Loud: Mitral stenosis (MS), short PR interval, hyperkinetic heart, thin chest wall (Fig. 110-2). Soft: Long PR interval, heart failure, mitral regurgitation, thick chest wall, pulmonary emphysema.
Heart sounds. A. Normal. S1, first heart sound; S2, second heart sound; A2, aortic component of the second heart sound; P2, pulmonic component of the second heart sound. B. Atrial septal defect with fixed splitting of S2. C. Physiologic but wide splitting of S2 with right bundle branch block. D. Reversed or paradoxical splitting of S2 with left bundle branch block. E. Narrow splitting of S2 with pulmonary hypertension. (From NO Fowler: Diagnosis of Heart Disease. New York, Springer-Verlag, 1991, p 31.)
Normally A2 precedes P2 and splitting increases with inspiration; abnormalities include:
Widened splitting: Right bundle branch block, PS, mitral regurgitation
Fixed splitting (no respiratory change in splitting): Atrial septal defect
Narrow splitting: Pulmonary hypertension
Paradoxical splitting (splitting narrows with inspiration): Aortic stenosis, left bundle branch block, heart failure
Loud A2: Systemic hypertension
Soft A2: Aortic stenosis (AS)
Loud P2: Pulmonary arterial hypertension
Soft P2: Pulmonic stenosis (PS)
Low-pitched, heard best with bell of stethoscope at apex, following S2; normal in children; after age 30–35, indicates LV failure or volume overload.
Low-pitched, heard best with bell at apex, preceding S1; reflects atrial contraction into a noncompliant ventricle; found in AS, hypertension, hypertrophic cardiomyopathy, and coronary artery disease (CAD).
High-pitched; follows S2 (by 0.06–0.12 s), heard at lower left sternal border and apex in MS; the more severe the MS, the shorter the S2–OS interval.
High-pitched sounds following S1 typically loudest at left sternal border; observed in dilation of aortic root or pulmonary artery, congenital AS or PS; when due to the latter, click decreases with inspiration.
At lower left sternal border and apex, often followed by late systolic murmur in mitral valve prolapse.
May be “crescendo-decrescendo” ejection type, pansystolic, or late systolic; right-sided murmurs (e.g., tricuspid regurgitation) typically increase with inspiration (Fig. 110-3; Tables 110-1 and 110-2).
A. Schematic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP), and left atrial pressure (LAP). The gray areas indicated a transvalvular pressure difference during systole. HSM, holosystolic murmur; MSM, midsystolic murmur. B. Graphic representation of ECG, AOP, LVP, and LAP with gray areas indicating transvalvular diastolic pressure difference. EDM, early diastolic murmur; MDM, middiastolic murmur; PSM, presystolic murmur.
TABLE 110-1HEART MURMURS ||Download (.pdf) TABLE 110-1HEART MURMURS
|Systolic Murmurs |
|Ejection-type ||Aortic outflow tract |
| || Aortic valve stenosis |
| || Hypertrophic obstructive cardiomyopathy |
| || Aortic flow murmur |
| ||Pulmonary outflow tract |
| || Pulmonic valve stenosis |
| || Pulmonic flow murmur |
|Holosystolic ||Mitral regurgitation |
| ||Tricuspid regurgitation |
| ||Ventricular septal defect |
|Late-systolic ||Mitral or tricuspid valve prolapse |
|Diastolic Murmurs |
|Early diastolic ||Aortic valve regurgitation |
| ||Pulmonic valve regurgitation |
|Mid-to-late diastolic ||Mitral or tricuspid stenosis |
| ||Flow murmur across mitral or tricuspid valves |
|Continuous ||Patent ductus arteriosus |
| ||Coronary AV fistula |
| ||Ruptured sinus of Valsalva aneurysm |
TABLE 110-2EFFECTS OF PHYSIOLOGIC AND PHARMACOLOGIC INTERVENTIONS ON THE INTENSITY OF HEART MURMURS AND SOUNDS ||Download (.pdf) TABLE 110-2EFFECTS OF PHYSIOLOGIC AND PHARMACOLOGIC INTERVENTIONS ON THE INTENSITY OF HEART MURMURS AND SOUNDS
|Systolic murmurs due to TR or pulmonic blood flow through a normal or stenotic valve and diastolic murmurs of TS or PR generally increase with inspiration, as do right-sided S3 and S4. Left-sided murmurs and sounds usually are louder during expiration, as is the pulmonic ejection sound. |
|Valsalva Maneuver |
|Most murmurs decrease in length and intensity. Two exceptions are the systolic murmur of HCM, which usually becomes much louder, and that of MVP, which becomes longer and often louder. Following release of the Valsalva maneuver, right-sided murmurs tend to return to control intensity earlier than left-sided murmurs. |
|After VPB or AF |
|Murmurs originating at normal or stenotic semilunar valves increase in the cardiac cycle following a VPB or in the cycle after a long cycle length in AF. By contrast, systolic murmurs due to AV valve regurgitation either do not change, diminish (papillary muscle dysfunction), or become shorter (MVP). |
|Positional Changes |
|With standing, most murmurs diminish, two exceptions being the murmur of HCM, which becomes louder, and that of MVP, which lengthens and often is intensified. With squatting, most murmurs become louder, but those of HCM and MVP usually soften and may disappear. Passive leg raising usually produces the same results. |
|Murmurs due to blood flow across normal or obstructed valves (e.g., PS, MS) become louder with both isotonic and submaximal isometric (handgrip) exercise. Murmurs of MR, VSD, and AR also increase with handgrip exercise. However, the murmur of HCM often decreases with near maximum handgrip exercise. Left-sided S4 and S3 are often accentuated by exercise, particularly when due to ischemic heart disease. |
Early diastolic murmurs: Begin immediately after S2, are high-pitched, and are usually caused by aortic or pulmonary regurgitation.
Mid-to-late diastolic murmurs: Low-pitched, heard best with bell of stethoscope; observed in MS or TS; less commonly due to atrial myxoma.
Continuous murmurs: Present in systole and diastole (envelops S2); found in patent ductus arteriosus and sometimes in coarctation of aorta; less common causes are systemic or coronary AV fistula, aortopulmonary septal defect, ruptured aneurysm of sinus of Valsalva.
For a more detailed discussion, see O’Gara PT, Loscalzo J: Physical Examination of the Cardiovascular System, Chap. 267, p. 1442, in HPIM-19.