AUSCULTATION HEART SOUNDS AND MURMURS James A. Shaver, MD OBJECTIVES Knowledge The student should be able to: a. draw the relationship between intracardiac and arterial pressures versus the normal and abnormal heart sounds; b. classify the types of systolic and diastolic murmurs on a pathophysiologic basis; c. list the factors that influence the intensity of normal and abnormal heart sounds Comprehension The student should be able to: a. understand the mechanisms of production of normal and abnormal heart sounds; b. appreciate the relationship between driving pressure, flow velocity, and the resultant turbulence in the production of murmurs; c. appreciate the concept of pulmonary and systemic vascular impedance and how it affects the timing and intensity of the second heart sound Application The student should be able to: a. predict the effect of altered hemodynamics on the timing and intensity of heart sounds and murmurs Analysis The student should be able to: a. differentiate systolic ejection murmurs versus pansystolic regurgitant murmurs by both their “murmur envelopes” as well as by their response to physiologic and pharmacologic maneuvers b. differentiate diastolic rumble and pandiastolic regurgitant murmurs by both their “murmur envelopes” as well as by their response to physiologic and pharmacologic maneuvers c. diagram the ausculatory findings of common valvular heart abnormalities Synthesis The student should be able to: a. diagnose the valvular lesion, given the diagram of the abnormal heart sounds and murmurs; b. predict alterations of intracardiac systolic and diastolic pressures on the basis of abnormal heart sounds and murmurs Evaluation The student should be able to: a. appreciate the value of cardiac auscultation in the overall evaluation of the cardiac patient CARDIAC AUSCULTATION Heart Murmurs A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of varying intensity (loudness), frequency (pitch), quality, configuration, and duration. Most authorities now agree that turbulence is the prime factor responsible for most murmurs; it occurs when blood velocity becomes critically high. The clinician’s description of a murmur should include its timing (systolic, diastolic, or continuous), location, radiation, and intensity. The location and radiation of a murmur are multifactorially determined by the site of origin, intensity, and direction of blood flow. The intensity of the murmur as heard at the chest wall is determined by the transmission characteristics of the tissue intervening between the source of the murmur and the stethoscope. Obesity, emphysema, and significant pleural or pericardial effusions will decrease the intensity of the murmur, whereas a thin, ascetic body type will often accentuate it. Systolic Murmurs. Systolic murmurs may be classified as systolic ejection or pansystolic regurgitant. Systolic ejection murmurs (SEM) are caused by forward flow across the left or right ventricular outflow tract, whereas pansystolic regurgitant murmurs are caused by retrograde flow from a high-pressure chamber into a lower-pressure chamber (Figure 1). A more detailed breakdown of this classification based on the physiologic mechanisms of production of these murmurs is shown in Figure 2. Classification of Murmurs Based on Physiologic Mechanism of Production Systolic murmurs are graded from 1 to 6. A grade 1 murmur is audible only after the listener has tuned in. Grade 2 is the faintest systolic murmur audible immediately after placing the stethoscope on the chest. Grade 5 is a loud murmur that cannot be heard with the stethoscope removed from the chest wall but can be heard with just the edge of the stethoscope touching the skin. A grade 6 murmur is audible with the stethoscope removed from the chest wall. Grade 3 and 4 are intermediate. Systolic murmurs of grade 3 or more in intensity are usually hemodynamically significant. Systolic thrills are usually associated with grade 4 or louder murmurs. A murmur’s intensity varies directly with the velocity of blood flow, which in turn is directly related to the pressure head that propels the blood across the murmur-producing area. Systolic ejection murmur. The midsystolic ejection murmur begins shortly after the left or right ventricular pressure exceeds aortic or pulmonary diastolic pressure sufficiently to open the aortic or pulmonic valve (Figure 3). Left Ventricular Ejection Dynamics Figure 3 Left ventricular ejection dynamics are illustrated by simultaneous recording of left ventricular and aortic pressure, aortic flow velocity and tine intensity envelope of murmur. During normal left ventricular ejection (left panel), peak flow velocity is early, with two-thirds of ventricular volume ejected during first half of systole. Murmur threshold may be exceeded during early peak flow and the corresponding murmur envelope is inscribed. Center panel shows exaggeration of the normal left ventricular ejection pattern, with