A SEMINAR PRESENTATION

ON

CARDIAC ARREST

BY

DEPARTMENT OF ANATOMY,

FACULTY OF BASIC MEDICAL SCIENCES,

LADOKE AKINTOLA UNIVERSITY OF TECHNOLOGY, OGBOMOSO, OYO

STATE, NIGERIA.

IN PARTIAL FULFILMENT OF THE AWARD OF BACHELOR OF

TECHNOLOGY (B.TECH) IN HUMAN ANATOMY.

JANUARY, 2024.
 TABLE OF CONTENT

TITLE PAGE

TABLE OF CONTENT

CHAPTER ONE

1.0 INTRODUCTION TO CARDIAC ARREST

CHAPTER TWO

2.1 SIGNS AND SYMPTOM OF CARDIAC ARREST

2.2 RISK FACTORS OF CARDIAC ARREST

2.3 CAUSES

2.4 MECHANISMS

2.5 DIAGNOSIS

2.6 PREVENTION

2.7 TREATMENT

CHAPTER THREE

3.0 CONCLUSION

REFERENCES
 CHAPTER ONE
INTRODUCTION
1.0 CARDIAC ARREST
As defined by the American Heart Association and the American College
of Cardiology, "(sudden) cardiac arrest is the sudden cessation of cardiac
activity so that the victim becomes unresponsive, with no normal breathing and
no signs of circulation. If corrective measures are not taken rapidly, this
condition progresses to sudden death. Cardiac arrest should be used to signify
an event as described above, that is reversed, usually by
CPR and/or defibrillation or cardioversion, or cardiac pacing. Sudden cardiac
death should not be used to describe events that are not fatal." (Kuller, 1980)

Those suffering from cardiac arrest may or may not have previously
diagnosed with heart disease. The cause of cardiac arrest varies by population
and age, most commonly occurring in those with a previous diagnosis of heart
disease. Most of all cardiac deaths are sudden and usually unexpected, which
has proven to be uniformly fatal in the past. However, bystander
Cardiopulmonary Resuscitation (CPR) and advances within Emergency Medical
Services (EMS) have proven life-saving interventions. Despite this,
approximately 10% of those suffering from cardiac arrest leave the hospital
alive, most of which are neurologically impaired. (Wong, 2014)

In the United States, approximately 535,000 cases occur annually (about

13 per 10,000 people). Of these, 326,000 (61%) experience cardiac arrest
outside of a hospital setting, while 209,000 (39%) occur within a
hospital. Cardiac arrest becomes more common with age and affects males
more often than females. Twice as many black men die from a cardiac arrest
than white men. Asian and Hispanic people are not as frequently affected as
white people. (Kronick et al. 2015)
 CHAPTER TWO

2.0 SIGNS AND SYMPTOMS OF CARDIAC ARREST

Cardiac arrest is not preceded by any warning symptoms in approximately

50 percent of people. For individuals who do experience symptoms, the
symptoms are usually nonspecific to the cardiac arrest. This can present in the
form of new or worsening:

 Chest Pain
 Fatigue
 Blackouts
 Dizziness
 Shortness of Breath
 Weakness
When cardiac arrest is suspected by a layperson due to signs of
unconsciousness and abnormal breathing, it should be assumed that the victim
is in cardiac arrest, and CPR should be initiated. If suspected by a trained
healthcare professional, they should attempt to feel for a pulse for 10 seconds
before initiating CPR. As a result of loss of blood flow to the brain, the person
will rapidly lose consciousness and can stop breathing. Coma can result from a
reversed cardiac arrest when the brain has been without oxygen for too
long. Near-death experiences are reported by 10 to 20 percent of people who
survived cardiac arrest, which demonstrates that a certain level of cognition is
still active during resuscitation. (Parnia et al., 2007)

2.1 RISK FACTORS OF CARDIAC ARREST

The risk factors for cardiac arrest are similar to those of coronary artery
disease and include age, cigarette smoking, high blood pressure, high
cholesterol, lack of physical exercise, obesity, diabetes, family history,
and cardiomyopathy. A statistical analysis of many of these risk factors
determined that approximately 50% of all cardiac arrests occur in 10% of the
population perceived to be at greatest risk due to aggregate harm of multiple risk
factors, demonstrating that cumulative risk of multiple comorbidities exceeds the
sum of each risk individually. (Mann et al., 2015)

