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. Occasionally, more specialized tests such as cardiac catheterization or nuclear studies are necessary.
History and Signalment
For patients with suspected heart disease, the signalment (age, breed, sex) helps provide a differential diagnosis list. The signalment influences the relative importance of possible heart diseases (eg, endocarditis is rare in cats and dogs but more common in cows and horses) as well as some specific abnormalities (eg, breed predispositions for certain congenital defects).
Animals presenting with heart disease may have no clinical signs or have a history of exercise intolerance, weakness, dyspnea, tachypnea, abdominal distention (ascites), syncope (fainting), cyanosis, or anorexia and weight loss. Other historical findings are more species specific, including peripheral or ventral edema (horses and cows). Cats rarely demonstrate cough with heart disease and more commonly present with a history of dyspnea (which may be subtle and go unnoticed by the owner) and anorexia. Dogs with congestive heart failure (CHF), in contrast, commonly demonstrate cough and dyspnea as a presenting complaint.
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. In addition to auscultation of the thorax, palpation should be performed to assess for the presence of thrills (low frequency vibrations that can be palpated with the fingertips) and alterations in intensity or location of the impulse beat. Concurrent auscultation and palpation of pulses should also be performed. Mucous membrane color and refill time, as well as assessment for jugular pulsation and excessive distention, is recommended. Limbs should be examined for the presence of edema, and the abdomen should be assessed for the presence of ascites. Because there are many causes of ascites, it is imperative to evaluate the jugular veins in every case in which ascites is present. If cardiac disease is the cause of the ascites, there is an obligatory distension of the jugular veins because cardiogenic abdominal effusion is caused by elevated right heart pressures. If ascites is present without jugular venous distension, then extracardiac causes of the ascites should be pursued.
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 ausculted. The first heart sound (S1) is associated with closure of the atrioventricular (AV) valves, and the second heart sound (S2) is associated with closure of the semilunar (aortic and pulmonic) valves. The third heart sound (S3) occurs in early diastole and is a result of rapid cessation of ventricular filling, while the fourth heart sound (S4) is associated with atrial systole (atrial contraction or atrial “kick”). In horses, all 4 sounds are normally audible. In cattle, typically only S1 and S2 are audible in normal individuals, although S3 or S4 can sometimes be heard. IV fluid administration in cattle can result in accentuation of S3 and/or S4. In dogs, cats, and ferrets, S1 and S2 are the only heart sounds normally audible. Less is known about goats, sheep, and pigs; however, only S1 and S2 are believed to be audible in these species.
Gallop Heart Sounds
A gallop heart sound is the presence of S1 and S2 accompanied by an interceding sound that is either an accentuated S3 or 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 ventricular dilatation from cardiac diseases such as dilated cardiomyopathy, degenerative valve disease, or left-to-right shunts such as patent ductus arteriosis. An S4 gallop heart sound (presystolic) is caused by atrial contraction pushing blood into a relatively high pressure ventricle. This is most commonly audible in cats with cardiomyopathy, especially hypertrophic cardiomyopathy. Because the heart rate commonly exceeds 160–180 bpm in cats, it is difficult to determine if the gallop sound is due to an S3 or S4 gallop on physical examination. However, the presence of an S3 gallop in a cat is much less common than an S4 gallop due to the common cardiac diseases of cats. A systolic click is a short, sharp, often transient sound that can occur during mid- to late systole. These clicks are uncommon in dogs and probably in other domestic species. However, when present, systolic clicks are most commonly noted in dogs with early myxomatous degeneration of the mitral valve with prolapse of one of the mitral leaflets. They usually are single but may be multiple and can vary in intensity (even completely disappearing) depending on cardiac loading conditions.