large stroke volume as seen high –output states. With critical left ventricular outflow obstruction (right panel), rapid early ejection is no longer possible; flow velocity is increased and a contour becomes rounded and prolonged, producing a typical diamond-shaped murmur of aortic obstruction. The contour of the time-intensity pattern, or murmur envelope, parallels the contour of flow velocity, and the murmur is heard when the sound produced by the peak turbulence exceeds the audible threshold. The intensity of SEMs is related directly to peak flow velocity during ventricular ejection. Any condition that increases forward flow, such as exercise, anxiety, or the increased stroke volume associated with a long diastolic pause following a premature beat (Figure 4), will increase the intensity of the murmur. Likewise, conditions that decrease stroke volume or its rate of ejection (congestive heart failure or negative inotropic drugs) will decrease the intensity of the murmur. Figure 4 Figure 4 Left ventricular ejection dynamics are demonstrated with a The effect of a premature ventricular contraction (PVC) on simultaneous flow probe in the central aorta, together with peak aortic flow velocity and the intensity of a systolic the aortic phonocardiogram. Note that at rest, a very short ejection murmur. Following a long diastolic filling period ejection murmur is recorded simultaneously with peak flow with a greater filling of the left ventricle, there is a more in the central aorta. Following exercise, there is a marked forceful contraction resulting in larger stroke volume and increase in the peak aortic flow, and associated with this is a peak flow, and in turn, resulting in a louder systolic significant increase in the systolic ejection murmur due to the ejection murmur. Beat-to-beat variations in the intensity turbulence produced by the high flow during early ejection. of a systolic murmur caused by premature atrial or Any maneuver which increased flow during systole will ventricular contractions, and in patients with atrial increase the intensity of a systolic ejection murmur. fibrillation, allow differentiation between ejection and pansystolic regurgitant murmurs. Innocent Murmurs Innocent murmurs are systolic ejection in nature and are found in patients without evidence of physiologic or structural abnormalities of the cardiovascular system (Figure 5). This definition excludes murmurs produced by minor structural abnormalities such as a prolapsing mitral valve, even if such murmurs are hemodynamically insignificant. Although systolic murmurs produced by high cardiac output are functional, physiologic, and flow related, they are excluded from this definition because of the associated altered physiologic state. Innocent murmurs are less than grade 3 in intensity and vary considerably with body position and level of activity, and from one examination to another. They are found in approximately 30% to 50% of all children and are common in adolescents and young adults. In elderly persons, innocent murmurs caused by flow across the left ventricular outflow tract may have a musical quality and are frequently heard best at the apex. Figure 5 This is an example of an innocent systolic ejection murmur (SEM) as recorded in a 16 year old boy. The murmur is soft, crescendo- decrescendo, and ends well before S2. Normal physiologic splitting is present, and no diastolic filling sounds are recorded. The carotid pulse is normal. The murmur was recorded in the pulmonary artery during diagnostic catheterization by intracardiac phonocardiography, confirming its right- sided origin. Because both innocent murmurs and systolic ejection murmurs associated with physiologic or structural abnormalities of the cardiovascular system have the same mechanism of production, it is not the nature of the murmur itself that allows the differential diagnosis, but rather the associated cardiac findings. Therefore, the “company the murmur keeps” establishes the proper diagnosis; the innocent murmur must be found in the setting of an otherwise normal cardiovascular examination (Figure 6). Right and LV Outflow Obstruction A prominent systolic ejection murmur is almost always present with obstruction to right or left ventricular outflow, which may be located at the valvular, supravalvular, or subvalvular level. These murmurs are crescendo-decrescendo in nature, and their murmur envelope closely parallels the instantaneous ventricular-great vessel pressure gradient (Figure 7). As long as the cardiac output is maintained, the intensity and duration of the murmur increase as the stenotic lesion progressively narrows. When cardiac output decreases, the intensity of the murmur decreases, although careful auscultation will usually reveal that the murmur still has a prolonged duration. Figure 7 Simultaneous phonocardiogram, left ventricular and central aortic pressure are recorded in a 23 year old patient with