NAVLE Cardiovascular

Equine Cardiac Arrhythmias – NAVLE Study Guide

Cardiac arrhythmias are disturbances in the normal rhythm, rate, or electrical conduction of the heart and are more common in horses than in any other large animal species.

Overview and Clinical Importance

Cardiac arrhythmias are disturbances in the normal rhythm, rate, or electrical conduction of the heart and are more common in horses than in any other large animal species. Approximately 25% of horses with no evidence of heart disease may have cardiac arrhythmias detectable during routine examination or with electrocardiography (ECG). Understanding equine arrhythmias is critical for NAVLE success because they directly impact performance assessment, pre-purchase examinations, and anesthetic risk evaluation.

The unique cardiovascular physiology of horses, including their large atrial size and high vagal tone, predisposes them to certain arrhythmias, particularly atrial fibrillation. Additionally, arrhythmias in horses may be brought on by excitement, fever, toxemia, colic, electrolyte imbalance, congenital defects, myocarditis, and valvular heart disease.

Parameter Normal Value Clinical Significance
Heart Rate 26-50 bpm at rest Less than 24 bpm = pathologic bradycardia
P Wave Duration Less than 0.16 sec Often bifid; prolongation suggests atrial enlargement
PR Interval 0.22-0.56 sec Prolongation indicates first-degree AV block
QRS Duration 0.08-0.14 sec Widening greater than 0.14 sec suggests ventricular origin
QT Interval 0.44-0.64 sec Varies with heart rate
T Wave Variable polarity May be positive, negative, or biphasic; changes with exercise/excitement

Normal Equine Cardiac Conduction

In normal sinus rhythm, the electrical impulse is initiated in the sinoatrial node (SA node) and transmitted across the atrial myocardium, generating the P wave. The impulse is delayed at the atrioventricular node (AV node), creating the PR interval. Rapid conduction then occurs through the His bundle, bundle branches, and Purkinje fiber network, activating the ventricular myocardium and generating the QRS complex. Ventricular repolarization produces the T wave.

High-YieldThe equine P wave is often bifid (two small humps) due to the large atria causing slightly asynchronous depolarization. The first peak represents right atrial depolarization and the second represents left atrial depolarization. This is a normal finding and should not be confused with P mitrale.

Normal Equine ECG Parameters (Base-Apex Lead)

Physiologic (Benign) Arrhythmias Pathologic Arrhythmias
Second-degree AV block (resolves with exercise) Sinus arrhythmia (respiratory variation) Sinus block/pause (resolves with exercise) Wandering atrial pacemaker (P wave morphology varies) Atrial fibrillation (most common pathologic arrhythmia) Ventricular tachycardia (life-threatening) Third-degree AV block (complete heart block) Frequent VPCs/APCs (especially if multiform or during exercise)

Classification of Equine Arrhythmias

Equine arrhythmias can be classified as physiologic (benign) or pathologic. Physiologic arrhythmias are associated with high vagal tone at rest and typically disappear with exercise or excitement. Pathologic arrhythmias require further investigation and may indicate underlying cardiac or systemic disease.

Arrhythmia Classification Summary

NAVLE TipThe key distinguishing feature of physiologic arrhythmias is that they DISAPPEAR with light exercise or excitement. If an arrhythmia persists during exercise, it is pathologic until proven otherwise. Always perform an exercise test when evaluating equine arrhythmias.
Type Definition and Clinical Features
Paroxysmal AF Terminates spontaneously, usually within 48 hours; may recur; often difficult to diagnose due to intermittent nature
Persistent AF Lasts more than 7 days; requires intervention for cardioversion; most common presentation in clinical practice
Permanent AF Does not respond to treatment or treatment is not attempted in long-standing cases
Lone AF No underlying structural cardiac disease; most common form in horses; best prognosis for treatment
Secondary AF Associated with underlying cardiac disease (valvular insufficiency, atrial enlargement) or systemic conditions; poorer prognosis

Physiologic Arrhythmias

Second-Degree Atrioventricular Block

Second-degree AV block is the most common physiologic arrhythmia in horses and is considered a normal finding when occurring at rest. It results from high vagal tone that slows conduction of impulses from the SA node through the AV node. The electrical impulse from the atria intermittently fails to conduct to the ventricles.

Clinical Features

  • Auscultation: Regular rhythm interrupted by pauses; fourth heart sound (S4) audible before the pause as the atria contract without ventricular response
  • ECG findings: P wave not followed by QRS complex; P-P intervals remain regular; blocked beats occur intermittently
  • Exercise response: Should COMPLETELY disappear with light exercise (trotting)
  • Clinical significance: Normal variation requiring NO treatment; if persistent during exercise, investigate for underlying pathology

Sinus Block and Sinus Arrhythmia

Sinus block occurs when high vagal tone blocks the pacing cells of the SA node itself. Unlike second-degree AV block, the atria do not contract during the pause (no S4 audible), and the ECG shows an absence of both P waves and QRS complexes during the pause. Sinus arrhythmia is less common in horses than in dogs but represents normal physiologic variation related to respiratory cycle changes in autonomic tone.