Previous adverse cardiac events, non-sustained ventricular

tachycardia (NSVT), syncope, and left ventricular hypertrophy (LVT) have been
shown to predict sudden cardiac death in children. Current cigarette smokers
with coronary artery disease were found to have a two to threefold increase in
the risk of sudden death between ages 30 and 59. Furthermore, it was found
that former smokers' risk was closer to that of those who had never smoked.
(Jonas et al., 2003)

Functional changes in the heart such as reduced ejection fraction or

cardiac arrhythmia have been shown to increase the risk of cardiac arrest and
act independently from the aforementioned risk factors. Conditions that produce
these functional changes can be acquired following previous cardiac injury or
inherited through familial history of arrhythmogenic disorders. (Mann et al.,
2015)

2.2 CAUSES OF CARDIAC ARREST

Sudden cardiac arrest can result from cardiac and non-cardiac causes
including the following:

Cardiac Causes
2.2.1 Coronary artery disease

Normal vs blocked coronary artery (Wikipedia, 2023)

 Coronary artery disease (CAD), also known as ischemic heart disease, is
responsible for 62 to 70 percent of all sudden cardiac deaths. CAD is a much
less frequent cause of sudden cardiac death in people under the age of
40. Cases have shown that the most common finding at postmortem
examination of sudden cardiac death is chronic high-grade stenosis of at least
one segment of a major coronary artery, an artery that supplies the heart muscle
with its blood supply. (Shah 2005)

This stenosis is often the result of narrowing and hardening of the arteries
following deposition of cholesterol plaques and inflammation over several years.
This accumulation and remodeling of the coronary vessels along with other
systemic blood vessels characterizes the progression of Atherosclerotic
Cardiovascular Disease. (Pahwa and Jialal, 2021)

When a stable plaque ruptures, it can block the flow of blood and oxygen
through small arteries resulting in ischemic injury as a result. The injury to tissue
following ischemia can lead to structural and functional changes preventing the
heart from continuing normal conduction cycles and altering heart rate. (Mann et
al., 2015)

2.2.2 Non-atherosclerotic coronary artery abnormalities

Abnormalities of the coronary arteries not related to atherosclerosis include

congenital coronary artery anomalies (most commonly anomalous origin of the
left coronary artery from the pulmonary artery), inflammation known as
coronary arteritis, embolism, vasospasm, and mechanical abnormalities related
to connective tissue diseases or trauma. These conditions account for 10-15%
of cardiac arrest and sudden cardiac death. (Mann et al., 2015)

 Coronary arteritis commonly results from a pediatric febrile inflammatory

condition known as Kawasaki disease. Other types of vasculitis can also
contribute to an increased risk of sudden cardiac death.
 Embolism, or clotting, of the coronary arteries most commonly occurs from
septic emboli secondary to endocarditis with involvement of the aortic valve,
tricuspid valve, or prosthetic valves.
 Coronary vasospasm may result in cardiac arrhythmias, altering the heart's
electrical conduction with a risk of complete cardiac arrest from severe or
prolonged rhythm changes.
 Mechanical abnormalities with an associated risk of cardiac arrest may arise
from coronary artery dissection, which can be attributed to Marfan
Syndrome or trauma. (Mann et al., 2015)
2.2.3 Structural heart disease

(Wikipedia, 2023)

Short axis view of the heart demonstrating wall thickening in left ventricular hypertrophy

Structural heart diseases unrelated to coronary artery disease account for 10%
of all sudden cardiac deaths. Examples of these include: cardiomyopathies
(hypertrophic, dilated, or arrhythmogenic), cardiac rhythm disturbances,
myocarditis, hypertensive heart disease, and congestive heart failure. (Zheng et
al., 2001)

Left ventricular hypertrophy is thought to be a leading cause of sudden

cardiac deaths in the adult population. This is most commonly the result of
longstanding high blood pressure, or hypertension, which has caused a
maladaptive change to the wall of the heart's main pumping chamber, the left
ventricle. Increased blood pressure means the heart must pump harder to
adequately circulate blood throughout the body. If the heart does this for a
prolonged period of time due to uncontrolled hypertension, the left ventricle can
experience hypertrophy (grow larger) in a way that decreases the heart's
effectiveness. Left ventricular hypertrophy can be demonstrated on
an echocardiogram and electrocardiogram (EKG). (Bornstein et al., 2021)

