Equine Cardiology Essentials

Course Information

Course Description

Equine Cardiology Essentials is a two-hour continuing education program for veterinary professionals. The first lecture reviews a systematic approach to the equine cardiac examination in general practice—including physical examination, auscultation, and electrocardiography—with emphasis on recognizing findings that may warrant advanced diagnostics. The second lecture reviews important equine cardiac diseases, recommended diagnostic evaluation, treatment options, and practical management steps. These notes cover four core areas:

• Equine Cardiac Anatomy and Electrophysiology: The remarkable efficiency of the equine heart, the relationship between heart size and athletic capacity, and how the electrical events of the cardiac cycle (P-QRS-T) map onto the audible heart sounds (S1–S4).
• The Systematic Cardiac Examination: Why the cardiac examination is far more than auscultation, the tools that support it, valve points of maximal intensity, and a disciplined approach to listening to both sides of the chest.
• Murmurs — Physiologic versus Pathologic: The high prevalence of murmurs in athletic horses, murmur characterisation and grading, distinguishing physiologic from pathologic murmurs, and the thresholds that warrant further work-up.
• Arrhythmias and Important Cardiac Diseases: A structured method for reading an equine ECG, the common physiologic arrhythmias of the resting horse, the surprising frequency of exercising arrhythmias, and when an arrhythmia signals genuine disease.

Equine Cardiac Anatomy and Electrophysiology

Presenter: Dr. Sian Durward-Akhurst, BVMS, MS, PhD, DACVIM (LAIM)

The equine heart is one of the most efficient pumps of any species. Horses are extraordinary athletes, and even the average Thoroughbred racehorse possesses cardiac potential that dwarfs the ability of the best human sprinters. A horse can drive heart rate from a resting 24–40 beats per minute to as high as 240 beats per minute, with cardiac output rising into the range of several hundred millilitres per kilogram per minute and aerobic capacity reaching approximately 200 ml/kg/min—far beyond the human equivalent of roughly 40 ml/kg/min. This physiology is the backdrop against which every cardiac finding must be interpreted, because what is normal for a fit equine athlete may look abnormal by the standards of other species.

Heart Size and Athletic Capacity

The equine heart weighs approximately one percent of body weight, but several of the most successful racehorses have carried hearts considerably larger than this typical figure. There is a demonstrable correlation between heart size and cardiac output, yet heart size alone does not predict which horse will win the Triple Crown—performance is multifactorial. Selective breeding for athletic potential and larger heart size carries a notable upside: the common degenerative cardiac conditions of small-animal and human medicine, such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and congenital degenerative valve disease, are rare to virtually unheard of in horses. The trade-off is that intense selection reduces genetic diversity and may be associated with conditions such as exercise-induced pulmonary haemorrhage, valvular incompetence, and an increased predisposition to arrhythmia.

What We Assess from the Outside

When we assess the heart from the outside of the horse, four elements dominate: the valves (the mitral and tricuspid atrioventricular valves and the aortic and pulmonic semilunar valves), the heart rate (whether it is within the normal range and appropriate for the horse's level of excitement or exercise), and the rhythm. A useful reference for equine cardiac anatomy is Marr and Bowen's Cardiology of the Horse. Keeping valves, rate, and rhythm in mind gives the examination a consistent structure regardless of the presenting complaint.

The Electrical Cycle and the Heart Sounds

Understanding auscultation requires mapping the electrical events of the ECG onto the four heart sounds. The P wave represents atrial depolarisation, as electrical activity spreads from the sinoatrial node across the atria to the atrioventricular node. The PR interval reflects conduction through the atrioventricular node, after which the wave travels down the Purkinje fibres and up across the ventricles. The QRS complex represents ventricular depolarisation and marks the onset of ventricular systole, while the T wave represents ventricular repolarisation.

The audible sounds align with these events. S1, the loudest and longest sound, is closure of the atrioventricular valves at the onset of systole and is present in every horse with a heartbeat. S2, quieter, shorter, and higher pitched than S1, is closure of the semilunar valves at the onset of diastole and is frequently split in normal horses. S3 corresponds to rapid ventricular filling; it is quieter than S2, is not always present, but can be heard in fit horses. S4 is atrial contraction—blood vibrating against the ventricular wall—and although not always audible, it is not uncommon in fit horses. Systole runs from the R wave to the end of the T wave, with S1 at its onset and S2 at its end; S3 and S4 fall within diastole. Recognising that healthy equine athletes commonly produce audible S3 and S4 gallop sounds prevents misclassifying normal physiology as disease.

