PEMICU I KEGAWATDARURATAN

ALFINDRA SEPALAWANDIKA
 LEARNING OBJECTIVE
• ACS (Acute Coronary syndrome)
• Syok Kardiogenik
• Aritmia
• Krisis Hipertensi
• Cardiac Arrest
ACUTE CORONARY SYNDROME
 ISCHEMIC HEART DISEASE

Coronary Artery
Disease
Ischemic Heart
UA & NSTEMI
Disease
Acute Coronary
Syndromes
STEMI

Harrison’s Principle of Internal Medicine 18th Ed

 ISCHEMIC HEART DISEASE
• Main symptom : Angina Pectoris
– Stable : chest/arm discomfort reprudicibly
associated with physical exertion or stress and is
relieved within 5-10mins by rest or sublingual
nutroglycerin
– Unstable : at least have one of three features
• Occurs at rest, lasting >10mins
• Severe and new onset
• Crescendo pattern

Harrison’s Principle of Internal Medicine 18th Ed

ISCHEMIC HEART DISEASE

Rosen’s Emergency Medicine 7th Ed

ACUTE CORONARY SYNDROMES

Harrison’s Principle of Internal Medicine 18th Ed

UNSTABLE ANGINA & NON-ST-
ELEVATION MYOCARDIAL INFARCTION
PATHPHYSIOLOGY

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CLINICAL PRESENTATION
• History & Physical Examination
– Chest pain in substernal or epigastrium region
radiates to neck, left arm, left shoulder
– Large infarction  diaphoresis, pale cool skin,
sinus tachycardia, 3rd and 4th heart sound, basilar
rales, LVD  hypotension
• ECG
– ST : depression or transient elevation
– T –waves inversion

Harrison’s Principle of Internal Medicine 18th Ed

 CLINICAL PRESENTATION
• Cardiac Biomarkers
– CKMB and Troponin, if elevated  NSTEMI, if not
elevated  UA

Harrison’s Principle of Internal Medicine 18th Ed

DIAGNOSTIC EVALUATION AND RISK
STRATIFICATION

Harrison’s Principle of Internal Medicine 18th Ed

CLINICAL CLASSIFICATION
DIFFERENTIAL DIAGNOSIS

Rosen’s Emergency Medicine 7th Ed

 MANAGEMENT
• Combination of Bed Rest, Nitrates, Beta
Blocker, + Continuous ECG Monitoring
• Antithrombotic Therapy
• Long term therapy consist of
– Beta Blockers + Statin + ACEi + Aspirin +
Clopidogrel for 12 months
– Aspirin continued to prevent thrombosis

Harrison’s Principle of Internal Medicine 18th Ed

 MANAGEMENT
• Drugs
– Nitrates
• Sublingual or IV
• Avoid in hypotension, patients with sildenafil

– Beta Blockers
• Used in unstable angina
• Avoid when : PR interval >0,24s, AV block, HR<60x, BP
<90mmHg, Shock, LV Failure, Airway disease

Harrison’s Principle of Internal Medicine 18th Ed

 MANAGEMENT
– CCB
• If both above drugs cannot relieve symptoms
• Avoid in Pulmonary Edema and LV dysfunction
– Morphine
• Analgesics, if pain persist after 3 nitroglycerin
• Avoid in hypotension, Respiratory distress, confusion,
obtudantion.
– Antithrombotic Agents

Harrison’s Principle of Internal Medicine 18th Ed

MANAGEMENT
Harrison’s Principle of Internal Medicine 18th Ed
 PRINZMETAL ANGINA
• A syndrome of ischemic pain that occurs at
rest but not usually with exertion and
associated with transient ST elevation
• Caused by focal spasm of coronal artery 
severe myocardial infacrtion
• Managed by Nitrates and CCB. Avoid aspirin.

Harrison’s Principle of Internal Medicine 18th Ed

ST-ELEVATION MYOCARDIAL
INFARCTION
 PATHOPHYSIOLOGY
• Thrombotic occlusion of Coronary artery with
atherosclerosis  Coronary blood flow ↓
• Coronary artery thrombus develop rapidly at
vascular injury site
• Affected by : Smoking, HT, Lipid accumulation
• Atherosclerotic plaque disrupted 
thrombogenesis (collagen, ADP, epinefrin,
serotonin) + Thromboxane A2  platelet
active
Harrison’s Principle of Internal Medicine 18th Ed
 PATHPHYSIOLOGY
• Myocardial damage depends on
– Territory supplied by affected vessel
– Whether or not the vessel become total occluded
– Duration of occlusion
– Quantity of blood supplied by collateral vessels
– Demand of oxygen
– Native factors that can produce spontaneous lysis
– Adequacy of reperfusion after flow restored

