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.
History and Signalment
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, myxomatous valve degeneration, etc).
Animals presenting with heart disease may have no clinical signs or have a history of tachypnea, dyspnea, abdominal distension (ascites), subcutaneous edema, weakness, syncope (fainting), cyanosis, exercise intolerance, or weight loss. A few historical findings are more species specific, including peripheral or ventral (subcutaneous) edema in horses and cattle. 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 occur due to pulmonary edema, but many more dogs that cough do so because of lung disease (eg, chronic bronchitis), so extreme care must be taken when evaluating dogs (especially older, small-breed dogs) with a cough and a heart murmur because most are not in heart failure.
A complete physical examination should be performed on any animal being evaluated for heart disease or that presents with signs that could be attributable to heart disease. The cardiac physical examination should start with auscultation of the heart. Auscultation should be done in as quiet of an environment as possible. In all cats, small dogs, and small mammals, a pediatric stethoscope should be used and only the diaphragm of the stethoscope needs to be used, because heart sounds, including gallop sounds, in animals 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 ausculted. In a young animal suspected of having congenital heart disease, the right base and along the neck should also be ausculted.
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 below). Mucous membrane color and refill time should be assessed but are often 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 presence of ascites (palpation and ballottement). The jugular veins should be examined with the animal in a standing or sitting position for presence of abnormal distension 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 and are associated with valve closure. Four heart sounds can potentially be ausculted. The first heart sound (S1) is associated with closure of the atrioventricular (mitral and tricuspid) valves, and the second heart sound (S2) with closure of the semilunar (aortic and pulmonic) valves. The third heart sound (S3) occurs in early diastole and is a result of the ventricles vibrating at the frequency heard at the time of rapid cessation of ventricular filling, and the fourth heart sound (S4) is in late diastole and associated with atrial systole (atrial contraction). All four sounds can be heard in a healthy horse. In healthy cattle, typically only S1 and S2 are audible, although S3 or S4 can sometimes be heard. IV fluid administration in cattle can be used to accentuate S3 and/or S4. In dogs, cats, and ferrets, S1 and S2 are the only heart sounds normally audible. Less is known about heart sounds in goats, sheep, and pigs; however, only S1 and S2 are believed to be audible in these species.
Three-Heart-Sound Rhythms (Gallop Heart Sounds and Systolic Clicks):
A gallop heart sound (rhythm) is the presence of S1 and S2 accompanied by an interceding sound or sounds in diastole (between S2 and S1) that is either an accentuated third heart sound (S3) or fourth heart sound (S4), or both. These are classified as protodiastolic (S3), presystolic (S4), or summation gallop heart sounds (fusion of S3 and S4). The most common gallop heart sound noted in dogs is a result of an accentuated S3 and typically occurs secondary to a normal quantity of blood "dumping" into a stiff left ventricle (eg, dilated cardiomyopathy), or a massive amount of blood "dumping" into a normal left ventricle in early diastole (eg, mitral regurgitation and patent ductus arteriosis). An S4 gallop heart sound is caused by 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 S3 or S4 gallop; often, it is a summation of the two.
Gallop rhythms are not the only three-heart-sound rhythms that can be ausculted. Systolic clicks also occur in dogs and cats and 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, they occur mostly in middle-aged to older small-breed dogs and are thought to be evidence of early myxomatous AV valve degeneration causing mitral valve prolapse (as they are in people). A systolic murmur may or may not also be present. Although systolic clicks are reasonably easy to distinguish from a gallop sound in a dog (they are usually relatively loud and high pitched whereas a gallop sound is soft and low-pitched), they often sound identical to a gallop sound in a cat. Thoracic radiographs can be used to help make the distinction between the two. In cats, gallop sounds are heard only in those with severe heart disease. Systolic clicks are usually heard in cats with an otherwise normal heart. So if the heart is not enlarged, the sound is more likely a systolic click. Systolic clicks usually are single but may be multiple and can vary in intensity (even completely disappearing) depending on cardiac loading conditions. Rarely, a three-heart-sound rhythm can be caused by a bigeminal rhythm.
Splitting of S1 or S2:
Splitting of S1 is caused by 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. Splitting of S1 can also occur 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 S2. Splitting of S2 can be a normal finding in horses during respiration. Abnormal splitting of S2 has been associated with pulmonary hypertension, as in pulmonary emphysema of 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 S2) might be heard with left bundle-branch block or premature ventricular ectopic beats of right ventricular origin. A split second heart sound is a subtle finding that usually cannot be appreciated by someone who has not heard it previously.
Heart murmurs are audible vibrations (sound) emanating from the heart or major blood vessels. The vast majority are due to turbulent blood flow brought on by high velocity blood flow that produces a mixed-frequency murmur. Much less commonly, they 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 (grade I-VI), and location (eg, left apex, left base) but can also be characterized by frequency (pitch), quality (eg, musical), and configuration (eg, crescendo-decrescendo).
A systolic murmur is classically 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. They 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 caused by 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 that caused by aortic valve infective endocarditis in dogs or degenerative disease in horses). In horses, the murmur of aortic insufficiency is most commonly musical, although "musical" in this context is a technical term (single frequency). They 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 (second heart sound) and then decreasing in intensity through diastole. A 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. Often, a systolic heart murmur is heard in a cat 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 (<3 mo old) and may be the result of a relative increase in stroke volume (stroke volume/aortic cross-sectional area) .