The Systematic Cardiac Examination

Presenter: Dr. Sian Durward-Akhurst, BVMS, MS, PhD, DACVIM (LAIM)

The cardiac examination is not just listening to the heart. A complete assessment begins with the signalment and history and with simple tools—a stethoscope and a thermometer—before progressing, where indicated, to electrocardiography. Watching the horse and observing its demeanour is the first step. The mucous membranes should be evaluated for colour and capillary refill time. A pulse should be palpated for rhythm, rate, and quality (strength), using the index and middle fingers (not the thumb) over the facial artery at the mandible or the transverse facial artery. The examiner should look for a jugular pulse—normal up to the bottom third of the neck with the head held up—and check for ventral oedema. Respiratory rate and any signs of respiratory distress or froth at the nostrils should be noted, and a rectal temperature is always worth taking, because concurrent fever materially changes the interpretation of a murmur or arrhythmia.

Tools That Support the Examination

Beyond the basic stethoscope and thermometer, a range of tools can extend the examination, including amplified and recording electronic stethoscopes and smartphone-based single-lead ECG devices. These are particularly valuable for documenting an irregular rhythm or characterising a murmur, allowing findings to be captured, replayed, and shared. The fundamentals, however, remain palpation and disciplined auscultation.

Auscultation and Valve Points of Maximal Intensity

Begin by feeling for the apex beat, located approximately where the mitral valve projects, and assess for a thrill and the rhythm. The valve points of maximal intensity on the left side of the chest follow a consistent map. The mitral valve is heard at the fifth intercostal space, dorsal to the halfway point between the shoulder and the sternum. The aortic valve is at the fourth intercostal space, ventral to the point of the shoulder and slightly cranial to the caudal border of the triceps. The pulmonic valve lies at the third intercostal space, just ventral to the point of the shoulder. It does not matter in which order the valves are auscultated, provided the examiner is consistent every time.

S1 and S2 are usually loudest at the apex beat, marking the beginning and end of systole; if the examiner is unsure which sound is which, palpating a pulse simultaneously resolves the ambiguity, because the pulse follows S1. S2 is often split when listening over the pulmonic valve at low heart rates. S3 is heard at the end of ventricular relaxation, usually caudal and dorsal to the apex beat. Critically, the right side must not be neglected: the tricuspid valve is auscultated at the third to fourth intercostal space in the ventral third of the thorax on the right. A complete examination always includes both sides of the chest, since right-sided findings carry their own diagnostic thresholds.

Murmurs: Physiologic versus Pathologic

Presenter: Dr. Sian Durward-Akhurst, BVMS, MS, PhD, DACVIM (LAIM)

Murmurs are common in athletic horses: approximately thirty to forty percent of healthy Thoroughbreds have heart murmurs. The clinically relevant questions are whether a given murmur is significant, how it should be managed, and what effect—if any—it has on performance. Many of these murmurs are entirely physiologic, so the examiner's task is to characterise each murmur carefully and apply consistent thresholds rather than reacting to the mere presence of a sound.

Characterising and Grading a Murmur

Murmur assessment rests on location (the point of maximal intensity), timing within the cardiac cycle, and grade; palpating the pulse simultaneously can help anchor the timing. Grading runs from one to six on a standardised scale.

Timing places a murmur within the cardiac cycle relative to S1–S4. Systolic murmurs (between S1 and S2) raise the possibility of mitral or tricuspid regurgitation, a subarterial ventricular septal defect, or a physiologic flow murmur. Diastolic murmurs raise the possibility of aortic or pulmonic regurgitation, a perimembranous ventricular septal defect, a physiologic murmur, or an aorto-cardiac fistula. Mapping the murmur to the correct part of the cycle therefore narrows the differential before any advanced imaging is considered.

