Ventricular fibrillation

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Ventricular fibrillation showing coarse, unformed QRS complexes[1]

Ventricular fibrillation is an uncommon life-threatening heart disease of dogs characterized by a lethal rhythm of multiple re-entrant circuits causing chaotic electrical activity in the ventricles.

Ventricular fibrillation is associated with a high mortality rate and sudden death.

The mechanism which initiates ventricular fibrillation is not completely understood but thought to involve the presence of multiple, independent wavefronts or single, dominant wavefronts that activate adjacent tissue[2]. This may affect the fibrillation threshold which dictates the duration of episode, defined as either short-duration ventricular fibrillation or and long-duration ventricular fibrillation (sustained)[3].

Like atrial fibrillation, the ventricles have no coordinated mechanical activity in the presence of uncoordinated electrical activation and cannot function as a pump. Ventricular flutter, which appears as rapid sine-wave activity on the ECG, may precede fibrillation. Ventricular fibrillation may be coarse (larger ECG oscillations) or fine.

Ventricular fibrillation can occur as a result of:

Regardless of cause, ventricular fibrillation leads to a rapid decline in ventricular fibrillation rate, emergence of inexcitable regions, and eventual global asystole followed by death[4], underscoring the importance of rapid diagnosis and treatment of this condition.

Diagnosis is usually based on clinical presentation of acute collapse, few audible cardiac sounds on auscultation and an ECG usually showing an irregularly undulating baseline.

This rapidly fatal rhythm requires immediate cardiac conversion and patients will die without use of a defibrillator to restore normal heart rhythm[5], followed by intravenous constant rate infusion of lidocaine[6]. Epinephrine (adrenalin) is given at the same time either intravenously or intracardiac at 0.2 mg/kg. If the patient is successfully cardioconverted, lidocaine is administered to minimize the risk of refibrillation or development of ventricular tachycardia.

Cardioconversion requires an external counter-shock (1 - 10 ws/kg) or internal counter-shock (0.1 - 1.0 ws/kg). Treatment of concurrent hypothermia, hyperkalemia and acid-base disturbances is required as well.

Prevention is difficult, unless there is a history of predisposition in particular canine patients. Endurance exercise training has been shown to reduce susceptible to recurrent ventricular fibrillation in susceptible canine patients[7].

References

  1. University of Pennsylvania
  2. Jalife J (2000) Ventricular fibrillation: mechanisms of initiation and maintenance. Annu Rev Physiol 62:25–50
  3. Wu L et al (2011) The effects of acute amiodarone on short- and long-duration ventricular defibrillation threshold in canines. J Cardiovasc Pharmacol 58(4):432-438
  4. Taylor TG et al (2012) Role of KATP channel in electrical depression and asystole during long-duration ventricular fibrillation in ex vivo canine heart. Am J Physiol Heart Circ Physiol 302(11):H2396-H2409
  5. Pariaut R et al (2011) Implantable cardioverter-defibrillator in a German shepherd dog with ventricular arrhythmias. J Vet Cardiol 13(3):203-210
  6. Prosek R (2010) Electrical cardioversion of sustained ventricular tachycardia in three Boxers. J Am Vet Med Assoc 236(5):554-557
  7. Kukielka M et al (2011) Endurance exercise training reduces cardiac sodium/calcium exchanger expression in animals susceptible to ventricular fibrillation. Front Physiol 2:3