Heart murmur intensity is classified as follows: Grade I—the lowest intensity murmur that can be heard, typically detected only while auscultation is performed in a quiet room; Grade II—a faint murmur, easily audible, and restricted to a localized area; Grade III—a murmur immediately audible when auscultation begins; Grade IV—a loud murmur immediately heard at the beginning of auscultation but not accompanied by a thrill; Grade V—a very loud murmur with a palpable thrill; and Grade VI—an extremely loud murmur with a thrill and that can be heard when the stethoscope is just removed from the chest wall.
Arrhythmias are abnormalities of the rate, regularity, or site of cardiac impulse formation and are noted during auscultation. Other terms such as dysrhythmia and ectopic rhythm are also used to describe arrhythmias. 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 clinically insignificant and require no specific therapy. 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. (For discussion of specific arrhythmias, see Common Tachyarrhythmias.) 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 ECG should be performed.
The arterial pulse is the rhythmic expansion of an artery that can be digitally palpated (or visualized) during physical examination. Physiologically, the pulse pressure is the systolic pressure minus the diastolic pressure. The arterial pulse can be felt best in several different locations. For example, in dogs and cats, the arterial pulse is typically palpated at the femoral artery. In horses, the facial artery is usually used. To feel the maximum pulse, an examiner must first occlude the artery with his or her fingers and then gradually decrease the digital pressure until the maximum pulse is felt. A weak pulse (a reduction in pulse pressure) is usually caused by 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 with 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 reduced 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 heart beat and is thus detected during simultaneous auscultation and pulse palpation. This often occurs as the result of a premature beat that occurs so early that the ventricles are unable to fill sufficiently, resulting in a reduced 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. This is a normal occurrence 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 caused by 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 (increased rate 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 ausculted in animals with pulmonary edema, but 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 distension 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 are not 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 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 distension and with a negative hepatojugular reflux test, then extracardiac causes of the ascites should be considered.
Synchronous Diaphragmatic Flutter
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. It is most common in horses and dogs. It is seen most commonly in dogs in association with hypocalcemia and electrolyte disturbances induced by GI disease. Similarly, in horses it is seen with hypocalcemia and in endurance horses that are dehydrated and electrolyte depleted.
Thoracic radiographs frequently provide valuable information in the assessment of animals with or suspected of having heart disease. However, thoracic radiography is rarely performed in horses or cows to evaluate heart disease because of the animal's large size and body conformation, which reduces the quality of the images. In dogs, in which numerous different body types must be dealt with, chest conformation must always be assessed before attempting to evaluate cardiac size. On the lateral view, dogs can be normal, shallow-chested, or deep-chested. On the dorsoventral (DV) or ventrodorsal (VD) views, they can be normal, narrow-chested, or barrel-chested. Many small breeds of dogs are shallow-chested. This makes the cardiac silhouette appear to be enlarged on the lateral view and often necessitates relying on the DV view to obtain an accurate assessment of size and shape. In deep-chested breeds, even severe cardiomegaly can look normal on the lateral view and, because the heart sits more upright in the chest, can also mask its presence on the DV view (eg, in Doberman Pinschers with dilated cardiomyopathy). Obesity also interferes with accurate reading of cardiac size by the presence of intrapericardial fat or by pushing the diaphragm forward, reducing the size of the thoracic space and pushing the heart into the cranial and narrower aspect of the thoracic cavity. Because of the marked variation in chest conformation, the changes seen between inspiration and expiration, and the changes seen between systole and diastole, only relatively dramatic changes in overall cardiac size can be identified in most dogs. Consequently, things such as mild generalized cardiomegaly cannot be identified on thoracic radiographs. The one chamber where mild, moderate, and severe enlargement can be relatively accurately identified is the left atrium. Finding enlargement of specific cardiac chambers and great vessels makes the presence of heart disease more likely and may also provide clues as to the specific disease present.
Cardiogenic pulmonary edema is a common finding in animals with CHF and may be associated with pulmonary venous congestion. However, the identification of pulmonary edema is often difficult and may not be possible in some dogs and even some cats. Cardiogenic pulmonary edema in dogs is typically found in the caudodorsal aspects of the lungs. In many cases, this region has an interstitial density that is enhanced by age and by expiration, giving a false impression that pulmonary edema is present or masking the presence of pulmonary edema. Digital radiography units, especially if not set up perfectly (to match analog units), have made the diagnosis even harder in many cases. In animals with chronic left heart failure, the left atrium is usually severely and always at least moderately enlarged. In acute heart failure (eg, chorda tendineae rupture), the left atrium may not be enlarged. Pleural effusion can usually be readily identified radiographically. In most species, this is seen with right or biventricular heart failure. However, in cats it is seen most commonly with left heart failure. Resolution of these abnormalities on subsequent thoracic radiographs can be used as one indication of efficacy of therapy. The presence of pulmonary edema or pleural effusion does not definitively confirm a cardiogenic origin or exclude another origin .
