Heart disease is defined as any functional, structural, or electrical abnormality of the heart. It encompasses a wide range of abnormalities, including congenital anomalies , as well as anatomical and physiologic disorders of varying causes. Heart disease can be classified by various characteristics, including presence at birth (eg, congenital or acquired), cause (eg, infectious, degenerative, genetic, or heritable), duration (eg, chronic or acute), clinical status (eg, left heart failure, right heart failure, or biventricular failure), anatomic malformation (eg, ventricular septal defect), or electrical disturbance (eg, atrial fibrillation, ventricular premature complexes).
The diagnosis of heart disease typically involves evaluating the signalment, history, and physical-examination findings, as well as results of diagnostic tests such as radiography, electrocardiography, and echocardiography. Rarely, more specialized tests, such as cardiac catheterization, CT, MRI, or nuclear studies, are necessary.
For animals with suspected heart disease, the signalment (age, breed, sex) helps formulate a differential diagnosis list. The signalment influences the relative importance of possible heart diseases (eg, endocarditis is rare in cats and small dogs but more common in cows and large dogs), as well as many specific abnormalities (eg, breed predispositions for certain congenital defects, dilated cardiomyopathy [DCM], myxomatous valve degeneration , etc).
Animals presenting with heart disease often have no clinical signs. Animals in heart failure may have :
Some findings are more common in some species, such as peripheral or ventral (subcutaneous) edema in horses and cattle in right heart failure , as opposed to ascites in dogs in right heart failure. Cats rarely cough with heart failure and more commonly present with a history of tachypnea/dyspnea (which may be subtle and go unnoticed by the owner) and anorexia. In dogs, coughing can be due to pulmonary edema; however, coughing in dogs is much more commonly due to lung disease (eg, chronic bronchitis). Therefore, extreme care must be taken when evaluating dogs (especially older, small-breed dogs) with a cough and a heart murmur, because many are not in heart failure.
A complete physical examination should be performed on any animal that is being evaluated for heart disease or that presents with clinical signs possibly attributable to heart disease. The cardiac physical examination should start with auscultation of the heart. Auscultation should be done in as quiet an environment as possible. In all cats, small dogs, and small mammals, a pediatric stethoscope should be used. In addition, only the diaphragm of the stethoscope needs to be used, because heart sounds, including gallop sounds, in animals of this size are not low enough in frequency to require the bell. In large dogs and large animals, the bell should also be used. In general, the left apex beat should first be located by palpation, then the head of the stethoscope placed over it (mitral area). The stethoscope head then should be inched forward and upward to the left base (pulmonic and aortic area). In any young animal, care should also be taken to place the stethoscope head farther forward (left axillary region) to listen for a continuous murmur (patent ductus arteriosus). Then the right apical region should be auscultated. In a young animal suspected of having congenital heart disease, the right base and along the neck should also be auscultated.
In addition to auscultation of the thorax, palpation of the ventral thorax should be performed to assess for the presence of a thrill (vibration created by turbulent blood flow that can be palpated with the fingertips) and alterations in intensity or location of the apex beat. Concurrent auscultation and palpation of the pulse should also be performed to identify pulse deficits (premature beats, atrial fibrillation) and to assess the strength and character of the systemic arterial pulse.
Pulmonary auscultation should be performed (see Respiratory Sounds ). Mucous membrane color and refill time should be assessed, but often they are normal even in animals with severe heart failure. Cyanosis may be present if the animal is severely hypoxemic. Limbs should be examined for the presence of edema, and the abdomen should be assessed for the presence of ascites (through palpation and ballottement). With the animal in a standing or sitting position, the jugular veins should be examined for the presence of abnormal distention and pulsation. A normal jugular vein will be distended and may pulsate when an animal is laterally recumbent.
Heart sounds are generated by the rapid acceleration and deceleration of blood and secondary vibrations in the cardiohemic system. Four heart sounds can potentially be auscultated:
In dogs, cats, and ferrets, S 1 and S 2 are the only heart sounds normally audible.