Congestive heart failure increases the risk of sudden cardiac death

fivefold. Structural abnormalities of the cardiac conduction system (notably
the Atrioventricular Node and His-Purkinje system) may predispose an individual
to arrhythmias with a risk of progressing to sudden cardiac arrest, albeit this risk
remains low. Many of these conduction blocks can be treated with internal
cardiac defibrillators for those determined to be at high risk due to severity of
fibrosis or severe electrophysiologic disturbances. (Mann et al., 2015)

2.2.4 Inherited Arrhythmia Syndromes

Arrhythmias not due to structural heart disease account for 5 to 10% of

sudden cardiac arrests. These are frequently caused by genetic disorders. The
genetic mutations often affect specialized proteins known as ion channels that
conduct electrically charged particles across the cell membrane, and this group
of conditions is therefore often referred to as channelopathies. Examples of
these inherited arrhythmia syndromes include Long QT syndrome
(LQTS), Brugada Syndrome, Catecholaminergic polymorphic ventricular
tachycardia, and Short QT syndrome. Many are also associated with
environmental or neurogenic triggers such as response to loud sounds that can
initiate lethal arrhythmias. Other conditions that promote arrhythmias but are not
caused by genetic mutations include Wolff-Parkinson-White syndrome. (Podrid,
2022)

Long QT syndrome, a condition often mentioned in young people's deaths,

occurs in one of every 5000 to 7000 newborns and is estimated to be
responsible for 3000 deaths annually compared to the approximately 300,000
cardiac arrests seen by emergency services. These conditions are a fraction of
the overall deaths related to cardiac arrest but represent conditions that may be
detected prior to arrest and may be treatable. The symptomatic expression of
Long-QT syndrome is quite broad and more often presents with syncope rather
than cardiac arrest. The risk of cardiac arrest is still present, and people with
family histories of sudden cardiac arrests should be screened for LQTS and
other treatable causes of lethal arrhythmia. Higher levels of risk for cardiac
arrest are associated with female sex, more significant QT prolongation, history
of unexplained syncope (fainting spells), or premature sudden cardiac
death. Additionally, individuals with LQTS should avoid certain medications that
carry the risk of increasing the severity of this conduction abnormality, such as
certain anti-arrhythmic, anti-depressant, and quinolone or macrolide antibiotics.
(Fazio et al., 2013)

2.2.5 Non-cardiac Causes

Non-cardiac causes account for 15 to 25% of cardiac arrests. Non-cardiac

causes are most commonly, respiratory arrest, diabetes, certain medications,
and blunt trauma. Respiratory arrest will be followed by cardiac arrest unless
promptly treated. Respiratory arrest can be caused by choking, drowning,
trauma, drug overdose, and poisoning.

Diabetes causes changes to electrolyte levels which raise the risk of

cardiac arrest. Certain medications including some antibiotics, diuretics, and
heart medications can worsen an existing arrhythmia. Trauma to the chest,
commonly from a blow to the upper left chest above the heart usually occurring
in a number of ball games. Other causes include types of bleeding such as
an intracranial bleed, or aortic rupture; hypovolemic shock, and pulmonary
embolism. Poisoning instances can include the stings of certain jellyfish. A
mnemonic for the many reversible causes is known as the Hs and Ts. (Raab et
al., 2018)

2.2.6 Children
 In children, the most common cause of cardiopulmonary arrest
is shock or respiratory failure that has not been treated. Heart arrhythmia is not
the most common cause in children. When there is a cardiac arrhythmia, it is
most often asystole or bradycardia, in contrast to ventricular
fibrillation or tachycardia as seen in adults. Other causes can include drugs such
as cocaine and methamphetamine or overdose of medications such as
antidepressants in a child who was previously healthy but is now presenting with
a dysrhythmia that has progressed to cardiac arrest. Common causes of sudden
unexplained cardiac arrest in children include hypertrophic cardiomyopathy,
coronary artery abnormalities, and arrhythmias. (Topjian et al., 2021)

