Holodiastolic Aortic Regurgitant Murmurs
The early diastolic murmur of aortic regurgitation is blowing and high-pitched in character and is often more difficult to record than to hear because of its high-frequency content. Since isovolumic relaxation of the left ventricle is very rapid, a large gradient quickly develops between the aortic and LV diastolic pressures, and the murmur builds up to maximum intensity almost immediately after A2. As diastole progresses, the gradient between the two chambers falls slowly, and the murmur envelope closely parallels the pressure drop in a decrescendo fashion up to Sj. When the aortic regurgitation is valvular in origin, the murmur is usually best heard at the third and fourth left parasternal areas. The finding that the murmur is heard best to the right of the sternum should alert the clinician to an aortic root etiology of the regurgitation.315 It should be pointed out that this finding is helpful only if present, since most patients with aortic regurgitation secondary to dilatation of the aortic root have the usual radiation with peak intensity to the left of the sternum. Although the frequency content of the murmur is in a range advantageous to the human ear, the amplitude of the vibrations may be quite small and the murmur quite faint. Therefore, the murmur may be overlooked if the examiner does not listen with the patient sitting up and leaning forward and does not listen with the diaphragm of the stethoscope pressed firmly against the chest wall. In addition, one should listen while the patient holds his or her breath after deep expiration.
The degree of aortic regurgitation is directly proportional to the pressure head driving the flow in a retrograde fashion. Maneuvers or pharmacologic agents that increase or decrease the diastolic aortic-left ventricular pressure gradient will increase or decrease the intensity of the regurgitant murmur. Prompt squatting often will bring out a very faint aortic regurgitant blowing murmur at the bedside, and inhalation of amyl nitrite will markedly decrease its intensity. It should be remembered that the murmur of mild aortic regurgitation often disappears during the latter stages of pregnancy due to the low peripheral vascular resistance. Pure aortic regurgitation without associated valvular stenosis may present with a prominent systolic ejection murmur as well as an Austin Flint rumble at the apex. The carotid pulse is rapid-rising and has a large volume. The A2 is often diminished or even absent when the regurgitation is valvular in origin due to inadequate coaptation and checking of the retrograde blood column by the deformed leaflets.
The etiology of the aortic regurgitation usually cannot be determined by the quality of the murmur. An exception to this rule is the presence of a "cooing dove" or musical diastolic murmur, which usually denotes a rupture or retroversion of an aortic cusp. Such ruptures occur secondary to trauma, bacterial endocarditis, and occasionally in the presence of arteriosclerotic involvement of the aortic valve. Retroversion and subsequent rupture of the aortic valve with a musical murmur are also a complication of syphilitic aortic regurgitation (see Chap. 56).
The murmur of very mild aortic regurgitation may be abbreviated and may end by middiastole. This is particularly true of the functional aortic regurgitant murmur of systemic arterial hypertension. As the volume of blood in the aorta decreases during diastole, the aortic annulus becomes smaller, and coupled with the decreasing aortic-left ventricular diastolic gradient, retrograde flow ceases, and the murmur disappears.
The murmur of aortic regurgitation also may be abbreviated if the aortic regurgitation is acute. Acute regurgitation of blood into a ventricle that has not had time to adapt to a large-volume load results in marked elevation of the LV end-diastolic pressure and equilibration of the aortic and LV diastolic pressures. With this, retrograde flow ceases, and the murmur disappears in the latter part of diastole. In the syndrome of acute aortic regurgitation, there may be preclosure of the mitral valve, resulting in a soft or absent S1 as well as absence of the presystolic component of the Austin Flint murmur. The auscultatory findings of acute versus chronic aortic regurgitation are contrasted in Fig. 10-85. Common causes of acute aortic regurgitation include aortic valve endocarditis, trauma, acute aortic dissection, and dehiscence of an aortic valve prosthesis (see Chap. 56).
Pulmonic regurgitation is found most commonly in the setting of severe pulmonary hypertension and dilatation of the pulmonary artery with inadequate coaptation of the leaflets of the pulmonic valve. The functional murmur of pulmonic regurgitation (Graham Steell murmur)316 is similar in both frequency and contour to that of aortic regurgitation because the hemodynamics responsible for their production are identical. The differential diagnosis is made by the "company the murmur keeps," and when it is associated with the peripheral signs of hemodynamically significant aortic regurgitation or with the findings of severe pulmonary hypertension, there is rarely a problem. However, when rheumatic mitral stenosis is the primary lesion, the semilunar regurgitant murmur may be secondary either to associated rheumatic aortic regurgitation or to the Graham Steell murmur if the pulmonary hypertension is severe. Careful investigation of the semilunar blowing murmur in the setting of mitral stenosis has shown that it is almost always due to aortic regurgitation, even when significant pulmonary hypertension is present.317 More common causes of the Graham Steell murmur of functional pulmonary regurgitation are primary pulmonary hypertension and Eisenmenger's syndrome.
Early diastolic murmurs occasionally are heard in end-stage renal failure, particularly when there is concurrent anemia, hypertension, and fluid overload. Doppler echocardiography demonstrated that these murmurs are usually pulmonic in origin.318 They are often transient in nature and are related to fluid overload. Such murmurs are diminished by extracellular fluid removal and reflect correctable pulmonary hypertension.318
The murmur of organic (non-pulmonary hypertensive) pulmonary regurgitation is quite different in quality and duration as compared with either aortic regurgitation or the Graham Steell murmur of pulmonary hypertension.3^ The murmur is delayed from P2 by a short interval and then builds up quickly to a crescendo followed by a decrescendo that ends well before Sj. In organic pulmonic regurgitation, the pulmonary artery pressure may be normal, and the diastolic gradient between the pulmonary artery and right ventricle may be very small, resulting in low-velocity retrograde flow and a lower-pitched murmur. The murmur is heard only during the period of maximal gradient in early and middle diastole, as the pulmonary artery pressure begins to equilibrate with the RV end-diastolic pressure in the latter part of diastole. This type of murmur may be congenital or acquired, as with pulmonary valve endocarditis, carcinoid syndrome, or surgical procedures on the pulmonic valve. It is often associated with a prominent systolic ejection murmur secondary to the large RV stroke volume.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...