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A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of varying intensity (loudness), frequency (pitch), quality, configuration, and duration.273 Although the exact physical principles that govern the production of murmurs have been debated for years, most authorities now agree that turbulence is the prime factor responsible for most murmurs. Turbulence arises when blood velocity becomes critically high due to high flow, flow through an irregular or narrow area, or a combination of both. Leatham has attributed the production of murmurs to three main factors: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these factors is operative.

While the intensity of a systolic murmur is not always proportional to the hemodynamic disturbance, grading the loudness of a murmur from 1 to 6 as described by Freeman and Levine274 is generally used. A grade 1 murmur is so faint that it can be heard only with special effort. A grade 2 murmur is faint but can be heard easily. A grade 3 murmur is moderately loud, a grade 4 murmur is very loud, and a grade 5 murmur is extremely loud and can be heard if only the edge of the stethoscope is in contact with the skin but cannot be heard if the stethoscope is removed from the skin. A grade 6 murmur is exceptionally loud and can be heard with the stethoscope just removed from contact with the chest. Experience has shown that systolic murmurs of grade 3 or more in intensity are usually hemodynamically significant.275 Systolic thrills usually are associated with murmurs of grade 4 or louder. The intensity of the murmur varies directly with the velocity of blood flow across the area of murmur production. The velocity, in turn, is directly related to the pressure head that drives the blood across the murmur-producing area. For example, high velocity of flow through a small VSD produces a loud murmur, whereas a large flow at low velocity through an ASD produces no murmur. The intensity of a murmur as auscultated at the chest wall is also determined by the transmission characteristics of the tissues intervening between the source of the murmur and the stethoscope. Obesity, emphysema, and the presence of significant pericardial or pleural effusion will decrease the intensity of a murmur, whereas a thin, asthenic body habitus often will accentuate it.



The frequency of a murmur bears a direct relationship to the velocity of blood flow, as does the intensity of the murmur. The low-velocity flow resulting from a small pressure head across a stenotic mitral valve produces a low-pitched rumbling murmur, whereas the large diastolic pressure gradient across a regurgitant aortic valve causes a high-pitched murmur. A recent study has further demonstrated that the dominant frequencies contained in heart murmurs due to stenotic lesions are directly related to the instantaneous jet velocities distal to the associated obstruction. Occasionally, the frequency composition of the same systolic murmur may vary, depending on the area auscultated. For example, the systolic murmur of aortic stenosis frequently sounds higher-pitched at the apex than at the base.276 Some murmurs such as the "cooing dove" regurgitant murmur of a ruptured or retroverted aortic cusp, the systolic "whoop" or "honk" of mitral valve prolapse, or the high-pitched systolic murmur of a degenerated bioprosthetic valve-have a very distinctive musical quality.

In addition to the intensity and frequency of murmurs, their timing also should be described. There is seldom any difficulty distinguishing between systole and diastole, since systole is considerably shorter at normal heart rates. At rapid heart rates, however, the durations of these two intervals approach each other. Under such circumstances, the examiner usually can time the murmur by simultaneous palpation of the lower right carotid artery or can rely on the fact that the second heart sound (S2) is usually the louder sound at the base. Once S2 is identified, murmurs can be located properly in the cardiac cycle as systolic or diastolic. If the murmur in question is at the apex, the proper timing can be ensured by the "inching" technique popularized by Harvey and Levine.215 This consists of slowly moving the stethoscope down from the base to the apex while repeatedly fixing the cardiac cycle in mind, using S2 as a reference point. With sinus tachycardia, carotid sinus pressure may temporarily slow the rate and make it possible to differentiate systole from diastole. Continuous murmurs are heard throughout the cardiac cycle in systole and diastole and usually have their peak intensity around S2.

The location and radiation of a murmur are determined multifactorially by the site of origin, intensity, and direction of blood flow, as well as by the physical characteristics of the chest. The duration and time intensity contour (murmur envelope) of a specific murmur are intimately related to the instantaneous pattern of blood flow velocity causing the murmur.

