Part 2
Systems of Care
Introduction
Cardiopulmonary Resuscitation
Quality Improvement in Resuscitation Systems,
Processes, and Outcomes
A Systems Approach
Measurement
Benchmarking and Feedback
Change
Summary
Acute Coronary Syndromes
Starts “On the Phone” With Activation of EMS
EMS Components
Hospital-Based Components
Acute Stroke
Regionalization of Stroke Care
Community and Professional Education
EMS
Post–Cardiac Arrest Care
Targeted Temperature Management
Hemodynamic and Ventilation Optimization
Immediate Coronary Reperfusion With PCI
Glycemic Control
Neurologic Care and Prognostication
Education, Implementation, and Teams
The Need for Teams
Cardiac Arrest Teams (In-Hospital)
Rapid Response System
Published Studies
Implementation of a Rapid Response System
Part 3
Effective High-Performance Team Dynamics
Introduction
Roles of the Leader and Members of a High-
Performance Team
Role of the Team Leader
Role of the Team Member
Elements of Effective High-Performance Team
Dynamics
Roles
What to Communicate
How to Communicate
Part 4
The Systematic Approach
Introduction
The Systematic Approach
Overview of the Systematic Approach
The BLS Assessment
Overview of the BLS Assessment
The Primary Assessment
Overview of the Primary Assessment
The Secondary Assessment
Overview of the Secondary Assessment
H’s and T’s
Diagnosing and Treating Underlying Causes
Introduction
Conditions and Management
Hypovolemia
Cardiac and Pulmonary Conditions
Drug Overdoses or Toxic Exposures
Part 5
The ACLS Cases

Overview of the Cases

Respiratory Arrest Case
Introduction
Case Drugs
Normal and Abnormal Breathing
Identification of Respiratory Problems by
Severity
Respiratory Distress
Respiratory Failure
Respiratory Arrest
The BLS Assessment
Assess and Reassess the Patient
Ventilation and Pulse Check
The Primary Assessment
Airway Management in Respiratory Arrest
Ventilations
Management of Respiratory Arrest
Overview
Giving Supplementary Oxygen
Maintain Oxygen Saturation
Opening the Airway
Common Cause of Airway Obstruction
Basic Airway Opening Techniques
Airway Management
Providing Basic Ventilation
Basic Airway Skills
Bag-Mask Ventilation
 Basic Airway Adjuncts: Oropharyngeal Airway
Introduction
Technique of OPA Insertion
Basic Airway Adjuncts: Nasopharyngeal Airway
Introduction
Technique of NPA Insertion
Suctioning
Introduction
Soft vs Rigid Catheters
Oropharyngeal Suctioning Procedure
Endotracheal Tube Suctioning Procedure
Providing Ventilation With an Advanced Airway
Introduction
Ventilation Rates
Laryngeal Mask Airway
Laryngeal Tube
Esophageal-Tracheal Tube
Endotracheal Tube
Precautions for Trauma Patients
Summary
Acute Coronary Syndromes Case
Introduction
Rhythms for ACS
Drugs for ACS
Goals for ACS Patients
Pathophysiology of ACS
Managing ACS: The Acute Coronary Syndromes
Algorithm
Overview of the Algorithm
Important Considerations
 Application of the ACS Algorithm
Identification of Chest Discomfort Suggestive of
Ischemia
Signs and Conditions
Starting With Dispatch
EMS Assessment, Care, and Hospital Preparation
Introduction
Monitor and Support ABCs
Administer Oxygen and Drugs
Obtain a 12-Lead ECG
Immediate ED Assessment and Treatment
Introduction
The First 10 Minutes
Patient General Treatment
Classify Patients According to ST-Segment
Deviation
Classify Into 3 Groups Based on ST-Segment
Deviation
STEMI
Introduction
Early Reperfusion Therapy
Use of PCI
Use of Fibrinolytic Therapy
Adjunctive Treatments
Acute Stroke Case
Introduction
Potential Arrhythmias With Stroke
Drugs for Stroke
Approach to Stroke Care
Introduction
Goals of Stroke Care
 Critical Time Periods
Application of the Suspected Stroke Algorithm
Identification of Signs of Possible Stroke
Warning Signs and Symptoms
Activate EMS System Immediately
Stroke Assessment Tools
Critical EMS Assessments and Actions
Introduction
Critical EMS Assessments and Actions
In-Hospital, Immediate General Assessment and
Stabilization
Introduction
Immediate General Assessment and
Stabilization
Immediate Neurologic Assessment by Stroke Team
or Designee
Overview
Establish Symptom Onset
Neurologic Examination
CT Scan: Hemorrhage or No Hemorrhage
Introduction
Decision Point: Hemorrhage or No
Hemorrhage
Fibrinolytic Therapy
Introduction
Evaluate for Fibrinolytic Therapy
Potential Adverse Effects
Patient Is a Candidate for Fibrinolytic Therapy
Extended IV rtPA Window 3 to 4.5 Hours
Intra-arterial rtPA
Endovascular Therapy
 Introduction
Intra-arterial rtPA
Mechanical Clot Disruption/Stent Retrievers
Systems of Care
General Stroke Care
Introduction
Begin Stroke Pathway
Monitor Blood Glucose
Monitor for Complications of Stroke and
Fibrinolytic Therapy
Hypertension Management in rtPA Candidates
Cardiac Arrest: VF/Pulseless VT Case
Introduction
Measurement
Benchmarking and Feedback
Change
Rhythms for VF/Pulseless VT
Drugs for VF/Pulseless VT
Managing VF/Pulseless VT: The Adult Cardiac Arrest
Algorithm
Overview
VF/pVT (Left Side)
Asystole/PEA (Right Side)
Summary
Application of the Adult Cardiac Arrest Algorithm:
VF/pVT Pathway
Introduction
Minimal Interruption of Chest Compressions
Deliver 1 Shock
Purpose of Defibrillation
Principle of Early Defibrillation
Resume CPR
 Rhythm Check
Self-Adhesive Pads
Shock and Vasopressors
Rhythm Check
Shock and Antiarrhythmics
Cardiac Arrest Treatment Sequences
Physiologic Monitoring During CPR
Treatment of VF/pVT in Hypothermia
Routes of Access for Drugs
Priorities
Intravenous Route
Intraosseous Route
Endotracheal Route
Fluid Administration
Vasopressors
Introduction
Vasopressors Used During Cardiac Arrest
Epinephrine
Antiarrhythmic Agents
Introduction
Amiodarone
Lidocaine
Magnesium Sulfate
Steroids in Cardiac Arrest
Respiratory or Cardiac Arrest Associated With
Opioid Overdose
Extracorporeal CPR (for VF/Pulseless
VT/Asystole/PEA)
Extracorporeal Membrane Oxygenation
Ultrasound (for VF/Pulseless VT/Asystole/PEA)
Ultrasound Use in Cardiac Arrest
Cardiac Arrest: Pulseless Electrical Activity Case
Introduction
Rhythms for PEA
Drugs for PEA
Description of PEA
Introduction
Historical Perspective
Managing PEA: The Adult Cardiac Arrest Algorithm
Overview
The PEA Pathway of the Cardiac Arrest
Algorithm
Decision Point: Rhythm Check
Administer Epinephrine
Nonshockable Rhythm
Decision Point: Shockable Rhythm
Asystole and PEA Treatment Sequences
Identification and Correction of Underlying
Cause
Cardiac Arrest: Asystole Case
Introduction
Rhythms for Asystole
Drugs for Asystole
Approach to Asystole
Introduction
Patients With DNAR Orders
Asystole as an End Point
Managing Asystole
Overview
Adult Cardiac Arrest Algorithm
Identification and Correction of Underlying
Cause
 Application of the Adult Cardiac Arrest Algorithm:
Asystole Pathway
Introduction
Confirmed Asystole
Administer Epinephrine
Decision Point: Rhythm Check
Nonshockable Rhythm
Shockable Rhythm
Asystole and PEA Treatment Sequences
TCP Not Recommended
Routine Shock Administration Not
Recommended
When in Doubt
Terminating Resuscitative Efforts
Terminating In-Hospital Resuscitative Efforts
Terminating Out-of-Hospital Resuscitative
Efforts
Duration of Resuscitative Efforts
Asystole: An Agonal Rhythm?
Ethical Considerations
Transport of Patients in Cardiac Arrest
Bradycardia Case
Introduction
Rhythms for Bradycardia
Drugs for Bradycardia
Description of Bradycardia
Definitions
Symptomatic Bradycardia
Signs and Symptoms
Managing Bradycardia: The Bradycardia Algorithm
Overview of the Algorithm
 Application of the Bradycardia Algorithm
Introduction
Identification of Bradycardia
Primary Assessment
Are Signs or Symptoms Caused by
Bradycardia?
Decision Point: Adequate Perfusion?
Treatment Sequence Summary
Treatment Sequence: Atropine
Treatment Sequence: Pacing
Treatment Sequence: Epinephrine, Dopamine
Next Actions
Transcutaneous Pacing
Introduction
Indications
Precautions
Technique
Assess Response to Treatment
Bradycardia With Escape Rhythms
Standby Pacing
Tachycardia: Stable and Unstable
Introduction
Rhythms for Unstable Tachycardia
Drugs for Unstable Tachycardia
The Approach to Unstable Tachycardia
Introduction
Definitions
Pathophysiology of Unstable Tachycardia
Signs and Symptoms
Rapid Recognition Is the Key to Management
Severity
Indications for Cardioversion
Managing Unstable Tachycardia: The Tachycardia
Algorithm
Introduction
Overview
Summary
Application of the Tachycardia Algorithm to the
Unstable Patient
Introduction
Assess Appropriateness for Clinical Condition
Identify and Treat the Underlying Cause
Decision Point: Is the Persistent
Tachyarrhythmia Causing Significant Signs
or Symptoms?
Perform Immediate Synchronized
Cardioversion
Determine the Width of the QRS Complex
Cardioversion
Introduction
Unsynchronized vs Synchronized Shocks
Potential Problems With Synchronization
Recommendations
Energy Doses for Cardioversion
Synchronized Cardioversion Technique
Introduction
Technique
Stable Tachycardias
Rhythms for Stable Tachycardia
Drugs for Stable Tachycardia
Approach to Stable Tachycardia
Introduction
Questions to Determine Classification
 Managing Stable Tachycardia: The Tachycardia
Algorithm
Introduction
Overview
Application of the Tachycardia Algorithm to the
Stable Patient
Introduction
Patient Assessment
BLS and ACLS Assessments
Decision Point: Stable or Unstable
IV Access and 12-Lead ECG
Decision Point: Narrow or Wide
Wide-Complex Tachycardias
Narrow QRS, Regular Rhythm
Tachycardia Algorithm: Advanced
Management Steps
Immediate Post–Cardiac Arrest Care Case
Introduction
Rhythms for Post–Cardiac Arrest Care
Drugs for Post–Cardiac Arrest Care
Multiple System Approach to Post–Cardiac
Arrest Care
Overview of Post–Cardiac Arrest Care
Managing Post–Cardiac Arrest Care: The Post–
Cardiac Arrest Care Algorithm
Application of the Immediate Post–Cardiac Arrest
Care Algorithm
Introduction
Optimize Ventilation and Oxygenation
Treat Hypotension (SBP Less Than 90 mm Hg)
STEMI Is Present or High Suspicion of AMI
Coronary Reperfusion
 Following Commands
Targeted Temperature Management
Advanced Critical Care
Post–Cardiac Arrest Maintenance Therapy
Appendix

Testing Checklists and Learning Station Checklists

ACLS Pharmacology Summary Table
2015 Science Summary Table
Glossary

Note on Medication Doses

Emergency cardiovascular care is a dynamic science. Advances in
treatment and drug therapies occur rapidly. Readers should use the
following sources to check for changes in recommended doses, indications,
and contraindications: the ECC Handbook, available as optional
supplementary material, and the package insert product information sheet
for each drug and medical device.
 Introduction
Course Description and Goal
The Advanced Cardiovascular Life Support (ACLS) Provider Course is designed for
healthcare providers who either direct or participate in the management of
cardiopulmonary arrest or other cardiovascular emergencies. Through didactic
instruction and active participation in simulated cases, students will enhance their skills
in the recognition and interventxion of cardiopulmonary arrest, immediate post–cardiac
arrest, acute arrhythmia, stroke, and acute coronary syndromes (ACS).
The goal of the ACLS Provider Course is to improve outcomes for adult patients of
cardiac arrest and other cardiopulmonary emergencies through early recognition and
interventions by high-performance teams.

Course Objectives
Upon successful completion of this course, students should be able to

• Apply the Basic Life Support (BLS), Primary, and Secondary Assessment
sequences for a systematic evaluation of adult patients
• Perform prompt, high-quality BLS, including prioritizing early chest compressions
and integrating early automated external defibrillator (AED) use
• Recognize respiratory arrest
• Perform early management of respiratory arrest
• Discuss early recognition and management of ACS, including appropriate
disposition
• Discuss early recognition and management of stroke, including appropriate
disposition
• Recognize bradyarrhythmias and tachyarrhythmias that may result in cardiac arrest
or complicate resuscitation outcome
• Perform early management of bradyarrhythmias and tachyarrhythmias that may
result in cardiac arrest or complicate resuscitation outcome
• Recognize cardiac arrest
• Perform early management of cardiac arrest until termination of resuscitation or
transfer of care, including immediate post–cardiac arrest care
 • Evaluate resuscitative efforts during a cardiac arrest through continuous
assessment of cardiopulmonary resuscitation (CPR) quality, monitoring the
patient’s physiologic response, and delivering real-time feedback to the team
• Model effective communication as a member or leader of a high-performance team
• Recognize the impact of team dynamics on overall team performance
• Discuss how the use of a rapid response team or medical emergency team may
improve patient outcomes
• Define systems of care

Course Design
To help you achieve these objectives, the ACLS Provider Course includes practice
learning stations and a Megacode evaluation station.
The practice learning stations give you an opportunity to actively participate in a variety
of learning activities, including

• Simulated clinical scenarios

• Demonstrations by instructors or video
• Discussion and role playing
• Practice in effective high-performance team behaviors

In these learning stations, you will practice essential skills both individually and as part
of a high-performance team. This course emphasizes effective team skills as a vital part
of the resuscitative effort. You will have the opportunity to practice as a member and as
a leader of a high-performance team.
At the end of the course, you will participate in a Megacode evaluation station to
validate your achievement of the course objectives. A simulated cardiac arrest scenario
will evaluate the following:

• Knowledge of core case material and skills

• Knowledge of algorithms
• Understanding of arrhythmia interpretation
• Use of appropriate basic ACLS drug therapy
• Performance as an effective leader of a high-performance team

Course Prerequisites and Preparation

The American Heart Association (AHA) limits enrollment in the
ACLS Provider Course to healthcare providers who direct or
participate in the resuscitation of a patient either in or out of
hospital. Participants who enter the course must have the basic
knowledge and skills to participate actively with the instructor and
other students.
 Before the course, please read the ACLS Provider
Manual, complete the mandatory Precourse Self-Assessment
modules on the Student Website (www.heart.org/eccstudent),
identify any gaps in your knowledge, and remediate those gaps
by studying the applicable content in the ACLS Provider
Manual or other supplementary resources, including the Student
Website. A passing score for the self-assessment is 70%, and
you may take it an unlimited number of times to achieve a passing
score. You will need to bring your Precourse Self-
Assessment certificate with you to class.
The following knowledge and skills are required for successful
course completion:

• BLS skills
• Electrocardiogram (ECG) rhythm interpretation for core
ACLS rhythms
• Knowledge of airway management and adjuncts
• Basic ACLS drug and pharmacology knowledge
• Practical application of ACLS rhythms and drugs
• Effective high-performance team skills

BLS Skills The foundation of advanced life support is strong BLS skills. You
must pass the high-quality BLS Testing Station to complete the
ACLS course. Make sure that you are proficient in BLS skills
before attending the course.

Watch the High-Quality BLS Skills video found on the

Student Website (www.heart.org/eccstudent). Review the High-
Quality BLS Skills Testing Checklist located in the Appendix..

ECG Rhythm The basic cardiac arrest and periarrest algorithms require
Interpretation for students to recognize these ECG rhythms:
Core ACLS
Rhythms • Sinus rhythm
• Atrial fibrillation and flutter
• Bradycardia
• Tachycardia
• Atrioventricular (AV) block
• Asystole
• Pulseless electrical activity (PEA)
• Ventricular tachycardia (VT)
 • Ventricular fibrillation (VF)

You will need to complete the ACLS Precourse Self-

Assessment, which contains ECG rhythm identification, on the
Student Website (www.heart.org/eccstudent). At the end of the
assessment, you will receive your score and feedback to help you
identify areas of strength and weakness. Remediate any gaps in
your knowledge before entering the course. During the course,
you must be able to identify and interpret rhythms during practice
as well as during the final Megacode evaluation station.

Basic ACLS Drug You must know the drugs and doses used in the ACLS
and Pharmacology algorithms. You will also need to know when to use which drug
Knowledge based on the clinical situation.

You will need to complete the ACLS Precourse Self-

Assessment, which contains pharmacology questions, on the
Student Website (www.heart.org/eccstudent). At the end of the
assessment, you will receive your score and feedback to help you
identify areas of strength and weakness. Remediate any gaps in
your knowledge before entering the course.

Course Materials

Course materials consist of the ACLS Provider Manual, Student

Website (www.heart.org/eccstudent), 2 Pocket Reference Cards, and
Precourse Preparation Checklist. The icon on the left directs you to
additional supplementary information on the Student Website.

ACLS The ACLS Provider Manual contains the basic information you need for
Provider effective participation in the course. This important material includes the
Manual systematic approach to a cardiopulmonary emergency, effective high-
performance team communication, and the ACLS cases and
algorithms. Please review this manual before attending the course.
Bring it with you for use and reference during the course.
The manual is organized into the following parts:
Part 1 Introduction
Part 2 Systems of Care
 Part 3 Effective High-Performance Team
Dynamics
Part 4 The Systematic Approach
Part 5 The ACLS Cases
Appendix Testing Checklists and Learning Station
Checklists
ACLS Pharmacology Basic ACLS drugs, doses, indications and
Summary Table contraindications, and side effects
2015 Science Summary Highlights of 2015 science changes in the
Table ACLS Provider Course
Glossary Alphabetical list of terms and their
definitions

The AHA requires that students complete and pass the Precourse
Self-Assessment found on the Student Website and print their scores for
submission to their ACLS Instructor. The Precourse Self-Assessment
allows students to understand gaps in knowledge required to participate in
and pass the course. Supplementary topics located on the Student Website
are useful but not essential for successful completion of the course.
Call-out Boxes
The ACLS Provider Manual contains important information presented in
call-out boxes that require the reader’s attention. Please pay particular
attention to the call-out boxes, listed below:
Critical Pay particular attention to the Critical
Concepts Concepts boxes that appear in the ACLS Provider
Manual. These boxes contain the most important
information that you must know.

Caution Caution boxes emphasize specific risks associated

with interventions.

FYI 2015 FYI 2015 Guidelines boxes contain the new 2015
Guidelines AHA Guidelines Update for CPR and Emergency
Cardiovascular Care (ECC) information.
 Foundational Foundational Facts boxes contain basic information
Facts that will help you understand the topics covered in the
course.

Life Is Why Life Is Why boxes describe why taking this course
matters.

Student Website

The ACLS Student Website (www.heart.org/eccstudent) contains the following

self-assessment and supplementary resources:
Resource Description How to Use
Mandatory The Precourse Self- Complete before the course to
Precourse Self- Assessment evaluates a help evaluate your proficiency
Assessment student’s knowledge in 3 and determine the need for
sections: rhythm, additional review and practice
pharmacology, and practical before the course
application
ACLS • Basic Airway Management Additional information to
Supplementary • Advanced Airway supplement basic concepts
Information Management presented in the ACLS course
• ACLS Core Rhythms
• Defibrillation Some information is
• Access for Medications supplementary; other areas
• Acute Coronary Syndromes are for the interested student
• Human, Ethical, and Legal or advanced provider
Dimensions of ECC and
ACLS
• Web-Based Self-
Assessment: Drugs Used in
Algorithms

High-Quality BLS • High-quality BLS

video • Compressions
• Ventilations
 • AED use

ACS video • ST-segment elevation

myocardial infarction
(STEMI)
• Chain of Survival
• Supplementary oxygen
• 12-lead ECG
• Reperfusion
• Percutaneous coronary
intervention
• Fibrinolytic therapy

Stroke video • Acute stroke

• Chain of Survival
• 8 D’s of Stroke Care
• Fibrinolytic therapy

Airway • Airway adjuncts

Management • Advanced airways
video • Confirmation devices

Pocket The Pocket Reference Cards are 2 stand-alone cards that are included
Reference with the ACLS Provider Manual.These cards can be used for quick
Cards reference on the following topics:
Topic Reference Cards
Cardiac arrest, • Adult Cardiac Arrest Algorithms
arrhythmias, and • Table with drugs and dosage
treatment reminders
• Adult Immediate Post–Cardiac
Arrest Care Algorithm
• Adult Bradycardia With a Pulse
Algorithm
• Adult Tachycardia With a Pulse
Algorithm

ACS and stroke • Acute Coronary Syndromes

Algorithm
• Fibrinolytic Checklist for STEMI
• Fibrinolytic Contraindications for
STEMI
• Adult Suspected Stroke Algorithm
 • Stroke Assessment—Cincinnati
Prehospital Stroke Scale
• Use of IV rtPA for Acute Ischemic
Stroke
• Hypertension Management in
Acute Ischemic Stroke

Precourse The Precourse Preparation Checklist is included with the ACLS

Preparation Provider Manual and can be found on the ACLS Student Website
Checklist (www.heart.org/eccstudent). Please print, review, and check the
boxes after you have completed preparation for each section.

Requirements for Successful Course Completion

To successfully complete the ACLS Provider Course and obtain your course completion
card, you must

• Pass the Adult High-Quality BLS Skills Test

• Pass the Bag-Mask Ventilation Skills Test, including oropharyngeal
airway/nasopharyngeal airway insertion
• Demonstrate competency in learning station skills
• Pass the Megacode Test
• Pass the open-resource exam with a minimum score of 84%

Life Is Saving Lives Is Why

Why Cardiac arrest remains a leading cause of death, so the AHA trains millions
of people each year to help save lives both in and out of the hospital. This
course is a key part of that effort.

ACLS Provider Manual Abbreviations

A
ACE Angiotensin-converting enzyme
ACLS Advanced cardiovascular life support
ACS Acute coronary syndromes
AED Automated external defibrillator
AHF Acute heart failure
AIVR Accelerated idioventricular rhythm
AMI Acute myocardial infarction
aPTT Activated partial thromboplastin time
AV Atrioventricular
B
BLS Basic life support: Check responsiveness, activate emergency response
system, check carotid pulse, provide defibrillation
C
CARES Cardiac Arrest Registry to Enhance Survival
CCF Chest compression fraction
CPR Cardiopulmonary resuscitation
CPSS Cincinnati Prehospital Stroke Scale
CQI Continuous quality improvement
CT Computed tomography
D
DNAR Do not attempt resuscitation
E
ECG Electrocardiogram
ED Emergency department
EMS Emergency medical services
ET Endotracheal
F
FDA Food and Drug Administration
FIO2 Fraction of inspired oxygen
G
GI Gastrointestinal
I
ICU Intensive care unit
INR International normalized ratio
IO Intraosseous
IV Intravenous
 L
LV Left ventricle or left ventricular
M
mA Milliamperes
MACE Major adverse cardiac events
MET Medical emergency team
MI Myocardial infarction
mm Hg Millimeters of mercury
N
NIH National Institutes of Health
NIHSS National Institutes of Health Stroke Scale
NINDS National Institute of Neurological Disorders and Stroke
NPA Nasopharyngeal airway
NSAID Nonsteroidal anti-inflammatory drug
NSTE- Non–ST-segment elevation acute coronary syndromes
ACS
NSTEMI Non–ST-segment elevation myocardial infarction
O
OPA Oropharyngeal airway
P
PaCO2 Partial pressure of carbon dioxide in arterial blood
PCI Percutaneous coronary intervention
PE Pulmonary embolism
PEA Pulseless electrical activity
PETCO2 Partial pressure of end-tidal carbon dioxide
PT Prothrombin time
pVT Pulseless ventricular tachycardia
R
ROSC Return of spontaneous circulation
RRT Rapid response team
rtPA Recombinant tissue plasminogen activator
 RV Right ventricle or right ventricular
S
SBP Systolic blood pressure
STEMI ST-segment elevation myocardial infarction
SVT Supraventricular tachycardia
T
TCP Transcutaneous pacing
TTM Targeted temperature management
U
UA Unstable angina
V
VF Ventricular fibrillation
VT Ventricular tachycardia

Advanced Cardiovascular Life Support

ACLS providers face an important challenge—functioning as a team that implements
and integrates both basic and advanced life support to save a person’s life. The 2015
AHA Guidelines Update for CPR and ECCreviewed evidence that shows that in both the
in-hospital and out-of-hospital settings, many cardiac arrest patients do not receive
high-quality CPR, and the majority do not survive. One study of in-hospital cardiac
arrest showed that the quality of CPR was inconsistent and did not always meet
guidelines recommendations.1 Over the years, however, patient outcomes after cardiac
arrest have improved. Table 1shows the recent trends in survival in both out-of-hospital
and in-hospital cardiac arrest in the United States.2
Table 1. Recent Cardiac Arrest Survival Data
In-Hospital Cardiac
Out-of-Hospital Cardiac Arrest
Arrest
Statistical Survival Survival
Update Bystander
Incidence, Rate* Incidence,† Rate*
CPR
n (Overall), n (Adults),
(Overall), %
% %
2015 326 200 45.9 10.6 209 000 25.5
2014 424 000 40.8 10.4 209 000 22.7
2013 359 400 40.1 9.5 209 000 23.9
2012 382 800 41.0 11.4 209 000 23.1
 Baseline 31 7.9 19
*Survival to hospital discharge.
†Extrapolated incidence based on the same 2011 Get With The Guidelines-

Resuscitation study.
To analyze these findings, a “back-to-basics” evidence review refocused on the
essentials of CPR, the links in the Chain of Survival, and the integration of BLS with
ACLS. Minimizing the interval between stopping chest compressions and delivering a
shock (ie, minimizing the preshock pause) improves the chances of shock success 3 and
patient survival.4 Experts believe that high survival rates from both out-of-hospital and
in-hospital sudden cardiac death are possible with strong systems of care.
High survival rates in studies are associated with several common elements:

• Training of knowledgeable healthcare providers

• Planned and practiced response
• Rapid recognition of sudden cardiac arrest
• Prompt provision of CPR
• Defibrillation as early as possible and within 3 to 5 minutes of collapse
• Organized post–cardiac arrest care

When trained persons implement these elements early, ACLS has the best chance of
producing a successful outcome.
Critical Optimization of ACLS
Concepts ACLS is optimized when a team leader effectively integrates high-quality
CPR and minimal interruption of high-quality chest compressions with
advanced life support strategies (eg, defibrillation, medications, advanced
airway).

Critical Minimize Interruptions in Compressions

Concepts Studies have shown that a reduction in the interval between stopping
compressions and shock delivery can increase the predicted shock
success. Interruptions in compressions should be limited to critical
interventions (rhythm analysis, shock delivery, intubation, etc), and even
then, these should be minimized to 10 seconds or less.

Closing the Gaps

Quality Assessment, Every emergency medical service (EMS) and hospital system
Review, and should perform continuous quality improvement to assess its
Translational resuscitation interventions and outcomes through a defined
Science process of data collection and review. There is now widespread
consensus that the best way to improve either community or in-
hospital survival from sudden cardiac arrest is to start with the
 standard “quality improvement model” and then modify that
model according to the Chain of Survival metaphor. Each link in
the chain comprises structural, process, and outcome variables
that can be examined, measured, and recorded. System
managers can quickly identify gaps that exist between observed
processes and outcomes and local expectations or published
“gold standards.”
Life Is Life Is Why
Why At the American Heart Association, we want people to experience more of
life’s precious moments. What you learn in this course can help build
healthier, longer lives for everyone.
References
1. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary
resuscitation during in-hospital cardiac arrest. JAMA. 2005;293(3):305-310.
2. Mozaffarian D, Benjamin EJ, Go AS, et al; on behalf of the American Heart
Association Statistics Committee and Stroke Statistics Subcommittee. Heart
disease and stroke statistics—2015 update: a report from the American Heart
Association. Circulation. 2015;131(4):e29-e322.
3. Edelson DP, Abella BS, Kramer-Johansen J, et al. Effects of compression depth
and pre-shock pauses predict defibrillation failure during cardiac
arrest. Resuscitation. 2006;71(2):137-145.
4. Edelson DP, Litzinger B, Arora V, et al. Improving in-hospital cardiac arrest process
and outcomes with performance debriefing. Arch Intern Med. 2008;168(10):1063-
1069.
 Systems of Care

Introduction A system is a group of regularly interacting and interdependent

components. The system provides the links for the chain and determines
the strength of each link and the chain as a whole. By definition, the
system determines the ultimate outcome and provides collective support
and organization. The ideal work flow to accomplish resuscitation
successfully is highly dependent on the system of care as a whole.

Cardiopulmonary Resuscitation
Quality Improvement in CPR is a series of lifesaving actions that improve the chance
Resuscitation Systems, of survival after cardiac arrest. Although the optimal
Processes, and approach to CPR may vary, depending on the rescuer, the
Outcomes patient, and the available resources, the fundamental
challenge remains how to achieve early and effective CPR.

A Systems Approach In this part, we will focus on 2 distinct systems of care: the
system for patients who arrest inside of the hospital and the
one for those who arrest outside of it. We will set into context
the building blocks for a system of care for cardiac arrest,
with consideration of the setting, team, and available
resources, as well as continuous quality improvement (CQI)
from the moment the patient becomes unstable until after the
patient is discharged.
Healthcare delivery requires structure (eg, people,
equipment, education) and process (eg, policies, protocols,
procedures), which, when integrated, produce a system (eg,
programs, organizations, cultures) leading to outcomes (eg,
patient safety, quality, satisfaction). An effective system of
care comprises all of these elements—structure, process,
 system, and patient outcomes—in a framework of CQI
(Figure 1).

Figure 1. Taxonomy of systems of care.

Successful resuscitation after cardiac arrest requires an integrated set of coordinated
actions represented by the links in the system-specific Chains of Survival (Figure 2).
Effective resuscitation requires an integrated response known as a system of care.
Fundamental to a successful resuscitation system of care is the collective appreciation
of the challenges and opportunities presented by the Chain of Survival. Thus,
individuals and groups must work together, sharing ideas and information, to evaluate
and improve their resuscitation system. Leadership and accountability are important
components of this team approach.
To improve care, leaders must assess the performance of each system component.
Only when performance is evaluated can participants in a system effectively intervene
to improve care. This process of quality improvement consists of an iterative and
continuous cycle of

• Systematic evaluation of resuscitation care and outcome

• Benchmarking with stakeholder feedback
• Strategic efforts to address identified deficiencies

While the care for all postresuscitation patients, regardless of where the arrest occurred,
converges in the hospital, generally in an intensive care unit (ICU), the structure and
process elements before that convergence vary highly for the 2 patient populations.
Patients with out-of-hospital cardiac arrest (OHCA) depend on their community for
support. Lay rescuers are expected to recognize a patient’s distress, call for help, and
initiate CPR and public-access defibrillation (PAD) until a team of professionally trained
EMS providers assumes responsibility and transports the patient to an emergency
department (ED) and/or cardiac catheterization lab before the patient is transferred to
an ICU for continued care.
In contrast, patients with in-hospital cardiac arrest (IHCA) depend on a system of
appropriate surveillance and prevention of cardiac arrest. When they do arrest, they
depend on the smooth interaction of the institution’s various departments and services
and on a multidisciplinary team of professional providers, which includes physicians,
nurses, respiratory therapists, pharmacists, counselors, and others.

Figure 2. System-specific Chains of Survival.

Foundational Medical Emergency Teams and Rapid Response Teams
Facts
• Many hospitals have implemented the use of METs or RRTs. The
purpose of these teams is to improve patient outcomes by identifying
and treating early clinical deterioration (Figure 3). IHCA is commonly
preceded by physiologic changes. In recent studies, nearly 80% of
hospitalized patients with cardiorespiratory arrest had abnormal vital
signs documented for up to 8 hours before the actual arrest. Many of
these changes can be recognized by monitoring routine vital signs.
Intervention before clinical deterioration or cardiac arrest may be
possible.
 • Consider this question: “Would you have done anything differently if
you knew 15 minutes before the arrest that…?”

Figure 3. Management of life-threatening emergencies requires integration of

multidisciplinary teams that can involve RRTs, cardiac arrest teams, and intensive care
specialties to achieve survival of the patient. Team leaders have an essential role in
coordination of care with team members and other specialists.
The classic resuscitation Chain of Survival concept linked the community to EMS and
EMS to hospitals, with hospital care as the destination.1 But patients with a cardiac
emergency may enter the system of care at one of many different points (Figure 4).
They can present anywhere, anytime—on the street or at home, yes, but also in the
hospital’s ED, inpatient bed, ICU, operating suite, catheterization suite, or imaging
department. The system of care must be able to manage cardiac emergencies
wherever they occur.

Figure 4. Patient’s point of entry. Abbreviations: EMS, emergency medical services;

IHCA, in-hospital cardiac arrest; SOC, system of care; DC, discharge.
Measurement Continual efforts to improve resuscitation outcomes are impossible
without data capture. The collection of resuscitation process measures
is the underpinning of a system of care’s quality improvement efforts.
Quality improvement relies on valid assessment of resuscitation
performance and outcome.
Utstein-style guidelines and templates have been prepared for reporting
resuscitation outcomes after trauma and drowning.2

• The Utstein Guidelines3 provide guidance for core performance

measures, including
o – Rate of bystander CPR
o – Time to defibrillation
o – Time to advanced airway management
o – Time to first administration of resuscitation medication
o – Survival to hospital discharge

Monitors to measure CPR performance are now widely available. 4 They

provide rescuers with invaluable real-time feedback on the quality of
CPR delivered during resuscitative efforts, data for debriefing after
resuscitation, and retrospective information for system-wide CPR CQI
programs. Without CPR measurement and subsequent understanding
of CPR performance, improvement and optimized performance cannot
occur. Providing CPR without monitoring performance can be likened to
flying an airplane without an altimeter.
Routinely available feedback on CPR performance characteristics
includes chest compression rate, depth, and recoil.4 Currently, certain
important parameters (chest compression fraction and preshock,
perishock, and postshock pauses) can be reviewed only retrospectively,
whereas others (ventilation rate, airway pressure, tidal volume, and
inflation duration) cannot be assessed adequately by current
technology. Additionally, accelerometers are insensitive to mattress
compression, and current devices often prioritize the order of feedback
by use of a rigid algorithm in a manner that may not be optimal or
realistic (eg, an accelerometer cannot measure depth if there is too
much leaning, so the device will prioritize feedback to correct leaning
before correcting depth). Although some software (automated
algorithms) and hardware (smart backboard, dual accelerometers,
reference markers, and others) solutions currently exist, continued
development of optimal and widely available CPR monitoring is a key
component to improved performance.
Life Is High-Quality CPR Is Why
Why
 Early recognition and CPR are crucial for survival from cardiac arrest. By
learning high-quality CPR, you’ll have the ability to improve patient outcomes
and save more lives.

Benchmarking Data should be systematically reviewed and compared internally to

and Feedback prior performance and externally to similar systems. Existing
registries can facilitate this benchmarking effort. Examples include

• Cardiac Arrest Registry to Enhance Survival (CARES) for

OHCA
• Get With The Guidelines®-Resuscitation program for IHCA

Change Simply measuring and benchmarking care can positively influence

outcome. However, ongoing review and interpretation are necessary
to identify areas for improvement, such as

• Increased bystander CPR response rates

• Improved CPR performance
• Shortened time to defibrillation
• Citizen awareness
• Citizen and healthcare professional education and training

Summary Over the past 50 years, the modern-era BLS fundamentals of early
recognition and activation, early CPR, and early defibrillation have
saved hundreds of thousands of lives around the world. However,
we still have a long road to travel if we are to fulfill the potential
offered by the Chain of Survival. Survival disparities presented a
generation ago appear to persist. Fortunately, we currently possess
the knowledge and tools—represented by the Chain of Survival—to
address many of these care gaps, and future discoveries will offer
opportunities to improve rates of survival.

Acute Coronary Syndromes

The primary goals of therapy for patients with acute coronary
syndromes (ACS) are to

1. Reduce the amount of myocardial necrosis that occurs in

patients with acute myocardial infarction, thus preserving left
 ventricular function, preventing heart failure, and limiting other
cardiovascular complications
2. Prevent major adverse cardiac events: death, nonfatal
myocardial infarction, and the need for urgent
revascularization
3. Treat acute, life-threatening complications of ACS, such as
ventricular fibrillation (VF), pulseless VT (pVT), unstable
tachycardias, symptomatic bradycardias, pulmonary edema,
cardiogenic shock, and mechanical complications of acute
myocardial infarction

Starts “On the Prompt diagnosis and treatment offers the greatest potential
Phone” With benefit for myocardial salvage. Thus, it is imperative that
Activation of EMS healthcare providers recognize patients with potential ACS to
initiate evaluation, appropriate triage, and management as
expeditiously as possible.

EMS Components • Prehospital ECGs

• Notification of the receiving facility of a patient with possible
ST-segment elevation myocardial infarction (“STEMI alert”)
• Activation of the cardiac catheterization team to shorten
reperfusion time
• Continuous review and quality improvement

Hospital-Based • ED protocols
Components o – Activation of the cardiac catheterization laboratory
o – Admission to the coronary ICU
o – Quality assurance, real-time feedback, and healthcare
provider education
• Emergency physician
o – Empowered to select the most appropriate reperfusion
strategy
o – Empowered to activate the cardiac catheterization team as
indicated
• Hospital leadership
o – Must be involved in the process and committed to support
rapid access to STEMI reperfusion therapy
Acute Stroke
The healthcare system has achieved significant improvements in
stroke care through integration of public education, emergency
dispatch, prehospital detection and triage, hospital stroke system
development, and stroke unit management. Not only have the
rates of appropriate fibrinolytic therapy increased over the past 5
years, but overall stroke care has also improved, in part through
the creation of stroke centers.

Regionalization of With the National Institute of Neurological Disorders and Stroke

Stroke Care recombinant tissue plasminogen activator (rtPA) trial,5 the crucial
need for local partnerships between academic medical centers
and community hospitals became clear. The time-sensitive nature
of stroke requires such an approach, even in densely populated
metropolitan centers.

Community and Community and professional education is essential and has

Professional successfully increased the proportion of stroke patients treated
Education with fibrinolytic therapy.

• Patient education efforts are most effective when the

message is clear and succinct.
• Educational efforts need to couple the knowledge of the
signs and symptoms of stroke with action—activate the
emergency response system.

EMS The integration of EMS into regional stroke models is crucial for
improvement of patient outcomes.6

• EMS response personnel trained in stroke recognition

• Stroke-prepared hospitals–primary stroke centers
• Access to stroke expertise via telemedicine from the nearest
stroke center

Post–Cardiac Arrest Care

The healthcare system should implement a comprehensive,
structured, multidisciplinary system of care in a consistent
manner for the treatment of post–cardiac arrest patients.
Programs should address targeted temperature management
 (TTM), hemodynamic and ventilation optimization, immediate
coronary reperfusion with percutaneous coronary intervention
(PCI) for eligible patients, neurologic care and prognostication,
and other structured interventions.
Patients who achieve return of spontaneous circulation (ROSC)
after cardiac arrest in any setting have a complex combination of
pathophysiologic processes described as post–cardiac arrest
syndrome, which includes postarrest brain injury, postarrest
myocardial dysfunction, systemic ischemia or reperfusion
response, and persistent acute and chronic pathology that may
have precipitated the cardiac arrest.7 Post–cardiac arrest
syndrome plays a significant role in patient mortality.
Individual hospitals with a high frequency of treating cardiac
arrest patients show an increased likelihood of survival when
these interventions are provided.8,9

Targeted The 2015 AHA Guidelines Update for CPR and

Temperature ECC recommends that TTM interventions be administered to
Management comatose (ie, lacking meaningful response to verbal commands)
adult patients with ROSC after cardiac arrest, by selecting and
maintaining a constant temperature between 32°C and 36°C
(89.6°F and 95.2°F) for at least 24 hours.

