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CHAPER 11: SUDDEN CARDIAC DEATH

INTRODUCTION
CLINICAL DISEASE
1) Coronary Artery Disease
2) Cardiomyopathy
3) Congenital Heart Disease
4) Valvular Heart Disease
5) Cardiac Pacemaker and Conducting System Disease
6) Hereditary Channelopathies
 Sudden Arrhythmic Death Syndrome
 Ion Channel Disease
 Brugada Syndrome
 Early Repolarization Syndrome
 Long QT Syndrome
 Short QT Syndrome
 Catecholaminergic Polymorphic Ventricular Tachycardia
PREVENTION OF SUDDEN CARDIAC DEATH
Antiarrhythmic drug and device therapy
SUDDEN CARDIAC DEATH RESCUE
Pulseless Ventricular Tachycardia/ Ventricular Fibrillation
Pulseless Electrical Activity

INTRODUCTION:

1) Most episodes of sudden cardiac arrest at public places have V. Fib.


2) Arrest at public places have higher survival than at home.
3) Sudden cardiac arrest is more common among lower social economic
status Hypertrophic cardiomyopathy is the [mc] cardiovascular cause of sudden
4) There is a circadian pattern of sudden cardiac death and acute cardiac death in young athletes, accounting for a third of such events.
myocardial infarction. Usually occurring within the first few hours after
awakening from sleep due to increased sympathetic stimulation. Indications for implantable cardioverter-defibrillator placement:
5) Bimodal peaks in sudden cardiac death: infancy (SIDS) and males age  Prior documented cardiac arrest
>45.  Ventricular fibrillation
6) Undiagnosed CAD is a major cause of sudden cardiac death in adults.  Hemodynamically significant or non-sustained ventricular tachycardia
 Patients with a first degree relative who has had sudden cardiac
CLINICAL DISEASES: death
1) Coronary artery disease  Unexplained episodes of syncope
 most commonly due to an acute plaque rupture.  A maximum left ventricular wall thickness >30mm
 A documented initial cardiac arrest rhythm of V. Fib (or shockable  An abnormal BP response to exercise in the presence of other RFs.
rhythm) suggests that an ACS is the cause but is not conclusive.  High risk children with unexplained syncope
 Massive left ventricular hypertrophy
2) Cardiomyopathy  FMHx of sudden cardiac death
Severe Left Ventricular dysfunction with reduced ejection fraction (EF <35) is
the best predictor of sudden cardiac death. Arrhythmogenic right ventricular cardiomyopathy is a hereditary form of
cardiac muscle disease characterized by right-sided heart failure. Ventricular
Cardiomyopathy with reduced EF regardless of cause or presence of arrhythmia of right ventricular origin, syncope and sudden cardiac death.
decompensation.  The ECG shows T-wave inversion in the right precordial leads (V1-V3)
 The Dilated ventricles create islands of ventricular tissue that
depolarize and polarize at different rates (circus movement reentry).
 Hx of myocardial infarction or ischemia
 Left ventricular hypertrophy (hypertension or vascular disease)
 Conduction disturbances (RBBB and LBBB)
 V. Fib is the [mc] rhythm disturbance in heart failure patients
 NYHA II and III – [mc] sudden cardiac death vs.
 NYHA IV – [mc] pump failure
 e.g.. Brugada syndrome, Early repolarization syndrome (ERS), Long QT
Table 11-2 CHD commonly associated with sudden cardiac death: ALCAPA, syndrome (LQTS), Short QT syndrome (SQTS) and Catecholaminergic
AS, CoA. ToF, TGA, Ebstein A, Single Ventricle polymorphic ventricular tachycardia (CPVT)

Brugada Syndrome – Brugada syndrome most commonly affects men and


consists of a prominent J-wave with a characteristic down sloping ST-
segment elevation in electrocardiogram leads V1-V3.
 Commonly looks like an RBBB and is associated with polymorphic
ventricular tachycardia that degenerates into ventricular fibrillation
and sudden cardiac death.
 Pathology: Autosomal Dominant, a sodium channel disorder.
 [mc] in south east asia called sudden unexplained nocturnal death
syndrome “bangungut – Philippines”, “pokkuri – Japan ” and “lai tai –
Thailand”
 IMPORTANT: identify the condition in ECG Figure 11-1 page 61
3) Congenital Heart Disease because the risk of sudden cardiac death is high and can be
 Sudden cardiac death is a frequent case of morbidity and mortality in prevented by internal cardioverter-defibrillator placement.
CHD patients who survive to adulthood.
 The most frequent coronary artery anomaly associated with sudden
cardiac death is anomalous origin of the left coronary artery from the
pulmonary artery [ALCAPA] syndrome. The left coronary artery
traverses between the aorta and the main pulmonary artery.
 The greatest risk of sudden cardiac death in children and adults with
congenital heart disease exists in those with left heart obstructive
lesions (e.g. Aortic stenosis and aortic coarctation) and cyanotic Early Repolarization Syndrome: It is [mc] seen in 100% of endurance
defects. athletes with unestablished clinical significance.
 Most sudden deaths occur during exercise usually resulting to  Classic ECG: prominent, notch-like J wave on the QRS down-slope,
Ventricular Fibrillation. followed by upsloping ST-segment elevation. (Fig 11-2)