2.3 MECHANISM OF CARDIAC ARREST

The definitive electrical mechanisms of cardiac arrest, which may arise
from any of the functional, structural, or physiologic abnormalities mentioned
above, are characterized by tachyarrhythmic or bradyarrhythmic events that do
not result in systole. The tachyarrhythmias can be further classified
as Ventricular fibrillation (V-fib) and pulseless or sustained Ventricular
tachycardia (V-tach), both of which are rapid and erratic arrhythmias that alter
the circulatory pathway such that adequate blood flow cannot be sustained and
is inadequate to meet the body's needs. (Mann et al., 2015)

The mechanism responsible for the majority of sudden cardiac deaths

is ventricular fibrillation. Ventricular fibrillation is a tachyarrhythmia characterized
by turbulent electrical activity in the ventricular myocardium leading to a heart
rate too disorganized and rapid to produce any meaningful cardiac output, thus
resulting in insufficient perfusion of the brain and essential organs. In ventricular
tachycardia, the heart also beats faster than normal, which may prevent the
heart chambers from properly filling with blood. Some of the electrophysiologic
mechanisms underpinning ventricular fibrillations include ectopic automaticity,
re-entry, and triggered activity. (Szabo et al., 2020) Structural changes in the
diseased heart as a result of inherited factors (mutations in ion-channel coding
genes, for example) cannot explain the suddenness of sudden cardiac death.
(Rubart and Zipes et al., 2005)

Both ventricular fibrillation and ventricular tachycardia can result in the

heart ineffectively pumping blood to the body. Ventricular tachycardia is
characterized by an altered QRS complex and a heart rate greater than 100
beats per minute. (AlMahameed and Ziv et al., 2019) When V-tach is sustained
(lasts for at least 30 seconds), inadequate blood flow to heart tissue can lead to
cardiac arrest. (Baldzizhar et al., 2016)

Bradyarrhythmias occur following dissociation of spontaneous electrical

conduction and the mechanical function of the heart resulting in pulseless
electrical activity (PEA) or through complete absence of electrical activity of the
heart resulting in asystole. Similar to the result of tachyarrhythmias, these
conditions lead to an inability to sustain adequate blood flow as well, though in
the case of bradyarrhythmias, the underlying cause is an absence of mechanical
activity rather than rapid beats leading to disorganization. (Mann et al., 2015)

2.4 DIAGNOSIS OF CARDIAC ARREST

Cardiac arrest is synonymous with clinical death. Historical information

and a physical exam can diagnose cardiac arrest and inform the potential cause
and prognosis. The provider taking the person's clinical history should try to
learn whether the episode was observed by anyone else, when it happened,
what the patient was doing (in particular whether there was any trauma), and
whether drugs were involved. The physical examination to diagnose cardiac
arrest focuses on the absence of a pulse. In many cases, lack of a carotid
pulse is the gold standard. Lack of a pulse in the periphery (radial/pedal) may
also result from other conditions (e.g. shock) or be the rescuer's
misinterpretation. Rescuers may often make a mistake when checking the
carotid pulse in an emergency, whether they are professionals or laymen. (Walls
et al., 2009)
 Point-of-care ultrasound (POCUS) is a tool that can be used to examine
the movement of the heart and its force of contraction at the patient's
bedside. POCUS can accurately diagnose cardiac arrest in hospital settings,
overcoming some of the shortcomings of diagnosis through checking the central
pulse (carotid arteries or subclavian arteries), as well as detecting movement
and contractions of the heart. (Long et al., 2018)

Using POCUS, clinicians can have limited, two-dimensional views of

different parts of the heart during arrest. These images can help clinicians
determine whether electrical activity within the heart is pulseless or pseudo-
pulseless, as well as help them diagnose the potentially reversible causes of an
arrest. Published guidelines from the American Society of
Echocardiography, American College of Emergency Physicians, European
Resuscitation Council, and the American Heart Association, as well as the 2018
preoperative Advanced Cardiac Life Support guidelines, have recognized the
potential benefits of using POCUS in diagnosing and managing cardiac arrest.
(Paul and Panzer, 2021)

Owing to the inaccuracy of this method of diagnosis, some bodies like the
European Resuscitation Council (ERC) have de-emphasized its importance.
Instead, the current guidelines prompt individuals to begin CPR on any
unconscious person with absent or abnormal breathing. The Resuscitation
Council in the United Kingdom stands in line with the ERC's recommendations
and those of the American Heart Association. They have suggested that the
technique to check carotid pulses should be used only by healthcare
professionals with specific training and expertise, and even then that it should be
viewed in conjunction with other indicators like agonal respiration. (Paul and
Panzer, 2021)