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 certain ectopic ventricular beats. Splitting of S1 can also occur in normal healthy, large-breed dogs. Delayed closure of the pulmonic valve (in relation to the aortic valve) results in splitting of S2. This may be seen during inspiration in dogs (especially large-breed dogs) as the increase in negative intrathoracic pressure increases right ventricular filling. Splitting of S2 can be a normal finding in horses during either inspiration or expiration. Abnormal splitting of S2 has been associated with pulmonary hypertension, as in pulmonary emphysema of horses and heartworm infestation of dogs. Other possible causes include atrial septal defect, right bundle-branch block, or ventricular ectopic beats of left ventricular origin. Delayed closure of the aortic valve (paradoxical splitting of S2) could be seen with left bundle-branch block or ventricular ectopic beats of right ventricular origin.
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 and occurs frequently in eclampsia. It is seen most commonly in dogs in association with electrolyte disturbances induced by GI disease.
Heart murmurs are audible vibrations emanating from the heart or major blood vessels and generally are the result of turbulent blood flow or vibrations of cardiac structures such as part of a valve leaflet or chordal structure. Murmurs are typically defined relative to timing, intensity, and location but can also be characterized by frequency (pitch), quality (eg, musical), and configuration (eg, crescendo-decrescendo).
A systolic murmur occurs during systole and is typically either ejection (crescendo-decrescendo) or regurgitant (holosystolic, plateau). Ejection systolic murmurs demonstrate the greatest intensity during mid-systole and appear diamond-shaped on phonocardiography. They can be produced by stenotic lesions at the semilunar valves (eg, pulmonic stenosis or subaortic stenosis). Regurgitant systolic murmurs demonstrate a constant intensity throughout systole and can be caused by mitral or tricuspid regurgitation (eg, myxomatous degeneration of the mitral valve) or a ventricular septal defect. Diastolic murmurs are typically decrescendo (decreasing in intensity through diastole) and a result of aortic or pulmonic insufficiency (such as that caused by aortic valve infective endocarditis in dogs or degenerative disease in horses). Continuous murmurs are most commonly a result of patent ductus arteriosus (a congenital cardiac defect) and occur throughout systole and diastole. Continuous murmurs vary in intensity over time, typically being most intense at the end of ventricular ejection and decreasing in intensity through diastole. A to-and-fro murmur occurs in animals that demonstrate both a systolic murmur and a diastolic murmur and can occur in animals 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 seen in healthy, young horses. Occasionally, systolic murmurs are noted in some cats secondary to an increase in right midventricular flow velocity without significant structural heart disease. Innocent cardiac murmurs are also commonly noted in immature cats and dogs (<6 mo old) as a result of increased stroke volume.
Heart murmurs are 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; or Grade VI—an extremely loud murmur 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; 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 Heart Disease and Heart Failure: Arrhythmias.)
A pulse is the rhythmic expansion of an artery that can be digitally palpated (or visualized) during physical examination. Physiologically, the pulse pressure is the difference between systolic and diastolic pressures. In dogs and cats, pulses are typically palpated at the femoral artery. Pulse deficits are absent pulses despite auscultation of a heart beat and are thus detected during simultaneous auscultation and pulse palpation. These occur as a result of ectopic contractions (arrhythmias) that occur so prematurely that the ventricles are unable to fill sufficiently, resulting in a reduced stroke volume that produces either a weak pulse or no pulse. Bounding pulses (an increase in pulse pressure) are usually caused by a reduced diastolic pressure and can be noted with aortic insufficiency or patent ductus arteriosus. Weak pulses (a reduction in pulse pressure) are usually caused by a decrease in systolic pressure and can be noted with systolic dysfunction, pericardial tamponade, or subaortic stenosis.
Dogs with severe subaortic stenosis may demonstrate 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 usually too subtle to observe on physical examination. Animals with pericardial effusion and cardiac tamponade, however, demonstrate an exaggeration of this finding. 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 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. These pulses typically do not extend beyond a third of the distance up the neck of an animal in a standing position.
Pulmonary edema may develop as a result of CHF. On physical examination, this may manifest as respiratory crackles and wheezes. Dyspnea or tachypnea may also be noted. A decrease in air movement is commonly present during thoracic auscultation in animals that have developed pleural effusion as a result of heart disease. This results in decreased respiratory sounds, especially ventrally. However, respiratory diseases or pleural effusion secondary to other underlying disease can also result in these clinical signs.
