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



INTRODUCTION — Acute decompensated heart failure (ADHF) is a common and potentially fatal cause of acute respiratory distress. The clinical syndrome is characterized by the development of dyspnea, generally associated with rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of acutely elevated cardiac filling pressures (cardiogenic pulmonary edema) [1]. ADHF can also present as elevated left ventricular filling pressures and dyspnea without pulmonary edema.

ADHF is most commonly due to left ventricular (LV) systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema due to an elevated pulmonary capillary wedge pressure in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, particularly renovascular hypertension, and severe renal disease.

Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure [1]. This disorder is discussed elsewhere. (See "Noncardiogenic pulmonary edema".)

General issues related to the management of ADHF in patients with and without acute myocardial infarction (MI) will be reviewed here. The pathophysiology and evaluation of patients with ADHF is presented separately. (See "Evaluation of acute decompensated heart failure".)

Treatment of ADHF and cardiogenic shock in the setting of acute coronary syndrome is discussed separately. Management of right ventricular MI which typically presents with hypotension and clear lungs is also discussed separately. (See "Treatment of acute decompensated heart failure in acute coronary syndromes".) and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction-I" and (see "Right ventricular myocardial infarction".

GENERAL APPROACH — The following recommendations are generally in agreement with those published in the 2009 focused updated of the 2005 American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines and the 2006 in the Heart Failure Society of America (HFSA) guidelines for ADHF [2,3]. Similar recommendations were provided in the 2008 European Society of Cardiology (ESC) guidelines for acute heart failure [4].

Hospitalization — The 2006 HFSA guidelines recommend hospital admission for patients with ADHF with the following clinical conditions [3]:

* Evidence of severely decompensated HF including hypotension, worsening renal function, or altered mentation. As noted in the 2009 ACC/AHA focused update, patients with rapid decompensation and hypoperfusion associated with decreasing urine output and other manifestations of shock should receive rapid intervention to improve systemic perfusion [2].
* Dyspnea at rest which is typically reflected by resting tachypnea and less commonly reflected by oxygen saturation <90 percent.
* Hemodynamically significant arrhythmia including new onset of atrial fibrillation with rapid ventricular response.
* Acute coronary syndromes.

The guidelines recommend that hospitalization should be considered for patients with ADHF with the following clinical conditions:

* Worsened congestion, even if without dyspnea; typically reflected by a weight gain of ≥5 kg
* Signs and symptoms of pulmonary or systemic congestion, even in the absence of weight gain
* Major electrolyte disturbance
* Associated comorbid conditions such as pneumonia, pulmonary embolus, diabetic ketoacidosis, or symptoms suggestive of transient ischemic attack or stroke
* Repeated ICD firings
* Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion

Inpatient monitoring — Patients who are admitted to the hospital for the management of ADHF are at risk for hemodynamic instability and arrhythmias, so close monitoring is necessary [2,3]. The HFSA guidelines recommend more than daily monitoring of vital signs (including orthostatic blood pressure) and at least daily monitoring of weight, fluid intake and output, symptoms and signs of congestion, serum electrolytes, BUN, and serum creatinine [3]. Routine tests include blood glucose, troponin, complete blood count, oxygen saturation, and the INR if warfarin is used. Evaluation of BNP or NT-proBNP, liver function tests, urinalysis, D-dimer, and arterial blood gases is recommended as clinically indicated.

ADHF is associated with an exceptionally high rate of readmissions, which is due in part to inadequate fluid removal during the initial admission [5,6]. Persistent congestion may be difficult to discern and accurate intake and output assessments are often difficult to maintain.

Daily assessment of patient weight may be the most effective method for documenting effective diuresis [2]. For accurate comparisons, daily measurements should use the same scale and should be performed at the same time each day, usually in the morning, prior to eating and after voiding. Weight comparisons may require adjustment for variations in food intake.

Telemetry is usually continued for at least 24 to 48 hours. This may be discontinued once the patients's hemodynamics, medication regimen, and electrolytes are stable.

