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MEDICINE II
1.1E CARDIAC ARREST AND SUDDEN CARDIAC DEATH

Term
Death

Cardiac Arrest

Cardiovascular
Collapse

DEFINITION OF TERMS
Definition
Qualifiers or
Exceptions
Irreversible cessation
None
of all biologic
functions
Abrupt cessation of
Rare spontaneous
cardiac pump
reversions; likelihood
function, which may
of successful
be reversible but will
intervention relates to
lead to death in the
mechanism of arrest,
absence of prompt
clinical setting and
intervention
time of intervention
A (sudden) loss of
Nonspecific term that
effective blood flow
includes cardiac
caused by cardiac
arrest and its
and/or peripheral
consequences and
vascular factors that
also events that revert
may revert
spontaneously
spontaneously (such
as syncope) or only
with intervention

CARDIAC ARREST
Cardiac arrest is expected:
- Life threatening illness
- Severe injuries
Cardiac arrest is not expected
- Sudden cardiac death
SUDDENT CARDIAC DEATH (SCD)
Natural death from cardiac causes, heralded by an abrupt loss
of consciousness within 1 hour after the onset of an acute
change in CV status
Pre-existing heart disease may or may not have been known to
be present but the time and mode of death are unexpected

TIME REFERENCES IN SUDDEN CARDIAC DEATH


Prodromes
Onset of terminal
Cardiac arrest
Biological
event
death
New or
Abrupt change in
Sudden
Failure of
worsening
clinical status
collapse
resuscitation
cardiovascular
OR failure of
Arrhythmia
Loss of
symptoms
electrical,
effective
Hypotension
mechanical
Chest pain
circulation
Chest pain
or CNS
Palpitations
Loss of
Dyspnea
function after
consciousne
Dyspnea
Lightheadedness
initial
ss
Fatiguability
resuscitation
Days to months
Up to 1 hour
Minutes to weeks

SUDDEN CARDIAC DEATH: EPIDEMIOLOGY


>300,000 cases of SCD per year in US
Account for 50% of all cardiac deaths
Peak incidence:
- Birth to 6 months: Sudden Infant Death Syndrome (SIDS)
- > 45 years: 88% of deaths are cardiac in origin
Male: Female = 4:1

RISK OF SCD BY DECILE OF MULTIVARIATE RISK


SELECTED
RISK FACTORS:
Age
Cigarettes
Diabetes
Heredity
Hyperlipidemia
Hypertension
Obesity
Sedentary
STRUCTURAL CAUSES OF CARDIAC ARRESY AND SUDDENT
CARDIAC DEATH
Coronary heart disease
80%
- Coronary artery abnormalities
- Myocardial ischemia and infarction
Myocardial hypertrophy
10-15%
- Secondary
- Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Inflammatory and infiltritive diseases
- Myocarditis
- Infiltritive diseases
Valvular heart disease
5-10%
Electrographic abnomalities
- Long QT syndrome
- Short QT syndrome
- Brugada syndrome (Sleep death in Southeast Asians;
bangungot)
- WPW syndrome
- Conduction abnormalities
AGE-RELATED & DISEASE SPECIFIC RISK FOR SCD
Usual causes:
Myocarditis
Hypertrophic CM
Long QT syndromes
Right ventricular
dysplasia
Anomalous coronary
artery
Brugada syndrome
Idiopathic VF

Usual causes:
Coronary atherosclerosis
Dilated cardiomyopathy
Infiltrative heart disease
Valvular heart disease

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Medicine II

1.1D ACUTE CORONARY SYNDROME

PATHOPHYSIOLOGY OF SCD IN CORONARY DISEASE

HYPERTROPHIC CARDIOMYOPATHY
The heart muscle
(myocardium) becomes
abnormally thick
(hypertrophied). The
thickened heart muscle
can make it harder for the
heart to pump blood.

DILATED CARDIOMYOPATHY
Usually starting in your
heart's main pumping
chamber (left ventricle). The
ventricle stretches and thins
(dilates) and can't pump
blood as well as a healthy
heart can.