Systolic Murmurs

Systolic murmurs may be classified into two basic categories-ejection (midsystolic) murmurs and regurgitant murmurs. This simple classification is attractive because it has a physiologic as well as a descriptive basis. Systolic ejection murmurs are due to forward flow across the LV or RV outflow tract, whereas systolic regurgitant murmurs are due to retrograde flow from a high-pressure cardiac chamber to a low-pressure chamber.277


The systolic ejection murmur begins shortly after the pressure in the left or right ventricle exceeds the aortic or pulmonic diastolic pressure sufficiently to open the aortic or pulmonic valve. As a result, there is a delay between the Sj, which occurs shortly after AV pressure crossover, and the beginning of the murmur (Fig. i0-ZZ). The murmur then waxes and wanes in a crescendo-decrescendo fashion often described as "diamond shaped" or "spindle shaped" in configuration. The murmur ends before the semilunar valve closure on the side from which it originates. The contour of the time-intensity pattern or envelope of the murmur corresponds to the contour of the flow velocity, and the murmur is heard when the sound produced during the peak turbulence exceeds the audible threshold. Thus not only is the overall intensity of the murmur proportional to the rate of ventricular ejection, but also its shape depends on the instantaneous flow velocity during the period of ejection. As can be seen in Fig. j0-78, during normal LV ejection, a disproportionately large volume flow occurs in early systole. If velocity of flow exceeds the murmur threshold, a short midsystolic or ejection murmur results, and its envelope corresponds to the flow velocity pattern. If the stroke volume of the ventricle is increased, this pattern of ejection persists in an exaggerated fashion; the resulting murmur has a tendency to peak early in systole and fade out about halfway through the ejection phase. Such murmurs have been referred to as "kite shaped" and are common in high-output states or conditions such as aortic regurgitation or heart block, where stroke volume is high.

Decreased Ejection

Figure 10-77: Midsystolic ejection murmurs are caused by forward flow across the LV or RV outflow tract, whereas pansystolic regurgitant murmurs are caused by retrograde flow from a high-pressure cardiac chamber to a low-pressure one. (Left) Diagrammatic representation of the midsystolic ejection murmur and the pansystolic regurgitant murmur, as related to LV, aortic, and left atrial (LA) pressures. The systolic ejection murmur occurs during the period of LV ejection; the onset of the murmur is separated from S1 by the period of isovolumic contraction and the crescendo-decrescendo murmur terminates before A2. The pansystolic regurgitant murmur begins with, or may replace, S1, and the murmur continues up to and through A2 as LV pressure exceeds left atrial pressure during the period of isovolumic relaxation. The murmur has a plateau configuration and varies little with respiration. (Right) Flow diagram. (Left panel reproduced from Reddy PS, Shaver JA, Leonard JJ. Cardiac systolic murmurs: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971; 14:19. Entire figure reproduced with permission from Shaver JA. Systolic murmurs. Heart Dis Stroke 1993; 2:10.)

Figure 10-77: Midsystolic ejection murmurs are caused by forward flow across the LV or RV outflow tract, whereas pansystolic regurgitant murmurs are caused by retrograde flow from a high-pressure cardiac chamber to a low-pressure one. (Left) Diagrammatic representation of the midsystolic ejection murmur and the pansystolic regurgitant murmur, as related to LV, aortic, and left atrial (LA) pressures. The systolic ejection murmur occurs during the period of LV ejection; the onset of the murmur is separated from S1 by the period of isovolumic contraction and the crescendo-decrescendo murmur terminates before A2. The pansystolic regurgitant murmur begins with, or may replace, S1, and the murmur continues up to and through A2 as LV pressure exceeds left atrial pressure during the period of isovolumic relaxation. The murmur has a plateau configuration and varies little with respiration. (Right) Flow diagram. (Left panel reproduced from Reddy PS, Shaver JA, Leonard JJ. Cardiac systolic murmurs: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971; 14:19. Entire figure reproduced with permission from Shaver JA. Systolic murmurs. Heart Dis Stroke 1993; 2:10.)