congenital Valvular aortic Stenosis. After a premature ventricular contraction (PVC) note the marked increase in the Pansystolic Regurgitation This increased gradient results in an peak left ventricular pressure and the gradient across the stenotic aortic valve. Murmur increase in the stroke volume across the stenotic valve and results in a marked increase in the intensity and duration of the systolic ejection murmur. The murmur envelope of the systolic ejection murmur corresponds to the instantaneous pressure difference between the left ventricle and central aorta. Also note the marked decrease in the intensity of the murmur during the premature systole which correlates with the markedly decreased pressure gradient on this beat. Pansystolic regurgitant murmurs are produced from retrograde flow from a chamber of high pressure to one of low pressure (Figure 1). Because there is usually a large pressure differential between the two chambers throughout systole, the murmurs are pansystolic in duration, high pitched in blowing and quality and plateau-like in configuration. The pansystolic murmur of mitral regurgitation is heard best at the apex, often radiating into the axilla. There is a good correlation between the intensity of the murmur and the degree of mitral regurgitation which is closely related to the pressure gradient causing the regurgitant flow from the left ventricle into the left atrium (Figure 8). Interventions at increased left ventricular pressure such as hand grip, the squatting position of vasoconstrictor drugs increase the intensity of the regurgitant murmur where as measures which decrease the left ventricular pressure (inhalation of amyl nitrite) decrease the intensity of the murmur. In contrast to systolic ejection murmurs, these murmurs very little with changes and forward cardiac output or beat-to-beat changes in stroke volume (Figure 9). Figure 8 The simultaneous apex phonocardiogram, left ventricular and left atrial pressures are recorded in a patient with moderately severe mitral regurgitation. During the control observation, there is a significant pressure gradient between the left ventricle and the left atrium and this is associated with a Grade IV pansystolic murmur which is recorded well at the apex. Following the inhalation of amyl nitrite, the peak left ventricular pressure, the height of the left atrial V wave and the left ventricular left atrial pressure gradient are markedly decreased. Associated with this is a marked decrease in the intensity of the pansystolic murmur. In contrast, following the infusion of phenylephrine, a potent peripheral vascular constrictor, there is a marked increase in the peak left ventricular pressure, the height of the left atrial V wave, and the pressure differential between the left ventricle and the left atrium. Associated with this is a marked increase in the intensity of the apical pansystolic murmur due to the increased retrograde flow as a result of the increased pressure gradient between the left ventricle and left atrium. Figure 9 There is little variation in the intensity of the pansystolic murmur with variation in cycle. This lack of marked variation is very helpful in differentiating apical pansystolic murmurs vs ejection murmurs that are also heard at the apex, particularly in the elderly patient. left sternal border; however when a large right ventricle occupies the apex, it may be heard well lateral to the midclavicular line. It is usually easily identified by its typical augmentation and intensity with inspiration (Figure 10). Simultaneous observation of the JVP while listening to this murmur will help define its right-sided origin, revealing prominent V waves with rapid Y descents that augment with inspiration. The murmur of a ventricular septal defect is heard at the parasternal border of the fourth, fifth and sixth intercostals spaces, frequently associated with a systolic thrill. In contrast to mitral regurgitation, the murmur does not radiate well to the axilla and its intensity does not correlate with the degree of left to right shunting, nor does it have any respiration variation characteristic of tricuspid regurgitation. Figure 10 The murmur of severe tricuspid regurgitation (TR) increases in intensity with inspiration and is associated with a very prominent V wave, having a rapid Y descent. The onset of the V wave in severe tricuspid regurgitation is early, as shown by a prominent systolic (S) wave. Not all regurgitant murmurs are pansystolic. Common variants of regurgitant murmurs are illustrated in Figure 11, and the typical response of the late systolic murmur of mitral prolapse to postural changes is shown in Figure 12. Figure 11 In addition to the classic pansystolic regurgitant murmur seen in mitral regurgitation, tricuspid regurgitation and ventricular septal defect variants exist. In patients with small ventricular septal defects, the murmur which starts with S1 may suddenly