Abdominal swelling may occur as a result of gas, soft tissue, or fluid accumulation. Animals with heart disease and right-sided heart failure (eg, those with heartworm disease, tricuspid valve dysplasia, pericardial tamponade) can develop ascites. In these circumstances, the ascites is associated with jugular venous distension.
Thoracic radiographs frequently provide valuable information in the assessment of animals suspected of having heart disease. However, thoracic radiography is rarely performed in horses or cows because of their large size and body conformation, which reduces the quality of the images. Finding generalized cardiomegaly or enlargement of specific cardiac chambers 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 is associated with pulmonary venous congestion; pleural effusion may also be noted, but this typically indicates biventricular failure except in cats, in which it can be seen with left-sided CHF. Resolution of these abnormalities on subsequent thoracic radiographs can be used as one indication of efficacy of therapy. The presence of pulmonary edema does not definitively confirm a cardiogenic origin or rule out another origin such as pulmonary disease. 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.
Electrocardiography is the recording of cardiac electrical activity from the body surface. It can be used to identify not only cardiac arrhythmias and conduction disturbances but also chamber enlargement. However, small animals differ from large animals in that large animals have a category B type heart (small animals have category A), in which there is a richly penetrating Purkinje cell population. This results in reduced complexes on the surface ECG, impairing the ability of the ECG to accurately detect changes in cardiac size. Therefore, the most common form of ECG performed in large animals is a base-apex rhythm analysis, in which the recorded deflections are much larger and the diagnostic focus is rhythm determination.
Chamber enlargement can be indicated by waveform abnormalities. In lead II in dogs and cats, wide or notched P waves suggest left atrial enlargement, whereas tall P waves suggest right atrial enlargement. Evidence for left ventricular enlargement includes tall R waves in leads that have the positive electrode on the left side of the heart (leads I, II, aVF, CV6LL, and CV6LU). Right ventricular enlargement is suggested by 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. Wide QRS complexes can occur in patients with either right or left ventricular enlargement; however, they can also be due to conduction disturbances (see Heart Disease and Heart Failure: Conduction Disturbances). While the ECG may suggest chamber enlargement, thoracic radiographs and echocardiography are more sensitive.
The sinus node initiates each cardiac contraction in a normal animal, sets the normal rate and rhythm, and is called the pacemaker of the heart. Normal sinus rhythm is a rhythm that is regular and originates at the sinus node, indicated on the ECG by a P wave that precedes each normal QRS complex. Sinus bradycardia is a regular sinus rhythm that is slower than expected for that species. Sinus bradycardia may be noted in animals that are overdosed with anesthesia or agents that can result in elevated vagal tone or reduced sympathetic tone (eg, xylazine, digoxin), hypothermic animals, hypothyroid animals, animals with sick sinus syndrome, or in animals with elevated 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 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 an excessive rate. Causes include stress (resulting in high sympathetic drive), 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 associated with respiratory cycling. 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 common in cats in their home environment. Sinus arrhythmia is characterized by increases in heart rate with inspiration and decreases with expiration. The variation in heart rhythm is associated with variation in the intensity of vagal tone. It is abolished by reduced vagal tone resulting from excitement, exercise, or administration of vagolytics 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 shorter or flatter P waves during slower rates.
Sinoatrial 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 pause is caused by a delayed discharge from the SA node. This results in a break in sinus rhythm in which the P-P interval surrounding the break is not an exact multiple of the normal P-P interval.
Sinus arrest is the absence of P waves on the ECG for a short period of time (typically accepted as a pause exceeding twice the normal P-P interval). Sinus arrest can be caused by prolonged SA nodal arrest or pause.