Aorta Flow Velocity
Figure 10-78: The simultaneous time-intensity course of the murmur "envelope," aortic flow velocity, and

LV and central aortic pressure. During normal LV ejection (left), peak flow velocity is early, with two-thirds of the ventricular volume ejected during the first half of systole. The murmur threshold may be exceeded during the early peak flow and the corresponding murmur envelope inscribed. (Center) Exaggeration of the normal pattern of LV ejection with a high stroke volume, as in high-output states. With critical aortic stenosis (right), rapid early ejection is no longer possible; the flow velocity is increased, and the contour becomes rounded and prolonged, producing the typical diamond-shaped murmur of aortic stenosis. (Modified from Reddy PS, et al. Cardiac systolic murmurs: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971; 14:4. Reproduced with permission from the publisher and the authors.)

The flow characteristics of normal RV ejection are somewhat different. Early ejection rates are not nearly as high, and the flow curve peaks somewhat later, having a more rounded contour. This flow pattern may well explain some of the long systolic ejection murmurs heard in ASDs and the straight-back syndrome, where only minimal gradients are found across the RV outflow tract.278 With true valvular obstruction, rapid early ejection is no longer possible; the aortic flow velocity patterns become rounded, resulting in the more symmetric murmur of aortic stenosis. In such cases, the instantaneous flow pattern is determined by the instantaneous pressure head with the resulting high correlation between the contour of the pressure gradient and the murmur envelope. If LV or RV obstruction is severe, systole is prolonged, and closure sound of the semilunar valve is delayed. The murmur, however, always stops before the closure sound on the side from which it originates, although it may envelop the closure sound of the opposite side of the circulation. Because of the high correlation between the shape of the murmur and its underlying flow velocity characteristics, careful attention must be given during auscultation to the shape and duration of the murmur as well as to its intensity.

The intensity of ejection murmurs closely parallels changes in cardiac output. Any condition that increases forward flow-such as exercise, anxiety, fever, or increased stroke volume associated with the long diastolic filling period after a premature beat-increases the intensity of the murmur. Likewise, conditions that decrease cardiac output-congestive heart failure, beta blockade, or other negative inotropic agents-will decrease the intensity of the ejection murmur. This intimate relationship to flow, particularly with beat-to-beat variations, usually will allow the clinician to differentiate a systolic ejection murmur from a systolic regurgitant murmur. Furthermore, definitive diagnosis of the systolic murmur often can be made during auscultation by careful attention to the response of the murmur to various bedside maneuvers that alter the flow and loading conditions of the heart.279 These maneuvers include respiration, the strain and release phases of the Valsalva maneuver, standing, squatting, passive leg elevation, isometric hand-grip exercise, inhalation of amyl nitrite, and transient arterial occlusion.

Innocent Murmurs

Innocent murmurs are always systolic ejection in nature and occur without evidence of physiologic or structural abnormalities in the cardiovascular system when peak flow velocity in early systole exceeds the murmur threshold.275 These murmurs are almost always less than grade 3 in intensity and vary considerably from examination to examination and with body position and level of physical activity. They are not associated with a thrill or with radiation to the carotid arteries or axillae. They may arise from flow across either the normal LV or RV outflow tract and always end well before semilunar valve closure.

Innocent murmurs are found in approximately 30 to 50 percent of all children. In young children, especially children aged 3 to 8 years, the vibratory systolic (Still's) murmur is common. It has a very distinctive quality described as "groaning," "croaking," "buzzing," or "twanging." It is heard best along the left sternal border at the third or fourth interspace and disappears by puberty. Considerable controversy exists as to the origin of the vibratory systolic murmur. Regardless of the exact cause, most authorities agree that this murmur originates from flow in the LV outflow tract.