Various other methods for detecting circulation and therefore diagnosing

cardiac arrest have been proposed. Guidelines following the 2000 International
Liaison Committee on Resuscitation (ILCOR) recommendations were for
rescuers to look for "signs of circulation" but not specifically the pulse. These
signs included coughing, gasping, color, twitching, and movement. Per evidence
that these guidelines were ineffective, the current ILCOR recommendation is
that cardiac arrest should be diagnosed in all casualties who are unconscious
and not breathing normally, a similar protocol to that which the European
Resuscitation Council has adopted. In a non-acute setting where the patient is
expired, diagnosis of cardiac arrest can be done via molecular autopsy or
postmortem molecular testing, which uses a set of molecular techniques to find
the ion channels that are cardiac defective. This could help elucidate the cause
of death in the patient. (Glatter et al., 2006)

Other physical signs or symptoms can help determine the potential cause
of the cardiac arrest. Below is a chart of the clinical findings and signs/symptoms
a person may have and potential causes associated with them.

Physical findings related to potential causes (Walls et al., 2009)

Location Findings Possible Causes

General Pale skin Hemorrhage

Decreased body temperature Hypothermia

Airway Presence of secretions, vomit, blood Aspiration

Tension pneumothorax
Inability to provide positive pressure ventilation
Airway obstruction

Tension pneumothorax

Neck Distension of the neck veins Cardiac tamponade

Pulmonary embolism

Trachea shifted to one side Tension pneumothorax

Chest Scar in the middle of the sternum Cardiac disease

 Tension pneumothorax

Lungs Breath sounds only on one side Right mainstem intubation

Aspiration

Esophageal intubation
No breath sounds or distant breath sounds
Airway obstruction

Aspiration

Wheezing Bronchospasm

Pulmonary edema

Aspiration

Rales Pulmonary edema

Pneumonia

Hypovolemia

Cardiac tamponade
Heart Decreased heart sounds
Tension pneumothorax

Pulmonary embolus

Ruptured abdominal aortic aneurysm

Abdomen Distended and dull
Ruptured ectopic pregnancy

Distended and tympanic Esophageal intubation

Rectal Blood present Gastrointestinal hemorrhage

Extremities Asymmetrical pulses Aortic dissection

Skin Needle tracks Drug abuse

2.5 PREVENTION OF CARDIAC ARREST

With the lack of positive outcomes following cardiac arrest, efforts have
been spent finding effective strategies to prevent cardiac arrest. With the prime
causes of cardiac arrest being ischemic heart disease, efforts to promote
a healthy diet, exercise, and smoking cessation are important. For people at risk
of heart disease, measures such as blood pressure control, cholesterol lowering,
and other medico-therapeutic interventions are used. A Cochrane
review published in 2016 found moderate-quality evidence to show that blood
pressure-lowering drugs do not reduce the risk of sudden cardiac
death. Exercise is an effective preventative measure for cardiac arrest in the
general population but may be risky for those with pre-existing conditions. The
risk of a transient catastrophic cardiac event increases in individuals with heart
disease during and immediately after exercise. The lifetime and acute risks of
cardiac arrest are decreased in people with heart disease who perform regular
exercise, perhaps suggesting the benefits of exercise outweigh the risks.
(Fanous and Dorian 2019)

2.6 TREATMENT OF CARDIAC ARREST

Sudden cardiac arrest may be treated via attempts at resuscitation. This is

usually carried out based on basic life support, Advanced Cardiac Life
Support (ACLS), Pediatric Advanced Life Support (PALS), or Neonatal
Resuscitation Program (NRP) guidelines.
2.6.1 Cardiopulmonary Resuscitation

CPR training on a mannequin

Early Cardiopulmonary Resuscitation (CPR) is essential to surviving

cardiac arrest with good neurological function. It is recommended that it be
started as soon as possible with minimal interruptions once begun. The
components of CPR that make the greatest difference in survival are chest
compressions and defibrillating shockable rhythms. After defibrillation, chest
compressions should be continued for two minutes before another rhythm
check. This is based on a compression rate of 100-120 compressions per
minute, a compression depth of 5–6 centimeters into the chest, full chest recoil,
and a ventilation rate of 10 breath ventilations per minute. (Walls et al., 2009)

