Nonpathologic Heart Murmurs

Young, often large and giant breed dogs without underlying cardiac disease may have soft, grade I to III/VI left basilar systolic murmurs. These innocent murmurs are usually midsystolic, high-frequency, and devoid of substantial radiation. Although uncertain, their origin is thought to be increased blood flow velocity and turbulence through the right or left ventricular outflow tract (LVOT). Innocent murmurs are usually nonprogressive and typically disappear in early adulthood. Similar to innocent murmurs, physiologic or functional murmurs are often grade I to III/VI midsystolic left basilar murmurs. Conditions associated with high cardiac output (i.e., fever, sepsis, high sympathetic tone) or decreased blood viscosity (i.e., anemia) may contribute to the development of an audible murmur. These murmurs generally resolve after the underlying disease process is corrected. Unfortunately not all soft murmurs are nonpathologic. Mild SAS, large nonrestrictive VSDs, and atrial septal defects (ASDs) may similarly display soft, systolic murmurs that could be confused with nonpathologic murmurs. Therefore common sense, the patient’s clinical status and intended use, and the client’s wishes must dictate whether diagnostics to assess the cardiac status are indicated.

Pathologic Heart Murmurs

Compared with innocent and functional murmurs, the murmurs that accompany many CHDs are louder (grade III/VI and beyond), longer in duration, and may obscure the normal heart sounds. Although murmurs of this intensity and duration are invariably indicators of underlying pathology that requires investigation, it is impossible to perfectly correlate the intensity of the murmur with the severity of the disease. Restrictive VSDs and small, restrictive left-to-right shunting PDA may produce minimal hemodynamic burden yet be accompanied by very intense murmurs. Continuous murmurs and diastolic murmurs should always be considered pathologic, no matter their intensity.

Concurrent palpation of the femoral arterial pulses during auscultation may help detect rhythm disturbances or provide useful information for distinguishing conditions with similar auscultatory findings (i.e., PS and SAS). A weak and late-to-rise femoral pulse, combined with a left basilar systolic murmur, suggests moderate to severe SAS. Bounding, or water hammer, pulses are often produced by widening of the pulse pressure subsequent to diastolic runoff in dogs with left-to-right PDA. Other conditions associated with diastolic runoff and bounding pulses include aortic insufficiency and peripheral arteriovenous fistulas.

Aortic Stenosis

SAS has likely replaced PDA as the most common congenital cardiac lesion in areas with a high population of large breed dogs. Although any breed of dog may be affected, evidence suggests Newfoundlands, Rottweilers, Boxers, Golden Retrievers, German Shepherd Dogs, and Bloodhounds have an increased relative risk for SAS. Valvular and supravalvular aortic stenosis are seen infrequently or rarely in dogs, and although uncommon, cats have been described with all three forms of fixed LVOT obstruction. SAS has been most thoroughly investigated in Newfoundlands, for whom breeding studies suggest an autosomal dominant mode of transmission with modifying genes or a polygenic mechanism. These same studies found that SAS may not be present at birth but instead begins to develop during the first 4 to 8 weeks of life. Because SAS lesions may progress as animals grow, it is not uncommon for the severity of the lesion and the associated murmur and cardiac changes to worsen from birth until young adulthood. Detection of mild disease is difficult; therefore ultimately genetic counseling is difficult.

The pathophysiologic consequences of aortic stenosis include left ventricular and in some instances left atrial hypertrophy, myocardial fibrosis, and aortic arch abnormalities. The hypertrophy and fibrosis produce a stiff, noncompliant left ventricle that ultimately necessitates higher atrial pressures to fill. Elevated left atrial, and hence pulmonary venous and pulmonary capillary hydrostatic, pressures may contribute to the development of pulmonary edema.

