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 pulmonaryembolism has not been previously reported in the medical literature. We present and discuss the mechanisms of pulsus alternans and its clinical implications. 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 are usually associated with left ventricular alternans, right ventricular dysfunction, pulmonary embolism, and pulmonary hypertension. B exactnumber of 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 has been a subject of investigation and conjecture since the nineteenth century. The first, based on the Frank-Starling mechanism, the beat-to-beat alteration in end-diastolic volume accounted for the alternating contractile force. The secon d 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.