Overall cardiac size can be assessed using the vertebral heart scale or score. This is most commonly done using the lateral projection. The maximal diameter of the cardiac silhouette from cranial to caudal is measured, as well as the distance from the carina to the apex of the cardiac silhouette (dorsal to ventral). These lengths are added together and measured in terms of thoracic vertebral bodies, so they are normalized for the size of the animal. The vertebral bodies are measured from the fourth thoracic vertebra caudally. The normal range is 8.5–10.5 vertebral bodies in dogs and 6.9–8.1 in cats. In many cases, it is more important to try to accurately assess the size of the left atrium than the overall size of the cardiac silhouette.
Electrocardiography is the recording of cardiac electrical activity from the body surface (surface ECG). It should primarily be used to identify cardiac arrhythmias. It can also identify conduction disturbances that do not alter rhythm and has been used to identify chamber enlargement in dogs and cats. However, its inaccuracy in identifying chamber enlargement and the advent of diagnostic ultrasound have diminished this role. As opposed to small animals in which the Purkinje fibers penetrate only ~1/3 of the way into the myocardium, Purkinje fibers in horses and cattle penetrate throughout the myocardium, resulting in "burst" depolarization of the ventricles and reduced waveform production and complexes on the surface ECG. Consequently, there is no relationship between complex height on a surface ECG and chamber enlargement. The most common ECG lead used in large animals is a base-apex that produces large deflections and is used for rhythm analysis. ECGs should be used only to characterize an arrhythmia in an animal with an auscultatory arrhythmia and to monitor rhythm during anesthesia; they should never be used as screening tools, as they are in human medicine (primarily for changes secondary to coronary artery disease).
Chamber enlargement can be indicated by waveform abnormalities in dogs and cats, but these abnormalities are commonly absent when there is chamber enlargement and are sometimes present when the heart is normal. In lead II in dogs and cats, wide or notched P waves suggest left atrial enlargement, whereas tall P waves suggest right atrial enlargement. Tall R waves in leads that have the positive electrode on the left and/or caudal aspect of the body (leads I, II, aVF, CV6LL, and CV6LU) are evidence of left ventricular enlargement. Deep S waves in the same leads in which the positive electrode is on the left side of the heart or the presence of a right-axis deviation suggest right ventricular enlargement. Wide QRS complexes can be seen in animals with either right or left ventricular enlargement; however, they can also be due to conduction disturbances (see AV Conduction Disturbances). The ECG is very insensitive at identifying mild to moderate changes in chamber size and unacceptably insensitive for detecting severe enlargement. Although false-positive findings are less frequent than false-negative findings, they do occur. Consequently, the accuracy is unacceptable, especially when compared with echocardiography and even with thoracic radiography.
Sinus Rhythm and Sinus Node Abnormalities
The sinus node initiates depolarization of the rest of the heart in a healthy animal, sets the normal rate and rhythm, and is called the normal pacemaker of the heart. It functions as the pacemaker because it is automatic (depolarizes on its own) and does so at a rate faster than the other automatic sites in the heart (AV node and Purkinje fibers). Normal sinus rhythm is regular and originates at the sinus node, indicated on the ECG by a P wave that precedes each normal QRS complex. The rate that the sinus node fires at varies tremendously from species to species and situation to situation. For example, a healthy horse can have a heart rate of 30 bpm at rest and 250 bpm during maximal exercise. Similarly, a healthy dog can have a heart rate in the teens when asleep and ≥250 bpm during maximal exercise. A healthy cat can have a heart rate of 240 bpm at rest in an examination room.
Sinus bradycardia is a regular sinus rhythm that is slower than expected for that species and for the situation the animal is in. Sinus bradycardia may be noted in animals overdosed with anesthesia or agents that can result in increased vagal tone (primary or secondary) or reduced sympathetic tone (eg, xylazine, β-adrenergic blocker), hypothermic animals, hypothyroid animals, animals with sick sinus syndrome, or in animals with increased vagal tone secondary to systemic disease (such as respiratory, neurologic, ocular, GI, or urinary tract disease). Treatment for sinus bradycardia is typically not needed unless clinical signs associated with the bradycardia, such as exercise intolerance, weakness, or collapse, are noted. In dogs and cats, atropine (0.04 mg/kg, IV, IM, or SC) may be considered for treatment of bradycardia. The initiating cause should also be corrected.
Sinus tachycardia is the finding of a regular sinus rhythm at a rate faster than normal but generally appropriate for the situation the animal is in (eg, stress, exercise, heart failure). If the rate is inappropriately high, (eg, 200 bpm in an otherwise healthy dog at rest at home), another form of tachycardia (eg, atrial or ventricular) should be considered. Causes include stress (resulting in high sympathetic drive), exercise, hyperthyroidism, fever, pain, hypovolemia, cardiac tamponade, heart failure, or administration of agents that can increase the rate of sinus node discharge (eg, catecholamines). Treatment involves resolving the underlying cause.
