Pulseless ventricular tachycardia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]


Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity. Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.

In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.



The normal physiology of Pulseless ventricular tachycardia/ventricular tachycardia can be understood as follows:


Pathophysiology of ventricular tachycardia can be better studied depending upon the subclass:[1][2][3][4]

Cellular level

  • Electrical reentry or abnormal automaticity is the main reason behind ventricular tachycardia.
    • Myocardial scarring from any process increases the likelihood of electrical reentrant circuits.
    • These circuits generally include a zone where normal electrical propagation is slowed by the scar.
    • Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT.
  • VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity.
  • Torsade de pointes seen in the long QT syndromes is likely a combination of triggered activity and ventricular reentry.
  • During VT cardiac output is reduced as a consequence of decreased ventricular filling from the rapid heart rate and the lack of properly timed or coordinated atrial contraction.
  • Ischemia and mitral insufficiency may also contribute to decreased ventricular stroke output and hemodynamic intolerance.
  • Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or when heart rates are very rapid.
  • Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to ventricular fibrillation (VF), resulting in sudden death.
  • In patients with monomorphic VT, mortality risk correlates with the degree of structural heart disease. Underlying structural heart diseases such as ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, and right ventricular dysplasia have all been associated with degeneration of monomorphic or polymorphic VT to VF.
  • Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.
  • If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.

Monomorphic Ventricular Tachycardia

Polymorphic Ventricular Tachycardia


Autosomal-dominant mutations in ryanodine receptor type 2 ( ryr2) have been complicated in a type of ventricular tachycardia known as catecholaminergic polymorphic ventricular tachycardia.[5]

Associated Conditions

Conditions associated with [disease name] include:


  1. Martin CA, Lambiase PD (October 2017). "Pathophysiology, diagnosis and treatment of tachycardiomyopathy". Heart. 103 (19): 1543–1552. doi:10.1136/heartjnl-2016-310391. PMC 5629945. PMID 28855272.
  2. Simons GR, Klein GJ, Natale A (February 1997). "Ventricular tachycardia: pathophysiology and radiofrequency catheter ablation". Pacing Clin Electrophysiol. 20 (2 Pt 2): 534–51. doi:10.1111/j.1540-8159.1997.tb06209.x. PMID 9058854.
  3. Brunckhorst C, Delacretaz E (April 2004). "[Ventricular tachycardia--etiology, mechanisms and therapy]". Ther Umsch (in German). 61 (4): 257–64. doi:10.1024/0040-5930.61.4.257. PMID 15137521.
  4. Srivathsan K, Ng DW, Mookadam F (July 2009). "Ventricular tachycardia and ventricular fibrillation". Expert Rev Cardiovasc Ther. 7 (7): 801–9. doi:10.1586/erc.09.69. PMID 19589116.
  5. Pan X, Philippen L, Lahiri SK, Lee C, Park SH, Word TA, Li N, Jarrett KE, Gupta R, Reynolds JO, Lin J, Bao G, Lagor WR, Wehrens X (September 2018). "In Vivo Ryr2 Editing Corrects Catecholaminergic Polymorphic Ventricular Tachycardia". Circ. Res. 123 (8): 953–963. doi:10.1161/CIRCRESAHA.118.313369. PMC 6206886. PMID 30355031. Vancouver style error: initials (help)

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