INTRODUCTION — Patients with acute decompensated heart failure (ADHF) often have coronary artery disease with or without an acute coronary syndrome (ACS) . The acute onset of severe myocardial ischemia can lead to a sudden impairment in systolic and/or 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 (MI) and may occur in the absence of chest pain.
Specific considerations apply to treatment of ADHF in patients presenting with ACS. The recommendations presented here are generally in agreement with those published in the 2004 American College of Cardiology/American Heart Association (ACC/AHA) ST-elevation MI (STEMI) guidelines with 2007 focused update, the 2007 ACC/AHA unstable angina/non-ST-elevation MI (UA/NSTEMI) guideline, and the 2009 focused update of the 2005 ACC/AHA HF guidelines [2-5].
Overall management of ACS 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 acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Prognosis and treatment 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 UA/NSTEMI and HF. As recommended in the 2009 focused update of the 2005 American College of Cardiology/American Heart Association 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 . (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Non-ST-elevation acute coronary syndromes: Selecting an approach to revascularization" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy".)
●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]. The routine performance of PCI within 3 to 24 hours after fibrinolytic therapy has been referred to as pharmacoinvasive strategy. For patients who have received fibrinolytic therapy, a strategy of coronary angiography with intent to perform PCI (or emergency coronary artery bypass graft surgery) is recommended for patients in the following clinical settings:
•Cardiogenic shock who are <75 years of age who are candidates for revascularization
•Severe HF and/or pulmonary edema
•Hemodynamically compromising ventricular arrhythmias
In addition, a pharmacoinvasive strategy is a reasonable option in the following settings:
•Cardiogenic shock with ≥75 years of age and who are suitable candidates for revascularization
•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):
•Refractory or recurrent angina
•Signs or symptoms of HF or new or worsening mitral regurgitation
•Reduced left ventricular (LV) systolic function (LV ejection fraction [LVEF] <40 percent)
Diuretic use — A diuretic (low- to intermediate-dose furosemide, 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, or even hypovolemic, particularly those without prior LV dysfunction and those who have not received fluid loading. In such patients, diuresis may lead to hypotension and potentially a worsening of ischemia.
Supplemental oxygen — As for treatment of ADHF, generally, supplemental oxygen should be administered to patients with myocardial infarction (MI) with arterial oxygen desaturation and assisted ventilation should be provided as needed. It is reasonable to administer oxygen to all patients with MI during the first six hours after presentation [2,4].
For patients requiring supplemental oxygen, we suggest initial therapies in the following order:
●Non-rebreather face mask delivering high-flow percent oxygen.
●If respiratory distress, respiratory acidosis, and/or hypoxia persist, we suggest noninvasive ventilation (NIV) as the preferred initial modality of assisted ventilation as long as the patient does not have a contraindication (table 1).
This approach is supported by evidence from meta-analyses and randomized trials in patients with cardiogenic pulmonary edema, indicating that NIV decreases the need for intubation and improves respiratory parameters.
In addition, a meta-analysis found that continuous positive airway pressure decreases in-hospital mortality . This beneficial effect on mortality was greater in trials with higher proportions of patients with ischemia or MI. These issues and conflicting data on a possible impact on mortality are discussed in detail separately.
●Patients with respiratory failure who fail NIV, or do not tolerate or have contraindications to NIV (table 1) should be intubated for conventional mechanical ventilation. In such patients, positive end-expiratory pressure is often useful to improve oxygenation. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit" and "Positive end-expiratory pressure (PEEP)".)
Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.
Morphine sulfate — In the setting of STEMI, morphine sulfate is recommended as the analgesic of choice for ischemic pain relief 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 with STEMI because observational data have 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) . The adverse effect of nitroprusside in patients with acute MI may be attributable to reflex tachycardia and/or 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 "Acute myocardial infarction: Role of beta blocker therapy".)