Innocent systolic ejection murmurs also have been attributed to flow in the normal RV outflow tract and have been termed innocent pulmonic systolic murmurs because the site of their maximal intensity is auscultated best in the pulmonic area at the second left interspace with radiation along the left sternal border. These are low to medium in pitch, with a blowing quality, and are common in children, adolescents, and young adults. Stein et al.,280 who used high-fidelity catheter-tipped micromanometers to record intracardiac sound and pressure in the aorta and pulmonary artery in adults with normal valves, invariably recorded the ejection murmur in the region of the aortic valve. They concluded that these murmurs, despite their precordial location, were aortic in origin.

In adults over age 50, innocent murmurs due to flow in the LV outflow tract are often heard and may be of a higher frequency, with a musical quality, and frequently loudest at the apex. They may be associated with a tortuous, dilated sclerotic aortic root, often in the setting of systolic hypertension. Mild sclerosis of the aortic valve also may be present.

The preceding descriptive breakdown of innocent murmurs is based primarily on age, precordial location, and distinctive acoustic qualities. Since all these murmurs are equally innocent, and because there is considerable overlap among them with respect to origin, transmission, and frequency composition, they are best characterized as systolic ejection murmurs without associated abnormalities of the cardiovascular system. Since both innocent and pathologic ejection murmurs have the same mechanism of production, it is "the company the murmur keeps" that affords the differential diagnosis of the pathologic systolic ejection murmur from the innocent murmur2^! Fig. 10-79).

For a murmur to be considered innocent, the examination of the cardiovascular system must disclose no abnormalities. Blood pressure and contour of the carotid, femoral, and brachial arteries always should be evaluated carefully. For example, a seemingly innocent murmur in the setting of hypertension, particularly in a younger patient, always should suggest the diagnosis of coarctation of the aorta, which can be diagnosed readily by palpation of weak or nearly absent femoral pulses and confirmed by taking the blood pressure in the lower extremities. There should be no elevation of the jugular venous pulse, and the contour of the jugular pulse should be normal, without exaggeration of either the a or v wave. Evidence of cardiac enlargement on physical examination should be absent, and palpation of the apex in the left lateral position should show no evidence of a presystolic impulse, sustained systolic motion, or hyperdynamic circulation. On auscultation, normal physiologic splitting should be present. A physiologic S3 is often present in association with an innocent murmur in children and young adults but should not be heard after age 30. An S4 is rarely heard in normal children and adults (younger than 50 years) and always should be considered to be abnormal when associated with a presystolic impulse. Systolic ejection sounds of valvular origin as well as midsystolic nonejection sounds should be absent because their presence points to minor abnormalities of the semilunar and AV valves, respectively (see Fig. 10-79). The remainder of the physical examination should show no evidence of a cardiac cause of pulmonary or systemic congestion. In almost all patients with innocent murmurs, the ECG and the cardiac silhouette on chest x-ray should be normal.

The supraclavicular arterial murmur or bruit is a common finding in normal individuals, particularly children and adolescents. These murmurs are maximal in intensity above the clavicles and tend to be louder on the right, although they are often heard bilaterally. The bruit begins shortly after S1, is diamond-shaped, and is of brief duration, usually occupying less than half of systole. Although the exact mechanism is unknown, it is related to peak flow velocity near the origin of the normal subclavian, innominate, or carotid artery. When particularly prominent, this murmur may transmit to the basal region of the heart and simulate a systolic ejection murmur. However, unlike the cardiac ejection murmur, the supraclavicular murmur is always louder above the clavicles than below them. Complete compression of the subclavian artery may cause the murmur to disappear completely, whereas partial compression occasionally may intensify it. Hyperextension of the shoulders is a simple bedside maneuver that may decrease the intensity of the murmur and cause it to disappear completely. In the adult, the supraclavicular murmur must be distinguished from the murmur of true organic carotid obstruction, this latter murmur being longer, often extending through S2, and frequently associated with a history suggestive of transient ischemic attacks.