Hemodynamic monitoring — The role of invasive hemodynamic monitoring in patients with ADHF is discussed separately.(See "Evaluation of acute decompensated heart failure", section on Swan-Ganz catheter and.) (See "Management of refractory heart failure", section on 'Hemodynamic monitoring',In patients with adequate acoustic windows, echocardiography may provide a noninvasive means of estimating filling pressures. (See "Tissue Doppler echocardiography", section on 'Estimation of LV filling pressures'.)

Treatment goals for acute versus chronic HF — It is important to distinguish the management of ADHF from that of chronic HF. The treatment of chronic HF, particularly when due to systolic dysfunction, is built around therapies that have been shown to reduce long-term mortality (eg, ACE inhibitors and beta blockers).

In contrast, the goals of the initial management of ADHF are hemodynamic stabilization, support of oxygenation and ventilation, and symptom relief [7]. Some of the cornerstones of chronic HF therapy should be avoided or used with caution in ADHF (eg, beta blockers), particularly during the period of initial stabilization. Such therapies may be initiated or reinstituted later in a patient's course.

The HFSA guidelines recommend the following treatment goals for patients admitted for ADHF [3]:

* Improve symptoms
* Optimize volume status
* Identify etiology
* Identifying precipitating factors
* Optimize chronic oral therapy
* Minimize side effects
* Identify patients who might benefit from revascularization (see "Treatment of acute decompensated heart failure in acute coronary syndromes")
* Educate patients concerning medications and self assessment of HF,
* Consider and, where possible, initiate a disease management program. (See "Prognosis of heart failure", section on 'Disease management programs'.)

Systolic versus diastolic dysfunction — Among patients with chronic HF, long-term management strategies differ according to whether or not the patient has significant systolic dysfunction. (See "Overview of the therapy of heart failure due to systolic dysfunction" and "Treatment and prognosis of diastolic heart failure".)

In the acute setting, however, some of the initial therapies are similar in systolic and diastolic HF, including the following:

* Diuresis
* Supplemental oxygen and assisted ventilation, if necessary
* Vasodilator therapy in selected patients
* Morphine sulfate in selected patients

Some components of the initial treatment strategy are approached differently in patients with systolic versus diastolic HF. Among patients with systolic dysfunction, some medications should be avoided or used with caution in the acute setting (eg, ACE inhibitors and beta blockers). In contrast, for patients with primarily diastolic dysfunction, treatment of hypertension and tachycardia is particularly important. Thus, ACE inhibitors and beta blockers may be useful in acute as well as chronic HF in patients with primarily diastolic dysfunction. Inotropic agents are not indicated in patients with diastolic dysfunction with preserved systolic function.

COMPONENTS OF THERAPY FOR ADHF

Initial stabilization — Patients presenting with acute dyspnea from ADHF should be rapidly assessed and stabilized. Stabilization measures include

* Airway assessment to assure adequate oxygenation and ventilation, including continuous pulse oximetry
* Vital signs assessment with attention to hypotension or hypertension
* Continuous cardiac monitoring
* Intravenous access
* Seated posture
* Diuretic therapy
* Vasodilator therapy
* Urine output monitoring (perhaps with urethral catheter placement)

Following airway and oxygenation assessment, initial stabilization includes the initiation of therapies aimed at the rapid correction of hemodynamic and intravascular volume abnormalities. The mainstay of therapy for these abnormalties in the acute setting is vasodilator and diuretic therapy. The aggressiveness of each depends on the patient's hemodymic and volume status. Patients with flash pulmonary edema due to hypertension, for instance, require aggressive vasodilatory therapy. Patients with normotension and volume overload best respond to a combination of diuretic therapy and vasodilators. Patients with hypotension and intravascular overload cannot tolerate vasodilators, and may respond either to diuretics alone or in combination with inotropes. It is important to tailor the therapy to the individual patient.

Supplemental oxygen and assisted ventilation — Supplemental oxygen therapy and assisted ventilation should be provided as needed. The 2009 focused update of the 2005 ACC/AHA guidelines recommend oxygen therapy to relieve symptoms related to hypoxemia. The 2006 HFSA guidelines note that routine administration of supplemental oxygen in the absence of hypoxia is NOT recommended [3].