Sinus arrhythmia occurs as a result of irregular discharge of the sinus node most commonly associated with the respiratory cycle. The site of impulse formation remains the sinus node; however, the frequency of the discharge varies. Sinus arrhythmia is a normal finding in dogs and horses; it is abnormal in cats in the hospital setting, although it appears to be more common in cats in their home environment. Respiratory sinus arrhythmia is characterized by an increase in heart rate with inspiration and a decrease with expiration. In dogs, sinus arrhythmia can also be seen that is not in sync with respiration. The variation in heart rate is associated with variation in the intensity of vagal tone. It is abolished by reduced vagal tone resulting from excitement, exercise, or administration of vagolytic drugs such as atropine. It may be associated with a wandering pacemaker, which is characterized on the ECG by taller P waves during faster rates and smaller P waves during slower rates.
Sinoatrial (SA) block occurs when the impulse from the SA node fails to be conducted through the surrounding tissue to the atria and ventricles. Thus, no P waves or QRS complexes are noted on the ECG, and the P-P interval surrounding the break in sinus rhythm is an exact multiple of the normal P-P interval. This is often difficult to diagnose in dogs because sinus arrhythmia is common, resulting in a variable normal P-P interval.
Sinus arrest (sinoatrial arrest, sinus pause) is the absence of P waves on the ECG for a short period (typically accepted as a pause exceeding twice the normal P-P interval). Sinus arrest is caused by excessive vagal tone, inherent sinus node disease, or both. This is usually due to some form of sick sinus syndrome (see below).
Atrial standstill is characterized as the complete absence of P waves on the ECG and occurs as a result of the atria being unable to be depolarized from the SA node discharge. This occurs either because the atrial myocardium is functionally unable to be depolarized (usually due to hyperkalemia), or because it has been destroyed by a cardiomyopathy or myocarditis (persistent atrial standstill). In hyperkalemia, the sinus node continues to depolarize, and the electrical tracts from the sinus node to the AV node (internodal tracts) continue to function, so the sinus node controls the rate (albeit at a slower rate). With persistent atrial standstill, the sinus node is destroyed, so the animal usually has an AV nodal (junctional) escape rhythm with a heart rate in the 40–65 bpm range (dog).
Sick sinus syndrome is a constellation of abnormalities, including ECG changes (sinus arrest, junctional or ventricular escape complexes, and possibly supraventricular tachycardia) and possible weakness or syncope from the bradycardia (usual) or tachycardia (rare). With this clinical syndrome, the principal problem either lies within the SA node or perinodal tissue, or is due to increased vagal tone, or both. In some instances, other portions of the specialized conduction tissue of the myocardium, including the AV node, can also be affected. Therefore, evidence for AV block may also be seen (see below). This condition is commonly noted in geriatric dogs, including Miniature Schnauzers and American Cocker Spaniels. Medical therapy consisting of parasympatholytics (eg, propantheline bromide, 0.25–0.5 mg/kg, PO, bid-tid) or sympathomimetics (eg, extended-release theophylline, 10 mg/kg, PO, bid; terbutaline, 0.14 mg/kg, PO, bid-tid in dogs) to increase heart rate can be tried, but these are often ineffective or are effective for only a relatively short time or with unacceptable adverse effects. These drugs may also worsen supraventricular tachyarrhythmias that can occur with sick sinus syndrome. The most effective treatment for the bradycardia is pacemaker implantation.
AV Conduction Disturbances
Atrioventricular (AV) block refers to alteration of impulse conduction through the AV node from the atria to the ventricles. In first-degree AV block (prolonged conduction), the conduction time is increased and is recognized on an ECG as an increased PR interval. This is clinically silent. In second-degree AV block (intermittent conduction), occasional impulses fail to be conducted through the AV node, bundle of His, or both bundle branches and is characterized by occasional P waves not followed by QRS complexes. During the block, there is no S1 or S2 and no arterial pulse. In horses, the sound associated with atrial contraction (S4) is commonly heard, and the occurrence of S4 not followed by other heart sounds is diagnostic for second-degree heart block. S4 may also be audible in dogs with second-degree AV block, but this is much less common. When the PR intervals preceding the dropped beat progressively lengthen, the condition is known as Mobitz type I second-degree AV block or Wenckebach phenomenon. This is usually due to high vagal tone and is the most common type of second-degree AV block seen in horses and puppies. No treatment is indicated. If the PR intervals do not change, the condition is known as a Mobitz type II second-degree AV block. Again, no treatment is indicated, but closer surveillance may be warranted to see whether the block progresses to a more severe form. A third type of second-degree AV block, high-grade second-degree AV block, refers to the situation when the block occurs with every other beat (2:1 [ie, two P waves for every QRS complex]) or more (3:1, 4:1, etc). High-grade second-degree AV block is distinguished from third-degree AV block by identifying an association between the QRS complexes and the P wave preceding each one (same PR interval for each). Dogs with high-grade second-degree AV block can have signs the same as dogs with third-degree AV block (eg, syncope) and are also at increased risk of sudden death.
In third-degree AV or complete heart block, none of the impulses is conducted from the atria to the ventricles. The atrial rhythm (P waves) occurs more rapidly and independently from the ventricular rhythm (QRS complexes; a form of AV dissociation), which originates from subsidiary pacemakers (AV node or Purkinje fibers in the ventricles; nodal and ventricular escape beats, respectively). The heart and pulse rates are usually regular but slow and generally unresponsive to factors or agents that usually increase heart rate (eg, exercise, excitement, atropine). The difference in timing between atrial and ventricular contractions results in variation in ventricular filling and consequent variation in intensity of S1(bruit de canon) and possibly arterial pulse pressure. Periodically, the atria contract when the ventricle is in systole, which results in a pulsation in the jugular vein (cannon A wave).