Physiologic Murmurs

Systolic physiologic murmurs arise from turbulent blood flow in the aorta and pulmonary artery during early systole. Their point of maximal intensity is over the left-side third or fourth intercostal space; they occur in early to mid systole, have a crescendo-decrescendo or decrescendo quality, may change in intensity with exercise, and are usually grade 1–3 of 6. Diastolic physiologic murmurs arise from turbulent blood flow during ventricular filling. Their point of maximal intensity is the left-side fifth intercostal space or the right-side fourth intercostal space; they occur in early diastole (between S2 and S3) or late diastole (between S4 and S1), are often musical or squeaky in character, and are likewise usually grade 1–3 of 6. Recognising these benign patterns prevents unnecessary referral.

When Further Work-up Is Indicated

Further work-up of a murmur is indicated when any of the following are present: a murmur of grade 3 of 6 or louder on the left side, or grade 4 of 6 or louder on the right side; a new-onset loud murmur; a continuous murmur; a suspected congenital murmur; or a murmur associated with clinical signs. Those clinical signs include poor performance, weak or bounding pulses, jugular distension or pulsation, resting tachycardia, a concurrent arrhythmia, or concurrent fever without an obvious underlying cause. The presence of any of these features moves a horse from monitoring toward echocardiography and a fuller cardiac evaluation.

Arrhythmias and Important Cardiac Diseases

Presenter: Dr. Sian Durward-Akhurst, BVMS, MS, PhD, DACVIM (LAIM)

An arrhythmia is an irregular heart rhythm, which may be regularly irregular or irregularly irregular and may reflect premature or delayed depolarisation. Quantitatively, an arrhythmia is suggested at rest by a deviation of at least twenty percent in the RR interval and during exercise by a deviation of at least five percent. Distinguishing a benign physiologic arrhythmia from a pathologic one is one of the central skills of the equine cardiac examination.

A Structured Approach to Reading an ECG

Reading an equine ECG should follow a disciplined sequence of questions. What is the heart rate? Is there a P wave for every QRS complex, and a QRS for every P? Do all QRS complexes appear normal and the same as one another? Are all P waves normal and the same? Is the RR interval regular? Are the PR, QRS, and QT durations within normal limits? Working through these questions in the same order each time makes it far harder to overlook a dropped beat, an ectopic complex, or an abnormal conduction interval. Premature complexes can be characterised on morphology: a supraventricular premature complex is premature but of similar morphology to the normal beats, whereas a ventricular premature complex is premature and appears wide, tall, and bizarre. Multiple ventricular premature complexes—bigeminy (every other beat abnormal), couplets, and triplets—move the picture toward complex arrhythmia.

Exercising Arrhythmias Are Surprisingly Common

The frequency of exercising arrhythmias is remarkably high in athletic horses: across Standardbreds, Thoroughbreds, and sport horses (dressage, show jumping, and eventing), premature depolarisations and supraventricular and ventricular arrhythmias are reported in a substantial proportion of clinically normal animals. Importantly, the clinical significance of many is unknown. In one body of work there was no difference in time to fatigue or maximal speed between horses with and without complex arrhythmias; paradoxically, horses with improved treadmill performance were roughly four times more likely to have had complex arrhythmias and more likely to have had at least one premature depolarisation. This raises a genuine challenge—how many horses with premature depolarisations are truly abnormal?—and reinforces that an isolated arrhythmia must always be interpreted in clinical context.

Common Physiologic Arrhythmias

Several arrhythmias are physiologic in the resting horse and characteristically disappear with excitement or exercise. Second-degree atrioventricular block is the most common arrhythmia seen at rest in healthy horses. It is regularly irregular: the RR interval is regular until a longer pause occurs that is about twice the length of the surrounding intervals, and on close inspection a P wave is present without a following QRS-T complex, because the atrial impulse is blocked and not transmitted to the ventricles—most likely due to the high vagal tone that is normal in horses. Critically, second-degree atrioventricular block should resolve with exercise, so jogging the horse in a circle for a few strides should restore a normal sinus rhythm. Sinus block is likewise regularly irregular and disappears with excitement or exercise. Sinus arrhythmia describes a heart rate that varies with breathing—increasing on inspiration as the vagus nerve relaxes its grip and decreasing on expiration as vagal tone rises—and is again physiologic, abating with excitement or exercise.