For patients requiring supplemental oxygen, we suggest considering initial therapies in the following order:

* Non-rebreather face mask delivering 100 percent oxygen.
* If respiratory distress, respiratory acidosis, and/or hypoxia persist, we suggest noninvasive positive pressure ventilation (NPPV) 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 NPPV decreases the need for intubation and improves respiratory parameters, such as dyspnea, hypercapnia, acidosis, and heart rate. NPPV may be particularly beneficial in patients with hypercapnia. These issues and conflicting data on a possible impact on mortality are discussed in detail separately. (See "Noninvasive positive pressure ventilation in acute respiratory failure in adults", section on 'Cardiogenic pulmonary edema'.)

Patients with respiratory failure who fail NPPV, or do not tolerate or have contraindications to NPPV (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 mechanical ventilation" and "Positive end-expiratory pressure (PEEP)", section on Cardiac disease.)

Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.

Diuretics — Patients with ADHF are usually volume overloaded. Even in the less common situation in which cardiogenic pulmonary edema develops without significant volume overload (eg, with hypertensive emergency, acute aortic or mitral valvular insufficiency), fluid removal with intravenous diuretics can relieve symptoms and improve oxygenation.

Although the safety and efficacy of diuretics have not been established in randomized, controlled trials, extensive observational experience has demonstrated that they effectively relieve congestive symptoms. (See "Use of diuretics in heart failure".)

Patients with ADHF and evidence of volume overload, regardless of etiology, should be treated with intravenous diuretics as part of their initial therapy [2,3,8]. Rare exceptions include patients with severe hypotension or cardiogenic shock. In such cases, the underlying cause for hemodynamic instability should be sought and the patient may require hemodynamic and mechanical ventilatory support. Patients with aortic stenosis with volume overload should be diuresed with caution. As noted in the 2009 focused update of the 2005 ACC/AHA HF guidelines, patients admitted with significant fluid overload should receive diuretic therapy without delay in the emergency department or outpatient clinic as early intervention may produce better outcomes [2]. (See 'Inotropic agents' below and 'Mechanical cardiac assistance' below and "Treatment and prognosis of cardiogenic shock complicating acute myocardial infarction", section on 'Circulatory support' and "Overview of mechanical ventilation", ).

Intravenous rather than oral administration is recommended because of greater and more consistent drug bioavailability.

Diuretic dosing — Common initial intravenous doses of loop diuretics in patients with normal renal function include the following:

* Furosemide — 40 mg intravenously
* Bumetanide — 1 mg intravenously
* Torsemide — 10 to 20 mg intravenously

Diuretic dosing should be individualized and titrated according to response and patient status. Patients who are treated with loop diuretics chronically are usually treated with a higher dose in the acute setting; diuresis may be achieved with an intravenous dose that is at least equivalent in milligrams to their maintenance oral dose (eg, 80 mg of intravenous furosemide for a patient who takes 80 mg orally daily) [2].

Peak diuresis typically occurs 30 minutes after administration. Most patients will require additional diuresis through the course of their care. Diuretic administration two or more times per day may be necessary.

Later transition from intravenous to oral diuretics should be made with careful attention to HF status, supine and upright hypotension, renal function and electrolytes [2].

Monitoring — Volume status and urine output should be continually reassessed. In addition, side effects (including worsening renal function, electrolyte abnormalities (with associated arrhythmia risk), and symptomatic hypotension) should be carefully monitored. (See "Optimal dosage and side effects of loop diuretics".)

Serum potassium and magnesium levels should be monitored at least daily and maintained in the normal range. Severe muscle cramps may occur with overly rapid diuresis and should be treated with potassium repletion if indicated [3].

Hemodynamic effects — By reducing intravascular volume, diuresis will eventually lower central venous and pulmonary capillary wedge pressures. In addition, furosemide and possibly other loop diuretics also have an initial morphine-like effect in acute pulmonary edema, causing venodilation that can decrease pulmonary congestion prior to the onset of diuresis [9]. This effect appears to be mediated by enhanced release of prostaglandins. (See "Use of diuretics in heart failure", section on Morphine-like effect in acute pulmonary edema.)

Reductions in right and left heart filling pressures with diuresis are frequently associated with augmented forward stroke volume and cardiac output related to decreases in functional tricuspid and mitral regurgitation and reduction in right ventricular volume with relief of left ventricular compression and improved left ventricular distensibility [3].