Harrison’s Principle of Internal Medicine 18th Ed

 CLINICAL PRESENTATION
• Precipitating factor
– Physical exercise, emotional stress,
medical/surgical illness
– Symptoms does not subsides after rest / nitrates
• General Appearance
– Anxious, distress, chest pain radiates to left arm
and neck and jaw, Levine Sign, weakness,
sweating, nausea, vomiting

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CLINICAL PRESENTATION
• Heart Rate
– May vary from bradycardia or tachycardia
– When in pain  tachycardia
• Blood Pressure
– Uncomplicated  normotensive
– Systolic ↓ Diastolic ↑
– When in pain  hypertension
– LV dysfunction  hypotension

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CLINICAL PRESENTATION
• Temperature & Respiration
– Fever (38oC - 39oC) in 24-48h, subsides in 4-5days
– RR elevated when STEMI occurs
• Carotid pulse
– Small pulse  Reduced Stroke Volume
– Sharp Brief  mitral regurgitation, ventricular
septum rupture
– Pulsus alternans  LV dysfunction

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CLINICAL PRESENTATION
• Cardiac Examination
– ↓ intensity of 1st heart sound
– 3rd or 4th heart sound may be audible
– Murmur or friction rubs

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CLINICAL PRESENTATION
• Laboratory Findings
– ECG  ST evelation, Evolve Q waves
– Cardiac Biomarkers (Table on next slide)
– PMN Leukocytosis (12000-15000)
– ESR N in 1st and 2nd day, elevated in 4th day
– Imaging
• Echocardiography : abnormal wall motion
• Radionuclide Imaging Techniques
• High Resolution MRI + contrast

Harrison’s Principle of Internal Medicine 18th Ed

CLINICAL PRESENTATION

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 CARDIAC BIOMARKERS

Braunwald’s Hearts Disease : Textbook of

Cardiovascular Medicine 9th Ed
Rosen’s Emergency Medicine 7th Ed
 MANAGEMENT
• Initial Management
– Prehospital care
– Management in Emergency Department
– Control of Discomfort
– Management strategies
– Limitation of Infarc size
– Reperfusion (PCI or Fibrinolytic)
– Hospital Care Management
– Pharmacotherapy
Harrison’s Principle of Internal Medicine 18th Ed
 PREHOSPITAL CARE
• Major elements
– Recognition of symptoms
– Rapid deployment of EMS
– Expeditious transportation
– Expeditious implementation of reperfusion

Harrison’s Principle of Internal Medicine 18th Ed

MAJOR COMPONENTS OF TIME DELAY

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 STEMI
ALGORYTHM

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 MANAGEMENT IN EMERGENCY
DEPARTMENT
• Face mask oxygen
• Aspirin 160-235mg chewed
• To relief discomfort
– Sublingual nitroglycerin : 3x0,4mg /5mins, avoided
when BP <90mmHg
– Morphine : analgesic, may cause constriction, AV
block  atropine
– IV beta blocker  metoprolol 3x5mg/2-5mins

Harrison’s Principle of Internal Medicine 18th Ed

MANAGEMENT STRATEGY

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

LIMITATION OF INFARC SIZE

Rosen’s Emergency Medicine 7th Ed

 REPERFUSION THERAPY
• Primary Percutaneous Coronary Intervention
– Angioplasty or stenting
– More effective than fibrinolysis
– Better short and long term outcomes
– Preffered when diagnosis in doubt, cardiogenic
shock, bleeding risk, symptoms have been present
for 2-3h
– Very expensive

Harrison’s Principle of Internal Medicine 18th Ed

 REPERFUSION THERAPY
• Fibrinolysis
– Agents : tPA, streptokinase, TNK, rPA
– Initiated within 30mins
– Benefits seen if administered in 1-6hrs
– More preffered if symptoms still in 1st hour
– tPA 15mg bolus  50mg IV / 30mins  35mg IV /
60 mins
– Contraindication (next slide)

Harrison’s Principle of Internal Medicine 18th Ed

CONTRAINDICATIONS OF FIBRINOLYSIS

CLEAR / ABSOLUTE RELATIVE

• History of Cerebrovascular • Current use of
hemorrhage antucoagulants
• Marked Hypertension • Recent invasive surgical
procedure
• Suspicion of aortic disection
• Prolonged cardiopulmonary
• Active internal bleeding ressucitation
• Known bleeding diathesis,
pregnancy, DM,
hemmorhagic ophtalmic
• History of severe HT

Harrison’s Principle of Internal Medicine 18th Ed

 PHARMACOTHERAPY
• Antithrombotic Agents
– Aspirin + Clopidogrel
– G IIB/IIIA receptor inhibitor
– UFH / LMWH, warfarin
• Beta Blockers
– Acute IV Beta blockers
– Long term therapy