Hemodynamic and Although providers often use 100% oxygen while performing the
Ventilation initial resuscitation, providers should titrate inspired oxygen
Optimization during the post–cardiac arrest phase to the lowest level required
to achieve an arterial oxygen saturation of 94% or greater, when
feasible. This helps to avoid any potential complications
associated with oxygen toxicity.
Avoid excessive ventilation of the patient because of potential
adverse hemodynamic effects when intrathoracic pressures are
increased and because of potential decreases in cerebral blood
flow when partial pressure of carbon dioxide in arterial blood
(PaCO2) decreases.
Healthcare providers may start ventilation rates at 10/min.
Normocarbia (partial pressure of end-tidal carbon dioxide
[PETCO2] of 30 to 40 mm Hg or PaCO2 of 35 to 45 mm Hg) may
be a reasonable goal unless patient factors prompt more
individualized treatment. Other PaCO2 targets may be tolerated
for specific patients. For example, a higher PaCO2 may be
permissible in patients with acute lung injury or high airway
pressures. Likewise, mild hypocapnia might be useful as a
temporary measure when treating cerebral edema, but
 hyperventilation could cause cerebral vasoconstriction.
Providers should note that when a patient’s temperature is below
normal, laboratory values reported for PaCO2 might be higher
than the actual values.
Healthcare providers should titrate fluid administration and
vasoactive or inotropic agents as needed to optimize blood
pressure, cardiac output, and systemic perfusion. The optimal
post–cardiac arrest blood pressure remains unknown; however,
a mean arterial pressure of 65 mm Hg or greater is a reasonable
goal.

Immediate Coronary After ROSC in patients in whom coronary artery occlusion is

Reperfusion With suspected, rescuers should transport the patient to a facility
PCI capable of reliably providing coronary reperfusion (eg, PCI) and
other goal-directed post–cardiac arrest care therapies. The
decision to perform PCI can be made irrespective of the
presence of coma or the decision to induce hypothermia,
because concurrent PCI and hypothermia are feasible and safe
and have good outcomes.

Glycemic Control Healthcare providers should not attempt to alter glucose

concentration within a lower range (80 to 110 mg/dL [4.4 to 6.1
mmol/L]), because of the increased risk of hypoglycemia.
The 2015 AHA Guidelines Update for CPR and ECC does not
recommend any specific target range of glucose management in
adult patients with ROSC after cardiac arrest.

Neurologic Care The goal of post–cardiac arrest management is to return patients

and Prognostication to their prearrest functional level. Reliable early prognostication
of neurologic outcome is an essential component of post–
cardiac arrest care, but the optimal timing is important to
consider. In patients treated with TTM, prognostication using
clinical examination should be delayed until at least 72 hours
after return to normothermia. For those not treated with TTM, the
earliest time is 72 hours after cardiac arrest and potentially
longer if the residual effect of sedation or paralysis confounds
the clinical examination.
Education, Implementation, and Teams
The Chain of Survival is a metaphor used to organize and
describe the integrated set of time-sensitive coordinated actions
necessary to maximize survival from cardiac arrest. The use of
evidence-based education and implementation strategies can
optimize the links in the chain.

The Need for Teams Mortality from IHCA remains high. The average survival rate is
approximately 24%, despite significant advances in treatments.
Survival rates are particularly poor for arrest associated with
rhythms other than VF/pVT. Non-VF/pVT rhythms are present in
more than 82% of arrests in the hospital.10
Many in-hospital arrests are preceded by easily recognizable
physiologic changes, many of which are evident with routine
monitoring of vital signs. In recent studies, nearly 80% of
hospitalized patients with cardiorespiratory arrest had abnormal
vital signs documented for up to 8 hours before the actual arrest.
This finding suggests that there is a period of increasing
instability before the arrest.

Cardiac Arrest Cardiac arrest teams are unlikely to prevent arrests because
Teams their focus has traditionally been to respond only after the arrest
(In-Hospital) has occurred. Unfortunately, the mortality rate is more than 75%
once the arrest occurs.10
Over the past few years, hospitals have expanded the focus to
include patient safety and prevention of arrest. The best way to
improve a patient’s chance of survival from a cardiorespiratory
arrest is to prevent it from happening.
Poor-quality CPR should be considered a preventable harm.4 In
healthcare environments, variability in clinician performance has
affected the ability to reduce healthcare-associated
complications,11 and a standardized approach has been
advocated to improve outcomes and reduce preventable
harms.12 Doing so requires a significant cultural shift within
institutions. Actions and interventions need to be proactive with
the goal of improving rates of morbidity and mortality rather than
reacting to a catastrophic event.
Rapid assessment and intervention for many abnormal
physiologic variables can decrease the number of arrests
occurring in the hospital.
Rapid Response The wide variability in incidence and location of cardiac arrest in
System the hospital suggests potential areas for standardization of
quality and prevention of at least some cardiac arrests. More
than half of cardiac arrests in the hospital are the result of
respiratory failure or hypovolemic shock, and the majority of
these events are foreshadowed by changes in physiology, such
as tachypnea, tachycardia, and hypotension. As such, cardiac
arrest in the hospital often represents the progression of
physiologic instability and a failure to identify and stabilize the
patient in a timely manner. This scenario is more common on the
general wards, outside of critical care and procedural areas,
where patient-to-nurse ratios are higher and monitoring of
patients less intense. In this setting, intermittent manual vital sign
monitoring with less frequent direct observation by clinicians may
increase the likelihood of delayed recognition.
Over the past decade, hospitals in several countries have
designed systems to identify and treat early clinical deterioration
in patients. The purpose of these rapid response systems is to
improve patient outcomes by bringing critical care expertise to
patients. The rapid response system has several components:

• Event detection and response triggering arm

• A planned response arm, such as the RRT
• Quality monitoring
• Administrative support

Many rapid response systems allow activation by a nurse,

physician, or family member who is concerned that the patient is
deteriorating. Some rapid response systems use specific
physiologic criteria to determine when to call the team. These
parameters may be weighted, combined, and scored as part of
an early warning sign system. The following list gives examples
of such criteria for adult patients:

• Threatened airway
• Respiratory rate less than 6/min or more than 30/min
• Heart rate less than 40/min or greater than 140/min
• Systolic blood pressure less than 90 mm Hg
• Symptomatic hypertension
• Unexpected decrease in level of consciousness
• Unexplained agitation
• Seizure
• Significant fall in urine output
• Subjective concern about the patient
 Medical Emergency Teams and Rapid Response
Teams
RRTs, or METs, were established for early intervention in
patients whose conditions were deteriorating, with the goal of
preventing IHCA.13,14 They can be composed of varying
combinations of physicians, nurses, and respiratory therapists.
These teams are usually summoned to patient bedsides when
an acute deterioration is recognized by other hospital staff.
Monitoring and resuscitation equipment and drug therapies often
accompany the team.
The rapid response system is critically dependent on early
identification and activation to immediately summon the team to
the patient’s bedside. These teams typically consist of healthcare
providers with both the critical care or emergency care
experience and skills to support immediate intervention for life-
threatening situations. These teams are responsible for
performing a rapid patient assessment and initiating appropriate
treatment to reverse physiologic deterioration and prevent a poor
outcome.

Published Studies The majority of published before-and-after studies of METs or

rapid response systems have reported a 17% to 65% drop in the
rate of cardiac arrests after the intervention. Other documented
benefits of these systems include

• A decrease in unplanned emergency transfers to the ICU

• Decreased ICU and total hospital length of stay
• Reductions in postoperative morbidity and mortality rates
• Improved rates of survival from cardiac arrest

The recently published Medical Emergency Response

Improvement Team (MERIT) trial is the only randomized
controlled trial comparing hospitals with an MET with those
without one. The study did not show a difference in the
composite primary outcome (cardiac arrest, unexpected death,
unplanned ICU admission) between the 12 hospitals in which an
MET system was introduced and 11 hospitals that had no MET
system in place. Further research is needed about the critical
details of implementation and the potential effectiveness of METs
in preventing cardiac arrest or improving other important patient
outcomes.
Implementation of a Implementing any type of rapid response system will require a
Rapid Response significant cultural change in most hospitals. Those who design
System and manage the system must pay particular attention to issues
that may prevent the system from being used effectively.
Examples of such issues are insufficient resources, poor
education, fear of calling the team, fear of losing control over
patient care, and resistance from team members.
Implementation of a rapid response system requires ongoing
education, impeccable data collection and review, and feedback.
Development and maintenance of these programs requires a
long-term cultural and financial commitment from the hospital
administration. Hospital administrators and healthcare
professionals need to reorient their approach to emergency
medical events and develop a culture of patient safety with a
primary goal of decreasing morbidity and mortality.
Life Is Education Is Why
Why Heart disease is the No. 1 cause of death in the world—with more than 17
million deaths per year. That’s why the AHA is continuously transforming our
training solutions as science evolves, and driving awareness of how
everyone can help save a life.
References
1. Cummins RO, Ornato JP, Thies WH, Pepe PE. Improving survival from sudden
cardiac arrest: the “chain of survival” concept. A statement for health professionals
from the Advanced Cardiac Life Support Subcommittee and the Emergency
Cardiac Care Committee, American Heart
Association. Circulation. 1991;83(5):1832-1847.
2. Jacobs I, Nadkarni V, Bahr J, et al; International Liaison Committee on
Resuscitation; American Heart Association; European Resuscitation Council;
Australian Resuscitation Council; New Zealand Resuscitation Council; Heart and
Stroke Foundation of Canada; InterAmerican Heart Foundation; Resuscitation
Councils of Southern Africa; ILCOR Task Force on Cardiac Arrest and
Cardiopulmonary Resuscitation Outcomes. Cardiac arrest and cardiopulmonary
resuscitation outcome reports: update and simplification of the Utstein templates for
resuscitation registries: a statement for healthcare professionals from a task force
of the International Liaison Committee on Resuscitation (American Heart
Association, European Resuscitation Council, Australian Resuscitation Council,
New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada,
InterAmerican Heart Foundation, Resuscitation Councils of Southern
Africa). Circulation. 2004;110(21):3385-3397.
3. Cummins RO, Chamberlain D, Hazinski MF, et al. Recommended guidelines for
reviewing, reporting, and conducting research on in-hospital resuscitation: the in-
hospital “Utstein style.” American Heart Association. Circulation. 1997;95(8):2213-
2239.
4. Meaney PA, Bobrow BJ, Mancini ME, et al; CPR Quality Summit Investigators, the
American Heart Association Emergency Cardiovascular Care Committee, the
Council on Cardiopulmonary, Critical Care Perioperative Resuscitation.
Cardiopulmonary resuscitation quality: [corrected] improving cardiac resuscitation
outcomes both inside and outside the hospital: a consensus statement from the
American Heart Association. Circulation. 2013;128(4):417-435.
5. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study
Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J
Med.1995;333(24):1581-1587.
6. Acker JE III, Pancioli AM, Crocco TJ, et al; American Heart Association, American
Stroke Association Expert Panel on Emergency Medical Services Systems, Stroke
Council. Implementation strategies for emergency medical services within stroke
systems of care: a policy statement from the American Heart Association/American
Stroke Association Expert Panel on Emergency Medical Services Systems and the
Stroke Council. Stroke. 2007;38(11):3097-3115.
7. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,
pathophysiology, treatment, and prognostication. A consensus statement from the
International Liaison Committee on Resuscitation (American Heart Association,
Australian and New Zealand Council on Resuscitation, European Resuscitation
Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation,
Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa);
the American Heart Association Emergency Cardiovascular Care Committee; the
Council on Cardiovascular Surgery and Anesthesia; the Council on
 Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical
Cardiology; and the Stroke Council. Circulation. 2008;118(23):2452-2483.
8. Carr BG, Kahn JM, Merchant RM, Kramer AA, Neumar RW. Inter-hospital
variability in post-cardiac arrest mortality. Resuscitation. 2009;80(1):30-34.
9. Callaway CW, Schmicker R, Kampmeyer M, et al. Receiving hospital
characteristics associated with survival after out-of-hospital cardiac
arrest. Resuscitation.2010;81(5):524-529.
10. Go AS, Mozaffarian D, Roger VL, et al; American Heart Association Statistics
Committee, Stroke Statistics Subcommittee. Heart disease and stroke statistics—
2013 update: a report from the American Heart
Association. Circulation. 2013;127(1):e6-e245.
11. Gurses AP, Seidl KL, Vaidya V, et al. Systems ambiguity and guideline compliance:
a qualitative study of how intensive care units follow evidence-based guidelines to
reduce healthcare-associated infections. Qual Saf Health Care. 2008;17(5):351-
359.
12. Pronovost PJ, Bo-Linn GW. Preventing patient harms through systems of
care. JAMA. 2012;308(8):769-770.
13. Devita MA, Bellomo R, Hillman K, et al. Findings of the first consensus conference
on medical emergency teams. Crit Care Med. 2006;34(9):2463-2478.
14. Peberdy MA, Cretikos M, Abella BS, et al; International Liaison Committee on
Resuscitation, American Heart Association, Australian Resuscitation Council,
European Resuscitation Council, Heart Stroke Foundation of Canada,
InterAmerican Heart Foundation, Resuscitation Council of Southern Africa, New
Zealand Resuscitation Council, American Heart Association Emergency
Cardiovascular Care Committee, American Heart Association Council on
Cardiopulmonary Perioperative Critical Care, Interdisciplinary Working Group on
Quality of Care and Outcomes Research. Recommended guidelines for monitoring,
reporting, and conducting research on medical emergency team, outreach, and
rapid response systems: an Utstein-style scientific statement: a scientific statement
from the International Liaison Committee on Resuscitation (American Heart
Association, Australian Resuscitation Council, European Resuscitation Council,
Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation,
Resuscitation Council of Southern Africa, and the New Zealand Resuscitation
Council); the American Heart Association Emergency Cardiovascular Care
Committee; the Council on Cardiopulmonary, Perioperative, and Critical Care; and
the Interdisciplinary Working Group on Quality of Care and Outcomes
Research. Circulation. 2007;116(21):2481-2500.
 Effective High-Performance Team Dynamics

Introduction Successful resuscitation attempts often require healthcare providers to

simultaneously perform a variety of interventions. Although a CPR-trained
bystander working alone can resuscitate a patient within the first
moments after collapse, most attempts require the concerted efforts of
multiple healthcare providers. Effective teamwork divides the tasks while
multiplying the chances of a successful outcome.
Successful high-performance teams not only have medical expertise and
mastery of resuscitation skills, but they also demonstrate effective
communication and team dynamics. Part 3 of this manual discusses the
importance of team roles, behaviors of effective team leaders and team
members, and elements of effective high-performance team dynamics.
During the course, you will have an opportunity to practice performing
different roles as a member and as a leader of a simulated high-
performance team.
Foundational Understanding Team Roles
Facts Whether you are a team member or a team leader during a
resuscitation attempt, you should understand not only your role but
also the roles of other members. This awareness will help you
anticipate

• What actions will be performed next

• How to communicate and work as a member or as a leader of a high-
performance team
Roles of the Leader and Members of a High-Performance Team
Role of the The role of the team leader is multifaceted. The team leader
Team
Leader • Organizes the group
• Monitors individual performance of team members
• Backs up team members
• Models excellent team behavior
• Trains and coaches
• Facilitates understanding
• Focuses on comprehensive patient care

Every high-performance team needs a leader to organize the efforts of the

group. The team leader is responsible for making sure everything is done
at the right time in the right way by monitoring and integrating individual
performance of team members. The role of the team leader is similar to
that of an orchestra conductor directing individual musicians. Like a
conductor, the team leader does not play the instruments but instead
knows how each member of the orchestra fits into the overall music.
The role of the team leader also includes modeling excellent team
behavior and leadership skills for the team and other people involved or
interested in the resuscitation. The team leader should serve as a teacher
or guide to help train future team leaders and improve team effectiveness.
After resuscitation, the team leader can facilitate analysis, critique, and
practice in preparation for the next resuscitation attempt.
The team leader also helps team members understand why they must
perform certain tasks in a specific way. The team leader should be able to
explain why it is essential to

• Push hard and fast in the center of the chest

• Ensure complete chest recoil
• Minimize interruptions in chest compressions
• Avoid excessive ventilation

Whereas members of a high-performance team should focus on their

individual tasks, the team leader must focus on comprehensive patient
care.

Role of the Team members must be proficient in performing the skills authorized by
Team their scope of practice. It is essential to the success of the resuscitation
Member attempt that members of a high-performance team are

• Clear about role assignments

• Prepared to fulfill their role responsibilities
 • Well practiced in resuscitation skills
• Knowledgeable about the algorithms
• Committed to success

Elements of Effective High-Performance Team Dynamics

Roles Clear Roles and Responsibilities
Every member of the team should know his or her role and responsibilities. Just
as different-shaped pieces make up a jigsaw puzzle, each team member’s role is
unique and critical to the effective performance of the team. Figure 5A identifies
6 team roles for resuscitation. When fewer than 6 people are present, these
tasks must be prioritized and assigned to the healthcare providers
present. Figure 5B shows how multiple providers can take on high-priority tasks
seamlessly as more team members get to the patient.
Figure 5. A, Suggested locations of team leader and team members during case
simulations and clinical events. B, Priority-based multiple-rescuer response. This figure
illustrates a potential seamless, time-sensitive, integrated team-based approach to
resuscitation where roles and interventions are prioritized and distributed as more
resources arrive to the patient. Times (in seconds) may vary based on circumstances,
response times, and local protocols. *With 2 or more rescuers, one healthcare provider
(HCP) should assume the role of team leader.
When roles are unclear, team performance suffers. Signs of unclear
roles include

• Performing the same task more than once

• Missing essential tasks
• Team members having multiple roles even if there are enough
providers

To avoid inefficiencies, the team leader must clearly delegate tasks.

Team members should communicate when and if they can handle
additional responsibilities. The team leader should encourage team
members to participate in leadership and not simply follow directions
blindly.
Do
 Team • Clearly define all team member roles in the clinical
leader setting

Team • Seek out and perform clearly defined tasks

members appropriate to your level of competence
• Ask for a new task or role if you are unable to
perform your assigned task because it is beyond
your level of experience or competence

Don’t
Team • Neglect to assign tasks to all available team
leader members
• Assign tasks to team members who are unsure of
their responsibilities
• Distribute assignments unevenly, leaving some
with too much to do and others with too little

Team • Avoid taking assignments

members • Take assignments beyond your level of
competence or expertise

Knowing Your Limitations

Not only should everyone on the team know his or her own limitations
and capabilities, but the team leader should also be aware of them.
This allows the team leader to evaluate team resources and call for
backup of team members when assistance is needed. High-
performance team members should anticipate situations in which they
might require assistance and inform the team leader.
During the stress of an attempted resuscitation, do not practice or
explore a new skill. If you need extra help, request it early. It is not a
sign of weakness or incompetence to ask for help; it is better to have
more help than needed rather than not enough help, which might
negatively affect patient outcome.
Do
Team leader and • Call for assistance early rather than waiting
team members until the patient deteriorates to the point that
help is critical
• Seek advice from more experienced
personnel when the patient’s condition
worsens despite primary treatment

Don’t
 Team leader • Reject offers from others to carry out an
and team assigned task you are unable to complete,
members especially if task completion is essential to
treatment

Team members • Use or start an unfamiliar treatment or therapy

without seeking advice from more experienced
personnel
• Take on too many assignments at a time when
assistance is readily available

Constructive Interventions
During a resuscitation attempt, the leader or a member of a high-
performance team may need to intervene if an action that is about to
occur may be inappropriate at the time. Although constructive
intervention is necessary, it should be tactful. Team leaders should
avoid confrontation with team members. Instead, conduct a debriefing
afterward if constructive criticism is needed.
Do
Team leader • Ask that a different intervention be started if it
has a higher priority

Team • Suggest an alternative drug or dose in a

members confident manner
• Question a colleague who is about to make a
mistake

Don’t
Team leader • Fail to reassign a team member who is trying to
function beyond his or her level of skill

Team • Ignore a team member who is about to administer

members a drug incorrectly

What to Knowledge Sharing

Communicate Sharing information is a critical component of effective team
performance. Team leaders may become trapped in a specific
treatment or diagnostic approach; this common human error is called
a fixation error. Examples of 3 common types of fixation errors are
“Everything is OK.”
“This and only this is the correct path.”
“Do anything but this.”
When resuscitative efforts are ineffective, go back to the basics and
talk as a team, with conversations like, “Well, we’ve observed the
following on the Primary Assessment… Have we missed something?”
Members of a high-performance team should inform the team leader
of any changes in the patient’s condition to ensure that decisions are
made with all available information.
Do
Team • Encourage an environment of information sharing
leader and ask for suggestions if uncertain of the next
best interventions
• Ask for good ideas for differential diagnoses
• Ask if anything has been overlooked (eg,
intravenous access should have been obtained or
drugs should have been administered)

Team • Share information with other team members

members
Don’t
Team leader • Ignore others’ suggestions for treatment
• Overlook or fail to examine clinical signs that are
relevant to the treatment

Team • Ignore important information to improve your role

members
Summarizing and Reevaluating
An essential role of the team leader is monitoring and reevaluating

• The patient’s status

• Interventions that have been performed
• Assessment findings

A good practice is for the team leader to summarize this information

out loud in a periodic update to the team. Review the status of the
resuscitation attempt and announce the plan for the next few steps.
Remember that the patient’s condition can change. Remain flexible to
changing treatment plans and revisiting the initial differential diagnosis.
Ask for information and summaries from the timer/recorder as well.
Do
Team leader • Draw continuous attention to decisions about
differential diagnoses
 • Review or maintain an ongoing record of
drugs and treatments administered and the
patient’s response

Team leader and • Clearly draw attention to significant changes

team members in the patient’s clinical condition
• Increase monitoring (eg, frequency of
respirations and blood pressure) when the
patient’s condition deteriorates

Don’t
Team • Fail to change a treatment strategy when new
leader information supports such a change
• Fail to inform arriving personnel of the current status
and plans for further action

How to Closed-Loop Communications

Communicate When communicating with high-performance team members, the team
leader should use closed-loop communication by taking these steps:

1. The team leader gives a message, order, or assignment to a team

member.
2. By receiving a clear response and eye contact, the team leader
confirms that the team member heard and understood the
message.
3. The team leader listens for confirmation of task performance from
the team member before assigning another task.

Do
Team • Assign another task after receiving oral
leader confirmation that a task has been completed, such
as, “Now that the IV is in, give 1 mg of epinephrine”

Team • Close the loop: Inform the team leader when a task
members begins or ends, such as, “The IV is in”

Don’t
 Team • Give more tasks to a team member without asking
leader or receiving confirmation of a completed
assignment

Team • Give drugs without verbally confirming the order

members with the team leader
• Forget to inform the team leader after giving the
drug or performing the procedure

Clear Messages
Clear messages consist of concise communication spoken with
distinctive speech in a controlled tone of voice. All healthcare
providers should deliver messages and orders in a calm and direct
manner without yelling or shouting. Unclear communication can lead
to unnecessary delays in treatment or to medication errors.
Yelling or shouting can impair effective high-performance team
interaction. Only one person should talk at any time.
Do
Team leader • Encourage team members to speak clearly

Team leader • Repeat the medication order

• Question an order if the slightest doubt exists

Don’t
Team leader • Mumble or speak in incomplete sentences
• Give unclear messages and drug/medication
orders
• Yell, scream, or shout

Team • Feel patronized by distinct and concise

members messages

Mutual Respect
The best high-performance teams are composed of members who
share a mutual respect for each other and work together in a collegial,
supportive manner. To have a high-performance team, everyone must
abandon ego and respect each other during the resuscitation attempt,
regardless of any additional training or experience that the team leader
or specific team members may have.
Do
Team leader and • Speak in a friendly, controlled tone of
team members voice
• Avoid shouting or displaying aggression if
you are not understood initially

Team leader • Acknowledge correctly completed

assignments by saying, “Thanks—good
job!”

Don’t
Team leader and • Shout or yell at team members—when one
team members person raises his voice, others will respond
similarly
• Behave aggressively or confuse directive
behavior with aggression
• Be uninterested in others
 The Systematic Approach

Introduction Healthcare providers use a systematic approach to assess and treat

arrest and acutely ill or injured patients for optimal care. The goal of the
high-performance team’s interventions for a patient in respiratory or
cardiac arrest is to support and restore effective oxygenation, ventilation,
and circulation with return of intact neurologic function. An intermediate
goal of resuscitation is return of spontaneous circulation (ROSC). The
actions used are guided by the following systematic approaches:

• BLS Assessment
• Primary Assessment (A, B, C, D, and E)
• Secondary Assessment (SAMPLE, H’s and T’s)

The Systematic Approach

Overview of the After determination of scene safety, the systematic approach

(Figure 6) first requires ACLS providers to determine the patient’s
Systematic
level of consciousness. As you approach the patient,
Approach
• If the patient appears unconscious
o – Use the BLS Assessment for the initial evaluation
o – After completing all of the appropriate steps of the BLS
Assessment, use the Primary and Secondary Assessments
for more advanced evaluation and treatment
• If the patient appears conscious
o – Use the Primary Assessment for your initial evaluation
 Before conducting these assessments, make sure the scene
is safe.

Figure 6. The systematic approach.

The details of the BLS Assessment and Primary and Secondary Assessments are
described below.

The BLS Assessment

Foundational Starting CPR When You Are Not Sure About a Pulse
Facts If you are unsure about the presence of a pulse, begin cycles of
compressions and ventilations. Unnecessary compressions are less
 harmful than failing to provide compressions when needed. Delaying or
failing to start CPR in a patient without a pulse reduces the chance of
survival.

Overview of the The BLS Assessment is a systematic approach to BLS that any
trained healthcare provider can perform. This approach
BLS
stresses early CPR and early defibrillation. It does not include
Assessment advanced interventions, such as advanced airway techniques or drug
administration. By using the BLS Assessment, healthcare providers
may achieve their goal of supporting or restoring effective
oxygenation, ventilation, and circulation until ROSC or initiation of
ACLS interventions. Performing the actions in the BLS Assessment
substantially improves the patient’s chance of survival and a good
neurologic outcome.
Remember: Assess…then perform appropriate action.

Caution Agonal Gasps

• Agonal gasps are not normal breathing. Agonal gasps may be present in
the first minutes after sudden cardiac arrest.
• A patient who gasps usually looks like he is drawing air in very quickly.
The mouth may be open and the jaw, head, or neck may move with gasps.
Gasps may appear forceful or weak. Some time may pass between gasps
because they usually happen at a slow rate. The gasp may sound like a
snort, snore, or groan. Gasping is not normal breathing. It is a sign of
cardiac arrest.

Although the BLS Assessment requires no advanced equipment, healthcare providers

can use any readily available universal precaution supplies or adjuncts, such as a bag-
mask ventilation device. Whenever possible, place the patient on a firm surface in a
supine position to maximize the effectiveness of chest compressions. Table 2 is an
overview of the BLS Assessment, and Figures 7through 11 illustrate the steps needed
during the BLS Assessment. Before approaching the patient, ensure scene safety. A
rapid scene survey should be performed to determine if any reason exists not to initiate
CPR, such as a threat to safety of the provider.

For more details, watch the High-Quality BLS video on the Student Website
(www.heart.org/eccstudent).

Table 2. The BLS Assessment

 Assess Assessment
Technique and
Action
Check • Tap and
responsiveness shout, “Are you
OK?”

Figure 7. Check responsiveness.

Shout for nearby • Shout for nearby
help/activate the help
emergency • Activate the
response system emergency
and get the response system
AED/defibrillator • Get an AED if one
is available, or
send someone to
activate the Figure 8. Shout for nearby
emergency help/activate the emergency response
response system system/get an AED.
and get an AED or
defibrillator

Check breathing • Check for absent

and pulse or abnormal
breathing (no
breathing or only
gasping) by
looking at
or scanning the
chest for
movement for
Figure 9. Check breathing and pulse
simultaneously.
 about 5 to 10
seconds

Ideally, the pulse

check is performed
simultaneously with
the breathing check
to minimize delay in
Figure 10. Checking a carotid pulse.
detection of cardiac
arrest and initiation
of CPR

• Check pulse for 5

to 10 seconds
• If no pulse within
10 seconds, start
CPR, beginning
with chest
compressions
• If there is a pulse,
start rescue
breathing at 1
breath every 5 to 6
seconds. Check
pulse about every
2 minutes

Defibrillation • If no pulse, check

for a shockable
rhythm with an
AED/defibrillator
as soon as it
arrives
• Provide shocks as
indicated Figure 11. Defibrillation.
• Follow each shock
immediately with
CPR, beginning
with compressions
 CriticalMinimizing Interruptions
Concepts ACLS providers must make every effort to minimize any interruptions
in chest compressions. Try to limit interruptions in chest compressions
(eg, defibrillation and rhythm analysis) to no longer than 10 seconds, except
in extreme circumstances, such as removing the patient from a dangerous
environment. When you stop chest compressions, blood flow to the brain
and heart stops. See Figure 12.
Avoid:

• Prolonged rhythm analysis

• Frequent or inappropriate pulse checks
• Taking too long to give breaths to the patient
• Unnecessarily moving the patient

Figure 12. Relationship of quality CPR to coronary perfusion pressure demonstrating

the need to minimize interruptions in compressions.
Coronary perfusion pressure (CPP) is aortic relaxation (“diastolic”) pressure minus right
atrial relaxation (“diastolic”) pressure. During CPR, CPP correlates with both myocardial
blood flow and ROSC. In 1 human study, ROSC did not occur unless a CPP of 15 mm
Hg or greater was achieved during CPR.
Critical Concepts Quality Compressions

• Compress the chest at least 2 inches (5 cm).

• Compress the chest at a rate of 100 to 120/min.
 • Allow complete chest recoil after each compression.

Foundational Chest Compression Depth

Facts Chest compressions are more often too shallow than too deep.
However, research suggests that compression depth greater than 2.4
inches (6 cm) in adults may not be optimal for survival from cardiac
arrest and may cause injuries. If you have a CPR quality feedback
device, it is optimal to target your compression depth from 2 to 2.4
inches (5 to 6 cm).

Foundational Single Healthcare Provider May Tailor Response

Facts
• Single healthcare providers may tailor the sequence of rescue actions
to the most likely cause of arrest. For example, if a lone healthcare
provider sees an adolescent suddenly collapse, it is reasonable to
assume that the patient has suffered a sudden cardiac arrest.
• A single rescuer should call for help (activate the emergency
response system), get an AED (if nearby), return to the patient to
attach the AED, and then provide CPR.
• On the other hand, if hypoxia is the presumed cause of the cardiac
arrest (such as in a drowning patient), the healthcare provider may
give approximately 2 minutes of CPR before activating the
emergency response system.

Critical Concepts High-Quality CPR

• Compress the chest hard and fast.

• Allow complete chest recoil after each compression.
• Minimize interruptions in compressions (10 seconds or less).
• Avoid excessive ventilation.
• Switch compressor about every 2 minutes or earlier if fatigued.*

*Switch should take 5 seconds or less.

The Primary Assessment

Overview of the For unconscious patients in arrest (cardiac or respiratory):

Primary
• Healthcare providers should conduct the Primary Assessment
Assessment after completing the BLS Assessment.

For conscious patients who may need more advanced assessment

and management techniques:

• Healthcare providers should conduct the Primary Assessment

first.

In the Primary Assessment, you continue to assess and perform an

action as appropriate until transfer to the next level of care. Many
times, members of a high-performance team perform assessments
and actions in ACLS simultaneously.
Remember: Assess…then perform appropriate action.
Table 3 provides an overview of the Primary Assessment.

Table 3. The Primary Assessment

Assess Action as Appropriate
Airway • Maintain airway patency in unconscious patients by
use of the head tilt–chin lift, oropharyngeal airway, or
• Is the airway patent? nasopharyngeal airway
• Is an advanced • Use advanced airway management if needed (eg,
airway indicated? laryngeal mask airway, laryngeal tube, esophageal-
• Is proper placement tracheal tube, endotracheal tube)
of airway device
confirmed? Healthcare providers must weigh the benefit of advanced
• Is tube secured and airway placement against the adverse effects of
placement interrupting chest compressions. If bag-mask ventilation is
reconfirmed adequate, healthcare providers may defer insertion of an
frequently? advanced airway until the patient does not respond to
initial CPR and defibrillation or until spontaneous
circulation returns. Advanced airway devices such as a
laryngeal mask airway, laryngeal tube, or esophageal-
tracheal tube can be placed while chest compressions
continue.
If using advanced airway devices:
 • Confirm proper integration of CPR and ventilation
• Confirm proper placement of advanced airway
devices by
o – Physical examination
o – Quantitative waveform capnography
• Secure the device to prevent dislodgment
• Monitor airway placement with continuous
quantitative waveform capnography

Breathing •Give supplementary oxygen when indicated

o – For cardiac arrest patients, administer 100%
• Are ventilation and oxygen
oxygenation o – For others, titrate oxygen administration to achieve
adequate? oxygen saturation values of 94% or greater by pulse
• Are quantitative oximetry
waveform • Monitor the adequacy of ventilation and
capnography and oxygenation by
oxyhemoglobin o – Clinical criteria (chest rise and cyanosis)
saturation monitored? o – Quantitative waveform capnography
o – Oxygen saturation
• Avoid excessive ventilation

Circulation • Monitor CPR quality

o – Quantitative waveform capnography (if PETCO2 is
• Are chest less than 10 mm Hg, attempt to improve CPR quality)
compressions o – Intra-arterial pressure (if relaxation phase
effective? [diastolic] pressure is less than 20 mm Hg, attempt to
• What is the cardiac improve CPR quality)
rhythm? • Attach monitor/defibrillator for arrhythmias or
• Is defibrillation or cardiac arrest rhythms(eg, ventricular fibrillation [VF],
cardioversion pulseless ventricular tachycardia [PVT], asystole,
indicated? pulseless electrical activity [PEA])
• Has IV/IO access • Provide defibrillation/cardioversion
been established? • Obtain IV/IO access
• Is ROSC present? • Give appropriate drugs to manage rhythm and blood
• Is the patient with a pressure
pulse unstable? • Give IV/IO fluids if needed
• Check glucose and temperature
• Are medications • Check perfusion issues
needed for rhythm or
blood pressure?
• Does the patient need
volume (fluid) for
resuscitation?

Disability • Check for neurologic function

• Quickly assess for responsiveness, levels of
consciousness, and pupil dilation
• AVPU: Alert, Voice, Painful, Unresponsive

Exposure • Remove clothing to perform a physical

examination, looking for obvious signs of trauma,
bleeding, burns, unusual markings, or medical alert
bracelets

PETCO2 is the partial pressure of CO2 in exhaled air at the end of the exhalation phase.

The Secondary Assessment

Overview of the The Secondary Assessment involves the differential diagnosis,

including a focused medical history and searching for and treating
Secondary
underlying causes (H’s and T’s). Gathering a focused history of the
Assessment patient is recommended. Ask specific questions related to the
patient’s presentation. Consider using the memory aid SAMPLE:
Signs and symptoms
Allergies
Medications (including the last dose taken)
Past medical history (especially relating to the current illness)
Last meal consumed
Events
The answers to these questions can help you quickly rule in or rule
out suspected diagnoses. Look for and treat the underlying cause by
considering the H’s and T’s to ensure you are not overlooking a
dangerous or likely possibility. The H’s and T’s create a road map for
possible diagnoses and interventions for your patient.
H’s and T’s Table 4 shows the potential reversible causes of cardiac arrest as
well as emergency cardiopulmonary conditions (H’s and T’s). The
ACLS cases provide details on these components.
PEA is associated with many conditions. Healthcare providers should
memorize the list of common causes to keep from overlooking an
obvious cause of PEA that might be reversed by appropriate
treatment.
The most common causes of cardiac arrest are presented as H’s and
T’s in the table below.

Table 4. The Most Common Causes of Cardiac Arrest

H’s T’s
Hypovolemia Tension pneumothorax
Hypoxia Tamponade (cardiac)
Hydrogen ion (acidosis) Toxins
Hypo-/hyperkalemia Thrombosis (pulmonary)
Hypothermia Thrombosis (coronary)

Critical Common Underlying Causes of PEA

Concepts
• Hypovolemia and hypoxia are the 2 most common underlying and
potentially reversible causes of PEA.
• Be sure to look for evidence of these problems as you assess the
patient.

Diagnosing and Treating Underlying Causes

Introduction Patients in cardiac arrest (VF/pVT/asystole/PEA) need rapid

assessment and management. Cardiac arrest may be caused by an
underlying and potentially reversible problem. If you can quickly
identify a specific condition that has caused or is contributing to PEA
and correct it, you may achieve ROSC. The identification of the
underlying cause is of paramount importance in cases of PEA and
asystole.
In the search for the underlying cause, do the following:
 • Consider frequent causes of PEA by recalling the H’s and T’s
• Analyze the ECG for clues to the underlying cause
• Recognize hypovolemia
• Recognize drug overdose/poisonings

Conditions and The H’s and T’s are a memory aid for the most common and
potentially reversible causes of periarrest and cardiopulmonary
Management
arrest (Table 4).

Hypovolemia Hypovolemia, a common cause of PEA, initially produces the classic

physiologic response of a rapid, narrow-complex tachycardia (sinus
tachycardia) and typically produces increased diastolic and
decreased systolic pressures. As loss of blood volume continues,
blood pressure drops, eventually becoming undetectable, but the
narrow QRS complexes and rapid rate continue (ie, PEA).
You should consider hypovolemia as a cause of hypotension, which
can deteriorate to PEA. Providing prompt treatment can reverse the
pulseless state by rapidly correcting the hypovolemia. Common
nontraumatic causes of hypovolemia include occult internal
hemorrhage and severe dehydration. Consider volume infusion for
PEA associated with a narrow-complex tachycardia.

Cardiac and Acute coronary syndromes involving a large amount of heart muscle
can present as PEA. That is, occlusion of the left main or proximal
Pulmonary
left anterior descending coronary artery can present with cardiogenic
Conditions shock rapidly progressing to cardiac arrest and PEA. However, in
patients with cardiac arrest and without known pulmonary embolism
(PE), routine fibrinolytic treatment given during CPR shows no
benefit and is not recommended.
Massive or saddle PE obstructs flow to the pulmonary vasculature
and causes acute right heart failure. In patients with cardiac arrest
due to presumed or known PE, it is reasonable to administer
fibrinolytics.
Pericardial tamponade may be a reversible condition. In the
periarrest period, volume infusion in this condition may help while
 definitive therapy is initiated. Tension pneumothorax can be
effectively treated once recognized.
Note that cardiac tamponade, tension pneumothorax, and massive
PE cannot be treated unless recognized. Bedside ultrasound, when
performed by a skilled provider, may aid in rapid identification of
tamponade and PE. There is growing evidence that pneumothorax
can be identified by using bedside ultrasound as well. Treatment for
cardiac tamponade may require pericardiocentesis. Tension
pneumothorax requires needle aspiration and chest tube placement.
These procedures are beyond the scope of the ACLS Provider
Course.