The significance of the AV block varies by species. Both first- and second-degree AV block may be present without outward evidence of cardiac disease. First-degree AV block may result from excessive vagal tone and usually is not significant in dogs or horses unless other evidence of heart disease or pathologic cause of increased vagal tone (eg, CNS or pulmonary disease) or AV nodal disease is present. In all species, second-degree AV block may be indicative of heart disease. However, in horses, Mobitz type I is common and is a normal physiologic response resulting from increased vagal tone. Mobitz type II second-, high-grade second-, and third-degree (complete) AV blocks are always abnormal in all species.
Second- and third-degree AV blocks may be caused by fibrosis, neoplasia, or injury to the AV node, or hypoxia, increased vagal tone, or electrolyte abnormalities. The ideal treatment would be to correct the underlying cause, although this is not usually possible. High-grade second-degree AV block and third-degree AV block can cause exercise intolerance or, more commonly, weakness, collapse, and syncope. Oral therapy with extended-release theophylline (10 mg/kg, PO, bid), terbutaline (0.14 mg/kg, PO, bid-tid in dogs), or propantheline bromide (0.25–0.5 mg/kg, PO, bid-tid) may occasionally be useful in animals with second-degree AV block, but more aggressive therapy (pacemaker implantation) is usually indicated in symptomatic (eg, syncopal) animals. Third-degree heart block is usually associated with irreversible lesions; the only effective treatment in dogs is pacemaker implantation. Dogs with third-degree AV block are at risk of sudden death and so should have a pacemaker implanted regardless of clinical signs. In cats, third-degree AV block often produces no clinical signs and so requires no therapy. However, problems can arise if it is not identified before anesthesia, and some cats will faint and thus require pacemaker implantation. Third-degree AV block is rare in horses and other species. Pacemakers have been implanted successfully in species other than dogs and cats but has rarely been done.
Tachyarrhythmias can be divided into supraventricular and ventricular based on their site of origin. Supraventricular premature complexes are premature complexes (as seen on an ECG) that originate from ectopic (nonautomatic) sites above the ventricles (eg, atrial myocardium and AV node). They may also be called atrial or nodal premature complexes/depolarizations/contractions/beats. Possible sites for ectopic depolarizations include the SA node (rare), atrial myocardium (very common), and AV node (AV junction). Electrocardiographically, supraventricular premature complexes are identified by a QRS complex that usually appears relatively normal but occurs earlier than the next expected normal QRS complex. Variable P wave morphologies may be noted before or after the supraventricular premature complex or may be hidden in the preceding sinus complex or within the premature complex. Supraventricular premature complexes are most commonly a result of atrial enlargement/disease, stress, or other causes of increased sympathetic tone. Supraventricular tachycardia (SVT) is a series of supraventricular premature complexes occurring consecutively. It may be short (nonsustained) or occur for prolonged periods (called sustained when >30 sec). SVT most commonly ranges in rate from 200–350 bpm in dogs. At rates closer to 200 bpm, it may be indistinguishable from sinus tachycardia on a surface ECG. Vagal maneuvers (ocular pressure, carotid sinus massage), precordial blow (chest thump), and IV drug administration (eg, diltiazem) often "break" an SVT into sinus rhythm and either do not change or more gradually slow a sinus tachycardia. Diltiazem (0.5–4 mg/kg, PO, tid) is the most common drug used to treat SVT long-term, but it can also be used IV to break the SVT into sinus rhythm (0.25 mg/kg IV bolus administered over 2 min, followed 15 min later by up to 0.35 mg/kg IV bolus administered over 2 min, if needed). Digoxin and β-blockers are also used. An accessory pathway (bypass tract) is a congenital abnormality that forms an electrical connection between an atrium and a ventricle outside the normal connection (AV node/bundle of His). These pathways have been recognized in dogs and cats and may result in supraventricular tachycardia (eg, orthodromic reciprocating tachycardia). Treatment may include radiofrequency catheter (heat) ablation of the bypass tract or, more commonly, oral medications such as procainamide, sotalol, or diltiazem.
Atrial flutter is a rare arrhythmia that often progresses to atrial fibrillation. It is most commonly caused by a reentrant loop within the atria and is classically characterized on the ECG by a “saw-toothed” baseline with relatively normal QRS complexes that can appear in a regular or irregular rhythm. The atrial rate of discharge is very rapid (>400 bpm). Only intermittent atrial impulses are conducted through the AV node because of its normal long refractory period, so the ventricular rate is slower than the atrial rate.