ACE inhibitor and ARB therapy — Initiation of an oral angiotensin converting enzyme (ACE) inhibitor is recommended in patients with an acute MI who have heart failure (HF) or systolic dysfunction (LVEF ≤40 percent) unless the systolic blood pressure is <100 mmHg or >30 mmHg below baseline or there are other contraindications. Therapy should be administered orally and titrated starting with a low initial dose. It should be noted that aggressive ACE inhibitor therapy prior to percutaneous intervention for acute MI or prior to hemodynamic stabilization has been associated with an increased risk of cardiogenic shock.
ACE inhibitors should be initiated before discharge for secondary prevention and continued indefinitely in certain MI patients, including those with HF, LVEF ≤40 percent, hypertension, diabetes, or chronic kidney disease.
An angiotensin II receptor blocker (ARB) should be administered to MI patients with HF, LVEF ≤40, or hypertension who are intolerant of ACE inhibitors.
ACE inhibitor or ARB therapy should continue indefinitely. Careful blood pressure monitoring is required when using either agent. 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 — Inpatient initiation of long-term aldosterone blockade (spironolactone or eplerenone) is recommended in post-MI patients with LVEF ≤40 and symptomatic HF and/or diabetes 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 "Acute myocardial infarction: Patients with 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, intraaortic 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 in acute myocardial infarction" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Intraaortic balloon pump counterpulsation" and "Acute myocardial infarction: Mechanical complications".)
Inotropic agents — Patients with myocardial infarction (MI), pulmonary congestion, and marginal or low blood pressure often require circulatory support with inotropic and vasopressor agents and/or intraaortic balloon counterpulsation to relieve pulmonary congestion and maintain adequate perfusion. (See "Intraaortic balloon pump counterpulsation".)
The 2004 American College of Cardiology/American Heart Association (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 .
Dopamine — Dopamine is recommended for hypotensive STEMI patients with clinical evidence of shock as noted in the 2004 ACC/AHA guidelines. Its actions are complex and dose-dependent:
●At low doses of 1 to 3 mcg/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric artery beds . Low doses of dopamine may decrease arterial pressure due to redistribution of blood flow.
●At 3 to 10 mcg/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 heart failure (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 mcg/kg per min .
Dopamine in medium-to-high doses should be reserved for hypotensive patients for whom an increase in arterial pressure is considered a priority.
Use of low-dose dopamine in patients with ADHF is discussed separately. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Inotropic agents'.)
Dobutamine — Use of dobutamine in ADHF is discussed separately. (See "Treatment of acute decompensated heart failure: General considerations".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)
SUMMARY AND RECOMMENDATIONS
●Patients with acute decompensated heart failure (ADHF) often have coronary artery disease with or without an acute coronary syndrome (ACS). Acute onset of myocardial ischemia with or without infarction can cause systolic and/or diastolic dysfunction, resulting in decreased cardiac output, elevated filling pressures, and/or the development of pulmonary edema. (See 'Introduction' above.)
●Urgent revascularization is a major component of therapy for patients presenting with ST-elevation myocardial infarction (STEMI) and is particularly important for those with HF. Early revascularization is indicated for patients presenting with unstable angina/non-ST-elevation MI and HF. (See 'Revascularization' above.)
●Medical therapy of ADHF with ACS includes judicious use of diuretics, supplemental oxygen and ventilatory support as needed, and vasodilator therapy. (See 'Medical therapy' above.)
●Initiation of oral angiotensin converting enzyme inhibitor is recommended within the first 24 hours of an acute MI in patients with pulmonary congestion or a left ventricular ejection fraction ≤40 percent. Beta blocker therapy within the first 24 hours is generally recommended for patients presenting with MI but initiation should be deferred in patients with HF. Inpatient initiation of long-term aldosterone antagonist therapy is also recommended in selected patients. (See 'Medical therapy' above and "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)
●Patients with MI, pulmonary congestion, and marginal or low blood pressure often require circulatory support with inotropic and vasopressor agents and/or intraaortic balloon counterpulsation to relieve pulmonary congestion and maintain adequate perfusion. (See 'Management of low output states' above and "Intraaortic balloon pump counterpulsation".)
●In the setting of STEMI, dopamine is recommended in hypotensive patients with clinical evidence of shock and dobutamine is recommended in hypotensive patients without clinical evidence of shock. (See 'Inotropic agents' above.)
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