Drug Overdoses Certain drug overdoses and toxic exposures may lead to peripheral
vascular dilatation and/or myocardial dysfunction with resultant
or Toxic
hypotension. The approach to poisoned patients should be
Exposures aggressive because the toxic effects may progress rapidly and may
be of limited duration. In these situations, myocardial dysfunction
and arrhythmias may be reversible. Numerous case reports confirm
the success of many specific limited interventions with one thing in
common: they buy time.
Treatments that can provide this level of support include

• Prolonged basic CPR in special resuscitation situations

• Extracorporeal CPR
• Intra-aortic balloon pumping
• Renal dialysis
• Intravenous lipid emulsion
• Specific drug antidotes (digoxin immune Fab, glucagon,
bicarbonate)
• Transcutaneous pacing
• Correction of severe electrolyte disturbances (potassium,
magnesium, calcium, acidosis)
• Specific adjunctive agents

Remember, if the patient shows signs of ROSC, post–cardiac

arrest care should be initiated.
 The ACLS Cases
Overview of the Cases
The ACLS simulated cases are designed to review the knowledge and skills you need
to successfully participate in course events and pass the Megacode skills test. Each
case contains the following topics:

• Introduction
• Rhythms and drugs
• Descriptions or definitions of key concepts
• Overview of algorithm
• Algorithm figure
• Application of the algorithm to the case
• Other related topics

This part contains the following cases:

• Respiratory Arrest
• Acute Coronary Syndromes
o – STEMI
• Acute Stroke
• Cardiac Arrest
o – VF/Pulseless VT
o – Asystole
o – PEA
• Bradycardia
• Tachycardia (Stable and Unstable)
• Immediate Post–Cardiac Arrest Care

Respiratory Arrest Case

Introduction This case reviews appropriate assessment, intervention, and
management options for an unconscious, unresponsive adult
patient in respiratory arrest. Respirations are completely absent or
 clearly inadequate to maintain effective oxygenation and
ventilation. A pulse is present. (Do not confuse agonal gasps with
adequate respirations.) The BLS Assessment and the Primary and
Secondary Assessments are used even though the patient is in
respiratory arrest and not in cardiac arrest.

Case Drugs This case involves the following drugs:

• Oxygen

Systems or facilities using rapid sequence intubation may consider

additional drugs.

Normal and The average respiratory rate for an adult is about 12 to 16/min.
Abnormal Normal tidal volume of 8 to 10 mL/kg maintains normal
Breathing oxygenation and elimination of CO2.
Tachypnea is a respiratory rate above 20/min and bradypnea is a
respiratory rate below 12/min. A respiratory rate below 6/min
(hypoventilation) requires assisted ventilation with a bag-mask
device or advanced airway with 100% oxygen.

Identification of Identifying the severity of a respiratory problem will help you decide
Respiratory the most appropriate interventions. Be alert for signs of
Problems by
Severity • Respiratory distress
• Respiratory failure

Respiratory Respiratory distress is a clinical state characterized by abnormal

Distress respiratory rate (eg, tachypnea) or effort. The respiratory effort may
be increased (eg, nasal flaring, retractions, and use of accessory
muscles) or inadequate (eg, hypoventilation or bradypnea).
Respiratory distress can range from mild to severe. For example, a
patient with mild tachypnea and a mild increase in respiratory effort
with changes in airway sounds is in mild respiratory distress. A
patient with marked tachypnea, significantly increased respiratory
effort, deterioration in skin color, and changes in mental status is
in severe respiratory distress. Severe respiratory distress can be
an indication of respiratory failure.
 Clinical signs of respiratory distress typically include some or all of
the following:

• Tachypnea
• Increased respiratory effort (eg, nasal flaring, retractions)
• Inadequate respiratory effort (eg, hypoventilation or
bradypnea)
• Abnormal airway sounds (eg, stridor, wheezing, grunting)
• Tachycardia
• Pale, cool skin (note that some causes of respiratory distress,
like sepsis, may cause the skin to get warm, red, and
diaphoretic)
• Changes in level of consciousness/agitation
• Use of abdominal muscles to assist in breathing

These indicators may vary in severity.

Respiratory distress is apparent when a patient tries to maintain
adequate gas exchange despite airway obstruction, reduced lung
compliance, or lung tissue disease. As the patient tires or as
respiratory function or effort or both deteriorate, adequate gas
exchange cannot be maintained. When this happens, clinical signs
of respiratory failure develop.

Respiratory Respiratory failure is a clinical state of inadequate oxygenation,

Failure ventilation, or both. Respiratory failure is often the end stage of
respiratory distress. If there is abnormal central nervous system
control of breathing or muscle weakness, the patient may show
little or no respiratory effort despite being in respiratory failure. In
these situations, you may need to identify respiratory failure based
on clinical findings. Confirm the diagnosis with objective
measurements, such as pulse oximetry or blood gas analysis.
Suspect probable respiratory failure if some of the following signs
are present:

• Marked tachypnea
• Bradypnea, apnea (late)
• Increased, decreased, or no respiratory effort
• Poor to absent distal air movement
• Tachycardia (early)
• Bradycardia (late)
• Cyanosis
• Stupor, coma (late)
 Respiratory failure can result from upper or lower airway
obstruction, lung tissue disease, and disordered control of
breathing (eg, apnea or shallow, slow respirations). When
respiratory effort is inadequate, respiratory failure can occur
without typical signs of respiratory distress. Respiratory failure is a
clinical state that requires intervention to prevent deterioration to
cardiac arrest. Respiratory failure can occur with a rise in arterial
carbon dioxide levels (hypercapnia), a drop in blood oxygenation
(hypoxemia), or both.

Respiratory Respiratory arrest is the cessation (absence) of breathing.

Arrest Respiratory arrest is usually caused by an event such as drowning
or head injury. For an adult in respiratory arrest, providing a tidal
volume of approximately 500 to 600 mL (6 to 7 mL/kg) should
suffice. This is consistent with a tidal volume that produces visible
chest rise.
Patients with airway obstruction or poor lung compliance may
require high pressures to be properly ventilated (to make the chest
visibly rise). A pressure-relief valve on a resuscitation bag-mask
device may prevent the delivery of a sufficient tidal volume in these
patients. Ensure that the bag-mask device allows you to bypass
the pressure-relief valve and use high pressures, if necessary, to
achieve visible chest expansion.
Excessive ventilation is unnecessary and can cause gastric
inflation and its resultant complications, such as regurgitation and
aspiration. More important, excessive ventilation can be harmful
because it increases intrathoracic pressure, decreases venous
return to the heart, and diminishes cardiac output and survival.
Healthcare providers should avoid excessive ventilation (too many
breaths or too large a volume) during respiratory arrest and cardiac
arrest.

The BLS Assessment

When evaluating a patient, proceed with the BLS Assessment after
determining that the scene is safe as described in “Part 4: The
Systematic Approach.”

Assess and The systematic approach is assessment, then action, for each step in
Reassess the the sequence.
Patient Remember: Assess…then perform appropriate action.
In this case, you assess and find that the patient has a pulse, so you
do not use the AED or begin chest compressions.
Ventilation In the case of a patient in respiratory arrest with a pulse, deliver
and Pulse ventilations once every 5 to 6 seconds with a bag-mask device or any
Check advanced airway device. Recheck the pulse about every 2 minutes.
Take at least 5 seconds but no more than 10 seconds for a pulse
check.

The Primary Assessment

Airway If bag-mask ventilation is adequate, providers may defer insertion
Management in of an advanced airway. Healthcare providers should make the
Respiratory decision to place an advanced airway during the Primary
Arrest Assessment.
Advanced airway equipment includes the laryngeal mask airway,
the laryngeal tube, the esophageal-tracheal tube, and the
endotracheal (ET) tube. If it is within your scope of practice, you
may use advanced airway equipment in the course when
appropriate and available.

Ventilations In this case, the patient is in respiratory arrest but continues to

have a pulse. You should ventilate the patient once every 5 to 6
seconds. Each breath should take 1 second and achieve visible
chest rise. Be careful to avoid excessive ventilation (too many
breaths per minute or too large a volume per breath).
FYI 2015 Guidelines Correct
Placement of
ET Tube
The AHA
recommends
continuous
waveform
capnography in
addition to
clinical
assessment as
the most
reliable method
of confirming
and monitoring
correct
placement of
an ET tube.
Management of Respiratory Arrest
Overview Management of respiratory arrest includes both BLS and ACLS
interventions. These interventions may include

• Giving supplementary oxygen

• Opening the airway
• Providing basic ventilation
• Using basic airway adjuncts (OPA and NPA)
• Suctioning
 According to the 2015 AHA Guidelines Update for CPR and
ECC, for patients with a perfusing rhythm, ventilations
should be delivered once every 5 to 6 seconds.
Critical Avoiding Excessive Ventilation
Concepts When using any form of assisted ventilation, you must avoid delivering
excessive ventilation (too many breaths per minute or too large a volume
per breath). Excessive ventilation can be harmful because it increases
intrathoracic pressure, decreases venous return to the heart, and
diminishes cardiac output. It may also cause gastric inflation and
predispose the patient to vomiting and aspiration of gastric contents. In
addition, hyperventilation may cause cerebral vasoconstriction,
reducing blood flow to the brain.

Giving Supplementary Oxygen

Maintain Give oxygen to patients with acute cardiac symptoms or respiratory

Oxygen distress. Monitor oxygen saturation and titrate supplementary oxygen to
Saturation maintain a saturation of 94% or greater. For patients in respiratory or
cardiac arrest, striving for 100% oxygen would be more appropriate.

See the Student Website (www.heart.org/eccstudent) for

details on use of oxygen in patients not in respiratory or cardiac arrest.

Opening the Airway

Common Cause Figure 13 demonstrates the anatomy of the airway. The most
of Airway common cause of upper airway obstruction in the
Obstruction unconscious/unresponsive patient is loss of tone in the throat
muscles. In this case, the tongue falls back and occludes the airway
at the level of the pharynx (Figure 14A).

Figure 13. Airway anatomy.

Figure 14. Obstruction of the airway by the tongue and epiglottis. When a patient is
unresponsive, the tongue can obstruct the airway. The head tilt–chin lift relieves
obstruction in the unresponsive patient. A, The tongue is obstructing the airway. B, The
head tilt–chin lift lifts the tongue, relieving the obstruction. C, If cervical spine trauma is
suspected, healthcare providers should use the jaw thrust without head extension.

Basic Airway Basic airway opening techniques will effectively relieve airway
Opening obstruction caused either by the tongue or from relaxation of muscles
Techniques in the upper airway. The basic airway opening technique is head tilt
with anterior displacement of the mandible, ie, head tilt–chin lift
(Figure 14B).
In the trauma patient with suspected neck injury, use a jaw thrust
without head extension (Figure 14C). Because maintaining an open
airway and providing ventilation is a priority, use a head tilt–chin lift
maneuver if the jaw thrust does not open the airway. ACLS providers
should be aware that current BLS training courses teach the jaw-
thrust technique to healthcare providers but not to lay rescuers.

Airway Proper airway positioning may be all that is required for patients who
Management can breathe spontaneously. In patients who are unconscious with no
cough or gag reflex, insert an OPA or NPA to maintain airway
patency.
If you find an unconscious/unresponsive patient who was known to
be choking and is now unresponsive and in respiratory arrest, open
the mouth wide and look for a foreign object. If you see one, remove
it with your fingers. If you do not see a foreign object, begin CPR.
Each time you open the airway to give breaths, open the mouth wide
and look for a foreign object. Remove it with your fingers if present. If
there is no foreign object, resume CPR.
Providing Basic Ventilation
Basic Airway Basic airway skills used to ventilate a patient are
Skills
• Head tilt–chin lift
• Jaw thrust without head extension (suspected cervical spine
trauma)
• Mouth-to-mouth ventilation
• Mouth-to-nose ventilation
• Mouth-to–barrier device (using a pocket mask) ventilation
• Bag-mask ventilation (Figures 15 and 16)

Figure 15. E-C clamp technique for holding the mask while lifting the jaw. Position
yourself at the patient’s head. Circle the thumb and first finger around the top of the
mask (forming a “C”) while using the third, fourth, and fifth fingers (forming an “E”) to lift
the jaw.

Figure 16. Two-rescuer use of the bag-mask device. The rescuer at the patient’s head
tilts the patient’s head and seals the mask against the patient’s face, with the thumb and
first finger of each hand creating a “C,” to provide a complete seal around the edges of
the mask. The rescuer uses the remaining 3 fingers (the “E”) to lift the jaw (this holds
the airway open). The second rescuer slowly squeezes the bag (over 1 second) until the
chest rises. Both providers should observe chest rise.
Bag-Mask A bag-mask ventilation device consists of a ventilation bag attached to a
Ventilation face mask. These devices have been a mainstay of emergency ventilation
for decades. Bag-mask devices are the most common method of
providing positive-pressure ventilation. When using a bag-mask device,
deliver approximately 600 mL tidal volume sufficient to produce chest rise
over 1 second. Bag-mask ventilation is not the recommended method of
ventilation for a single healthcare provider during CPR. (A single
healthcare provider should use a pocket mask to give ventilation, if
available.) It is easier for 2 trained and experienced rescuers to provide
bag-mask ventilation. One rescuer opens the airway and seals the mask
to the face while the other squeezes the bag, with both rescuers watching
for visible chest rise.
The universal connections present on all airway devices allow you to
connect any ventilation bag to numerous adjuncts. Valves and ports may
include

• One-way valves to prevent the patient from rebreathing exhaled air

• Oxygen ports for administering supplementary oxygen
• Medication ports for administering aerosolized and other medications
• Suction ports for clearing the airway
• Ports for quantitative sampling of end-tidal CO2

You can attach other adjuncts to the patient end of the valve, including a
pocket face mask, laryngeal mask airway, laryngeal tube, esophageal-
tracheal tube, and ET tube.

See the Student Website

(www.heart.org/eccstudent) for more information on bag-mask
ventilation.

Basic Airway Adjuncts: Oropharyngeal Airway

Introduction The OPA is used in patients who are at risk for developing airway
obstruction from the tongue or from relaxed upper airway muscles.
This J-shaped device (Figure 17A) fits over the tongue to hold it and
the soft hypopharyngeal structures away from the posterior wall of the
pharynx.
 The OPA is used in unconscious patients if procedures to open the
airway (eg, head tilt–chin lift or jaw thrust) fail to provide and maintain
a clear, unobstructed airway. An OPA should not be used in a
conscious or semiconscious patient because it may stimulate gagging
and vomiting. The key assessment is to check whether the patient has
an intact cough and gag reflex. If so, do not use an OPA.
The OPA may be used to keep the airway open during bag-mask
ventilation when providers might unknowingly push down on the chin,
blocking the airway. The OPA is also used during suctioning of the
mouth and throat and in intubated patients to prevent them from biting
and occluding the ET tube.

Technique of Step Action

OPA Insertion
1 Clear the mouth and pharynx of secretions, blood, or vomit
by using a rigid pharyngeal suction tip if possible.
2 Select the proper size OPA. Place the OPA against the side
of the face (Figure 17B). When the flange of the OPA is at
the corner of the mouth, the tip is at the angle of the
mandible. A properly sized and inserted OPA results in
proper alignment with the glottic opening.
3 Insert the OPA so that it curves upward toward the hard
palate as it enters the mouth.
4 As the OPA passes through the oral cavity and approaches
the posterior wall of the pharynx, rotate it 180° into the
proper position (Figure 17C). The OPA can also be inserted
at a 90° angle to the mouth and then turned down toward the
posterior pharynx as it is advanced. In both methods, the
goal is to curve the device around the tongue so that the
tongue is not inadvertently pushed back into the pharynx
rather than being pulled forward by the OPA.
An alternative method is to insert the OPA straight in while
using a tongue depressor or similar device to hold the tongue
forward as the OPA is advanced.
After insertion of an OPA, monitor the patient. Keep the head and jaw
positioned properly to maintain a patent airway. Suction the airway as
needed.
Caution Be Aware of the Following When Using an
OPA
 • OPAs that are too large may obstruct the
larynx or cause trauma to the laryngeal
structures.
• OPAs that are too small or inserted
improperly may push the base of the tongue
posteriorly and obstruct the airway.
• Insert the OPA carefully to avoid soft tissue
trauma to the lips and tongue.

Remember to use the OPA only in the

unresponsive patient with no cough or gag
reflex. If the patient has a cough or gag reflex,
the OPA may stimulate vomiting and
laryngospasm.

Figure 17. Oropharyngeal airways. A, Oropharyngeal airway

devices. B, Oropharyngeal airway device measurement. C, Oropharyngeal airway
device inserted.

Basic Airway Adjuncts: Nasopharyngeal Airway

Introduction The NPA is used as an alternative to an OPA in patients who need a
basic airway management adjunct. The NPA is a soft rubber or plastic
uncuffed tube (Figure 18A) that provides a conduit for airflow between the
nares and the pharynx.
Unlike oral airways, NPAs may be used in conscious, semiconscious, or
unconscious patients (patients with an intact cough and gag reflex). The
NPA is indicated when insertion of an OPA is technically difficult or
dangerous. Examples include patients with a gag reflex, trismus, massive
trauma around the mouth, or wiring of the jaws. The NPA may also be
used in patients who are neurologically impaired with poor pharyngeal
tone or coordination leading to upper airway obstruction.
Figure 18. Nasopharyngeal airways. A, Nasopharyngeal airway
devices. B, Nasopharyngeal airway device measurement. C, Nasopharyngeal airway
device inserted.

Technique of Step Action

NPA
1 Select the proper size NPA.
Insertion
• Compare the outer circumference of the NPA with the inner
aperture of the nares. The NPA should not be so large that
it causes sustained blanching of the nostrils. Some
providers use the diameter of the patient’s smallest finger as
a guide to selecting the proper size.
• The length of the NPA should be the same as the distance
from the tip of the patient’s nose to the earlobe (Figure
18B).

2 Lubricate the airway with a water-soluble lubricant or

anesthetic jelly.
3 Insert the airway through the nostril in a posterior direction
perpendicular to the plane of the face. Pass it gently along the
floor of the nasopharynx (Figure 18C).
If you encounter resistance:

• Slightly rotate the tube to facilitate insertion at the angle of

the nasal passage and nasopharynx.
 • Attempt placement through the other nostril because
patients have different-sized nasal passages.

Reevaluate frequently. Maintain head tilt by providing anterior

displacement of the mandible by using a chin lift or jaw thrust. Mucus,
blood, vomit, or the soft tissues of the pharynx can obstruct the NPA,
which has a small internal diameter. Frequent evaluation and suctioning
of the airway may be necessary to ensure patency.
Caution Be Aware of the Following When Using an NPA

• Take care to insert the airway gently to avoid complications. The airway
can irritate the mucosa or lacerate adenoidal tissue and cause bleeding,
with possible aspiration of clots into the trachea. Suction may be
necessary to remove blood or secretions.
• An improperly sized NPA may enter the esophagus. With active
ventilation, such as bag-mask ventilation, the NPA may cause gastric
inflation and possible hypoventilation.
• An NPA may cause laryngospasm and vomiting, even though it is
commonly tolerated by semiconscious patients.
• Use caution in patients with facial trauma because of the risk of
misplacement into the cranial cavity through a fractured cribriform plate.

Caution Precautions for OPAs and NPAs

Take the following precautions when using an OPA or NPA:

• Always check spontaneous respirations immediately after insertion of

either an OPA or an NPA.
• If respirations are absent or inadequate, start positive-pressure
ventilations at once with an appropriate device.
• If adjuncts are unavailable, use mouth-to-mask barrier device ventilation.

Suctioning
Introduction Suctioning is an essential component of maintaining a patient’s
airway. Providers should suction the airway immediately if there
are copious secretions, blood, or vomit.
Suction devices consist of both portable and wall-mounted units.

• Portable suction devices are easy to transport but may not

provide adequate suction power. A suction force of −80 to
−120 mm Hg is generally necessary.
 • Wall-mounted suction units should be capable of providing an
airflow of greater than 40 L/min at the end of the delivery tube
and a vacuum of more than −300 mm Hg when the tube is
clamped at full suction.
• Adjust the amount of suction force for use in children and
intubated patients.

Soft vs Rigid Both soft flexible and rigid suctioning catheters are available.
Catheters Soft flexible catheters may be used in the mouth or nose. Soft
flexible catheters are available in sterile wrappers and can also be
used for ET tube deep suctioning.
Rigid catheters (eg, Yankauer) are used to suction the oropharynx.
These are better for suctioning thick secretions and particulate
matter.
Catheter Use for
Type
Soft • Aspiration of thin secretions from the
oropharynx and nasopharynx
• Performing intratracheal suctioning
• Suctioning through an in-place airway (ie, NPA)
to access the back of the pharynx in a patient
with clenched teeth

Rigid • More effective suctioning of the oropharynx,

particularly if there is thick particulate matter

Oropharyngeal Follow the steps below to perform oropharyngeal suctioning.

Suctioning Step Action
Procedure
1 • Measure the catheter before suctioning and do not
insert it any further than the distance from the tip of
the nose to the earlobe.
• Gently insert the suction catheter or device into the
oropharynx beyond the tongue.

2 • Apply suction by occluding the side opening of the

catheter while withdrawing with a rotating or twisting
motion.
• If using a rigid suction device (eg, Yankauer suction),
place the tip gently into the oral cavity. Advance by
 pushing the tongue down to reach the oropharynx if
necessary.

Endotracheal Patients with pulmonary secretions may require suctioning even

Tube Suctioning after ET intubation. Follow the steps below to perform ET tube
Procedure suctioning:
Step Action
1 • Use sterile technique to reduce the likelihood of airway
contamination.

2 • Gently insert the catheter into the ET tube. Be sure the

side opening is not occluded during insertion.
• Insertion of the catheter beyond the tip of the ET tube
is not recommended because it may injure the ET
mucosa or stimulate coughing or bronchospasm.

3 • Apply suction by occluding the side opening only while

withdrawing the catheter with a rotating or twisting
motion.
• Suction attempts should not exceed 10
seconds. To avoid hypoxemia, precede and follow
suctioning attempts with a short period of
administration of 100% oxygen.

Monitor the patient’s heart rate, pulse, oxygen saturation, and

clinical appearance during suctioning. If bradycardia
develops, oxygen saturation drops, or clinical appearance
deteriorates, interrupt suctioning at once. Administer high-
flow oxygen until the heart rate returns to normal and the
clinical condition improves. Assist ventilation as needed.

Providing Ventilation With an Advanced Airway

Introduction Selection of an advanced airway device depends on the training,
scope of practice, and equipment of the providers on the high-
performance team. Advanced airways include but are not limited to

• Laryngeal mask airway

• Laryngeal tube
• Esophageal-tracheal tube
 • ET tube

Because a small proportion of patients cannot be ventilated with a

laryngeal mask airway, providers who use this device should have an
alternative airway management strategy. A bag-mask device can be
this alternate strategy.
This course will familiarize you with types of advanced airways.
Instruction in the skilled placement of these airways is beyond the
scope of the basic ACLS Provider Course. To be proficient in the use
of advanced airway devices, you must have adequate initial training
and ongoing experience. Providers who insert advanced airways must
participate in a process of CQI to document and minimize
complications.
In this course, you will practice ventilating with an advanced airway in
place and integrating ventilation with chest compressions.

Ventilation Airway Ventilation During Ventilation During

Rates Devices Cardiac Arrest Respiratory Arrest
Any advanced Once every 6 seconds Once every 5 to 6
airway seconds

Laryngeal The laryngeal mask airway is an advanced airway alternative to ET

Mask Airway intubation and provides comparable ventilation. It is acceptable to use
the laryngeal mask airway as an alternative to an ET tube for airway
management in cardiac arrest. Only experienced providers should
perform laryngeal mask airway insertion.

See the Student Website (www.heart.org/eccstudent) for

more information on the laryngeal mask airway.

Laryngeal The advantages of the laryngeal tube are similar to those of the
Tube esophageal-tracheal tube; however, the laryngeal tube is more
compact and less complicated to insert.
Healthcare professionals trained in the use of the laryngeal tube may
consider it as an alternative to bag-mask ventilation or ET intubation
for airway management in cardiac arrest. Only experienced providers
should perform laryngeal tube insertion.
 See the Laryngeal Intubation section on the Student
Website (www.heart.org/eccstudent) for more information on this
procedure.

Esophageal- The esophageal-tracheal tube is an advanced airway alternative to ET

Tracheal Tube intubation. This device provides adequate ventilation comparable to an
ET tube. It is acceptable to use the esophageal-tracheal tube as an
alternative to an ET tube for airway management in cardiac
arrest. Only providers experienced with its use should perform
esophageal-tracheal tube insertion.

See the Student Website (www.heart.org/eccstudent) for

more information on the esophageal-tracheal tube.

Endotracheal A brief summary of the basic steps for performing ET intubation is

Tube given here to familiarize the ACLS provider who may assist with the
procedure.

• Prepare for intubation by assembling the necessary equipment.

• Perform ET intubation (see the Student Website).
• Inflate cuff or cuffs on the tube.
• Attach the ventilation bag.
• Confirm correct placement by physical examination and a
confirmation device. Continuous waveform capnography is
recommended (in addition to clinical assessment) as the most
reliable method of confirming and monitoring correct placement of
an ET tube. Healthcare providers may use colorimetric and
nonwaveform carbon dioxide detectors when waveform
capnography is not available.
• Secure the tube in place.
• Monitor for displacement.

Only experienced providers should perform ET intubation.

See the Endotracheal Intubation section on the Student

Website (www.heart.org/eccstudent) for more information on this
procedure.
 Caution Use of Cricoid Pressure

• The routine use of cricoid pressure in cardiac arrest is not recommended.

• Cricoid pressure in nonarrest patients may offer some measure of
protection to the airway from aspiration and gastric insufflation during bag-
mask ventilation. However, it also may impede ventilation and interfere
with placement of a supraglottic airway or intubation.

Precautions for Trauma Patients

Summary When providing assisted ventilation for patients with known or suspected
cervical spine trauma, avoid unnecessary spine movement. Excessive head
and neck movement in patients with an unstable cervical spinal column can
cause irreversible injury to the spinal cord or worsen a minor spinal cord
injury. Approximately 2% of patients with blunt trauma serious enough to
require spinal imaging in the ED have a spinal injury. This risk is tripled if the
patient has a head or facial injury. Assume that any patient with multiple
trauma, head injury, or facial trauma has a spine injury. Be particularly
cautious if a patient has suspected cervical spine injury. Examples are
patients who have been involved in a high-speed motor vehicle collision,
have fallen from a height, or were injured while diving.
Follow these precautions if you suspect cervical spine trauma:

• Open the airway by using a jaw thrust without head extension. Because
maintaining a patent airway and providing adequate ventilation are
priorities, use a head tilt–chin lift maneuver if the jaw thrust is not
effective.
• Have another team member stabilize the head in a neutral position
during airway manipulation. Use manual spinal motion restriction
rather than immobilization devices. Manual spinal immobilization is
safer. Cervical collars may complicate airway management and may
even interfere with airway patency.
• Spinal immobilization devices are helpful during transport.

Acute Coronary Syndromes Case

Introduction The ACLS provider must have the basic knowledge to assess and
stabilize patients with ACS. Patients in this case have signs and
symptoms of ACS, including possible AMI. You will use the ACS
Algorithm as the guide to clinical strategy.
The initial 12-lead ECG is used in all ACS cases to classify patients into
1 of 3 ECG categories, each with different strategies of care and
management needs. These 3 ECG categories are ST-segment elevation
 suggesting ongoing acute injury, ST-segment depression suggesting
ischemia, and nondiagnostic or normal ECG. These are outlined in the
ACS Algorithm, but STEMI with time-sensitive reperfusion strategies is
the focus of this course (Figure 20).
Key components of this case are

• Identification, assessment, and triage of acute ischemic chest

discomfort
• Initial treatment of possible ACS
• Emphasis on early reperfusion of the patient with ACS/STEMI

Rhythms for Sudden cardiac death and hypotensive bradyarrhythmias may occur
ACS with acute ischemia. Providers will understand to anticipate these
rhythms and be prepared for immediate attempts at defibrillation and
administration of drug or electrical therapy for symptomatic
bradyarrhythmias.
Although 12-lead ECG interpretation is beyond the scope of the ACLS
Provider Course, some ACLS providers will have 12-lead ECG reading
skills. For them, this case summarizes the identification and
management of patients with STEMI.

Drugs for Drug therapy and treatment strategies continue to evolve rapidly in the
ACS field of ACS. ACLS providers and instructors will need to monitor
important changes. The ACLS Provider Course presents only basic
knowledge focusing on early treatment and the priority of rapid
reperfusion, relief of ischemic pain, and treatment of early life-
threatening complications. Reperfusion may involve the use of
fibrinolytic therapy or coronary angiography with PCI (ie, balloon
angioplasty/stenting). When used as the initial reperfusion strategy for
STEMI, PCI is called primary PCI.
Treatment of ACS involves the initial use of drugs to relieve ischemic
discomfort, dissolve clots, and inhibit thrombin and platelets. These
drugs are

• Oxygen
• Aspirin
• Nitroglycerin
• Opiates (eg, morphine)
• Fibrinolytic therapy (overview)
• Heparin (UFH, LWMH)
 Additional agents that are adjunctive to initial therapy and will not be
discussed in the ACLS Provider Course are

• β-Blockers
• Adenosine diphosphate (ADP) antagonists (clopidogrel, prasugrel,
ticagrelor)
• Angiotensin-converting enzyme (ACE) inhibitors
• HMG-CoA reductase inhibitors (statin therapy)
• Glycoprotein IIb/IIIa inhibitors

Goals for ACS Patients

Foundational OHCA Response
Facts Half of the patients who die of ACS do so before reaching the hospital.
VF or pulseless VT is the precipitating rhythm in most of these deaths.
VF is most likely to develop during the first 4 hours after onset of
symptoms.
Communities should develop programs to respond to OHCA. Such
programs should focus on

• Recognizing symptoms of ACS

• Activating the EMS system, with EMS advance notification of the
receiving hospital
• Providing early CPR
• Providing early defibrillation with AEDs available through public
access defibrillation programs and first responders
• Providing a coordinated system of care among the EMS system, the
ED, and Cardiology

The primary goals are

• Identification of patients with STEMI and triage for early

reperfusion therapy
• Relief of ischemic chest discomfort
• Prevention of MACE, such as death, nonfatal MI, and the need
for urgent postinfarction revascularization
• Treatment of acute, life-threatening complications of ACS,
such as VF/pulseless VT, symptomatic bradycardias, and
unstable tachycardias

Reperfusion therapy opens an occluded coronary artery with either

mechanical means or drugs. PCI, performed in the heart
catheterization suite after coronary angiography, allows balloon
dilation and/or stent placement for an occluded coronary artery.
 “Clot-buster” drugs are called fibrinolytics, a more accurate term
than thrombolytics.

Pathophysiology Patients with coronary atherosclerosis may develop a spectrum of

of ACS clinical syndromes representing varying degrees of coronary artery
occlusion. These syndromes include non-ST elevation ACS
(NSTE-ACS) and STEMI. Sudden cardiac death may occur with
each of these syndromes. Figure 19 illustrates the pathophysiology
of ACS.
Figure 19. Pathophysiology of ACS.
Figure 20. The Acute Coronary Syndromes Algorithm.
Managing ACS: The Acute Coronary Syndromes Algorithm
Overview of the The Acute Coronary Syndromes Algorithm (Figure 20) outlines the
Algorithm assessment and management steps for a patient presenting with
symptoms suggestive of ACS. The EMS responder in the out-of-
hospital environment can begin immediate assessments and
actions. These include giving oxygen, aspirin, nitroglycerin, and
morphine if needed, and obtaining an initial 12-lead ECG (Step 2).
Based on the ECG findings, the EMS provider may complete a
fibrinolytic therapy checklist and notify the receiving ED of a
potential AMI-STEMI when appropriate (Step 3). If out-of-hospital
providers are unable to complete these initial steps before the
patient’s arrival at the hospital, the ED provider should implement
this component of care.
Subsequent treatment occurs on the patient’s arrival at the hospital.
ED personnel should review the out-of-hospital 12-lead ECG if
available. If not performed, acquisition of the 12-lead ECG should
be a priority. The goal is to analyze the 12-lead ECG as soon as
possible within 10 minutes of the patient’s arrival in the ED (Step
4). Hospital personnel should categorize patients into 1 of 3 groups
according to analysis of the ST segment or the presence of left
bundle branch block (LBBB) on the 12-lead ECG. Treatment
recommendations are specific to each group.

• STEMI
• NSTE-ACS
• Low-/intermediate-risk ACS

The ACS Case will focus on the early reperfusion of the STEMI
patient, emphasizing initial care and rapid triage for reperfusion
therapy.

Important The ACS Algorithm (Figure 20) provides general guidelines that
Considerations apply to the initial triage of patients based on symptoms and the
12-lead ECG. Healthcare personnel often obtain serial cardiac
markers (CK-MB, cardiac troponins) in most patients that allow
additional risk stratification and treatment recommendations. Two
important points for STEMI need emphasis:

• The ECG is central to the initial risk and treatment stratification

process.
• Healthcare personnel do not need evidence of elevated
cardiac markers to make a decision to administer fibrinolytic
 therapy or perform diagnostic coronary angiography with
coronary intervention (angioplasty/stenting) in STEMI patients.

Application of the The steps in the algorithm guide assessment and treatment:
ACS Algorithm
• Identification of chest discomfort suggestive of ischemia (Step
1)
• EMS assessment, care, transport, and hospital prearrival
notification (Step 2)
• Immediate ED assessment and treatment (Step 3)
• Classification of patients according to ST-segment analysis
(Steps 5, 9, and 11)
• STEMI (Steps 5 through 8)

Identification of Chest Discomfort Suggestive of Ischemia

Signs and You should know how to identify chest discomfort suggestive of
Conditions ischemia. Conduct a prompt and targeted evaluation of every patient
whose initial complaints suggest possible ACS.
The most common symptom of myocardial ischemia and infarction is
retrosternal chest discomfort. The patient may perceive this discomfort
more as pressure or tightness than actual pain.
Symptoms suggestive of ACS may also include

• Uncomfortable pressure, fullness, squeezing, or pain in the center of

the chest lasting several minutes (usually more than a few minutes)
• Chest discomfort spreading to the shoulders, neck, one or both
arms, or jaw
• Chest discomfort spreading into the back or between the shoulder
blades
• Chest discomfort with light-headedness, dizziness, fainting,
sweating, nausea, or vomiting
• Unexplained, sudden shortness of breath, which may occur with or
without chest discomfort

Consider the likelihood that the presenting condition is ACS or one of its
potentially lethal mimics. Other life-threatening conditions that may
cause acute chest discomfort are aortic dissection, acute pulmonary
embolism (PE), acute pericardial effusion with tamponade, and tension
pneumothorax.
Foundational STEMI Chain of Survival
Facts The STEMI Chain of Survival (Figure 21) described by the AHA is
similar to the Chain of Survival for sudden cardiac arrest. It links actions
to be taken by patients, family members, and healthcare providers to
maximize STEMI recovery. These links are

• Rapid recognition and reaction to STEMI warning signs

• Rapid EMS dispatch and rapid EMS system transport and prearrival
notification to the receiving hospital
• Rapid assessment and diagnosis in the ED (or cath lab)
• Rapid treatment

Figure 21. The STEMI Chain of Survival.

Starting All dispatchers and EMS providers must receive training in ACS symptom
With recognition along with the potential complications. Dispatchers, when
Dispatch authorized by medical control or protocol, should tell patients with no
history of aspirin allergy or signs of active or recent gastrointestinal (GI)
bleeding to chew aspirin (160 to 325 mg) while waiting for EMS providers
to arrive.

EMS Assessment, Care, and Hospital Preparation

Introduction EMS assessment, care, and hospital preparation are outlined in Step
2. EMS responders may perform the following assessments and
actions during the stabilization, triage, and transport of the patient to
an appropriate facility:

• Monitor and support airway, breathing, and circulation (ABCs).

• Administer aspirin and consider oxygen if O2 saturation is less
than 90%, nitroglycerin, and morphine if discomfort is
unresponsive to nitrates.
• Obtain a 12-lead ECG; interpret or transmit for interpretation.
 • Complete a fibrinolytic checklist if indicated.
• Provide prearrival notification to the receiving facility if ST
elevation.

Monitor and Monitoring and support of ABCs includes

Support ABCs
• Monitoring vital signs and cardiac rhythm
• Being prepared to provide CPR
• Using a defibrillator if needed

Administer Providers should be familiar with the actions, indications, cautions, and
Oxygen and treatment of side effects.
Drugs Oxygen
High inspired-oxygen tension will tend to maximize arterial oxygen
saturation and, in turn, arterial oxygen content. This will help support
oxygen delivery (cardiac output × arterial oxygen content) when
cardiac output is limited. This short-term oxygen therapy does not
produce oxygen toxicity.
EMS providers should administer oxygen if the patient is dyspneic, is
hypoxemic, has obvious signs of heart failure, has an arterial oxygen
saturation less than 90%, or the oxygen saturation is unknown.
Providers should titrate oxygen therapy to a noninvasively monitored
oxyhemoglobin saturation 90% or greater. Because its usefulness has
not been established in normoxic patients with suspected or confirmed
ACS, providers may consider withholding supplementary oxygen
therapy in these patients.
Aspirin (Acetylsalicylic Acid)
A dose of 160 to 325 mg of non–enteric-coated aspirin causes
immediate and near-total inhibition of thromboxane A2 production by
inhibiting platelet cyclooxygenase (COX-1). Platelets are one of the
principal and earliest participants in thrombus formation. This rapid
inhibition also reduces coronary reocclusion and other recurrent
events independently and after fibrinolytic therapy.
If the patient has not taken aspirin and has no history of true aspirin
allergy and no evidence of recent GI bleeding, give the patient aspirin
(160 to 325 mg) to chew. In the initial hours of an ACS, aspirin is
absorbed better when chewed than when swallowed, particularly if
morphine has been given. Use rectal aspirin suppositories (300 mg)
for patients with nausea, vomiting, active peptic ulcer disease, or other
disorders of the upper GI tract.
Nitroglycerin (Glyceryl Trinitrate)
Nitroglycerin effectively reduces ischemic chest discomfort, and it has
beneficial hemodynamic effects. The physiologic effects of nitrates
cause reduction in LV and right ventricular (RV) preload through
peripheral arterial and venous dilation.
Give the patient 1 sublingual nitroglycerin tablet (or spray “dose”)
every 3 to 5 minutes for ongoing symptoms if it is permitted by medical
control and no contraindications exist. Healthcare providers may
repeat the dose twice (total of 3 doses). Administer nitroglycerin only if
the patient remains hemodynamically stable: SBP is greater than 90
mm Hg or no lower than 30 mm Hg below baseline (if known) and the
heart rate is 50 to 100/min.
Nitroglycerin is a venodilator and needs to be used cautiously or not at
all in patients with inadequate ventricular preload. These situations
include

• Inferior wall MI and RV infarction. RV infarction may complicate

an inferior wall MI. Patients with acute RV infarction are very
dependent on RV filling pressures to maintain cardiac output and
blood pressure. If RV infarction cannot be ruled out, providers
must use caution in administering nitrates to patients with inferior
STEMI. If RV infarction is confirmed by right-sided precordial
leads or clinical findings by an experienced provider, nitroglycerin
and other vasodilators (morphine) or volume-depleting drugs
(diuretics) are contraindicated as well.
• Hypotension, bradycardia, or tachycardia. Avoid use of
nitroglycerin in patients with hypotension (SBP less than 90 mm
Hg), marked bradycardia (less than 50/min), or tachycardia.
• Recent phosphodiesterase inhibitor use. Avoid the use of
nitroglycerin if it is suspected or known that the patient has taken
sildenafil or vardenafil within the previous 24 hours or tadalafil
within 48 hours. These agents are generally used for erectile
dysfunction or in cases of pulmonary hypertension and in
combination with nitrates may cause severe hypotension
refractory to vasopressor agents.

Opiates (eg, Morphine)

Give an opiate (eg, morphine) for chest discomfort unresponsive to
sublingual or spray nitroglycerin if authorized by protocol or medical
control. Morphine is indicated in STEMI when chest discomfort is
unresponsive to nitrates. Use morphine with caution in NSTE-ACS
because of an association with increased mortality.
Morphine may be utilized in the management of ACS because it
 • Produces central nervous system analgesia, which reduces the
adverse effects of neurohumoral activation, catecholamine
release, and heightened myocardial oxygen demand
• Produces venodilation, which reduces LV preload and oxygen
requirements
• Decreases systemic vascular resistance, thereby reducing LV
afterload
• Helps redistribute blood volume in patients with acute pulmonary
edema

Remember, morphine is a venodilator. Like nitroglycerin, use smaller

doses and carefully monitor physiologic response before administering
additional doses in patients who may be preload dependent. If
hypotension develops, administer fluids as a first line of therapy.
Critical Pain Relief With Nitroglycerin
Concepts Relief of pain with nitroglycerin is neither specific nor a useful diagnostic
tool to determine the etiology of symptoms in ED patients with chest pain or
discomfort. GI etiologies as well as other causes of chest discomfort can
“respond” to nitroglycerin administration. Therefore, the response to nitrate
therapy is not diagnostic of ACS.

