While the importance of the equine heart is undeniable, particularly for athletes, many practitioners are uncomfortable diagnosing cardiac conditions. The goals of this article are to look at anatomy and function to help understand common cardiac conditions, to break down the most common findings, to better understand when to refer, and to understand how to manage common scenarios.
The Equine Heart: An Amazing Machine
A horse’s heart is a major contributor to its athletic prowess. In a pair of studies comparing steers and horses of similar size, lung capacity and cardiac output were found to be twice as large in the horse, with a maximal oxygen consumption rate (VO2 max) 2.6 times higher.
Thoroughbred racehorses have larger hearts than even warmbloods of much larger size. A great deal of work has been done to correlate the size of the heart to racing performance, with methods of predicting “heart score” used to determine performance capabilities.
Anatomy
Regional Anatomy
The heart, sitting in the cranial thorax, sits largely behind the triceps musculature, located approximately from the 3rd-6th intercostal spaces (ICS), with the pulmonic, aortic, and mitral valves distributed on the left side in the 3rd, 4th, and 5th ICS, and the tricuspid valve in the 3rd-4th right ICS.
Gross Anatomy
General cardiac anatomy is similar in most mammalian species, with the classic four-chamber layout. The musculature of each of the chambers reflects the job needed: The atria have the thinnest walls, then the right ventricle, then the left ventricle with the most muscular walls, needing to supply the entire body.
The shape of the ventricles is also different, with the left being relatively conical, having its ejection through the aorta relatively centrally located. The right ventricle essentially spirals around the front of the heart, having its ejection through the pulmonary artery towards the left side.
These different shapes are an adaptation to the different pressures required by the systemic and pulmonary circuits.
Valvular Anatomy
Cardiac valves are, for the most part, passive structures pushed out of the way during forward flow. After contraction of the corresponding chamber, a pressure gradient develops, causing backflow, which under normal circumstances pushes the valves backward, where they are held taught either through their connections to the wall as in the aortic and pulmonic valve leaflets, or through the anchoring chordae tendineae as in the AV valves.
The mitral valve separates the left atrium and ventricle, and the tricuspid valve separates the right atrium and ventricle. The aortic valve separates the aortic root from the left ventricular outflow tract, and the pulmonic valve separates the pulmonic arterial root from the right ventricular outflow tract.
Electrical Anatomy
The P cells of the sino-atrial (SA) node on the right side of the atrium generate an electrical impulse. The impulse is transmitted through the myocytes of the atria, moving in a generally downward wave-like fashion in normal circumstances until contacting the atrioventricular (AV) node.
The P cells of the AV node generate a new electrical impulse, which is transmitted rapidly to the apex of the heart through the bundle of His. From the apex, the impulse is divided into left and right bundle branches. Physiologically, this anatomy allows for the wave of contraction of myocytes in the ventricles to progress in an upward fashion from the apex toward the base of the heart and the great vessels.
Purkinje fibers travel into the subendocardium in all mammals, but they go deeper into the myocardium of horses and other ungulates, including the distantly related cetaceans. This myocardial penetration of Purkinje fibers allows for a more instantaneous contraction and facilitates the high exercising heart rates achievable in horses.
Examination
Physical Exam
Auscultation of the heart is the main tool veterinarians use to evaluate cardiac function in the field. However, palpation of arterial pulses, evaluation of jugular pulses, capillary refill time, dependent edema, and lung function all play roles in the physical exam.
Heart rate itself can be an important factor. A horse with a loud murmur but a resting heart rate of 36, for example, is unlikely to be in left-sided heart failure. Information from auscultation can be enhanced by using a high-quality stethoscope, finding a quiet space to work, and listening carefully for an extended period over each of the valve regions.
When assessing rhythm, it can be helpful to tap your foot along to the expected rhythm. Most horses have a quite regular sinus rhythm (unlike humans and dogs), so irregularly timed beats stand out. This technique is also helpful during long pauses to assess whether there were one or two dropped beats.
Heart Sounds
Up to four normal heart sounds are audible, with the most notable being S1 and S2, the classic lub-dub. S4 is often audible, particularly prior to a dropped beat with 2nd-degree AV block.
Electrocardiography
During a full evaluation, a specialist can perform a 12-lead ECG to evaluate the horse for nuanced abnormalities. But, a standard base-apex ECG delivers a significant amount of information, and the number of simple, compact, but effective devices on the market now make this an essential tool to have on the truck. In addition, several exercising ECG systems are now available that mount on the girth and deliver true ECG or at least heart rate, which can be helpful for aerobic training.
Heart Murmurs
What Is a Murmur?
It is important to remember that a murmur is only a sound, not a specific diagnosis. Instead of laminar flow, we hear turbulence created by backflow or (much less commonly in horses) restriction of flow. Some murmurs are normal (physiologic flow), while some more severe diseases may occasionally only create a mild sound.
Many factors can have a temporary effect in creating a transient murmur, including colic and dehydration among other things. For this reason, multiple auscultations are helpful.