However, during diuresis some patients experience symptomatic hypotension with decreasing cardiac output and systemic blood pressure due to a lag in reequilibration of intravascular volume via movement of fluid from the interstitial space. Patients with HF with preserved LV ejection fraction (LVEF) or restrictive physiology may be more sensitive to diuresis-induced reductions in preload. Diuretics may enhance the hypotensive effects of ACE inhibitor or angiotensin receptor blocker (ARB) therapy even when volume overload persists. Careful monitoring during diuresis is required to prevent adverse hemodynamic effects.

Renal effects — Renal function frequently deteriorates during diuretic treatment and careful monitoring is recommended. The main mechanism is a decrease in cardiac output as cardiac filling pressures are reduced. Worsening renal function during diuretic treatment of HF is an indicator of poor prognosis and may occur before euvolemic status is achieved. (See "Predictors of survival in heart failure due to systolic dysfunction", section on 'Reduced GFR and elevated BUN'.)

Guidelines for management of patients with ADHF with abnormal or rising serum creatinine and/or BUN include the following [3]:

* If serum creatinine rises modestly in the face of continued signs and symptoms of congestion, diuresis is generally continued.
* If increases in serum creatinine appear to reflect intravascular volume depletion, then reduction or temporary discontinuation of diuretic or vasodilator therapy should be considered. Adjunctive inotropic therapy should be considered.
* Patients with moderate to severe renal dysfunction and evidence of intravascular fluid overload should continue to be treated with diuretics. In the presence of severe fluid overload, renal function may improve with diuresis.
* If substantial congestion persists and diuresis cannot be achieved without an unacceptable degree of azotemia, then ultrafiltration or dialysis should be considered. (See 'Ultrafiltration' below and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Indications, timing, and dialysis dose".)

Inadequate response to diuretic therapy — For patients who do not respond adequately to initial loop diuretic therapy, options include [2,3]:

* Sodium and fluid restriction. Sodium restriction to a limit of <2 g daily may be considered in patients with refractory volume overload [3]. (See 'Sodium and fluid restriction' below.)

* Doubling the diuretic dose until diuresis ensues or the maximum recommended dose is reached. (See "Optimal dosage and side effects of loop diuretics", section on 'Maximum effective dose'.)

* Addition of a thiazide diuretic to potentiate the effects of the loop diuretic. Chlorothiazide is the only thiazide that can be given intravenously; however, its availability may be limited and a rapidly absorbed oral preparation, such as hydrochlorothiazide, is an alternative. A potassium-sparing diuretic (such as spironolactone) can also be added, more to prevent potassium wasting than to significantly increase the diuresis. (See "Treatment of refractory edema", section on 'Enhanced tubular sodium reabsorption'.)

The HFSA and ACC/AHA guidelines recommend oral metolazone or spironolactone or intravenous chlorothiazide as the second diuretic agent to add when diuretic response is inadequate. Although it has been suggested that metolazone is the thiazide of choice in refractory patients with advanced renal failure (GFR below 20 mL/min), there is at present no convincing evidence that metolazone has unique efficacy among the thiazides when comparable doses are given. (See "Treatment of refractory edema", section on 'Enhanced tubular sodium reabsorption'.)

* A continuous intravenous infusion of the loop diuretic. A Cochrane review of eight trials in 254 patients found that urine output was significantly greater with a continuous infusion than with bolus administration, although the difference was modest (mean difference 271 mL per 24 hours) [10]. Less tinnitus and hearing loss occurred with continuous infusion. The review concluded that the available data were insufficient to confidently assess the relative merits of the two approaches.

In addition, ultrafiltration may be considered. (See 'Ultrafiltration' below.)

Sodium and fluid restriction — Dietary sodium restriction is an important component of therapy to restore euvolemia and greater restriction may be feasible in hospital than in the outpatient setting [3]. The HFSA guidelines on ADHF recommend a low sodium diet (2 g daily) and consideration of stricter sodium restriction in patients with recurrent or refractory volume overload.

Mild hyponatremia is common among HF patients and a low serum sodium is an adverse prognostic indicator. (See "Hyponatremia in heart failure", section on 'Effect on prognosis'.)