Caution Use of Nonsteroidal Anti-inflammatory Drugs

Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is contraindicated
(except for aspirin) and should be discontinued. Both nonselective as well as
COX-2 selective drugs should not be administered during hospitalization for
STEMI because of the increased risk of mortality, reinfarction, hypertension,
heart failure, and myocardial rupture associated with their use.

Obtain a EMS providers should obtain a 12-lead ECG. The AHA recommends out-of-
12-Lead hospital 12-lead ECG diagnostic programs in urban and suburban EMS
ECG systems.
EMS Action Recommendation
12-Lead ECG if The AHA recommends routine use of 12-lead out-of-
available hospital ECGs for patients with signs and symptoms of
possible ACS.
Prearrival Prearrival notification of the ED shortens the time to
hospital treatment (10 to 60 minutes has been achieved in
notification for clinical studies) and speeds reperfusion therapy with
STEMI fibrinolytics or PCI or both, which may reduce mortality
and minimize myocardial injury.
 Fibrinolytic If STEMI is identified on the 12-lead ECG, complete a
checklist if fibrinolytic checklist if appropriate.
appropriate

See the Student Website (www.heart.org/eccstudent) for a sample

fibrinolytic checklist.

Immediate ED Assessment and Treatment

Introduction The high-performance team should quickly evaluate the patient with
potential ACS on the patient’s arrival in the ED. Within the first 10
minutes, obtain a 12-lead ECG (if not already performed before arrival)
and assess the patient.
The 12-lead ECG (example in Figure 22) is at the center of the
decision pathway in the management of ischemic chest discomfort
and is the only means of identifying STEMI.
A targeted evaluation should be performed and focus on chest
discomfort, signs and symptoms of heart failure, cardiac history, risk
factors for ACS, and historical features that may preclude the use of
fibrinolytics. For the patient with STEMI, the goals of reperfusion are to
give fibrinolytics within 30 minutes of arrival or perform PCI within 90
minutes of arrival.

Figure 22. Anterior STEMI on a 12-lead ECG.

Figure 23 shows how to measure ST-segment deviation.
Figure 23. How to measure ST-segment deviation. A, Inferior MI. The ST segment has
no low point (it is covered or concave). B, Anterior MI.

The First 10 Assessment and stabilization of the patient in the first 10 minutes
Minutes should include the following:

• Check vital signs and evaluate oxygen saturation.

• Establish IV access.
• Take a brief focused history and perform a physical examination.
• Complete the fibrinolytic checklist and check for contraindications,
if indicated.
• Obtain a blood sample to evaluate initial cardiac marker levels,
electrolytes, and coagulation.
• Obtain and review portable chest x-ray (less than 30 minutes after
the patient’s arrival in the ED). This should not delay fibrinolytic
therapy for STEMI or activation of the PCI team for STEMI.
 Note: The results of cardiac markers, chest x-ray, and laboratory
studies should not delay reperfusion therapy unless clinically
necessary, eg, suspected aortic dissection or coagulopathy.

Patient Unless allergies or contraindications exist, 4 agents may be considered

General in patients with ischemic-type chest discomfort:
Treatment
• Oxygen if hypoxemic (O2 % less than 90%) or signs of heart failure
• Aspirin
• Nitroglycerin
• Opiate (eg, morphine if ongoing discomfort or no response to
nitrates)

Because these agents may have been given out of hospital, administer
initial or supplementary doses as indicated. (See the discussion of
these drugs in the previous section, EMS Assessment, Care, and
Hospital Preparation.)
Critical Oxygen, Aspirin, Nitrates, and Opiates
Concepts
• Unless contraindicated, initial therapy with oxygen if needed, aspirin,
nitrates, and, if indicated, morphine is recommended for all patients
suspected of having ischemic chest discomfort.
• The major contraindication to nitroglycerin and morphine is hypotension,
including hypotension from an RV infarction. The major
contraindications to aspirin are true aspirin allergy and active or recent
GI bleeding.

Classify Patients According to ST-Segment Deviation

Classify Into 3 Review the initial 12-lead ECG (Step 4) and classify patients into 1 of
Groups Based the 3 following clinical groups (Steps 5, 9, and 11):
on ST-Segment General Group Description
Deviation STEMI ST elevation
NSTE-ACS ST depression or dynamic T-wave
inversion
Low-/intermediate-risk Normal or nondiagnostic ECG
ACS
 • STEMI is characterized by ST-segment elevation in 2 or more
contiguous leads or new LBBB. Threshold values for ST-
segment elevation consistent with STEMI are J-point elevation
greater than 2 mm (0.2 mV) in leads V2 and V3* and 1 mm or
more in all other leads or by new or presumed new LBBB.
*2.5 mm in men younger than 40 years; 1.5 mm in all women.
• NSTE-ACS is characterized by ischemic ST-segment depression
0.5 mm (0.05 mV) or greater or dynamic T-wave inversion with
pain or discomfort. Nonpersistent or transient ST elevation 0.5
mm or greater for less than 20 minutes is also included in this
category.
• Low-/intermediate-risk ACS is characterized by normal or
nondiagnostic changes in the ST segment or T wave that are
inconclusive and require further risk stratification. This
classification includes patients with normal ECGs and those with
ST-segment deviation in either direction of less than 0.5 mm
(0.05 mV) or T-wave inversion ≤2 mm or 0.2 mV. Serial cardiac
studies and functional testing are appropriate. Note that
additional information (troponin) may place the patient into a
higher risk classification after initial classification.

The ECG classification of ischemic syndromes is not meant to be

exclusive. A small percentage of patients with normal ECGs may be
found to have MI, for example. If the initial ECG is nondiagnostic and
clinical circumstances indicate (eg, ongoing chest discomfort), repeat
the ECG.

STEMI
Introduction Patients with STEMI usually have complete occlusion of an epicardial
coronary artery.
The mainstay of treatment for STEMI is early reperfusion therapy
achieved with primary PCI or fibrinolytics.
Reperfusion therapy for STEMI is perhaps the most important
advancement in treatment of cardiovascular disease in recent years.
Early fibrinolytic therapy or direct catheter-based reperfusion has been
established as a standard of care for patients with STEMI who present
within 12 hours of onset of symptoms with no contraindications.
Reperfusion therapy reduces mortality and saves heart muscle; the
shorter the time to reperfusion, the greater the benefit. A 47% reduction in
mortality was noted when fibrinolytic therapy was provided in the first
hour after onset of symptoms.
 Critical Delay of Therapy
Concepts
• Routine consultation with a cardiologist or another physician should not
delay diagnosis and treatment except in equivocal or uncertain cases.
Consultation delays therapy and is associated with increased hospital
mortality rates.
• Potential delay during the in-hospital evaluation period may occur
from door to data (ECG), from datato decision, and
from decision to drug (or PCI). These 4 major points of in-hospital
therapy are commonly referred to as the “4 D’s.”
• All providers must focus on minimizing delays at each of these points.
Out-of-hospital transport time constitutes only 5% of delay to treatment
time; ED evaluation constitutes 25% to 33% of this delay.

Early Rapidly identify patients with STEMI and quickly screen them for
Reperfusion indications and contraindications to fibrinolytic therapy by using a
Therapy fibrinolytic checklist if appropriate.
The first qualified physician who encounters a patient with STEMI
should interpret or confirm the 12-lead ECG, determine the risk/benefit
of reperfusion therapy, and direct administration of fibrinolytic therapy
or activation of the PCI team. Early activation of PCI may occur with
established protocols. The following time frames are recommended:

• For PCI, this goal for ED door–to–balloon inflation time is 90

minutes. In patients presenting to a non–PCI-capable hospital,
time from first medical contact to device should be less than 120
minutes when primary PCI is considered.
• If fibrinolysis is the intended reperfusion, an ED door-to-needle
time (needle time is the beginning of infusion of a fibrinolytic agent)
of 30 minutes is the medical system goal that is considered the
longest time acceptable. Systems should strive to achieve the
shortest time possible.
• Patients who are ineligible for fibrinolytic therapy should be
considered for transfer to a PCI facility regardless of delay. The
system should prepare for a door-to-departure time of 30 minutes
when a transfer decision is made.

Adjunctive treatments may also be indicated.

Use of PCI The most commonly used form of PCI is coronary intervention with
stent placement. Optimally performed primary PCI is the preferred
reperfusion strategy over fibrinolytic administration. Rescue PCI is used
early after fibrinolytics in patients who may have persistent occlusion of
 the infarct artery (failure to reperfuse with fibrinolytics), although this
term has been recently replaced and included by the
term pharmacoinvasive strategy. PCI has been shown to be superior to
fibrinolysis in the combined end points of death, stroke, and reinfarction
in many studies for patients presenting between 3 and 12 hours after
onset. However, these results have been achieved in experienced
medical settings with skilled providers (performing more than 75 PCIs
per year) at a skilled PCI facility (performing more than 200 PCIs for
STEMI with cardiac surgery capabilities).
Considerations for the use of PCI include the following:

• PCI is the treatment of choice for the management of STEMI when

it can be performed effectively with a door-to-balloon time of less
than 90 minutes from first medical contact by a skilled provider at a
skilled PCI facility.
• Primary PCI may also be offered to patients presenting to non–
PCI-capable centers if PCI can be initiated promptly within 120
minutes from first medical contact. The TRANSFER AMI (Trial of
Routine Angioplasty and Stenting After Fibrinolysis to Enhance
Reperfusion in Acute Myocardial Infarction) trial supports the
transfer of high-risk patients who receive fibrinolysis in a non-PCI
center within 12 hours of symptom onset to a PCI center within 6
hours of fibrinolytic administration to receive routine early coronary
angiography and PCI if indicated.
• For patients admitted to a hospital without PCI capabilities, there
may be some benefit associated with transfer for PCI versus
administration of on-site fibrinolytics in terms of reinfarction, stroke,
and a trend to lower mortality when PCI can be performed within
120 minutes of first medical contact.
• PCI is also preferred in patients with contraindications to
fibrinolytics and is indicated in patients with cardiogenic shock or
heart failure complicating MI.

Use of A fibrinolytic agent or “clot-buster” is administered to patients with J-

Fibrinolytic point ST-segment elevation greater than 2 mm (0.2 mV) in leads
Therapy V2 and V3 and 1 mm or more in all other leads or by new or presumed
new LBBB (eg, leads III, aVF; leads V3, V4; leads I and aVL) without
contraindications. Fibrin-specific agents are effective in achieving
normal flow in about 50% of patients given these drugs. Examples of
fibrin-specific drugs are rtPA, reteplase, and tenecteplase.
Streptokinase was the first fibrinolytic used widely, but it is not fibrin
specific.
Considerations for the use of fibrinolytic therapy are as follows:
 • In the absence of contraindications and in the presence of a
favorable risk-benefit ratio, fibrinolytic therapy is one option for
reperfusion in patients with STEMI and onset of symptoms within
12 hours of presentation with qualifying ECG findings and if PCI is
not available within 90 minutes of first medical contact.
• In the absence of contraindications, it is also reasonable to give
fibrinolytics to patients with onset of symptoms within the prior 12
hours and ECG findings consistent with true posterior MI.
Experienced providers will recognize this as a condition where ST-
segment depression in the early precordial leads is equivalent to
ST-segment elevation in others. When these changes are
associated with other ECG findings, it is suggestive of a “STEMI”
on the posterior wall of the heart.
• Fibrinolytics are generally not recommended for patients
presenting more than 12 hours after onset of symptoms. But they
may be considered if ischemic chest discomfort continues with
persistent ST-segment elevation.
• Do not give fibrinolytics to patients who present more than 24
hours after the onset of symptoms or patients with ST-segment
depression unless a true posterior MI is suspected.

Adjunctive Other drugs are useful when indicated in addition to oxygen, sublingual
Treatments or spray nitroglycerin, aspirin, morphine, and fibrinolytic therapy. These
include

• Unfractionated or low-molecular-weight heparin

• Bivalirudin
• P2Y12 inhibitors
• IV nitroglycerin
• β-Blockers
• Glycoprotein IIb/IIIa inhibitors

IV nitroglycerin and heparin are commonly used early in the

management of patients with STEMI. These agents are briefly
discussed below. Use of bivalirudin, P2Y12 inhibitors, β-blockers, and
glycoprotein IIb/IIIa inhibitors will not be reviewed. Use of these agents
requires additional risk stratification skills and a detailed knowledge of
the spectrum of ACS and, in some instances, continuing knowledge of
the results of clinical trials.
Heparin (Unfractionated or Low-Molecular-Weight)
Heparin is routinely given as an adjunct for PCI and fibrinolytic therapy
with fibrin-specific agents (rtPA, reteplase, tenecteplase). It is also
indicated in other specific high-risk situations, such as LV mural
thrombus, atrial fibrillation, and prophylaxis for venous
thromboembolism in patients with prolonged bed rest and heart failure
complicating MI. If you use these drugs, you must be familiar with
dosing schedules for specific clinical strategies.
The inappropriate dosing and monitoring of heparin therapy has
caused excess intracerebral bleeding and major hemorrhage in
STEMI patients. Providers using heparin need to know the
indications, dosing, and use in the specific ACS categories.
The dosing, use, and duration have been derived from use in
clinical trials. Specific patients may require dose modification. See
the ECC Handbook for weight-based dosing guidelines, intervals
of administration, and adjustment of low-molecular-weight heparin
in renal function. See the ACC/AHA guidelines for detailed
discussion in specific categories.
IV Nitroglycerin
Routine use of IV nitroglycerin is not indicated and has not been shown
to significantly reduce mortality in STEMI. IV nitroglycerin is indicated
and used widely in ischemic syndromes. It is preferred over topical or
long-acting forms because it can be titrated in a patient with potentially
unstable hemodynamics and clinical condition. Indications for initiation
of IV nitroglycerin in STEMI are

• Recurrent or continuing chest discomfort unresponsive to

sublingual or spray nitroglycerin
• Pulmonary edema complicating STEMI
• Hypertension complicating STEMI

Treatment goals using IV nitroglycerin are as follows:

Treatment Goal Management
Relief of ischemic chest • Titrate to effect
discomfort • Keep SBP greater than 90 mm Hg
• Limit drop in SBP to 30 mm Hg
below baseline in hypertensive
patients

Improvement in pulmonary • Titrate to effect

edema and hypertension • Limit drop in SBP to 10% of
baseline in normotensive patients
• Limit drop in SBP to 30 mm Hg
below baseline in hypertensive
patients
 Acute Stroke Case
Introduction The identification and initial management of patients with acute
stroke is within the scope of an ACLS provider. This case
covers principles of out-of-hospital care and fundamental aspects of
initial in-hospital acute stroke care.
Out-of-hospital acute stroke care focuses on

• Rapid identification and assessment of patients with stroke

• Rapid transport (with prearrival notification) to a facility capable
of providing acute stroke care

In-hospital acute stroke care includes the

• Ability to rapidly determine patient eligibility for fibrinolytic

therapy
• Administration of fibrinolytic therapy to appropriate candidates,
with availability of neurologic medical supervision within target
times
• Consideration of new treatment options like endovascular
therapy
• Initiation of the stroke pathway and patient admission to a stroke
unit if available

The target times and goals are recommended by the NINDS, which
has recommended measurable goals for the evaluation of stroke
patients. These targets or goals should be achieved for at least 80%
of patients with acute stroke.

Potential The ECG does not take priority over obtaining a computed
Arrhythmias tomography (CT) scan. No arrhythmias are specific for stroke, but the
With Stroke ECG may identify evidence of a recent AMI or arrhythmias such as
atrial fibrillation as a cause of an embolic stroke. Many patients with
stroke may demonstrate arrhythmias, but if the patient is
hemodynamically stable, most arrhythmias will not require treatment.
There is general agreement to recommend cardiac monitoring during
the first 24 hours of evaluation in patients with acute ischemic stroke
to detect atrial fibrillation and potentially life-threatening arrhythmias.

Drugs for This case involves these drugs:

Stroke
• Approved fibrinolytic agent (rtPA)
• Glucose (D50)
 • Labetalol
• Nicardipine
• Enalaprilat
• Aspirin
• Nitroprusside

Foundational Major Types of Stroke

Facts Stroke is a general term. It refers to acute neurologic impairment that
follows interruption in blood supply to a specific area of the brain.
Although expeditious stroke care is important for all patients, this case
emphasizes reperfusion therapy for acute ischemic stroke.
The major types of stroke are

• Ischemic stroke: Accounts for 87% of all strokes and is usually

caused by an occlusion of an artery to a region of the brain (Figure
24).
• Hemorrhagic stroke: Accounts for 13% of all strokes and occurs when
a blood vessel in the brain suddenly ruptures into the surrounding
tissue. Fibrinolytic therapy is contraindicated in this type of stroke.
Avoid anticoagulants.

Figure 24. Types of stroke. Eighty-seven percent of strokes are ischemic and
potentially eligible for fibrinolytic therapy if patients otherwise qualify. Thirteen percent of
strokes are hemorrhagic, and the majority of these are intracerebral. The male-to-
female incidence ratio is 1.25 in persons 55 to 64 years of age, 1.50 in those 65 to 74,
1.07 in those 75 to 84, and 0.76 in those 85 and older. Blacks have almost twice the risk
of first-ever stroke compared with whites.

Approach to Stroke Care

Introduction Each year in the United States, about 795 000 people have a new or
recurrent stroke. Stroke remains a leading cause of death in the United
States.
 Early recognition of acute ischemic stroke is important because IV
fibrinolytic treatment should be provided as early as possible, generally
within 3 hours of onset of symptoms, or within 4.5 hours of onset of
symptoms for selected patients. Endovascular therapy may be given
within 6 hours of onset of symptoms, but better outcomes are associated
with shorter times to treatment. Most strokes occur at home, and only half
of acute stroke patients use EMS for transport to the hospital. Stroke
patients often deny or try to rationalize their symptoms. Even high-risk
patients, such as those with atrial fibrillation or hypertension, fail to
recognize the signs of stroke. This delays activation of EMS and
treatment, resulting in increased morbidity and mortality.
Community and professional education is essential, and it has been
successful in increasing the proportion of eligible stroke patients treated
with fibrinolytic therapy. Healthcare providers, hospitals, and communities
must continue to develop systems to improve the efficiency and
effectiveness of stroke care.
Foundational Stroke Chain of Survival
Facts The goal of stroke care is to minimize brain injury and maximize the
patient’s recovery. The Stroke Chain of Survival (Figure 25) described
by the AHA and the American Stroke Association is similar to the Chain
of Survival for sudden cardiac arrest. It links actions to be taken by
patients, family members, and healthcare providers to maximize stroke
recovery. These links are

• Rapid recognition and reaction to stroke warning signs

• Rapid EMS dispatch
• Rapid EMS system transport and prearrival notification to the
receiving hospital
• Rapid diagnosis and treatment in the hospital

Figure 25. The Stroke Chain of Survival.

 Foundational The 8 D’s of Stroke Care
Facts The 8 D’s of Stroke Care highlight the major steps in diagnosis and
treatment of stroke and key points at which delays can occur:

• Detection: Rapid recognition of stroke symptoms

• Dispatch: Early activation and dispatch of EMS by 9-1-1
• Delivery: Rapid EMS identification, management, and transport
• Door: Appropriate triage to stroke center
• Data: Rapid triage, evaluation, and management within the ED
• Decision: Stroke expertise and therapy selection
• Drug/Device: Fibrinolytic or endovascular therapy
• Disposition: Rapid admission to the stroke unit or critical care unit

For more information on these critical elements, see the Adult

Suspected Stroke Algorithm (Figure 26).

Goals of The Suspected Stroke Algorithm (Figure 26) emphasizes important elements
Stroke of out-of-hospital care for possible stroke patients. These actions include a
Care stroke scale or screen and rapid transport to the hospital. As with ACS, prior
notification of the receiving hospital speeds the care of the stroke patient
upon arrival.
The NINDS has established critical in-hospital time goals for assessment
and management of patients with suspected stroke. This algorithm reviews
the critical in-hospital time periods for patient assessment and treatment:

1. Immediate general assessment by the stroke team, emergency

physician, or another expert within 10 minutes of arrival; order urgent
noncontrast CT scan
2. Neurologic assessment by the stroke team or designee and CT scan
performed within 25 minutes of hospital arrival
3. Interpretation of the CT scan within 45 minutes of ED arrival
4. Initiation of fibrinolytic therapy in appropriate patients (those without
contraindications) within 1 hour of hospital arrival and 3 hours from
symptom onset
5. Door-to-admission time of 3 hours

Foundational The National Institute of Neurological Disorders and Stroke

Facts The NINDS is a branch of the National Institutes of Health (NIH). Its
mission is to reduce the burden of neurologic disease by supporting and
conducting research. NINDS researchers have studied stroke and
reviewed data leading to recommendations for acute stroke care. The
NINDS has set critical time goals for assessment and management of
stroke patients based on experience obtained in large studies of stroke
patients.
Critical Patients with acute ischemic stroke have a time-dependent benefit for
Time fibrinolytic therapy similar to that of patients with ST-segment elevation MI,
Periods but this time-dependent benefit is much shorter.
The critical time period for administration of IV fibrinolytic therapy begins
with the onset of symptoms. Critical time periods from hospital arrival are
summarized below:
Immediate general assessment 10 minutes

Immediate neurologic assessment 25 minutes

Acquisition of CT of the head 25 minutes

Interpretation of the CT scan 45 minutes

Administration of fibrinolytic therapy, 60 minutes

timed from ED arrival

Administration of fibrinolytic therapy, 3 hours, or 4.5 hours

timed from onset of symptoms in selected patients

Administration of endovascular 6 hours in selected

therapy, timed from onset of symptoms patients

Admission to a monitored bed 3 hours

Figure 26. The Adult Suspected Stroke Algorithm.
Application of the We will now discuss the steps in the algorithm, as well as
Suspected Stroke other related topics:
Algorithm
• Identification of signs and symptoms of possible
stroke and activation of emergency response (Step
1)
• Critical EMS assessments and actions (Step 2)
• Immediate general assessment and stabilization
(Step 3)
• Immediate neurologic assessment by the stroke
team or designee (Step 4)
• CT scan: hemorrhage or no hemorrhage (Step 5)
• Fibrinolytic therapy risk stratification if candidate
(Steps 6, 8, and 10)
• General stroke care (Steps 11 and 12)

Identification of Signs of Possible Stroke

Warning Signs The signs and symptoms of a stroke may be subtle. They include
and Symptoms
• Sudden weakness or numbness of the face, arm, or leg,
especially on one side of the body
• Sudden confusion
• Trouble speaking or understanding
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking
• Dizziness or loss of balance or coordination
• Sudden severe headache with no known cause

Activate EMS Stroke patients and their families must be educated to activate EMS
System as soon as they detect potential signs or symptoms of stroke.
Immediately Currently half of all stroke patients are driven to the ED by family or
friends.
EMS provides the safest and most efficient method of emergency
transport to the hospital. The advantages of EMS transport include
the following:

• EMS personnel can identify and transport a stroke patient to a

hospital capable of providing acute stroke care and notify the
hospital of the patient’s impending arrival.
 • Prearrival notification allows the hospital to prepare to evaluate
and manage the patient efficiently.

Emergency medical dispatchers also play a critical role in timely

treatment of potential stroke by

• Identifying possible stroke patients

• Providing high-priority dispatch
• Instructing bystanders in lifesaving CPR skills or other supportive
care if needed while EMS providers are on the way

Stroke The AHA recommends that all EMS personnel be trained to recognize
Assessment stroke by using a validated, abbreviated out-of-hospital neurologic
Tools evaluation tool such as the Cincinnati Prehospital Stroke Scale
(CPSS) (Table 5).
Cincinnati Prehospital Stroke Scale
The CPSS identifies stroke on the basis of 3 physical findings:

• Facial droop (have the patient smile or try to show teeth)

• Arm drift (have the patient close eyes and hold both arms out,
with palms up)
• Abnormal speech (have the patient say, “You can’t teach an old
dog new tricks”)

By using the CPSS, medical personnel can evaluate the patient in

less than 1 minute. The presence of 1 finding on the CPSS has a
sensitivity of 59% and a specificity of 89% when scored by prehospital
providers.
With standard training in stroke recognition, paramedics
demonstrated a sensitivity of 61% to 66% for identifying patients with
stroke. After receiving training in use of a stroke assessment tool,
paramedic sensitivity for identifying patients with stroke increased to
86% to 97%.
Table 5. The Cincinnati Prehospital Stroke Scale
Test Findings
Facial droop: Have the patient Normal—both sides of face
show teeth or smile (Figure 27) move equally
Abnormal—one side of face
does not move as well as the
other side
 Arm drift: Patient closes eyes Normal—both arms move the
and extends both arms straight same or both arms do not move
out, with palms up, for 10 at all (other findings, such as
seconds (Figure 28) pronator drift, may be helpful)
Abnormal—one arm does not
move or one arm drifts down
compared with the other
Abnormal speech: Have Normal—patient uses correct
patient say, “you can’t teach an words with no slurring
old dog new tricks”
Abnormal—patient slurs words,
uses the wrong words, or is
unable to speak
Interpretation: If any 1 of these 3 signs is abnormal, the probability
of a stroke is 72%. The presence of all 3 findings indicates that the
probability of stroke is greater than 85%.
Modified from Kothari RU, Pancioli A, Liu T, Brott T, Broderick J.
Cincinnati Prehospital Stroke Scale: reproducibility and validity. Ann
Emerg Med. 1999;33(4):373-378. With permission from Elsevier.

Figure 27. Facial droop.

Figure 28. One-sided motor weakness (right arm).

Critical EMS Assessments and Actions

Introduction Prehospital EMS providers must minimize the interval between the
onset of symptoms and patient arrival in the ED. Specific stroke
therapy can be provided only in the appropriate receiving hospital
ED, so time in the field only delays (and may prevent) definitive
therapy. More extensive assessments and initiation of supportive
therapies can continue en route to the hospital or in the ED.

Critical EMS To provide the best outcome for the patient with potential stroke, do
Assessments the following:
and Actions Identify Signs Define and Recognize the Signs of Stroke
(Step 1)
 Support Support the ABCs and provide supplementary
ABCs oxygen to hypoxemic (eg, oxygen saturation
less than 94%) stroke patients or those patients
with unknown oxygen saturation.
Perform Perform a rapid out-of-hospital stroke
stroke assessment (CPSS, Table 5).
assessment
Establish time Determine when the patient was last known to
be normal or at neurologic baseline. This
represents time zero. If the patient wakes from
sleep with symptoms of stroke, time zero is the
last time the patient was seen to be normal.
Triage to Transport the patient rapidly and consider triage
stroke center to a stroke center. Support cardiopulmonary
function during transport. If possible, bring a
witness, family member, or caregiver with the
patient to confirm time of onset of stroke
symptoms.
Alert hospital Provide prearrival notification to the receiving
hospital.
Check During transport, check blood glucose if
glucose protocols or medical control allows.
The patient with acute stroke is at risk for respiratory compromise
from aspiration, upper airway obstruction, hypoventilation, and
(rarely) neurogenic pulmonary edema. The combination of poor
perfusion and hypoxemia will exacerbate and extend ischemic brain
injury, and it has been associated with worse outcome from stroke.
Both out-of-hospital and in-hospital medical personnel should
provide supplementary oxygen to hypoxemic (ie, oxygen saturation
less than 94%) stroke patients or patients for whom oxygen
saturation is unknown.
Foundational Stroke Centers and Stroke Units
Facts Initial evidence indicates a favorable benefit from triage of stroke
patients directly to designated stroke centers, but the concept of routine
out-of-hospital triage of stroke patients requires continued evaluation.
Each receiving hospital should define its capability for treating patients
with acute stroke and should communicate this information to the EMS
system and the community. Although not every hospital has the
resources to safely administer fibrinolytics or endovascular therapy,
every hospital with an ED should have a written plan that describes how
 patients with acute stroke will be managed in that institution. The plan
should

• Detail the roles of healthcare providers in the care of patients with

acute stroke, including identifying sources of neurologic expertise
• Define which patients to treat with fibrinolytics or endovascular
therapy at that facility
• Describe when patient transfer to another hospital with a dedicated
stroke unit is appropriate

Patients with stroke should be admitted to a stroke unit when a stroke

unit with a multidisciplinary team experienced in managing stroke is
available within a reasonable transport interval.
Studies have documented improvement in 1-year survival rate,
functional outcomes, and quality of life when patients hospitalized for
acute stroke receive care in a dedicated unit with a specialized team.

In-Hospital, Immediate General Assessment and Stabilization

Introduction Once the patient arrives in the ED, a number of assessments and
management activities must occur quickly. Protocols should be used
to minimize delay in definitive diagnosis and therapy.
The goal of the stroke team, emergency physician, or other
experts should be to assess the patient with suspected stroke
within 10 minutes of arrival in the ED: “time is brain” (Step 3).

Immediate ED providers should do the following:

General Step Actions
Assessment and
Assess ABCs Assess the ABCs and evaluate baseline vital
Stabilization signs.
Provide oxygen Provide supplementary oxygen to hypoxemic
(eg, oxyhemoglobin saturation less than 94%)
stroke patients or those patients with unknown
oxygen saturation.
Establish IV Establish IV access and obtain blood samples
access and for baseline blood count, coagulation studies,
obtain blood and blood glucose. Do not let this delay
samples obtaining a CT scan of the brain.
Check glucose Promptly treat hypoglycemia.
 Perform Perform a neurologic screening assessment.
neurologic Use the NIH Stroke Scale (NIHSS) or a similar
assessment tool.
Activate the Activate the stroke team or arrange
stroke team consultation with a stroke expert based on
predetermined protocols.
Order CT brain Order an emergent CT scan of the brain. Have
scan it read promptly by a qualified physician.
Obtain 12-lead Obtain a 12-lead ECG, which may identify a
ECG recent or ongoing AMI or arrhythmias (eg,
atrial fibrillation) as a cause of embolic stroke.
A small percentage of patients with acute
stroke or transient ischemic attack have
coexisting myocardial ischemia or other
abnormalities. There is general agreement to
recommend cardiac monitoring during the first
24 hours of evaluation in patients with acute
ischemic stroke to detect atrial fibrillation and
potentially life-threatening arrhythmias.
Life-threatening arrhythmias can follow or
accompany stroke, particularly intracerebral
hemorrhage. If the patient is hemodynamically
stable, treatment of non–life-threatening
arrhythmias (bradycardia, VT, and
atrioventricular [AV] conduction blocks) may
not be necessary.
Do not delay the CT scan to obtain the
ECG.

Immediate Neurologic Assessment by Stroke Team or Designee

Overview The stroke team, neurovascular consultant, or emergency physician
does the following:

• Reviews the patient’s history, performs a general physical

examination, and establishes time of symptom onset
• Performs a neurologic examination (eg, NIHSS)

The goal for neurologic assessment is within 25 minutes of the

patient’s arrival in the ED: “time is brain” (Step 4).
Establish Establishing the time of symptom onset may require interviewing out-
Symptom of-hospital providers, witnesses, and family members to determine
Onset the time the patient was last known to be normal.

Neurologic Assess the patient’s neurologic status by using one of the more
Examination advanced stroke scales. Following is an example:
National Institutes of Health Stroke Scale
The NIHSS uses 15 items to assess the responsive stroke patient.
This is a validated measure of stroke severity based on a detailed
neurologic examination. A detailed discussion is beyond the scope of
the ACLS Provider Course.

CT Scan: Hemorrhage or No Hemorrhage

Introduction A critical decision point in the assessment of the patient with acute
stroke is the performance and interpretation of a noncontrast CT
scan to differentiate ischemic from hemorrhagic stroke.
Assessment also includes identifying other structural abnormalities
that may be responsible for the patient’s symptoms or that
represent contraindication to fibrinolytic therapy. The initial
noncontrast CT scan is the most important test for a patient with
acute stroke.

• If a CT scan is not readily available, stabilize and promptly

transfer the patient to a facility with this capability.
• Do not give aspirin, heparin, or rtPA until the CT scan has
ruled out intracranial hemorrhage.

The CT scan should be completed within 25 minutes of the

patient’s arrival in the ED and should be read within 45
minutes from ED arrival: “time is brain” (Step 5).

Decision Point: Additional imaging techniques such as CT perfusion, CT

Hemorrhage or No angiography, or magnetic resonance imaging scans of patients
Hemorrhage with suspected stroke should be promptly interpreted by a
physician skilled in neuroimaging interpretation. Obtaining these
studies should not delay initiation of IV rtPA in eligible patients.
The presence of hemorrhage versus no hemorrhage determines
the next steps in treatment (Figures 29A and B).
Yes, Hemorrhage Is Present
If hemorrhage is noted on the CT scan, the patient is not a
candidate for fibrinolytics. Consult a neurologist or neurosurgeon.
Consider transfer for appropriate care (Step 7).
No, Hemorrhage Is Not Present
If the CT scan shows no evidence of hemorrhage and no sign of
other abnormality (eg, tumor, recent stroke), the patient may be a
candidate for fibrinolytic therapy (Steps 6 and 8).
If hemorrhage is not present on the initial CT scan and the patient
is not a candidate for fibrinolytics for other reasons, consider giving
aspirin (Step 9) either rectally or orally after performing a
swallowing screen (see below). Although aspirin is not a time-
critical intervention, it is appropriate to administer aspirin in the ED
if the patient is not a candidate for fibrinolysis. The patient must be
able to safely swallow before aspirin is given orally. Otherwise, use
the suppository form.
Figure 29. Occlusion in a cerebral artery by a thrombus. A, Area of infarction
surrounding immediate site and distal portion of brain tissue after occlusion. B, Area of
ischemic penumbra (ischemic, but not yet infarcted [dead] brain tissue) surrounding
areas of infarction. This ischemic penumbra is alive but dysfunctional because of altered
membrane potentials. The dysfunction is potentially reversible. Current stroke treatment
tries to keep the area of permanent brain infarction as small as possible by preventing
the areas of reversible brain ischemia in the penumbra from transforming into larger
areas of irreversible brain infarction.

Fibrinolytic Therapy
Introduction Several studies have shown a higher likelihood of good to excellent
functional outcome when rtPA is given to adults with acute ischemic
stroke within 3 hours of onset of symptoms, or within 4.5 hours of
onset of symptoms for selected patients. But these results are
obtained when rtPA is given by physicians in hospitals with a stroke
protocol that rigorously adheres to the eligibility criteria and
therapeutic regimen of the NINDS protocol. Evidence from
prospective randomized studies in adults also documents a greater
likelihood of benefit the earlier treatment begins.
The AHA and stroke guidelines recommend giving IV rtPA to
patients with acute ischemic stroke who meet the NINDS eligibility
criteria if it is given by

• Physicians using a clearly defined institutional protocol

• A knowledgeable interdisciplinary team familiar with stroke
care
• An institution with a commitment to comprehensive stroke care
and rehabilitation

The superior outcomes reported in both community and tertiary

care hospitals in the NINDS trials can be difficult to replicate in
hospitals with less experience in, and institutional commitment to,
acute stroke care. There is strong evidence to avoid all delays and
treat patients as soon as possible. Failure to adhere to protocol is
associated with an increased rate of complications, particularly risk
of intracranial hemorrhage.

Evaluate for If the CT scan is negative for hemorrhage, the patient may be a
Fibrinolytic candidate for fibrinolytic therapy. Immediately perform further
Therapy eligibility and risk stratification:

• If the CT scan shows no hemorrhage, the probability of acute

ischemic stroke remains. Review inclusion and exclusion
 criteria for IV fibrinolytic therapy (Table 6) and repeat the
neurologic exam(NIHSS or Canadian Neurological Scale).
• If the patient’s neurologic function is rapidly improving toward
normal, fibrinolytics may be unnecessary.

Table 6. Inclusion and Exclusion Characteristics of Patients

With Ischemic Stroke Who Could Be Treated With rtPA Within
3 Hours From Symptom Onset*
Inclusion Criteria
• Diagnosis of ischemic stroke causing measurable neurologic
deficit
• Onset of symptoms <3 hours before beginning treatment
• Age ≥18 years

Exclusion Criteria
• Significant head trauma or prior stroke in previous 3 months
• Symptoms suggest subarachnoid hemorrhage
• Arterial puncture at noncompressible site in previous 7 days
• History of previous intracranial hemorrhage
o – Intracranial neoplasm, arteriovenous malformation, or
aneurysm
o – Recent intracranial or intraspinal surgery
• Elevated blood pressure (systolic >185 mm Hg or diastolic
>110 mm Hg)
• Active internal bleeding
• Acute bleeding diathesis, including but not limited to
o – Platelet count <100 000/mm3
o – Heparin received within 48 hours, resulting in aPTT greater
than the upper limit of normal
o – Current use of anticoagulant with INR >1.7 or PT >15
seconds
o – Current use of direct thrombin inhibitors or direct factor Xa
inhibitors with elevated sensitive laboratory tests (such as
aPTT, INR, platelet count, and ECT; TT; or appropriate factor
Xa activity assays)
• Blood glucose concentration <50 mg/dL (2.7 mmol/L)
• CT demonstrates multilobar infarction (hypodensity >1/3
cerebral hemisphere)

Relative Exclusion Criteria

Recent experience suggests that under some circumstances—
with careful consideration and weighing of risk to benefit—
 patients may receive fibrinolytic therapy despite 1 or more relative
contraindications. Consider risk to benefit of rtPA administration
carefully if any one of these relative contraindications is present:

• Only minor or rapidly improving stroke symptoms (clearing

spontaneously)
• Pregnancy
• Seizure at onset with postictal residual neurologic impairments
• Major surgery or serious trauma within previous 14 days
• Recent gastrointestinal or urinary tract hemorrhage (within
previous 21 days)
• Recent acute myocardial infarction (within previous 3 months)

Notes

• The checklist includes some US FDA–approved indications

and contraindications for administration of rtPA for acute
ischemic stroke. Recent AHA/ASA guideline revisions may
differ slightly from FDA criteria. A physician with expertise in
acute stroke care may modify this list.
• Onset time is either witnessed or last known normal.
• In patients without recent use of oral anticoagulants or heparin,
treatment with rtPA can be initiated before availability of
coagulation study results but should be discontinued if INR is
>1.7 or PT is elevated by local laboratory standards.
• In patients without history of thrombocytopenia, treatment with
rtPA can be initiated before availability of platelet count but
should be discontinued if platelet count is <100 000/mm 3.

Abbreviations: aPTT, activated partial thromboplastin time; CT,

computed tomography; ECT, ecarin clotting time; FDA, Food and
Drug Administration; INR, international normalized ratio; PT,
prothrombin time; rtPA, recombinant tissue plasminogen activator;
TT, thrombin time.
*Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early
management of patients with acute ischemic stroke: a guideline for
healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. 2013;44(3):870-
947.

Potential As with all drugs, fibrinolytics have potential adverse effects. At this
Adverse Effects point, weigh the patient’s risk for adverse events against the
potential benefit and discuss with the patient and family.
 • Confirm that no exclusion criteria are present (Table 6).
• Consider risks and benefits.
• Be prepared to monitor and treat any potential complications.

The major complication of IV rtPA for stroke is intracranial

hemorrhage. Other bleeding complications may occur and may
range from minor to major. Angioedema and transient hypotension
may occur.

Patient Is a If the patient remains a candidate for fibrinolytic therapy (Step 8),
Candidate for discuss the risks and potential benefits with the patient or family if
Fibrinolytic available (Step 10). After this discussion, if the patient or family
Therapy members decide to proceed with fibrinolytic therapy, give the
patient rtPA. Begin your institution’s stroke rtPA protocol, often
called a “pathway of care.”
Do not administer anticoagulants or antiplatelet treatment for
24 hours after administration of rtPA, typically until a follow-up
CT scan at 24 hours shows no intracranial hemorrhage.