Description of Murmurs
At a minimum, murmurs should be categorized by timing within the cycle: systolic or diastolic. Murmurs are more fully described by grade, timing/duration, character, location, and degree of radiation.
An example of the description of murmurs in a horse with aortic regurgitation might be “a grade III/VI, holo-diastolic, decrescendo, musical murmur heard loudest over the left 4th intercostal space, radiating dorsally and caudally ~10cm, with a similar grade I-II/VI murmur audible on the right.”
Significance of Cardiac Murmurs
The vast majority of equine murmurs are caused by backflow through valves (regurgitation). Stenotic lesions in horses are extremely rare, seen primarily in uncommon developmental disorders. Valvular fibrosis, which blunts the valve edge and decreases its surface area, is a common age-related change found in the aortic and mitral valves.
Left-Sided Systolic Murmurs
Physiologic flow murmurs are relatively common in young, fit horses and are most commonly heard as a focal grade III/VI or less soft-blowing systolic murmur, typically in the left 3rd ICS, reflecting turbulence caused as a large volume of blood is ejected through the aorta. Murmurs heard in colicky horses are thought to be associated with an increased sympathetic tone.
Mitral regurgitation (MR) is heard as a left-sided systolic murmur, typically centered over the 5th ICS. Generally speaking, the loudness of the murmur correlates with severity, but some loud murmurs can be clinically insignificant. The character is typically “band-shaped,” meaning there is a relatively uniform intensity throughout. A crescendo murmur is uncommon and typically indicates mitral valve prolapse.
The clinical significance of MR depends largely on the effects of backpressure into the atrium and the pulmonary tree. Horses have a good capacity for managing increased pulmonary pressures if this accommodation can happen over time. Typical slowly progressing valve degeneration allows for this time, but a sudden rupture of chordae tendineae could cause rapid decompensation and classic signs of left-heart failure including pulmonary edema and death.
A more common sequela is an enlargement of the left atrium to a point where atrial fibrillation can occur (see section on arrhythmias).
Left-Sided Diastolic Murmurs
Aortic regurgitation (AR) is a common finding, particularly in older horses, and is typically heard loudest in the left 4th ICS. In most horses, it is a decrescendo murmur, reflecting the decreasing pressure gradient of the continually ejecting aorta. In horses with 2nd-degree AV block, the murmur typically continues through the entire pause.
Commonly, you can hear a musical “dive-bomber” sound, although it can be harsh as well. The loudness of the murmur, particularly musical ones, does not always correlate with the degree of regurgitation. Louder murmurs will sometimes radiate widely over the left thorax, occasionally being audible through the withers or manubrium.
Aortic regurgitation is generally tolerated well and is more commonly something that horses die with but not from. Significant AR causes left ventricular enlargement, which can lead to stretching of the mitral annulus, which then causes (or increases pre-existing) mitral regurgitation. Enlargement of the left ventricle can also lead to decreased function.
Diastolic physiologic flow murmurs occur as squeaky, early diastolic murmurs, thought to be associated with rapid ventricular filling.
Right-Sided Systolic Murmurs: Tricuspid Regurgitation
Regurgitation through the tricuspid valve is less common than through the aortic or mitral valves in most horses. The exception is in racehorses, particularly Standardbreds, where the sustained exertion causes dilation of the tricuspid annulus, causing a functional separation of otherwise normal valve leaflets. Most tricuspid murmurs are between grade I-IV and band-shaped.
Tricuspid regurgitation (TR) is generally well tolerated but can lead to right atrial enlargement, which can also be a risk factor for atrial fibrillation. The presence of jugular pulses and dependent edema is common with significant TR.
Ventricular Septal Defect
Ventricular septal defects (VSD) are the most common congenital cardiac abnormality. These can occur in isolation or as part of a complex of congenital issues. VSDs are typically harsh right-sided murmurs caused by the differential in pressures between the left and right ventricles. A palpable thrill is common.
Horses presenting with a VSD later in life typically have isolated VSDs of relatively small size, which may be well tolerated. Larger VSDs, or those associated with other congenital abnormalities, typically present with clinical signs such as elevated heart and/or respiratory rate, exercise intolerance, etc. These more significant clinical cases have a poor prognosis.
Arrhythmias
An arrhythmia is any alteration of the normal electrical conduction, which is heard as an irregular rhythm. It includes non-pathologic arrhythmias such as sinus arrhythmia and 2nd-degree AV block. The term dysrhythmia is sometimes used to denote pathologic irregular rhythms such as atrial fibrillation. Most information can be readily obtained with a hand-held ECG reader such as the AliveCor by Kardia Mobile or a similar device.
Non-Pathologic Arrhythmias
Sinus arrhythmia is not common in adult horses. This alteration in rhythm is associated with respiration and the variation of vagal tone causing mild acceleration/deceleration of rate with the respiratory cycle.
