Heart murmurs and sounds

Auscultation typically starts in the aortic area, continuing in clockwise fashion: first over the pulmonic, then the mitral (or apical), and finally the tricuspid areas ( Fig. 2.1 ). Because murmurs may radiate widely, they often become audible in areas outside those historically assigned to them. Hence, “inching” the stethoscope (i.e., slowly dragging it from site to site) can be the best way to avoid missing important findings. The typical sequence of auscultation of the heart is illustrated in Fig. 2.2 .

The intensity or loudness of a murmur is traditionally graded by the Levine system (no relation to this book’s editor) from 1/6 to 6/6. Everything else being equal, increased intensity usually reflects increased flow turbulence. Thus a louder murmur is more likely to be pathologic and severe. The grading system is summarized in Table 2.1 .

Ejection: Increased “forward” flow over the aortic or pulmonic valve. This can be:

• Physiologic: Normal valve but flow high enough to cause turbulence (anemia, exercise, fever, and other hyperkinetic heart syndromes).

• Pathologic: Abnormal valve with or without outflow obstruction (i.e., aortic stenosis [AS] vs. aortic sclerosis).

Regurgitation: “Backward” flow from a high- to a low-pressure bed. Although this is usually due to incompetent atrioventricular (AV) valves (mitral or tricuspid), it can also be due to ventricular septal defect (VSD).

Common causes of systolic murmurs include mitral regurgitation (MR), AS, tricuspid regurgitation, hypertrophic cardiomyopathy (HCM), VSD, and “functional” murmurs.

Causes of diastolic murmurs include aortic regurgitation (AR), pulmonic regurgitation, mitral stenosis (MS), and tricuspid stenosis.

Continuous murmurs can be caused by patent ductus arteriosus (PDA), coronary arteriovenous (AV) fistula, ruptured sinus of Valsalva aneurysm, and other etiologies.

• Causes of systolic, diastolic, and continuous murmurs are given in Table 2.2 .

  Table 2.2

  Principal Causes of Heart Murmurs

  From Braunwald, E., & Perloff, J. K. (2005). Physical examination of the heart and circulation. In D. P. Zipes, P. Libby, R. O. Bonow, & E. Braunwald (Eds.), Braunwald’s heart disease: a textbook of cardiovascular medicine (7th ed., pp. 77–106). Philadelphia, PA: Saunders; Norton, P. J., & O’Rourke, R. A. (2003). Approach to the patient with a heart murmur. In E. Braunwald & L. Goldman (Eds.), Primary cardiology (2nd ed., pp. 151–168). Philadelphia, PA: Elsevier.

  Systolic Murmurs

  Early Systolic

  Mitral—acute MR VSD Muscular Nonrestrictive with pulmonary hypertension Tricuspid—TR with normal pulmonary artery pressure

  Midsystolic

  Aortic Obstructive Supravalvular—supravalvular aortic stenosis, coarctation of the aorta Valvular—aortic stenosis and sclerosis Subvalvular—discrete, tunnel, or HCM Increased flow, hyperkinetic states, AR, complete heart block Dilation of ascending aorta, atheroma, aortitis Pulmonary Obstructive Supravalvular—pulmonary artery stenosis Valvular—pulmonic valve stenosis Subvalvular—infundibular stenosis (dynamic) Increased flow, hyperkinetic states, left-to-right shunt (e.g., ASD) Dilation of pulmonary artery

  Late Systolic

  Mitral—MVP, acute myocardial ischemia Tricuspid—tricuspid valve prolapsed

  Holosystolic

  Atrioventricular valve regurgitation (MR, TR) Left-to-right shunt at ventricular level (VSD)

  Diastolic Murmurs

  Early Diastolic

  Aortic regurgitation Valvular—congenital (bicuspid valve), rheumatic deformity, endocarditis, prolapse, trauma, postvalvulotomy Dilation of valve annulus—aortic dissection, annuloaortic ectasia, cystic medial degeneration, hypertension, ankylosing spondylitis Widening of commissures—syphilis Pulmonic regurgitation Valvular—postvalvulotomy, endocarditis, rheumatic fever, carcinoid Dilation of valve annulus—pulmonary hypertension, Marfan syndrome Congenital—isolated or associated with tetralogy of Fallot, VSD, pulmonic stenosis