Harrison’s Principle of Internal Medicine 18th Ed

 PHARMACOTHERAPY
• ACEi
– Reduce ventricular dysfunction
– Reduce risk of CHF
– Reduce risk of reocclusion
– ARB for intolerance patients
• Others
– Strict control of blood glucose, serum magnesium,
etc

Harrison’s Principle of Internal Medicine 18th Ed

CARDIAC ARREST
DEFINITION

Harrison’s Principle of Internal Medicine 18th Ed

CAUSES OF CARDIAC ARREST

Rosen’s Emergency Medicine 7th Ed

CARDIOGENIC SHOCK AND DEATH

Braunwald’s Hearts Disease : Textbook of Cardiovascular Medicine 9th Ed

 ALGORITHM
FOR
VF / VT

Harrison’s Principle of Internal Medicine 18th Ed

 Pulseless Electrical Activity (PEA)
• Cardiac conduction impulses occur in organized pattern, but this
fails to produce myocardial contraction (former “electromechanical
dissociation”); or insufficient ventricular filling during diastole; or
ineffective contractions
• Occur 5% of in-hospital cardiac arrest

• ECG: Rhythm displays organized electrical activity (not VF/pulseless

VT)
• Seldom as organized as normal sinus rhythm
• Poor prognosis
• Clinical Manifestations:
– Collapse; unconscious
– Agonal respirations or apnea
– No pulse detectable by arterial palpation
• Etiologies
– Hypovolemia
– “Tablets” (drug OD, ingestions)
– Tamponade, cardiac
• Treatment:
– Per PEA algorithm
– Primary ABCD (basic CPR)
– Secondary
• AB (advanced airway and ventilation);
• C (IV, epinephrine, atropine if electrical activity <60
complexes per minute);
• D (identify and treat reversible causes)
 ASYSTOLE
• Occur in 25% of in-hospital cardiac arrest
• Occur 10% of out-side hospital cardiac arrest
• Characterized by ventricular standstill due to suppression of
the cardiac peacemaker by myocardial disease, anoxia,
electrolyte imbalance,or drugs

• ECG shows flat traces

• Often represent massive heart damage
• Survival less than 4%
• Clinical Manifestations:
– Early may see agonal respirations; unconscious;
unresponsive
– No pulse; no blood pressure
– Cardiac arrest
• Etiologies:
– End of life (death)
– Ischemia/hypoxia from many causes
– Acute respiratory failure (no oxygen; apnea; asphyxiation)
– Massive electrical shock: electrocution; lightning strike
– Postdefibrillatory shocks
• Treatment:
– Always check for status
– Primary ABCD survey (basic CPR)
– Secondary ABCD survey
 ALGORYTHM
FOR
BRADYCARDIA
OR ASYSTOLE

