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Cardiac Arrest and Sudden

Cardiac Death
Definition
• Cardiac arrest, (also known as
cardiopulmonary arrest or circulatory arrest)
is the cessation of normal circulation of the
blood due to failure of the heart to contract
effectively
• Cardiac arrest is a medical emergency that, in
certain situations, is potentially reversible if
treated early.
• Unexpected cardiac arrest sometimes leads to
death almost immediately; this is called
sudden cardiac death (SCD).
Distinction between Cardiovascular Collapse, Cardiac Arrest, and Death
Term Definition Qualifiers or Exceptions
Cardiovascular A sudden loss of effective blood Nonspecific term that includes
collapse flow due to cardiac and/or cardiac arrest and its
peripheral vascular factors which consequences and also events
may reverse spontaneously (e.g., that characteristically revert
neurocardiogenic syncope; spontaneously
vasovagal syncope) or only with
interventions (e.g., cardiac arrest)
Cardiac arrest Abrupt cessation of cardiac pump Rare spontaneous reversions;
function which may be reversible likelihood of successful
by a prompt intervention but will interventions relates to
lead to death in its absence mechanism of arrest, clinical
setting, and prompt return of
circulation
Death Irreversible cessation of all None
biologic functions
Etiology
Structural Causes
I. Coronary heart disease
A. Coronary artery abnormalities
1. Chronic atherosclerotic lesions
2. Acute (active) lesions (plaque fissuring, platelet aggregation, acute
thrombosis)
3. Anomalous coronary artery anatomy
B. Myocardial infarction
1. Healed
2. Acute
II. Myocardial hypertrophy
A. Secondary
B. Hypertrophic cardiomyopathy
1. Obstructive
2. Nonobstructive
Structural cause
III. Dilated cardiomyopathy—primary muscle disease
IV. Inflammatory and infiltrative disorders
A. Myocarditis
B. Noninfectious inflammatory diseases
C. Infiltrative diseases
D. Right ventricular dysplasia
V. Valvular heart disease
VI. Electrophysiologic abnormalities, structural
A. Anomalous pathways in Wolff-Parkinson-White syndrome
B. Conducting system disease
VII. Inherited disorders of molecular structure associated with
electrophysiologic abnormalities (e.g., congenital long QT syndromes,
Brugada syndrome)
Functional Contributing Factors
I. Alterations of coronary blood flow
A. Transient ischemia
B. Reperfusion after ischemia
II. Low cardiac output states
A. Heart failure
1. Chronic
2. Acute decompensation
B. Shock
III. Systemic metabolic abnormalities
A. Electrolyte imbalance (e.g., hypokalemia)
B. Hypoxemia, acidosis
Functional Contributing Factors
IV. Neurophysiologic disturbances
A. Autonomic fluctuations: central, neural, humoral
B. Receptor function
V. Toxic responses
A. Proarrhythmic drug effects
B. Cardiac toxins (e.g., cocaine, digitalis intoxication)
C. Drug interactions
History
• Obtaining a thorough history from the patient,
family members, or other witnesses is necessary
to obtain insight into the events surrounding the
sudden death.
• Patients at risk for SCD may have prodromes of
chest pain, fatigue, palpitations, and other
nonspecific complaints.
• History and associated symptoms, to some
degree depend on the underlying etiology of SCD.
Risk Factors
• Risk factors that relate to coronary artery
disease and subsequent myocardial infarction
and ischemic cardiomyopathy also are
important and include a family history of
premature coronary artery disease, smoking,
dyslipidemia, hypertension, diabetes, obesity,
and a sedentary lifestyle.
Risk Factors
• Coronary artery disease
– Previous cardiac arrest
– Syncope
– Prior myocardial infarction, especially within 6
months
– Ejection fraction less than 30-35%
– History of frequent ventricular ectopy (more than
10 PVCs per h or nonsustained VT)
Risk Factors
• Dilated cardiomyopathy
– Previous cardiac arrest
– Syncope
– Ejection fraction less than 30-35%
– Use of inotropic medications
Risk Factors
• Hypertrophic cardiomyopathy
– Previous cardiac arrest
– Syncope
– Family history of SCD
– Symptoms of heart failure
– Drop in SBP or ventricular ectopy upon stress
testing
– Palpitations
– Most are asymptomatic
Risk Factors
• Valvular disease
– Valve replacement within 6 months
– Syncope
– History of frequent ventricular ectopy
– Symptoms associated with severe uncorrected
aortic stenosis or mitral stenosis
Risk Factors
• Long QT syndrome
– Family history of long QT and SCD
– Medications that prolong the QT interval
– Bilateral deafness
• Wolff-Parkinson-White (WPW) syndrome
(with atrial fibrillation or atrial flutter with
extremely rapid ventricular rates)
– With extremely rapid conduction over an
accessory pathway, degeneration to VF can occur.
The Cardiac Arrest Score
• ED SBP greater than 90 mm Hg = 1 point
• ED SBP less than 90 mm Hg = 0 points
• Time to ROSC less than 25 minutes = 1 point
• Time to ROSC more than 25 minutes = 0 points
• Neurologically responsive = 1 point
• Comatose = 0 point
• Maximum score = 3 points
Patients with a score of 3 points can be expected to have
an 89% chance of neurologic recovery and an 82% chance
of survival to discharge (see the image below).
Differential Diagnoses
• Aortic Stenosis • Myocardial Infarction
• Cardiomyopathy, • Myocardial Ischemia
Dilated • Tetralogy of Fallot
• Cardiomyopathy, • Torsade de Pointes
Hypertrophic • Ventricular Fibrillation
• Coronary Artery • Ventricular Premature
Atherosclerosis Complexes
• Ebstein Anomaly • Ventricular Tachycardia
• Lown-Ganong-Levine • Wolff-Parkinson-White
Syndrome Syndrome
Laboratory Studies
• Cardiac enzymes (creatine kinase, myoglobin,
troponin): Elevations in these enzyme levels
may indicate ischemia and MI.
The extent of myocardial damage usually can be
correlated to the extent of elevation in the
enzyme levels. Patients are at increased risk for
arrhythmia in the peri-infarct period.
Laboratory Studies
• Electrolytes, calcium, and magnesium: Severe
metabolic acidosis, hypokalemia,
hyperkalemia, hypocalcemia, and
hypomagnesemia are some of the conditions
that can increase the risk for arrhythmia and
sudden death.
Laboratory Studies
• Quantitative drug levels (quinidine,
procainamide, tricyclic antidepressants,
digoxin): Drug levels higher than the levels
indicated in the therapeutic index may have a
proarrhythmic effect.
• Toxicology screen: Looking for drugs, such as
cocaine, that can lead to vasospasm-induced
ischemia is warranted if suspicion exists.
Laboratory Studies
• Thyroid-stimulating hormone:
Hyperthyroidism can lead to tachycardia and
tachyarrhythmias.
Over a period of time, it also can lead to heart
failure. Hypothyroidism can lead to QT
prolongation.
Laboratory Studies
• Brain natriuretic peptide (BNP): BNP has
predictive value especially in post MI patients
and in patients with heart failure.
Imaging Studies
• Chest radiography
• Echocardiography
• Nuclear imaging techniques
CardioPulmonary Resuscitation
• Cardiopulmonary resuscitation (CPR) is an
emergency procedure which is performed in
an effort to manually preserve intact brain
function until further measures are taken to
restore spontaneous blood circulation and
breathing in a person in cardiac arrest.
CardioPulmonary Resuscitation
• CPR alone is unlikely to restart the heart; its
main purpose is to restore partial flow of
oxygenated blood to the brain and heart.
• The objective is to delay tissue death and to
extend the brief window of opportunity for a
successful resuscitation without permanent
brain damage.
• Posisikan tangan tegak lurus korban
Basic Life Support &
Automated External
Defibrillation Course
CHAIN OF SURVIVAL
APPROACH SAFELY!

