Clinical Vignette

An apparently healthy 5-month-old mixed-breed dog presents to you for a routine wellness examination. According to the owner, the puppy is showing no signs of exercise intolerance, weakness, coughing, or respiratory distress.

Clinical Examination

A grade 5/6 left basilar systolic murmur is noted on thoracic auscultation. There is wide radiation of the murmur over right cranial thorax. Mucous membranes are pink with a normal capillary refill time. Femoral pulses are strong and regular.

What are your differential diagnoses for the type of murmur auscultated on physical examination? How would you prioritize your differential list? What is your diagnostic plan for this patient?

Problem Definition

Normal Physiology

In normal small animal patients, the only transient sounds heard are the first (S1) and second (S2) heart sounds. The first heart sound is associated with closure of the left and right atrioventricular valves (mitral and tricuspid, respectively), and signifies the onset of systole. It is best heard over the right and left apices. The first heart sound is longer, louder, and of lower frequency than the second heart sound. The second heart sound signifies the end of systole and is associated with the closure of the semilunar (aortic and pulmonic) valves. It is higher pitched and of slightly shorter duration compared with the first heart sound (Sisson and Ettinger 1999; Prosek 2005). The second heart sound is best heard over the aortic and pulmonic valve regions. Normally, the aortic component (A₂) precedes the pulmonic component (P₂) by an inaudible interval of time. Both S1 and S2 are relatively high-frequency sounds and are best heard with the diaphragm of the stethoscope. Proper identification of both S1 and S2 is critical for timing of abnormal cardiac sounds, including both transient sounds and murmurs.

Normally, blood flow through the heart is laminar. Turbulent blood flow creates vibrations and occurs when laminar flow is disturbed. Such sound vibrations arise from high-velocity flow through the great vessels, ejection of blood into a dilated great vessel, or decreased viscosity of blood (e.g., anemia). Murmurs may also result from flow disturbances within the heart, including valve insufficiency, valvular stenosis, or shunts. Reynold’s number describes the relationship between murmurs and blood viscosity, velocity of blood flow, and vessel diameter. This equation describes the probability of a flow disturbance creating a murmur, with a higher value representing an increased probability of producing turbulence that would result in murmur (Rushmer 1970):

Pathophysiology

The first heart sound may be split into two components, the mitral and tricuspid elements, due to asynchronous contraction of the left and right ventricles. Splitting of S1 occurs occasionally in healthy, large-breed dogs. More commonly, a split S1 occurs as a result of electrical disturbances, including a right or left bundle branch block, right ventricular pacing, or ventricular ectopy (Sisson and Ettinger 1999; Prosek 2005). Splitting of the second heart sound occurs in a variety of patients. Physiologic splitting of S2 occurs in young, healthy, large-breed dogs during inspiration. Inspiration decreases intrathoracic pressure and augments venous filling of the right side of the heart. The increased volume of blood within the right ventricle requires a slightly prolonged ejection time, delaying the pulmonic component (P2) compared to the aortic component (A2) of S2. During expiration, the difference in right and left ventricular ejection times is not apparent (Ettinger and Suter 1970; Smetzer et al. 1970; Sisson and Ettinger 1999; Braunwald and Perloff 2005). Pathologic splitting of the second heart sound is due to either the delay of A₂ or further delay of P₂. A delay of the aortic component is referred to as “paradoxical splitting of S2,” and can occur secondary to aortic stenosis, conduction disturbances (i.e., left bundle branch block), systemic hypertension, right ventricular pacing, or ventricular ectopy. Splitting of S2 secondary to a delayed P₂ may also occur secondary to conduction disturbances (i.e., right bundle branch block) or ventricular ectopy. The most common cause of a split S2 is pulmonary hypertension secondary to advanced heartworm disease or associated with certain congenital defects, such as a reversed patent ductus arteriosus (PDA) (Fig. 18-1). A tympanic S2 may also be heard in patients with severe pulmonary hypertension. “Fixed” splitting of S2 occurs with atrial septal defects (ASDs). Unlike patients with pulmonary hypertension, the interval between A₂ and P₂ does not vary with the phase of respiration (Ettinger and Suter 1970; Sisson and Ettinger 1999; Braunwald and Perloff 2005; Prosek 2005).

FIGURE 18-1. Split second heart sound in a patient with severe pulmonary hypertension associated with a reversed patent ductus arteriosus. S1, first heart sound; A2, aortic component of second heart sound; P2, pulmonic component of second heart sound.

