Clay A. Calvert
PROBLEM DEFINITION AND RECOGNITION
Murmurs are audible successive sounds with distinct duration, as opposed to normal heart sounds, which are short transitory events. Cardiac murmurs result from turbulence created in laminar blood flow. When the flow velocity of fluid within a pipe exceeds a certain value, turbulence develops and energy is dissipated, which generates audible vibrations. Turbulence may also arise when fluid passes through a small hole in a plate that partially occludes a pipe, when the pipe diameter changes abruptly, or when a jet of fluid strikes a surface. A critical level of turbulence must be achieved to produce a sound that is clinically evident. The characteristics of the murmur depend upon the velocity of blood flow and the surrounding structures that are caused to vibrate. Blood velocity and blood density variations can also produce turbulence within the heart and arteries.
Heart murmurs may be classified as (1) innocent, (2)
functional, or (3) pathologic (Table 1). It is useful to describe
murmurs on the basis of five auscultatory criteria (Table 2).
First, they may be categorized according to their timing in the cardiac cycle (Table 3);
accordingly, murmurs are identified as being systolic, diastolic, or continuous. A second
aspect of the description of a heart murmur is its intensity (Table 4).a Unfortunately,
murmur intensity does not necessarily indicate flow volume. Thus, although a very small
jet does not usually generate a loud murmur, torrential flow through a large hole, as in a
large ventricular septal defect, occasionally produces no murmur. The ear perceives
higher-frequency noises as being louder than those of the same amplitude but of lower
frequency. Third, the frequency, or pitch, of the murmur over each of the heart valves and
at the thoracic inlet should be characterized. The fourth aspect of the characterization
of a murmur is the modulation or shape of the murmur. Although the holosystolic plateau
murmur of mitral insufficiency (regurgitation) is relatively easy to recognize, not all
plateau or ejection (crescendo-decrescendo, also called diamond-shaped) murmurs are easily
discerned. A phonocardiogram is necessary to confirm the modulation of many murmurs. Last,
the location of the murmur where the intensity is loudest and the area of radiation should
be succinctly described. The classification of systolic murmurs" into systolic
ejection murmurs and holosystolic (regurgitant systolic) murmurs is of clinical value.
TABLE 1. Classification of Heart Murmurs and Examples
Functional I/VI-III/VI Medium to high Systolic ejection Anemia
High cardiac output
Pathologic I/VI-VI/VI Low to high Systolic anterior
mitral valve motion
AV valve annulus
Congenital heart defects,
Acquired valvular disease,
Aortic outflow tract obstruction,
Continuous Crescendo-decrescendo PDA
TABLE 2. Description of Cardiac Murmurs Based on Auscultatory Criteria
Timing (see Table 22-3) Systolic
Intensity I/VI-VI/VI Frequency (pitch) Low
Modulation (shape) Plateau
TABLE 3. Cardiac Murmurs Based on Location Within the Cardiac Cycle (Timing) and Characte (Modulation) Timing
(diamond-shaped ejection murmur)
Congenital pulmonic stenosia
Congenital aortic stenosis
Mitral regurgitation (insufficiency)
Tricuspid regurgitation. (insufficiency)
Ventricular septal defect
Aortic regurgitation (insufficiency)
Aortic valve bacterial endocarditis Secondary to chronic aortic stenosis Secondary to a high ventricular
Continuous Patent ductus arteriosis
|TABLE 4. Classification of Cardiac Murmurs by Degree of Intensity|
|Audible after a few seconds of auscultation, low intensity|
|Immediately audible, moderate intensity|
|Loud intensity without a precordial thrill|
|Loud intensity with a precordial thrill|
|Loudest intensity, precordial thrill, audible with stethoscope slightly away from thoracic wall|
Systolic ejection murmurs imply turbulent blood flow at the time of right or left ventricular ejection into its corresponding great artery. They are typical of the murmurs produced by congenital aortic and pulmonic stenosis. The origin of such murmurs is likely to be along the ventricular outflow at the semilunar valve level or at the immediate artery (pulmonary or aorta). Since actual blood flow is an essential ingredient in the genesis of turbulence responsible for the murmurs, the murmur begins after semilunar valve opening and ends upon cessation of flow with the closure of the same semilunar valve. Such murmurs are known as crescendo-decrescendo, or diamond-shaped.