Extended IV rtPA Treatment of carefully selected patients with acute ischemic stroke
Window 3 to 4.5 with IV rtPA between 3 and 4.5 hours after onset of symptoms has
Hours also been shown to improve clinical outcome, although the degree
of clinical benefit is smaller than that achieved with treatment within
3 hours. Data supporting treatment in this time window come from a
large, randomized trial (ECASS-3 [European Cooperative Acute
Stroke Study]) that specifically enrolled patients between 3 and 4.5
hours after symptom onset, as well as a meta-analysis of prior
trials.
At present, use of IV rtPA within the 3- to 4.5-hour window has not
yet been approved by the US Food and Drug Administration (FDA),
although it is recommended by an AHA/American Stroke
Association science advisory. Administration of IV rtPA to patients
with acute ischemic stroke who meet the NINDS or ECASS-3
eligibility criteria (Table 7) is recommended if rtPA is administered
by physicians in the setting of a clearly defined protocol, a
knowledgeable team, and institutional commitment.
Table 7. Additional Inclusion and Exclusion Characteristics of
Patients With Acute Ischemic Stroke Who Could Be Treated
With IV rtPA Within 3 to 4.5 Hours From Symptom Onset*
Inclusion Criteria
 • Diagnosis of ischemic stroke causing measurable neurologic
deficit
• Onset of symptoms 3 to 4.5 hours before beginning treatment

Exclusion Criteria
• Age >80 years
• Severe stroke (NIHSS score >25)
• Taking an oral anticoagulant regardless of INR
• History of both diabetes and prior ischemic stroke

Abbreviations: INR, international normalized ratio; NIHSS, National

Institutes of Health Stroke Scale; rtPA, recombinant tissue
plasminogen activator.
*Del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr, American Heart
Association Stroke Council. Expansion of the time window for
treatment of acute ischemic stroke with intravenous tissue
plasminogen activator: a science advisory from the American Heart
Association/American Stroke Association. Stroke. 2009;40(8):2945-
2948.

Intra-arterial rtPA Improved outcome from use of cerebral intra-arterial rtPA has been
documented. For patients with acute ischemic stroke who are not
candidates for standard IV fibrinolysis, consider intra-arterial
fibrinolysis in centers with the resources and expertise to provide it
within the first 6 hours after onset of symptoms. Intra-arterial
administration of rtPA is not yet approved by the FDA.

Endovascular Therapy
Introduction Substantial new high-quality evidence regarding the clinical
efficacy of endovascular treatments of acute ischemic stroke
has recently become available. To this end, while IV rtPA
remains as the first-line treatment, the AHA now recommends
endovascular therapy for select patients with acute ischemic
stroke.
As with fibrinolytic therapy, patients must meet inclusion criteria
to be considered for this treatment. Similarly, better clinical
outcomes are associated with reduced times from symptom
onset to reperfusion, but these new treatment options offer the
added benefit of expanding the treatment window up to 6 hours
from the onset of symptoms.
Intra-arterial rtPA Improved outcomes from use of cerebral intra-arterial rtPA has
been documented. For patients with acute ischemic stroke who
are not candidates for standard IV fibrinolysis, consider intra-
arterial fibrinolysis in centers with the resources and expertise to
provide it within the first 6 hours after onset of symptoms. Intra-
arterial administration of rtPA has not yet been approved by the
FDA.

Mechanical Clot Mechanical clot disruption or retrieval with a stent has been
Disruption/Stent demonstrated to provide clinical benefit in selected patients with
Retrievers acute ischemic stroke.
Patients should receive endovascular therapy with a stent
retriever if they meet all the following criteria:

• Prestroke mRS score of 0 to 1

• Acute ischemic stroke receiving intravenous rtPA within 4.5
hours of onset according to guidelines from professional
medical societies
• Causative occlusion of the internal carotid artery or
proximal MCA (M1)
• Age 18 years or older
• NIHSS score of 6 or greater
• ASPECTS of 6 or greater
• Treatment can be initiated (groin puncture) within 6 hours of
symptom onset

Systems of Care Recent clinical trials suggest that all patients eligible for
endovascular therapy should be considered for this treatment in
addition to IV rtPA. Systems of care for acute ischemic stroke
need to be in place so that eligible patients can be quickly
transported to comprehensive stroke centers that offer these
treatments.

General Stroke Care

Introduction The general care of all patients with stroke includes the following:

• Begin stroke pathway.

• Support airway, breathing, and circulation.
 • Monitor blood glucose.
• Monitor blood pressure.
• Monitor temperature.
• Perform dysphagia screening.
• Monitor for complications of stroke and fibrinolytic therapy.
• Transfer to general intensive care if indicated.

Begin Stroke Admit patients to a stroke unit (if available) for careful observation
Pathway (Step 11), including monitoring of blood pressure and neurologic
status. If neurologic status worsens, order an emergent CT scan.
Determine if cerebral edema or hemorrhage is the cause; consult
neurosurgery as appropriate.
Additional stroke care includes support of the airway,
oxygenation, ventilation, and nutrition. Provide normal saline to
maintain intravascular volume (eg, approximately 75 to 100 mL/h)
if needed.

Monitor Blood Hyperglycemia is associated with worse clinical outcome in

Glucose patients with acute ischemic stroke. But there is no direct
evidence that active glucose control improves clinical outcome.
There is evidence that insulin treatment of hyperglycemia in other
critically ill patients improves survival rates. For this reason,
consider giving IV or subcutaneous insulin to lower blood glucose
in patients with acute ischemic stroke when the serum glucose
level is greater than 185 mg/dL.

Monitor for Prophylaxis for seizures is not recommended. But treatment of

Complications of acute seizures followed by administration of anticonvulsants to
Stroke and prevent further seizures is recommended. Monitor the patient for
Fibrinolytic signs of increased intracranial pressure. Continue to control blood
pressure to reduce the potential risk of bleeding.
Therapy

Hypertension Although management of hypertension in stroke patients is

Management in controversial, patients who are candidates for fibrinolytic therapy
rtPA Candidates should have their blood pressure controlled to lower the risk of
intracerebral hemorrhage after administration of rtPA. General
guidelines for the management of hypertension are outlined
in Table 8.
If a patient is eligible for fibrinolytic therapy, blood pressure must
be 185 mm Hg or less systolic and 110 mm Hg or less diastolic to
limit the risk of bleeding complications. Because the maximum
interval from onset of stroke until effective treatment of stroke with
rtPA is limited, most patients with sustained hypertension above
these levels will not be eligible for IV rtPA.
The management of arterial hypertension in patients not
undergoing reperfusion strategies remains challenging. Data to
guide recommendations for treatment are inconclusive or
conflicting. Many patients have spontaneous declines in blood
pressure during the first 24 hours after onset of stroke. Until more
definitive data are available, the benefit of treating arterial
hypertension in the setting of acute ischemic stroke is not well
established (Class IIb; Level of Evidence C).1 Patients who have
malignant hypertension or other medical indications for
aggressive treatment of blood pressure should be treated
accordingly (revised from the previous guideline).2
Table 8. Potential Approaches to Arterial Hypertension in
Acute Ischemic Stroke Patients Who Are Potential
Candidates for Acute Reperfusion Therapy*
Patient otherwise eligible for acute reperfusion therapy except
that blood pressure is >185/110 mm Hg:

• Labetalol 10-20 mg IV over 1-2 minutes, may repeat × 1

time, or
• Nicardipine IV 5 mg/h, titrate up by 2.5 mg/h every 5-15
minutes, maximum 15 mg/h; when desired blood pressure is
reached, adjust to maintain proper blood pressure limits, or
• Other agents (hydralazine, enalaprilat, etc) may be
considered when appropriate

If blood pressure is not maintained at or below 185/110 mm Hg,

do not administer rtPA. Management of blood pressure during
and after rtPA or other acute reperfusion therapy:

• Monitor blood pressure every 15 minutes for 2 hours from

the start of rtPA therapy, then every 30 minutes for 6 hours,
and then every hour for 16 hours.

If systolic blood pressure 180-230 mm Hg or diastolic blood

pressure 105-120 mm Hg:

• Labetalol 10 mg IV followed by continuous IV infusion 2-8

mg/min, or
 • Nicardipine IV 5 mg/h, titrate up to desired effect by 2.5 mg/h
every 5-15 minutes, maximum 15 mg/h

If blood pressure not controlled or diastolic blood pressure

>140 mm Hg, consider sodium nitroprusside.
*Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early
management of patients with acute ischemic stroke: a guideline
for healthcare professionals from the American Heart
Association/American Stroke
Association. Stroke. 2013;44(3):870-947.

Cardiac Arrest: VF/Pulseless VT Case

Introduction This case focuses on the assessment and actions used for a cardiac
arrest due to VF or pulseless VT that is refractory (unresponsive) to
the first shock.
In this case and during the course, you will have an opportunity to
demonstrate effective high-performance team behaviors while
performing the assessment and action skills. During the BLS
Assessment, team members will perform continuous high-quality
CPR with effective chest compressions and ventilation. The team
leader will conduct the Primary Assessment, including rhythm
recognition (shockable versus nonshockable), defibrillation using a
manual defibrillator, resuscitation drugs, a discussion of
IV/intraosseous (IO) access, and advanced airways.
The success of any resuscitation attempt is built on a strong base of
high-quality CPR and defibrillation when required by the patient’s
ECG rhythm. To improve care, leaders must assess the
performance of each system component. Only when performance is
evaluated can participants in a system effectively intervene to
improve care. This process of quality improvement consists of an
iterative and continuous cycle of

• Systematic evaluation of resuscitation care and outcome

• Benchmarking with stakeholder feedback
• Strategic efforts to address identified deficiencies

Another characteristic of high-quality CPR is minimal interruptions in

chest compressions. Studies demonstrate that healthcare providers
interrupt compressions far too often and for too long, in some cases
spending 25% to 50% of a resuscitation attempt without delivering
chest compressions.
Chest compression fraction (CCF) is the proportion of time during
cardiac arrest resuscitation when chest compressions are
performed. CCF should be as high as possible: at least 60% and
 ideally greater than 80%. Data suggest lower CCF is associated with
decreased ROSC and survival to hospital discharge.

Measurement Quality improvement relies on valid assessment of resuscitation

performance and outcome.

• The Utstein guidelines provide guidance for core performance

measures, including
o – Rate of bystander CPR
o – Time to defibrillation
o – Survival to hospital discharge
• It is important to share information among all links in the system
of care, including
o – Dispatch records
o – EMS patient care report
o – Hospital records

Benchmarking Data should be systematically reviewed and compared internally to

and Feedback prior performance and externally to similar systems. Existing
registries can facilitate this benchmarking effort. Examples include
the

• CARES for OHCA

• Get With The Guidelines®-Resuscitation program for IHCA

Change Simply measuring and benchmarking care can positively influence

outcome. However, ongoing review and interpretation are necessary
to identify areas for improvement, such as

• Citizen awareness
• Citizen and healthcare professional education and training
• Increased bystander CPR response rates
• Improved CPR performance
• Shortened time to defibrillation
Rhythms for VF/ This case involves these ECG rhythms:
Pulseless VT
• VF (example in Figure 30)
• VT
• ECG artifact that looks like VF
• New LBBB

Figure 30. Example of ventricular fibrillation.

Drugs for VF/ This case involves these drugs:

Pulseless VT
• Epinephrine
• Norepinephrine
• Amiodarone
• Lidocaine
• Magnesium sulfate
• Dopamine
• Oxygen
• Other medications, depending on the cause of the
VT/pulseless VT arrest

Managing VF/Pulseless VT: The Adult Cardiac Arrest Algorithm

Overview The Adult Cardiac Arrest Algorithm (Figure 31) is the most important
algorithm to know for adult resuscitation. This algorithm outlines all
assessment and management steps for the pulseless patient who does not
initially respond to BLS interventions, including a first shock from an AED.
The algorithm consists of the 2 pathways for a cardiac arrest:

• A shockable rhythm (VF/pulseless VT) displayed on the left side of the

algorithm
• A nonshockable rhythm (asystole/PEA) displayed on the right side of
the algorithm
Throughout the case discussion of the Cardiac Arrest Algorithm, we will refer
to Steps 1 through 12. These are the numbers assigned to the steps in the
algorithm.
Figure 31. The Adult Cardiac Arrest Algorithm.
VF/pVT (Left Because many patients with sudden cardiac arrest demonstrate VF at
Side) some point in their arrest, it is likely that ACLS providers will
frequently follow the left side of the Cardiac Arrest Algorithm (Figure
31). Rapid treatment of VF according to this sequence is the best
approach to restoring spontaneous circulation.
Pulseless VT is included in the algorithm because it is treated as VF.
VF and pulseless VT require CPR until a defibrillator is available.
Both are treated with high-energy unsynchronized shocks.

Asystole/PEA The right side of the algorithm outlines the sequence of actions to
(Right Side) perform if the rhythm is nonshockable. You will have an opportunity to
practice this sequence in the Asystole and PEA Cases.

Summary The VF/Pulseless VT Case gives you the opportunity to practice

performing rapid treatment of VF/pVT by following the steps on the
left side of the Cardiac Arrest Algorithm (Steps 1 through 8).

Application of the Adult Cardiac Arrest Algorithm: VF/pVT Pathway

Introduction This case discusses the assessment and treatment of a patient
with refractory VF or pulseless VT. This algorithm assumes that
healthcare providers have completed the BLS Assessment,
including activation of the emergency response system,
performing CPR, attaching the manual defibrillator, and delivering
the first shock (Steps 1 through 4).
The ACLS high-performance team now intervenes and conducts
the Primary Assessment. In this case, the team assesses the
patient and takes actions as needed. The team leader
coordinates the efforts of the high-performance team as they
perform the steps listed in the VF/pVT pathway on the left side of
the Cardiac Arrest Algorithm.

Minimal A team member should continue to perform high-quality CPR

Interruption of until the defibrillator arrives and is attached to the patient. The
Chest team leader assigns roles and responsibilities and organizes
Compressions interventions to minimize interruptions in chest compressions.
This accomplishes the most critical interventions for VF or
pulseless VT: CPR with minimal interruptions in chest
compressions and defibrillation during the first minutes of arrest.
 The AHA does not recommend continued use of an AED (or the
automatic mode) when a manual defibrillator is available and the
provider’s skills are adequate for rhythm interpretation. Rhythm
analysis and shock administration with an AED may result in
prolonged interruptions in chest compressions.
Figure 32 demonstrates the need to minimize interruptions in
compressions. CPP is aortic relaxation (“diastolic”) pressure
minus right atrial relaxation (“diastolic”) pressure. During CPR,
CPP correlates with both myocardial blood flow and ROSC. In 1
human study, ROSC did not occur unless a CPP 15 mm Hg or
greater was achieved during CPR.

Figure 32. Relationship of quality CPR to coronary perfusion pressure (CPP)

demonstrating the need to minimize interruptions in compressions.
Foundational Resume CPR While Manual Defibrillator Is Charging
Facts
• Shortening the interval between the last compression and the shock
by even a few seconds can improve shock success (defibrillation and
ROSC). Thus, it is reasonable for healthcare providers to practice
efficient coordination between CPR and defibrillation to minimize the
hands-off interval between stopping compressions and administering
the shock.
• For example, after verifying a shockable rhythm and initiating the
charging sequence on the defibrillator, another provider should
resume chest compressions and continue until the defibrillator is fully
charged. The defibrillator operator should deliver the shock as soon
as the compressor removes his or her hands from the patient’s chest
and all providers are “clear” of contact with the patient.
• Use of a multimodal defibrillator in manual mode may reduce the
duration of chest compression interruption required for rhythm
analysis compared with automatic mode but could increase the
frequency of inappropriate shock. Individuals who are not comfortable
interpreting cardiac rhythms can continue to use an AED.
 • For an AED, follow the device’s prompts or know your device-specific
manufacturer’s recommendations.
• It is important that healthcare providers be knowledgeable of how
their defibrillator operates, and if possible, limit pauses in chest
compressions to rhythm analysis and shock delivery.

Deliver 1 Shock Step 3 directs you to deliver 1 shock. The appropriate energy dose is
determined by the identity of the defibrillator—monophasic or
biphasic. See the column on the right of the algorithm.
If you are using a monophasic defibrillator, give a single 360-J shock.
Use the same energy dose for subsequent shocks.
Biphasic defibrillators use a variety of waveforms, each of which is
effective for terminating VF over a specific dose range. When using
biphasic defibrillators, providers should use the manufacturer’s
recommended energy dose (eg, initial dose of 120 to 200 J). Many
biphasic defibrillator manufacturers display the effective energy dose
range on the face of the device. If you do not know the effective dose
range, deliver the maximal energy dose for the first and all
subsequent shocks.
If the initial shock terminates VF but the arrhythmia recurs later in the
resuscitation attempt, deliver subsequent shocks at the previously
successful energy level.
Immediately after the shock, resume CPR, beginning with chest
compressions. Give 2 minutes of CPR.

Purpose of Defibrillation does not restart the heart. Defibrillation stuns the heart
Defibrillation and briefly terminates all electrical activity, including VF and pVT. If
the heart is still viable, its normal pacemakers may eventually resume
electrical activity (return of spontaneous rhythm) that ultimately results
in a perfusing rhythm (ROSC).
In the first minutes after successful defibrillation, however, any
spontaneous rhythm is typically slow and may not create pulses or
adequate perfusion. The patient needs CPR (beginning with chest
compressions) for several minutes until adequate heart function
resumes. Moreover, not all shocks will lead to successful defibrillation.
This is why it is important to resume high-quality CPR, beginning with
chest compressions immediately after a shock.

Principle of The interval from collapse to defibrillation is one of the most important
Early determinants of survival from cardiac arrest. Early defibrillation is
Defibrillation
 critical for patients with sudden cardiac arrest for the following
reasons:

• A common initial rhythm in out-of-hospital witnessed sudden

cardiac arrest is VF. Pulseless VT rapidly deteriorates to VF.
When VF is present, the heart quivers and does not pump blood.
• Electrical defibrillation is the most effective way to treat VF
(delivery of a shock to stop the VF).
• The probability of successful defibrillation decreases quickly over
time.
• VF deteriorates to asystole if not treated.

The earlier defibrillation occurs, the higher the survival rate. When VF
is present, CPR can provide a small amount of blood flow to the heart
and brain but cannot directly restore an organized rhythm. The
likelihood of restoring a perfusing rhythm is optimized with immediate
CPR and defibrillation within a few minutes of the initial arrest (Figure
33).
For every minute that passes between collapse and defibrillation, the
chance of survival from a witnessed VF sudden cardiac arrest
declines by 7% to 10% per minute if no bystander CPR is
provided.3 When bystanders perform CPR, the decline is more
gradual and averages 3% to 4% per minute.3-6 CPR performed early
can double3,7 or triple8 survival from witnessed sudden cardiac arrest
at most defibrillation intervals.
Lay rescuer AED programs increase the likelihood of early CPR and
attempted defibrillation. This helps shorten the time between collapse
and defibrillation for a greater number of patients with sudden cardiac
arrest.

Figure 33. Relationship between survival from ventricular fibrillation sudden cardiac
arrest and time from collapse to defibrillation.
Foundational Clearing for Defibrillation
Facts To ensure safety during defibrillation, always announce the shock
warning. State the warning firmly and in a forceful voice before
delivering each shock (this entire sequence should take less than 5
seconds):

• “Clear. Shocking.”
o – Check to make sure you are clear of contact with the patient, the
stretcher, or other equipment.
o – Make a visual check to ensure that no one is touching the patient
or stretcher.
o – Be sure oxygen is not flowing across the patient’s chest.
• When pressing the shock button, the defibrillator operator should
face the patient, not the machine. This helps to ensure coordination
with the chest compressor and to verify that no one resumed contact
with the patient.

You do not need to use these exact words, but you must warn others
that you are about to deliver shocks and that everyone must stand clear
of the patient.

Resume • Immediately resume CPR, beginning with chest compressions.

CPR • Do not perform a rhythm or pulse check at this point unless the patient
is showing signs of life or advanced monitoring indicates ROSC.
• Establish IV/IO access.

The Guidelines recommend that healthcare providers tailor the sequence of

rescue actions based on the presumed etiology of the arrest. Moreover,
ACLS providers functioning within a high-performance team can choose the
optimal approach for minimizing interruptions in chest compressions (thereby
improving chest compression fraction). Use of different protocols, such as 3
cycles of 200 continuous compressions with passive oxygen insufflation and
airway adjuncts, compression-only CPR in the first few minutes after arrest,
and continuous chest compressions with asynchronous ventilation once
every 6 seconds with the use of a bag-mask device, are a few examples of
optimizing CCF and high-quality CPR. A default compression-to-ventilation
ratio of 30:2 should be used by less-trained healthcare providers or if 30:2 is
the established protocol. Figure 34 shows the progression from lay rescuers
to highly trained and proficient healthcare providers.
Figure 34. Progression from lay rescuers to highly trained healthcare providers for CPR
delivery.

Rhythm Check Conduct a rhythm check after 2 minutes of CPR. Be careful to

minimize interruptions in chest compressions.
The pause in chest compressions to check the rhythm should
not exceed 10 seconds.

• If a nonshockable rhythm is present and the rhythm is organized,

a team member should try to palpate a pulse. If there is any
doubt about the presence of a pulse, immediately resume CPR.

Remember: Perform a pulse check—preferably during rhythm

analysis—only if an organized rhythm is present.

• If the rhythm is organized and there is a palpable pulse, proceed

to post–cardiac arrest care.
• If the rhythm check reveals a nonshockable rhythm and there is
no pulse, proceed along the asystole/PEA pathway on the right
side of the Cardiac Arrest Algorithm (Steps 9 through 11).
• If the rhythm check reveals a shockable rhythm, give 1 shock and
resume CPR immediately for 2 minutes after the shock (Step 6).

Self-Adhesive The AHA recommends routine use of self-adhesive pads. Using

Pads conductive materials (gel pads or self-adhesive pads) during the
 defibrillation attempt reduces transthoracic impedance, or the
resistance that chest structures have on electrical current.

Shock and For persistent VF/pulseless VT, give 1 shock and resume CPR
Vasopressors immediately for 2 minutes after the shock.
Immediately after the shock, resume CPR, beginning with chest
compressions. Give 2 minutes of CPR.
When IV/IO access is available, give epinephrine during CPR after
the second shock as follows:

• Epinephrine 1 mg IV/IO—repeat every 3 to 5 minutes

Note: If additional team members are available, they should anticipate

the need for drugs and prepare them in advance.
Epinephrine hydrochloride is used during resuscitation primarily for
its α-adrenergic effects, ie, vasoconstriction. Vasoconstriction
increases cerebral and coronary blood flow during CPR by increasing
mean arterial pressure and aortic diastolic pressure. In previous
studies, escalating and high-dose epinephrine administration did not
improve survival to discharge or neurologic outcome after
resuscitation from cardiac arrest.
No known vasopressor (epinephrine) increases survival from
VF/pulseless VT. Because these medications can improve aortic
diastolic blood pressure, coronary artery perfusion pressure, and the
rate of ROSC, the AHA continues to recommend their use.
FYI 2015 Vasopressin
Guidelines Vasopressin has been removed from the 2015 AHA Guidelines Update
for CPR and ECC.
The 2015 AHA Guidelines Update for CPR and ECC states that
“vasopressin offers no advantage as a substitute for epinephrine in
cardiac arrest.” As such, it has been removed from the 2015 updated
Adult Cardiac Arrest Algorithm.

Rhythm Check Conduct a rhythm check after 2 minutes of CPR. Be careful to

minimize interruptions in chest compressions.
Interruption in compressions to conduct a rhythm analysis
should not exceed 10 seconds.

• If a nonshockable rhythm is present and the rhythm is

organized, a team member should try to palpate a pulse. If
there is any doubt about the presence of a pulse,
immediately resume CPR.
 • If the rhythm check is organized and there is a palpable
pulse, proceed to post–cardiac arrest care.
• If the rhythm check reveals a nonshockable rhythm and there
is no pulse, proceed along the asystole/PEA pathway on the
right side of the Cardiac Arrest Algorithm (Steps 9 through
11).
• If the rhythm check reveals a shockable rhythm, resume
chest compressions if indicated while the defibrillator is
charging (Step 8). The team leader is responsible for team
safety while compressions are being performed and the
defibrillator is charging.

Shock and Give 1 shock and resume CPR beginning with chest
Antiarrhythmics compressions for 2 minutes immediately after the shock.
Healthcare providers may consider giving antiarrhythmic drugs,
either before or after the shock. Research is still lacking on the
effect of antiarrhythmic drugs given during cardiac arrest on
survival to hospital discharge. If administered, amiodarone is the
first-line antiarrhythmic agent given in cardiac arrest because it
has been clinically demonstrated that it improves the rate of
ROSC and hospital admission in adults with refractory
VF/pulseless VT.

• Amiodarone 300 mg IV/IO bolus, then consider an additional

150 mg IV/IO once
o – Amiodarone is considered a class III antiarrhythmic drug,
but it possesses electrophysiologic characteristics of the
other classes. Amiodarone blocks sodium channels at rapid
pacing frequencies (class I effect) and exerts a
noncompetitive antisympathetic action (class II effect). One
of the main effects of prolonged amiodarone administration is
lengthening of the cardiac action potential (class III effect).

If amiodarone is not available, providers may administer lidocaine.

• Lidocaine 1 to 1.5 mg/kg IV/IO first dose, then 0.5 to 0.75

mg/kg IV/IO at 5- to 10-minute intervals, to a maximum dose
of 3 mg/kg
o – Lidocaine suppresses automaticity of conduction tissue in
the heart, by increasing the electrical stimulation threshold of
the ventricle, His-Purkinje system, and spontaneous
depolarization of the ventricles during diastole by a direct
action on the tissues.
 o – Lidocaine blocks permeability of the neuronal membrane
to sodium ions, which results in inhibition of depolarization
and the blockade of conduction.

Providers should consider magnesium sulfate for torsades de

pointes associated with a long QT interval.

• Magnesium sulfate for torsades de pointes, loading dose 1

to 2 g IV/IO diluted in 10 mL (eg, D5W, normal saline) given
as IV/IO bolus, typically over 5 to 20 minutes
o – Magnesium can be classified as a sodium/potassium
pump agonist.
o – Magnesium has several electrophysiological effects,
including suppression of atrial L- and T-type calcium
channels, and ventricular after-depolarizations.

Routine administration of magnesium sulfate in cardiac arrest is

not recommended unless torsades de pointes is present.
Search for and treat any treatable underlying cause of cardiac
arrest. See the column on the right of the algorithm. See Table
4 in Part 4 for more information on the H’s and T’s.

Cardiac Arrest The Adult Cardiac Arrest Circular Algorithm (Figure 35)
Treatment summarizes the recommended sequence of CPR, rhythm checks,
Sequences shocks, and delivery of drugs based on expert consensus. The
optimal number of cycles of CPR and shocks required before
starting pharmacologic therapy remains unknown. Note that
rhythm checks and shocks are organized around 5 cycles of
compressions and ventilations, or 2 minutes if a provider is timing
the arrest.
Figure 35. The Adult Cardiac Arrest Circular Algorithm. Do not delay shock. Continue
CPR while preparing and administering drugs and charging the defibrillator. Interrupt
chest compressions only for the minimum amount of time required for ventilation (until
advanced airway placed), rhythm check, and actual shock delivery.

Physiologic The AHA recommends using quantitative waveform capnography in

Monitoring intubated patients to monitor CPR quality (Figure 36), optimize chest
During CPR compressions, and detect ROSC during chest compressions (Figure
37). Although placement of invasive monitors during CPR is not
generally warranted, physiologic parameters such as intra-arterial
relaxation pressures (Figures 36A and B) and central venous oxygen
saturation (SCVO2), when available, may also be helpful for
optimizing CPR and detecting ROSC.
Animal and human studies indicate that PETCO2, CPP, and
SCVO2 monitoring provides valuable information on both the patient’s
condition and the response to therapy. Most important, PETCO2,
CPP, and SCVO2correlate with cardiac output and myocardial blood
flow during CPR. When chest compressions fail to achieve identified
threshold values, ROSC is rarely achieved. Furthermore, an abrupt
increase in any of these parameters is a sensitive indicator of ROSC
that can be monitored without interrupting chest compressions.
Although no clinical study has examined whether titrating
resuscitative efforts to physiologic parameters improves outcome, it is
reasonable to use these parameters, if available, to optimize
compressions and guide vasopressor therapy during cardiac arrest.
End-Tidal CO2
The main determinant of PETCO2 during CPR is blood delivery to the
lungs. Persistently low PETCO2 values less than 10 mm Hg during
CPR in intubated patients (Figure 36B) suggest that ROSC is
unlikely. If PETCO2 abruptly increases to a normal value of 35 to 40
mm Hg, it is reasonable to consider this an indicator of ROSC.

• If the PETCO2 is less than 10 mm Hg during CPR, it is

reasonable to try to improve chest compressions and
vasopressor therapy.

Coronary Perfusion Pressure or Arterial Relaxation

Pressure
Increased CPP correlates with both myocardial blood flow and
ROSC. A reasonable surrogate for CPP during CPR is arterial
relaxation (“diastolic”) pressure, which can be measured by using an
intra-arterial catheter.

• If the arterial relaxation pressure is less than 20 mm Hg (Figure

36B), it is reasonable to try to improve chest compressions and
vasopressor therapy.

Central Venous Oxygen Saturation

If oxygen consumption, arterial oxygen saturation, and hemoglobin
are constant, changes in SCVO2 reflect changes in oxygen delivery
due to changes in cardiac output. SCVO2 can be measured
continuously by using oximetric tipped central venous catheters
placed in the superior vena cava or pulmonary artery. Normal range
is 60% to 80%.

• If the SCVO2 is less than 30%, it is reasonable to try to improve

chest compressions and vasopressor therapy.
Figure 36. Physiologic monitoring during CPR. A, High-quality compressions are shown
through waveform capnography and intra-arterial relaxation pressure. PETCO2 values
less than 10 mm Hg in intubated patients or intra-arterial relaxation pressures less than
20 mm Hg indicate that cardiac output is inadequate to achieve ROSC. In either of
those cases, it is reasonable to consider trying to improve quality of CPR by optimizing
chest compression parameters or giving a vasopressor or both. B, Ineffective CPR
compressions shown through intra-arterial relaxation pressure and waveform
capnography.

Figure 37. Waveform capnography during CPR with ROSC. This capnography tracing
displays PETCO2 in millimeters of mercury on the vertical axis over time. This patient is
intubated and receiving CPR. Note that the ventilation rate is approximately 10/min.
Chest compressions are given continuously at a rate slightly faster than 100/min but are
not visible with this tracing. The initial PETCO2 is less than 12.5 mm Hg during the first
minute, indicating very low blood flow. PETCO2 increases to between 12.5 and 25 mm
Hg during the second and third minutes, consistent with the increase in blood flow with
ongoing resuscitation. ROSC occurs during the fourth minute. ROSC is recognized by
the abrupt increase in PETCO2 (visible just after the fourth vertical line) to greater than
50 mm Hg, which is consistent with a substantial improvement in blood flow.

Treatment of Defibrillation is appropriate for the cardiac arrest patient in VF/pVT

VF/pVT in who has severe hypothermia and a body temperature of less than
Hypothermia 30°C (less than 86°F). If the patient does not respond to the initial
shock, it is reasonable to perform additional defibrillation attempts
according to the usual BLS guidelines while engaging in active
rewarming. The hypothermic patient may have a reduced rate of
drug metabolism, raising concern that drug levels may accumulate
to toxic levels with standard dosing regimens. Although the
evidence does not support the use of antiarrhythmic drug therapy in
hypothermic patients in cardiac arrest, it is reasonable to consider
administration of a vasopressor according to the standard ACLS
algorithm concurrent with rewarming strategies.
ACLS treatment of the patient with severe hypothermia in cardiac
arrest in the hospital should be aimed at rapid core rewarming.
For patients in cardiac arrest with moderate hypothermia (30°C to
34°C [86°F to 93.2°F]), start CPR, attempt defibrillation, give
medications spaced at longer intervals, and, if in hospital, provide
active core rewarming.
Routes of Access for Drugs
Priorities Priorities during cardiac arrest are high-quality CPR and early
defibrillation. Insertion of an advanced airway and drug administration
are of secondary importance. No drug given during cardiac arrest has
been studied adequately to show improved survival to hospital
discharge or improved neurologic function after cardiac arrest.
Historically in ACLS, providers have administered drugs either via the
IV or ET route. ET absorption of drugs is poor and optimal drug
dosing is not known. For this reason, the IV or IO route is preferred.

Intravenous A peripheral IV is preferred for drug and fluid administration unless

Route central line access is already available.
Central line access is not necessary during most resuscitation
attempts. Central line access may cause interruptions in CPR and
complications during insertion, including vascular laceration,
hematomas, and bleeding. Insertion of a central line in a
noncompressible vessel is a relative (not absolute) contraindication to
fibrinolytic therapy in patients with ACS.
Establishing a peripheral line does not require interruption of CPR.
Drugs, however, typically require 1 to 2 minutes to reach the central
circulation when given by the peripheral IV route.
If a drug is given by the peripheral venous route, administer it as
follows:

• Give the drug by bolus injection unless otherwise specified.

• Follow with a 20-mL bolus of IV fluid.
• Elevate the extremity for about 10 to 20 seconds to facilitate
delivery of the drug to the central circulation.

Intraosseous Drugs and fluids during resuscitation can be delivered safely and
Route effectively via the IO route if IV access is not available. Important
points about IO access are

• IO access can be established in all age groups.

• IO access often can be achieved in 30 to 60 seconds.
• The IO route of administration is preferred over the ET route and
may be easier to establish in cardiac arrest.
• Any ACLS drug or fluid that is administered IV can be given IO.

IO cannulation provides access to a noncollapsible marrow venous

plexus, which serves as a rapid, safe, and reliable route for
 administration of drugs, crystalloids, colloids, and blood during
resuscitation. The technique uses a rigid needle, preferably a
specially designed IO or bone marrow needle from an IO access kit.

For more information on IO access, see the Access for

Medications section on the Student Website
(www.heart.org/eccstudent).

Endotracheal IV and IO administration routes are preferred over the ET

Route administration route. When considering administration of drugs via the
ET route during CPR, keep these concepts in mind:

• The optimal dose of most drugs given by the ET route is

unknown.
• The typical dose of drugs administered via the ET route is 2 to
2½ times the IV route.
• CPR will need to be stopped transiently so drug does not
regurgitate up the ET tube.

Studies demonstrate that epinephrine, vasopressin, and lidocaine are

absorbed into the circulatory system after administration via the ET
route. When giving drugs via the ET route, dilute the dose in 5 to 10
mL of sterile water or normal saline. Inject the drug directly into the ET
tube.

Fluid Healthcare providers should titrate fluid administration and vasoactive

Administration or inotropic agents as needed to optimize blood pressure, cardiac
output, and systemic perfusion. The optimal post–cardiac arrest blood
pressure remains unknown; however, a mean arterial pressure 65
mm Hg or greater is a reasonable goal.
In hypovolemic patients, the ECF volume is typically restored with
normal saline or lactated Ringer’s solution. Avoid D5W because it will
reduce serum sodium too rapidly. Serum electrolytes should be
appropriately monitored.

Vasopressors
Introduction While there is evidence that the use of vasopressors favors initial
resuscitation with ROSC, research is still lacking on the effect of
the routine use of vasopressors at any stage during management
of cardiac arrest on the rates of survival to hospital discharge.
Vasopressors Vasopressors optimize cardiac output and blood pressure. The
Used During vasopressor used during cardiac arrest is
Cardiac Arrest
• Epinephrine: 1 mg IV/IO (repeat every 3 to 5 minutes)

If IV/IO access cannot be established or is delayed, give

epinephrine 2 to 2.5 mg diluted in 5 to 10 mL of sterile water or
normal saline and injected directly into the ET tube. Remember,
the ET route of drug administration results in variable and
unpredictable drug absorption and blood levels.

Epinephrine Although healthcare providers have used epinephrine for years in

resuscitation, few studies have been conducted to address the
question of whether it improves outcome in humans. Epinephrine
administration improves ROSC and hospital admission rates;
however, large studies have not been conducted to evaluate
whether survival is improved. Because there are no large studies
to confirm longer-term outcome, we rely on the positive short-term
effects of increased ROSC and increased hospital admission to
support the use in cardiac arrest. No studies demonstrate
improved rates of survival to hospital discharge or neurologic
outcome when comparing standard epinephrine doses with initial
high-dose or escalating-dose epinephrine. Therefore, the AHA
does not recommend the routine use of high-dose or escalating
doses of epinephrine.
Epinephrine is thought to stimulate adrenergic receptors,
producing vasoconstriction, increasing blood pressure and heart
rate, and improving perfusion pressure to the brain and heart.
Repeat epinephrine 1 mg IV/IO every 3 to 5 minutes during
cardiac arrest.
Remember, follow each dose given by peripheral injection
with a 20-mL flush of IV fluid and elevate the extremity above
the level of the heart for 10 to 20 seconds.

Antiarrhythmic Agents
Introduction As with vasopressors, research is still lacking on the effect of routine
antiarrhythmic drug administration during human cardiac arrest and
survival to hospital discharge. Amiodarone, however, has been
shown to increase short-term survival to hospital admission when
compared with placebo or lidocaine.
Amiodarone • Consider amiodarone for treatment of VF or pulseless VT
unresponsive to shock delivery, CPR, and a vasopressor.
• Amiodarone is a complex drug that affects sodium, potassium,
and calcium channels. It also has α-adrenergic and β-
adrenergic blocking properties.
• During cardiac arrest, consider amiodarone 300 mg IV/IO push
for the first dose. If VF/pulseless VT persists, consider giving a
second dose of 150 mg IV/IO in 3 to 5 minutes.

Lidocaine • Lidocaine is an alternative antiarrhythmic of long-standing and

widespread familiarity. However, it has no proven short-term or
long-term efficacy in cardiac arrest. Providers may consider
giving lidocaine when amiodarone is not available.
• The initial lidocaine dose is 1 to 1.5 mg/kg IV/IO. Repeat if
indicated at 0.5 to 0.75 mg/kg IV/IO over 5- to 10-minute
intervals to a maximum of 3 mg/kg.
• If no IV/IO access is available, the dose for ET administration is
2 to 4 mg/kg.

Magnesium • IV magnesium may terminate or prevent recurrent torsades de

Sulfate pointes in patients who have a prolonged QT interval during
normal sinus rhythm. When VF/pulseless VT cardiac arrest is
associated with torsades de pointes, give magnesium sulfate at
a loading dose of 1 to 2 g IV/IO diluted in 10 mL (eg, D5W,
normal saline) given over 5 to 20 minutes. If a prearrest 12-lead
ECG is available for review, check the QT interval for
prolongation.
• Remember that pulseless VT is treated with an immediate high-
energy shock, whereas magnesium is an adjunctive agent used
to prevent recurrent or treat persistent VT associated with
torsades de pointes.
• Magnesium sulfate is also indicated for patients with known or
suspected low serum magnesium, such as patients with
alcoholism or other conditions associated with malnutrition or
hypomagnesemic states. For patients in refractory VF/pulseless
VT, check the patient’s history, if available, for one of these
conditions that suggests the presence of a reversible electrolyte
abnormality.
Steroids in • The use of steroids in cardiac arrest has been assessed in both
Cardiac Arrest the out-of-hospital and in-hospital settings. In IHCA, steroids
were combined with a vasopressor bundle or cocktail of
epinephrine and vasopressin.
• In an initial randomized controlled trial (RCT) involving 100
IHCA patients, the use of a combination of methylprednisolone,
vasopressin, and epinephrine during cardiac arrest and
hydrocortisone after ROSC for those with shock significantly
improved survival to hospital discharge compared with the use
of only epinephrine and placebo.9 In a subsequent study
published in 2013,10 136 in 268 patients with IHCA, the same
combination of methylprednisolone, vasopressin, and
epinephrine during cardiac arrest (and hydrocortisone in those
with post-ROSC shock), significantly improved the survival to
discharge with good neurologic outcome compared with only
epinephrine and placebo.
• The same 2 RCTs provided evidence that the use of
methylprednisolone and vasopressin in addition to epinephrine
improved ROSC rates compared with the use of placebo and
epinephrine alone.
• In OHCA, steroids have been evaluated in 1 RCT 11 and 1
observational study.12 In these studies, steroids were not
bundled as they were in the IHCA but studied as a sole
treatment. When dexamethasone was given during cardiac
arrest, it did not improve survival to hospital discharge or ROSC
or survival to discharge, as compared with placebo. The
observational study showed no benefit in survival to discharge
but did show an association of improved ROSC with
hydrocortisone compared with no hydrocortisone.
• In light of the data presented, no recommendation can be made
on the routine use of steroids alone in IHCA. However, the
combination of intra-arrest vasopressin, epinephrine, and
methylprednisolone and postarrest hydrocortisone may be
considered for IHCA patients.
• For OHCA patients, use of steroids during CPR is of uncertain
benefit.

