pansystolic murmur

**Definition:** A murmur that starts at S1 and extends through S2. It is plateau-shaped (constant intensity) and is often high-pitched and "blowing." It is also called a holosystolic murmur.

**Pathophysiology:** The murmur is produced by regurgitant or shunt flow between two chambers whose pressure gradient persists throughout systole. This includes the isovolumetric contraction phase, so the murmur begins right at S1 instead of after the aortic or pulmonic valve opens. Ejection murmurs, such as aortic stenosis, are different. They are crescendo-decrescendo and start after S1.

**Classic causes** 1. **Mitral regurgitation (MR)** - Heard best at the apex and radiates to the axilla. - Louder with expiration, handgrip, and squatting (increased afterload). - Often accompanied by a soft S1 and a possible S3 from volume overload. - Causes: - Acute: papillary muscle rupture after MI (days 3–5, inferior MI/posteromedial papillary muscle), infective endocarditis, chordae rupture. - Chronic: mitral valve prolapse, rheumatic heart disease, LV dilation/functional MR, connective tissue disease (Marfan, Ehlers-Danlos). - Mitral valve prolapse has a mid-systolic click followed by a late systolic murmur. It is not typically pansystolic. 2. **Tricuspid regurgitation (TR)** - Heard best at the left lower sternal border. - Louder with inspiration (Carvallo sign). - Associated with prominent v waves in the JVP and pulsatile hepatomegaly. - Causes: right ventricular dilation or pulmonary hypertension, IV drug use endocarditis (*S. aureus*), carcinoid syndrome, Ebstein anomaly (maternal lithium), rheumatic heart disease. 3. **Ventricular septal defect (VSD)** - Heard best at the left lower sternal border, with a harsh quality and an associated thrill. - Louder with handgrip (increased afterload increases the left-to-right shunt). - Small restrictive VSDs have louder murmurs than large ones. - It is the most common congenital heart defect and is associated with fetal alcohol syndrome and trisomies. It can also occur after MI from septal rupture (days 3–5, LAD territory). - Untreated large VSDs lead to pulmonary hypertension, reversal of the shunt (Eisenmenger syndrome), cyanosis, and clubbing. The murmur disappears when the shunt reverses.

**Dynamic maneuvers (high-yield)** - **Inspiration** increases right-sided murmurs (TR). - **Expiration** increases left-sided murmurs (MR). - **Handgrip/squatting** increases afterload and so increases MR and VSD murmurs. - **Valsalva and standing** decrease venous return and so decrease most murmurs. The exceptions are HCM and mitral valve prolapse, whose murmurs increase.

**Clinical pearls** - Acute severe MR can produce a soft or short murmur because of rapid LA-LV pressure equalization, along with pulmonary edema and hypotension or shock. - Chronic MR leads to eccentric LV hypertrophy and LA enlargement, with atrial fibrillation as a possible consequence. - Management depends on the cause and severity. It includes afterload reduction and diuretics, and valve repair or replacement for severe symptomatic disease. For a VSD, small defects often close spontaneously and large defects need surgery. - Diagnosis is confirmed with echocardiography with Doppler.

**Differential for murmur timing:** The murmur of aortic stenosis is a systolic crescendo-decrescendo ejection murmur. HCM has a systolic murmur that increases with decreased preload. Diastolic murmurs are not pansystolic (AR, MS).