4) Valvular Heart Disease


 Hemodynamically sever aortic stenosis can cause effort-induced
dyspnea myocardial ischemia and ventricular arrhythmias, which can
trigger syncope and sudden cardiac death.
 [mc] of aortic stenosis are congenital bicuspid aortic valve (mid-
adulthood) and tricuspid aortic valve calcification (>70-80 yrs of age).
 A harsh, late-peaking systolic murmur at the upper-right sternal border
with radiation to the neck is a typical finding in hemodynamically Long QT Syndrome – the Long QT syndrome is characterized by prolongation
significant aortic stenosis. of the corrected QT interval (QTc), syncope, and sudden death caused by
torsades de pointes and ventricular fibrillation.
5) Cardiac pacing and conducting system  Calculate: Bazett’s equation which corrects the measured QT interval
 Sick sinus syndrome, a degenerative disorder, affects the heart’s to a HR of 60bpm
primary pacemakers and conduction systems and can cause  Prolongation of the QTc represents dispersion in ventricular
intermittent lightheadedness, syncope, or sudden cardiac death. repolarization and can be hereditary or acquired (hypokalemia,
 Due to degradation of the sinoatrial node, may also involve AV node hypomagnesemia, hypocalcemia, anorexia, ischemia, CNS,
and other conduction tissues. terfenadine-ketoconazole combination, antipsychotics or
 Lenegre’s disease – idiopathic sclerodegeneration of the AV node antiarrythmics)
and bundle branches  Management: avoidance of QT-prolonging drugs and avoidance of high
 Lev’s disease – fibrosis and calcification of the conduction system intensity sports, as well as a cardiology referral.
 Symptomatic bradycardia is treated with pacemaker placement.  Tx: B Blockers as sudden death prophylaxis. Persistence of syncope
despite B-blocker Tx warrants implantable cardioverter-defibrillator.
6) Hereditary Channelopathies  Autosomal Recessive: Jervell and Lange-Nielsen syndrome
Sudden Arrhythmic Death Syndrome – characterized by sudden cardiac  Autosomal Dominant: Romano-ward syndrome without nerve
death occurring out of hospital in relatively young adults [mc] men, often deafness.
during sleep or at rest, usually without any premonitory symptoms
(including syncope)and with no anatomic abnormality identified at autopsy. Short QT syndrome – an abnormally short QTc (<.34s) can be secondary to
hypercalcemia, hyperkalemia, acidosis, systemic inflammatory syndrome,
Ion Channel Disease – Cardiovascular and genetic examination of first- myocardial ischemia, or increase vagal tone or can be inherited.
degree relatives show familial cardiac diseases “channelopathy” or “ion  Classic ECG: early repolarization in inferolateral leads.
channel disease”.
Catecholaminergic Polymorphic Ventricular Tachycardia
 Pathology: Defective myocardial cellular calcium handling
 S/Sx: exercise and stress related v. tach + syncope and sudden cardiac
death. [mc] presents with epilepsy as the cause of recurrent syncope.
 Classic ECG: none but! most individual exhibit unexplain sinus
bradycardia.

PREVENTION OF SUDDEN CARDIAC DEATH


 Prodromal symptoms are uncommon.
 [mc] symptoms, if present, chest dyscomfort, dyspnea and “not
feeling well”
 Screening: no sensitive and specific test. (options: early detection of  Problem: compromised cardiac output.
ventricular late potentials, inducibility of v.tach, presence of T-wave  Outcome: despite intervention bradyasystolic rhythms have poor
alternans. outcomes.
 The only opportunity for prevention is to recognize signs and  Bardycardia occurs frequently during cardiac arrest
symptoms of syndromes that place a patient at higher risk of sudden  To ensure that ventricular fibrillation is not masquerading as asystole,
cardiac death and to admit or refer such patient for proper evaluation rescuers can switch to another lead whenever a “flat line” is recorded
and prophylaxis. on the ECG during resuscitation or use US if available.
 Antiarrythmic drug and device therapy:
 Avoid: Class I antiarrythmics are proarythmogenic
 Implantable cardio-defib are superior vs. B-blocker and amiodarone

SUDDEN CARDIAC DEATH RESCUE


 [mc] is either pulseless V.tach or V.fib
 Survival is inversely related to duration of event. (onset and
termination of abnormal rhythm)
 EMS and In-hospital resuscitation systems are the most effective
rescue interventions.
 Early CPR, ACLS, Defibrillation and drug therapy.
 Early Defibrillation confers the best survival among the interventions.
 By-standers capable of using external defibrillators reduces mortality
by half compared to CPR alone.

Pulseless Ventricular Tachycardia/ Ventricular Fibrillation


 Two rhythms with highest survivability: V. tach and V. fib.
 Unwitnessed Asystolic patients usually have neurologic deficits.
 Exception: witnessed cardiac arrest with asystole due to increase
vagal tone or hypoxia of brief duration.

Pulseless Electrical Activity


 Defined as an organized rhythm without a pulse.
 Tx: directed at identifying and treating the underlying cause or
causes.
 Bradyasystole: defined as a ventricular rate <60 bpm or period of
absent heart rhythm. Can be with or without a pulse.
 Primary Bradyasystole: heart fails to general electrical activity to
generate ventricular depolarizations that maintain end organ
function.
 Secondary Bradyasystole: factors external to the heart eg. Hypoxia.