Heart: dysrhythmia (arrhythmia)

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• Most dysrhythmias are clinically unimportant.
• Abnormalities of heart rate +/- conduction (rhythm).
• Cause : systemic disease, primary cardiac disease.
• Signs : many are subclinical, frequent finding in cardiac disease.
• Diagnosis : auscultation, ECG, must make accurate diagnosis before considering treatment.
• Treatment : may be inappropriate - anti-dysrhythmic drugs if necessary.
• Prognosis : often depends on etiology.

• Incidental with concurrent heart failure and systemic disease.

• Lethargy.
• Exercise intolerance.
• Weakness.

• Syncope.
• Sudden death.

• Older female Miniature Schnauzer  (sick sinus syndrome).

• Brachycephalic breeds        (sinus arrest  ).
• Older female Miniature Schnauzer  (sick sinus syndrome).
• Cocker Spaniel .
• Dachshund .

• Giant breeds (predisposed to dilated cardiomyopathy   and atrial fibrillation .
• Springer Spaniel  (atrial standstill).
• Labrador Retriever  (supraventricular tachycardias).

• Sotalol/mexiletine can be expensive.
• Repeat Holter evaluation.

Pathogenesis

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• May occur as a primary entity or secondary to systemic or cardiac disease.

• 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.
• Ectopy:
  • Myocardial hypoxia, electrolyte imbalances or sympathetic stimulation  ectopic foci.
  • 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.
• Can be classified according to site of origin.

Supraventricular

• Sinus arrhythmia (sinus tachycardia, sinus bradycardia).
• Atrial tachycardia.
• Junctional escape rhythms.
• Atrial standstill.
• Atrial fibrillation/flutter .
• Atrial premature contraction (APCs) .
• Sinoatrial block  or SA arrest.

Atrioventricular nerve block

• First degree AV block .
• Second degree AV block .
• Third degree AV block .

Ventricular

• Accelerated idioventricular rhythm .
• Ventricular tachycardia .
• Ventricular fibrillation .
• Ventricular premature contractions (VPCs) .
• Atrioventricular dissociation.
• Escape rhythms.

Diagnosis

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• Weakness and collapse.
• Lethargy.
• Syncope.
• Sudden death.

• Abnormal heart rhythm often apparent on auscultation.
• Pulse deficits, ie presence of heart sound with no palpable peripheral pulse in some tachydysrhythmias.
  It is important to palpate the femoral pulse at the SAME time as auscultating the heart to detect any pulse deficits.

• Varying pulse intensity.
• Signs of underlying heart disease  or other systemic illness.

• Poor peripheral pulses in some cases, especially with tachydysrythmias.

• See ECG overview .
• For definitive diagnosis of dysrhythmia type.
• Holter monitor - it may be necessary to fit a portable ECG (Holter) to detect intermittent or infrequent dysrhythmias.
• Further tests aimed at identifying underlying cause.

• Thoracic radiographs  are taken to rule out underlying cardiac disease particularly atrial or ventricular enlargement.
• Abdominal radiographs  may be useful in identifying significant pathology, eg splenic neoplasia .

• Ultrasonography  to detect underlying cardiac pathology.

• Electrolyte assay:
  • Potassium  : hyperkalemia  may  bradycardia, hypokalemia  ECG abnormalities.
  • Calcium  : hypercalcemia  may  ventricular dysrhythmia (rare), hypocalcemia  ECG abnormalities.
• Magnesium: hypomagnesemia  ventricular dysrhythmias.

• Electrocardiography.
• Electrophysiologic (EP) study (rare in animals).

Treatment

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• Identify and treat underlying non-cardiac causes.
• Correct electrolyte imbalances  and treat congestive heart failure  if present.
• Ensure adequate oxygenation.
• Provide adequate analgesia.
• Select appropriate anti-dysrhythmic drug if indicated.
  Inappropriate anti-dysrhythmic therapy is often worse than no treatment.

• Reverse excess vagal activity with atropine  or glycopyrrolate .
• If due to glycoside toxicity, withdraw or reduce dose.
• Pacemaker implantation  if bradydysrhythmia with clinical signs.

• Cardiac glycoside, eg digoxin  for atrial fibrillation.
• Calcium channel blockers, eg verapamil  or diltiazem .
• Beta-blockers, eg propranolol  if no myocardial dysfunction.

• Lidocaine  or procainamide  intravenously.
• Beta-blockers if no myocardial failure.
• Sotalol  for Boxer arrhythmias without myocardial failure.
• Mexiletine  often with atenolol  or metoprolol.

• Clinical condition of animal is often best guide to assessing significance of dysrhythmia.

• Repeat ambulatory electrocardiography (Holter) at regular intervals to ensure resolution.

Sequelae

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• Depends on dysrhythmia and underlying disease.
• Varies from poor to good so important to make accurate diagnosis.

• Reduced frequency of dysrhythmia on electrocardiogram.
• Normalizing of heart rate.
• Improving clinical condition.

Sources

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• Moise N S (1998) Autonomic influences on cardiac rhythms in dogs. JSAP 39 , 460-468.

• Knight D (1999) Reason must supercede dogma in the management of ventricular arrhthymias. In: Kirk's Current Veterinary Therapy 13. Ed J Bonagura. Saunders Co. pp 730-733.
• Moise N S (1999) CVT update - ventricular arrhythmias. In: Kirk's Current Veterinary Therapy 13. Ed J Bonagura. Saunders Co. pp 733-737.

• Serena Brownlie BVM&S PhD CertSAC MRCVS , Broadacres, Bedford Road, Little Houghton, Northampton NN7 1AW, UK.
• Dr Mark Rishniw DVM DipACVIM , VRT Box 34, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.

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