Respiratory or • In the United States in 2013, 16 235 people died of prescription

Cardiac Arrest opioid toxicity, and an additional 8257 died of heroin
Associated With overdose.13,14 In the United States in 2012, opioid overdose
Opioid Overdose became the leading cause of unintentional injurious death in
 people aged 25 to 60 years, accounting for more deaths than
motor vehicle collisions.15 A majority of these deaths are
associated with prescription opioids. Statistics are similar in
Canada.16
• Isolated opioid toxicity is associated with central nervous
system (CNS) and respiratory depression that can progress to
respiratory and cardiac arrest. Most opioid deaths involve the
coingestion of multiple drugs or medical and mental health
comorbidities.17-20 In addition, methadone and propoxyphene
can cause torsades de pointes, and cardiotoxicity has been
reported with other opioids.21-27 Except in specific clinical
settings (eg, unintended opioid overdose during a medical
procedure), rescuers cannot be certain that the patient’s clinical
condition is due to opioid-induced CNS and respiratory
depression toxicity alone.
• Naloxone is a potent opioid receptor antagonist in the brain,
spinal cord, and GI system. Naloxone has an excellent safety
profile and can rapidly reverse CNS and respiratory depression
in a patient with an opioid-associated resuscitative emergency.
Based on the rescuer’s training and clinical circumstance,
naloxone can be administered intravenously,28-
31 intramuscularly,28,29,32 intranasally,30,32-36 or subcutaneously37;

nebulized for inhalation38,39; or instilled into the bronchial tree

via ET tube.40
• For patients with known or suspected opioid overdose who are
in respiratory arrest, healthcare providers should give naloxone
as soon as it is available. It may be given at a dose of 2 mg IN
or 0.4 mg IM/IV, which may be repeated every 4 minutes if
necessary. Figure 38 shows the algorithm for opioid overdose.
While this algorithm was designed for lay rescuers, ACLS
providers will follow the ACLS systematic approach, which
includes a pulse check.
Figure 38. The Opioid-Associated Life-Threatening (Adult) Emergency Algorithm.
Extracorporeal CPR (for VF/Pulseless VT/Asystole/PEA)
Extracorporeal Extracorporeal CPR (ECPR) refers to venoarterial extracorporeal
Membrane membrane oxygenation during cardiac arrest, including
Oxygenation extracorporeal membrane oxygenation and cardiopulmonary
bypass. These techniques require adequate vascular access and
specialized equipment. The use of ECPR may allow providers
additional time to treat reversible underlying causes of cardiac
arrest (eg, acute coronary artery occlusion, PE, refractory VF,
profound hypothermia, cardiac injury, myocarditis,
cardiomyopathy, congestive heart failure, drug intoxication) or
serve as a bridge for LV assist device implantation or cardiac
transplantation.
While there are currently no data from RCTs on the use of ECPR
for cardiac arrest, evidence reviewed for the 2015 AHA Guidelines
Update for CPR and ECC suggests a benefit to survival and
favorable neurologic outcome with the use of ECPR when
compared with conventional CPR in patients with refractory
cardiac arrest.
In settings where ECPR can be rapidly implemented,
providers may consider its use among select cardiac arrest
patients with potentially reversible causes of cardiac arrest
who have not responded to initial conventional CPR.

Ultrasound (for VF/Pulseless VT/Asystole/PEA)

Ultrasound Ultrasound may be applied to patients receiving CPR to help assess
Use in Cardiac myocardial contractility and to help identify potentially treatable causes
Arrest of cardiac arrest, such as hypovolemia, pneumothorax, pulmonary
thromboembolism, or pericardial tamponade. However, it is unclear
whether important clinical outcomes are affected by the routine use of
ultrasound among patients experiencing cardiac arrest. If a qualified
sonographer is present and use of ultrasound does not interfere with
the standard cardiac arrest treatment protocol, then ultrasound may be
considered as an adjunct to standard patient evaluation.

Cardiac Arrest: Pulseless Electrical Activity Case

Introduction This case focuses on assessment and management of a cardiac arrest
patient with PEA. During the BLS Assessment, high-performance team
members will demonstrate high-quality CPR with effective chest
compressions and ventilation with a bag-mask device. In the Primary
Assessment, the team leader will recognize PEA and implement the
appropriate interventions outlined in the Cardiac Arrest Algorithm.
Because correction of an underlying cause of PEA, if present and
 identified, is critical to patient outcome, the team leader will verbalize the
differential diagnosis while leading the high-performance team in the
search for and treatment of reversible causes.

Rhythms for You will need to recognize the following rhythms:

PEA
• Rate—too fast or too slow
• Width of QRS complexes—wide versus narrow

Drugs for This case involves these drugs:

PEA
• Epinephrine
• Other medications, depending on the cause of the PEA arrest

Description of PEA
Introduction PEA encompasses a heterogeneous group of rhythms that are
organized or semiorganized but lack a palpable pulse. PEA includes

• Idioventricular rhythms
• Ventricular escape rhythms
• Postdefibrillation idioventricular rhythms
• Sinus rhythm
• Other

Any organized* rhythm without a pulse is defined as PEA. Even sinus

rhythm without a detectable pulse is called PEA. Pulseless rhythms that
are excluded by definition include VF, pVT, and asystole.
*An organized rhythm consists of QRS complexes that are similar in
appearance from beat to beat (ie, each has a uniform QRS
configuration). Organized rhythms may have narrow or wide QRS
complexes, they may occur at rapid or slow rates, they may be regular
or irregular, and they may or may not produce a pulse.

Historical Previously, high-performance teams used the term electromechanical

Perspective dissociation (EMD) to describe patients who displayed electrical activity
on the cardiac monitor but lacked apparent contractile function because
of an undetectable pulse. That is, weak contractile function is present—
 detectable by invasive monitoring or echocardiography—but the cardiac
function is too weak to produce a pulse or effective cardiac output. This
is the most common initial condition present after successful
defibrillation. PEA also includes other conditions where the heart is
empty because of inadequate preload. In this case, the contractile
function of the heart is adequate, but there is inadequate volume for the
ventricle to eject. This may occur as a result of severe hypovolemia, or
as a result of decreased venous return from PE or pneumothorax.

Managing PEA: The Adult Cardiac Arrest Algorithm

Overview As described earlier, the Cardiac Arrest Algorithm consists of 2
cardiac arrest pathways (Figure 39). The left side of the algorithm
outlines treatment for a shockable rhythm (VF/ pVT). The right
side of the algorithm (Steps 9 through 11) outlines treatment for a
nonshockable rhythm (asystole/PEA). Because of the similarity in
causes and management, the Cardiac Arrest Algorithm combines
the asystole and PEA pathways, although we will review these
rhythms in separate cases. In both pathways, therapies are
organized around periods (2 minutes) of uninterrupted, high-
quality CPR.
The ability to achieve a good resuscitation outcome with return of
a perfusing rhythm and spontaneous respirations depends on the
ability of the high-performance team to provide effective CPR and
to identify and correct a cause of PEA if present.
Everyone on the high-performance team must carry out the steps
outlined in the algorithm and at the same time focus on the
identification and treatment of reversible causes of the arrest.

The PEA Pathway In this case, the patient is in cardiac arrest. High-performance
of the Cardiac team members initiate and perform high-quality CPR throughout
Arrest Algorithm the BLS Assessment and the Primary and Secondary
Assessments. The team interrupts CPR for 10 seconds or less for
rhythm and pulse checks. This patient has an organized rhythm
on the monitor but no pulse. The condition is PEA (Step 9). Chest
compressions resume immediately. The team leader now directs
the team in the steps outlined in the PEA pathway of the Cardiac
Arrest Algorithm (Figure 39), beginning with Step 10.
IV/IO access is a priority over advanced airway management
unless bag-mask ventilation is ineffective or the arrest is caused
by hypoxia. All high-performance team members must
simultaneously conduct a search for an underlying and treatable
cause of the PEA in addition to performing their assigned roles.
Decision Point: Conduct a rhythm check and give 2 minutes of CPR after
Rhythm Check administration of the drugs. Be careful to minimize interruptions in
chest compressions.
The pause in CPR to conduct a rhythm check
should not exceed 10 seconds.

Administer • Give epinephrine as soon as IV/IO access becomes

Epinephrine available.
o – Epinephrine 1 mg IV/IO—repeat every 3 to 5 minutes

Administer drugs during CPR. Do not stop CPR to

administer drugs.

• Consider advanced airway and capnography.

Nonshockable • If no electrical activity is present (asystole), go back to Step

Rhythm 10.
• If organized electrical activity is present, try to palpate a
pulse. Take at least 5 seconds but do not take more than 10
seconds to check for a pulse.
• If no pulse is present, or if there is any doubt about the
presence of a pulse, immediately resume CPR for 2 minutes,
starting with chest compressions. Go back to Step 10 and
repeat the sequence.
• If a palpable pulse is present and the rhythm is organized,
begin post–cardiac arrest care.
Figure 39. The Adult Cardiac Arrest Algorithm.
Decision Point: • If the rhythm check reveals a shockable rhythm, resume CPR
Shockable Rhythm with chest compressions while the defibrillator is charging if
possible.
• Switch to the left side of the algorithm and perform steps
according to the VF/pVT sequence starting with Step 5 or 7.

Asystole and PEA Figure 39 summarizes the recommended sequence of CPR,

Treatment rhythm checks, and delivery of drugs for PEA and asystole based
Sequences on expert consensus.

Identification and Treatment of PEA is not limited to the interventions outlined in the
Correction of algorithm. Healthcare providers should attempt to identify and
Underlying Cause correct an underlying cause if present. Healthcare providers must
stop, think, and ask, “Why did this person have this cardiac arrest
at this time?” It is essential to search for and treat reversible
causes of PEA for resuscitative efforts to be potentially
successful. Use the H’s and T’s to recall conditions that could
have contributed to PEA.
Critical Common Underlying Causes of PEA
Concepts Hypovolemia and hypoxia are the 2 most common underlying and
potentially reversible causes of PEA. Be sure to look for evidence of these
problems as you assess the patient.

Cardiac Arrest: Asystole Case

Introduction In this case, the patient is in cardiac arrest. High-performance team
members initiate and perform high-quality CPR throughout the BLS
Assessment and the Primary and Secondary Assessments. The team
interrupts CPR for 10 seconds or less for a rhythm check. This patient
has no pulse and the rhythm on the monitor is asystole. Chest
compressions resume immediately. The team leader now directs the
team in the steps outlined in the asystole pathway of the Cardiac Arrest
Algorithm (Figure 31 in the section Managing VF/Pulseless VT: The
Adult Cardiac Arrest Algorithm), beginning with Step 10.
IV/IO access is a priority over advanced airway management unless
bag-mask ventilation is ineffective or the arrest is caused by hypoxia.
 All high-performance team members must simultaneously conduct a
search for an underlying and treatable cause of the asystole in addition
to performing their assigned roles.
At the end of this case, the team will discuss the criteria for terminating
resuscitative efforts; in some cases, we must recognize that the patient
is dead and that it would be more appropriate to direct efforts to
supporting the family.

Rhythms for You will need to recognize the following rhythms:

Asystole
• Asystole (example in Figure 40)
• Slow PEA terminating in bradyasystolic rhythm

Figure 40. Example of asystole.

Drugs for This case involves these drugs:

Asystole
• Epinephrine
• Other medications, depending on the cause of the asystole
arrest

Approach to Asystole
Introduction Asystole is a cardiac arrest rhythm associated with no discernible
electrical activity on the ECG (also referred to as flat line). You should
confirm that the flat line on the monitor is indeed “true asystole” by
validating that the flat line is

• Not another rhythm (eg, fine VF) masquerading as a flat line

• Not the result of an operator error

Foundational Asystole and Technical Problems

Facts
 Asystole is a specific diagnosis, but flat line is not. The term flat line is
nonspecific and can result from several possible conditions, including
absence of cardiac electrical activity, lead or other equipment failure,
and operator error. Some defibrillators and monitors signal the operator
when a lead or other equipment failure occurs. Some of these problems
are not applicable to all defibrillators.
For a patient with cardiac arrest and asystole, quickly rule out any other
causes of an isoelectric ECG, such as

• Loose leads or leads not connected to the patient or

defibrillator/monitor
• No power
• Signal gain (amplitude/signal strength) too low

Patients During the BLS, Primary, and Secondary Assessments, you should be
With DNAR aware of reasons to stop or withhold resuscitative efforts. Some of these
Orders are

• Rigor mortis
• Indicators of do-not-attempt-resuscitation (DNAR) status (eg,
bracelet, anklet, written documentation)
• Threat to safety of providers

Out-of-hospital providers need to be aware of EMS-specific policies and

protocols applicable to these situations. In-hospital providers and high-
performance teams should be aware of advance directives or specific
limits to resuscitation attempts that are in place. That is, some patients
may consent to CPR and defibrillation but not to intubation or invasive
procedures. Many hospitals will record this in the medical record.

Asystole as Often, asystole represents the final rhythm. Cardiac function has
an End diminished until electrical and functional cardiac activity finally stop and
Point the patient dies. Asystole is also the final rhythm of a patient initially in VF
or pVT.
Prolonged efforts are unnecessary and futile unless special resuscitation
situations exist, such as hypothermia and drug overdose. Consider
stopping if ETCO2 is less than 10 after 20 minutes of CPR.
Managing Asystole
Overview The management of asystole consists of the following
components:

• Implementing the steps in the Cardiac Arrest Algorithm

• Identifying and correcting underlying causes
• Terminating efforts as appropriate

Adult Cardiac As described in the VF/Pulseless VT and PEA Cases, the Cardiac
Arrest Algorithm Arrest Algorithm consists of 2 pathways (Figures 31 and 39). The
left side of the algorithm outlines treatment for a shockable rhythm
(VF/pulseless VT). The right side of the algorithm (Steps 9
through 11) outlines treatment for a nonshockable rhythm
(asystole/PEA). In both pathways, therapies are designed around
periods (2 minutes) of uninterrupted, high-quality CPR. In this
case, we will focus on the asystole component of the
asystole/PEA pathway.

Identification and Treatment of asystole is not limited to the interventions outlined in

Correction of the algorithm. Healthcare providers should attempt to identify and
Underlying Cause correct an underlying cause if present. Healthcare providers must
stop, think, and ask, “Why did this person have this cardiac arrest
at this time?” It is essential to search for and treat reversible
causes of asystole for resuscitative efforts to be potentially
successful. Use the H’s and T’s to recall conditions that could
have contributed to asystole.

Application of the Adult Cardiac Arrest Algorithm: Asystole Pathway

Introduction In this case, you have a patient in cardiac arrest. High-quality
CPR is performed throughout the BLS, Primary, and Secondary
Assessments. Interrupt CPR for 10 seconds or less while you
perform a rhythm check. You interpret the rhythm on the monitor
as asystole. CPR beginning with chest compressions for 2
minutes resumes immediately. You now conduct the steps
outlined in the asystole pathway of the Cardiac Arrest Algorithm
beginning with Step 9. At the same time, you are searching for a
possible underlying cause of the asystole.
Confirmed Asystole Give priority to IV/IO access. Do not interrupt CPR while
establishing IV or IO access.

Administer • Continue high-quality CPR, and as soon as IV/IO access is

Epinephrine available, give epinephrine as follows:
o – Epinephrine 1 mg IV/IO—repeat every 3 to 5 minutes

Administer drugs during CPR. Do not stop CPR to

administer drugs.

• Consider advanced airway and capnography.

Decision Point: Check the rhythm after 2 minutes of CPR.

Rhythm Check Interruption of chest compressions to conduct a
rhythm check should not exceed 10 seconds.

Nonshockable • If no electrical activity is present (asystole), go back to Step

Rhythm 10 or 11.
• If electrical activity is present and organized, try to palpate a
pulse.
• If no pulse is present or if there is any doubt about the
presence of a pulse, continue CPR, starting with chest
compressions for 2 minutes. Go back to Step 10 and repeat
the sequence.
• If a good pulse is present and the rhythm is
organized, begin post–cardiac arrest care.

Shockable Rhythm If the rhythm check reveals a shockable rhythm, prepare to

deliver a shock (resuming chest compressions during charging if
appropriate). Refer to the left side of the algorithm and perform
steps according to the VF/pVT sequence, starting with Step 5 or
7.
Asystole and PEA The diagram in Figure 39 (the Cardiac Arrest Algorithm)
Treatment summarizes the recommended sequence of CPR, rhythm
Sequences checks, and delivery of drugs for PEA and asystole based on
expert consensus.

TCP Not Several randomized controlled trials failed to show benefit from
Recommended attempted TCP for asystole. The AHA does not recommend the
use of TCP for patients with asystolic cardiac arrest.

Routine Shock There is no evidence that attempting to “defibrillate” asystole is

Administration Not beneficial. In one study, the group that received shocks had a
Recommended trend toward worse outcome. Given the importance of minimizing
interruption of chest compressions, there is no justification for
interrupting chest compressions to deliver a shock to patients
with asystole.

When in Doubt If it is unclear whether the rhythm is fine VF or asystole, an initial

attempt at defibrillation may be warranted. Fine VF may be the
result of a prolonged arrest. At this time, the benefit of delaying
defibrillation to perform CPR before defibrillation is unclear. EMS
system medical directors may consider implementing a protocol
that allows EMS responders to provide CPR while preparing for
defibrillation of patients found by EMS personnel to be in VF.

Terminating Resuscitative Efforts

Terminating In- If healthcare providers cannot rapidly identify an underlying cause
Hospital and the patient does not respond to the BLS and ACLS
Resuscitative interventions, termination of all resuscitative efforts should be
Efforts considered.
The decision to terminate resuscitative efforts rests with the
treating physician in the hospital and is based on consideration of
many factors, including

• Time from collapse to CPR

• Time from collapse to first defibrillation attempt
• Comorbid disease
• Prearrest state
• Initial arrest rhythm
• Response to resuscitative measures
 • ETCO2 less than 10 after 20 minutes of CPR

None of these factors alone or in combination is clearly predictive

of outcome. However, the duration of resuscitative efforts is an
important factor associated with poor outcome. The chance that
the patient will survive to hospital discharge and be neurologically
intact diminishes as resuscitation time increases. Stop the
resuscitation attempt when you determine with a high degree of
certainty that the patient will not respond to further ACLS and
ECPR is not indicated or not available.

Terminating Out- Continue out-of-hospital resuscitative efforts until one of the

of-Hospital following occurs:
Resuscitative
Efforts • Restoration of effective, spontaneous circulation and
ventilation
• Transfer of care to a senior emergency medical professional
• The presence of reliable criteria indicating irreversible death
• The healthcare provider is unable to continue because of
exhaustion or dangerous environmental hazards or because
continued resuscitation places the lives of others in jeopardy
• A valid DNAR order is presented
• Online authorization from the medical control physician or by
prior medical protocol for termination of resuscitation

Duration of The final decision to stop resuscitative efforts can never be as

Resuscitative simple as an isolated time interval. If ROSC of any duration
Efforts occurs, it may be appropriate to consider extending the
resuscitative effort.
Experts have developed clinical rules to assist in decisions to
terminate resuscitative efforts for in-hospital and out-of-hospital
arrests. You should familiarize yourself with the established policy
or protocols for your hospital or EMS system.
Continue out-of-hospital resuscitative efforts until one of the
following occurs:

• Restoration of effective, spontaneous circulation and

ventilation
• Transfer of care to a senior emergency medical professional
• The presence of reliable criteria indicating irreversible death
 • The rescuer is unable to continue because of exhaustion or
dangerous environmental hazards or because continued
resuscitation places the lives of others in jeopardy
• A valid DNAR order is presented
• Online authorization from the medical control physician or by
prior medical protocol for termination of resuscitation

It may also be appropriate to consider other issues, such as drug

overdose and severe prearrest hypothermia (eg, submersion in
icy water) when deciding whether to extend resuscitative efforts.
Special resuscitation interventions and prolonged resuscitative
efforts may be indicated for patients with hypothermia, drug
overdose, or other potentially reversible causes of arrest.

Asystole: An You will see asystole most frequently in 2 situations:

Agonal Rhythm?
• As a terminal rhythm in a resuscitation attempt that started
with another rhythm
• As the first rhythm identified in a patient with unwitnessed or
prolonged arrest

Persistent asystole represents extensive myocardial ischemia

and damage from prolonged periods of inadequate coronary
perfusion. Prognosis is poor unless a special resuscitation
circumstance or immediately reversible cause is present. Survival
from asystole is better for in-hospital than for out-of-hospital
arrests according to data from Get With The Guidelines®-
Resuscitation, formerly the National Registry of CPR
(www.heart.org/resuscitation).

Ethical The high-performance team must make a conscientious and

Considerations competent effort to give patients “a trial of CPR and ACLS,”
provided the patient had not expressed a decision to forego
resuscitative efforts and the victim is not obviously dead (eg, rigor
mortis, decomposition, hemisection, decapitation) (see the DNAR
discussion on the Student Website). The final decision to stop
resuscitative efforts can never be as simple as an isolated time
interval.

See Human, Ethical, and Legal Dimensions of CPR on the

Student Website (www.heart.org/eccstudent).
Transport of Emergency medical response systems should not require field
Patients in Cardiac personnel to transport every patient in cardiac arrest back to a
Arrest hospital or to an ED. Transportation with continuing CPR is
justified if interventions available in the ED cannot be performed
in the out-of-hospital setting and they are indicated for special
circumstances (ie, cardiopulmonary bypass or extracorporeal
circulation for patients with severe hypothermia).
After OHCA with ROSC, transport the patient to an appropriate
hospital with a comprehensive post–cardiac arrest treatment
system of care that includes acute coronary interventions,
neurologic care, critical care, and hypothermia. Transport the in-
hospital post–cardiac arrest patient to an appropriate critical care
unit capable of providing comprehensive post–cardiac arrest
care.

Bradycardia Case
Introduction This case discusses assessment and management of a patient with
symptomatic bradycardia (heart rate less than 50/min).
The cornerstones of managing bradycardia are to

• Differentiate between signs and symptoms that are caused by the

slow rate versus those that are unrelated
• Correctly diagnose the presence and type of AV block
• Use atropine as the drug intervention of first choice
• Decide when to initiate transcutaneous pacing (TCP)
• Decide when to start epinephrine or dopamine to maintain heart
rate and blood pressure
• Know when to call for expert consultation about complicated
rhythm interpretation, drugs, or management decisions

In addition, you must know the techniques and cautions for using TCP.

Rhythms for This case involves these ECG rhythms:

Bradycardia
• Sinus bradycardia
• First-degree AV block
• Second-degree AV block
o – Type I (Wenckebach/Mobitz I)
o – Type II (Mobitz II)
• Third-degree AV block
You should know the major AV blocks because important treatment
decisions are based on the type of block present (Figure 41). Complete
AV block is generally the most important and clinically significant
degree of block. Also, complete or third-degree AV block is the degree
of block most likely to cause cardiovascular collapse and require
immediate pacing. Recognition of a symptomatic bradycardia due to
AV block is a primary goal. Recognition of the type of AV block is a
secondary goal.
Figure 41. Examples of AV block. A, Sinus bradycardia with borderline first-degree AV
block. B, Second-degree AV block type I. C, Second-degree AV block type
II. D,Complete AV block with a ventricular escape pacemaker (wide QRS: 0.12 to 0.14
second). E, Third-degree AV block with a junctional escape pacemaker (narrow QRS:
less than 0.12 second).
Drugs for Bradycardia This case involves these drugs:

• Atropine
• Dopamine (infusion)
• Epinephrine (infusion)

Description of Bradycardia
Definitions Definitions used in this case are as follows:
Term Definition
Bradyarrhythmia or Any rhythm disorder with a heart rate less
bradycardia* than 60/min—eg, third-degree AV block—or
sinus bradycardia. When bradycardia is the
cause of symptoms, the rate is generally
less than 50/min.
Symptomatic Signs and symptoms due to the slow heart
bradyarrhythmia rate
*For the purposes of this case, we will use the
term bradycardia interchangeably with bradyarrhythmiaunless
specifically defined.

Symptomatic Sinus bradycardia may have multiple causes. Some are physiologic
Bradycardia and require no assessment or therapy. For example, a well-trained
athlete may have a heart rate in the range of 40 to 50/min or
occasionally lower.
In contrast, some patients have heart rates in the normal sinus range,
but these heart rates are inappropriate or insufficient for them. This is
called a functional or relative bradycardia. For example, a heart rate of
70/min may be relatively too slow for a patient in cardiogenic or septic
shock.
This case will focus on the patient with a bradycardia and heart rate
less than 50/min. Key to the case management is the determination of
symptoms or signs due to the decreased heart rate. A symptomatic
bradycardia exists clinically when 3 criteria are present:

1. The heart rate is slow.

2. The patient has symptoms.
3. The symptoms are due to the slow heart rate.
Signs and You must perform a focused history and physical examination to
Symptoms identify the signs and symptoms of a bradycardia.
Symptoms include chest discomfort or pain, shortness of breath,
decreased level of consciousness, weakness, fatigue, light-
headedness, dizziness, and presyncope or syncope.
Signs include hypotension, drop in blood pressure on standing
(orthostatic hypotension), diaphoresis, pulmonary congestion on
physical examination or chest x-ray, frank congestive heart failure or
PE, and bradycardia-related (escape) frequent premature ventricular
complexes or VT.

Managing Bradycardia: The Bradycardia Algorithm

Overview of The Adult Bradycardia With a Pulse Algorithm (Figure 42) outlines the
the steps for assessment and management of a patient presenting with
Algorithm symptomatic bradycardia with pulse. Implementation of this algorithm
begins with the identification of bradycardia (Step 1); the heart rate is
less than 50/min. First steps include the components of the BLS
Assessment and the Primary Assessment, such as supporting
circulation and airway management, giving oxygen if indicated,
monitoring the rhythm and vital signs, establishing IV access, and
obtaining a 12-lead ECG if available (Step 2). In the differential
diagnosis, you determine if the patient has signs or symptoms of poor
perfusion and if these are caused by the bradycardia (Step 3).
The primary decision point in the algorithm is the determination of
adequate perfusion. If the patient has adequate perfusion, you observe
and monitor (Step 4). If the patient has poor perfusion, you administer
atropine (Step 5). If atropine is ineffective, prepare for TCP or consider
dopamine or epinephrine infusion (Step 5). If indicated, you prepare for
transvenous pacing, search for and treat contributing causes, and seek
expert consultation (Step 6).
The treatment sequence in the algorithm is determined by the severity of
the patient’s condition. You may need to implement multiple
interventions simultaneously. If cardiac arrest develops, go to the
Cardiac Arrest Algorithm.
Figure 42. The Adult Bradycardia With a Pulse Algorithm.

Application of the Bradycardia Algorithm

Introduction In this case, you have a patient presenting with symptoms of
bradycardia. You conduct appropriate assessment and
interventions as outlined in the Bradycardia Algorithm. At the
same time, you are searching for and treating possible
contributing factors.
Identification of Identify whether the bradycardia is
Bradycardia
• Present by definition, ie, heart rate less than 50/min
• Inadequate for the patient’s condition (functional or relative)

Primary Next, perform the Primary Assessment, including the following:

Assessment A Maintain patent airway.
B Assist breathing as needed; give oxygen in case of
hypoxemia; monitor oxygen saturation.
C Monitor blood pressure and heart rate; obtain and review a
12-lead ECG; establish IV access.
D Conduct a problem-focused history and physical
examination; search for and treat possible contributing
factors.

Are Signs or Step 3 prompts you to consider if the signs or symptoms of poor
Symptoms Caused perfusion are caused by the bradycardia.
by Bradycardia? The key clinical questions are

• Are there “serious” signs or symptoms?

• Are the signs and symptoms related to the slow heart rate?

Look for adverse signs and symptoms of the bradycardia:

• Symptoms (eg, chest discomfort, shortness of breath,

decreased level of consciousness, weakness, fatigue, light-
headedness, dizziness, presyncope or syncope)
• Signs (eg, hypotension, congestive heart failure, ventricular
arrhythmias related to the bradycardia)

Sometimes the “symptom” is not due to the bradycardia. For

example, hypotension associated with bradycardia may be due
to myocardial dysfunction rather than the bradycardia. Keep this
in mind when you reassess the patient’s response to treatment.

Critical Bradycardia
Concepts The key clinical question is whether the bradycardia is causing the
patient’s symptoms or some other illness is causing the bradycardia.
Decision You must now decide if the patient has adequate or poor perfusion.
Point:
Adequate • If the patient has adequate perfusion, observe and monitor (Step
Perfusion? 4).
• If the patient has poor perfusion, proceed to Step 5.

Treatment If the patient has poor perfusion secondary to bradycardia, the

Sequence treatment sequence is as follows:
Summary Give atropine as first-line Atropine 0.5 mg IV—may repeat to a
treatment total dose of 3 mg
If atropine is ineffective
Transcutaneous or Dopamine 2 to 20 mcg/kg per minute
pacing (chronotropic or heart rate dose)
Epinephrine 2 to 10 mcg/min
The treatment sequence is determined by the severity of the patient’s
clinical presentation. For patients with symptomatic bradycardia, move
quickly through this sequence. These patients may be “pre–cardiac
arrest” and may need multiple interventions simultaneously.
Avoid relying on atropine in type II second-degree or third-degree AV
block or in patients with third-degree AV block with a new wide QRS
complex where the location of the block is likely to be in infranodal
tissue (such as in the bundle of His or more distal conduction system).
These bradyarrhythmias are not likely to be responsive to reversal of
cholinergic effects by atropine and are preferably treated with TCP or β-
adrenergic support as temporizing measures while the patient is
prepared for transvenous pacing. Atropine administration should not
delay implementation of external pacing or β-adrenergic infusion for
patients with impending cardiac arrest.
Although not a first-line agent for treatment of symptomatic bradycardia,
a β-adrenergic infusion (ie, dopamine, epinephrine) is an alternative
when a bradyarrhythmia is unresponsive to, or inappropriate for,
treatment with atropine, or as a temporizing measure while the patient
is prepared for transvenous pacing.
No known vasopressor (epinephrine) increases survival from
bradycardia. Because these medications can improve aortic diastolic
 blood pressure, coronary artery perfusion pressure, and the rate of
ROSC, the AHA continues to recommend their use.
Alternative drugs may also be appropriate in special circumstances
such as the overdose of a β-blocker or calcium channel blocker.
Healthcare providers should not wait for a maximum dose of atropine if
the patient is presenting with second-degree or third-degree block;
rather, they may move to a second-line treatment after 2 to 3 doses of
atropine.

Treatment In the absence of immediately reversible causes, atropine remains the

Sequence: first-line drug for acute symptomatic bradycardia. Atropine sulfate acts
Atropine by reversing cholinergic-mediated decreases in the heart rate and AV
node conduction. Dopamine and epinephrine may be successful as an
alternative to TCP.
For bradycardia, give atropine 0.5 mg IV every 3 to 5 minutes to a total
dose of 0.04 mg/ kg (maximum total dose of 3 mg). Atropine doses of
less than 0.5 mg may paradoxically result in further slowing of the heart
rate.
Use atropine cautiously in the presence of acute coronary ischemia or
MI. An atropinemediated increase in heart rate may worsen ischemia or
increase infarct size.
Do not rely on atropine in Mobitz type II second-degree or third-degree
AV block or in patients with third-degree AV block with a new wide QRS
complex.

Treatment TCP may be useful for treatment of symptomatic bradycardia. TCP is

Sequence: noninvasive and can be performed by ACLS providers.
Pacing Healthcare providers should consider immediate pacing in unstable
patients with high-degree heart block when IV access is not available. It
is reasonable for healthcare providers to initiate TCP in unstable
patients who do not respond to atropine.
After initiation of pacing, confirm electrical and mechanical capture.
Because heart rate is a major determinant of myocardial oxygen
consumption, set the pacing rate to the lowest effective rate based on
clinical assessment and symptom resolution. Reassess the patient for
symptom improvement and hemodynamic stability. Give analgesics and
sedatives for pain control. Note that many of these drugs may further
decrease blood pressure and affect the patient’s mental status. Try to
identify and correct the cause of the bradycardia.
Some limitations apply. TCP can be painful and may not produce
effective electrical and mechanical capture. If symptoms are not caused
by the bradycardia, pacing may be ineffective despite capture. Because
 TCP is painful and not as reliable as transvenous pacing, it should be
considered as an emergent bridge to transvenous pacing in patients
with significant sinus bradycardia or AV block.
If you chose TCP as the second-line treatment and it is also ineffective
(eg, inconsistent capture), begin an infusion of dopamine or
epinephrine and prepare for possible transvenous pacing by obtaining
expert consultation.
Foundational Sedation and Pacing
Facts Most conscious patients should be given sedation before pacing. If the
patient is in cardiovascular collapse or rapidly deteriorating, it may be
necessary to start pacing without prior sedation, particularly if drugs for
sedation are not immediately available. The clinician must evaluate the
need for sedation in light of the patient’s condition and need for
immediate pacing. A review of the drugs used is beyond the scope of
the ACLS Provider Course. The general approach could include the
following:

• Give parenteral benzodiazepine for anxiety and muscle contractions.

• Give a parenteral narcotic for analgesia.
• Use a chronotropic infusion once available.
• Obtain expert consultation for transvenous pacing.

Treatment Although β-adrenergic agonists with rate-accelerating effects are

Sequence: not first-line agents for treatment of symptomatic bradycardia,
Epinephrine, they are alternatives to TCP or in special circumstances such as
Dopamine overdose with a β-blocker or calcium channel blocker.
Because epinephrine and dopamine are vasoconstrictors, as well
as chronotropes, healthcare providers must assess the patient’s
intravascular volume status and avoid hypovolemia when using
these drugs.
Both epinephrine and dopamine infusions may be used for
patients with symptomatic bradycardia, particularly if associated
with hypotension, for whom atropine may be inappropriate or after
atropine fails.
Begin epinephrine infusion at a dose of 2 to 10 mcg/min and
titrate to patient response.
Begin dopamine infusion at 2 to 20 mcg/kg per minute and titrate
to patient response. At lower doses, dopamine has a more
selective effect on inotropy and heart rate; at higher doses
(greater than 10 mcg/kg per minute), it also has vasoconstrictive
effects.
Next Actions After consideration of the treatment sequence in Step 5, you may
need to

• Prepare the patient for transvenous pacing

• Treat the contributing causes of the bradycardia
• Consider expert consultation—but do not delay treatment if
the patient is unstable or potentially unstable

Transcutaneous Pacing
Introduction A variety of devices can pace the heart by delivering an electrical
stimulus, causing electrical depolarization and subsequent cardiac
contraction. TCP delivers pacing impulses to the heart through the
skin by use of cutaneous electrodes. Most manufacturers have added
a pacing mode to manual defibrillators.
The ability to perform TCP is now often as close as the nearest
defibrillator. Providers need to know the indications, techniques, and
hazards for using TCP.

Indications Indications for TCP are as follows:

• Hemodynamically unstable bradycardia (eg, hypotension,

acutely altered mental status, signs of shock, ischemic chest
discomfort, acute heart failure [AHF] hypotension)
• Unstable clinical condition likely due to the bradycardia
• For pacing readiness in the setting of AMI as follows:
o – Symptomatic sinus bradycardia
o – Mobitz type II second-degree AV block
o – Third-degree AV block
o – New left, right, or alternating bundle branch block or
bifascicular block
• Bradycardia with symptomatic ventricular escape rhythms

Precautions Precautions for TCP are as follows:

• TCP is contraindicated in severe hypothermia and is not

recommended for asystole.
• Conscious patients require analgesia for discomfort unless delay
for sedation will cause/contribute to deterioration.
 • Do not assess the carotid pulse to confirm mechanical capture;
electrical stimulation causes muscular jerking that may mimic the
carotid pulse.

Technique Perform TCP by following these steps:

Step Action
1 Place pacing electrodes on the chest according to package
instructions.
2 Turn the pacer on.
3 Set the demand rate to approximately 60/min. This rate can
be adjusted up or down (based on patient clinical response)
once pacing is established.
4 Set the current milliamperes output 2 mA above the dose at
which consistent capture is observed (safety margin).
External pacemakers have either fixed rates (asynchronous mode)
or demand rates.

Assess Rather than target a precise heart rate, the goal of therapy is to
Response to ensure improvement in clinical status (ie, signs and symptoms related
Treatment to the bradycardia). Signs of hemodynamic impairment include
hypotension, acutely altered mental status, signs of shock, ischemic
chest discomfort, AHF, or other signs of shock related to the
bradycardia. Start pacing at a rate of about 60/min. Once pacing is
initiated, adjust the rate based on the patient’s clinical response. Most
patients will improve with a rate of 60 to 70/min if the symptoms are
primarily due to the bradycardia.
Consider giving atropine before pacing in mildly symptomatic
patients. Do not delay pacing for unstable patients, particularly those
with high-degree AV block. Atropine may increase heart rate, improve
hemodynamics, and eliminate the need for pacing. If atropine is
ineffective or likely to be ineffective or if establishment of IV access or
atropine administration is delayed, begin pacing as soon as it is
available.
Patients with ACS should be paced at the lowest heart rate that
allows clinical stability. Higher heart rates can worsen ischemia
because heart rate is a major determinate of myocardial oxygen
demand. Ischemia, in turn, can precipitate arrhythmias.
An alternative to pacing if symptomatic bradycardia is unresponsive
to atropine is a chronotropic drug infusion to stimulate heart rate:
 • Epinephrine: Initiate at 2 to 10 mcg/min and titrate to patient
response
• Dopamine: Initiate at 2 to 20 mcg/kg per minute and titrate to
patient response

Bradycardia A bradycardia may lead to secondary bradycardia-dependent

With Escape ventricular rhythms. When the heart rate falls, an electrically unstable
Rhythms ventricular area may “escape” suppression by higher and faster
pacemakers (eg, sinus node), especially in the setting of acute
ischemia. These ventricular rhythms often fail to respond to drugs.
With severe bradycardia, some patients will develop wide-complex
ventricular beats that can precipitate VT or VF. Pacing may increase
the heart rate and eliminate bradycardia-dependent ventricular
rhythms. However, an accelerated idioventricular rhythm (sometimes
called AIVR) may occur in the setting of inferior wall MI. This rhythm
is usually stable and does not require pacing.
Patients with ventricular escape rhythms may have normal
myocardium with disturbed conduction. After correction of electrolyte
abnormalities or acidosis, rapid pacing can stimulate effective
myocardial contractions until the conduction system recovers.

Standby Pacing Several bradycardic rhythms in ACS are caused by acute ischemia of
conduction tissue and pacing centers. Patients who are clinically
stable may decompensate suddenly or become unstable over
minutes to hours from worsening conduction abnormalities. These
bradycardias may deteriorate to complete AV block and
cardiovascular collapse.
Place TCP electrodes in anticipation of clinical deterioration in
patients with acute myocardial ischemia or infarction associated with
the following rhythms:

• Symptomatic sinus node dysfunction with severe and

symptomatic sinus bradycardia
• Asymptomatic Mobitz type II second-degree AV block
• Asymptomatic third-degree AV block
• Newly acquired left, right, or alternating bundle branch block or
bifascicular block in the setting of AMI
 Tachycardia: Stable and Unstable
Introduction If you are the team leader in this case, you will conduct the
assessment and management of a patient with a rapid, unstable
heart rate. You must be able to classify the tachycardia and
implement appropriate interventions as outlined in the Tachycardia
Algorithm. You will be evaluated on your knowledge of the factors
involved in safe and effective synchronized cardioversion as well as
your performance of the procedure.

