ISSN 2398-2950      

Ventricular fibrillation

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Synonym(s): VF


Introduction

  • Cause: can occur as electrophysiological complication of other "malignant" (ie prefibrillatory) ventricular arrhythmia such as very fast and sustained ventricular tachycardia (VT Ventricular tachycardia) in the presence of severe organic myocardial disease (eg hypertrophic cardiomyopathy).
    • In severe heart failure, when diastolic function is poor, intraventricular diastolic filling pressure is high, and myocardial hypoxia is present, VT can be a precursor to VF.
  • Untreated ventricular fibrillation    →   hemodynamic cardiac arrest and death.
  • May be induced by lengthy or deep-planed general anesthesia (eg when lengthy and severe myocardial hypoxia present) or at onset of anesthesia induction, either in severely diseased patients or (rarely) in healthy animals.
  • Respiratory arrest and ventilatory failure can lead to VF.
  • Diagnosis: electrocardiography. Chaotic/random, irregular, low-amplitude oscillations or undulations at a rate ranging between 150 and 300, or even >400 cycles/minute, with no distinct P waves (despite continuation of organized atrial electrical and mechanical activity), QRS complexes or T waves.
  • Undulations either coarse (and relatively more amenable for cardioversion) or fine (less amenable for cardioversion).
  • Many malignant ventricular arrhythmias that electrocardiographically and hemodynamically appear to be asystole (see Differential Diagnosis) are, in fact, fine VF. Therefore, open-chest heart massage and direct observation of myocardial activity may be warranted early with this arrhythmia.
  • Treatment: direct current (DC) electrical countershock (defibrillation) only effective therapy.
  • Prognosis: in the severely diseased, poor to grave, often even if promptly and successfully treated.
  • More favorable if defibrillation performed immediately in otherwise normal animal with chemical etiology, eg drug toxicity:
    • Anesthetic overdose such as halothane or barbiturates.
    • Drug-drug interaction.

Pathogenesis

Predisposing factors

General

Primary cardiac disease

Extra-cardiac disease

  • Severe, terminal systemic disease (eg neoplastic/traumatic/endocrine).
  • Hyperkalemia Hyperkalemia (>11 mEq/L)
  • Severe acid-base imbalance Acid base imbalance (eg metabolic or respiratory alkalosis or acidosis).
  • Progressive (eg anemia Anemia: overview) or acute (eg severe hemorrhage or prolonged ventilatory arrest) severe hypoxia/anoxia.
  • Extreme hypothermia Hypothermia or hyperthermia Hyperthermia.
  • A surge (or an iatrogenic bolus at a toxic dose) of circulating cathecholamines, especially when myocardium has been previously sensitized.
  • Acute, severe intoxication/drug toxicity (eg digoxin Digoxin).
  • Electrocution Electrocution/lightning strike.

Pathophysiology

  • Both ventricles "quiver" rather than contract, therefore stroke volume and cardiac output drop to zero even if some minimal, disorganized and non-coordinated myocardial mechanical activity still takes place.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Crowe D T, Fox P R, Devey J J & Spreng D (1999) Cardiopulmonary and cerebral resuscitation. In: Textbook of Canine and Feline Cardiology. Principals and Clinical Practice. 2nd Edn. Eds: P R Fox, D Sisson D and N S Moise. WB Saunders Co, Philadelphia. pp 427-445.
  • Kittleson M D (1998) Diagnosis and treatment of arrhythmias (dysrhythmias). In: Small Animal Cardiovascular Medicine. Eds: M D Kittleson and R D Kienle. Mosby Inc, St Louis. pp 449-494.
  • Labato M A (1995) Cardiopulmonary arrest and resuscitation. In: Textbook of Veterinary Internal Medicine. diseases of the Dog and Cat.1 , Eds: S J Ettinger and E C Feldman. WB Saunders Co, Philadelphia. pp.71-79.
  • The Merck Veterinary Manual, Eighth Edition, Published by Merck & Co Inc, Whitehouse Station, NJ, USA. In cooperation with MERIAL LIMITED, a Merck and Aventis Company:http://www.merckvetmanual.com/(All rights reserved).

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