Author
Wilson S Colucci, MD
Section Editors
Stephen S Gottlieb, MD
James Hoekstra, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC



INTRODUCTION — Patients with acute decompensated heart failure (ADHF) commonly have coronary artery disease with or without an acute coronary syndrome [1]. The acute onset of severe myocardial ischemia can lead to a sudden impairment in systolic and diastolic function, resulting in a decreased cardiac output, elevated filling pressures and the development of pulmonary edema. Flash pulmonary edema can result from myocardial ischemia with or without myocardial infarction.

Specific considerations apply to treatment of ADHF in patients presenting with acute coronary syndromes (ACS). The recommendations presented here are generally in agreement with those published in the 2004 American College of Cardiology/American Heart Association (ACC/AHA) STEMI guidelines with 2007 focused update, the 2007 ACC/AHA UA/NSTEMI guideline and the 2009 focused update of the 2005 ACC/AHA heart failure guidelines [2-5].

Overall management of acute coronary syndrome and acute MI (including fuller discussion of all therapies including anticoagulant and antiplatelet agents), cardiogenic shock in the setting of acute MI and general treatment of ADHF are discussed separately. (See "Overview of the management of acute ST elevation myocardial infarction" and "Overview of the management of unstable angina and acute non-ST elevation myocardial infarction" and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction".)

Management of right ventricular MI which typically presents with hypotension and clear lungs is discussed separately (see "Right ventricular myocardial infarction".

REVASCULARIZATION — Urgent revascularization is a major component of therapy for patients presenting with STEMI, and is particularly important for those with HF. Early revascularization is indicated for patients presenting with unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) and HF. As recommended in the 2009 focused update of the 2005 ACC/AHA HF guidelines, urgent cardiac catheterization and revascularization is reasonable when it is likely to prolong meaningful survival in patients with acute HF and known or suspected acute myocardial ischemia due to occlusive coronary disease, especially when there are signs and symptoms of systemic hypoperfusion [5]. (See "Overview of the management of acute ST elevation myocardial infarction" and "Overview of the management of unstable angina and acute non-ST elevation myocardial infarction" and "Coronary arteriography and revascularization for unstable angina or non-ST elevation acute myocardial infarction".)

* Primary percutaneous coronary intervention (PCI) is recommended in patients with STEMI when it can be performed within 90 minutes of first medical contact [2,3]. In addition, it is reasonable to promptly (within 30 minutes of arrival) transfer patients with STEMI with severe HF to facilities capable of rapid revascularization.
* Fibrinolytic therapy is recommended for patients with STEMI when timely primary PCI cannot be performed [2,3]. For patients who have received fibrinolytic therapy, a strategy of coronary angiography with intent to perform PCI (or emergency CABG) is recommended for certain patients including those with

- Cardiogenic shock who are < 75 years of age who are candidates for revascularization

- Severe HF and/or pulmonary edema OR

- Hemodynamically compromising ventricular arrhythmias.

A strategy of rescue revascularization is reasonable for patients with STEMI with cardiogenic shock who are ≥75 years of age who are suitable candidates for revascularization and rescue PCI is also reasonable for patients with hemodynamic instability and/or persistent ischemic symptoms.

* A strategy of early coronary angiography with intent to perform revascularization is indicated in certain UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures) including those with the following (as well as others discussed separately):

- Hemodynamic instability

- Refractory or recurrent angina

- Signs or symptoms of HF or new or worsening mitral regurgitation

- Reduced left ventricular systolic function (LVEF <40 percent) .

MEDICAL THERAPY

Diuretic use — Diuretic (low to intermediate dose furosemide or torsemide or bumetanide) should be administered to treat pulmonary congestion if there is associated volume overload. However, caution is advised to avoid unnecessary or excessive diuresis since some patients are normovolemic, particularly those without prior LV dysfunction and those who have not received fluid loading.

Supplemental oxygen — As for treatment of ADHF generally, supplemental oxygen should be administered to patients MI with arterial oxygen desaturation. It is reasonable to administer oxygen to all patients with MI during the first six hours.

Morphine sulfate — In the setting of STEMI, morphine sulfate is recommend as the analgesic of choice for ischemic pain relief in addition to serving as a treatment for pulmonary edema, provided that additional therapy is used to manage the underlying ischemia. In UA/NSTEMI, it is reasonable to administer morphine if there is uncontrolled ischemic pain, provided that additional therapy is used to manage the underlying ischemia. The recommendation for morphine is less strong in UA/NSTEMI as compared to STEMI because observational data has raised concern about excess mortality in UA/NSTEMI patients receiving morphine.

Vasodilator therapy — Nitroglycerin is recommended for MI patients to treat ischemic pain, hypertension, or pulmonary congestion unless the systolic blood pressure is <100 mmHg or ≥30 mmHg below baseline.