In dogs and cats, atrial fibrillation is an even more rapid (>600–700 atrial depolarizations/min) atrial rhythm that results in a slower (in the 80–300 bpm range in dogs) and always irregular ventricular rhythm. As in atrial flutter, the AV node is bombarded by frequent atrial depolarizations. The AV node acts as a filter, allowing only some of the depolarizations to reach the ventricles but always in an irregular fashion. In dogs and cats, atrial fibrillation is characterized on the ECG by a supraventricular (normal-appearing QRS complexes) and an irregular ventricular rhythm that is most commonly fast. Once those characteristics are identified, the next thing to look for is the absence of P waves and an undulating baseline that can appear almost flat (fine) or very rough (coarse). The irregular rhythm results in variation in the diastolic filling period of the ventricles, resulting in variability in stroke volume and thus variability in pulse character, including pulse deficits. This also causes variation in the intensity of the heart sounds, especially the second heart sound, creating a heart that sounds like "tennis shoes in a dryer" on auscultation in dogs. In dogs, atrial fibrillation is most commonly associated with underlying cardiac disease. The notable exception occurs in some giant dog breeds, such as Irish Wolfhounds, Scottish Deerhounds, Great Danes, and others, in which the rhythm can develop with an otherwise normal heart (so-called lone or primary atrial fibrillation). Lone atrial fibrillation is the most common form seen in horses (see below). All cats in atrial fibrillation have severe underlying heart disease.
The goal of treatment of atrial fibrillation in most dogs and all cats is control of the ventricular rate, ie, the frequency with which QRS complexes are generated from the fibrillatory depolarization waves. Rate control is usually accomplished with digoxin alone, diltiazem alone, or a combination of the two. Diltiazem alone is generally more effective then digoxin alone, and the combination is generally more effective than either alone. A β-blocker, such as atenolol, may also be used but never in combination with diltiazem. These drugs prolong the refractory period of the AV node and slow AV nodal conduction, resulting in fewer atrial depolarizations crossing the AV node to the ventricles. Amiodarone has also been used to control the ventricular response rate, but its adverse effects (hepatic and thyroid toxicities) limit its use to second-line therapy in animals refractory to the digoxin and diltiazem/atenolol protocol. In rare instances, electrical cardioversion (defibrillation of the heart that is synced to the ECG to prevent causing ventricular fibrillation) is used to convert atrial fibrillation to sinus rhythm. This is generally more rational in a dog with lone atrial fibrillation but has also been done in dogs with severe cardiac disease. In those instances, sinus rhythm commonly reverts back to atrial fibrillation within weeks to months, necessitating reconversion or rate control. Cardioversion is frequently combined with amiodarone administration in an attempt to prolong the time until reversion to atrial fibrillation.
In ruminants, atrial fibrillation is usually paroxysmal and associated with GI tract disorders (eg, vagal indigestion), but it also may be persistent and occur as a sequela of cor pulmonale or with other cardiac diseases.
In horses, atrial fibrillation can usually be diagnosed by identifying an undulating baseline. It most often occurs in the absence of underlying cardiac disease (primary or lone atrial fibrillation) and is associated with the normally high vagal tone found in horses that most likely have some predisposition for the arrhythmia. However, it may also occur secondary to cardiac disease such as mitral insufficiency, aortic insufficiency, myocarditis, pericarditis, or untreated congenital cardiac defects. The resting heart rate is usually within the normal range when there is no underlying cardiac disease, whereas it is typically increased with underlying disease; this may help identify the cause of the arrhythmia on physical examination. Most horses with primary atrial fibrillation exhibit no clinical signs at rest or with moderate exercise/work; however, more strenuous exercise or work may result in evidence of reduced cardiac output. This can be seen in racehorses who are evaluated for a sudden reduction in race performance. In this setting, the clinical signs could also be due to paroxysmal atrial fibrillation, which can be identified only during the exercise period. In horses with primary atrial fibrillation, conversion to sinus rhythm with quinidine at a dosage of 22 mg/kg, PO, every 2 hr until conversion, is still the treatment of choice. The success rate for conversion is greatest in horses with atrial fibrillation of shorter duration. The chance for success is considered excellent if the duration is <4 mo and relatively good if >4 mo, although conversion may take longer and quinidine toxicity is more likely to develop. Horses with atrial fibrillation can also be successfully converted to sinus rhythm electrically (cardioversion). This requires the careful placement of electrode catheters in a pulmonary artery and the right atrium (via the jugular vein) of an awake horse followed by anesthesia. Electrical shocks of increasing intensity are then delivered through the catheters. This method is very successful but is time-consuming and expensive. Most horses can return to successful racing performance after conversion. However, some will revert to atrial fibrillation over time. Conversion to sinus rhythm is not indicated in horses with severe underlying cardiac disease, because the likelihood of conversion, or maintenance of sinus rhythm if converted, is very low.
Ventricular premature complexes arise from a site within the ventricular myocardium or specialized conduction system. On the ECG, the QRS complex usually appears wide and is followed by a large T wave that is opposite in polarity to the QRS complex. This produces a large, bizarre complex when compared with normally sinus-driven QRS complexes, occurs earlier than the next expected sinus-driven QRS complex (ie, premature), and does not have an associated preceding P wave, although unassociated P waves going at a slower rate (AV dissociation) may be seen. Most commonly, these complexes occur from noncardiac causes such as anesthesia, age, electrolyte abnormalities, acute toxicities, neoplasia (eg, splenic hemangiosarcoma in dogs), gastric distension (eg, gastric dilation and volvulus syndrome in dogs), or trauma. They may also be associated with ventricular myocardial diseases such as dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (Boxer cardiomyopathy), and myocarditis.