A gallop heart sound (rhythm) is the presence of S 1 and S 2 accompanied by an interceding sound or sounds in diastole (between S 2 and S 1 ) that is either an accentuated third heart sound (S 3 ) or fourth heart sound (S 4 ), or both. Gallop heart sounds are classified as protodiastolic (S 3 ), presystolic (S 4 ), or summation (fusion of S 3 and S 4 ). The most common gallop heart sound noted in dogs is a result of an accentuated S 3 and typically occurs secondary to a normal quantity of blood "dumping" into a stiff left ventricle (as in DCM ), or a massive amount of blood "dumping" into a normal left ventricle in early diastole (as in mitral regurgitation and patent ductus arteriosis ). An S 4 gallop heart sound is due to the action of atrial contraction pushing blood into a stiff left ventricle. In cats with cardiomyopathy , especially hypertrophic cardiomyopathy , the left ventricle is stiff, so both third and fourth heart sounds can be heard. However, because the heart rate commonly exceeds 160–180 bpm in cats in an examination room, it is usually impossible via auscultation to determine whether the gallop sound is due to an S 3 or an S 4 gallop; often, it is a summation of the two.
Gallop rhythms are not the only three-heart-sound rhythms that can be auscultated. Systolic clicks also occur in dogs and cats, and they are much more common than gallop rhythms in dogs. A systolic click is a short, sharp sound that occurs during mid to late systole. In dogs, systolic clicks occur mostly in middle-aged to older small breeds, and they are thought to be evidence of early myxomatous AV valve degeneration , causing mitral valve prolapse (as they are in humans). A systolic murmur may or may not also be present. Although systolic clicks are reasonably easy to distinguish from a gallop sound in dogs (they are usually relatively loud and high pitched, whereas a gallop sound is soft and low pitched), in cats they often sound identical to a gallop sound. Thoracic radiographs can be used to help distinguish between the two. In cats, gallop sounds are heard when severe heart disease is present. Systolic clicks are usually heard in cats that have an otherwise normal heart. So, if the heart is not enlarged, the sound is more likely a systolic click. Systolic clicks usually are single; however, they may be multiple, and they can vary in intensity (even completely disappearing), depending on cardiac loading conditions. Rarely, a three-heart-sound rhythm is a bigeminal rhythm (in which every other beat is premature).
Split heart sounds are rare, subtle, and seldom clinically noteworthy in small animals. Splitting of S 1 is due to discordant closure of the mitral and tricuspid valves, which can occur when there is asynchronous contraction of the ventricles, as in left or right bundle-branch block, cardiac pacing, and ectopic premature ventricular beats. S 1 can also be split in healthy, large-breed dogs and in large animals.
Delayed closure of the pulmonic valve (in relation to the aortic valve) results in splitting of S 2 . Splitting of S 2 can be a normal finding in horses during respiration. Abnormal splitting of S 2 has been associated with pulmonary hypertension, as in pulmonary emphysema in horses and severe heartworm disease in dogs. Other possible causes include a large atrial septal defect , right bundle-branch block, or premature ventricular ectopic beats of left ventricular origin. Delayed closure of the aortic valve (paradoxical splitting of S 2 ) might be heard with left bundle-branch block or premature ventricular ectopic beats of right ventricular origin. It has never been described in small animals. A split S 2 is a subtle finding that usually must be heard several times along with a mentor before it can be appreciated.
Heart murmurs are audible vibrations (sound) emanating from the heart or major blood vessels. The vast majority are due to turbulence created by high-velocity blood flow that produces a mixed-frequency murmur. Much less commonly, murmurs are due to vibrations of cardiac structures such as part of a valve leaflet or chordal structure that produces a single frequency (musical) murmur. Murmurs are typically defined relative to timing (systole, diastole, continuous); intensity (grades 1–6); and location (eg, left apex, left base). They can also be characterized by frequency (pitch); quality (eg, musical); and configuration (eg, crescendo-decrescendo).
Phonocardiogram, murmur of subaortic stenosis, dogCourtesy of Dr. Mark D. Kittleson.