When an Arrhythmia Warrants Further Work-up

Further work-up of an arrhythmia is indicated when complex arrhythmias are present—atrial fibrillation, or supraventricular or ventricular tachycardia—or when an arrhythmia is associated with clinical signs such as poor performance, staggering or collapse, weak or bounding pulses, jugular distension or pulsation, a concurrent murmur, or concurrent fever. An unexpectedly elevated resting heart rate, or a heart rate that falls outside the expected range during and after exercise (for example, well above roughly 100 bpm fifteen minutes into recovery), is a further trigger for investigation.

Summary

The equine cardiac examination integrates the mucous membranes, pulse rate, rhythm, and quality, jugular distension or pulsation, ventral oedema, respiratory rate, and temperature, together with auscultation of rate, rhythm, and murmurs on both sides of the chest. The findings that should raise concern are a murmur of typically grade 3 of 6 or louder, a non-physiologic arrhythmia or a physiologic arrhythmia that does not resolve with exercise, any complex arrhythmia, and any arrhythmia or murmur accompanied by clinical signs. Used systematically, this framework reliably identifies the minority of horses that genuinely require advanced diagnostics while sparing the many normal equine athletes whose murmurs and arrhythmias are simply a feature of their remarkable cardiovascular physiology.

Post-Lecture Addition: Congenital Cardiac Disease

Congenital heart disease is rare in horses, with the lecture citing an estimated prevalence of approximately 0.03–0.2% and a necropsy prevalence of approximately 0.5% in one equine necropsy population. The presenter cautioned that the true prevalence may be underestimated because not every foal that dies undergoes necropsy. Familial or breed risk is suspected: Arabians were described as the classic congenital heart disease breed signal, while Welsh ponies and Standardbreds are overrepresented for ventricular septal defects. The underlying cause is likely a mixture of genetic and environmental factors, and the genetics of equine congenital cardiac disease are not yet fully defined.

Suspicion for congenital disease is highest early in life. Foals may present within the first 24–48 hours, though some present later. Concerning signs include failure to thrive, dyspnoea, cyanosis, syncope, pneumonia, dysmaturity, sepsis-like illness, abnormal mucous membrane colour, abnormal respiratory rate or effort, poor pulse quality, or abnormal jugular veins. The live discussion added a practical bedside pearl: if a foal is already receiving oxygen, briefly assessing mucous membrane colour off oxygen, when clinically appropriate and safe, may reveal cyanosis that is otherwise hidden. Bilateral auscultation matters in foals because congenital murmurs can be loud enough to hear on both sides, but a lesion may still be missed if only one side of the chest is examined.

Ventricular Septal Defect (VSD)

VSD was presented as the most common known congenital cardiac disease in horses. Most commonly, the turbulent flow is heard more strongly on the right side because the shunt travels from the left ventricle toward the right ventricle, near the tricuspid region. Although the shunt direction is left-to-right, the overload is primarily left-sided because the extra blood moves through the pulmonary circulation and returns to the left atrium. Foals with clinically important VSDs may therefore show left-sided congestive signs such as pulmonary oedema.

Diagnosis and prognosis are based on echocardiography, not murmur loudness. In foals, a VSD-to-aorta ratio greater than 0.4 was described as more guarded, particularly when clinical signs of heart failure, congestive heart failure, or pulmonary oedema are present. In adult horses, a defect greater than approximately 2.5 cm or a VSD-to-aorta ratio greater than 0.4 is more likely to be clinically significant. Small defects may close spontaneously, but the presenter emphasised that murmur intensity is a poor stand-alone severity marker: a small VSD can create a very loud murmur because flow velocity and turbulence are high, while a larger defect can be quieter because the same pressure difference moves through a larger opening.

Other Congenital Shunts and Valve Defects

Patent ductus arteriosus was framed as persistence of normal fetal circulation. The ductus arteriosus should close within 72 hours postpartum, and many are no longer audible by the routine 24-hour foal examination. If a continuous PDA-type murmur is heard in a foal without clinical signs, a short-interval recheck can be appropriate; persistent or clinically significant findings warrant further evaluation. PDA, like VSD, causes left-sided overload because excess blood returns through the pulmonary veins to the left atrium. Atrial septal defects are rarer and produce right-sided overload because blood moves from the left atrium into the right atrium and through the right side of the heart. Tetralogy of Fallot was described as a right-to-left shunt syndrome with right ventricular outflow tract obstruction, right ventricular hypertrophy, VSD, and overriding aorta; long-term consequences can include erythrocytosis and hyperviscosity, and athletic performance is unlikely.