Harrison’s Principle of Internal Medicine 18th Ed

CARDIOGENIC SHOCK
 Description
• Inadequate tissue perfusion due to cardiac
dysfunction
• Underlying mechanisms in acute myocardial
infarction (AMI):
– Pump failure:
• left ventricle (LV) infarct
• Infarct in pre-existing LV dysfunction
• Reinfarction
 Description
– Mechanical complications:
• Acute mitral regurgitation
• Ventricular septal defect
• LV rupture
• Pericardial tamponade
– Right ventricular (RV) infarction
 Etiology
• AMI
• Sepsis
• Myocarditis
• Cardiomyopathy
• Drug toxicity:
– Beta-blocker
– Calcium channel blocker
– Adriamycin
• etc
 Signs and Symptoms
• General:
– Cyanosis
– Pallor
– Diaphoresis
– Dulled sensorium
– Decrease in body temperature
– Urine flow of less than 20 mL/h
 Signs and Symptoms
• Cardiac:
– Ischemic chest pain
– Systolic apical blowing murmur
– Gallop rhythm:
• S3 reflects severe myocardial dysfunction
• S4 is present in 80% patients in sinus rhythm with AMI
– Systolic click:
• Suggests rupture of the chordae tendinae
 Signs and Symptoms
• Neck:
– Jugular venous distention
• Abdominal:
– Epigastric pain
– Nausea and vomiting
• Neurologic:
– Obtundation
 Test
Electrocardiogram
• Normal ECG does not rule out AMI.
• Findings of AMI (ST-elevations in two or more
contiguous leads)
• May occur in non-ST-elevation acute coronary
syndrome
• Dysrhythmias
• LV hypertrophy
 Test
Chest Radiography
• Pulmonary congestion
• Pleural effusion
• Cardiomegaly
• Pneumonia
• Pneumothorax
• Pericardial effusion
 Test
Emergent Echocardiography
• Transthoracic echocardiography (TTE) with color Doppler
• LV contractility looking for hypokinesis, akinesis or
dyskinesis
• Acute mitral regurgitation or septal defects
• RV dilatation, tricuspid insufficiency, high pulmonary artery
and RV pressures suggest pulmonary embolism
• RV hypokinesis or akinesis, RV dilatation, normal
pulmonary pressures suggest RV infarction
• Pericardial effusion, right atrium or RV diastolic collapse
suggest cardiac tamponade
 Lab
• B-type natriuretic peptide (BNP):
– Diagnostic and prognostic value
• Creatine kinase (CK), CK-Mb, troponin
• Electrolytes and renal function
– Acute renal failure is a strong predictor of
mortality
• CBC:
– Identify anemia or elevated WBC
• Drug levels (e.g., digoxin)
 Differential Diagnosis
• Obstructive shock
• Distributive shock
• Hypovolemic shock
 Treatment
Pre Hospital
• CABs, IV access, O2, monitor
• Consider fluid bolus if no crackles.
• Aspirin
• Nitroglycerin or morphine sulfate for chest
pain in absence of hypotension
• Transport AMI patients to facility with 24-hour
cardiac revascularization capability.
 Treatment
Initial Stabilization
• CABs
• Two large bore peripheral IV lines
• Cardiac monitor
• Endotracheal intubation for airway compromise:
– Consider etomidate for induction (minimal effect on
blood pressure)
• Fluid challenge (100–250 mL normal saline) in
absence of pulmonary congestion
• Foley catheter to monitor urine output
 Treatment
Medication (Drugs)
• Dobutamine
• Dopamine
• Furosemide
• Milrinone
• Nitroglycerin
• Nitroprusside
• Norepinephrine
BASIC LIFE SUPPORT
CPR
BLS pada dewasa
 Definition
• CPR is an organized, sequential response to
cardiac arrest, including
– Recognition of absent breathing and circulation
– Basic life support with chest compression and rescue
breathing
– Advanced cardiac life support (ACLS) with definitive
airway and rhythm control
– Postresuscitative care
• Prompt initiation of chest compression and early
defibrillation (when indicates) are the key of
success.
 When to start CPR
Anyone who initiate resuscitation knowledge and skills to
initiate CPR when dealing with cases of cardiac arrest.

A. Incidence of cardiac arrest who witnessed

– If we are witnessing the cardiac arrest, was should immediately
started CPR. However, there are circumstances like this some
underlying unnecessary
CPR started:
– There is evidence of demand for family
– CPR efforts will harm people who helped
– Possible CPR can restore spontaneous circulation is very small
– Cardiac arrest happened on terminal illness who have been
treated to the maximum
B. Incidence of cardiac arrest was not witnessed
• Helper ill cardiac know how long it's been going
on. For something like this we do not need to
start doing CPR if the state finds as follows:
– There is a sign that death does not change like rigor
mortis / bruised corpse
– It's getting no signs of decay
– Patients experiencing trauma that can not be saved,
such as charred, decapitation
 When to stop CPR
There are several compelling reasons for rescuers to stop CPR
among other things:
• Helpers are doing basic and advanced life support optimal
included:
• CPR, defibrillation in patients with VF / VT without a pulse, vasopressin
/ epinephrine IV, open the airway, ventilation and oxygenation using
airway aid and all levels lanut rhythm after treatment performed.
• Helpers are considering whether there is a hypothermia
patient. Helpers has established the presence / absence of
hypothermia by measuring body temperature.
• Helpers have considered whether patients
exposed to toxic materials or an overdose that
inhibits CNS.
• Helper was recorded through a monitor
systolic settled for 10 minutes or more.
• The time interval pd cardiac resuscitation
efforts were unsuccessful witnessed restore
spontaneous circulation was 25-30 minutes.
 General Technique of CPR continued
• If alone, alternate 30 chest compressions and
2 ventilations for any age patient
• In two-rescuer CPR for infant/child, alternate
15 compressions and 2 ventilations
– Chest-encircling method in infant
• Give each ventilation over 1 second
• Follow local protocol regarding oxygen
Put hand(s) in correct position
for chest compressions
Give 30 chest compressions at
rate of 100 per minute
Then give 2 ventilations
 AHA 2013
• Post- Cardiac Arrest Care
– Change:New 5th link in the chain of survival

– Why : Emphasize importance of comprehensive

multidisciplinary care through hospital discharge and
beyond

– Includes : Optimizing vital organ perfusion

• Titration of FiO2 to maintain O2 sat ≥ 94% and < 100%
• Transport to comprehensive post-arrest system of care
• Emergent coronary reperfusion for STEMI or high suspicion of AMI
• Temperature control
• Anticipation, treatment, and prevention of multiple organ dysfunction
 Treatment
• the initial response and basic life support
• public access defibrillation (if available)
• advanced life support
• postresuscitation care
• long-term management