When are vasoactive agents indicated in acute heart failure?

The Hospitalist. 2008 October;2008(10):

October 1, 2008|The Hospitalist

Prashant Vaishnava, MD;Sylvia C. McKean, MD;Anju Nohria, MD;Kenneth L. Baughman, MD

Case

A 72-year-old retired nurse with known nonischemic dilated cardiomyopathy with an ejection fraction of approximately 20% and status-post cardiac resynchronization therapy presents to the emergency department with dyspnea with minimal activity, three-pillow orthopnea, and paroxysmal nocturnal dyspnea.

She had been hospitalized twice during the past 60 days for similar symptoms. Her medications included losartan (20 mg po q daily), carvedilol (3.125 mg twice daily), spironolactone (25 mg daily), digoxin (0.125 mg daily), and furosemide (80 mg twice daily). Vital signs are notable for a blood pressure of 90/50 mmHg and an irregular pulse of 90 beats per minute. Physical examination is notable for marked jugular venous distension, lungs clear to auscultation bilaterally, biventricular heaves, a markedly displaced left ventricular point of maximal impulse, and a prominent S3 gallop.

Despite treatment with intravenous furosemide and temporary withdrawal of carvedilol, the patient remains symptomatic with persistent jugular venous distension.

Should she be given a vasoactive agent?

Key Points

Acute heart failure syndrome (AHFS) is the most common cause of hospitalization in patients over the age of 65 in the United States.
Initial management of AHFS depends on definition of the patient’s hemodynamic profile, in terms of elevation of filling pressures and adequacy of perfusion.
In the absence of symptomatic hypotension, intravenous vasodilators (nitroglycerin, nitroprusside, or nesiritide) may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms.
There is little evidence from randomized controlled trials guiding the use of inotropes and their use is generally limited to the following indications: short-term treatment for AHFS that is unresponsive to adequate doses of diuretics and especially when associated with systemic hypotension, bridge to recovery (as following myocarditis) or to definitive treatment (such as transplantation), or for palliation when relief of symptoms is the agreed upon goal.
Dobutamine and milrinone, the most commonly used inotropes, are associated with improvement in hemodynamic response and symptomatic relief, at the expense of increased mortality.

Additional Reading

Adams KF, Lindenfield J, Arnold J, et al. Executive summary: HFSA 2006 comprehensive heart failure practice guidelines. J Card Fail 2006;12:10-38.
Allen LA and O’Connor CM. Management of acute decompensated heart failure. CMAJ. 2007;176(6):797-805.
Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: The Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J 2005;26:384-416.
Mebazaa A, Gheorghiade M, Pina IL, et al. Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Crit Care Med. 2008;36(Suppl.):S129-S139.

Overview

Acute heart failure syndrome (AHFS), defined as a gradual or rapid change in heart failure signs and symptoms, is the most common cause of hospitalization in the United States1. It is associated with an average in-hospital mortality of 4% to 5%, a 30-day mortality of 7% to11%, and a one-year mortality of 33%2.

In patients with previously established myocardial dysfunction, AHFS commonly reflects exacerbation of symptoms after a period of stability. The clinical presentation and severity of AHFS may range from mild volume overload to life-threatening cardiogenic shock and multi-organ failure unresponsive to pharmacologic therapy.2

Initial management of AHFS depends on definition of the patient’s hemodynamic profile. To guide initial therapy, classify patients into one of four hemodynamic profiles during a brief bedside assessment that relies on evaluation of filling pressures (wet or dry) and adequacy of perfusion (hot or cold) (see figure 1).3