A systolic murmur is typically described as either ejection (crescendo-decrescendo) or regurgitant (holosystolic, plateau). However, making this distinction is often difficult, even for an experienced examiner, especially when the heart rate is fast. Ejection-quality systolic murmurs typically demonstrate the greatest intensity during mid systole and appear diamond shaped on phonocardiography. Systolic murmurs are most commonly produced by stenotic lesions at the semilunar valves (eg, pulmonic stenosis or subaortic stenosis ). A classic regurgitant systolic murmur demonstrates a constant intensity throughout systole and is commonly due to mitral or tricuspid regurgitation (eg, myxomatous degeneration of the mitral valve ) or a ventricular septal defect . However, these murmurs may also change intensity during systole.
Diastolic murmurs are typically decrescendo (decreasing in intensity through diastole) and usually the result of aortic insufficiency (such as the insufficiency due to aortic valve infectious endocarditis in dogs or degenerative disease in horses). Diastolic murmurs may sound like a dive-bomber or grunting.
A continuous murmur is most commonly the result of patent ductus arteriosus and occurs throughout systole and diastole. A continuous murmur varies in intensity over time, typically being most intense at the end of ventricular ejection (the second heart sound) and then decreasing in intensity through diastole. The term "to-and-fro murmur" describes a murmur that occurs both in systole and in diastole (eg, in an animal with subaortic stenosis and aortic insufficiency).
In horses, early systolic and diastolic murmurs can be noted in the absence of heart disease or anemia. The point of maximal intensity is typically located over the left heart base. A short, high-pitched, squeaking, early diastolic cardiac murmur is sometimes heard in healthy, young horses. In cats, systolic heart murmurs are often heard without cardiac disease. Some of these systolic murmurs are due to an increase in right outflow tract flow velocity (dynamic right ventricular outflow tract obstruction ). Innocent cardiac murmurs are also sometimes noted in immature cats and dogs (
Heart murmur intensity is classified as follows:
A soft systolic heart murmur (grades 1 and 2) usually either is not due to heart disease or is due to mild heart disease. An exception would be a large atrial septal defect . A very loud systolic heart murmur is commonly associated with severe heart disease (eg, severe subaortic stenosis in dogs almost always creates a loud systolic heart murmur), but that is not always the case. For example, a small ventricular septal defect usually produces a loud systolic heart murmur on the right side of the chest, and even some dogs with mild mitral regurgitation have a loud heart murmur. Grades 3 and 4 heart murmurs are generally not predictive of heart disease severity.
Grading murmur severity is subjective and the differences between grades 1 and 2, grades 3 and 4, and grades 5 and 6 are difficult to discern, vary from individual to individual, and provide no useful information. Consequently, it may be better to describe them as soft, moderately loud to loud, and palpable.
Arrhythmias (also called dysrhythmias or ectopic rhythms) are abnormalities of the rate, regularity, or site of cardiac impulse formation and are noted during auscultation. The presence of a cardiac arrhythmia does not necessarily indicate the presence of heart disease; some arrhythmias are normal, such as sinus arrhythmia in a dog and second-degree AV block in a horse; many cardiac arrhythmias are not clinically important and require no specific treatment. Some arrhythmias, however, may cause severe clinical signs, such as syncope, or lead to sudden death. Numerous systemic disorders may be associated with abnormal cardiac rhythms. Common auscultatory findings in animals with an arrhythmia are a rate that is too slow (bradycardia), a rate that is too fast (tachycardia), premature beats (a beat is heard too early), an irregular rhythm, and pauses in the rhythm. Whenever an abnormal rhythm is heard, an electrocardiogram (ECG) should be performed.
The arterial pulse is the rhythmic expansion of an artery by blood flow/pressure that can be digitally palpated (or visualized) during physical examination. Physiologically, the pulse pressure (the pulse one feels) is the systolic pressure minus the diastolic pressure. The best place to feel the arterial pulse depends on the species;.in dogs and cats the arterial pulse is typically palpated at the femoral artery, whereas in horses, the facial artery is usually used. To feel the maximum pulse, examiners should first occlude the artery with their fingers and then gradually decrease the digital pressure until the maximum pulse is felt.