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. Even though there are no P waves present, the QRS complexes are most often triggered by the wave of depolarization that comes from the SA node resulting in a sinoventricular rhythm. In some cases, the ventricular rhythm can be variable because of the concurrent presence of a sinus arrhythmia. The heart rate is typically slow (40–80 bpm) in affected dogs, depending on the precise etiology. Causes include hyperkalemia (transient atrial standstill), in which the elevated potassium precludes atrial myocardial depolarization; myocarditis; and specific forms of cardiomyopathy (atrioventricular cardiomyopathy), in which the atrial myocardium is replaced by fibrous tissue (persistent atrial standstill). Resolution of the hyperkalemia will convert the atrial standstill into a normal sinus rhythm.
Sick sinus syndrome is a constellation of clinical signs, including ECG changes (sinus pause or block, sinus arrest, junctional or ventricular escape complexes, and possibly supraventricular tachycardias) and weakness or syncope from the bradycardia (most common) or tachycardia (less common). With this clinical syndrome, the principal problem lies within the SA node or perinodal tissue; however, 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 disease is commonly noted in geriatric dogs, including Miniature Schnauzers and 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 period of 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 remains pacemaker implantation.
Atrioventricular (AV) block refers to alteration of impulse conduction 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. In second-degree AV block (intermittent conduction), occasional impulses fail to be conducted through the AV junction, 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- or third-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. If the PR intervals do not change, the condition is known as a Mobitz type II second-degree AV block.
In third-degree AV block or complete heart block, none of the impulses are conducted from the atria to the ventricles. The atrial rhythm (P waves) occurs more rapidly and independently from the ventricular rhythm (QRS complexes), which originates from subsidiary pacemakers within the ventricles. The heart and pulse rates are 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 large pulsations in the jugular vein (cannon A waves).
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 generally is not considered significant in dogs or horses unless other evidence of heart disease or pathologic cause of increased vagal tone (eg, CNS or pulmonary 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- and third-degree (complete) AV block is always abnormal in all species.
Second- and third-degree AV block may be caused by fibrosis, neoplasia, other injuries to the AV node, hypoxia, agents that increase 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 (many nonconducted P waves) and third-degree AV block are frequently associated with exercise intolerance or 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 animals. Third-degree heart block is usually associated with irreversible lesions; the only effective treatment is pacemaker implantation.
Arrhythmias can be divided into bradyarrhythmias, in which the heart rate is excessively slow, and tachyarrhythmias, in which the heart rate is excessively rapid. The former includes sinus bradycardia, sinus arrest, SA block, AV block, and atrial standstill (see above). Tachyarrhythmias can be divided into supraventricular and ventricular based on their site of origin. Supraventricular premature depolarizations are premature depolarizations that originate from above the ventricles. They may also be called atrial premature complexes/depolarizations. Possible sites for ectopic depolarizations include the SA node, atrial myocardium, and supraventricular AV nodal junction. Electrocardiographically, supraventricular premature depolarizations include a QRS complex that 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 depolarization or may be hidden in the preceding sinus complex or within the premature depolarization. Supraventricular premature depolarizations are most commonly a result of atrial enlargement, stress, or other causes of increased sympathetic tone. Supraventricular tachycardia is a series of supraventricular premature depolarizations occurring consecutively for a relatively prolonged period of time. Accessory pathways are congenital abnormalities that allow an electrical connection between the atria and ventricles outside the normal connection (AV node/bundle of His). These pathways or bypass tracts have been recognized in dogs and cats and may result in supraventricular tachyarrhythmias. Treatment may involve radiofrequency catheter ablation of the bypass tract or oral medications such as procainamide, sotalol, or diltiazem.
Atrial flutter is a rare, usually transient arrhythmia that either reverts to sinus rhythm or progresses to atrial fibrillation. It is caused by a large circular reentrant loop within the atria and is 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 (often >400 bpm) so that only intermittent atrial impulses are conducted across the AV node because of prolonged AV nodal refractoriness.