Approach safely
Scene Check response
Shout for help
Rescuer
Open airway
Victim Check breathing
Call 112
Bystanders 30 chest compressions
2 rescue breaths
CHECK RESPONSE

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
CHECK RESPONSE

Shake shoulders gently


Ask “Are you all right?”
If he/she responds
• Find out what is wrong.
• Reassess regularly.
SHOUT FOR HELP

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
OPEN AIRWAY

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
Checking Vital Signs
• A – Airway
–Open the airway
–Head tilt chin lift
CHECK BREATHING

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
CHECK BREATHING

• Look, listen and feel for


NORMAL breathing
– No longer than 10
seconds seconds

• Do not confuse agonal


breathing with
NORMAL breathing
AGONAL BREATHING

• Occurs shortly after the heart stops


in up to 40% of cardiac arrests

• Described as barely, heavy, noisy or gasping


breathing

• Recognise as a sign of cardiac arrest


Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
• Kneeling on the right side of the
patients
CHEST COMPRESSIONS
• Place the heel of one hand in
the centre of the chest
• Place other hand on top
• Interlock fingers
• Place yourself vertically above
the patient’s chest
• Compress the chest
– Rate 100x/minute
– Depth 4-5 cm
– Equal compression : relaxation
• When possible change CPR
operator every 2 min
30 CHEST COMPRESSIONS

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
How CPR Works
• Effective CPR provides 1/4 to 1/3 normal
blood flow
• Rescue breaths contain 16% oxygen
(21%)
• If the compression is right, you can feel
the carotid pulse
RESCUE BREATHS

Approach safely
Check response
Shout for help
Open airway
Check breathing
Call 112
30 chest compressions
2 rescue breaths
RESCUE BREATHS

• Pinch the nose


• Take a normal breath
• Place lips over mouth
• Blow until the chest
rises
• Take about 1 second
• Allow chest to fall
• Repeat
CONTINUE CPR

30 2
• Continue the CPR, starting with
the compression.
Indikasi RJP/BLS efektif
• Jika resusitasi berhasil
– Konstriksi pupil
– Perbaikan warna kulit
– Detak jantung kembali secra spontan
– Pernafasan spontan terjadi
– Pergerakan lengan dan tungkai
– Usaha untuk menelan
– Kesadaran pulih
Kapan RJP dihentikan?
• Bntuan profesional datang mengambil alih
• RJP berhasil
• Penyelamat kelelahan

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