stop during early or mid-systole. The proposed explanation is that as ventricular volume becomes smaller after maximal ejection, the defect seals shut and the murmur ceases. In acute mitral regurgitation, the regurgitant murmur may end well before A2 as the results of an extremely high left atrial V wave that abolishes the left ventricular –left atrial pressure gradient during late systole. S1 may be soft if a flair mitral leaflet is present and is preceded by a prominent S2. Audible expiratory splitting with an accentuated P 2 is present. Mid-to late systolic regurgitation murmurs may be due to papillary muscle dysfunction as well as to prolapsed of them mitral or tricuspid valve. In the latter conditions, the valve is competent in early systole, but as ventricular volume decreases, the leaflets become incompetent and the murmur begins and builds in late systole to become maximal at the same S 2. FINDINGS IN MITRAL VALVE PROLAPSE ARE ACTUALLY QUITE DIFFERENT FROM THOSE IN CONDITIONS CAUSING EJECTUR MURMURS Figure 12 Diastolic Murmurs. Diastolic murmurs are caused by either structural abnormalities of the atrioventricular and semilunar valves or increased flow across anatomically normal atrioventricular valves. In contrast to some systolic ejection murmurs that are innocent, diastolic murmurs should never be considered innocent. They have two basic mechanisms of production. Diastolic filling murmurs or rumbles are due to forward flow across the atrioventricular valves, whereas diastolic regurgitant murmurs are due to retrograde flow across an incompetent semilunar valve (Figure 13). A further breakdown of this classification based on the mechanism of production of each murmur is shown in Figure 14. Diastolic filling murmurs (rumbles). Diastolic rumbles are caused by forward flow across the atrioventricular valves, and their onset is delayed from their respective semilunar closure sound by the isovolumic relaxation period (Figure 13). When the atrial pressure exceeds the declining ventricular pressure, the atrioventricular valves open and filling begins. There are two phases of rapid ventricular filling, early diastole and presystole, the time at which these murmurs tend to be most prominent. Heart Murmurs Figure 13 Right panel: Flow diagram. Diastolic filling murmurs or rumbles are caused by forward flow across the atrioventricular valves, where as diastolic regurgitant murmurs are caused by retrograde flow across an incompetent semilunar valve. Left panel: Diagrammatic representation of the diastolic filling murmur and the diastolic regurgitant murmur as related to high-fidelity left ventricular (LV), aortic, and left atrial (LA) pressure. The diastolic filling murmur occurs during the diastolic filling period and is separated from the second heart sound (S2) by the isovolumic relaxation period (IRP). The rumbling murmur is most prominent during rapid early ventricular filling and presystole, terminated with the first heart sound (S1). The diastolic regurgitant murmur begins immediately after S2 and continues in a decrescendo fashion up to S1, closely paralleling the aortic-left ventricular diastolic pressure gradient. Classification of Murmurs Based on Physiologic Mechanism of Production The diastolic rumble of the stenotic mitral valve is heard best at the apex. As long as the stenotic valve has mobility, the murmur is introduced by an opening snap and is most prominent during the two phases of rapid ventricular filling (Figure 15). The duration of the mitral rumble correlates well with the duration of the diastolic gradient across the mitral valve, whereas its intensity is related to both the severity of the obstruction and the forward flow across the stenotic valve. In normal sinus rhythm, the presystolic murmur crescendos up to S1. The diastolic rumble of the stenotic tricuspid valve is usually heard in Figure 15 xiphoid area just off the left sternal border. In In mild mitral Stenosis, the diastolic gradient across valve is limited to the phases of rapid ventricular filling in early contrast to the presystolic murmur of mitral diastole and presystole. The rumble occurs during either or stenosis, which crescendos up to the both periods. As the stenotic process becomes severe, a large gradient develops across the valve during the entire diastolic filling period and the rumble persists through out the diastolic filling period. As the left atrial pressure becomes higher, the time from aortic valve closure sound (2) to the opening snap (OS) shortens. In severe mitral Stenosis, secondary pulmonary hypertension results in a louder pulmonic valve closure sound (P2) and splitting interval usually narrows. S1, first heart sound; S2, second heart sound. loud S1, the earlier onset of right atrial systole relative to left atrial systole results in a presystolic tricuspid murmur with a crescendo-decrescendo configuration, which ends before S1 and increases with inspiration (Figure 16). The Effect of Respiration on the Murmur of Tricuspid Stenosis Figure 16 In tricuspid stenosis (TR), note the crescendo-decrescendo presystolic murmur of TS is coincident with the rapid rise and decline of the A wave. Short mid-diastolic flow rumbles, often introduced by S3, are also produced by high flow across the normal or regurgitant atrioventricular valve (Figure 17). Diastolic Flow Rumbles Figure 17 Diastolic flow rumbles are caused by high flow across the atrioventricular valves in patients having atrial septal defect (ASD), ventricular septal defect (VSD), and patient ductus arteriosus. Shunting through the atrial septal defect results in high flow across the tricuspid valve, producing the tricuspid flow rumble (TFR). In both VSD and PDA, left-to-right shunting through the VSD or PDA, causes high flow across the mitral valve, resulting in a mitral flow rumble (MFR). With both MR and TR, the large regurgitation volume causes increased flow during early diastole across the atrio ventricular valve, resulting in MFR and TRF, respectively, both being introduced by a prominent third heart sound (S3). With inspiration, there is a significant increase in the intensity of the pansystolic regurgitant tricuspid murmur (PRM), the S3, and the TFR. No significant changes in the intensity of the diastolic flow rumbles occur with inspiration in patients have ADS, VDS, PDA or MR. A 2, aortic valve closure sound; M1, mitral valve closure sound; P2, pulmonary valve closure sound; SEM, systolic ejection murmur, T1, tricuspid valve closure sound. Pandiastolic aortic regurgitant murmurs. When the aortic valve becomes incompetent, a blowing high-pitched decrescendo diastolic murmur develops (Figure 13). The murmur of aortic regurgitation resulting from deformity of the aortic valve is usually best heard in the third and fourth left parasternal areas. When the murmur is heard best to the right of the sternum (Harvey’s sign), however, the clinician should be alerted to a possible aortic root etiology for the regurgitation. The murmur of mild aortic regurgitation is frequently quite faint and may be overlooked if the examiner does not listen with the patient sitting up and leaning forward, with the diaphragm of the stethoscope pressed firmly against the chest wall during held forced expiration. Pharmacological agents or maneuvers that increase or decrease the diastolic aortic left ventricular pressure gradient will increase or decrease the intensity of the regurgitant murmur. For example, prompt squatting or hand grip often elicits a faint aortic regurgitant murmur at the bedside, whereas inhalation of amyl nitrite will markedly decrease an easily heard aortic regurgitant murmur. In many patients, combined aortic stenosis and regurgitation are present when the deformed aortic valve is both obstructive and incompetent. In this situation, the classic to-fro murmur of aortic stenosis and regurgitation is present (Figure 18). Unlike a continuous murmur that reaches its peak intensity at about the time of S2, the to-fro murmur has two separate components that can be clearly distinguished by the presence of a silent period before the onset of the regurgitant component. Pulmonary regurgitation is most commonly found when severe pulmonary hypertension is present with dilation of the pulmonary artery. This type of pulmonary regurgitant murmur (Graham Steell’s murmur) is identical in contour and pitch to that of aortic regurgitation, both murmurs being produced by similar hemodynamics. Although these murmurs cannot be differentiated by their acoustic qualities, the Graham Steell’s murmur is almost always accompanied by physical findings of severe pulmonary hypertension. Figure 18 During abnormal communication between high-pressure and low-pressure systems, large pressure gradient exists throughout the cardiac cycle, producing continuous murmurs. A classic example is patent ductus arteriosus. At times, this type of murmur is confused with a to-fro murmur, which is a combination of a systolic ejection murmur and the murmur of semilunar valve incompetence. The classic example of to-fro murmur is aortic stenosis and regurgitation. The continuous murmur builds to a crescendo around second heart sound (S 2) where as the to-fro murmur has two components, a mid- systolic and early diastolic component with a silent period between the two murmurs. Continuous murmurs. A continuous murmur Table I is defined as one that begins in systole and Physiologic classifications of continuous extends through S2 into part or all of diastole. It murmurs does not necessarily have to occupy the entire cardiac cycle; thus a systolic murmur that extends into diastole without stopping at S2 is A Continuous murmurs caused by rapid blood flow 1. Venous hum considered to be continuous, even if it fades 2. Mammary souffle away before the subsequent S1. Continuous 3. Hemiangioma 4. Hyperthyroidism murmurs can be congenital or acquired. 