INTRODUCTION — Cardiac auscultation is one of the most useful investigative tools to detect alterations in cardiovascular anatomy and physiology. Physiologic maneuvers during auscultation (dynamic auscultation) may sufficiently alter the systemic hemodynamics to change the character, behavior, and intensity of heart sounds and murmurs, thereby improving the diagnostic accuracy of the physical examination (figure 1).
The most common maneuvers used during auscultation will be reviewed here (table 1).
LIMITATIONS AND SUBSEQUENT TESTING — Concerns about the use of these maneuvers are that they may be difficult to interpret and may not be reproducible, particularly when performed by nonexperts, and their diagnostic utility has rarely been validated.
In current clinical practice, echocardiography is the standard for establishing the cause of a murmur. As noted in major society guidelines, an echocardiogram is indicated for diagnosis and evaluation of patients with known or suspected valve disease [1,2]. Echocardiography is not needed in asymptomatic patients with a benign flow murmur but is appropriate in patients with cardiac symptoms and any cardiac murmur and asymptomatic patients with a diastolic murmur, a grade 3 or greater systolic murmur, or a systolic murmur in association with other abnormal exam findings, such as a systolic click or reduced carotid upstroke.
RESPIRATION — Venous return to the right ventricle increases during normal inspiration resulting in an increase in its volume. In contrast, inspiration causes a decrease in venous return to the left ventricle and a reduction in its volume. These changes in venous return can alter the intensity of murmurs and heart sounds, primarily those that originate from the right side of the heart. (See "Auscultation of cardiac murmurs in adults" and "Auscultation of heart sounds".)
●During inspiration there is an increase in the splitting of S2 as A2 and P2 are separated (due to longer right ventricular ejection time compared to left ventricular ejection time during inspiration).
●Third (S3) and fourth (S4) heart sounds of right ventricular origin usually diminish with expiration and increase with inspiration. An S3 and S4 originating from the left side of the heart may increase with expiration and decrease with inspiration.
●In tricuspid stenosis, the opening snap diminishes with expiration and increases with inspiration. In contrast, the opening snap of mitral stenosis increases with expiration and decreases with inspiration.
●Pulmonary ejection sound of valvular origin decreases in intensity during inspiration.
●Inspiration increases the intensity of murmurs originating from the right side of the heart, including the diastolic murmurs of tricuspid stenosis and pulmonary regurgitation, the systolic murmur of tricuspid regurgitation (Carvallo sign), and the presystolic murmur of Ebstein anomaly.
●In mitral valve prolapse, the inspiratory decrease in venous return to the left side of the heart reduces left ventricular volume; the murmur and click occur earlier and may diminish.
ABRUPT STANDING — Abrupt standing from the supine position decreases venous return to the heart and, consequently, right and left ventricular diastolic volumes and stroke volumes decline. There also may be a fall in arterial pressure and a reflex increase in heart rate. These hemodynamic changes are associated with changes in the following murmurs:
●Decrease in the intensity of the murmurs of pulmonary and aortic stenosis and of a benign flow murmur.
●Decrease in the intensity of the murmurs of mitral and tricuspid regurgitation.
●Earlier onset of the click and prolongation of systolic murmur of mitral valve prolapse.
●Decrease in the intensity of the systolic murmur in ventricular septal defect without significant pulmonary hypertension.
●In hypertrophic cardiomyopathy, a decrease in left ventricular outflow size is associated with an increase in the intensity of the ejection systolic murmur along with a decrease or unchanged carotid pulse volume (magnitude of arterial expansion).
SQUATTING — Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure. During this maneuver the patient should breath normally and avoid breath-holding or a Valsalva maneuver. Squatting from a standing position causes changes in the following murmurs:
●Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which favors the movement of blood in the left ventricle across the regurgitant mitral valve into the left atrium rather than entering the systemic circulation across the aortic valve.
●In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in intensity with squatting because of the increase in afterload.
●Increase in the magnitude of the left-to-right shunt in ventricular septal defect associated with an increased intensity of the systolic murmur.
●In patients with tetralogy of Fallot, the net effect of squatting is usually an increase in pulmonary flow, which is associated with increased intensity of the pulmonary ejection systolic murmur. (See "Tetralogy of Fallot (TOF): Pathophysiology, clinical features, and diagnosis", section on 'Cardiac auscultation'.)
●Intensity of the diastolic murmur of aortic regurgitation increases due to augmented regurgitation; intensity of the Austin-Flint murmur also may increase.
●In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur promptly declines because of an increased left ventricular volume and arterial pressure, which increase the effective orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may increase.
●Intensity of the murmur of valvular aortic stenosis shows variable changes, depending upon the type of hemodynamic response; a significant increase in systemic vascular resistance is associated with a decreased intensity of the murmur, an increased left ventricular volume with increased intensity of the murmur. There is usually no change or a decrease in the intensity of a benign flow murmur.
