Symptomatic Aortic Stenosis With Congestive Heart Failure

Jeffrey Tabas, MD


March 04, 2010


What is the optimal therapy for patients with acute congestive heart failure and severe aortic stenosis? What if the patient is hypotensive?

Response from Jeffrey Tabas, MD
Associate Professor, Department of Emergency Medicine, University of California, San Francisco; Director of Quality Assurance, San Francisco General Hospital, San Francisco, California

Symptomatic aortic stenosis (AS) can be a challenging condition to manage. Patients with AS may be asymptomatic, with the diagnosis made after investigation of a harsh crescendo/decrescendo murmur, heard best at the left upper sternal border and radiating to both carotid arteries. Patients may also present with symptoms related to the AS, such as exertional chest pain, syncope, or heart failure. The classic teaching is that the life expectancy for uncorrected, symptomatic AS is 5 years with chest pain (ischemia due to the increased work of pumping), 2 years with syncope (limitation of forward flow with increased demand), and 1 year with heart failure (severely limited forward flow without increased demand). The valve area marks the severity of AS and roughly correlates with symptoms. Severe AS is defined by a valve area of less than 1.0 cm2. Aortic valve replacement is indicated when patients with severe AS become symptomatic or left ventricular dysfunction develops.

Heart failure in the setting of AS is due to limitation of forward flow and, usually, left ventricular dysfunction. Heart failure with AS carries a poor prognosis and acute management is difficult. One of the important goals in management of AS is to avoid hypotension. Because AS causes fixed left ventricular forward flow, attempts to increase cardiac output through increased contractility or increased heart rate have little to no effect. Aortic stenosis is 1 of 2 underlying conditions that have the poorest prognosis in cardiac arrest (the other is pulmonary hypertension, which limits right ventricular forward flow).

In heart failure without AS, the management goals are to decrease preload and afterload, and increase inotropy. Treatment goals in patients with AS and heart failure are similar, but response is severely limited, due to the relatively fixed outflow obstruction. Additionally, recovery from hypotension is more problematic due to decreased responsiveness to pressors. Therefore, the practitioner should maintain a lower threshold for therapy escalation, such as intubation and intra-aortic balloon pump intervention. Practitioners should also consider the initial cause of deterioration, such as myocardial infarction, hypertensive crisis, valve dysfunction from infective endocarditis, and infection.

Nitroglycerin should be first line therapy, with the goal of afterload and preload reduction, if the blood pressure will tolerate (systolic blood pressure < 140 mm Hg is ideal). Sublingual delivery provides a rapid bolus of medication -- roughly 80 mcg per minute for 5 minutes, but should be used with caution, especially with lower systolic blood pressures. Intravenous nitroglycerin is often more appropriate because it can be delivered and titrated with much greater control. Even topical delivery might be preferred to sublingual delivery because it can be controlled more easily than the sublingual route.

Loop diuretics to treat volume overload may be appropriate if there is evidence of systolic dysfunction as suggested by the patient's history or previous reports, by examination findings such as bilateral lower extremity edema, or by bedside ultrasound. Patients generally experience better response to therapy when the heart failure is primarily due to impaired left ventricular function rather than severely limited forward flow from AS. In patients without AS who have heart failure, a trial of bilevel positive airway pressure may be appropriate; however, given the concerns for rapid deterioration and poor response to therapy with severe AS, physicians should have a lower threshold for intubation of these patients.

In the patient with severe AS who becomes hypotensive, treatment options are especially limited, and escalation of care should occur immediately, including consultation with a cardiothoracic surgeon. The practitioner should attempt a trial of pressors, and if heart failure is present, should proceed with intubation. The need for intra-aortic balloon pump support should be anticipated if there is inadequate response to pressor support.