As mentioned previously, S1 and S2 are the only transient heart sounds that can be auscultated in normal dogs and cats. The presence of a third (S3) or fourth (S4) heart sound signifies a gallop rhythm. The third and fourth heart sounds are low-frequency diastolic sounds that are best heard with the bell of the stethoscope. Both of these sounds are associated with decreased compliance of the ventricles. The third heart sound (S3) or ventricular gallop is associated with early ventricular filling and is heard in patients with diastolic dysfunction and very high filling pressures. Typical patients with an S3 gallop include dogs with congestive heart failure secondary to dilated cardiomyopathy, PDA, or severe mitral regurgitation (Prosek 2005). An atrial gallop (S4) is associated with atrial systole and is best heard in patients with impaired ventricular relaxation without significantly elevated filling pressures. In these patients, a vigorous atrial contraction is required to optimize ventricular filling and maintain cardiac output. Typical patients with an S4 gallop are cats with ventricular hypertrophy secondary to hyperthyroidism, systemic hypertension, or hypertrophic cardiomyopathy (Fig. 18-2) (Detweiler and Patterson 1967). An S4 gallop may also be audible in patients with third-degree atrioventricular block (Prosek 2005). Tachycardia may cause S3 and S4 gallops to be superimposed, resulting in a summation gallop (Detweiler and Patterson 1967; Ettinger and Suter 1970; Prosek 2005).

FIGURE 18-2. Phonocardiographic recording of a gallop rhythm in a cat diagnosed with hypertrophic cardiomyopathy. S1, first heart sound; S2, second heart sound; S4, fourth heart sound.

Clicks are high-pitched transient heart sounds that are heard during systole. Ejection clicks are best heard over the aortic or pulmonic valve region. These sounds occur secondary to great vessel dilatation or to systolic movements of abnormal semilunar valves. Ejection sounds are most commonly heard in patients with pulmonic stenosis when fused and thickened pulmonic leaflets dome during systole. Ejection sounds are usually recognized via phonocardiogram rather than by auscultation (Ettinger and Suter 1970; Sisson and Ettinger 1999). Midsystolic clicks are heard during early to midsystole over the mitral or tricuspid valve area (Fig. 18-3). Such clicks are heard in human patients with early degenerative valve disease in which valvular prolapse occurs. The vibrational sound likely results from the tensing of chordae tendinae or redundant valvular tissue. This is the same mechanism that is thought to be responsible for systolic clicks in canine patients. Systolic clicks may be intermittent and may change their position within systole from beat to beat (Smetzer et al. 1970; Braunwald and Perloff 2005; Prosek 2005). As degeneration of the valve increases in severity, the midsystolic click is obscured by the increasing intensity of the mitral regurgitant murmur. Midsystolic clicks can be distinguished from gallop sounds by recognizing that they are systolic and not diastolic in timing. Because clicks are higher frequency than gallop sounds, they are best heard with the diaphragm rather than with the bell of the stethoscope.

FIGURE 18-3. Phonocardiogram showing high-frequency systolic clicks occurring at various points within systole. Midsystolic clicks are caused by valvular prolapse in canine patients with degenerative valve disease. S1, first heart sound; S2, second heart sound; C, systolic click.

Early diastolic sounds are rare auscultatory findings in dogs and cats. A pericardial knock occurs with restrictive pericardial disease (e.g., constrictive pericarditis). It is caused by rapid ventricular filling that is suddenly halted by a restrictive pericardium. A tumor plop occurs with a mobile mass lesion within the atrial lumen. The sound is thought to result from abrupt movement of the mass into the atrioventricular valve orifice during diastole. Since such types of tumors are extremely rare in dogs and cats, this transient heart sound is very uncommon. An opening snap may be found in patients with mitral stenosis and is also exceedingly rare in small animals. This sound results from a mobile but tethered mitral leaflet that bows open during early diastole due to high filling pressures (Sisson and Ettinger 1999; Perloff 2000; Braunwald and Perloff 2005).

Cardiac Murmurs

The first step in classification is to provide a description of timing, intensity, point of maximal intensity (PMI), radiation, pitch (frequency), and shape of the murmur (Table 18-1).

