Classification of Cardiac Murmurs and Their Mechanisms
Cardiac murmurs are classified by their timing in the cardiac cycle, with each type having distinct pathophysiological mechanisms that reflect specific hemodynamic abnormalities or structural cardiac lesions. 1
Systolic Murmurs
Midsystolic (Ejection) Murmurs
- Mechanism: Generated by turbulent blood flow across normal or stenotic semilunar valves during ventricular ejection, typically crescendo-decrescendo in character 1
- Common causes include aortic stenosis, pulmonic stenosis, and benign flow murmurs 1
- These murmurs increase in intensity after a ventricular premature beat or during long cycle lengths in atrial fibrillation due to increased stroke volume 1
Early Systolic Murmurs
- Mechanism: Begin with S1 and end in midsystole, less common than other systolic murmurs 1
- Typically caused by tricuspid regurgitation without pulmonary hypertension or acute mitral regurgitation 1
- In large ventricular septal defects with pulmonary hypertension, the pressure equalization at end-systole eliminates the shunt, limiting the murmur to early systole 1
Pansystolic (Holosystolic) Murmurs
- Mechanism: Generated when blood flows between chambers maintaining widely different pressures throughout the entire systolic period, creating a plateau-shaped murmur from S1 to S2 2
- Three primary causes with distinct clinical implications:
- Mitral regurgitation: Backward flow from left ventricle to left atrium due to valve prolapse, rheumatic disease, papillary muscle dysfunction, or left ventricular dilation 2
- Tricuspid regurgitation: Backward flow from right ventricle to right atrium, often secondary to pulmonary hypertension or right ventricular failure 2
- Ventricular septal defect: Abnormal communication between ventricles with persistent left-to-right shunting throughout systole 2
- Clinical differentiation: Mitral regurgitation is best heard at the apex radiating to the axilla, while tricuspid regurgitation is loudest at the lower left sternal border and increases with inspiration 2
Late Systolic Murmurs
- Mechanism: Start well after ejection begins and end before or at S2, typically soft to moderately loud and high-pitched at the left ventricular apex 1
- Caused by apical tethering and malcoaptation of mitral leaflets due to anatomic and functional changes of the annulus and ventricle 1
- Classic association with mitral valve prolapse, where late systolic regurgitation occurs due to prolapse of leaflet(s) into the left atrium, often accompanied by midsystolic clicks 1
- Can occur without clicks in some cases 1
Diastolic Murmurs
Early Diastolic Murmurs
- Mechanism: Begin with or shortly after S2 when ventricular pressure drops sufficiently below aortic or pulmonary artery pressure 1
- High-pitched, decrescendo murmurs indicate aortic regurgitation or pulmonic regurgitation with pulmonary hypertension, reflecting rapid decline in regurgitant volume during diastole 1
- Low to medium-pitched murmurs suggest pulmonic regurgitation without pulmonary hypertension, with slightly delayed onset because regurgitant flow is minimal at valve closure when the reverse pressure gradient is minimal 1
- Common late after repair of tetralogy of Fallot 1
Middiastolic Murmurs
- Mechanism: Occur during early ventricular filling due to relative disproportion between valve orifice size and diastolic blood flow volume 1
- Usually originate from mitral and tricuspid valves 1
- Primary causes:
- Austin-Flint murmur: Low-pitched, rumbling diastolic murmur at the left ventricular apex in severe chronic aortic regurgitation, occurring without an opening snap 1
Presystolic Murmurs
- Mechanism: Begin during ventricular filling that follows atrial contraction, therefore requiring sinus rhythm 1
- Usually caused by mitral or tricuspid stenosis 1
- Right or left atrial myxoma can mimic these murmurs 1
Continuous Murmurs
- Mechanism: Arise from high-to-low pressure shunts that persist through end of systole and beginning of diastole 1
- Begin in systole, peak near S2, and continue into all or part of diastole 1
- Uncommon in valvular heart disease 1
- Can occur with aortic dissection creating fistulae between the dissecting aneurysm and cardiac chambers or pulmonary artery 3
Dynamic Auscultation for Differentiation
Respiratory Variation
- Right-sided murmurs increase with inspiration due to increased venous return 1
- Left-sided murmurs are louder during expiration 1
Valsalva Maneuver
- Most murmurs decrease in length and intensity 1
- Exceptions: Hypertrophic cardiomyopathy murmur becomes much louder, and mitral valve prolapse murmur becomes longer and often louder 1
- After release, right-sided murmurs return to baseline earlier than left-sided murmurs 1
Positional Changes
- Standing: Most murmurs diminish except hypertrophic cardiomyopathy (louder) and mitral valve prolapse (lengthens and intensifies) 1
- Squatting: Most murmurs become louder, but hypertrophic cardiomyopathy and mitral valve prolapse usually soften or disappear 1
Exercise
- Murmurs from flow across normal or obstructed valves (pulmonic stenosis, mitral stenosis) become louder with both isotonic and isometric exercise 1
- Mitral regurgitation, ventricular septal defect, and aortic regurgitation murmurs increase with handgrip exercise 1
Clinical Significance and Diagnostic Approach
- Pansystolic murmurs almost always indicate pathological conditions requiring further evaluation, as they can lead to heart failure, pulmonary hypertension, and arrhythmias if untreated 2
- Echocardiography is the gold standard for confirming the cause of murmurs and should be performed in all patients with pansystolic murmurs of unknown cause 4
- Diastolic and continuous murmurs are mostly pathologic and warrant further workup 5
- Innocent murmurs are minor (grade 1-2/6), crescendo-decrescendo, position-dependent, midsystolic murmurs without radiation that need no further workup in asymptomatic patients with normal physical capacity 5