Disorders of Cardiac Repolarization, Paroxysmal Tachycardia, and Ventricular Fibrillation

Disorders of Cardiac Repolarization, Paroxysmal Tachycardia diagram

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https://mednotesbyrazaullah.blogspot.com/2026/08/chapter-06-skeletal-muscle-fiber.html

Disorders of Cardiac Repolarization, Paroxysmal Tachycardia, and Ventricular Fibrillation

Ventricular repolarization represents a crucial physiological phase during which cardiac muscle fibers restore their resting membrane potential following depolarization. When electrical repolarization is delayed, the total ventricular action potential duration lengthens, creating a prolonged Q-T interval on the electrocardiogram. This prolonged repolarization phase significantly alters the electrical stability of the ventricles, predisposing the heart to severe and potentially life-threatening ventricular arrhythmias. Understanding the underlying genetic, metabolic, and pharmacological mechanisms of repolarization disorders helps clinicians prevent sudden cardiac collapse and manage complex electrical disturbances.

Additionally, ectopic foci and abnormal re-entrant circuits can induce sudden bursts of rapid cardiac rhythms, known as paroxysmal tachycardias, originating within the atria, the AV node, or the ventricular myocardium. If abnormal excitation cycles become uncoordinated, the electrical activity degenerates into chaotic re-entry movements termed ventricular fibrillation. During fibrillation, localized muscle regions contract independently without generating synchronized mechanical pumping, leading to instantaneous cessation of systemic blood flow. Diagnostic analysis of these rhythm disturbances allows medical professionals to apply targeted electrical and pharmacological interventions to restore normal cardiac rhythmicity.

Disorders of Cardiac Repolarization and Long QT Syndrome

  • Q wave corresponds to ventricular muscle depolarization.
  • T wave corresponds to ventricular muscle repolarization.
  • Q-T interval measures Q point to T wave end.
  • Delayed ventricular repolarization prolongs action potential duration.
  • Prolonged repolarization causes long QT syndrome (LQTS).
  • Delayed repolarization increases susceptibility to ventricular arrhythmias.
  • Torsades in the pointes means twisting of the points.
  • Torsades the  pointes alters QRS complex shape continuously.
  • Arrhythmia onset usually follows a premature beat.
  • Long Q-T intervals trigger rapid ventricular tachycardia.
  • Torsades the pointes can degenerate into ventricular fibrillation.
  • Congenital LQTS results from inherited gene mutations.
  • Mutations alter sodium or potassium ion channel genes.
  • Ten different channel gene mutations cause LQTS.
  • Acquired LQTS results from plasma electrolyte disturbances.
  • Hypomagnesemia, hypokalemia, and hypocalcemia cause LQTS.
  • Antiarrhythmic drugs like quinidine prolong Q-T interval.
  • Antibiotics like fluoroquinolones or erythromycin cause LQTS.
  • Fainting spells occur during exercise or anger.
  • Sudden loud noises can precipitate ventricular arrhythmias.
  • Acute LQTS treatment includes intravenous magnesium sulfate.
  • Long-term treatment utilizes beta-adrenergic receptor blockers.
  • Implantable cardiac defibrillators prevent sudden cardiac death.

Paroxysmal Tachycardia Mechanisms

  • Ectopic foci cause rapid rhythmical cardiac impulses.
  • Impulses spread rapidly in all cardiac directions.
  • Re-entrant circus feedback pathways cause local re-excitation.
  • Irritable focus becomes temporary primary cardiac pacemaker.
  • Paroxysmal means rapid rate begins very suddenly.
  • Paroxysms last seconds, minutes, hours, or longer.
  • Paroxysmal attacks end as suddenly as started.
  • Pacemaker instantly shifts back to sinus node.
  • Carotid sinus pressure elicits therapeutic vagal reflex.
  • Vagal reflex stimulation can stop paroxysmal attacks.
  • Quinidine depresses membrane sodium permeability during activation.
  • Lidocaine reduces sodium permeability to stop attack.
  • Depressing sodium influx blocks focal rhythmical discharge.

Atrial and Supraventricular Paroxysmal Tachycardia

  • Atrial tachycardia suddenly increases rate up to 150.
  • Inverted P waves appear before QRS-T complexes.
  • Abnormal P wave superimposes onto preceding T wave.
  • Abnormal P wave shape indicates non-sinus origin.
  • AV nodal tachycardia causes normal QRS-T complexes.
  • Missing or obscured P waves indicate nodal origin.
  • Atrial and AV nodal are supraventricular tachycardias.
  • Supraventricular tachycardia usually affects young healthy individuals.
  • Patients generally outgrow predisposition after adolescence period.
  • Attacks cause severe fright and temporary physical weakness.
  • Supraventricular tachycardia rarely causes permanent cardiac damage.

Ventricular Paroxysmal Tachycardia Characteristics

  • Ventricular tachycardia shows sequential ventricular premature beats.
  • Normal beats do not intersperse during paroxysm.
  • Ischemic ventricular damage usually causes ventricular tachycardia.
  • Repeated rapid stimulation initiates lethal ventricular fibrillation.
  • Digitalis toxicity causes irritable foci causing tachycardia.
  • Quinidine increases cardiac muscle refractory period duration.
  • Quinidine increases excitation threshold to block foci.

Ventricular Fibrillation and Cardiac Arrest

  • Ventricular fibrillation is most serious cardiac arrhythmia.
  • Fibrillation causes death within one to three minutes.
  • Cardiac impulses travel berserk within ventricular muscle.
  • Impulses feed back repeatedly to re-excite muscle.
  • Uncoordinated muscle contractions prevent synchronized pumping action.
  • Ventricular chambers remain in partial contraction state.
  • Fibrillating ventricles pump no effective blood output.
  • Unconsciousness occurs within four to five seconds.
  • Lack of cerebral blood flow causes rapid fainting.
  • Permanent tissue death occurs within a few minutes.
  • Sudden electrical shock frequently initiates ventricular fibrillation.
  • Cardiac muscle ischemia sparks dangerous ventricular fibrillation.

Phenomenon of Re-entry and Circus Movements

  • Normal cardiac impulses die after complete depolarization.
  • Refractory muscle cannot transmit a second impulse.
  • Impulse dies and awaits new sinus potential.
  • Circular muscle strips demonstrate re-entry impulse transmission.
  • Unidirectional impulse travels around circular muscle pathway.
  • Returning impulse dies if origin remains refractory.
  • Long pathway length permits origin refractory recovery.
  • Impulse continues traveling around circle repeatedly endlessly.
  • Decreased conduction velocity delays impulse return time.
  • Slow conduction allows muscle refractory period recovery.
  • Shortened refractory period allows continuous re-entry movement.
  • Continuous circus movement causes persistent ventricular fibrillation.

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