High-YieldTo differentiate second-degree AV block from sinus block: listen for S4 during the pause. Present = AV block (atria contracting). Absent = sinus block (atria not contracting). Both should resolve with exercise.
Treatment Protocol and Efficacy Side Effects/Considerations
Quinidine Sulfate (Oral) 22 mg/kg via nasogastric tube every 2 hours until conversion or max dose reached Therapeutic levels: 2-5 μg/mL Success rate: up to 88% Depression, muzzle edema Colic, diarrhea Hypotension, ataxia Severe arrhythmias (torsades de pointes) Laminitis, death (rare)
TVEC Catheter electrodes placed in RA and PA General anesthesia required Synchronized biphasic shocks Success rate: up to 98% Anesthetic risks Requires specialized equipment Available only at referral centers No antiarrhythmic drug side effects
Amiodarone (IV) Constant rate infusion after loading dose Success rate: approximately 60% Used in chronic AF cases Elevated liver enzymes Hindlimb weakness Severe diarrhea (with prolonged use greater than 36 hours)

Atrial Fibrillation

Atrial fibrillation (AF) is the most common performance-limiting pathologic arrhythmia in horses, with a reported incidence of up to 2.5% in some populations. It was first documented by ECG in horses in 1911. Horses are uniquely predisposed due to their large atrial size and high vagal tone, which create an ideal environment for sustaining AF once initiated.

Pathophysiology

In AF, the normal coordinated electrical and contractile mechanisms within the atria are lost. Multiple wavelets of electrical activity pass through the myocardium, interacting with each other and structural barriers. The atria fail to contract effectively and instead fibrillate (quiver). This results in loss of the atrial contribution to cardiac output (approximately 20% of stroke volume) and an irregularly irregular ventricular rhythm due to inconsistent transmission of impulses through the AV node.

Classification

Clinical Signs

  • Exercise intolerance: Most common presenting complaint; severity depends on athletic demands
  • Poor performance: More evident in horses working near maximal cardiovascular capacity (racehorses, eventers)
  • Exercise-induced pulmonary hemorrhage (EIPH): Has been associated with AF
  • Collapse: Rare but reported during exercise
  • Incidental finding: Some horses with lone AF show no clinical signs at rest or low-level work

Diagnosis

Auscultation

  • Irregularly irregular rhythm - hallmark finding
  • Absent fourth heart sound (S4) - atria not contracting
  • Variable intensity of S1 and S2 from beat to beat
  • Heart rate often normal at rest (high vagal tone provides additional AV nodal block)

ECG Findings (Definitive Diagnosis)

  • Absence of P waves
  • F (fibrillation) waves - irregular baseline undulations representing chaotic atrial activity; may be coarse or fine
  • Irregularly spaced QRS complexes - variable R-R intervals
  • QRS complexes usually normal in morphology (unless aberrant conduction or concurrent ventricular ectopy)
NAVLE TipAF can be confused with second-degree AV block on auscultation because both produce an irregular rhythm. Key differences: AF = irregularly IRREGULAR (no pattern), absent S4, abnormal ECG. Second-degree AV block = regularly IRREGULAR (predictable pattern), S4 present during pauses, ECG shows P waves with intermittent blocked beats, resolves with exercise.

Complete Diagnostic Workup

  • Resting ECG: Confirms diagnosis; evaluate for ventricular ectopy
  • Echocardiography: Assess for underlying cardiac disease, atrial size, valvular function, and ventricular function
  • Exercising ECG: Evaluate heart rate response and detect ventricular arrhythmias during exercise
  • Complete blood count and biochemistry: Rule out electrolyte abnormalities, especially hypokalemia and hypomagnesemia

Treatment of Atrial Fibrillation

Treatment is aimed at restoring sinus rhythm (cardioversion). Cardioversion is recommended for horses that will be used for athletic performance, especially those working at high cardiovascular demand. Treatment is typically not attempted during the first 48 hours due to possibility of spontaneous conversion in paroxysmal AF.

Treatment Options Comparison

High-YieldQuinidine toxicity monitoring is CRITICAL. Stop treatment if: (1) heart rate exceeds 80 bpm, (2) QRS duration exceeds 120% of baseline, (3) severe clinical signs develop. Watch for QRS widening as early sign of torsades de pointes.

"QUINIDINE = Q.U.I.N.I.D.I.N.E." QRS widening (monitor closely!) Upper respiratory stridor (nasal edema) Intestinal upset (colic, diarrhea) Neurologic signs (ataxia, depression) Increase heart rate (stop if greater than 80 bpm) Death (rare but possible) Inflammation of feet (laminitis) Nasal edema (muzzle swelling) Edema and hypotension