Nitroprusside is often used when pronounced afterload reduction is required (as in the setting of ventricular septal rupture). However, limited data are available on the efficacy and safety of nitroprusside use in the setting of acute MI. One report suggested that nitroprusside administration after MI has an equivocal impact on mortality (worsening of mortality with early administration and improvement of mortality with later treatment) [6]. The adverse effect of nitroprusside in patients with acute MI may be attributable to coronary steal.

Beta blocker therapy — Although initiation of beta-blocker therapy within the first 24 hours is generally recommended for patients presenting with MI, such therapy is contraindicated in patients with signs of HF, evidence of a low output state, increased risk of cardiogenic shock, or other contraindications such as heart block or reactive airways disease.

Beta blocker therapy should be initiated before discharge for secondary prevention and continued indefinitely in all patients who have had an MI or ACS, unless contraindicated. For those who remain in HF throughout the hospitalization, low doses should be initiated, with gradual titration on an outpatient basis.

Beta blocker therapy in patients with MI is discussed in detail separately. (See "Beta blockers in the management of acute coronary syndrome".)

ACE inhibitor and ARB therapy — Initiation of oral angiotensin converting enzyme (ACE) inhibitor within the first 24 hours is recommended in patients with an acute MI who have pulmonary congestion or an LVEF ≤40 unless the systolic blood pressure is <100 mmHg or >30 mmHg below baseline or there are other contraindications. Therapy should be titrated starting with a low initial dose.

ACE inhibitors should be initiated before discharge for secondary prevention and continued indefinitely in certain MI patients, including those with LVEF≤40 percent, hypertension, diabetes or chronic kidney disease.

An angiotensin II receptor blocker (ARB) should be administered to MI patients with HF or LVEF ≤40 who are intolerant of ACEI.

ACE inhibitor and ARB use in MI patients is discussed in detail separately. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)

Aldosterone antagonists — Long-term aldosterone blockade (spironolactone or eplerenone) is recommended in post-MI patients with symptomatic HF or diabetes and LVEF ≤40 without significant renal dysfunction (serum creatinine ≤2.5 mg/dL [221 micromol/L] in men and ≤2.0 mg/dL [177 micromol/L] in women) or hyperkalemia who are already receiving therapeutic doses of ACE inhibitor. (See "Overview of the management of acute ST elevation myocardial infarction", section on Aldosterone antagonists and.) (See "Overview of the management of unstable angina and acute non-ST elevation myocardial infarction", section on Aldosterone antagonists and.) (See "Treatment of acute myocardial infarction in diabetes mellitus", section on 'Aldosterone antagonists'.)

MANAGEMENT OF LOW OUTPUT STATES — A low output state may manifest as hypotension or preserved blood pressure with evidence of hypoperfusion and is not always accompanied by pulmonary congestion. Recommended treatments include inotropic support, intra-aortic counterpulsation, revascularization, and surgical correction of mechanical complications (such as ventricular septal rupture or papillary muscle rupture). (See "Clinical manifestations and diagnosis of cardiogenic shock complicating acute myocardial infarction" and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction" and "Intraaortic balloon pump counterpulsation" and "Mechanical complications of acute myocardial infarction".)

Inotropic agents — Patients with MI, pulmonary congestion and marginal or low blood pressure often require circulatory support with inotropic and vasopressor agents and/or intra-aortic balloon counterpulsation to relieve pulmonary congestion and maintain adequate perfusion. (See "Intraaortic balloon pump counterpulsation".)

The 2004 ACC/AHA STEMI guidelines suggest using dopamine in hypotensive patients with clinical evidence of shock and using dobutamine in hypotensive patients without clinical evidence of shock [2].

Dopamine — Although not mentioned in the 2006 HFSA ADHF guidelines, dopamine is recommended for hypotensive STEMI patients with clinical evidence of shock in the 2004 ACC/AHA guidelines. Its actions are complex and dose-dependent:

* At low doses of 1 to 3 µg/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric artery beds [7].
* At 3 to 10 µg/kg per min, dopamine also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate.
* At medium-to-high doses, dopamine also stimulates alpha-adrenergic receptors, producing arterial and venous constriction that may compromise systolic function and filling pressures. However, a study of 13 patients with class III or IV chronic HF with severe LV systolic dysfunction suggested that renal arterial vasodilation and improvement in cardiac output may persist as the dopamine dose is titrated up to 10 µg/kg per min [7].

Dopamine should be reserved for hypotensive patients without shock for whom an increase in arterial pressure is considered a priority.

Dobutamine — Use of dobutamine in ADHF is discussed separately.

Reference:
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