Puppies with mild to moderate SAS are often reported to be clinically normal at the time of immunization. Owners with severely affected dogs may report exercise intolerance, syncope, or a history consistent with left heart failure. In some cases sudden death occurs without premonitory signs. Auscultatory abnormalities are usually present in cases of moderate to severe SAS because the intensity and duration of the murmur tend to increase and lengthen, respectively, with more severe disease. Obstruction to blood flow through the LVOT produces an ejection, left basilar systolic murmur. The murmur tends to radiate up the carotid arteries and to the right so it can frequently be auscultated in the ventral cervical region, and in some cases the PMI is at the right heart base. Because SAS may progress through early adulthood, the murmur can increase in intensity between sequential physical examinations. Femoral pulse alterations, with palpably reduced and late rising pulse amplitudes, are often found in dogs with moderate to severe obstruction.

Although nonspecific, electrocardiographic changes that may accompany SAS include increased R wave amplitude and QRS duration consistent with left ventricular enlargement, as well as ST segment and T wave alterations suggestive of myocardial ischemia (Figure 32-1). VPCs may be evident on baseline electrocardiography (ECG), and studies of Holter examinations suggest the overall number and grade of VPCs display a modest correlation with pressure gradient. Ventricular tachycardia and ultimately fibrillation are the presumed mechanism for sudden death in dogs with SAS.

Figure 32-1 Lead II, 10 mm/mV, 50 mm/s. ST segment depression (arrows) >0.2 mV may suggest myocardial ischemia in dogs with concentric ventricular hypertrophy and reduced myocardial oxygen delivery.

Radiography is limited in the assessment of ventricular enlargement in dogs with SAS because it produces concentric rather than eccentric hypertrophy. Nonetheless assessment of the cardiac silhouette still proves useful in dogs with moderate to severe SAS for detection of poststenotic dilation of the aorta or left atrial enlargement.

Echocardiography provides a reliable method for identification of moderate to severe SAS. Common findings include left ventricular concentric hypertrophy, a subvalvular fibrous ring or band narrowing the LVOT, and poststenotic dilation of the aorta. Hyperechogenicity of the left ventricular endocardial surface and papillary muscles may be seen in dogs with myocardial ischemia and replacement fibrosis.

Although the exact velocity cutoff to distinguish mild, moderate, and severe SAS is uncertain, it is generally accepted that gradients more than 100 mm Hg represent severe disease with a high likelihood of complications. Currently available diagnostic methods seem incapable of identifying dogs with grade 1 lesions. Even dogs with grade 2 lesions may be difficult to accurately assess purely based on the LVOT velocities because of the likelihood of breed and examination condition variations.

Although many dogs with mild to moderate SAS live normal lifespans devoid of clinical consequences, the natural history and responses to therapy of severe SAS are disappointing. Commonly reported outcomes of dogs with severe SAS include exercise intolerance, syncope, sudden death (most commonly in the first 3 years of life), and the development of congestive heart failure and/or endocarditis. In general, dogs with mild to moderate disease do not require specific therapy and can often exercise normally. Antibiotic prophylaxis is recommended for surgical procedures in all dogs with SAS because they appear to be at increased risk for developing endocarditis; however, the effectiveness of this therapy is uncertain. Exercise restriction is prudent for dogs with moderate to severe SAS, and β-blockers (i.e., atenolol) are frequently administered in an effort to combat arrhythmogenesis, reduce myocardial oxygen demands, and limit tachycardia. Currently the survival benefit imparted by β-blockers is unknown. Additional antiarrhythmic medications may be necessary to treat VPCs, ventricular tachycardia, or atrial fibrillation if they complicate the clinical situation. Similarly standard therapy for left heart failure, including diuretics, angiotensin-converting enzyme inhibitors, and possibly positive inotropic agents, are indicated for animals that develop pulmonary edema.

Pulmonic Stenosis

Valvular PS is the most common congenital right ventricular outflow tract (RVOT) obstruction in dogs and is the third most common congenital cardiac defect encountered. PS is less commonly identified in cats, and both species have been reported to infrequently display sub- and supravalvular forms of RVOT obstruction. Breeds with an increased relative risk for PS include English Bulldogs, Terrier breeds, Miniature Schnauzers, Chihuahuas, and Samoyeds. PS has been identified as hereditary in breeding studies of Beagles with a spectrum of pulmonary valve abnormalities. Grade 1 lesions display mild leaflet thickening with commissural fusion producing a central orifice. More severe cases of PS tend to be grade 2 lesions with moderate to severe thickening of the valve leaflets with fusion or hypoplasia producing RVOT obstruction. Fibrous thickening at the base of the valve may accompany valvular dysplasia. Boxers and Bulldogs have been identified with coronary arterial abnormalities that contribute to a unique form of subvalvular PS that is difficult to address surgically.