Correctly performed bystander CPR has been shown to increase survival;

it is performed in fewer than 30% of out-of-hospital cardiac arrests (OHCAs) as
of 2007. If high-quality CPR has not resulted in return of spontaneous circulation
(ROSC) and the person's heart rhythm is in asystole, discontinuing CPR and
pronouncing the person's death is generally reasonable after 20
minutes. Exceptions to this include certain cases
with hypothermia or drowning victims. Some of these cases should have longer
and more sustained CPR until they are nearly normothermic. (Wang et al.,
2017) Longer durations of CPR may be reasonable in those who have cardiac
arrest while in hospital. Bystander CPR by the lay public before the arrival of
EMS also improves outcomes. (Kronick et al., 2015)
 Either a bag valve mask or an advanced airway may be used to help with
breathing particularly since vomiting and regurgitation are common, especially in
OHCA. If this occurs, then modification to existing oropharyngeal suction may be
required, such as the use of Suction Assisted Laryngoscopy Airway
Decontamination. High levels of oxygen are generally given during
CPR. Tracheal intubation has not been found to improve survival rates or
neurological outcomes in cardiac arrest and in the prehospital environment, may
worsen it. Endotracheal tubes and supraglottic airways appear equally
useful. When done by EMS, 30 compressions followed by two breaths appear
better than continuous chest compressions and breaths being given while
compressions are ongoing. (Zhan et al., 2017)

For bystanders, CPR that involves only chest compressions results in

better outcomes as compared to standard CPR for those who have gone into
cardiac arrest due to heart issues. Mouth-to-mouth as a means of providing
respirations to the patient has been phased out due to the risk of contracting
infectious diseases from the patient. Mechanical chest compressions (as
performed by a machine) are no better than chest compressions performed by
hand. It is unclear if a few minutes of CPR before defibrillation results in different
outcomes than immediate defibrillation. If cardiac arrest occurs after 20 weeks of
pregnancy, the uterus should be pulled or pushed to the left during CPR. If a
pulse has not returned by four minutes, an emergency Cesarean section is
recommended. (Lavonas et al., 2015)

2.6.2 Defibrillation

Defibrillation is indicated if an electric-shockable heart rhythm is present.

The two shockable rhythms are ventricular fibrillation and pulseless ventricular
tachycardia. In children, 2 to 4 J/Kg is recommended. (Berg et al., 2015)

In out-of-hospital arrests, the defibrillation is made by an automated

external defibrillator (AED), a portable machine that can be used by any user: it
provides voice instructions that guide the process, automatically checks the
victim's condition, and applies the appropriate electric shocks. Some
defibrillators even provide feedback on the quality of CPR compressions,
encouraging the lay rescuer to press the person's chest hard enough to circulate
blood.

In addition, there is increasing use of public access defibrillation. This

involves placing AEDs in public places and training staff in these areas on how
to use them. This allows defibrillation to occur prior to the arrival of emergency
services, which has been shown to increase chances of survival. It has been
shown that those who have arrests in remote locations have worse outcomes
following cardiac arrest. (Lyon et al., 2004)

2.6.3 Medications

As of 2016, medications other than epinephrine (adrenaline), while

included in guidelines, have not been shown to improve survival to hospital
discharge following OHCAs. This includes the use of atropine, lidocaine,
and amiodarone. (Wang et al., 2017)

Epinephrine in adults, as of 2019, appears to improve survival but does

not appear to improve neurologically normal survival. It is generally
recommended every three to five minutes. Epinephrine acts on the alpha-1
receptor, which in turn increases the blood flow that supplies the heart. This
would assist with providing more oxygen to the heart. Based on 2019 guidelines,
1 mg of epinephrine may be administered to patients every 3–5 minutes, but
doses higher than 1 mg of epinephrine are not recommended for routine use in
cardiac arrest. If the patient has a non-shockable rhythm, epinephrine should be
administered as soon as possible. For a shockable rhythm, epinephrine should
only be administered after an initial defibrillation attempt. (Berg et al., 2019)