FUNCTIONAL CAUSES OF CARDIAC ARREST


Alterations of coronary blood flow
- Transient ischemia
- Reperfusion after ischemia
Low cardiac output states
- Heart failure
- Shock
Systemic metabolic abnormalities
- Electrolyte imbalance (ex. Hypokalemia)
Neurophysiologic disturbances
- Autonomic fluctuations
Toxic responses
- Proarrhythmic drug effects
- Cardiac toxins (Ex. Cocaine, Digitalis intoxication)
- Drug interactions

BIOLOGICAL MODEL OF SUDDEN CARDIAC DEATH


STRUCTURE
FUNCTION
Myocardial infarction
Transient alterations of
- Acute
coronary blood flow
- Healed
Electrogenic
- Vasomotor dynamics
- Aneurysm
Theory
- Acute (transient) ischemia
- Reperfusion after ischemia
Hypertrophy
PVCs
- Secondary
Systemic factors
- Primary
- Hemodynamic factors
- Hypoxemia, acidosis
Myopathic ventricle
- Electrolyte imbalance
- Dilatation
VT/VF
Neurophysiological interactions
Structural electrical
- Transmitters, receptors
abnormality
- Central influences
Toxic effects
- Proarrhythmic drugs
- Cardiac toxicity
RISK OF SCD RELATED TO LEFT VENTRICULAR EJECTION
FRACTION

ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA

PROGNOSTIC SIGNIFICANCE OF VENTRICULAR ARRHYTHMIAS


AND LV EJECTION FRACTION AFTER MI

A rare form of cardiomyopathy in which the heart


muscle of the right ventricle (RV) is replaced by fat
and/or fibrous tissue.
The right ventricle is dilated and contracts poorly. As a
result, the ability of the heart to pump blood is usually
weakened.

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Medicine II

MECHANISMS OF CARDIAC ARREST


Arrhythmic events
- Ventricular fibrillation (VF)
62.4%
- Bradyarrhythmias (including AV block & asystole 16.5%
- Torsades des pointes
12.7%
- Primary ventricular tachycardia (VT)
8.3%
Pulseless electrical activity (PEA)
- Previously referred to as electromechanical dissociation

1.1D ACUTE CORONARY SYNDROME


VENTRICULAR TACHYCARDIA DUE TO MYOCARDIAL ISCHEMIA

VENTICULAR FIBRILLATION

SINUS ARREST / ASYSTOLE

VENTRICULAR TACHYCARDIA

TORSADES DE POINTES

CLINICAL PRESENTATION OF PATIENTS WITH VENTRICULAR


ARRYTHMIAS AND SUDDEN CARDIAC DEATH

Asymptomatic individuals with or without ECG abnormalities

Patients with symptoms potentially attributable to ventricular


arrythmias
- Palpitations
- Dyspnea
- Chest pains
- Syncope or presyncope

Hemodynamically stable VT

Hemodynamically unstable VT

Cardiac arrest
- Asystole (sinus arrest, high grade AV block)
- Ventricular tachycardia (VT)
- Ventricular fibrillation (VF)
- Pulseless electrical activity (PEA)
EMERGENCY MANAGEMENT OF SCD: CARDIOPULMONARY
RESUSCITATION

Basic life support


- Airway
> Head tilt
> Chin tilt
- Breathing
> Mouth-to-mouth
> Mas-to-mouth
>30:2 (ratio of chest compressions to breaths)
- Circulation
> High quality chest compression
- Hands maintain firm contact with lower sternum
- Sternum must be depressed by 11/2 - 2 inches
- Allow full chest recoil between compressions
- Compression rate of 100/minute

NEW BLS GUIDELINES


Compressions
- Effective, uninterrupted compressions alone result in equivalent
survival
Airway
Breathing
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Medicine II

1.1D ACUTE CORONARY SYNDROME

EXTERNAL CHEST COMPRESSIONS

CAUSES OF PULSELESS ELECTRICAL ACTIVITY


Hypoxia
Hypovolemia
Hydrogen ion (acidosis)
Hypothermia
Hypo / Hyperkalemia
Hypoglycemia
Tension pneumothorax
Tamponade (cardiac)
Thrombosis (coronary; pulmonary)
Toxins (drug overdose; poisoning)
Trauma
SURVIVAL AFTER OUT OF HOSPITAL CARDIAC ARREST

ADVANCED CARDIAC LIFE SUPPORT (ACLS) FOR VF PULSELESS


VT

PREVENTION OF SCD
Secondary prevention (postcardiac arrest survivors)
Primary prevention
- Advanced structural heart disease with LVEF < 35%
- Less advanced structural heart disease with LVEF > 35%
- Structurally normal heart with molecular disorders associated
with increased risk of ventricular arrhythmias
- General population
Implantable cardioverter defibrillator (ICD); treatment of choice
Pharmacologic therapy
- Beta-blockers
- Amiodarone
- Sotalol
SUCCESSFUL DEFIBRILLATION BY ICD

ADVANCED CARDIAC LIFE SUPPORT FOR PATIENTS WITH


BRADYARRHYTHMIC ASYSTOLIC ARRESTS AND PULSELESS
ELECTRICAL ACTIVITY

VT IN A PATIENT WITH BRUGADA SYNDROME

_________________________________________________________
END OF TRANX

"What you do today can improve all your tomorrows." - Ralph Marston

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