Ventricular tachycardia is the occurrence of three or more sequential ventricular premature complexes. These can again be nonsustained or sustained (>30 sec). They can also be divided into slower, benign ventricular tachycardias and faster, malignant ones. A slower, benign ventricular tachycardia is called an accelerated idioventricular rhythm (AIVR) and is commonly seen in dogs in the intensive care unit secondary to systemic (often intra-abdominal) disease or trauma. It is characterized on the ECG by the presence of a ventricular tachycardia that is relatively slow (usually <200 bpm). Sinus rhythm may be interspersed with the AIVR, with one rhythm taking control of the rhythm whenever it is slightly faster than the other.
Fusion beats (hybrid sinus beat and premature ventricular contraction [PVC]) can also be seen. This arrhythmia does not result in sudden death and usually dissipates on its own within 48–72 hr. As such, it only needs to be treated (eg, lidocaine) if it is causing hemodynamic instability.
Malignant ventricular tachycardia is most commonly found in dogs with severe underlying cardiac disease, usually either a cardiomyopathy (eg, dilated cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy) or severe semilunar valve stenosis (eg, subaortic stenosis, pulmonic stenosis). Malignant ventricular tachycardia predisposes the animal to sudden death due to the tachycardia degenerating into ventricular fibrillation. Frequently, this arrhythmia is not identified, so the first clinical sign seen is sudden death. Some dogs (especially Boxers and Doberman Pinschers) will experience syncope as the result of a very fast (often >400 bpm) ventricular tachycardia that spontaneously reverts back to sinus rhythm within seconds (must last >6 sec and usually lasts no more than 1 min) of its onset. Sotalol or a combination of atenolol and mexiletine effectively controls the arrhythmia in Boxers and usually stops the syncope and presumably prevents sudden death. β-blockers are frequently administered to dogs with severe subaortic stenosis and to some with severe pulmonic stenosis in an attempt to prevent sudden death. Proof of efficacy is lacking. Sotalol may be a more logical choice. Ventricular tachycardia must be distinguished from ventricular escape rhythm, as seen with third-degree AV block, and from idioventricular rhythm, a terminal ventricular escape rhythm. A ventricular escape rhythm is a slow rhythm (20–40 bpm) that occurs because higher pacemakers (SA and AV nodes) have failed. Suppression of a ventricular escape rhythm by drug therapy (eg, lidocaine) results in cessation of all cardiac electrical activity (ie, death).
Ventricular fibrillation is a result of microreentrant circuits within the ventricular myocardium, resulting in the absence of effective ventricular contractions; thus, it is a terminal rhythm. The only effective treatment is electrical defibrillation.
A detailed discussion of antiarrhythmic therapy is covered elsewhere (see Antiarrhythmics). Most antiarrhythmic drugs are administered to suppress ectopic premature depolarizations (eg, atrial and ventricular premature complexes, atrial and ventricular tachycardia) or to slow the ventricular rate in animals with atrial flutter or fibrillation. Many of these drugs are being supplanted by automatic implantable defibrillators in human medicine, so the manufacture of these drugs is waning. Some of the antiarrhythmics have negative inotropic effects, with the potential to worsen active CHF. This is most likely to occur with the use of β-blockers in the treatment of supraventricular tachyarrhythmias and with sotalol.
Atrial fibrillation is one of the most commonly treated tachyarrhythmias; it is imperative to decrease the ventricular rate to ≤160 bpm if the rate is faster than that in the clinic. In experimental situations, pacing the heart of a dog at a rate ≥180 bpm results in myocardial failure severe enough to cause CHF within weeks. Consequently, leaving the rate this high will cause further cardiac disease and decompensation. There are no firm data to suggest that keeping the heart rate even lower than 160 bpm is beneficial in dogs. Diltiazem (0.5-2 mg/kg, PO, tid) or a combination of diltiazem and digoxin are generally the preferred methods of controlling the ventricular rate in dogs with atrial fibrillation. A low dose of a β-blocker, such as atenolol (0.25 mg/kg, PO, bid), may also be used instead of diltiazem,but its use is uncommon. (Also see Antiarrhythmics).
Ventricular tachycardia can degenerate into ventricular fibrillation and cause sudden death. Fast ventricular tachycardia (>250 bpm) and ventricular tachycardia in animals with severe underlying cardiac disease, such as subaortic stenosis, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy ([ARVC] Boxers), are most vulnerable to dying suddenly from ventricular tachycardia. In Boxers with ARVC, sotalol (0.5–3 mg/kg, PO, bid; most commonly 80 mg/dog, PO, bid) or a combination of mexiletine (5–8 mg/kg, PO, tid) and atenolol (0.5–1 mg/kg, PO, bid) can effectively reduce or, more commonly, stop the syncope (usually due to a ventricular tachycardia firing at a rate of >400 bpm) seen in these dogs. It also obviously decreases the incidence of sudden death and so commonly results in years of survival. A minority of Boxers with ARVC develop true dilated cardiomyopathy and are also prone to sudden death. Doberman Pinschers with dilated cardiomyopathy also commonly die suddenly due to ventricular tachycardia. In these instances, the negative inotropic effects of sotalol can either push a dog into heart failure or make existing heart failure worse. Consequently, if sotalol is to be used in either of these patient populations, the dose must be started low and titrated upward carefully, with pimobendan administered concurrently. Mexiletine can also be used alone but, at least in theory, is not as effective at preventing sudden death. Amiodarone (12–15 mg/kg/day, PO, for 2 wk [loading dose] followed by 5–7 mg/kg/day, PO) is probably more efficacious at preventing sudden death than mexiletine but has many more adverse effects. Doberman Pinschers appear to be particularly susceptible to the hepatotoxic effects of the drug.