Physical examination of animals with PS often reveals a variable-intensity, left basilar, systolic, ejection murmur in a reportedly healthy puppy. Compared with murmurs of SAS, PS murmurs do not radiate as extensively to the right cranial thorax or up the carotid arteries. The femoral arterial pulse is usually normal. Jugular distention or abnormal pulsation should increase suspicion of right heart failure or concurrent cardiac defects (i.e., TVD). Many dogs with PS are reportedly asymptomatic during the first year of life when the murmur is initially detected. However, clinical signs, including exercise intolerance, syncope, and signs consistent with right heart failure often complicate severe cases of PS and have been reported in 34% to 83% of dogs evaluated.

In cases of moderate to severe PS, the ECG almost always displays criteria for right ventricular enlargement (Figure 32-2). The P waves are usually normal. Ventricular arrhythmias appear to be less common than in dogs with SAS.

Figure 32-2 Lead II, 5 mm/mV, 50 mm/s. Deep S waves frequently accompany dogs with moderate to severe pulmonic stenosis.

Radiography usually reveals moderate cardiomegaly with a right heart enlargement pattern (Figure 32-3). Poststenotic dilation of the main pulmonary artery produces loss of the cranial cardiac silhouette on the lateral view and dilation at approximately the 2 o’clock position on the dorsoventral (DV) view.

Figure 32-3 Lateral (A) and dorsoventral (B) radiographs from a dog with severe pulmonic stenosis. The lateral radiograph displays increased sternal contact with lifting of the apex off the sternum and loss of the cranial cardiac silhouette. Right heart enlargement and dilation of the main pulmonary artery (arrows) are evident on the dorsoventral view.

Echocardiography provides a method for definitive diagnosis and assessment of severity of PS, as well as identification of concurrent cardiac defects. Of the four cardiac valves, the pulmonary valve morphology tends to be the most difficult to clearly assess via transthoracic echocardiography. Therefore in some instances it is challenging to distinguish valvular PS from discrete subvalvular obstruction. Mild PS is usually categorized as a pressure gradient less than 50 mm Hg, whereas the cutoff for severe disease varies with peak gradients described more than 80 or 100 mm Hg. Contrast echocardiography may identify right-to-left shunting at the atrial level as RV diastolic dysfunction, and tricuspid insufficiency contributes to right atrial hypertension.

Although precise criteria for establishing a prognosis for dogs and cats with PS are lacking, it is generally accepted that dogs with uncomplicated mild to moderate PS often live normal, comfortable lives and do not require specific therapy. Serial echocardiographic examinations should be performed to determine whether the stenosis, right ventricular hypertrophy, tricuspid insufficiency, or right atrial dilation progresses. In animals with severe PS, clinical experience suggests they are more likely to develop exercise intolerance, right heart failure, or die suddenly. Surgical intervention is generally recommended even in asymptomatic dogs with severe PS.

Several techniques have been described and are available for the treatment of PS. Valvular PS with a normally developed pulmonary annulus is most often treated by percutaneous balloon valvuloplasty (Figure 32-4). The goals of intervention include improving survival and resolving clinical signs in symptomatic animals. Surgical success, defined as a reduction of the pressure gradient into the mild category, or in markedly severe cases as a reduction in the pressure gradient of more than 50%, is achievable in up to 80% of dogs. Valvuloplasty has been reported to reduce clinical signs and mortality compared with animals not undergoing surgery.

Figure 32-4 Fluoroscopic images obtained during balloon valvuloplasty of pulmonic stenosis. A guidewire is directed through the cranial vena cava, right atrium, and right ventricle into the pulmonary artery. Afterward a balloon dilation catheter is fed across the guidewire and is quickly inflated (A) until the stenotic lesion is stretched or torn when the balloon is fully inflated (B).

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