Functional Systolic Ejection Murmurs

Systolic ejection murmurs produced by high cardiac output states are functional and flow-related but are excluded from the category of innocent murmurs because of their associated altered physiologic state. These include the cardiac murmurs of thyrotoxicosis, pregnancy, anemia, fever, exercise, and peripheral arteriovenous fistula, which are best interpreted in light of the total presentation of the patient (see Fig. 1077). Although these murmurs are often grade 3 and occasionally grade 4 in intensity, they always end well before S2 and are only rarely confused with obstruction of the LV or RV outflow tract. The large stroke volume associated with high-degree heart block often produces a functional systolic murmur; when found in the setting of complete heart block, beat-to-beat variations in the intensity of the murmur are present due to the random contribution of atrial systole to LV filling.

The functional systolic murmur in patients with a hemodynamically significant ASD is due to the increased flow in the RV outflow tract secondary to the left-to-right shunt at the atrial level. It is easily diagnosed at the bedside "by the company it keeps." The hallmark of this condition is wide, fixed splitting of S2. When the shunt is large (more than 2.5:1), a hyperdynamic parasternal impulse is usually present, and a diastolic flow rumble is often heard in the tricuspid area. In addition, the tricuspid closure is loud, and prominent a and v waves are seen in the JVP. An important condition to be differentiated from an ASD is narrowing of the anteroposterior diameter of the bony thorax. Prominent systolic murmurs-often grade 3 or 4-are heard in patients having the straight-back syndrome and/or pectus excavatum.282 Audible expiratory splitting is frequently present and, coupled with a prominent pulmonary artery on the chest x-ray (secondary to the narrow anteroposterior diameter), can lead to additional unnecessary procedures to rule out an ASD. Careful attention at the bedside to the physical examination of the spine, thoracic cage, and sternum should be part of the routine evaluation of any patient with a murmur. Often, confirmation of the thoracic abnormality with a lateral chest film is all that is necessary for definitive evaluation. Similar systolic murmurs from the RV outflow tract are also present in patients having significant left-to-right shunting at the ventricular level.

Prominent systolic ejection murmurs are the rule in patients with significant aortic regurgitation secondary to the large forward stroke volume. Although no significant LV outflow gradient is found in these patients, the intensity of such murmurs may be grade 4 or 5, and occasionally they are associated with a thrill. They always end well before aortic closure and are clearly separated from the early regurgitant murmur. Such a murmur is rarely confused with significant valvular obstruction because of the peripheral findings of wide-open aortic regurgitation. When true valvular obstruction is present (mixed stenosis and regurgitation of the aortic valve), the longer systolic ejection murmur is often associated with a prominent thrill. Systolic ejection murmurs due to large RV stroke volume are also seen in severe organic pulmonic valvular regurgitation.

Ventricular ejection into a dilated great vessel is commonly associated with a systolic ejection murmur. In the elderly, such murmurs are due to ejection into a dilated, sclerotic aorta and often are best appreciated at the apex. Frequently, degenerative changes of the aortic valve are also present, and the clinician is faced with a difficult decision as to whether or not true obstruction exists. The presence of significant calcification on fluoroscopic examination favors true obstruction and can be confirmed when a significant gradient is demonstrated by Doppler studies. A systolic ejection murmur due to RV ejection into a massively dilated pulmonary artery is frequently present in idiopathic dilatation of the pulmonary artery (see Fig. 10-73), which is often confused with an ASD due to the wide auditory expiratory splitting present in this condition. The prominent pulmonary ejection sound also may be confused with a loud tricuspid closure sound of a patient with an ASD. Short systolic ejection murmurs, frequently associated with a prominent late pulmonary ejection sound, are also seen in dilated pulmonic arteries secondary to severe pulmonary hypertension of any cause. Physical findings of severe pulmonary hypertension are always present, including a prominent parasternal impulse and increased intensity of the pulmonic component of S2, which is well heard at the apex. Prominent a waves in the neck and a right-sided S4 that increases with inspiration are present if the ventricular septum is intact. If the pulmonary hypertension is associated with intracardiac shunting, cyanosis frequently is present. A high-pitched, early diastolic murmur of pulmonic regurgitation secondary to severe pulmonary hypertension often is present.