Vasopressin overall does not improve or worsen outcomes compared to

epinephrine. The combination of epinephrine, vasopressin,
and methylprednisolone appears to improve outcomes. Some of the lack of
long-term benefits may be related to delays in epinephrine use. While evidence
does not support its use in children, guidelines state its use is reasonable. (Scott
et al., 2015)

Lidocaine and amiodarone are also deemed reasonable in children with

cardiac arrest who have a shockable rhythm. The general use of sodium
bicarbonate or calcium is not recommended. The use of calcium in children has
been associated with poor neurological function as well as decreased
survival. Correct dosing of medications in children is dependent on weight. To
minimize time spent calculating medication doses, the use of a Broselow tape is
recommended. (Walls et al., 2017)

The 2010 guidelines from the American Heart Association no longer

contain the recommendation for using atropine in pulseless electrical
activity and asystole for lack of evidence supporting its use. Neither lidocaine
nor amiodarone, in those who continue in ventricular tachycardia or ventricular
fibrillation despite defibrillation, improves survival to hospital discharge, despite
both equally improving survival to hospital admission. (Sanfilippo et al., 2016)

Thrombolytics may cause harm but may be of benefit in those with a

confirmed pulmonary embolism as the cause of arrest. Evidence for use
of naloxone in those with cardiac arrest due to opioids is unclear, but it may still
be used. In those with cardiac arrest due to local anesthetic, lipid emulsion may
be used. (Lavonas et al., 2015)
2.6.4 Implantable Cardioverter Defibrillator

Illustration of an implantable cardioverter-defibrillator (ICD)

An Implantable Cardioverter-Defibrillator (ICD) is a battery-powered device

that monitors electrical activity in the heart, and when an arrhythmia is detected,
can deliver an electrical shock to terminate the abnormal rhythm. ICDs are used
to prevent Sudden Cardiac Death (SCD) in those who have survived a prior
episode of Sudden Cardiac Arrest (SCA) due to ventricular fibrillation or
ventricular tachycardia (secondary prevention). (Epstein et al., 2008) ICDs are
also used prophylactically to prevent sudden cardiac death in certain high-risk
patient populations (primary prevention). (Shun-Shin et al., 2017)

Numerous studies have been conducted on the use of ICDs for the
secondary prevention of SCD. These studies have shown improved survival with
ICDs compared to the use of anti-arrhythmic drugs. ICD therapy is associated
with a 50% relative risk reduction in death caused by an arrhythmia and a 25%
relative risk reduction in all-cause mortality. (Connolly et al., 2000)

Primary prevention of SCD with ICD therapy for high-risk patient

populations has similarly shown improved survival rates in several large studies.
The high-risk patient populations in these studies were defined as those with
severe ischemic cardiomyopathy (determined by a reduced left ventricular
ejection fraction (LVEF)). The LVEF criteria used in these trials ranged from less
than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT. (Shun-
Shin et al., 2017)

CHAPTER THREE

CONCLUSION AND RECOMMENDATION

3.0 CONCLUSION

Cardiac arrest, also known as sudden cardiac arrest, is when the heart
suddenly and unexpectedly stops beating. The most common cause of cardiac
arrest is an irregular heart rhythm (arrythmia), usually ventricular fibrillation (V-
fib), or ventricular tachycardia (V-tach). Heart problems are the main risk
factor. Less common, non-cardiac causes include major blood loss, lack of
oxygen, very low potassium, electrical injury, heart failure, and intense physical
exercise. CPR and defibrillation can reverse a cardiac arrest, leading to
the return of spontaneous circulation (ROSC), but without such intervention, it
will prove fatal, known as sudden cardiac death. Treatment for cardiac arrest
includes immediate CPR and, if a shockable rhythm is present,
defibrillation. Two protocols have been established for CPR: basic life
support (BLS) and advanced cardiac life support (ACLS).

3.1 RECOMMENDATION

The following are the recommendation to cardiac arrest in order to reduce

death. Encourage attendees to:

1. Call Emergency Services: Stress the importance of dialing emergency

services (911 or local equivalent) as the first step.

2. Start CPR: Discuss the basics of hands-only CPR, emphasizing chest

compressions at a rate of 100-120 per minute.

3. Use AEDs: Highlight the value of Automated External Defibrillators

(AEDs) if accessible, and the significance of early defibrillation.
 4. Raise Awareness: Promote awareness about recognizing signs of
cardiac arrest and the need for a quick response within the community.

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