Most HF patients with hyponatremia have volume overload, rather than volume depletion. The HFSA guidelines recommend fluid restriction (<2 L/day) in HF patients with moderate hyponatremia (serum sodium <130 meq/L) and volume overload and indicate that fluid restriction should be considered to assist in treatment of fluid overload in other patients [3]. Stricter fluid restriction may be considered in patients with severe (serum sodium <125 meq/L) or worsening hyponatremia, although patient tolerance of strict fluid restriction may be limited. (See "Hyponatremia in heart failure", section on 'Treatment'.)

Vasodilator therapy — In patients without hypotension with severely symptomatic fluid overload, vasodilators such as intravenous nitroglycerin, nitroprusside, or nesiritide can be beneficial when added to diuretics or in those who do not respond to diuretics alone [2]. Patients with systemic hypertension may require more aggressive vasodilator therapy (eg, up-titration of nitroglycerin) to assure more rapid reversal of dyspnea.

The 2006 HFSA guidelines provide the following recommendations for use of vasodilators [3]:

* In the absence of symptomatic hypotension, intravenous nitroglycerin, nitroprusside or nesiritide may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms in patients admitted with ADHF.
* Frequent blood pressure monitoring is recommended with vasodilator agents. Dosage of these agents should be decreased if symptomatic hypotension develops. Once symptomatic hypotension is resolved, reintroduction and titration may be considered.
* Intravenous nitroglycerin or nitroprusside and diuretics are recommended for rapid symptom relief in patients with acute pulmonary edema or severe hypertension.
* Intravenous nitroprusside, nitroglycerin or nesiritide may be considered in patients with ADHF and advanced HF who have persistent severe HF despite aggressive treatment with diuretics and standard oral therapies.

Nitrates — Nitrates are the most commonly used vasodilators. In patients without symptomatic hypotension, intravenous nitroglycerin added to diuretic therapy may contribute to rapid improvement in congestive symptoms [2,3]. Nitroglycerin reduces LV filling pressure primarily via venodilation. At higher doses the drug variably lowers systemic afterload and increases stroke volume and cardiac output.

The benefit of nitrate therapy was illustrated by a study in which 110 patients were randomly assigned to a combination of either high dose intravenous isosorbide dinitrate plus low dose intravenous furosemide or low dose isosorbide dinitrate plus high dose furosemide [11]. Patients receiving the high dose isosorbide dinitrate and low dose furosemide combination had a significantly lower combined risk of myocardial infarction, requirement for mechanical ventilation or death than those treated with the high dose diuretic and low dose isosorbide regimen.

Tachyphylaxis can occur within hours with administration of high doses of nitroglycerin and the strategy of nitrate-free interval used to reduce tolerance during chronic therapy could result in adverse hemodynamic effects in patients with ADHF. Potential adverse effects of nitroglycerin include hypotension and headache. Nitrate administration is contraindicated after use of PDE-5 inhibitors such as sildenafil. (See "Sexual activity in patients with heart disease", section on Adverse interaction with.) nitrates).

In patients with ADHF, we recommend intravenous rather than transdermal (ointment or patch) or oral nitrate administration for greater speed and reliability of delivery and ease of titration. An initial dose of 5 to 10 µg/min of intravenous nitroglycerin is recommended with the dose increased in increments of 5 to 10 µg/min every 3 to 5 minutes as required and tolerated (dose range 10 to 200 µg/min).

Similar benefits have been described with high-dose intravenous isosorbide dinitrate, where available [11,12]. However, if hypotension occurs, the longer half-life of isosorbide dinitrate compared to intravenous nitroglycerin (four hours versus three to five minutes) is a major disadvantage.

Nitroprusside is a potent vasodilator with balanced venous and arteriolar effects producing rapid reduction in pulmonary capillary wedge pressure and increase in cardiac output. A need for pronounced afterload reduction is an indication for nitroprusside (initial dose 5 to 10 µg/min, dose titrated up to every 5 minutes, dose range 5 to 400 µg/min) as opposed to nitroglycerin [13]. Examples of such settings include hypertensive emergency, acute aortic regurgitation, acute mitral regurgitation, or acute ventricular septal rupture. The dose is generally titrated to maintain a systolic blood pressure >90 mmHg or mean arterial pressure > 65 mmHg. (See "Drug treatment of hypertensive emergencies", section on 'Nitroprusside'.)