Rhythms for This case involves these ECG rhythms (examples in Figure 43):
Unstable
Tachycardia • Sinus tachycardia
• Atrial fibrillation
• Atrial flutter
• Reentry supraventricular tachycardia (SVT)
• Monomorphic VT
• Polymorphic VT
• Wide-complex tachycardia of uncertain type
Figure 43. Examples of tachycardias. A, Sinus tachycardia. B, Atrial fibrillation. C, Atrial
flutter. D, Supraventricular tachycardia. E, Monomorphic ventricular
tachycardia. F,Polymorphic ventricular tachycardia.

Drugs for Drugs are generally not used to manage patients with unstable
Unstable tachycardia. Immediate cardioversion is recommended. Consider
Tachycardia administering sedative drugs in the conscious patient. But do not
delay immediate cardioversion in the unstable patient.

The Approach to Unstable Tachycardia

Introduction A tachyarrhythmia (rhythm with heart rate greater than 100/min)

has many potential causes and may be symptomatic or
asymptomatic. The key to management of a patient with any
tachycardia is to determine whether pulses are present. If pulses
are present, determine whether the patient is stable or unstable
and then provide treatment based on patient condition and
rhythm.
If the tachyarrhythmia is sinus tachycardia, conduct a diligent
search for the cause of the tachycardia. Treatment and
correction of this cause will improve the signs and symptoms.

Definitions Definitions used in this case are as follows:

Term Definition
Tachyarrhythmia, Heart rate greater than 100/min
tachycardia*
Symptomatic Signs and symptoms due to the
tachyarrhythmia rapid heart rate
*For the purposes of this case, we will use the
term tachycardia interchangeably with tachyarrhythmia.Sinus
tachycardia will be specifically indicated.

Pathophysiology of Unstable tachycardia exists when the heart rate is too fast for the
Unstable patient’s clinical condition and the excessive heart rate causes
Tachycardia symptoms or an unstable condition because the heart is

• Beating so fast that cardiac output is reduced; this can

cause pulmonary edema, coronary ischemia, and
hypotension with reduced blood flow to vital organs (eg,
brain, kidneys)
 • Beating ineffectively so that coordination between the atrium
and ventricles or the ventricles themselves reduces cardiac
output

Signs and Unstable tachycardia leads to serious signs and symptoms that
Symptoms include

• Hypotension
• Acutely altered mental status
• Signs of shock
• Ischemic chest discomfort
• AHF

Rapid Recognition The 2 keys to management of patients with unstable tachycardia

Is the Key to are
Management
1. Rapid recognition that the patient is significantly
symptomatic or even unstable
2. Rapid recognition that the signs and symptoms are caused
by the tachycardia

You must quickly determine whether the patient’s

tachycardia is producing hemodynamic instability and
serious signs and symptoms or whether the signs and
symptoms (eg, the pain and distress of an AMI) are
producing the tachycardia.
This determination can be difficult. Many experts suggest that
when a heart rate is less than 150/min, it is unlikely that
symptoms of instability are caused primarily by the tachycardia
unless there is impaired ventricular function. A heart rate of
150/min or greater is usually an inappropriate response to
physiologic stress (eg, fever, dehydration) or other underlying
conditions.

Severity Assess for the presence or absence of signs and symptoms and
for their severity. Frequent patient assessment is indicated.
Indications for Rapid identification of symptomatic tachycardia will help you
Cardioversion determine whether you should prepare for immediate
cardioversion. For example:

• Sinus tachycardia is a physiologic response to extrinsic

factors, such as fever, anemia, or hypotension/shock, which
create the need for a compensatory and physiological
increase in heart rate. There is usually a high degree of
sympathetic tone and neurohormonal factors in these
settings. Sinus tachycardia will not respond to cardioversion.
In fact, if a shock is delivered, the heart rate often increases.
• If the patient with tachycardia is stable (ie, no serious signs
related to the tachycardia), patients may await expert
consultation because treatment has the potential for harm.
• Atrial flutter typically produces a heart rate of approximately
150/min (lower rates may be present in patients who have
received antiarrhythmic therapy). Atrial flutter at this rate is
often stable in the patient without heart or serious systemic
disease.
• At rates greater than 150/min, symptoms are often present
and cardioversion is often required if the patient is unstable.
• If the patient is seriously ill or has underlying cardiovascular
disease, symptoms may be present at lower rates.

You must know when cardioversion is indicated, how to prepare

the patient for it (including appropriate medication), and how to
switch the defibrillator/monitor to operate as a cardioverter.

Managing Unstable Tachycardia: The Tachycardia Algorithm

Introduction The Adult Tachycardia With a Pulse Algorithm simplifies initial
management of tachycardia. The presence or absence of pulses is
considered key to management of a patient with any tachycardia. If
pulses are present, determine whether the patient is stable or unstable
and then provide treatment based on the patient’s condition and rhythm.
If a pulseless tachycardia is present, then manage the patient according
to the Cardiac Arrest Algorithm (Figure 31 in the section Managing
VF/Pulseless VT: The Adult Cardiac Arrest Algorithm).
The ACLS provider should either be an expert or be able to obtain expert
consultation. Actions in the steps require advanced knowledge of ECG
rhythm interpretation and antiarrhythmic therapy and are intended to be
accomplished in the in-hospital setting with expert consultation available.
Overview The Tachycardia Algorithm (Figure 44) outlines the steps for assessment
and management of a patient presenting with symptomatic tachycardia
with pulses. Implementation of this algorithm begins with the identification
of tachycardia with pulses (Step 1). If a tachycardia and a pulse are
present, perform assessment and management steps guided by the BLS
Assessment and the Primary and Secondary Assessments (Step 2). The
key in this assessment is to decide if the tachycardia is stable or
unstable.
If signs and symptoms persist despite provision of supplementary oxygen
and support of airway and circulation and if significant signs or symptoms
are due to the tachycardia (Step 3), then the tachycardia is unstable and
immediate synchronized cardioversion is indicated (Step 4).
If the patient is stable, you will evaluate the ECG, and determine if the
QRS complex is wide or narrow and regular or irregular (Step 5). The
treatment of stable tachycardia is presented in the next case (Step 6).
A precise diagnosis of the rhythm (eg, reentry SVT, atrial flutter) may not
be possible at this time.
Figure 44. The Adult Tachycardia With a Pulse Algorithm.
Foundational Serious or Significant Symptoms
Facts Unstable Condition
Intervention is determined by the presence of significant symptoms or
by an unstable condition resulting from the tachycardia.*
Serious symptoms and signs include

• Hypotension
• Acutely altered mental status
• Signs of shock
• Ischemic chest discomfort
• AHF

*Ventricular rates less than 150/min usually do not cause serious

signs or symptoms.

Summary Your assessment and management of this patient will be guided by the
following key questions presented in the Tachycardia Algorithm:

• Are symptoms present or absent?

• Is the patient stable or unstable?
• Is the QRS narrow or wide?
• Is the rhythm regular or irregular?
• Is the QRS monomorphic or polymorphic?

Your answers to these questions will determine the next appropriate steps.

Application of the Tachycardia Algorithm to the Unstable Patient

Introduction In this case, you have a patient with tachycardia and a pulse.
You conduct the steps outlined in the Tachycardia Algorithm
to evaluate and manage the patient.

Assess • Tachycardia is defined as an arrhythmia with a rate

Appropriateness for greater than 100/min.
Clinical Condition • The rate takes on clinical significance at its greater
extremes and is more likely attributable to an arrhythmia
rate of 150/min or greater.
• It is unlikely that symptoms of instability are caused
primarily by the tachycardia when the heart rate is less
 than 150/min unless there is impaired ventricular
function.

Identify and Treat the Use the BLS, Primary, and Secondary Assessments to guide
Underlying Cause your approach.

• Look for signs of increased work of breathing

(tachypnea, intercostal retractions, suprasternal
retractions, paradoxical abdominal breathing) and
hypoxemia as determined by pulse oximetry.
• Give oxygen, if indicated, and monitor oxygen
saturation.
• Obtain an ECG to identify the rhythm.
• Evaluate blood pressure.
• Establish IV access.
• Identify and treat reversible causes.

If symptoms persist despite support of adequate oxygenation

and ventilation, proceed to Step 3.

Critical Unstable Patients

Concepts
• Healthcare providers should obtain a 12-lead ECG early in the
assessment to better define the rhythm.
• However, unstable patients require immediate cardioversion.
• Do not delay immediate cardioversion for acquisition of the 12-lead
ECG if the patient is unstable.

Decision Point: Is the Assess the patient’s degree of instability and determine if
Persistent the instability is related to the tachycardia.
Tachyarrhythmia Causing Unstable
Significant Signs or If the patient demonstrates rate-related cardiovascular
Symptoms? compromise with signs and symptoms such as
hypotension, acutely altered mental status, signs of
shock, ischemic chest discomfort, AHF, or other signs of
shock suspected to be due to a tachyarrhythmia,
proceed to immediate synchronized cardioversion (Step
4).
Serious signs and symptoms are unlikely if the
ventricular rate is less than 150/min in patients with a
healthy heart. However, if the patient is seriously ill or
has significant underlying heart disease or other
 conditions, symptoms may be present at a lower heart
rate.
Stable
If the patient does not have rate-related cardiovascular
compromise, proceed to Step 5. The healthcare provider
has time to obtain a 12-lead ECG, evaluate the rhythm,
determine the width of the QRS, and determine
treatment options. Stable patients may await expert
consultation because treatment has the potential for
harm.
Foundational Treatment Based on Type of Tachycardia
Facts You may not always be able to distinguish between supraventricular and
ventricular rhythms. Most wide-complex (broad-complex) tachycardias
are ventricular in origin (especially if the patient has underlying heart
disease or is older). If the patient is pulseless, treat the rhythm as VF
and follow the Cardiac Arrest Algorithm.
If the patient has a wide-complex tachycardia and is unstable, assume it
is VT until proven otherwise. The amount of energy required for
cardioversion of VT is determined by the morphologic characteristics.

• If the patient is unstable but has a pulse with regular uniform wide-
complex VT (monomorphic VT):
o – Treat with synchronized cardioversion and an initial shock of 100 J
(monophasic waveform).
o – If there is no response to the first shock, increasing the dose in a
stepwise fashion is reasonable.*
• Arrhythmias with a polymorphic QRS appearance (polymorphic VT),
such as torsades de pointes, will usually not permit synchronization. If
the patient has polymorphic VT:
o – Treat as VF with high-energy unsynchronized shocks (eg,
defibrillation doses).

If there is any doubt about whether an unstable patient has

monomorphic or polymorphic VT, do not delay treatment for further
rhythm analysis. Provide high-energy, unsynchronized shocks.
*No studies that addressed this issue had been identified at the time that
the manuscript for the 2015 AHA Guidelines Update for CPR and
ECC was in preparation. Thus, this recommendation represents expert
opinion.

Perform Immediate • If possible, establish IV access before cardioversion and

Synchronized administer sedation if the patient is conscious.
Cardioversion
 • Do not delay cardioversion if the patient is extremely
unstable.

Further information about cardioversion appears below.

If the patient with a regular narrow-complex SVT or a
monomorphic wide-complex tachycardia is not hypotensive,
healthcare providers may administer adenosine while
preparing for synchronized cardioversion.
If cardiac arrest develops, see the Cardiac Arrest Algorithm.

Determine the Width • If the width of the QRS complex is 0.12 second or more,
of the QRS Complex go to Step 6.
• If the width of the QRS complex is less than 0.12 second,
go to Step 7.

Cardioversion
Introduction You must know when cardioversion is indicated and what type
of shock to administer. Before cardioversion, establish IV
access and sedate the responsive patient if possible, but do
not delay cardioversion in the unstable or deteriorating patient.
This section discusses the following important concepts about
cardioversion:

• The difference between unsynchronized and synchronized

shocks
• Potential challenges to delivery of synchronized shocks
• Energy doses for specific rhythms

Unsynchronized vs Modern defibrillator/cardioverters are capable of delivering 2

Synchronized Shocks types of shocks:

• Unsynchronized shocks
• Synchronized shocks

An unsynchronized shock simply means that the electrical

shock will be delivered as soon as the operator pushes the
shock button to discharge the device. Thus, the shock may fall
randomly anywhere within the cardiac cycle. These shocks
 should use higher energy levels than synchronized
cardioversion.
Synchronized cardioversion uses a sensor to deliver a shock
that is synchronized with a peak of the QRS complex (eg, the
highest point of the R wave). When this option (the “sync”
option) is engaged, the operator presses the shock button to
deliver a shock. There will likely be a delay before the
defibrillator/cardioverter delivers a shock because the device
will synchronize shock delivery with the peak of the R wave in
the patient’s QRS complex. This synchronization may require
analysis of several complexes. Synchronization avoids the
delivery of a shock during cardiac repolarization (represented
on the surface ECG as the T wave), a period of vulnerability in
which a shock can precipitate VF. Synchronized cardioversion
uses a lower energy level than attempted defibrillation. Low-
energy shocks should always be delivered as synchronized
shocks to avoid precipitating VF.

Potential Problems In theory, synchronization is simple. The operator pushes the

With Synchronization sync control on the face of the defibrillator/cardioverter. In
practice, however, there are potential problems.
For example:

• If the R-wave peaks of a tachycardia are undifferentiated

or of low amplitude, the monitor sensors may be unable to
identify an R-wave peak and therefore will not deliver the
shock.
• Many cardioverters will not synchronize through the
handheld quick-look paddles. An unwary practitioner may
try to synchronize—unsuccessfully in that the machine will
not discharge—and may not recognize the problem.
• Synchronization can take extra time (eg, if it is necessary
to attach electrodes or if the operator is unfamiliar with the
equipment).

Recommendations When to Use Synchronized Shocks

Synchronized shocks are recommended for patients with

• Unstable SVT
• Unstable atrial fibrillation
• Unstable atrial flutter
 • Unstable regular monomorphic tachycardia with pulses

When to Use Unsynchronized Shocks

Unsynchronized high-energy shocks are recommended

• For a patient who is pulseless

• For a patient demonstrating clinical deterioration (in
prearrest), such as those with severe shock or
polymorphic VT, when you think a delay in converting the
rhythm will result in cardiac arrest
• When you are unsure whether monomorphic or
polymorphic VT is present in the unstable patient

Should the shock cause VF (occurring in only a very small

minority of patients despite the theoretical risk), immediately
attempt defibrillation.

Energy Doses for Select the energy dose for the specific type of rhythm.
Cardioversion For unstable atrial fibrillation:

• Monophasic cardioversion: Deliver an initial 200-J

synchronized shock.
• Biphasic cardioversion: Deliver an initial 120- to 200-J
synchronized shock.
• In either case, increase the energy dose in a stepwise
fashion for any subsequent cardioversion attempts.

A dose of 120 to 200 J is reasonable with a biphasic waveform.

Escalate the second and subsequent shock dose as needed.
Cardioversion of atrial flutter and SVT generally require less
energy. An initial energy dose of 50 to 100 J with a
monophasic or biphasic waveform is often sufficient.
Monomorphic VT (regular form and rate) with a pulse responds
well to monophasic or biphasic waveform cardioversion
(synchronized) shocks at an initial dose of 100 J. If there is no
response to the first shock, increase the dose in a stepwise
fashion. No studies were identified that addressed this issue.
Thus, this recommendation represents expert opinion.

Synchronized Cardioversion Technique

Introduction Synchronized cardioversion is the treatment of choice when a patient
has a symptomatic (unstable) reentry SVT or VT with pulses. It is also
 recommended to treat unstable atrial fibrillation and unstable atrial
flutter.
Cardioversion is unlikely to be effective for treatment of junctional
tachycardia or ectopic or multifocal atrial tachycardia because these
rhythms have an automatic focus arising from cells that are
spontaneously depolarizing at a rapid rate. Delivery of a shock
generally cannot stop these rhythms and may actually increase the
rate of the tachyarrhythmia.
In synchronized cardioversion, shocks are administered through
adhesive electrodes or handheld paddles. You will need to place the
defibrillator/monitor in synchronized (sync) mode. The sync mode is
designed to deliver energy just after the R wave of the QRS complex.

Technique Follow these steps to perform synchronized cardioversion. Modify the

steps for your specific device.
Step Action
1 Sedate all conscious patients unless unstable or deteriorating
rapidly.
2 Turn on the defibrillator (monophasic or biphasic).
3 Attach monitor leads to the patient (“white to right, red to ribs,
what’s left over to the left shoulder”) and ensure proper
display of the patient’s rhythm. Position adhesive electrode
(conductor) pads on the patient.
4 Press the sync control button to engage the synchronization
mode.
5 Look for markers on the R wave indicating sync mode.
6 Adjust monitor gain if necessary until sync markers occur with
each R wave.
7 Select the appropriate energy level.
Deliver monophasic synchronized shocks in the following
sequence:
If Initial Dose*
Unstable atrial fibrillation 200 J
Unstable monomorphic VT 100 J
Other unstable SVT/atrial
50 to 100 J
flutter
 Polymorphic VT (irregular Treat as VF with high-
form and rate) and energy shock (defibrillation
unstable doses)
*Biphasic waveforms using lower energy are acceptable if
documented to be clinically equivalent or superior to reports
of monophasic shock success. Extrapolation from elective
cardioversion of atrial fibrillation supports an initial biphasic
dose of 120 to 200 J with escalation as needed.
Consult the device manufacturer for specific
recommendations.
8 Announce to team members: “Charging defibrillator—stand
clear!”
9 Press the charge button.
10 Clear the patient when the defibrillator is charged. (See
“Foundational Facts: Clearing for Defibrillation” in the
VF/Pulseless VT Case.)
11 Press the shock button(s).
12 Check the monitor. If tachycardia persists, increase the
energy level (joules) according to the Electrical Cardioversion
Algorithm

(see Supplementary Materials on the ACLS Student

Website; www.heart.org/eccstudent).
13 Activate the sync mode after delivery of each synchronized
shock. Most defibrillators default back to the unsynchronized
mode after delivery of a synchronized shock.This default
allows an immediate shock if cardioversion produces VF.

Stable This case reviews assessment and management of a stable patient (ie,
Tachycardias no serious signs related to the tachycardia) with a rapid heart
rate. Patients with heart rates greater than 100/min have a
tachyarrhythmia or tachycardia. In this case, we will use the
terms tachycardia and tachyarrhythmia interchangeably. Note that
sinus tachycardia is excluded from the treatment algorithm. Sinus
tachycardia is almost always physiologic, developing in response to a
compromise in stroke volume or a condition that requires an increase
in cardiac output (eg, fever, hypovolemia). Treatment involves
identification and correction of that underlying problem.
 You must be able to classify the type of tachycardia (wide or narrow;
regular or irregular) and implement appropriate interventions as
outlined in the Tachycardia Algorithm. During this case you will

• Perform initial assessment and management

• Treat regular narrow-complex rhythms (except sinus tachycardia)
with vagal maneuvers and adenosine

If the rhythm does not convert, you will monitor the patient and
transport or obtain expert consultation. If the patient becomes clinically
unstable, you will prepare for immediate unsynchronized shock or
synchronized cardioversion as discussed in the Unstable Tachycardia
Case.

Rhythms for Tachycardias can be classified in several ways based on the

Stable appearance of the QRS complex, heart rate, and whether they are
Tachycardia regular or irregular:

• Narrow–QRS complex (SVT) tachycardias (QRS less than 0.12

second) in order of frequency
o – Sinus tachycardia
o – Atrial fibrillation
o – Atrial flutter
o – AV nodal reentry
• Wide–QRS complex tachycardias (QRS 0.12 second or more)
o – Monomorphic VT
o – Polymorphic VT
o – SVT with aberrancy
• Regular or irregular tachycardias
o – Irregular narrow-complex tachycardias are probably atrial
fibrillation

Drugs for This case involves the following drug:

Stable
Tachycardia • Adenosine

Several agents are also used to provide analgesia and sedation during
electrical cardioversion. These agents are not covered in the ACLS
Provider Course.
Approach to Stable Tachycardia
Introduction In this case, a stable tachycardia refers to a condition in
which the patient has

• A heart rate greater than 100/min

• No significant signs or symptoms caused by the
increased rate
• An underlying cardiac electrical abnormality that
generates the rhythm

Questions to Determine Classification of the tachycardia depends on the careful

Classification clinical evaluation of these questions:

• Are symptoms present or absent?

• Are symptoms due to the tachycardia?
• Is the patient stable or unstable?
• Is the QRS complex narrow or wide?
• Is the rhythm regular or irregular?
• Is the QRS monomorphic or polymorphic?
• Is the rhythm sinus tachycardia?

The answers guide subsequent diagnosis and treatment.

Foundational Understanding Sinus Tachycardia

Facts
• Sinus tachycardia is a heart rate that is greater than 100/min and is
generated by sinus node discharge. The heart rate in sinus
tachycardia does not exceed 220/min and is agerelated. Sinus
tachycardia usually does not exceed 120 to 130/min, and it has a
gradual onset and gradual termination. Reentry SVT has an abrupt
onset and termination.
• Sinus tachycardia is caused by external influences on the heart, such
as fever, anemia, hypotension, blood loss, or exercise. These are
systemic conditions, not cardiac conditions. Sinus tachycardia is a
regular rhythm, although the rate may be slowed by vagal maneuvers.
Cardioversion is contraindicated.
• β-Blockers may cause clinical deterioration if the cardiac output falls
when a compensatory tachycardia is blocked. This is because cardiac
output is determined by the volume of blood ejected by the ventricles
with each contraction (stroke volume) and the heart rate.

Cardiac output (CO) = Stroke volume (SV) × Heart rate

 • If a condition such as a large AMI limits ventricular function (severe
heart failure or cardiogenic shock), the heart compensates by
increasing the heart rate. If you attempt to reduce the heart rate in
patients with a compensatory tachycardia, cardiac output will fall and
the patient’s condition will likely deteriorate.

In sinus tachycardia, the goal is to identify and treat the underlying

systemic cause.

Managing Stable Tachycardia: The Tachycardia Algorithm

Introduction As noted in the Unstable Tachycardia Case, the key to management of a
patient with any tachycardia is to determine whether pulses are present,
and if pulses are present, to determine whether the patient is stable or
unstable and then to provide treatment based on patient condition and
rhythm. If the patient is pulseless, manage the patient according to the
Cardiac Arrest Algorithm (Figure 31 in the section Managing
VF/Pulseless VT: The Adult Cardiac Arrest Algorithm). If the patient has
pulses, manage the patient according to the Tachycardia Algorithm
(Figure 44).

Overview If a tachycardia and a pulse are present, perform assessment and

management steps guided by the BLS Assessment and the Primary and
Secondary Assessments. Determine if significant symptoms or signs are
present and if these symptoms and signs are due to the tachycardia. This
will direct you to either the stable (Steps 5 through 7) or unstable (Step
4) section of the algorithm.

• If significant signs or symptoms are due to the tachycardia, then the

tachycardia is unstable and immediate cardioversion is indicated
(see the Unstable Tachycardia Case).
• If the patient develops pulseless VT, deliver unsynchronized high-
energy shocks (defibrillation energy) and follow the Cardiac Arrest
Algorithm.
• If the patient has polymorphic VT, treat the rhythm as VF and deliver
high-energy unsynchronized shocks (ie, defibrillation energy).
 In this case, the patient is stable, and you will manage according to the
stable section of the Tachycardia Algorithm (Figure 44). A precise
identification of the rhythm (eg, reentry SVT, atrial flutter) may not be
possible at this time.

Application of the Tachycardia Algorithm to the Stable Patient

Introduction In this case, a patient has stable tachycardia with a pulse. Conduct
the steps outlined in the Tachycardia Algorithm to evaluate and
manage the patient.

Patient Step 1 directs you to assess the patient’s condition. Typically, a

Assessment heart rate greater than 150/min at rest is due to tachyarrhythmias
other than sinus tachycardia.

BLS and ACLS Using the BLS, Primary, and Secondary Assessments to guide your
Assessments approach, evaluate the patient and do the following as necessary:

• Look for signs of increased work of breathing and hypoxia as

determined by pulse oximetry.
• Give oxygen; monitor oxygen saturation.
• Support the airway, breathing, and circulation.
• Obtain an ECG to identify the rhythm; check blood pressure.
• Identify and treat reversible causes.

If symptoms persist, proceed to Step 3.

Decision Point: Unstable

Stable or If the patient is unstable with signs or symptoms as a result of the
Unstable tachycardia (eg, hypotension, acutely altered mental status, signs of
shock, ischemic chest discomfort, or AHF), go to Step 4 (perform
immediate synchronized cardioversion). See the Unstable
Tachycardia Case.
Stable
If the patient is stable, go to Step 5.

IV Access and If the patient with tachycardia is stable (ie, no serious signs or
12-Lead ECG symptoms related to the tachycardia), you have time to evaluate the
rhythm and decide on treatment options. Establish IV access if not
 already obtained. Obtain a 12-lead ECG (when available) or rhythm
strip to determine if the QRS is narrow (less than 0.12 second) or
wide (0.12 second or more).

Decision Point: The path of treatment is now determined by whether the QRS is
Narrow or Wide wide (Step 6) or narrow (Step 7), and whether the rhythm is regular
or irregular. If a monomorphic wide-complex rhythm is present and
the patient is stable, expert consultation is advised. Polymorphic
wide-complex tachycardia should be treated with immediate
unsynchronized cardioversion.
Foundational Treating Tachycardia
Facts
• You may not always be able to distinguish between supraventricular
(aberrant) and ventricular wide-complex rhythms. If you are unsure,
be aware that most wide-complex (broad-complex) tachycardias
are ventricular in origin.
• If a patient is pulseless, follow the Cardiac Arrest Algorithm.
• If a patient becomes unstable, do not delay treatment for further
rhythm analysis. For stable patients with wide-complex tachycardias,
transport and monitor or consult an expert, because treatment has
the potential for harm.

Wide-Complex Wide-complex tachycardias are defined as a QRS of 0.12 second or

Tachycardias more. Consider expert consultation.
The most common forms of life-threatening wide-complex
tachycardias likely to deteriorate to VF are

• Monomorphic VT
• Polymorphic VT

Determine if the rhythm is regular or irregular.

• A regular wide-complex tachycardia is presumed to be VT or

SVT with aberrancy.
• An irregular wide-complex tachycardia may be atrial fibrillation
with aberrancy, pre-excited atrial fibrillation (atrial fibrillation
using an accessory pathway for antegrade conduction), or
polymorphic VT/torsades de pointes. These are advanced
rhythms requiring additional expertise or expert consultation.

If the rhythm is likely VT or SVT in a stable patient, treat based on the

algorithm for that rhythm.
 If the rhythm etiology cannot be determined and is regular in its rate
and monomorphic, recent evidence suggests that IV adenosine is
relatively safe for both treatment and diagnosis. IV antiarrhythmic
drugs may be effective. We recommend procainamide, amiodarone,
or sotalol. See the right column of the Tachycardia Algorithm (Figure
44) for recommended doses.
In the case of irregular wide-complex tachycardia, management
focuses on control of the rapid ventricular rate (rate control),
conversion of hemodynamically unstable atrial fibrillation to sinus
rhythm (rhythm control), or both. Expert consultation is advised.
Caution Drugs to Avoid in Patients With Irregular Wide-Complex Tachycardia
Avoid AV nodal blocking agents such as adenosine, calcium channel
blockers, digoxin, and possibly β-blockers in patients with pre-excitation atrial
fibrillation, because these drugs may cause a paradoxical increase in the
ventricular response.

Narrow The therapy for narrow QRS with regular rhythm is

QRS,
Regular • Attempt vagal maneuvers
Rhythm • Give adenosine

Vagal maneuvers and adenosine are the preferred initial interventions for
terminating narrow-complex tachycardias that are symptomatic (but
stable) and supraventricular in origin (SVT). Vagal maneuvers alone
(Valsalva maneuver or carotid sinus massage) will terminate about 25%
of SVTs. Adenosine is required for the remainder.
If SVT does not respond to vagal maneuvers:

• Give adenosine 6 mg as a rapid IV push in a large (eg, antecubital)

vein over 1 second. Follow with a 20 mL saline flush and elevate the
arm immediately.
• If SVT does not convert within 1 to 2 minutes, give a second dose of
adenosine 12 mg rapid IV push following the same procedure above.

Adenosine increases AV block and will terminate approximately 90% of

reentry arrhythmias within 2 minutes. Adenosine will not terminate atrial
flutter or atrial fibrillation but will slow AV conduction, allowing for
identification of flutter or fibrillation waves.
Adenosine is safe and effective in pregnancy. Adenosine does, however,
have several important drug interactions. Larger doses may be required
for patients with significant blood levels of theophylline, caffeine, or
theobromine. The initial dose should be reduced to 3 mg in patients taking
dipyridamole or carbamazepine. There have been recent case reports of
prolonged asystole after adenosine administration to patients with
 transplanted hearts or after central venous administration, so lower doses
such as 3 mg may be considered in these situations.
Adenosine may cause bronchospasm; therefore, adenosine should
generally not be given to patients with asthma or chronic obstructive
pulmonary disease, particularly if patients are actively bronchospastic.
If the rhythm converts with adenosine, it is probable reentry SVT. Observe
for recurrence. Treat recurrence with adenosine or longer-acting AV nodal
blocking agents such as the non-dihydropyridine calcium channel
blockers (verapamil and diltiazem) or β-blockers. Typically, you should
obtain expert consultation if the tachycardia recurs.
If the rhythm does not convert with adenosine, it is possible atrial flutter,
ectopic atrial tachycardia, or junctional tachycardia. Obtain expert
consultation about diagnosis and treatment.
Caution What to Avoid With AV Nodal Blocking Agents
AV nodal blocking drugs should not be used for pre-excited atrial fibrillation
or flutter. Treatment with an AV nodal blocking agent is unlikely to slow the
ventricular rate and in some instances may accelerate the ventricular
response. Caution is advised when combining AV nodal blocking agents that
have a longer duration of action, such as calcium channel blockers or β-
blockers, because their actions may overlap if given serially, which can
provoke profound bradycardia.

Tachycardia Some ACLS providers may be familiar with the differential

Algorithm: diagnosis and therapy of stable tachycardias that do not respond
Advanced to initial treatment. The basic ACLS provider is expected to
Management Steps recognize a stable narrow-complex or wide-complex tachycardia
and classify the rhythm as regular or irregular. Regular narrow-
complex tachycardias may be treated initially with vagal
maneuvers and adenosine. If these are unsuccessful, the ACLS
provider should transport or seek expert consultation.
If ACLS providers have experience with the differential diagnosis
and therapy of stable tachycardias beyond initial management,
the Tachycardia Algorithm lists additional steps and
pharmacologic agents used in the treatment of these
arrhythmias, both for rate control and for termination of the
arrhythmia.
If at any point you become uncertain or uncomfortable
during the treatment of a stable patient, seek expert
consultation. The treatment of stable patients may await
expert consultation because treatment has the potential for
harm.
 Immediate Post–Cardiac Arrest Care Case

Introduction There is increasing recognition that systematic post–cardiac arrest

care after ROSC can improve the likelihood of patient survival with
good quality of life. Positive correlations have been observed
between the likelihood of survival and the number of cardiac arrest
cases treated at any individual hospital.41,42 Studies show most
deaths occur during the first 24 hours after resuscitation from
cardiac arrest.43,44 Post–cardiac arrest care has a significant
potential to reduce early mortality caused by hemodynamic
instability and later morbidity and mortality caused by multiorgan
failure and brain injury.45,46
There is a growing body of research focused on the identification
and optimization of practices that improve outcomes of patients
who achieve ROSC after cardiac arrest.47 Mere restoration of
blood pressure and gas exchange does not ensure survival and
functional recovery. Significant cardiovascular dysfunction can
develop after ROSC that requires active support of blood flow and
ventilation, including intravascular volume expansion, vasoactive
and inotropic drugs, and invasive devices. Targeted temperature
management (TTM) and treatment of the underlying cause of
cardiac arrest impact survival and neurologic outcome.
Hemodynamic optimization protocols have been introduced as part
of a bundle of care to improve survival.48-50 The data suggest that
proactive management of post–cardiac arrest physiology can
improve outcomes by ensuring organ oxygenation and perfusion
and by avoiding and managing complications.
This case focuses on the management and optimization of
cardiopulmonary function and perfusion of vital organs after
ROSC.
To ensure the success of post–cardiac arrest care, healthcare
providers must

• Optimize the patient’s hemodynamic and ventilation status

• Initiate TTM
• Provide immediate coronary reperfusion with PCI
• Provide neurologic care and prognostication and other
structured interventions

In this case, you will have an opportunity to use the 12-lead ECG
while using the assessment and action skills typically performed
after ROSC.
Rhythms for You will need to recognize the following rhythms:
Post–Cardiac
Arrest Care • Rate—too fast or too slow
• Width of QRS complexes—wide versus narrow

Drugs for Post– This case involves these drugs:

Cardiac Arrest
Care • Epinephrine infusion
• Dopamine infusion
• Norepinephrine infusions

Multiple System A comprehensive, structured, multidisciplinary system of care

Approach to should be implemented in a consistent manner for the treatment of
Post–Cardiac post–cardiac arrest patients. Programs should include TTM,
Arrest Care optimization of hemodynamics and gas exchange, immediate
coronary reperfusion when indicated for restoration of coronary
blood flow with PCI, neurologic diagnosis, critical care
management, and prognostication.
Clinicians should treat the precipitating cause of cardiac arrest
after ROSC and initiate or request studies that will further aid in
evaluation of the patient. It is essential to identify and treat any
cardiac, electrolyte, toxicologic, pulmonary, and neurologic
precipitants of arrest.

Overview of Post– Providers should ensure an adequate airway and support

Cardiac Arrest breathing immediately after ROSC. Unconscious patients usually
Care require an advanced airway for mechanical support of breathing.
Providers should also elevate the head of the bed 30° if tolerated
to reduce the incidence of cerebral edema, aspiration, and
ventilatory-associated pneumonia. Proper placement of an
advanced airway, particularly during patient transport, should be
monitored by waveform capnography as described in the 2015
AHA Guidelines Update for CPR and ECC. Oxygenation of the
patient should be monitored continuously with pulse oximetry.
Although 100% oxygen may have been used during initial
resuscitation, providers should titrate inspired oxygen to the lowest
level required to achieve an arterial oxygen saturation of 94% to
99% to avoid potential oxygen toxicity. Hyperventilation is common
after cardiac arrest and should be avoided because of the potential
for adverse hemodynamic effects. Hyperventilation increases
intrathoracic pressure, which decreases preload and lowers
cardiac output. The decrease in PaCO2 seen with hyperventilation
can also decrease cerebral blood flow directly. Ventilation should
be started at 10/min and titrated to achieve a PETCO2 of 35 to 40
mm Hg or a PaCO2 of 40 to 45 mm Hg.
Healthcare providers should frequently reassess vital signs and
monitor for recurrent cardiac arrhythmias by using continuous
ECG monitoring. If the patient is hypotensive (SBP less than 90
mm Hg), fluid boluses can be administered. If TTM is indicated,
cold fluids may be helpful for initial induction of hypothermia. If the
patient’s volume status is adequate, infusions of vasoactive agents
may be initiated and titrated to achieve a minimum SBP of 90 mm
Hg or greater or a mean arterial pressure of 65 mm Hg or more.
Some advocate higher mean arterial pressures to promote
cerebral blood flow.
Brain injury and cardiovascular instability are the major factors that
determine survival after cardiac arrest.51 Because TTM is currently
the only intervention demonstrated to improve neurologic recovery,
it should be considered for any patient who is comatose and
unresponsive to verbal commands after ROSC. The patient should
be transported to a location that reliably provides this therapy in
addition to coronary reperfusion (eg, PCI) and other goal-directed
postarrest care therapies.
Clinicians should treat the precipitating cause of cardiac arrest
after ROSC and initiate or request studies that will further aid in
evaluation of the patient. It is essential to identify and treat any
cardiac, electrolyte, toxicologic, pulmonary, and neurologic
precipitants of arrest. Overall, the most common cause of cardiac
arrest is cardiovascular disease and associated coronary
ischemia.52,53 Therefore, a 12-lead ECG should be obtained as
soon as possible to detect ST elevation or LBBB. Coronary
angiography should be performed emergently (rather than later in
the hospital stay or not at all) for OHCA patients with suspected
cardiac etiology of arrest and ST elevation on ECG. When there is
high suspicion of AMI, local protocols for treatment of AMI and
coronary reperfusion should be activated. Coronary angiography, if
indicated, can be beneficial in post–cardiac arrest patients
regardless of whether they are awake or comatose. Even in the
absence of ST elevation, emergent coronary angiography is
reasonable for patients who are comatose after OHCA of
suspected cardiac origin. Concurrent PCI and TTM are safe, with
good outcomes reported for some comatose patients who have
undergone PCI.
Critical care facilities that treat patients after cardiac arrest should
use a comprehensive care plan that includes acute cardiovascular
 interventions, use of TTM, standardized medical goal-directed
therapies, and advanced neurologic monitoring and care.
Neurologic prognosis may be difficult to determine during the first
72 hours after resuscitation. This should be the earliest time to
prognosticate a poor neurologic outcome in patients not treated
with TTM. For those treated with TTM, providers should wait 72
hours after the patient returns to normothermia before
prognosticating by using clinical examination where sedation or
paralysis can be a confounder. Many initially comatose survivors
of cardiac arrest have the potential for full
recovery.48,54,55 Therefore, it is important to place patients in a
hospital critical care unit where expert care and neurologic
evaluation can be performed and where appropriate testing to aid
prognosis is performed in a timely manner.

Managing Post–Cardiac Arrest Care: The Post–Cardiac Arrest Care

Algorithm
The Adult Immediate Post–Cardiac Arrest Care Algorithm (Figure 45) outlines all the
steps for immediate assessment and management of post–cardiac arrest patients with
ROSC. During this case, team members will continue to maintain good ventilation and
oxygenation with a bag-mask device or advanced airway. Throughout the case
discussion of the Post–Cardiac Arrest Care Algorithm, we will refer to Steps 1 through
8. These are the numbers assigned to the steps in the algorithm.
Use the H’s and T’s to recall conditions that could have contributed to the cardiac arrest.
See column on the right of the algorithm and “Part 4: The Systematic Approach” for
more information on the H’s and T’s, including clinical clues and suggested treatments.
Figure 45. The Adult Immediate Post–Cardiac Arrest Care Algorithm.

Application of the Immediate Post–Cardiac Arrest Care Algorithm

Introduction This case discusses the assessment and treatment of a patient who
had cardiac arrest and was resuscitated with the use of the BLS
 Assessment and the ACLS Primary and Secondary Assessments.
During rhythm check in the ACLS Primary Assessment, the patient’s
rhythm was organized and a pulse was detected (Step 12, Cardiac
Arrest Algorithm [Figure 31]). The team leader will coordinate the
efforts of the high-performance post–cardiac arrest care team as
they perform the steps of the Post–Cardiac Arrest Care Algorithm.

Optimize Step 2 directs you to ensure an adequate airway and support

Ventilation and breathing immediately after ROSC. An unconscious/unresponsive
Oxygenation patient will require an advanced airway for mechanical support of
breathing.

• Use continuous waveform capnography to confirm and monitor

correct placement of the ET tube (Figures 46 and 47).
• Use the lowest inspired oxygen concentration that will maintain
arterial oxyhemoglobin saturation 94% or greater. When titration
of inspired oxygen is not feasible (eg, in an out-of-hospital
setting), it is reasonable to empirically use 100% oxygen until
the patient arrives at the ED.
• Avoid excessive ventilation of the patient (do not ventilate too
fast or too much). Providers may begin ventilations at 10/min
and titrate to achieve a PETCO2 of 35 to 40 mm Hg or a
PaCO2 of 40 to 45 mm Hg.

To avoid hypoxia in adults with ROSC after cardiac arrest and if

appropriate equipment is available, providers may use the highest
available oxygen concentration until the arterial oxyhemoglobin
saturation or the partial pressure of arterial oxygen can be
measured. Decrease the fraction of inspired oxygen (FIO2) when
oxyhemoglobin saturation is 100%, provided the oxyhemoglobin
saturation can be maintained for 94% or greater.
Because an oxygen saturation of 100% may correspond to a
PaCO2 for a saturation of 100%, provided the patient can maintain
oxyhemoglobin saturation of 94% or greater.
Figure 46. Waveform capnography. A, Normal range of 35 to 45 mm Hg. B, 20 mm
Hg. C, 0 mm Hg.
Figure 47. Waveform capnography with an ET showing normal (adequate) ventilation
pattern: PETCO2 35 to 40 mm Hg.
Critical Waveform Capnography
Concepts In addition to monitoring ET tube position, quantitative waveform
capnography allows healthcare personnel to monitor CPR quality, optimize
chest compressions, and detect ROSC during chest compressions or when
a rhythm check reveals an organized rhythm.

