A 72-year-old man with long-standing dyspnea was seen in the clinic after experiencing an episode of syncope. Physical examination showed weak and slowly rising arterial pulses. Cardiac auscultation showed a harsh midsystolic murmur best heard at the second right intercostal space with decreased intensity of the second heart sound. Electrocardiogram and echocardiogram confirmed the diagnosis of severe aortic stenosis. Two months later, the patient comes to the emergency department with palpitations and increased shortness of breath. His blood pressure is 90/60 mm Hg and his heart rate is 130/min with an irregularly irregular rhythm. Electrocardiogram shows new-onset atrial fibrillation without significant ST-segment or T-wave changes. Chest x-ray shows bilateral pulmonary edema. Which of the following hemodynamic changes is most likely associated with this patient's current presentation?
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This patient's sudden-onset heart failure was most likely precipitated by acute atrial fibrillation, a condition that occurs in up to 10% of patients with severe aortic stenosis (AS). Patients with severe AS already have reduced cardiac output due to significant valvular obstruction, which can be exacerbated by the sudden loss of normal atrial contraction that contributes to ventricular filling. Atrial contraction is especially important for these patients as many have concentric left ventricular (LV) hypertrophy and therefore reduced LV compliance. As a result, they become dependent on atrial contraction to maintain adequate LV filling. Without atrial contraction, LV preload can decrease to the point of producing severe hypotension. In addition, loss of the atrial kick can result in significantly increased mean pulmonary venous pressure due to buildup of blood in the left atrium and pulmonary veins, leading to acute pulmonary edema. As a result, cardioversion is indicated for acute atrial fibrillation in patients with severe AS.
(Choice A) Cardiogenic pulmonary edema is characteristic of left, not right, heart failure. When the forward pumping function of the left heart is impaired, pressure can build up in the left atrium. This rise in pressure is transmitted to the pulmonary veins and capillaries, resulting in increased fluid transudation into the alveoli and pulmonary interstitium.
(Choices C and E) This patient has no evidence of myocardial ischemia on electrocardiogram, meaning that LV systolic function is most likely unchanged. Under these circumstances, an increase in LV filling (preload) would increase cardiac output and mean arterial pressure due to the Frank-Starling mechanism. This patient's decreased cardiac output is most likely due to decreased LV preload.
(Choice D) In a patient with AS, LV afterload is determined by the mean systolic blood pressure and the degree of transvalvular obstruction. In degenerative calcific AS and most other forms of adult AS, the transvalvular obstruction gradually increases over years to decades, making an acute increase in LV afterload unlikely. In addition, this patient's acute hypotension would actually cause a reduction in afterload.
Educational objective:
In patients with chronic aortic stenosis and concentric left ventricular hypertrophy, atrial contraction contributes significantly to left ventricular filling. Loss of atrial contraction due to atrial fibrillation can reduce left ventricular preload and cardiac output sufficiently to cause systemic hypotension. Decreased forward filling of the left ventricle can also result in backup of blood in the left atrium and pulmonary veins, leading to acute pulmonary edema.