  Middiastolic

  Mitral MS Carey Coombs murmur (middiastolic apical murmur in acute rheumatic fever) Increased flow across nonstenotic mitral valve (e.g., MR, VSD, PDA, high-output states, complete heart block) Tricuspid Tricuspid stenosis Increased flow across nonstenotic tricuspid valve (e.g., TR, ASD, anomalous pulmonary venous return) Left and right atrial tumors (myxoma) Severe or eccentric AR (Austin Flint murmur)

  Late Diastolic

  Presystolic accentuation of MS murmur Austin Flint murmur of severe or eccentric AR

  Continuous Murmurs

  PDA AV fistula Ruptured sinus of Valsalva aneurysm Aortic septal defect Cervical venous hum Anomalous left coronary artery Proximal coronary artery stenosis Mammary souffle of pregnancy Pulmonary artery branch stenosis Bronchial collateral circulation Small (restrictive) ASD with MS Intercostal arteriovenous fistula

  AR, Aortic regurgitation; ASD, atrial septal defect; AV, arteriovenous; HCM, hypertrophic cardiomyopathy; MR, mitral regurgitation; MS, mitral stenosis; MVP, mitral valve prolapse; PDA, patent ductus arteriosus; TR, tricuspid regurgitation; VSD, ventricular septal defect.

They are benign findings caused by turbulent ejection into the great vessels. Functional murmurs have no clinical relevance other than getting into the differential diagnosis of a systolic murmur.

The murmur of aortic sclerosis is common in the elderly. This early-peaking systolic murmur is extremely age related, affecting 21% to 26% of persons 65 years of age and 55% to 75% of octogenarians. (Conversely, the prevalence of AS in these age groups is 2% and 2.6%, respectively.) The murmur of aortic sclerosis may be due to either a degenerative change of the aortic valve or abnormalities of the aortic root. Senile degeneration of the aortic valve includes thickening, fibrosis, and occasionally calcification. This can stiffen the valve and yet not cause a transvalvular pressure gradient. In fact, commissural fusion is typically absent in aortic sclerosis. Abnormalities of the aortic root may be diffuse (such as a tortuous and dilated aorta) or localized (like a calcific spur or an atherosclerotic plaque that protrudes into the lumen, creating a turbulent bloodstream).

There are two golden and three silver rules, as follows:

• The first golden rule is to always judge (systolic) murmurs like people—by the company they keep. Hence, murmurs that keep bad company (like symptoms, extra sounds, thrill, and abnormal arterial or venous pulse or abnormal electrocardiogram/chest radiograph) should be considered pathologic until proven otherwise. These murmurs should receive extensive evaluation, including technology-based assessment.

• The second golden rule is that a diminished or absent S ₂ usually indicates a poorly moving and abnormal semilunar (aortic or pulmonic) valve. This is the hallmark of pathology. On the flip side, functional systolic murmurs are always accompanied by a well-preserved S ₂ , with normal split.

The three silver rules are these:

• All holosystolic (or late systolic) murmurs are pathologic.

• All diastolic murmurs are pathologic.

• All continuous murmurs are pathologic.

Thus functional murmurs should be systolic, short, soft (typically less than 3/6), early peaking (never passing midsystole), predominantly circumscribed to the base, and associated with a well-preserved and normally split second sound. They should be part of an otherwise normal cardiovascular examination and often disappear with sitting, standing, or straining (as, e.g., following a Valsalva maneuver).

Fig. 2.3 diagrams innocent (functional) and pathologic heart murmurs.

Valvular area must be reduced by at least 50% (the minimum for creating a pressure gradient at rest) for the AS murmur to become audible. Mild disease may produce loud murmurs too, but usually significant hemodynamic compromise (along with symptoms) does not occur until there is a 60% to 70% reduction in the valvular area. This means that early to mild AS may be subtle at rest. Exercise, however, may intensify the murmur by increasing the output and gradient.