●During phase 1, with the onset of the maneuver, there is a transient increase in left ventricular output.
●During the straining phase, phase 2, there is a decrease in venous return, right and left ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure; this is associated with a reflex increase in heart rate.
●During phase 3 (release of Valsalva), which only lasts for a few cardiac cycles, there is a further reduction in left ventricular volume.
●Phase 4 is characterized by an increase in stroke volume and arterial pressure and reflex slowing of heart rate (the overshoot).
Analysis of changes in the intensity and character of the murmur during phase 2 of the Valsalva maneuver is most useful and practical for the differential diagnosis.
●The intensity of flow murmurs, murmurs of aortic and pulmonary stenosis, tricuspid and mitral regurgitation, aortic and pulmonary regurgitation, and mitral and tricuspid stenosis decreases. The volume of the carotid pulse also decreases.
●The murmur of hypertrophic cardiomyopathy increases in intensity as the left ventricular outflow size decreases with a decreased venous return. The carotid pulse volume also declines.
●In mitral valve prolapse there is an early onset of the click and murmur due to the decrease in left ventricular volume. The opposite effects are observed during phase 4.
HAND GRIP — Sustained hand grip for 20 to 30 seconds leads to an increase in systemic vascular resistance, arterial pressure, cardiac output, and left ventricular volume and filling pressure. Hemodynamic changes during hand grip are variable and not always similar in all patients. As an example, the increase in arterial pressure may be relatively greater than the increase in heart rate or cardiac output. Thus, changes in intensity of murmurs are not always predictable.
Hand grip is most useful in differentiating between the ejection systolic murmur of aortic stenosis and the regurgitant murmur of mitral regurgitation. Intensity of the murmur of aortic stenosis tends to decrease along with a decreased transvalvular pressure gradient, while the severity and murmur of mitral regurgitation increase. Other murmurs change as follows:
●Increased severity and murmur of aortic regurgitation.
●Increased left-to-right shunt in ventricular septal defect with an increased intensity of the murmur.
●The diastolic murmur of mitral stenosis becomes accentuated because of an increased heart rate.
●In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur softens due to an increased left ventricular volume and arterial pressure.
●The click and the murmur of mitral valve prolapse are delayed because of the increased left ventricular volume.
POSTEXTRASYSTOLIC POTENTIATION — If premature beats occur during the clinical examination, analysis of changes in the intensity and character of the murmur during the postextrasystolic (postectopic) beat can provide clues to the diagnosis of valvular heart disease. The postectopic pause is associated with an increased ventricular volume; however, myocardial contractility also increases due to postextrasystolic potentiation. In most circumstances, the effect of increased contractility supersedes the effect of an increased ventricular volume, resulting in the following changes:
●Intensity of the ejection systolic murmur increases in aortic stenosis and hypertrophic cardiomyopathy. Carotid pulse volume increases in the former and decreases or remains unchanged in the latter. These findings in patients with hypertrophic cardiomyopathy reflect the Brockenbrough sign (postextrasystolic potentiation resulting in increased left ventricular outflow gradient and decreased or unchanged pulse pressure).
●The murmur of aortic regurgitation also may increase due to an increased arterial pressure that augments the regurgitant flow.
●Tricuspid regurgitation murmurs increase due to an increased right ventricular volume.
●The pansystolic murmur of mitral regurgitation, particularly of rheumatic origin, does not usually change.
●In mitral valve prolapse, postextrasystolic potentiation causes a rapid rate of ejection and, therefore, an earlier onset of the click and the murmur.
AMYL NITRITE — Amyl nitrite (a predominantly arteriolar dilator) was previously used as a bedside pharmacologic maneuver [3-6], but its use is no longer recommended given the utility of echocardiography for distinguishing various cardiac lesions.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease" and "Society guideline links: Cardiomyopathy".)
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●Respiration – Systemic venous return and pulmonary venous return change reciprocally with inspiration and expiration. These changes alter certain heart sounds and murmurs, primarily those that originate from the right side of the heart. (See 'Respiration' above.)
●Abrupt standing and squatting – Systemic venous return and systemic arterial pressure change reciprocally with abrupt standing and squatting. These changes alter certain heart sounds and murmurs such as the click and murmur of mitral valve prolapse and the ejection systolic murmur in hypertrophic cardiomyopathy. (See 'Abrupt standing' above and 'Squatting' above.)
●Valsalva maneuver – The straining phase of the Valsalva maneuver induces a decrease in intensity of the murmur of aortic stenosis and an increase in the intensity of the systolic ejection murmur of hypertrophic cardiomyopathy. (See 'Valsalva maneuver' above.)
●Hand grip – Hand grip induces an increase in systemic vascular resistance and tends to decrease the intensity of the murmur of aortic stenosis and increase the intensity of the murmur of mitral regurgitation. (See 'Hand grip' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges the late Kanu Chatterjee, MD, who contributed to an earlier version of this topic review.
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