Caution Things to Avoid During Ventilation

• When securing an advanced airway, avoid using ties that pass

circumferentially around the patient’s neck, thereby obstructing venous
return from the brain.
 • Excessive ventilation may potentially lead to adverse hemodynamic
effects when intrathoracic pressures are increased and because of
potential decreases in cerebral blood flow when PaCO2decreases.

Foundational Waveform Capnography

Facts
• End-tidal CO2 is the concentration of carbon dioxide in exhaled air at
the end of expiration. It is typically expressed as a partial pressure in
millimeters of mercury (PETCO2). Because CO2 is a trace gas in
atmospheric air, CO2 detected by capnography in exhaled air is
produced in the body and delivered to the lungs by circulating blood.
• Cardiac output is the major determinant of CO2 delivery to the lungs.
If ventilation is relatively constant, PETCO2 correlates well with
cardiac output during CPR.
• Providers should observe a persistent capnographic waveform with
ventilation to confirm and monitor ET tube placement in the field, in
the transport vehicle, on arrival at the hospital, and after any patient
transfer to reduce the risk of unrecognized tube misplacement or
displacement.
• Although capnography to confirm and monitor correct placement of
supraglottic airways (eg, laryngeal mask airway, laryngeal tube, or
esophageal-tracheal tube) has not been studied, effective ventilation
through a supraglottic airway device should result in a capnography
waveform during CPR and after ROSC.

Treat Box 3 directs you to treat hypotension when SBP is less than 90 mm
Hypotension Hg. Providers should obtain IV access if not already established.
(SBP Less Than Verify the patency of any IV lines. ECG monitoring should continue
90 mm Hg) after ROSC, during transport, and throughout ICU care until deemed
clinically not necessary. At this stage, consider treating any
reversible causes that might have precipitated the cardiac arrest but
persist after ROSC.
When IV is established, treat hypotension as follows:

• IV bolus 1-2 L normal saline or lactated Ringer’s

• Norepinephrine 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-
35 mcg per minute) IV infusion titrated to achieve a minimum
SBP of greater than 90 mm Hg or a mean arterial pressure of
greater than 65 mm Hg
• Epinephrine 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35
mcg per minute) IV infusion titrated to achieve a minimum SBP
 of greater than 90 mm Hg or a mean arterial pressure of greater
than 65 mm Hg
• Dopamine 5-10 mcg/kg per minute IV infusion titrated to
achieve a minimum SBP of greater than 90 mm Hg or a mean
arterial pressure of greater than 65 mm Hg

Norepinephrine (levarterenol) is a naturally occurring potent

vasoconstrictor and inotropic agent. It may be effective for
management of patients with severe hypotension (eg, SBP less than
70 mm Hg) and a low total peripheral resistance who do not respond
to less potent adrenergic drugs such as dopamine, phenylephrine,
or methoxamine.
Epinephrine can be used in patients who are not in cardiac arrest
but who require inotropic or vasopressor support.
Dopamine hydrochloride is a catecholamine-like agent and a
chemical precursor of nor-epinephrine that stimulates the heart
through both α- and β-adrenergic receptors.

STEMI Is Present Both in- and out-of-hospital medical personnel should obtain a 12-
or High lead ECG as soon as possible after ROSC to identify those patients
Suspicion of AMI with STEMI or a high suspicion of AMI. Once such patients have
been identified, hospital personnel should attempt coronary
reperfusion (Step 5).
EMS personnel should transport these patients to a facility that
reliably provides this therapy (Step 5).

Coronary Aggressive treatment of STEMI, including coronary reperfusion with

Reperfusion PCI, should begin if detected after ROSC, regardless of coma or
TTM. In the case of out-of-hospital STEMI, provide advance
notification to receiving facilities.

Following Step 4 directs you to examine the patient’s ability to follow verbal
Commands commands.
If the patient does not follow commands, the high-performance team
should consider implementing TTM (Step 7). If the patient is able to
follow verbal commands, move to Step 8.
Targeted To protect the brain and other organs, the high-performance team
Temperature should start TTM in patients who remain comatose (lack of
Management meaningful response to verbal commands) with ROSC after cardiac
arrest.
For TTM, healthcare providers should select and maintain a
constant target temperature between 32°C and 36°C for a period of
at least 24 hours. Although the optimal method of achieving the
target temperature is unknown, any combination of rapid infusion of
ice-cold, isotonic, non–glucose-containing fluid (30 mL/kg),
endovascular catheters, surface cooling devices, or simple surface
interventions (eg, ice bags) appears to be safe and effective.
Specific features of the patient may favor selection of one
temperature over another for TTM. Higher temperatures might be
preferred in patients for whom lower temperatures convey some risk
(eg, bleeding), and lower temperatures might be preferred when
patients have clinical features that are worsened at higher
temperatures (eg, seizures, cerebral edema). Of note, there are
essentially no patients for whom temperature control somewhere in
the range between 32°C and 36°C is contraindicated. Therefore, all
patients in whom intensive care is continued are eligible.
In the prehospital setting, routine cooling of patients after ROSC with
rapid infusion of cold IV fluids should not be done. Current evidence
indicates that there is no direct outcome benefit from these
interventions and that the IV fluid administration in the prehospital
setting may increase pulmonary edema and rearrest. Whether
different methods or devices for temperature control outside of the
hospital are beneficial is unknown.
Foundational Targeted Temperature Management
Facts
• TTM is the only intervention demonstrated to improve neurologic
recovery after cardiac arrest.
• The optimal duration of TTM is at least 24 hours. Comparative studies
of the duration of TTM have not been performed in adults, but
hypothermia for up to 72 hours was used safely in newborns.
• Healthcare providers should monitor the patient’s core temperature
during TTM by using an esophageal thermometer, bladder catheter in
nonanuric patients, or a pulmonary artery catheter if one is placed for
other indications. Axillary and oral temperatures are inadequate for
measurement of core temperature changes.
• TTM should not affect the decision to perform PCI, because
concurrent PCI and hypothermia are reported to be feasible and safe.
Advanced Critical After coronary reperfusion interventions or in cases where the
Care post–cardiac arrest patient has no ECG evidence or suspicion of
MI, the high-performance team should transfer the patient to an
ICU.

Post–Cardiac Arrest There is no evidence to support continued prophylactic

Maintenance administration of antiarrhythmic medications once the patient
Therapy achieves ROSC.

Life Is Science Is Why

Why Cardiovascular diseases claim more lives than all forms of cancer combined.
This unsettling statistic drives the AHA’s commitment to bring science to life
by advancing resuscitation knowledge and research in new ways.
References
1. Jauch EC, Saver JL, Adams HP Jr, et al; American Heart Association Stroke
Council, Council on Cardiovascular Nursing, Council on Peripheral Vascular
Disease, Council on Clinical Cardiology. Guidelines for the early management of
patients with acute ischemic stroke: a guideline for healthcare professionals from
the American Heart Association/American Stroke
Association. Stroke. 2013;44(3):870-947.
2. Adams HP Jr, del Zoppo G, Alberts MJ, et al; American Heart Association,
American Stroke Association Stroke Council, Clinical Cardiology Council,
Cardiovascular Radiology and Intervention Council, Atherosclerotic Peripheral
Vascular Disease Quality of Care Outcomes in Research Interdisciplinary Working,
Groups. Guidelines for the early management of adults with ischemic stroke: a
guideline from the American Heart Association/American Stroke Association Stroke
Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention
Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care
Outcomes in Research Interdisciplinary Working Groups: the American Academy of
Neurology affirms the value of this guideline as an educational tool for
neurologists. Stroke. 2007;38(5):1655-1711.
3. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP. Predicting survival from
out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med.1993;22(11):1652-
1658.
4. Valenzuela TD, Roe DJ, Cretin S, Spaite DW, Larsen MP. Estimating effectiveness
of cardiac arrest interventions: a logistic regression survival
model. Circulation. 1997;96(10):3308-3313.
5. Chan PS, Krumholz HM, Nichol G, Nallamothu BK. Delayed time to defibrillation
after in-hospital cardiac arrest. N Engl J Med. 2008;358(1):9-17.
6. Stiell IG, Wells GA, Field B, et al. Advanced cardiac life support in out-of-hospital
cardiac arrest. N Engl J Med. 2004;351(7):647-656.
7. Swor RA, Jackson RE, Cynar M, et al. Bystander CPR, ventricular fibrillation, and
survival in witnessed, unmonitored out-of-hospital cardiac arrest. Ann Emerg
Med. 1995;25(6):780-784.
8. Holmberg M, Holmberg S, Herlitz J. Incidence, duration and survival of ventricular
fibrillation in out-of-hospital cardiac arrest patients in
Sweden. Resuscitation.2000;44(1):7-17.
9. Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, et al. Vasopressin, epinephrine,
and corticosteroids for in-hospital cardiac arrest. Arch Intern Med.2009;169(1):15-
24.
10. Mentzelopoulos SD, Malachias S, Chamos C, et al. Vasopressin, steroids, and
epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a
randomized clinical trial. JAMA. 2013;310(3):270-279.
11. Paris PM, Stewart RD, Deggler F. Prehospital use of dexamethasone in pulseless
idioventricular rhythm. Ann Emerg Med. 1984;13(11):1008-1010.
12. Tsai MS, Huang CH, Chang WT, et al. The effect of hydrocortisone on the outcome
of out-of-hospital cardiac arrest patients: a pilot study. Am J Emerg
Med.2007;25(3):318-325.
13. Centers for Disease Control and Prevention. Injury prevention and control:
prescription drug overdose. http://www.cdc.gov/drugoverdose/index.html. Accessed
September 14, 2015.
14. Hedegaard H, Chen LH, Warner M. Drug-poisoning deaths involving heroin: United
States, 2000–2013. http://www.cdc.gov/nchs/data/databriefs/db190.htm. Accessed
September, 14, 2015.
15. Centers for Disease Control and Prevention. Fatal injury
data. http://www.cdc.gov/injury/wisqars/fatal.html. Accessed September 14, 2015.
16. Carter CI, Graham B. Opioid overdose prevention and response in
Canada. http://drugpolicy.ca/wp-
content/uploads/2014/07CDPC_OverdosePreventionPolicy_Final_July2014.pdf.
Accessed March 17, 2015.
17. Jones CM, Paulozzi LJ, Mack KA; Centers for Disease Control and Prevention
(CDC). Alcohol involvement in opioid pain reliever and benzodiazepine drug abuse-
related emergency department visits and drug-related deaths—United States,
2010. MMWR Morb Mortal Wkly Rep. 2014;63:881–885.
18. Madadi P, Hildebrandt D, Lauwers AE, Koren G. Characteristics of opioid-users
whose death was related to opioid-toxicity: a population-based study in Ontario,
Canada. PLoS One. 2013;8(4):e60600.
19. Webster LR, Cochella S, Dasgupta N, et al. An analysis of the root causes for
opioid-related overdose deaths in the United States. Pain Med. 2011;12 Suppl
2:S26-35.
20. Paulozzi LJ, Logan JE, Hall AJ, McKinstry E, Kaplan JA, Crosby AE. A comparison
of drug overdose deaths involving methadone and other opioid analgesics in West
Virginia. Addiction. 2009;104(9):1541-1548.
21. Krantz MJ, Kutinsky IB, Robertson AD, Mehler PS. Doserelated effects of
methadone on QT prolongation in a series of patients with torsade de
pointes. Pharmacotherapy. 2003;23(6):802-805.
22. Eap CB, Crettol S, Rougier JS, et al. Stereoselective block of hERG channel by
(S)-methadone and QT interval prolongation in CYP2B6 slow metabolizers. Clin
Pharmacol Ther. 2007;81(5):719-728.
23. Krantz MJ, Martin J, Stimmel B, Mehta D, Haigney MC. QTc interval screening in
methadone treatment. Ann Intern Med. 2009;150(6):387-395.
24. Stallvik M, Nordstrand B, Kristensen O, Bathen J, Skogvoll E, Spigset O. Corrected
QT interval during treatment with methadone and buprenorphine—relation to doses
and serum concentrations. Drug Alcohol Depend. 2013;129(1-2):88-93.
25. Chou R, Weimer MB, Dana T. Methadone overdose and cardiac arrhythmia
potential: findings from a review of the evidence for an American Pain Society and
College on Problems of Drug Dependence clinical practice guideline. J
Pain. 2014;15(4):338-365.
26. Lipski J, Stimmel B, Donoso E. The effect of heroin and multiple drug abuse on the
electrocardiogram. Am Heart J. 1973;86(5):663-668.
27. Labi M. Paroxysmal atrial fibrillation in heroin intoxication. Ann Intern
Med. 1969;71(5):951-959.
28. Leach M. Naloxone: a new therapeutic and diagnostic agent for emergency use. J
Amer Coll Emerg Phys. 1973;2:21-23.
29. Sporer KA, Firestone J, Isaacs SM. Out-of-hospital treatment of opioid overdoses in
an urban setting. Acad Emerg Med. 1996;3(7):660-667.
30. Robertson TM, Hendey GW, Stroh G, Shalit M. Intranasal naloxone is a viable
alternative to intravenous naloxone for prehospital narcotic overdose. Prehosp
Emerg Care. 2009;13(4):512-515.
31. Evans LE, Swainson CP, Roscoe P, Prescott LF. Treatment of drug overdosage
with naloxone, a specific narcotic antagonist. Lancet. 1973;1(7801):452-455.
32. Kelly AM, Kerr D, Dietze P, Patrick I, Walker T, Koutsogiannis Z. Randomised trial
of intranasal versus intramuscular naloxone in prehospital treatment for suspected
opioid overdose. Med J Aust. 2005;182(1):24-27.
33. Barton ED, Colwell CB, Wolfe T, et al. Efficacy of intranasal naloxone as a
needleless alternative for treatment of opioid overdose in the prehospital setting. J
Emerg Med. 2005;29(3):265-271.
34. Wolfe TR, Braude DA. Intranasal medication delivery for children: a brief review
and update. Pediatrics. 2010;126(3):532-537.
35. Loimer N, Hofmann P, Chaudhry HR. Nasal administration of naloxone is as
effective as the intravenous route in opiate addicts. Int J Addict. 1994;29(6):819-
827.
36. Doe-Simkins M, Walley AY, Epstein A, Moyer P. Saved by the nose: bystander-
administered intranasal naloxone hydrochloride for opioid overdose. Am J Public
Health. 2009;99(5):788-791.
37. Wanger K, Brough L, Macmillan I, Goulding J, MacPhail I, Christenson JM.
Intravenous vs subcutaneous naloxone for out-of-hospital management of
presumed opioid overdose. Acad Emerg Med. 1998;5(4):293-299.
38. Baumann BM, Patterson RA, Parone DA, et al. Use and efficacy of nebulized
naloxone in patients with suspected opioid intoxication. Am J Emerg
Med.2013;31(3):585-588.
39. Weber JM, Tataris KL, Hoffman JD, Aks SE, Mycyk MB. Can nebulized naloxone
be used safely and effectively by emergency medical services for suspected opioid
overdose? Prehosp Emerg Care. 2012;16(2):289-292.
40. Greenberg MI, Roberts JR, Baskin SI. Endotracheal naloxone reversal of
morphine-induced respiratory depression in rabbits. Ann Emerg
Med. 1980;9(6):289-292.
41. Callaway CW, Schmicker R, Kampmeyer M, et al. Receiving hospital
characteristics associated with survival after out-of-hospital cardiac
arrest. Resuscitation.2010;81(5):524-529.
42. Carr BG, Kahn JM, Merchant RM, Kramer AA, Neumar RW. Inter-hospital
variability in post-cardiac arrest mortality. Resuscitation. 2009;80(1):30-34.
43. Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial dysfunction in
survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol. 2002;40(12):2110-
2116.
44. Negovsky VA. The second step in resuscitation—the treatment of the “post-
resuscitation disease.” Resuscitation. 1972;1(1):1-7.
45. Safar P. Resuscitation from clinical death: pathophysiologic limits and therapeutic
potentials. Crit Care Med. 1988;16(10):923-941.
46. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,
pathophysiology, treatment, and prognostication. A consensus statement from the
International Liaison Committee on Resuscitation (American Heart Association,
Australian and New Zealand Council on Resuscitation, European Resuscitation
Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation,
Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa);
the American Heart Association Emergency Cardiovascular Care Committee; the
Council on Cardiovascular Surgery and Anesthesia; the Council on
Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical
Cardiology; and the Stroke Council. Circulation. 2008;118(23):2452-2483.
47. Skrifvars MB, Pettila V, Rosenberg PH, Castren M. A multiple logistic regression
analysis of in-hospital factors related to survival at six months in patients
resuscitated from out-of-hospital ventricular
fibrillation. Resuscitation. 2003;59(3):319-328.
48. Gaieski DF, Band RA, Abella BS, et al. Early goal-directed hemodynamic
optimization combined with therapeutic hypothermia in comatose survivors of out-
of-hospital cardiac arrest. Resuscitation. 2009;80(4):418-424.
49. Sunde K, Pytte M, Jacobsen D, et al. Implementation of a standardised treatment
protocol for post resuscitation care after out-of-hospital cardiac
arrest. Resuscitation. 2007;73(1):29-39.
50. Kirves H, Skrifvars MB, Vahakuopus M, Ekstrom K, Martikainen M, Castren M.
Adherence to resuscitation guidelines during prehospital care of cardiac arrest
patients. Eur J Emerg Med. 2007;14(2):75-81.
51. Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an
intensive care unit following cardiac arrest. Intensive Care Med. 2004;30(11):2126-
2128.
52. Anyfantakis ZA, Baron G, Aubry P, et al. Acute coronary angiographic findings in
survivors of out-of-hospital cardiac arrest. Am Heart J. 2009;157(2):312-318.
53. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary angiography in
survivors of out-of-hospital cardiac arrest. N Engl J Med. 1997;336(23):1629-1633.
54. Bunch TJ, White RD, Gersh BJ, et al. Long-term outcomes of out-of-hospital
cardiac arrest after successful early defibrillation. N Engl J Med.2003;348(26):2626-
2633.
55. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to
improve the neurologic outcome after cardiac arrest. N Engl J
Med.2002;346(8):549-556.
Airway Management

Skills Testing Checklist

Student Name ___________________ Date of Test ___________________

Critical Performance Steps ✓ if done correctly

BLS Assessment and Interventions

Checks for responsiveness •

• Taps and shouts, “Are you OK?”

Activates the emergency response system

• Shouts for nearby help/Activates the emergency response system and gets the AED

or

• Directs second rescuer to activate the emergency response system and get the AED

Checks breathing •

• Scans chest for movement (5-10 seconds)

Checks pulse (5-10 seconds)

Breathing and pulse check can be done simultaneously
Notes that pulse is present and does not initiate chest compressions or attach AED

Inserts oropharyngeal or nasopharyngeal airway

Administers oxygen

Performs effective bag-mask ventilation for 1 minute •

• Gives proper ventilation rate (once every 5-6 seconds)

• Gives proper ventilation speed (over 1 second)
• Gives proper ventilation volume (~half a bag)
Megacode Testing Checklist: Scenarios 1/3/8

Bradycardia ➔ Pulseless VT ➔ PEA ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if
Critical Performance Steps done
correctly

Team Leader

Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management

Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

Administers correct dose of atropine

Prepares for second-line treatment

Pulseless VT Management

Recognizes pVT

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

PEA Management

Recognizes PEA

Verbalizes potential reversible causes of PEA (H’s and T’s)

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm checks

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need for
endotracheal intubation and waveform capnography, and orders laboratory tests
 Considers targeted temperature management

Megacode Testing Checklist: Scenarios 2/5

Bradycardia ➔ VF ➔ Asystole ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if done
Critical Performance Steps
correctly

Team Leader
Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management
Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

Administers correct dose of atropine

Prepares for second-line treatment

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

Asystole Management
Recognizes asystole

Verbalizes potential reversible causes of asystole (H’s and T’s)

 Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm checks

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need
for endotracheal intubation and waveform capnography, and orders laboratory tests

Considers targeted temperature management

Megacode Testing Checklist: Scenarios 4/7/10

Tachycardia ➔ VF ➔ PEA ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if done
Critical Performance Steps
correctly

Team Leader
Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Tachycardia Management
Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes unstable tachycardia

Recognizes symptoms due to tachycardia

Performs immediate synchronized cardioversion

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

 Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

PEA Management
Recognizes PEA

Verbalizes potential reversible causes of PEA (H’s and T’s)

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm checks

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need
for endotracheal intubation and waveform capnography, and orders laboratory tests

Considers targeted temperature management

Megacode Testing Checklist: Scenarios 6/11

Bradycardia ➔ VF ➔ PEA ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if done
Critical Performance Steps
correctly
Team Leader
Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management
Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

 Administers correct dose of atropine

Prepares for second-line treatment

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

PEA Management
Recognizes PEA

Verbalizes potential reversible causes of PEA (H’s and T’s)

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm checks

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need
for endotracheal intubation and waveform capnography, and orders laboratory tests

Considers targeted temperature management

Megacode Testing Checklist: Scenario 9

Tachycardia ➔ PEA ➔ VF ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if done
Critical Performance Steps
correctly

Team Leader
Ensures high-quality CPR at all times
Assigns team member roles

Ensures that team members perform well

Tachycardia Management
Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes tachycardia (specific diagnosis)

Recognizes no symptoms due to tachycardia

Considers appropriate initial drug therapy

PEA Management
Recognizes PEA

Verbalizes potential reversible causes of PEA (H’s and T’s)

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm and pulse checks

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need
for endotracheal intubation and waveform capnography, and orders laboratory tests

Considers targeted temperature management

Megacode Testing Checklist: Scenario 12
Bradycardia ➔ VF ➔ Asystole/PEA ➔ PCAC

Student Name ___________________ Date of Test ___________________

✓ if done
Critical Performance Steps
correctly

Team Leader
Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management
Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

Administers correct dose of atropine

Prepares for second-line treatment

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug–rhythm check/shock–CPR

Administers appropriate drug(s) and doses

Asystole and PEA Management

Recognizes asystole and PEA

Verbalizes potential reversible causes of asystole and PEA (H’s and T’s)

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm checks

Post–Cardiac Arrest Care

Identifies ROSC

Ensures BP and 12-lead ECG are performed, O2 saturation is monitored, verbalizes need
for endotracheal intubation and waveform capnography, and orders laboratory tests
Considers targeted temperature management
Adult Cardiac Arrest Algorithm—2015 Update
Adult Cardiac Arrest Algorithm—2015 Update
Adult Bradycardia With a Pulse Algorithm
Adult Tachycardia With a Pulse Algorithm
Adult Immediate Post–Cardiac Arrest Care Algorithm—2015 Update
 ACLS Pharmacology Summary Table

Drug Indications Precautions/Contraindications Adult Dosage

Adenosine • First drug for most • Contraindicated in poison/drug- IV Rapid Push
forms of stable narrow- induced tachycardia or second-
complex SVT. or third-degree heart block • Place patient in
Effective in terminating • Transient side effects include mild reverse
those due to reentry flushing, chest pain or tightness, Trendelenburg
involving AV node or brief periods of asystole or position before
sinus node bradycardia, ventricular ectopy administration of
• May consider for • Less effective (larger doses may drug
unstable narrow- be required) in patients taking • Initial bolus of 6
complex reentry theophylline or caffeine mg given rapidly
tachycardia while • Reduce initial dose to 3 mg in over 1 to 3
preparations are made patients receiving dipyridamole seconds followed
for cardioversion or carbamazepine, in heart by NS bolus of
• Regular and transplant patients, or if given by 20 mL; then
monomorphic wide- central venous access elevate the
complex tachycardia, • If administered for irregular, extremity
thought to be or polymorphic wide-complex • A second dose
previously defined to tachycardia/VT, may cause (12 mg) can be
be reentry SVT deterioration (including given in 1 to 2
• Does not convert atrial hypotension) minutes if
fibrillation, atrial flutter, • Transient periods of sinus needed
or VT bradycardia and ventricular
• Diagnostic maneuver: ectopy are common after Injection
stable narrow-complex termination of SVT Technique
SVT • Safe and effective in pregnancy
• Record rhythm
strip during
administration
• Draw up
adenosine dose
and flush in 2
separate
syringes
• Attach both
syringes to the IV
injection port
closest to patient
• Clamp IV tubing
above injection
port
• Push IV
adenosine as
quickly as
 possible (1 to 3
seconds)
• While
maintaining
pressure on
adenosine
plunger, push NS
flush as rapidly
as possible after
adenosine
• Unclamp IV
tubing

Amiodarone Because its use is Caution: Multiple complex drug VF/pVT Cardiac
associated with toxicity, interactions Arrest
amiodarone is indicated Unresponsive to
for use in patients with • Rapid infusion may lead to CPR, Shock, and
life-threatening hypotension Vasopressor
arrhythmias when • With multiple dosing, cumulative
administered with doses >2.2 g over 24 hours are • First dose: 300
appropriate monitoring: associated with significant mg IV/IO push
hypotension in clinical trials • Second dose (if
• VF/pulseless VT • Do not administer with other needed): 150 mg
unresponsive to shock drugs that prolong QT interval IV/IO push
delivery, CPR, and a (eg, procainamide)
vasopressor • Terminal elimination is extremely Life-Threatening
• Recurrent, long (half-life lasts up to 40 days) Arrhythmias
hemodynamically Maximum
unstable VT cumulative
dose: 2.2 g IV over
With expert 24 hours. May be
consultation, amiodarone administered as
may be used for treatment follows:
of some atrial and
ventricular arrhythmias • Rapid
infusion: 150 mg
IV over first 10
minutes (15 mg
per minute). May
repeat rapid
infusion (150 mg
IV) every 10
minutes as
needed
• Slow
infusion: 360 mg
IV over 6 hours
(1 mg per
minute)
• Maintenance
infusion: 540 mg
 IV over 18 hours
(0.5 mg per
minute)

Atropine • First drug for • Use with caution in presence of Bradycardia

Sulfate symptomatic sinus myocardial ischemia and (With or Without
Can be given bradycardia hypoxia. Increases myocardial ACS)
via • May be beneficial in oxygen demand
endotracheal presence of AV nodal • Avoid in hypothermic bradycardia • 0.5 mg IV every 3
tube block. Not likely to be • May not be effective for to 5 minutes as
effective for type II infranodal (type II) AV block and needed, not to
second-degree or new third-degree block with wide exceed total dose
third-degree AV QRS complexes. (In these of 0.04 mg/kg
block or a block in patients, may cause paradoxical (total 3 mg)
nonnodal tissue slowing. Be prepared to pace or • Use shorter
• Routine use during give catecholamines) dosing interval (3
PEA or asystole is • Doses of atropine <0.5 mg may minutes) and
unlikely to have a result in paradoxical slowing of higher doses in
therapeutic benefit heart rate severe clinical
• Organophosphate (eg, conditions
nerve agent)
poisoning: extremely Organophosphate
large doses may be Poisoning
needed
Extremely large
doses (2 to 4 mg or
higher) may be
needed

Dopamine • Second-line drug for • Correct hypovolemia with volume IV Administration

IV infusion symptomatic replacement before initiating
bradycardia (after dopamine • Usual infusion
atropine) • Use with caution in cardiogenic rate is 2 to 20
• Use for hypotension shock with accompanying CHF mcg/kg per
(SBP ≤70 to 100 mm • May cause tachyarrhythmias, minute
Hg) with signs and excessive vasoconstriction • Titrate to patient
symptoms of shock • Do not mix with sodium response; taper
bicarbonate slowly

Epinephrine • Cardiac arrest: VF, • Raising blood pressure and Cardiac Arrest
Can be given pulseless VT, asystole, increasing heart rate may cause
via PEA myocardial ischemia, angina, • IV/IO dose: 1 mg
endotracheal • Symptomatic and increased myocardial (10 mL of 1:10
tube bradycardia: Can be oxygen demand 000 solution)
considered after • High doses do not improve administered
Available in atropine as an survival or neurologic outcome every 3 to 5
1:10 000 and alternative infusion to and may contribute to minutes during
1:1000 dopamine postresuscitation myocardial resuscitation.
concentrations • Severe dysfunction Follow each dose
hypotension: Can be • Higher doses may be required to with 20 mL flush,
used when pacing and treat poison/drug-induced shock elevate arm for
atropine fail, when
 hypotension 10 to 20 seconds
accompanies after dose
bradycardia, or with • Higher
phosphodiesterase dose: Higher
enzyme inhibitor doses (up to 0.2
• Anaphylaxis, severe mg/kg) may be
allergic used for specific
reactions: Combine indications (β-
with large fluid volume, blocker or
corticosteroids, calcium channel
antihistamines blocker
overdose)
• Continuous
infusion: Initial
rate: 0.1 to 0.5
mcg/kg per
minute (for 70-kg
patient: 7 to 35
mcg per minute);
titrate to
response
• Endotracheal
route: 2 to 2.5
mg diluted in 10
mL NS

Profound
Bradycardia or
Hypotension
2 to 10 mcg per
minute infusion;
titrate to patient
response

Lidocaine • Alternative to • Contraindication: Prophylactic Cardiac Arrest

Can be given amiodarone in cardiac use in AMI is contraindicated From VF/pVT
via arrest from VF/pVT • Reduce maintenance dose (not
endotracheal • Stable monomorphic loading dose) in presence of • Initial dose: 1 to
tube VT with preserved impaired liver function or LV 1.5 mg/kg IV/IO
ventricular function dysfunction • For refractory VF,
• Stable polymorphic VT • Discontinue infusion immediately may give
with normal baseline if signs of toxicity develop additional 0.5 to
QT interval and 0.75 mg/kg IV
preserved LV function push, repeat in 5
when ischemia is to 10 minutes;
treated and electrolyte maximum 3
balance is corrected doses or total of
• Can be used for stable 3 mg/kg
polymorphic VT with
baseline Perfusing
Arrhythmia
For stable VT, wide-
complex tachycardia
 • QT-interval of uncertain type,
prolongation if significant ectopy:
torsades suspected
• Doses ranging
from 0.5 to 0.75
mg/kg and up to
1 to 1.5 mg/kg
may be used
• Repeat 0.5 to
0.75 mg/kg every
5 to 10 minutes;
maximum total
dose: 3 mg/kg

Maintenance
Infusion
1 to 4 mg per minute
(30 to 50 mcg/kg per
minute)

Magnesium • Recommended for use • Occasional fall in blood pressure Cardiac Arrest
Sulfate in cardiac arrest only if with rapid administration (Due to
torsades de pointes or • Use with caution if renal failure is Hypomagnesemia
suspected present or Torsades de
hypomagnesemia is Pointes)
present 1 to 2 g (2 to 4 mL of
• Life-threatening a 50% solution
ventricular arrhythmias diluted in 10 mL [eg,
due to digitalis toxicity D5W, normal saline]
• Routine administration given IV/IO)
in hospitalized patients
with AMI is not Torsades de
recommended Pointes With a
Pulse or AMI With
Hypomagnesemia

• Loading dose of
1 to 2 g mixed in
50 to 100 mL of
diluent (eg, D5W,
normal saline)
over 5 to 60
minutes IV
• Follow with 0.5 to
1 g per hour IV
(titrate to control
torsades)
 2015 Science Summary Table
Topic 2010 2015
Systematic • 1-2-3-4 • Check responsiveness
Approach: BLS • Check responsiveness: o – Tap and shout
Assessment o – Tap and shout • Shout for nearby help/activate
(name change) o – Scan chest for movement emergency response system/get AED
• Activate the emergency response • Check breathing and pulse
system and get an AED (simultaneously)
• Circulation: Check the carotid pulse. • Defibrillation: If indicated, deliver a
If you cannot detect a pulse within 10 shock with an AED or defibrillator
seconds, start CPR, beginning with
chest compressions, immediately
• Defibrillation: If indicated, deliver a
shock with an AED or defibrillator

Systematic • Airway • Airway

Approach: • Breathing • Breathing
Primary • Circulation • Circulation
Assessment • Differential diagnosis (H’s and T’s) • Disability
(name change) • Exposure

Systematic • NA • SAMPLE
Approach: • H’s and T’s
Secondary
Assessment
(new)

BLS: High- • A rate of at least 100 chest • A rate of 100 to 120 chest
Quality CPR compressions per minute compressions per minute
• A compression depth of at least 2 • A compression depth of at least 2
inches in adults inches in adults*
• Allowing complete chest recoil after • Allowing complete chest recoil after
each compression each compression
• Minimizing interruptions in • Minimizing interruptions in
compressions (10 seconds or less) compressions (10 seconds or less)
• Avoiding excessive ventilation • Avoiding excessive ventilation
• Switching provddiac arrest with aiers • Chest compression fraction of at least
about every 2 minutes to avoid 60% but ideally greater than 80%
fatigue • Switch compressor about every 2
minutes or sooner if fatigued
• Use of audio and visual feedback
devices to monitor CPR quality
 *When a feedback device is available,
adjust to a maximum depth of 2.4 inches [6
cm]) in adolescents and adults.

ACLS: • Consider therapeutic hypothermia • Consider targeted temperature

Immediate Post– (32°C to 34°C for 12 to 24 hours) to management to optimize survival and
Cardiac Arrest optimize survival and neurologic neurologic recovery in comatose
Care recovery in comatose patients patients—cool to 32°C to 36°C for at
least 24 hours
• Out-of-hospital cooling of patients with
rapid infusion of cold IV fluids after
ROSC is not recommended

ACLS: Managing • For cardiac arrest with an advanced • For cardiac arrest with an advanced
the Airway airway in place, ventilate once every airway in place, ventilate once every 6
6 to 8 seconds seconds

ACLS: • Dopamine dosing: 2 to 10 mcg/kg per • Dopamine dosing: 2 to 20 mcg/kg per

Bradycardia minute minute

ACLS: ACS • NSTEMI • NSTE-ACS

• Titrate O2 saturation to ≥94% • Titrate O2 saturation to ≥90%

Topic 2015
ACLS: Cardiac • Removed vasopressin from the Cardiac Arrest Algorithm
Arrest • Administer epinephrine as soon as feasible after the onset of cardiac arrest due to
an initial nonshockable rhythm
• Added Opioid-Associated Life-Threatening Emergency (Adult) Algorithm
• Healthcare providers tailor the sequence of rescue actions based on the presumed
etiology of the arrest. Moreover, ACLS providers functioning within a high-
performance team can choose the optimal approach for minimizing interruptions in
chest compressions (thereby improving chest compression fraction [CCF]). Use of
different protocols, such as 3 cycles of 200 continuous compressions with passive
oxygen insufflation and airway adjuncts, compression-only CPR in the first few
minutes after arrest, and continuous chest compressions with asynchronous
ventilation once every 6 seconds with the use of a bag-mask device, are a few
examples of optimizing CCF and high-quality CPR. A default compression-to-
ventilation ratio of 30:2 should be used by less-trained healthcare providers or if
30:2 is the established protocol.
• Consider using ultrasound during arrest to detect underlying causes (eg, PE)
• Extracorporeal CPR may be considered among select cardiac arrest patients who
have not responded to initial conventional CPR, in settings where it can be rapidly
implemented
• Consider administering intravenous lipid emulsion, concomitant with standard
resuscitative care, to patients who have premonitory neurotoxicity or cardiac arrest
due to local anesthetic toxicity or other forms of drug toxicity and who are failing
standard resuscitative measures
ACLS: Stroke • Endovascular therapy (treatment window up to 6 hours)

Glossary
A
Acute Having a sudden onset and short course

Acute myocardial infarction The early critical stage of necrosis of heart muscle tissue caused by
(AMI) blockage of a coronary artery

Advanced cardiovascular Emergency medical procedures in which basic life support efforts of CPR
life support (ACLS) are supplemented with drug administration, IV fluids, etc

Asystole Absence of electrical and mechanical activity in the heart

Atrial fibrillation In atrial fibrillation the atria “quiver” chaotically and the ventricles beat
irregularly

Atrial flutter Rapid, irregular atrial contractions due to an abnormality of atrial excitation

Atrioventricular (AV) block A delay in the normal flow of electrical impulses that cause the heart to
beat

Automated external A portable device used to restart a heart that has stopped
defibrillator (AED)

B
Basic life support (BLS) Emergency treatment of a victim of cardiac or respiratory arrest through
cardiopulmonary resuscitation and emergency cardiovascular care

Bradycardia Slow heartbeat, whether physiologically or pathologically

C
Capnography The measurement and graphic display of CO2 levels in the airways, which
can be performed by infrared spectroscopy

Cardiac arrest Temporary or permanent cessation of the heartbeat

Cardiopulmonary A basic emergency procedure for life support, consisting of mainly manual
resuscitation (CPR) external cardiac massage and some artificial respiration

Coronary syndrome A group of clinical symptoms compatible with acute myocardial ischemia.
Also called coronary heart disease.

Coronary thrombosis The blocking of the coronary artery of the heart by a thrombus

E
Electrocardiogram (ECG) A test that provides a typical record of normal heart action

Endotracheal (ET) The passage of a tube through the nose or mouth into the trachea for
intubation maintenance of the airway
Esophageal-tracheal tube A double-lumen tube with inflatable balloon cuffs that seal off the
hypopharynx from the oropharynx and esophagus; used for airway
management

H
Hydrogen ion (acidosis) The accumulation of acid and hydrogen ions or depletion of the alkaline
reserve (bicarbonate content) in the blood and body tissues, decreasing
the pH

Hyperkalemia An abnormally high concentration of potassium ions in the blood. Also

called hyperpotassemia.

Hypoglycemia An abnormally low concentration of glucose in the blood

Hypokalemia An abnormally low concentration of potassium ions in the blood. Also

called hypopotassemia.

Hypothermia When the patient’s core body temperature is below 96.8°F (36°C)

Hypovolemia A decrease in the volume of circulating blood

Hypoxia A deficiency of oxygen reaching the tissues of the body

I
Intraosseous (IO) Within a bone

Intravenous (IV) Within a vein

M
Mild hypothermia When the patient’s core body temperature is between 93.2°F and 96.8°F

Moderate hypothermia When the patient’s core body temperature is from 86°F to 93.2°F

N
Nasopharyngeal Pertaining to the nose and pharynx

O
Oropharyngeal airway A tube used to provide free passage of air between the mouth and pharynx

P
Perfusion The passage of fluid (such as blood) through a specific organ or area of
the body (such as the heart)

Prophylaxis Prevention of or protection against disease

Pulmonary edema (PE) A condition in which fluid accumulates in the lungs

Pulseless electrical activity Continued electrical rhythmicity of the heart in the absence of effective
(PEA) mechanical function

R
Recombinant tissue A clot-dissolving substance produced naturally by cells in the walls of
plasminogen activator blood vessels
(rtPA)

S
Severe hypothermia When the patient’s core body temperature is below 86°F

Sinus rhythm The rhythm of the heart produced by impulses from the sinoatrial node

Supraglottic Situated or occurring above the glottis

Synchronized cardioversion Uses a sensor to deliver a shock that is synchronized with a peak in the
QRS complex

Syncope A loss of consciousness over a short period of time, caused by a

temporary lack of oxygen in the brain

T
Tachycardia Increased heartbeat, usually ≥100/min

Tamponade (cardiac) A condition caused by accumulation of fluid between the heart and the
pericardium, resulting in excess pressure on the heart. This impairs the
heart’s ability to pump sufficient blood.

Tension pneumothorax Pneumothorax resulting from a wound in the chest wall which acts as a
valve that permits air to enter the pleural cavity but prevents its escape

Thrombus A blood clot formed within a blood vessel

U
Unsynchronized shock An electrical shock that will be delivered as soon as the operator pushes
the shock button to discharge the defibrillator. Thus, the shock can fall
anywhere within the cardiac cycle.

V
Ventricular fibrillation (VF) Very rapid uncoordinated fluttering contractions of the ventricles

Ventricular tachycardia (VT) A rapid heartbeat that originates in one of the lower chambers (ventricles)
of the heart