Sudden cardiac death pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] José Eduardo Riceto Loyola Junior, M.D.[3] Edzel Lorraine Co, DMD, MD[4]

Overview

The pathogenesis of cardiac arrest is characterized by the myocardial inflammatory process in the setting of atherosclerosis, structural heart disease, genetic disorders, and environmental factors. The SCN5A, KCNH2, KCNQ1, RYR2, MYBPC3, PKP2, DSP genes mutation are associated with the development of inherited causes of cardiac arrest and sudden cardiac death.

Pathophysiology

• The pathogenesis of cardiac arrest is characterized by the myocardial inflammatory process in the setting of atherosclerosis, structural heart disease, genetic disorders, and environmental factors.
• The SCN5A, KCNH2, KCNQ1, RYR2, MYBPC3, PKP2, DSP genes mutation are associated with the development of inherited causes of cardiac arrest and sudden cardiac death.

Structural and functional causes of sudden cardiac death Coronary artery disease Cardiomyopathy Valvular heart disease Congenital heart disease Primary electrical abnormality Channelopathy

Trigger Myocardial infarction Myocardial ischemia/reperfusion Emotional, physical stress Hemodynamic decompensation Electrolyte imbalance Hypoxemia,acidosis Neurophysiological interactions Drugs

Arrhythmia mechanism Re-entry Automaticity Triggered activity Conduction block

Fatal arrhythmia Monomorphic ventricular tachycardia Polymorphic ventricular tachycardia Ventricular fibrillation Profound bradycardia Asystole Pulseless electrical activity

• The pathogenesis of cardiac arrest during defecation in patients with advanced cardiomyopathy and poor cardiac reserve is defined as increased parasympathetic tone during defecation rather than conduction system abnormalities leading to defecation induced bradyarrhythmia by these mechanisms:
  • Negative chronotropic and drotropic effects during defecation
  • Reduced venous return to the heart
  • Reduced cardiac output
  • Sympathetic efferent reflex stimulation by arterial baroreceptors to compensate for such changes
  • Inappropriate stimulation of cardiac mechanoreceptors (C-fibers) due to sympathetic response in a volume-depleted ventricle
  • C-fiber signal activates vasopressor neurons in the medulla causing parasympathetic stimulation and sympathetic withdraw
  • Parasympathetic stimulation results not only in negative chronotropic, dromnotropic and inotropic effects but also vascular tone instability.