Congenital valve defects are uncommon. Semilunar valve stenosis is more common than atrioventricular valve stenosis; mild pulmonic stenosis may permit some performance, usually reduced, whereas moderate to severe stenosis may lead to exercise intolerance, syncope, congestive heart failure, or death. Atrioventricular valve stenosis can produce atrial dilation, atrial arrhythmias, and congestive heart failure. In young horses with murmurs that are no longer in the immediate neonatal period, valvular stenosis or poor valve development should remain on the differential, and prognosis is often guarded when these lesions are confirmed.

Post-Lecture Addition: Disease-Specific Murmur Interpretation

Post-Lecture Addition: Pathologic Arrhythmias, AF, and Performance Risk

Atrial Fibrillation

Atrial fibrillation was identified as the most common pathologic arrhythmia in horses and the arrhythmia most clearly linked to poor performance. It is not necessarily the most common rhythm disturbance overall, but it is the one most important to recognise clinically. On auscultation it is classically irregularly irregular; the presenter used the practical analogy that a rhythm sounding like "tennis balls in a dryer" should be treated as atrial fibrillation until proven otherwise. ECG confirmation is required even when clinical suspicion is high, and echocardiography is almost always recommended because atrial fibrillation associated with structural disease carries a worse prognosis than lone or apparently structurally normal atrial fibrillation.

Many horses with paroxysmal or lone atrial fibrillation spontaneously return to sinus rhythm, typically within 24–48 hours of onset. This makes diagnosis challenging when the horse performs poorly during an event but is in normal rhythm the next day. Athletic horses that remain in atrial fibrillation and are expected to continue athletic work require treatment. After cardioversion, the lecture described follow-up with a 24-hour ECG and echocardiogram to confirm rhythm and cardiac function. If atrial fibrillation duration is short, return to training may occur relatively quickly under specialist guidance; longer or unknown-duration cases generally require longer restriction.

A key live-lecture safety point was activity restriction. Racehorses in atrial fibrillation should not race. Horses that are not treated should avoid exercise that produces consistent heart rates above 220 beats per minute. Lower-level uses may be possible for selected horses with informed riders and lower heart-rate demands, but high-intensity athletic work is not appropriate while the horse remains in atrial fibrillation.

Premature Atrial and Ventricular Depolarisations

Premature atrial depolarisations often show altered P-wave morphology because they do not originate from the sinoatrial node. A few isolated PADs often do not require treatment, but the gold-standard work-up discussed in the lecture includes a 24-hour ECG and investigation for underlying causes such as electrolyte abnormalities, cardiac disease, or thyroid-related issues. If PADs are overdriven by exercise or only occasional at exercise, the horse may be safe for use, while recognising that PADs can increase the risk of atrial fibrillation.

Premature ventricular depolarisations have no preceding P wave and altered QRS morphology and are often followed by a pause. The lecturer treated PVDs as somewhat more concerning than PADs. A 24-hour ECG is commonly recommended, and an underlying-cause search remains important. If occasional PVDs are overdriven by exercise, selected horses may be suitable for riding by an informed adult. However, horses with PVDs associated with collapse or with moderate to severe structural cardiac disease should not be ridden.

Ventricular Tachycardia and High-Risk Complexity

Ventricular tachycardia was defined as three or more consecutive premature depolarisations. Monomorphic runs have similar morphology; polymorphic runs vary because beats arise from multiple ventricular sites. Complexity becomes more concerning when there is polymorphic ventricular tachycardia, short coupling intervals, R-on-T timing, rapid ventricular rate greater than about 120 bpm, or repetitive ectopic activity. The presenter explained that very short coupling intervals can trigger ventricular fibrillation or other severe degenerative arrhythmias. These findings should not be treated as benign incidental discoveries, particularly when paired with distress, abnormal pulses, collapse, or heart-failure signs.