Animals with chronic bradyarrhythmias as seen with AV block (high-grade second or third degree) or sick sinus syndrome most commonly present with weakness, episodic weakness/collapse, and syncope. Pacemaker implantation is the treatment of choice. If pacemaker implantation is not a viable option, anticholinergics, PDE inhibitors, or sympathomimetics may be administered. Propantheline is a mild anticholinergic dosed at 0.25–0.5 mg/kg, PO, bid-tid. The parenteral formulation of atropine may be administered PO but must be diluted 10:1 with corn syrup at a dosage of 0.04 mg/kg, PO, tid-qid. Adverse effects include mydriasis, dry mucous membranes, tachycardia, and GI stasis. Theophylline is a nonselective PDE inhibitor with modest positive chronotropic effects. Extended-release tablets or capsules can be given at 10 mg/kg, PO, bid. If no adverse effects are seen and the desired clinical effect is not achieved, the dosage in dogs can be increased to 15 mg/kg, PO, bid, while monitoring for adverse effects, and in cats to 20 mg/kg, PO, every 24–48 hr. Adverse effects may include restlessness, excitability, tachycardia, or GI upset. Terbutaline is a β-agonist that has more potent positive chronotropic effects but with similar adverse effects to those seen with theophylline. It is dosed to effect at 1.25–5 mg/dog (not per kg), PO, tid, and 0.625 mg/cat, PO, bid. Attempts to overcome clinically significant bradyarrhythmias with oral therapy are often unrewarding, although overall clinical signs may improve in some animals.
Echocardiography, the use of diagnostic medical ultrasound to evaluate the heart and proximal great vessels, complements other diagnostic procedures by quantifying chamber dimensions, wall thicknesses, and the dynamic events of the cardiac cycle; it also allows visualization of the anatomy and motion of valves and visualization of congenital abnormalities ranging from a defect in the interventricular septum to a stenotic pulmonary valve. Blood flow velocity is also commonly measured, and turbulent blood flow is identified using Doppler echocardiography. Pressure gradients, blood flow volumes, and several indices of cardiac function can be calculated. Echocardiography can also identify changes in myocardial tissue texture indicative of ischemia and fibrosis and delineate masses, valvular vegetations, pericardial effusion, and many other features previously verifiable only with cardiac catheterization or at necropsy.
There are four main types of echocardiography: three-dimensional, two-dimensional, M-mode (one-dimensional), and Doppler. Two-dimensional echocardiography provides a wedge-shaped, two-dimensional image of the heart in real-time. Several standard long-axis and short-axis views obtained from standard imaging windows on the thorax have been developed for dogs, cats, horses, and cows. M-mode echocardiography is produced by a one-dimensional beam of ultrasound that penetrates the heart, providing an “ice-pick view” over time. The tissue interfaces that are encountered by the beam are then plotted on a screen. This mode of evaluation has been typically used to measure chamber dimensions, wall thickness, valve motion, and great vessel dimensions but, as frame rate of two-dimensional echocardiography has improved, this mode has lost some of its usefulness. Three-dimensional echocardiography is the newest modality and is still in its infancy. Doppler echocardiography uses the principle of changing frequency of the ultrasonic beam after it contacts a moving structure (eg, RBCs, cardiac wall) to measure velocity. Doppler echocardiography is further divided into spectral (pulsed and continuous wave), color flow, and tissue Doppler echocardiography. Color flow Doppler echocardiography is a form of pulsed Doppler echocardiography prone to aliasing when high velocity flow is encountered, allowing high velocity (and therefore turbulent) flow in the heart and great vessels to be detected. Continuous wave Doppler is used to quantitate high velocity flow and thus used to calculate pressure gradients, most commonly across the regions of valves, using the modified Bernoulli equation (4 × velocity2). Tissue Doppler imaging is used to measure the lower velocity motion of cardiac structures, most commonly ventricular walls, in an attempt to quantitate regional myocardial function. Variations include measuring strain and strain rate.
Cardiac catheterization involves the placement of catheters into cardiac chambers and surrounding great vessels to measure pressure, inject contrast agents, and place devices. The latter is commonly termed interventional cardiology. Indications include diagnostic evaluation (eg, when other diagnostic tests are insufficient to identify specific cardiac abnormalities or are unable to identify the severity of a lesion), presurgical evaluation (eg, to help diagnose constrictive pericarditis before surgery), therapeutic intervention, and clinical research. Diagnostic and presurgical cardiac catheterization, however, have largely been replaced by echocardiography. Currently, most cardiac catheterizations are interventional procedures to address cardiac defects (eg, closure of a patent ductus arteriosus).
Last full review/revision April 2015 by Mark D. Kittleson, DVM, PhD, DACVIM (Cardiology)