Felis ISSN 2398-2950

Heart: dysrhythmia

Synonym(s): Arrhythmia, Heart block, Ectopic beat

Contributor(s): Serena Brownlie, Phil Fox, Philip K Nicholls, Penny Watson

Introduction

  • Definition: abnormalities of rate and rhythm of the heartbeat.
  • Cause: primary cardiac disease - muscular or conduction abnormalities; systemic disease; trauma.
  • Signs: many are asymptomatic; syncope, sudden death, congestive heart failure.
  • Diagnosis: auscultation; electrocardiography (ECG).
  • Treatment: anti-arrhythmic drugs depending on type of arrhythmia; correction of metabolic factors.
  • Prognosis: depends on cause and response to therapy.
    Follow the diagnostic trees forCommon Cardiac Arrhythmias Common cardiac arrhythmias and Bradyarrhythmia & Tachyarrhythmia Bradyarrhythmia & Tachyarrhythmia.

Pathogenesis

Predisposing factors

General

  • Toxemia Shock: septic.
  • Hypoxia.
  • Myocardial wall abnormality.
  • Drugs.
  • Neurological abnormality, ie 'brain-heart syndrome'.
  • Systemic/metabolic diseases.
  • Cardiomyopathies.

Specific

Bradycardia

AV block in cats is always abnormal and needs investigation.

Tachycardia

  • Hyperthyroidism Hyperthyroidism.
  • Myocardial disease.
  • Drugs:
    • Atropine (parasympatholytics).
    • Anti-arrhythmics.
    • Anesthetic agents.
    • Cardiac glycoside toxicity (can   →   VPCs).
  • Electrolyte imbalance:
  • Hypomagnesemia.
  • Acidosis.
  • Nervousness/adrenaline.
  • Fever.
  • Pain.

Pathophysiology

  • Conduction abnormalities or development of ectopic foci   →   trigger dysrhythmias.
  • Depolarization of pacemaker cells in sino-atrial node (dictates intrinsic heart rate):
    • Increased by sympathetic stimulation (excitement, fear and pain).
    • Decreased by parasympathetic stimulation.
    • Altered by drugs, hormone levels, electrolytes.
    • Reflected by damage to conduction tissues   →   AV or branch bundle block.
  • Ectopia:
    • Myocardial disease (myocarditis, fibrosis or hypoxia), electrolyte imbalances, endotoxins or toxins released from reperfusion injury or sympathetic stimulation   →   ectopic foci.
  • Extracellular potassium affects heart rate:
    • Hypokalemia   →   faster depolarization.
    • Hyperkalemia   →   reduces resting membrane potential   →   slows conduction velocity and heart rate.
  • Intracellular calcium ion concentration affects the Na+/Ca++ exchange pump.
  • Abnormal automaticity refers to site of depolarization in non-pacemaker tissue.
  • Re-entry refers to second depolarization when part of impulse is delayed by passage through diseased tissue (due to hypoxia or fibrosis).
  • After-potentials are oscillations in resting membrane potential following repolarization which may reach threshold potential and trigger an impulse.
  • After-potentials are enhanced by adrenergic stimulation, digitalis toxicity and increased intracellular calcium.

Timecourse

  • Depends on cause.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rials S J, Wu Y, Ford N et al (1995) Effect of left ventricular hypertrophy and its regression on ventricular electrophysiology and vulnerability to inducible arrhythmia in the feline heart. Circulation 91 (2), 426-430 PubMed.
  • Kowey P R, O'Brien R, Wu Y et al (1992) Effect of gallopamil on electrophysiologic abnormalities and ventricular arrhythmias associated with ventricular hypertrophy in the feline heart. Am Heart J 124 (4), 898-905 PubMed.
  • Boyden P A, Tilley L P, Albala A et al (1984) Mechanisms for atrial arrhythmias associated with cardiomyopathy - a study of feline hearts with primary myocardial disease. Circulation 69 (5), 1036-1047 PubMed.


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