Holosystolic or regurgitant systolic murmurs, that is, those associated with mitral or tricuspid valve regurgitation (insufficiency), begin as soon as the atrioventricular valve closes and continue beyond semilunar valve closure. Because the pressure difference (gradient) between ventricle and recipient chamber(atrium) is considerable throughout systole, the murmur tends to have an even or plateau configuration. A holosystolic murmur is also typical of a ventricular septal defect.
Innocent systolic ejection murmurs are produced by normal turbulent flow through the proximal great arteries at the time of ventricular ejection. The intensity of the murmur, as influenced by stroke volume or velocity of ejection, and proximity of the great arteries to the chest wall determine whether the murmur is audible with the stethoscope. Such murmurs are typically heard when a tachycardia exists, and in puppies, kittens, and young lean dogs; these animals tend to have a brisk circulation and a smaller thoracic cage with a narrow transverse diameter. The murmur tends to be of medium frequency, peaks in early to midsystole, usually ends before the second heart sound, and is best heard on the left side over the mitral or aortic valve or at the thoracic inlet. The murmur may be the result of turbulent flow into the pulmonary artery or aorta, or both.
Functional systolic murmurs are produced by increased velocity of blood within the cardiovascular system and by extracardiac factors.' Pleural or pericardial effusion, anemia, fever, hyperthyroidism, and tachycardia of any cause may produce functional murmurs. Such murmurs are often detected during anesthesia when a sinus tachycardia exists due to atropine administration.
Decreased blood viscosity and increased velocity of blood flow produce turbulence if the blood hemoglobin level falls below 6 mg/dl (packed cell volume is usually less than 15% to 20%). The functional murmur of anemia is usually of low intensity and high frequency and occurs during early systole to midsystole. Anemic murmurs are best heard over the mitral valve or aortic valve area.Functional murmurs may be audible when states of high cardiac output exist. Chronic anemia can lead to increased cardiac output, although the exact pathophysiology is not completely understood. The increased cardiac output is produced by both tachycardia and increased stroke volume. Reduction of blood viscosity is an important aspect of the increased cardiac output of anemia,' as is decreased peripheral resistance. Thyrotoxicosis is characterized by an increased cardiac output. There is probably a direct effect of thyroid hormone on the heart, producing a tachycardia. In addition, there is an increased sensitivity to circulating catecholamines, and there may also be a decreased peripheral vascular resistance.
Murmurs in diastole are unusual and occur in dogs and cats, most often across the aortic valve. The murmur of aortic regurgitation (insufficiency) strongly implies the presence of aortic valvular bacterial endocarditis. The murmur begins immediately after aortic valve closure (second heart sound) and is usually of high frequency, with a decrescendo configuration.
A continuous murmur extends from systole into diastole. Such a murmur results from blood flow continuing from a high-pressure to a lower-pressure area, despite semilunar valve closure. Patent ductus arteriosus is the prototype, and only common example in dogs and cats, of a continuous murmur that peaks in intensity at the second heart sound.
The minimum data base for patients with cardiac murmurs is a complete physical examination and characterization of the murmur (timing, intensity, frequency, location, and modulation). If the murmur is considered to be due to anemia or pathologic conditions, then the data base is extended. The possibility of a cardiac murmur being due to a high cardiac output state (anemia, hyperthyroidism) depends on the history and physical examination findings.
