Felis ISSN 2398-2950

Heart: dysrhythmia

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 for Common 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.

• Cardiac glycoside toxicity Digoxin.
• Feline dysautonomia Feline dysautonomia.
• Hyperkalemia Hyperkalemia.
• Hypercalcemia Hypercalcemia: overview.
• Drugs (anti-arrhythmics, sedatives).
• Severe upper respiratory infections.

Tachycardia

• Hyperthyroidism Hyperthyroidism.
• Myocardial disease.
• Drugs:
  • Atropine (parasympatholytics).
  • Anti-arrhythmics.
  • Anesthetic agents.
  • Cardiac glycoside toxicity (can   →   VPCs).
• Electrolyte imbalance:
  • Hypokalemia Hypokalemia.
  • Hypocalcemia.
• 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

Treatment

Outcomes