Heart: dysrhythmia (Arrhythmia, Heart block, Ectopic beat)

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• 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.

• Incidental with concurrent heart failure or systemic disease.

• Lethargy.
• Exercise intolerance.
• Weakness.
• Syncope.

• Sudden death.

• Anesthesia - halothane increases myocardial sensitivity to adrenaline.
• Same as cardiac failure if signs are apparent .
• Any stress.

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

Bradycardia

 AV block in cats is always abnormal and needs investigation.

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

Tachycardia

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

• 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.

• Depends on cause.

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

• May be normal.

• Signs of cardiac failure.
• Syncope.
• Weakness, lethargy.

• Sinus bradycardia: heart rate <120 bpm.
• Sinus tachycardia: heart rate >240 bpm - physiological response to fear, stress, pain or excitement; also circulatory shock, fever, anemia, increased sympathetic tone, hyperthyroidism. Drugs: levothyroxine, some bronchodilators.

• Provides an indication of most dysrhythmias.
• Premature beats: common in congestive heart failure (CHF ), rare in normal cats.

Pulse

• Atrial or ventricular tachycardia weak pulse.
• Atrial fibrillation pulse deficit: common in CHF and cardiomyopathy .

Temperature

• Low temperature bradycardia.
   May also have low peripheral temperature if poor perfusion or tachycardia.

Bodyweight

• Low bodyweight associated with thyrotoxicosis or cardiac failure.

Evidence of trauma

• Chest trauma myocardial contusions.
• Head trauma altered autonomic control ('brain-heart syndrome').

• For definitive diagnosis .

• See thoracic radiography .
• For evidence of cardiac disease.

• Electrolyte assay:
  • Subnormal or elevated potassium .
  • Subnormal or elevated calcium .
  • Magnesium assay is also advisable if possible - hypomagnesemia causes refractory tachyarrhythmias and may be quite common in diabetic ketoacidosis or renal failure .
• Evidence of renal disease, ie urea and creatinine .
• Thyroid hormone assays: elevated levels thyroid hormone .

Hematology

• Severe anemia .
• Indications of infectious cause, ie left-shifted neutrophilia .

• Cardiac auscultation with concurrent palpation of femoral pulse.
• Hematology.
• Biochemistry.
• Thyroid hormone assays.
• History.
• Radiography.

• Electrocardiography.

• Conduction system lesions unremarkable grossly.

• If no gross lesions, fix entire heart for histopathology. AV bundle located at AV junction beneath attachment of right AV valve. Numerous serial or stepped histological sections are required to evaluate the conduction system, although myocardial disease may be more widespread in distribution.

• To rule out feline dysautonomia, fix autonomic ganglia, eg coeliacomesenteric ganglia located in connective tissue between adrenals and aorta (remove block of tissue from this area for fixation since ganglia are hard to identify grossly). Fix whole brain.

 Ectopia is secondary to cardiac or systemic disease hence correcting underlying cause may be sufficient, ie treat hyperthyroidism.

All Of Correct electrolyte imbalances .
And Treat congestive heart failure if present.
And Ensure adequate oxygenation .
And Provide adequate analgesia .

• Reverse excess vagal activity with atropine , or glycopyrrolate .
• Hypothermia - administer warm fluids to increase core temperature.

If due to hyperkalemia

• Renal failure (oliguric) .
• Hypoadrenocorticism .
• Reperfusion injury (also increased calcium).
• Severe metabolic acidosis.
• Hypoadrenocorticism (very rare):
  • Diagnose and treat cause.
  • Potassium-free intravenous fluids to increase urine output.
  • Emergency therapy to protect the heart - calcium gluconate , sodium bicarbonate , insulin , with dextrose infusion .

If due to neurological causes

• For example, raised intracranial pressure, meningoencephalitis:
• Diagnose and treat cause.
• Atropine to increase heart rate.

If due to drugs

• Alpha 2-adrenoceptor agonist sedatives - give alpha 2-adrenoceptor antagonists.
• Beta-adrenoceptor antagonists - give beta-adrenoceptor agonists.
• Calcium channel blockers - give intravenous calcium gluconate .
• Cardiac glycosides - reduce dose or discontinue.
• Phenothiazines (especially acepromazine ) - give atropine .

• Pacemaker if bradydysrhythmia with clinical signs.

• Stress: treat underlying disease.
• Myocardial irritability.

Atrial fibrillation

• Cardiac glycosides .
• Calcium channel blockers .
• Beta-adrenergic blockade .

Ventricular premature contractions

• Treat if causing clinical signs (weak pulse, poor peripheral perfusion, muscle weakness, depression):
  • Beta-blockers, eg propranolol .
  • Lidocaine .
   Do not use large intravenous doses as cats are more susceptible to CNS effects of lidocaine including respiratory arrest.
  • Procainamide .
  • Sofolol.

• Signs, if bradydysrhythmia with no clinical signs, may progress to more serious dysrhythmia.
• Tachydysrhythmias - aim for heart rate 150-200 bpm.

 CARE - drugs may interact toxicity.

• Cimetidine reduces hepatic clearance of many antiarrthyhmics increased concentration of other drugs.
• Some calcium channel blockers reduce the excretion of digoxin reduce dose digoxin if used together.
• Beta-blockers (beta-receptor antagonists should be used with care in myocardial disease as removing the sympathetic tone may uncover severe systolic dysfunction).
• Digoxin, calcium channel blockers (Verapamil), beta-blockers will be synergistic if used in combination.
• Lidocaine overdose seizures (which can be controlled with diazepam ) also causes CNS depression. Respiratory arrest and sinus arrest is possible.
• Propanolol reduces clearance of lidocaine reduce dose lidocaine if used together.
   Ventricular escape beats in third degree AV block should not be suppressed with anti-dysrhythmic drugs.

• Electrocardiography.

• Good: if cause can be identified and removed.
• Poor: in severe or progressive myocardial disease.
• Treatment in ventricular dysrhythmia may improve quality of life but not length, ie no reduction in incidence of sudden death.
• Venticular arrhythmia may progress to fibrillation which is rapidly fatal.

• Resolution of clinical signs.
• Resolution or improvement, ie less frequent VPCs, of ECG changes.

• Cardiac disease too severe or too far advanced.
• Unable to control other factors, eg toxemia, neurological disease.
• Standard reasons for failure .

• Recent references from 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), 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), 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), 1036-1047. PubMed

• Dr Serena Brownlie BVM&S PhD CertSAC MRCVS, Broadacres, Bedford Road, Little Houghton, Northampton NN7 1AW, UK.
• Dr P Fox DVM DipACVIM DipECVIM ACVECC, Animal Medical Centre, 510 East 62nd Street, New York, NY 10021, USA. E-mail: philip.fox@amcny.org.
• Dr Phil Nicholls BVSc BSc PhD MRCVS MRCPath, Division of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, WA 6150, Australia.
• P Watson MA VetMB CertVR DSAM MRCVS, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.

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