Atrial fibrillation is a rapid and very irregular atrial rhythm caused by disorganized depolarization of the atria. As in atrial flutter, the AV node is bombarded by frequent atrial depolarizations that result in prolonged AV nodal refractoriness and nonconduction of most of these atrial depolarizations. Atrial fibrillation is characterized on the ECG by the absence of P waves, an undulating baseline that can appear almost flat (fine) or very rough (coarse), and relatively normal appearing QRS complexes that occur with no identifiable pattern (irregularly irregular). The irregularity results in variation in the diastolic filling period of the ventricles. Along with a loss of the atrial contribution to filling, this causes variation of the intensity of the heart sounds and amplitude of the arterial pulses. In dogs and cats, atrial fibrillation is almost always associated with underlying cardiac disease. Notable exceptions occur in some giant dog breeds such as Irish Wolfhounds, Scottish Deerhounds, Great Danes, and others in which the rhythm can develop with otherwise normal hearts (lone or primary atrial fibrillation).
The goal of treatment of atrial fibrillation in dogs and cats is control of the ventricular response rate (ie, the frequency with which QRS complexes are generated from the fibrillatory depolarization waves) and not conversion to sinus rhythm, because this rhythm is usually associated with underlying cardiac disease. This is usually accomplished with digoxin combined with either diltiazem or a β-blocker such as atenolol. These drugs slow AV nodal conduction, resulting in fewer atrial depolarizations crossing the AV node to the ventricle. 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. Conversion to sinus rhythm in dogs with primary atrial fibrillation or recent onset atrial fibrillation secondary to cardiac disease can be attempted. Current pharmacologic choices include quinidine and amiodarone, while direct-current cardioversion has gained some popularity in teaching institutions.
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 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, while it is typically elevated 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 would 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 is currently 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. Most horses can return to successful racing performance after conversion. Conversion to sinus rhythm is not indicated in horses with underlying cardiac disease because the likelihood of conversion or maintenance of sinus rhythm if converted is very low.
Ventricular premature depolarizations arise from a site within the ventricular myocardium or specialized conduction system. On the ECG, the QRS complex usually appears wide and bizarre compared with normally sinus-driven QRS complexes, occurs earlier than the next expected sinus driven QRS complex, and does not have a consistently associated preceding P wave. Most commonly, these complexes occur from noncardiac causes such as electrolyte abnormalities, acute toxicities, neoplasia (eg, splenic hemangiosarcoma in dogs), gastric distention (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 sequential ventricular premature depolarizations over a prolonged period of time. These could be paroxysmal, nonsustained (4–10), or sustained. 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. An accelerated idioventricular rhythm is commonly seen in dogs in the intensive care unit secondary to illness or trauma. It is characterized on the ECG by the presence of a ventricular rhythm that is relatively slow (usually <120 bpm) and associated with atrioventricular dissociation, whereas sinus rhythm is seen when the sinus rate is faster than the ventricular rhythm. This is considered a relatively benign arrhythmia in most animals. While the underlying cause should be sought and treated as necessary, the arrhythmia itself typically results in no clinical signs, requires no specific therapy, and resolves once the underlying illness/trauma is corrected.
Echocardiography, the use of ultrasound to evaluate the heart and proximal great vessels, complements other diagnostic procedures by quantifying the dynamic events of the cardiac cycle. Cardiac chamber and wall dimensions can be determined; the anatomy and motion of valves can be visualized; and 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 3 main types of echocardiography: two-dimensional, M-mode, and Doppler. Two-dimensional echocardiography provides a wedge-shaped, two-dimensional image of the heart in real-time motion. 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.” The tissue interfaces that are encountered by the beam are then plotted on a screen. This mode of evaluation is typically used to measure chamber dimensions, wall thickness, valve motion, and great vessel dimensions. Doppler echocardiography uses the principle of changing frequency of the ultrasonic beam after it contacts a moving RBC to measure flow velocity and thus identify turbulent or high-velocity flow. This can locate cardiac murmurs.
Cardiac catheterization involves the placement of specialized catheters into the heart and surrounding great vessels. 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, therapeutic intervention, and in clinical research. Diagnostic and presurgical cardiac catheterization, however, have largely been replaced by echocardiography.
Last full review/revision July 2011 by Daniel F. Hogan