Murmurs are classified according to their timing within the cardiac cycle. Murmurs can be systolic, diastolic, or continuous in timing. Systolic murmurs start during or after the first heart sound, whereas diastolic murmurs begin during or following the second heart sound. All diastolic murmurs terminate prior to the onset of the first heart sound. Continuous murmurs are audible throughout the cardiac cycle. The timing of murmurs can be further classified according to their occurrence within a certain phase of the cardiac cycle, and as such are defined as “presystolic,” “holo-”/“pan-” (throughout), “proto-” (early), “meso-” (middle), and “tele-” (late). (Detweiler and Patterson 1967; Prosek 2005).

TABLE 18-1. Description of murmurs on the basis of auscultatory characteristics

Murmurs are also described according to their intensity (Table 18-2) (Ettinger and Suter 1970). This grading scale was modified from the original grading system described by Freeman and Levine in 1933 (Freeman and Levine 1933). Although such a scale is very subjective, grading of murmur-intensity facilitates communication between clinicians and assists in formulating differential diagnoses. It is important to remember that murmur intensity does not necessarily correlate with severity of disease. For example, a dog may have very severe myocardial dysfunction due to idiopathic dilated cardiomyopathy but may have no murmur or a minimally audible murmur.

The PMI refers to the location where the murmur is heard the loudest. Most descriptions of the PMI use valve regions (i.e., pulmonic, aortic, mitral, tricuspid) to name the location of murmurs in dogs. A more general description of apex versus base may also be used. Most clinicians find this description scheme impractical for cats. Instead, cat murmurs are more often described as sternal versus parasternal, cranial versus caudal, and left versus right. Radiation further qualifies the location of the murmur by describing the direction in which the murmur spreads across the thorax. Murmurs typically radiate in the direction of the flow disturbance responsible for the murmur. For example, the murmur of subaortic stenosis often radiates loudly cranially over the right thorax as well as over the carotid arteries.

TABLE 18-2. Classification of murmur intensity

TABLE 18-3. Murmur classification on the basis of timing and configuration

Pitch refers to the frequency of the murmur and is also a subjective assessment. Higher frequency murmurs are best heard with the diaphragm of a stethoscope, whereas lower frequency murmurs are most audible with the stethoscope bell. Most murmurs are of mixed frequency with no dominant frequency audible. Such murmurs are often described as “harsh.” Certain murmurs are referred to as “musical” and consist of a dominant frequency. Musical murmurs may be produced by vibration of a valve or vessel wall at a pure frequency.

Finally, murmurs are classified according to the shape of vibrations. The shape refers to the configuration or profile of the murmur as it is recorded on a phonocardiogram (Table 18-3). Commonly used terms include “plateau,” “crescendo,” “decrescendo,” and “crescendo–decrescendo.” Plateau murmurs maintain relatively the same intensity throughout their occurrence; such murmurs have a “band-shaped” configuration. Crescendo–decrescendo murmurs increase in intensity to a peak and then taper in intensity, creating a “diamond-shaped” configuration (Detweiler and Patterson 1967). Examples of these types of murmurs are provided throughout the remainder of the chapter.

Clinical Associations

There are many pathologic causes of cardiac murmurs. Such examples include blood flow through stenotic valves, incompetent valves, or abnormal connections between chambers or vessels. It is most logical to divide the common types of murmurs on the basis of timing (Table 18-3).

Systolic Murmurs

Mitral Regurgitation. The murmur of mitral insufficiency is harsh (mixed frequency) and begins immediately after the first heart sound. It increases in intensity until it reaches a constant intensity (“plateau”) that continues throughout systole (Fig. 18-4). Some examples of mitral regurgitant murmurs may be decrescendo if mild in severity. The murmur can be musical or high pitched and may change in quality within the same individual (Ettinger and Suter 1970). When mitral regurgitation is present, S1 becomes louder in intensity. If the mitral regurgitant murmur is loud enough and of long enough duration, it may obscure the second heart sound. Systemic hypertension will increase the intensity of the murmur, whereas hypotension will decrease the intensity of mitral regurgitation. Inspiration may decrease the intensity of mitral regurgitation, while expiration may increase the intensity (Smetzer et al. 1970). The PMI is over the left apex, but radiation dorsally and over the right thorax is common.

FIGURE 18-4. Phonocardiographic tracing of the plateau-shaped systolic murmur of mitral regurgitation. S1, first heart sound; S2, second heart sound; M, systolic murmur.

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