LV Outflow Tract Murmurs

Obstruction to LV outflow may be congenital or acquired and may be located at the valvular, supravalvular, or subvalvular level. Stenosis is occasionally present at more than one level. In the clinical evaluation, one should attempt to define the severity and the level of obstruction. A summary of this differential diagnosis can be found in Table 10-12 (see Chap. 56).

The murmur of fixed stenosis of the LV outflow tract, regardless of the site, is crescendo-decrescendo, and its contour closely parallels the instantaneous pressure gradient. As long as cardiac output is maintained, there is an excellent correlation between the intensity and length of the murmur with severity of obstruction. Although there is a tendency toward late peaking of the murmur with increasing severity of the obstruction, this delayed peaking has not been found to correlate as well with the severity of valvular obstruction in aortic stenosis as it has in pulmonic stenosis.283 The murmur of significant fixed LV outflow tract obstruction usually is best heard in the second right and second and third left interspaces near the sternum. It radiates widely into the neck and along the great vessels. With radiation to the apex, particularly in the elderly patient, the high-frequency components of the murmur predominate, and the apical murmur has a high pitch and often a musical quality. This characteristic change in the pitch between the proximal and distal radiation of the murmur is a repeated source of confusion on auscultation. There is an almost overpowering urge to call it a separate murmur of mitral regurgitation; however, observations repeatedly demonstrate that this murmur, regardless of its timbre or harmonics, retains a spindle-shaped configuration whenever it is heard or recorded. The murmur of aortic stenosis varies directly with the length of the preceding diastole; the longer the preceding ventricular filling period, the louder is the systolic murmur Fig. 10-80). In contrast, the apical murmur of mitral regurgitation is associated with little or no variation in intensity with varying cycle lengths. This observation is useful in patients with atrial fibrillation or frequent premature contractions and helps to identify whether an apical murmur is due to radiation of an ejection murmur or is an additional regurgitant murmur of mitral regurgitation. Beat-to-beat variations in the intensity of the murmur of aortic stenosis have been noted in both pulsus alternans and AV dissociation.

A loud early systolic valvular ejection sound or click is the hallmark of congenital valvular aortic stenosis, and its presence defines the obstruction at the valvular level (see Fig. ^-66). As discussed earlier in this chapter, its intensity correlates well with the motility of the valve, and there is little correlation with the severity of the obstruction. It disappears when the valve becomes immobile due to calcific fixation and is absent in fixed subaortic stenosis. With progressive increase in the severity of the outflow obstruction, the duration of LV ejection is prolonged, resulting in narrow, single, or reversed splitting of S2. Reversed splitting of S2 in aortic stenosis in the absence of LBBB is always associated with severe obstruction (see Chap. 56).

Regardless of the site of obstruction, significant stenosis always results in LV hypertrophy, with a decreased diastolic compliance. Clinically, this is manifest as a presystolic apical pulsation on palpation and as an S4 on auscultation (see Fig. jQ-76). In patients older than age j2, the S4 is generally associated with a LV diastolic pressure above U mmHg and a left atrial a-wave peak of about j3 mmHg. The relationship between the severity of obstruction and the presence of S4 gallops is indirect, reflecting hypertrophy and decreased compliance of the left ventricle rather than obstruction per se.

Because of the frequent coexistence of hypertensive or arteriosclerotic heart disease in elderly patients with calcific aortic stenosis, the presence of an S4 is nonspecific and correlates poorly with the severity of obstruction. The S3 gallops also may be heard in LV outflow tract obstruction, particularly when decompensation occurs (see Fig. j0-76).

The diagnosis of hemodynamically significant aortic stenosis in the elderly presents a particularly difficult problem. The murmur is often of low intensity due to the decreased cardiac output and poor LV function. An ejection sound or click is rarely present, due to calcific fixation of the valve leaflets, and S2 is of low amplitude. The murmur is often loudest at the apex, has a high-frequency content, and may be difficult to define as ejection in nature because Sj and A2 may be poorly heard and therefore lost as landmarks defining the onset and end of mechanical systole.283 In most patients with severe aortic stenosis, no A2 is heard, and the systolic murmur obliterates P2. In the elderly, the rate of rise of the carotid pulse may be nearly normal due to the hard, sclerotic vessels even with severe obstruction. As shown in Fig. 1080, the response of the murmur following a premature ventricular contraction (PVC) may be very helpful in confirming the ejection nature of the murmur. Differentiation from the benign murmur of mild aortic sclerosis may be difficult and often necessitates confirmation of obstruction and its quantitation by echo-Doppler examination284 (see also Chaps. j5 and 56).

