Official reprint from UpToDate®

www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Treatment of acute decompensated heart failure in acute

coronary syndromes
AUTHOR: Wilson S Colucci, MD
SECTION EDITORS: Stephen S Gottlieb, MD, James Hoekstra, MD
DEPUTY EDITOR: Todd F Dardas, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2023.

This topic last updated: Oct 11, 2021.

INTRODUCTION

Patients with acute decompensated heart failure (ADHF) often have coronary artery disease
with or without an acute coronary syndrome (ACS) [1]. 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 [5]. (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):

• Hemodynamic instability
• 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)

MEDICAL THERAPY

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 [6]. 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) [7]. 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 [2].

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 [8]. 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 [8].

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.)

Use of UpToDate is subject to the Terms of Use.

Topic 3498 Version 20.0

GRAPHICS

Contraindications to noninvasive ventilation

Absolute

The need for emergent intubation (eg, cardiac or respiratory arrest, severe respiratory distress, unstabl
cardiac arrhythmia)

Relative
Nonrespiratory organ failure that is acutely life-threatening

Severe encephalopathy (eg, GCS <10)

Severe upper gastrointestinal bleeding

Hemodynamic instability

Facial or neurological surgery, trauma, or deformity

Significant airway obstruction (eg, laryngeal mass or tracheal tumor)

Inability to cooperate, protect airway, or clear secretions (eg, patients at high risk or aspiration)

Anticipated prolonged duration of mechanical ventilation (eg, ≥4 to 7 days)

Recent esophageal or gastric anastomosis*

Multiple contraindications

Insufficient staffing support

GCS: Glasgow Coma Score.

* Esophageal or gastric distension from air may increase the risk of anastomotic dehiscence.

Adapted with permission from: International Consensus Conferences in Intensive Care Medicine: Noninvasive positive pressure
ventilation in acute respiratory failure. Am J Respir Crit Care Med 2001; 163:283. Copyright © 2001 American Thoracic Society.

Graphic 60442 Version 6.0