Minimum Data Base for Patients with Cardiac Murmurs Suspected
Sequential physical examination Sequential physical examination CBC, serum chemistry profile, UA if indicated by physical or historic findings
CBC, serum chemistry profile, UA Thoracic radiographs Electrocardiogram Special tests* *Phonocardiogram, echocardiogram, nonselective angiogram, selective cardiac catheterization
CBC, complete blood count; UA, urine analysis
If the cardiac murmur is thought to be pathologic, then the first steps that are indicated to generate a rank-ordered rule-out list are to consider the epizootiologic factors pertaining to the patient and to characterize the murmur. The age, breed (or type of dog), and historic evidence of a preexisting murmur should be assessed. Most puppies, kittens, and young dogs with loud murmurs (IV/VI to VI/VI) have a congenital heart defect. Most middle-aged to old, small, or miniature dog breeds, chondrodysplastic breeds, and beagles with heart murmurs have acquired mitral valvular insufficiency, often with concomitant tricuspid valvular insufficiency. However, even middle-aged dogs of any breed or type may have a congenital defect, and the client may or may not be aware of its presence; therefore, such a history should be ascertained. Unfortunately, because of incomplete physical examinations or poor skill on the part of the veterinarian, the absence of a history of a heart murmur in animals of any age does not rule out the possibility of a congenital defect.
Common Rule outs for Pathologic Heart Murmurs
Age and Type
Most Common Rule Outs
Puppies, kittens, young animals
Giant- and large-breed dog
Cardiomyopathy (dilated) Mitral insufficiency Tricuspid insufficiency Bacterial endocarditis
Mitral insufficiency Tricuspid insufficiency Bacterial endocarditis
Spaniels may develop heart murmurs due to either AV valvular fibrosis (endocardiosis), dilated cardiomyopathy, or both. Giant- and large-breed dogs, 4 years of age or older, may develop murmurs of mitral insufficiency secondary to dilated cardiomyopathy. Frequently, such dogs already manifest clinical signs of heart failure.
Most commonly, heart murmurs associated with bacterial endocarditis are aortic in origin, but systolic murmurs of mitral insufficiency are also common. The presence of a diastolic murmur should alert the clinician to the probability of bacterial endocarditis, especially when clinical and laboratory evidence is consistent with bacteremia. Fever, leukocytosis, monocytosis, lameness, hypoalbuminemia, increased serum alkaline phosphatase activity, hypoglycemia, and bacteriuria are variably present in dogs with bacteremia. "z The incidence of bacterial endocarditis in cats is unknown but is probably much lower than that in dogs.
Heart murmurs in middle-aged to older cats are most likely the result of cardiomyopathy, as are new murmurs in young adult cats. A careful history is necessary to rule out the possibility of the murmur having been present since birth (i.e., congenital heart defect).
The most likely disorders associated with many cardiac murmurs can be quickly rank-ordered based on epizootiologic factors. The characteristics of the heart murmur are then determined during the physical examination. The character of the murmur associated with a patent ductus arteriosus in young animals is pathognomonic, and the diagnosis can usually be supported by thoracic radiographic findings. Young dogs, especially those of a breed or type known to have an increased incidence of pulmonic stenosis, with cardiac murmurs that are clearly or suspected to be of pulmonic valve origin will usually have evidence of right ventricular hypertrophy and a right axis deviation on the electrocardiogram.
it is imperative that the patent ductus arteriosus and pulmonic stenosis be correctly diagnosed, since surgical correction or valvuloplasty is feasible. For most practical purposes, the mere diagnosis of a congenital defect of other types is adequate. Special tests are usually required for a specific diagnosis, and surgical intervention is seldom feasible.
The character of the acquired mitral insufficiency in older, small-breed dogs usually allows for the clinical diagnosis. Thoracic radiographs are indicated to assess the severity of cardiac enlargement and the therapeutic indications. The historic findings are also important in assessing the indications for treatments.
The historic and physical findings in dogs with dilated cardiomyopathy usually overshadow the significance of a cardiac murmur. The diagnosis is usually suspected during the physical examination and supported in most instances by radiographic and electrocardiographic abnormalities. Echocardiography is the safest and easiest method of confirming the diagnosis.
Feline cardiomyopathy and hyperthyroidism account for virtually all heart disease in the adult. The diagnosis is supported by abnormalities of thoracic radiographs or the electrocardiogram, or both. The diagnosis is confirmed by echocardiography and/or thyroid hormone assay.
Cyanosis in association with a heart murmur in a young animal is usually the result of a right-to-left shunt or severe left-sided congestive heart failure. In older dogs, cyanosis is associated with severe left-sided congestive heart failure.
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