Clinical meaning
Heart murmurs are produced by turbulent blood flow across abnormal valves, through structural defects, or across normal valves under high-flow conditions. Their timing in the cardiac cycle directly reflects the hemodynamic event producing them. Systolic murmurs occur between S1 (mitral and tricuspid valve closure) and S2 (aortic and pulmonic valve closure) and fall into two categories: systolic ejection (crescendo-decrescendo or diamond-shaped) murmurs result from blood being forced through a stenotic semilunar valve or outflow tract obstruction during ventricular ejection — the classic aortic stenosis murmur peaks in mid-systole as flow velocity peaks, best heard at the right upper sternal border radiating to the carotids. Holosystolic (pansystolic) murmurs are produced by a continuous pressure gradient throughout systole, as in mitral regurgitation (blood leaks from the high-pressure left ventricle back into the lower-pressure left atrium throughout systole, producing a blowing murmur at the apex radiating to the axilla) and ventricular septal defect (VSD). Diastolic murmurs occur between S2 and S1 and are almost always pathological. Early diastolic decrescendo murmurs result from aortic regurgitation: incompetent aortic valve allows retrograde flow from the high-pressure aorta into the ventricle immediately after S2, with intensity decreasing as the pressure gradient diminishes. Mid-to-late diastolic rumbling murmurs (best heard with the bell at the apex) result from mitral stenosis: blood must be forced through a narrowed mitral valve orifice from atrium to ventricle during diastolic filling, often preceded by an opening snap. Dynamic auscultation maneuvers alter preload and afterload to help differentiate murmurs: Valsalva and standing decrease preload, increasing the murmur of HOCM (worsening outflow obstruction) and mitral valve prolapse while decreasing most other murmurs; squatting increases preload and afterload, decreasing HOCM and MVP while increasing most other murmurs.