Bovis ISSN 2398-2993

Dysrhythmias

Contributor(s): Louise Cox-O’Shea , Gayle Hallowell

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Introduction

  • Definition: abnormalities of rate and rhythm of the heartbeat.
  • Cause: primary cardiac disease - muscular or conduction abnormalities; systemic disease- especially GI problems.
  • Signs: often no clinical signs; weakness, syncope, sudden death, congestive heart failure.
  • Diagnosis: auscultation; electrocardiography (ECG).
  • Treatment: anti-dysrhythmic drugs depending on type of rhythmdisturbance; correction of metabolic and electrolyte abnormalities; address underlying disease process.
  • Prognosis: depends on cause and response to therapy.

Pathogenesis

Etiology

  • Primary or secondary.
  • Physiological or pathological.

Predisposing factors

General

  • Systemic Inflammatory Response Syndrome (SIRS) or sepsis.
  • Hypoxia.
  • Myocardial wall abnormality, especially myocarditis and other cardiomyopathies.
  • Amyloidosis.
  • Drugs.
  • Systemic/metabolic diseases especially GI disease.
  • Neurological abnormality, ie 'brain-heart syndrome'.

Specific

Bradycardia
  • Hyperkalemia.
  • Hypercalcemia.
  • Drugs (sedatives, esp alpha-2 agonists, anti-dysrhythmics).
  • Severe upper respiratory infections.
Tachycardia
  • Myocardial disease.
  • Drugs: 
    • Anesthetic agents.
    • Atropine (parasympatholytics).
    • Anti-dysrhythmics.
  • Electrolyte imbalance: 
  • Acidosis.
  • Nervousness/adrenaline.
  • Fever.
  • Pain i.e. severe lameness.

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, SIRS or sepsis, reperfusion injury/ e.g. diseases like E. coli mastitis 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 and increased intracellular calcium.
Physiological dysrhythmias
  • The most common physiological dysrhythmia found in cattle is sinus dysrhythmia. Occasionally first and second degree atrio-ventricular blockade are identified either on auscultation or electrocardiogram. These will all resolve with physical activity or an increase in heart rate.
Supraventricular
  •  (sinus tachycardia, sinus bradycardia).
  • Atrial premature contractions (APCs).
  • Atrial fibrillation/flutter.
  • Atrial tachycardia.
  • Sinoatrial block or SA arrest.
  • Atrial standstill.
  • Functional escape rhythms.
Atrioventricular nerve block
  • Second degree AV block – can be physiological or pathological.
  • Third degree AV block.
Ventricular
  • Ventricular premature contractions (VPCs).
  • Ventricular tachycardia.
  • Atrioventricular dissociation.
  • Accelerated idioventricular rhythm.
  • Escape rhythms.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed And VetMedResource.
  • Rezakhani A, Paphan A A & Gheisari H R (2004) Cardiac dysrhythmias in clinically healthy heifers and cows. J Am Vet Med Assoc 182 (12), pp 1380-6
  • Moise N S (1998) Autonomic influences on cardiac rhythms in dogs. JSAP 39, pp 460-468 PubMed.
  • Wagner A E et al (1997) Arterial blood pressure monitoring in anesthetized animals. JAVMA 210 (9), pp 1279-1284 PubMed.
  • Rials S J 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), pp 426-430 PubMed.
  • Kowey P R 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), pp 898-905 PubMed.
  • Boyden P A (1984) Mechanisms for atrial arrhythmias associated with cardiomyopathy - a study of feline hearts with primary myocardial disease. Circulation 69 (5), pp 1036-1047 PubMed.
  • McGuirk S M, Muir W W, Sams R A & Rings D M (1983) Atrial fibrillation in cows: clinical findings and therapeutic considerations. J Am Vet Med Assoc 182 (12) pp 1380-6 PubMed.

Other sources of information

  • GOV.UK (2017) Veterinary Medicines Directorate. [online] Last accessed 27th November 2017. Available at: www.gov.uk.
  • Clark-Price S & Divers T J (2008) Anesthesia for Field Emergencies and Euthanasia. In: Equine Emergencies, Treatment and Procedures. Eds: Orsini J A & Divers T J. Saunders, Philadelphia. pp 661-670.
  • Taylor P M & Clarke K W (1999) Routine for Cardiopulmonary Resuscitation after Cardiac Arrest. In: Handbook of Equine Anaesthesia. Saunders, Philadelphia. pp 139-142.
  • Riebold T W, Geiser D R & Goble D O (1995) Large Animal Anesthesia. Principles and Techniques. 2nd edn. Iowa State University Press, Ames, IA, USA. pp 83-140 & 174-204.
  • Dugdale A (2010) Veterinary Anaesthesia. Eds: Wiley-Blackwell.
  • The Merck Veterinary Manual Merial.
  • Stephen A (2002) Veterinary Anaesthesia and Pain Management Secrets. 1st Edn. Ed: Greene
 


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