The major limitation to the use of nitroprusside is its metabolism to cyanide. The accumulation of nitroprusside metabolites can lead to the development of cyanide, or rarely thiocyanate, toxicity which may be fatal. Doses above 400 µg/min generally do not provide greater benefit and may increase the risk of thiocyanate toxicity. Nitroprusside administration requires close and continuous blood pressure monitoring, and may cause reflex tachycardia. Thus, the use of nitroprusside is limited to selected patients, usually for durations of less than 24 to 48 hours.

Nesiritide — Although plasma brain natriuretic peptide (BNP) levels are increased in patients with HF, such patients typically are sodium avid and have increased systemic vascular resistance, primarily due to high levels of vasoconstrictors, such as angiotensin II and norepinephrine. Exogenous administration of recombinant human BNP (nesiritide) to patients with HF further increases plasma BNP concentrations and produces arterial and venous vasodilation.

Initial clinical trials have demonstrated the efficacy of nesiritide in improving hemodynamic parameters and symptoms of heart failure. However, subsequent studies raised concerns about a potential adverse impact on mortality rate and a potential risk of worsening renal function. In addition nesiritide has a longer effective half-life than the nitrate vasodilators so hypotension may persist longer. (See "Nesiritide in the treatment of acute decompensated heart failure".)

Nesiritide is suggested as an alternative vasodilator therapy in patients with ADHF without hypotension with volume overload who remain dyspneic despite intravenous loop diuretics. Nesiritide is typically given as an initial intravenous bolus of 2 mcg/kg, followed by a continuous infusion of 0.01 mcg/kg per with subsequent dose adjustment as necessary. Close monitoring of hemodynamics, urine output, and renal function are necessary for effective clinical use and safety.

ACE inhibitors and ARBs — For patients with HF due to systolic dysfunction, ACE inhibitors and angiotensin receptor blockers (ARBs) are a mainstay of chronic therapy. (See "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use" and "Angiotensin II receptor blockers in heart failure due to systolic dysfunction: Therapeutic use".)

Among patients with ADHF, the role of angiotensin inhibition depends upon whether the patient is already receiving such therapy.

Continued therapy — For the majority of patients with systolic dysfunction who have been treated with chronic ACE inhibitor or ARB therapy, maintenance oral therapy can be cautiously continued during an episode of ADHF in the absence of hemodynamic instability or contraindications [2]. These medications should be decreased or discontinued in the following settings:

* Hypotension
* Acute renal failure
* Hyperkalemia

With regard to hypotension, two additional points should be considered:

* Some patients with chronic HF and severe left ventricular systolic dysfunction tolerate relatively low blood pressures (eg, systolic blood pressure 90 to 100 mmHg). Such patients often tolerate chronic ACE inhibitor or ARB therapy and may tolerate these drugs in the acute setting as well.
* Patients with acute pulmonary edema may initially be hypertensive due to high catecholamine levels during the early period of distress. With initial therapy, blood pressure may fall rapidly and patients may become relatively hypotensive, particularly if they are aggressively diuresed. Thus, long-acting drugs, such as ACE inhibitors and ARBs, should be administered with caution the first few hours of hospitalization.

Initiation of therapy — Although some have advocated early use of ACE inhibitor in patients with acute decompensated heart failure, we do not recommend this approach. There is limited data on the safety and efficacy of initiating new ACE inhibitor or ARB therapy in the early phase of therapy of ADHF (ie, the first 12 to 24 hours) [7].

Major concerns with early therapy include:

* Patients with ADHF may develop hypotension and/or worsening renal function during initial therapy. Determining the pathogenesis of such complications is more difficult if an ACE inhibitor or ARB has been given. Hypotension following administration of these agents may be prolonged given the long effective half-lives of these agents.
* The intravenous ACE inhibitor enalaprilat may have deleterious effects in patients with an acute myocardial infarction, especially when complicated by HF or aggressive diuresis [14,15].