Second degree AV block is a very common finding in horses with high vagal tone at rest. Most of the time, this is not clinically a concern. Under normal circumstances, it should resolve even with light exercise. Dropping two beats in a row is less common but can be clinically insignificant in some horses. Dropping more than two beats in a row, having only one beat between dropped beats, and not resolving with exercise are all signs of high-grade second-degree AV block which would warrant a further workup.
Veterinarians should use caution when using alpha-2 agonists for sedation or inhalant anesthetics, as these can cause bradycardia and enhance the block. Ketamine does not cause bradycardia. Sparing techniques through combined drug use can limit the use of these drugs. Atropine is effective at increasing heart rate but is not always carried in the field. N-butyl scopolamine bromide, a common anti-spasmodic drug, is also effective. Lower doses can be added gradually to the desired effect.
Pathologic Arrhythmias
Atrial fibrillation (AF) is the most common pathologic dysrhythmia. The classic form is described as an irregularly irregular beat akin to “tennis shoes in a dryer.” Unlike in humans, where approximately one in seven strokes is caused by AF, and these tend to be more severe than from other causes, horses can exercise at moderate intensities in AF without significant issues provided there are no other significant cardiac deficits. Racehorses and upper-level three-day eventers would not be able to reach the levels of exertion necessary to compete, but most horses would be OK.
Ideally, horses in AF should have a full echocardiogram and an exercising ECG to define any valvular pathology and to rule out other potential underlying dysrhythmias that could be more consequential. On ECG, horses in AF will have an underlying undulating baseline (f waves) with no P waves and an irregular R-R interval.
Supraventricular premature (atrial) depolarizations are common, particularly immediately post-exercise. These are unlikely to be of clinical significance in most horses but can be confusing during auscultation.
Premature ventricular depolarizations (VPD or VPC for contractions) are less common and generally signify a more serious condition. Exercising horses with VPDs are at risk for developing ventricular tachycardia, which can potentially convert to ventricular fibrillation and syncope or even death.
Horses with certain electrolyte abnormalities, such as hypomagnesemia, might be predisposed to ventricular premature beats, particularly in horses being treated after colic surgery. Toxins and scarring of the myocardium can also be risk factors that can be more difficult to manage.
On auscultation, these two types of premature beats can often be distinguished by the gap after the premature beat. In supraventricular premature beats, the beat following the premature beat will occur at the same interval as the preceding normal interval, so a foot-tap rhythm will switch from corresponding to the beat to falling regularly mid-beat immediately after the premature beat.
With ventricular premature beats, there is typically a short gap after the premature beat, and subsequent beats will again correspond to the foot-tap rhythm.
Myocarditis and Cardiomyopathy
Myocarditis is most commonly associated with viruses and bacterial infections but can also be caused by certain parasitic organisms. The influenza virus is the most likely viral cause, but EVA and EIA as well as other less-common viruses can also cause myocarditis. Cardiotoxins include certain plants, ionophore antibiotics, and certain components of snake venom. Oleander, all types of Yew trees, avocado leaves and branches, foxglove, milkweeds, and plants related to rhododendrons are all toxic to horses.
Pit vipers (rattlesnakes and related species like massasaugas and copperhead snakes), as well as coral snakes (the only dangerously venomous snakes in the US that are not pit vipers), can cause significant cardiotoxicity. Up to 70% of snake-bitten horses will develop an arrhythmia, and 40% show evidence of myocardial damage (elevated cardiac troponin-I, a cardiomyocyte-specific enzyme).
The bigger feed companies tend to use separate facilities to make feeds containing ionophores, so intoxication from equine-formulated feeds is rare. This type of toxicity is more typically accidental, but fatality rates are high.
Field vs. Referral
With the availability of good portable ECG equipment and high-quality portable ultrasound machines, veterinarians can perform good workups in the field. As with any type of examination, the amount of workup done in the field for cardiac cases depends on the clinician’s experience and confidence level and the equipment available. Referral is worthwhile in cases with a significant murmur or arrhythmia for workup by a specialist, as are cases with unexplained exercise intolerance.
References
- Jones JH, Longworth KE, Lindholm A, Conley KE, Karas RH, Kayar SR, Taylor CR. Oxygen transport during exercise in large mammals. I. Adaptive variation in oxygen demand. J Appl Physiol (1985). 1989 Aug;67(2):862-70. doi: 10.1152/jappl.1989.67.2.862. PMID: 2793686.
- Constantinopol M, Jones JH, Weibel ER, Taylor CR, Lindholm A, Karas RH. Oxygen transport during exercise in large mammals. II. Oxygen uptake by the pulmonary gas exchanger. J Appl Physiol (1985). 1989 Aug;67(2):871-8. doi: 10.1152/jappl.1989.67.2.871. PMID: 2793687.
- Reef VB, et al, Recommendations for Management of Equine Athletes with Cardiovascular Abnormalities. JVIM 2014 May/June;28(3):749-61.
This article originally ran in the FAEP’s quarterly publication, The Practitioner.
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