Prognosis

  • Lone AF: Good prognosis for return to full performance if sinus rhythm is restored
  • Recurrence rate: 15-20% (higher in Warmbloods and horses with prolonged AF duration before treatment)
  • Favorable prognostic factors: AF duration less than 4 months, lone AF, resting heart rate less than 60 bpm
  • Post-treatment: Rest period recommended; duration based on AF duration (longer AF = longer rest for reverse remodeling)
Drug Dosage Notes
Lidocaine Bolus: 0.5-1.5 mg/kg IV CRI: 25-50 μg/kg/min First-line for emergency treatment CNS excitation at toxic doses May cause hypotension
Magnesium Sulfate 2-4 mg/kg IV slowly Max: 50 mg/kg total Especially useful if hypomagnesemia suspected Adjunct therapy
Procainamide 1 mg/kg IV slowly Second-line if lidocaine refractory Use in conscious horses

Ventricular Arrhythmias

Ventricular Premature Complexes (VPCs)

Ventricular premature complexes (VPCs) arise from ectopic foci within the ventricular myocardium. Isolated VPCs can occur in approximately 14% of clinically normal horses during 24-hour Holter monitoring and may be observed immediately post-exercise. However, frequent VPCs or VPCs that occur during exercise are always pathologic.

ECG Characteristics

  • Wide, bizarre QRS complex (greater than 0.14 seconds) - impulse travels through slow ventricular myocardium rather than fast conduction pathways
  • No preceding P wave - ventricular origin
  • T wave usually opposite in direction to QRS (discordant)
  • Occurs earlier than expected (premature)
  • Followed by compensatory pause

Causes

  • Systemic disease: colic, toxemia, sepsis, hypoxia
  • Electrolyte imbalances: hypokalemia, hypomagnesemia
  • Myocardial disease: myocarditis, cardiomyopathy
  • Drug effects: halothane sensitization to catecholamines
  • Acid-base disturbances

Ventricular Tachycardia

Ventricular tachycardia (VT) is defined as four or more consecutive VPCs at a rate typically exceeding 100 bpm. VT is NEVER normal and represents a life-threatening arrhythmia with potential for degeneration to ventricular fibrillation and sudden death.

Classification

  • Monomorphic VT: Single ectopic focus; uniform QRS morphology; regular R-R intervals
  • Polymorphic VT: Multiple ectopic foci; variable QRS morphology; more unstable; higher risk of VF
  • Sustained VT: Lasts more than 30 seconds
  • Torsades de pointes: Polymorphic VT with characteristic twisting QRS pattern; associated with QT prolongation; can occur with quinidine toxicity

Clinical Signs

  • Tachycardia at rest (greater than 100 bpm)
  • Pulse deficits
  • Weakness, collapse, syncope
  • Signs of low cardiac output: weak pulses, prolonged CRT, cold extremities
  • Sustained VT leads to heart failure within 1-3 days (jugular pulsations, ventral edema)

Treatment of Ventricular Tachycardia

High-YieldAlways treat the underlying cause! VT in horses is often secondary to systemic disease (especially colic and GI disease). Correct electrolyte abnormalities, treat primary disease, and rest the horse. Most horses with VPCs will have spontaneous resolution after 4-8 weeks of rest if no primary cardiac disease is present.

Other Arrhythmias

Atrial Premature Complexes (APCs)

Atrial premature complexes (APCs) originate from an ectopic focus in the atria (not the SA node). Rare APCs or APCs immediately post-exercise may be normal. Frequent APCs require investigation and may progress to atrial fibrillation or atrial tachycardia.

ECG Characteristics

  • Premature beat (occurs earlier than expected)
  • P' wave with different morphology from normal sinus P waves
  • Normal QRS complex (conducted through normal pathways)
  • Four or more APCs in a row = atrial tachycardia

Third-Degree (Complete) AV Block

Third-degree AV block is rare in horses and represents complete failure of impulse conduction from atria to ventricles. The atria and ventricles beat independently (AV dissociation). This is a serious pathologic arrhythmia typically associated with myocarditis, structural cardiac disease, or degenerative changes in the conduction system.

ECG Characteristics

  • P waves present at regular intervals (atrial rate)
  • QRS complexes present at regular but slower rate (ventricular escape rhythm)
  • No consistent relationship between P waves and QRS complexes
  • QRS may be narrow (junctional escape) or wide (ventricular escape)

Clinical signs: Severe bradycardia, syncope, collapse, exercise intolerance. May require pacemaker implantation, which is technically possible but rarely performed in horses.

Memory Aids and Board Tips

Arrhythmia Quick Recognition

"FAT PAW" - Features of Atrial Fibrillation F - Fibrillation waves (irregular baseline) A - Absent P waves T - Tachycardia with exercise (exaggerated response) P - Poor performance A - Absent S4 (no atrial contraction) W - Wobbly irregular rhythm (irregularly irregular)

"WIDE and BIZARRE = VENTRICULAR" When you see wide (greater than 0.14 sec), bizarre QRS complexes without preceding P waves, think VENTRICULAR origin. Normal QRS = supraventricular (atrial or junctional) Wide QRS = ventricular OR aberrant conduction

"EXERCISE TEST is KEY" Physiologic arrhythmias (2nd-degree AV block, sinus arrhythmia, sinus block) = DISAPPEAR with exercise Pathologic arrhythmias (AF, VT, frequent ectopy) = PERSIST or WORSEN with exercise If in doubt, TROT the horse!

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