Pulsus Alternans: Echocardiographic Evidence of Reduced Venous Return and Alternating End-diastolic Fiber Length as Causative Factors

Abstract

The echocardiographic findings are described in a patient with left heart failure both before and after development of severe pulsus alternans (PA). Right ventricular dimension (RVD) before and after PA was 2.7 and 1.0 cm, respectively. Left atrial dimension (LAD) before and after PA was 4.8 cm and 2.7 cm, respectively. Left ventricular end-diastolic dimension (LVDd) without PA was 6.7 cm; with PA was 6.0 cm before the strong beat and 5.7 cm before the weak beat. End-diastolic thickness of the left ventricular wall (LVW) was 0.8 cm before the strong beat and 1.1 cm before the weak beat. Thus the weak beat was initiated from a shorter end-diastolic fiber length than the strong beat. The weak beat had no aortic valve opening, and the accompanying phonocardiogram revealed absence of the early ejection sound and aortic component of the second heart sound. Decreased blood volume owing to diuretic therapy most likely contributed to the development of PA, since the RVD, LAD, and LVDd became smaller, the heart rate did not change, and the rhythm was regular. The echocardiographic findings are described in a patient with left heart failure both before and after development of severe pulsus alternans (PA). Right ventricular dimension (RVD) before and after PA was 2.7 and 1.0 cm, respectively. Left atrial dimension (LAD) before and after PA was 4.8 cm and 2.7 cm, respectively. Left ventricular end-diastolic dimension (LVDd) without PA was 6.7 cm; with PA was 6.0 cm before the strong beat and 5.7 cm before the weak beat. End-diastolic thickness of the left ventricular wall (LVW) was 0.8 cm before the strong beat and 1.1 cm before the weak beat. Thus the weak beat was initiated from a shorter end-diastolic fiber length than the strong beat. The weak beat had no aortic valve opening, and the accompanying phonocardiogram revealed absence of the early ejection sound and aortic component of the second heart sound. Decreased blood volume owing to diuretic therapy most likely contributed to the development of PA, since the RVD, LAD, and LVDd became smaller, the heart rate did not change, and the rhythm was regular.