RV Outflow Tract Obstruction

Obstructions to RV outflow are congenital anomalies and may be at the level of the valve, infundibulum, and proximal or distal branches of the pulmonary artery. Isolated infundibular pulmonic stenosis with an intact septum is rare and is usually associated with a large VSD (tetralogy of Fallot). When the ventricular septum is intact, there is an excellent correlation between both the intensity and duration of the murmur and the severity of obstruction.285 Figure 10-81 contrasts the auscultatory findings of progressively more severe valvular pulmonic stenosis with an intact ventricular septum with those in tetralogy of Fallot with progressively more severe RV outflow obstruction.286 As with valvular aortic stenosis, an early systolic ejection sound defines the level of obstruction at the valve. In mild to moderate valvular obstruction, the intensity of this sound is markedly attenuated or may disappear with inspiration. In more severe valvular obstruction, this sound may fuse with S1 or actually may present as a presystolic click when the pressure generated by a forceful right atrial contraction exceeds RV end-diastolic pressure, causing doming of the stenotic valve in late diastole. Although obstruction to RV outflow in tetralogy of Fallot is usually at the infundibular level, valvular stenosis also may be present. In this setting, a pulmonary valvular ejection sound introduces a systolic murmur, and little variation in the intensity of the ejection sound is found with respiration.

The classic late peaking of the systolic ejection murmur of severe pulmonic stenosis with an intact ventricular septum is demonstrated in Fig. 10-82. Note that the late vibrations of the murmur completely envelop A2, whereas P2 is markedly delayed and decreases in intensity secondary to the low pulmonary artery closing pressure. In moderate to severe valvular pulmonic stenosis, an excellent correlation has been found between the A2-P2 interval and the RV peak pressure. When the ventricular septum is intact in severe RV outflow obstruction, prominent a waves are present in the JVP in association with a right-sided S4 that may increase with inspiration. Neither of these is present in uncomplicated tetralogy of Fallot. Occasionally, in very severe pulmonic stenosis, a low-pitched presystolic murmur may be present due to forward flow across the stenotic valve that has been opened prematurely by forceful right atrial contraction in late diastole. Such patients are often cyanotic due to right-to-left shunting through a patent foramen ovale.

In isolated infundibular obstruction, a pulmonic ejection sound is usually not encountered, and the pulmonic closure (P2) is usually not audible except in the mildest cases. Both valvular pulmonic stenosis and isolated infundibular pulmonic stenosis with an intact septum can be differentiated from tetralogy of Fallot by noting the marked intensification of the ejection murmur after the inhalation of amyl nitrite. In contrast, the murmur of tetralogy of Fallot shortens and decreases in intensity.

In branch stenosis of the pulmonary artery, there is a systolic murmur of varying intensity at the upper left sternal border that is widely transmitted to the right side of the chest, back, and both axillae. The murmur is usually less harsh and of higher pitch than the murmur of valvular stenosis. With more peripheral branch stenosis, systolic ejection murmurs or even continuous murmurs may be heard over the lung fields. The wide radiation of this murmur is particularly helpful in alerting the clinician to this type of right-sided obstruction.

Systolic Regurgitant Murmurs

Systolic regurgitant murmurs are produced by retrograde flow from a chamber of high pressure to a chamber of lower pressure. The classic examples of such murmurs are the holosystolic (pansystolic) murmur of mitral regurgitation, tricuspid regurgitation, and VSD. Since there is usually a high-pressure differential between the two chambers throughout systole, the murmurs are holosystolic in duration, high-pitched and blowing in quality, and plateaulike in configuration.

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