Thus, intravenous enalaprilat should be avoided in patients with an acute myocardial infarction and probably in those with other causes of HF [7,14]. Early initiation of oral ACE inhibitor therapy is also not recommended (except for those with acute infarction), and should be avoided in patients at high risk for hypotension (eg, low baseline blood pressure or hyponatremia, which is a marker for increased activation of the renin-angiotensin system and therefore increased dependence upon angiotensin II for blood pressure maintenance). In addition, the aggressive diuretic therapy typically given for acute pulmonary edema may increase sensitivity to ACE inhibition or angiotensin blockade, including risks of hypotension and renal dysfunction. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use" and "Pathophysiology of heart failure: Neurohumoral adaptations" and "Hyponatremia in heart failure".)

Once the patient is stable, chronic oral therapy with ACE inhibitor or ARB can be started. Initiation of these therapies known to improve outcomes is recommended in stable patients with systolic dysfunction prior to hospital discharge [2]. (See "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use" and "Angiotensin II receptor blockers in heart failure due to systolic dysfunction: Therapeutic use".)

Inotropic agents — The intravenous inotropic agents such as dobutamine and/or milrinone may be helpful in selected patients with severe LV systolic dysfunction and low output syndrome (diminished peripheral perfusion and end-organ dysfunction) for whom treatment may be limited by marginal systemic blood pressure or inadequate response to vasodilator and diuretic therapy [16,17].

As recommended in the 2009 ACC/AHA focused update, for patients with evidence of hypotension associated with hypoperfusion AND obvious evidence of elevated cardiac filling pressures (eg, elevated jugular venous pressure or elevated pulmonary artery wedge pressure), intravenous inotropic or vasopressor drugs are recommended to maintain systemic perfusion and preserve end-organ function while more definitive treatment is considered [2]. However, the usefulness of intravenous inotropic drugs to maintain systemic perfusion and preserve end-organ performance is uncertain for patients with severe systolic dysfunction, low blood pressure and evidence of low cardiac output.

Similarly, the 2006 HFSA guidelines for ADHF include the following recommendations for use of inotropes [3]:

* Intravenous inotropes (milrinone or dobutamine) may be considered to relieve symptoms and improve end-organ function in patients with advanced HF characterized by LV dilation, reduced LVEF, and diminished peripheral perfusion or end-organ dysfunction (low output syndrome), particularly if these patients have marginal systolic blood pressure (<90 mmHg), have symptomatic hypotension despite adequate filling pressure, or are unresponsive to, or intolerant of, intravenous vasodilators.
* Intravenous inotropes may be considered in similar patients (e.g. patients with depressed systolic function and marginal cardiac output) with evidence of fluid overload if they respond poorly to intravenous diuretics or manifest diminished or worsening renal function.
* When adjunctive therapy is needed in other patients with ADHF (e.g. patients with preserved cardiac output), administration of vasodilators should be considered instead of intravenous inotropes.
* Intravenous inotropes are not recommended unless left heart filling pressures are known to be elevated based on direct measurement or clear clinical signs.
* Administration of intravenous inotropes in the setting of ADHF should be accompanied by continuous or frequent blood pressure monitoring and continuous monitoring of cardiac rhythm.
* If symptomatic hypotension or worsening tachyarrhythmias develop during administration of these agents, discontinuation or dose reduction should be considered.

Inotropes are not indicated for treatment of ADHF in the setting of preserved systolic function.

Adverse effects — There is concern that inotropic agents may adversely impact outcomes in patients with ADHF with congestion without a low output state [18,19]. Inotropic agents may increase heart rate and myocardial oxygen consumption and thus provoke ischemia and potentially damage hibernating but viable myocardium, particularly in patients with ischemic heart disease. In addition, inotropic agents can increase atrial [18] and ventricular [20] arrhythmias. Given these concerns, careful patient selection is required for inotrope use. (See "Inotropic agents in heart failure due to systolic dysfunction", section on 'Intravenous therapy' and "Use of vasopressors and inotropes".)

Routine use of inotropes in patients hospitalized for heart failure was found to be harmful in the OPTIME-CHF trial [18]. In this trial, 949 patients admitted to the hospital with an acute exacerbation of chronic HF were randomly assigned to a 48 to 72 hour infusion of milrinone or placebo. Milrinone therapy was associated with significant increases in hypotension requiring intervention and atrial arrhythmias, and with nonsignificant increases in mortality in-hospital (3.8 versus 2.3 percent) and at 60 days (10.3 versus 8.9 percent). This trial did not evaluate patients whose treating physicians felt could not be randomized, but demonstrates overall adverse effects in noncritical patients despite improved symptoms.