Exercise-Associated Sudden Death and When to Suspect Cardiac Disease

The lecture framed exercise-associated sudden death as uncommon but clinically important. The cited Thoroughbred racing fatality rate was approximately 1.1–1.3 per 1,000 race starts, with roughly 20% considered sudden death. About half of sudden death cases may have no diagnosis at necropsy, and arrhythmias are usually undetectable at necropsy because they are electrical rather than structural abnormalities. In the presenter group's case series, all four horses wearing ECGs at the time of death died of an arrhythmia, and three of the four were in atrial fibrillation before leaving the stall.

Cardiac suspicion should rise when a horse finishes a long way behind the field, stops or does not finish, collapses, becomes an inconsistent performer, refuses expected work, or shows epistaxis and/or exercise-induced pulmonary haemorrhage. The presenter described Standardbred racehorses developing atrial fibrillation as often running well and then suddenly slowing, stopping, or dropping to the back of the field. These patterns are not diagnostic by themselves, but they justify cardiac evaluation when other explanations do not fully account for the performance change.

Annotated Post-Lecture Additions & Q&A

Q1. What murmur findings would make sedation for dentistry or routine care especially concerning?

Audience question: A practitioner asked whether there is a rule or red flag for geriatric horses with presumed age-related murmurs when sedation is needed for dental work and the owner declines further work-up.

Presenter clarification: The presenter would be particularly nervous about sedating a horse with a loud murmur, approximately grade 3–6/6, especially if the horse is tachycardic at rest. If heart rate is normal, mucous membranes are good, jugular veins fill normally without abnormal pulsation, and the horse has no clear exercise-intolerance history, sedation may still be considered after an explicit risk discussion and documentation, especially when the procedure cannot reasonably be performed without sedation. The practical approach described was to go gently with sedation and consider dental blocks so less sedation is needed.

Q2. If murmur loudness does not equal severity, which echo findings push recommendations toward restriction, monitoring, or intervention?

Audience question: Vet On It asked which echocardiographic findings most strongly influence whether to monitor versus intervene when murmur loudness alone is unreliable.

Presenter clarification: Moderate to severe mitral valve disease, especially in a younger horse, makes the long-term prognosis more concerning. Follow-up decisions are based on whether cardiac structure is deteriorating and on exercising ECG findings. Significant arrhythmias during exercise make the presenter much more likely to advise that a horse is not safe to ride. If a young horse has marked mitral valve disease but no major structural deterioration or significant arrhythmias yet, low-level use by an informed adult may be reasonable with cardiac monitoring about every six months. Aortic regurgitation can look dramatic on ultrasound without producing comparable clinical signs; if there is no significant aortic enlargement, no other concerning structural change, and no significant arrhythmias on ECG, monitoring may be favored over immediate retirement.

What was added in this post-lecture version?

• Congenital disease expansion: prevalence estimates, foal suspicion signs, oxygen/cyanosis pearl, VSD shunt physiology, VSD:Ao prognosis threshold, PDA closure timing, ASD overload direction, Tetralogy of Fallot summary, and congenital valve-defect prognosis.
• Disease-specific murmur interpretation: mitral, aortic, tricuspid, aorto-pulmonary, aorto-cardiac, and adult VSD murmur patterns with prognosis-reducing features.
• Pathologic arrhythmia expansion: atrial fibrillation diagnosis and activity restrictions, PAD/PVD work-up logic, ventricular tachycardia complexity markers, and sudden-death/performance-suspicion context.
• Annotated Q&A: sedation risk discussion for horses with murmurs and echo/ECG findings that influence monitoring versus restriction decisions.

Source References

• [BASE-E42]: Original Event 42 Equine Cardiology Essentials interactive lecture notes.
• [E42-LIVE]: Event 42 live lecture transcript, used for second-hour cardiology disease and arrhythmia additions.
• [E42-CHAT]: Event 42 live chat/Q&A, used for learner-question clarifications.
• [E42-DECK2]: Event 42 presenter cardiac-disease slide deck, used with the live transcript for disease-specific additions.

Version History

• v1: Original source-locked interactive lecture notes.
• v2: Enhanced with live-transcript, presenter-deck, and Q&A updates. Added source-cited Update 6/9/26 notes in context below the relevant base sections; cited presenter/live-lecture sources control where mismatches exist.