Pulsus alternans is characterized by regular rhythm with beat-to-beat alternation of systolic pressures. Left ventricular alternans is usually found in severe left ventricular dysfunction due to cardiomyopathy, coronary artery disease, systemic hypertension, and aortic stenosis. Right ventricular alternans is usually associated with left ventricular alternans, right ventricular dysfunction, pulmonary embolism, and pulmonary hypertension. Biventricular alternans is rare and associated with severe left ventricular dysfunction and left anterior descending coronary artery disease. The exact mechanism of pulsus alternans has not been clearly delineated, and it has been remained a subject of investigation and conjecture since the nineteenth century. Two fundamental mechanisms have been proposed to explain ventricular alteration. The first, based on the Frank-Starling mechanism, proposes beat-to-beat alteration in end-diastolic volume accounted for the alternating contractile force. The second proposed mechanism which explains the physiology of pulsus alternans involves the abnormal calcium handling by cardiac myocytes. To the best of our knowledge, biventricular alternans in pulmonary embolism has not been previously reported in the medical literature. We present and discuss the mechanisms of pulsus alternans and its clinical implications.

To assess the effect of rapid preload reduction on left ventricular performance in nonischemic cardiomyopathy, 11 patients were studied during inferior vena caval (IVC) balloon occlusion. Five developed sustained pulsus alternans. During pulsus alternans, the strong beats demonstrated systolic performance characteristics similar to baseline values, despite a drop in both left ventricular (LV) end-diastolic diameter (66 +/- 13 to 61 +/- 13 mm; p less than 0.05) and LV end-diastolic pressure (21 +/- 8 to 9 +/- 6 mmHg; p less than 0.05). In contrast, the weak beats demonstrated a reduction in peak systolic pressure (130 +/- 36 to 109 +/- 33 mmHg; p less than 0.02), fractional shortening (20% +/- 4% to 17% +/- 9%; p less than 0.05) and peak positive dP/dt (1,006 +/- 224 to 921 +/- 287 mmHg; p less than 0.05). Measures of diastolic performance (peak negative dP/dt, the time constant of LV relaxation, the length of diastasis, and LV end-diastolic stress) were not different between baseline beats and the strong beats; and only LV end-diastolic stress differed when baseline beats were compared to the weak beats. When the strong beats were compared to the weak beats during induced pulsus alternans, significant differences were observed in peak systolic pressure, peak positive dP/dt, and fractional shortening, but no differences in any measured diastolic parameter was observed. A slight difference was noted in the left ventricular end-diastolic diameters, with the weak beat consistently beginning at a slightly smaller diameter (61 +/- 13; mm vs 59 +/- 13; p less than 0.05). In summary, these data are consistent with an augmentation and deletion of intrinsic contractile forces in association with an alternation in preload on a beat-to-beat basis as best describing left ventricular performance during pulsus alternans.

The most recent patient in a 13-year experience with 14 patients suffering massive pulmonary thromboembolism requiring pulmonary thromboembolectomy is the focus of this report. This 40-year-old woman not only survived life-threatening acute hypoxemia and right heart failure, but was also found to have developed a unique transudative 700 cc pericardial effusion. Pulmonary artery pressure was 90/30 (mean 50 mmHg), accompanied by 17 mm right ventricular alternans. Systemic alternans and tamponade physiology were absent. This unusual natural model for acute right heart failure illustrates a novel mechanism for pericardial effusion physiology.

This investigation was performed to determine the presence of unilateral or bilateral pulsus alternans in the systemic and pulmonary circulations in heart failure and to estimate the prevalence of pulsus alternans in congestive cardiomyopathy. The subjects were 36 adult patients in heart failure due to a variety of cardiopulmonary diseases. We measured left- and right-sided systolic time intervals from simultaneous dual echocardiograms of both semilunar valves. The alternans was left-sided in seven patients, right-sided in one patient and bilateral in six patients. Pulsus alternans was induced by ventricular premature complexes (VPCs), except in one patient with bilateral and persistent alternans. For a VPC to precipitate alternans, the early beat itself must be associated with an abbreviated ejection time. Echophonocardiographic records of 100 patients with congestive cardiomyopathy were reviewed for evidence of pulsus alternans. We found persistent alternans in 10 patients and VPC-induced alternans in seven patients. We could not measure any difference in severity of disease in patients with pulsus alternans compared with those without.

The phenomenon of isolated mechanical alternans of the right ventricle is described in the setting of right ventricular infarction. We also discuss the resemblance of right ventricular infarction to cardiac tamponade or pericardial constriction.

Pulsus alternans of the pulmonary artery without systemic pulsus alternans is uncommon and is associated with multiple diseases. Two cases of pulmonary hypertension with pulmonary arterial pulsus alternans and right-sided heart failure are described. Primary pulmonary hypertension was demonstrated at autopsy in both cases. These two case reports constitute another previously unreported cause for pulsus alternans in the pulmonary circuit.