A weak pulse (a decrease in pulse pressure) is usually due to a decrease in systolic pressure and can be noted with decreased stroke volume in animals in heart failure, hypovolemic shock, or cardiac tamponade, as well as those with severe subaortic stenosis . However, a weak pulse can also be felt in a healthy animal if the artery is not palpated appropriately or in an obese or heavily muscled animal. A bounding pulse (an increase in pulse pressure) is usually caused primarily by a decreased diastolic pressure and can be noted with aortic insufficiency and patent ductus arteriosus . However, the pulse in a thin, athletic dog may also feel stronger than expected. The pulse felt with mitral regurgitation is often normal but at times may be termed "brisk."
A pulse deficit is an absent pulse despite auscultation of a heartbeat and is thus detected during simultaneous auscultation and pulse palpation. Pulse deficits are often due to a premature beat that occurs so early that the ventricles are unable to fill sufficiently, resulting in a decreased stroke volume that produces either a weak pulse or no pulse. Atrial fibrillation also produces pulse deficits, as well as alternating pulse strength.
Dogs with severe subaortic stenosis may have a pulse pressure that slowly increases during ventricular systole and reaches a peak pressure late in systole called pulsus parvus et tardus . Pulsus paradoxus is a decrease in pulse pressure during inspiration and an increase in pulse pressure during expiration. Pulsus paradoxus occurs normally in animals, but it is too subtle to observe on physical examination. Animals with cardiac tamponade (severe pericardial effusion), however, demonstrate an exaggeration of this finding, so it becomes detectable. Pulsus alternans is an alternating strong and weak pulse while the animal is in sinus rhythm; it can be noted (albeit rarely) in animals with severe (usually terminal) myocardial failure or tachyarrhythmias . Pulsus bigeminus is an alternating strong and weak pulse due to an arrhythmia such as ventricular bigeminy. The weaker pulse (during the ventricular premature contraction) typically follows a shorter time interval than the stronger pulse.
Jugular venous pulsation can be noted in normal animals but typically does not extend beyond the thoracic inlet.
Pulmonary edema may develop as a result of congestive heart failure (CHF). Animals with pulmonary edema will be hyperpneic (have an increased respiratory rate [tachypnea] and depth of respiration) and may be dyspneic. The increased depth of respiration may increase bronchovesicular sounds. Fine and, less commonly, coarse crackles might be auscultated in animals with pulmonary edema; however, fine crackles are usually heard only at the end of a deep inspiration. Coarse crackles in dogs are most commonly heard with chronic bronchitis. Pulmonary edema is often silent (no auscultatory abnormality). Respiratory sounds may be absent in animals with pleural effusion, especially ventrally.
Abdominal distention may occur as a result of gas, soft tissue, or fluid accumulation. Animals with right heart failure (eg, due to severe heartworm disease, severe tricuspid valve dysplasia , cardiac tamponade) can develop ascites. Because there are many causes of ascites, it is important to evaluate the jugular veins in every case in which ascites is present. If right heart failure is the cause of the ascites, the jugular veins may be distended (but often they are not distended in dogs and cats) by the increase in right atrial pressure. If the jugular veins are not distended in a dog or cat with ascites, a hepatojugular reflux test should be performed. To do this, one person examines the jugular veins with the animal standing or sitting, while another person places firm and steady pressure on the abdomen. In a dog or cat in right heart failure, the jugular veins should distend well up the neck with this maneuver. If ascites is present without jugular venous distention and with a negative hepatojugular reflux test, then extracardiac causes of the ascites should be considered.
The diaphragm may contract synchronously with the heart to produce loud thumping noises on auscultation and usually visible contraction in the flank area. The syndrome results from stimulation of the phrenic nerve by atrial depolarization and occurs primarily when there is a marked electrolyte or acid-base imbalance, particularly with hypocalcemia. Synchronous diaphragmatic flutter is most common in horses and dogs. In dogs it occurs most commonly in association with hypocalcemia and electrolyte disturbances induced by GI disease, although idiopathic cases also occur. Similarly, in horses it occurs with hypocalcemia, and in endurance horses it accompanies dehydration and electrolyte depletion.