5. Acute alcoholic hepatitis Although it is beyond the scope of this lecture to 6. Hyperemia of neoplasm (hepatoma renal cell carcinoma, Paget’s disease) detail the many conditions that may cause a B. Continuous murmurs caused by high-to-low pressure shunts continuous murmur, a few of the more common 1. Systemic artery to pulmonary artery (patent ductus arteriosus, aortopulmonary window, truncus arteriosus, clinical conditions are reviewed. A more pulmonary atresia, anomalous left coronary, complete physiologic classification of bronchiectasis, sequestration of the lung) 2. Systemic artery to right heart (ruptured sinus of valsalva, continuous murmurs is provided in Table I. coronary artery fistula) 3. Left-to-right atrial shunting (Lutembacher’s syndrome, mitral atresia plus atrial septal defect) The differential diagnosis of a continuous 4. Venovenous shunts (anomalous pulmonary veins, murmur should include the benign cervical portosystemic shunts) 5. Arteriovenous fistula (systemic or pulmonic) venous hum heard commonly in children, in C. Continuous murmurs secondary to localized arterial nearly all pregnant women, and in persons with obstruction 1. Coarctation of the aorta high cardiac output. This murmur is usually 2. Branch pulmonary stenosis poorly heard in the supine position, and its 3. Carotid occlusion 4. Ciliac mesenteric occlusion 5. Renal occlusion 6. Femoral occlusion 7. Coronary occlusion presence in an adult in this position strongly suggests a hyperdynamic circulatory rate. Its peak intensity is in the supraclavicular fossa just lateral to the sternocleidomastoid muscle and is usually more prominent on the right side, peaking in early diastole. A cervical venous hum can be terminated easily by digital compression of the JVP (Figure 19). Another benign continuous murmur is a mammary souffle, which occurs in 10% to 15% of pregnant women during the second and third trimesters and in early postpartum lactation. This murmur may be obliterated by firm pressure on the stethoscope or by digital pressure lateral to the site of auscultation. A patent ductus arteriosus is a classic example of a cardiovascular congenital anomaly in which there is shunting from a high-pressure systemic to the low- pressure pulmonary circulation, resulting in a large pressure gradient between the two circulations throughout the cardiac cycle. This murmur is heard best in the left infraclavicular area and the second left intercostal space, and peaks in intensity at the time of S2. Atriovenous fistulas between peripheral vessels produce a classic continuous murmur with systolic accentuation caused by the shunting of blood at high flow rates from a high-pressure artery into a low-pressure vein. This condition should always be considered as a potential cause for heart failure. These murmurs are best heard at the site of the fistula and local compression on the venous side decreases its intensity. Complete obliteration of the fistula abruptly terminates the murmur. Continuous murmurs in adults are also caused by severe localized arterial obstructions. Although partially occluded arteries usually have only a delayed systolic murmur, this murmur may be continuous if the obstruction is critical, and adequate collateral flow is not available. Such murmurs are commonly heard directly over the carotid, subclavian, and femoral arteries. Continuous murmurs caused by obstruction of the renal or mesenteric arteries can also be heard by careful auscultation over the back or abdomen, respectively. Questions: 1. All of the following statements regarding cardiac murmurs are true but one: a. The regurgitant murmur of aortic regurgitation will increase in intensity with an abrupt squatting. b. The pansystolic murmur of tricuspid regurgitation will increase in intensity with inspiration. c. The late systolic murmur of mitral valve prolapse will begin later in systole with the assumption of an upright posture. d. The systolic ejection murmur of severe calcific aortic stenosis may become nearly inaudible with congestive heart failure and low cardiac output. e. The continuous murmur of a patent ductus arteriosus peaks in intensity around the second heart sound while the to-fro murmur of aortic stenosis and aortic regurgitation is silent around the second heart sound. 2. All of the following statements regarding innocent murmurs are true but one: a. Innocent murmurs are always systolic ejection in nature. b. Innocent murmurs are frequently seen in “the company” of a physiologic S3 in adolescents. c. Innocent murmurs are frequently introduced by a loud ejection sound. d. Innocent murmurs are usually grade 1 to grade 3 in intensity and vary from exam to exam as well as with changes in position. e. The functional systolic ejection murmurs of anemia or thyrotoxicosis are not considered innocent because of the altered physiologic state, even though there is no structural cardiac abnormality.