The general role of inotropic agents in patients with heart failure is discussed separately. (See "Inotropic agents in heart failure due to systolic dysfunction", section on 'Intravenous therapy'.)

Specific agents — The 2006 HFSA guidelines recommend use of the following inotropes in patients with ADHF [3]:

* Milrinone — Milrinone is a phosphodiesterase inhibitor that increases myocardial inotropy by inhibiting degradation of cyclic AMP. Other direct effects of milrinone include reducing systemic vascular resistance (via inhibition of peripheral phosphodiesterase) and improving left ventricular diastolic compliance [21,22]. These changes lead to an increase in cardiac index and decrease in left ventricular afterload and filling pressures. Patients should receive a loading dose of 50 µg/kg over 10 minutes, followed by a maintenance dose of 0.375 to a maximum of 0.750 µg/kg per min. Dose adjustment is required in the presence of renal insufficiency, hypotension, or arrhythmias.
* Dobutamine — Dobutamine acts primarily on beta-1 adrenergic receptors, with minimal effects on beta-2 and alpha-1 receptors. The hemodynamic effects of dobutamine include increase in stroke volume, and cardiac output, and modest decreases in systemic vascular resistance and pulmonary capillary wedge pressure [23,24]. The 2004 ACC/AHA STEMI guidelines suggest using dobutamine in patients with hypotension who do not have clinical evidence of shock [14]. It should be started at 2.5 µg/kg per min and, if tolerated and needed, can be gradually increased to 15 µg/kg per min.

Use of dopamine is discussed separately. (See "Treatment of acute decompensated heart failure in acute coronary syndromes", section on 'Inotropic agents'.)

Beta blockers — Beta blockers reduce mortality when used in the long-term management of such patients, but must be used cautiously in patients with decompensated HF with systolic dysfunction because of the potential to worsen acute HF due to systolic dysfunction. (See "Use of beta blockers in heart failure due to systolic dysfunction".)

Thus, in patients with systolic dysfunction and ADHF, we approach the use of beta blockers in the following manner:

* For patients on chronic beta blocker therapy, if the degree of decompensation is mild without hypotension or evidence of hypoperfusion, continuation of beta blocker as tolerated is recommended [2]. Support for continuation of beta blocker therapy in this setting comes from retrospective analyses of patients enrolled in randomized trials [25,26] and reports from the OPTIMIZE-HF program and the Italian Survey on Acute Heart Failure [27,28]. Withdrawal of beta blocker therapy was associated with increased mortality as compared to continuation of such therapy. However, these retrospective analyses cannot definitively determine whether the discontinuation was the cause of the worse outcome. While the increase in mortality was only partially explained by greater clinical risk factors in the patients withdrawn from beta blocker therapy, such analyses cannot account for all factors. For more severely ill patients, halving of the dose of beta blockers or discontinuation may be necessary.
* For patients on chronic beta blocker therapy with moderate-to-severe decompensation or hypotension, we decrease or withhold beta blocker therapy during the early phase of treatment. In patients requiring inotropic support or those with severe volume overload, we withhold therapy [29].
* For patients who are not treated with beta blocker therapy chronically, we do not initiate a beta blocker in the early management of acute HF. However, the initiation of therapy prior to hospital discharge in stable patients improves long-term beta blocker compliance without an increase in side effects or drug discontinuation, so initiation prior to discharge is recommended in stable patients [2]. Prior to initiation of therapy, the patient should have no or minimal evidence of fluid retention and should not have required recent intravenous inotropic therapy. Beta blocker therapy should start with low doses. Particular caution is indicated in patient who have required inotropes during their hospitalization. (See "Use of beta blockers in heart failure due to systolic dysfunction", section on 'Initiation of therapy'.)

Morphine sulfate — Data are limited on the efficacy and safety of morphine therapy in ADHF. Morphine reduces patient anxiety and decreases the work of breathing. These effects diminish central sympathetic outflow, leading to arteriolar and venous dilatation with a resultant fall in cardiac filling pressures [30,31].

However, retrospective studies have found that morphine administration for ADHF is associated with increased frequency of mechanical ventilation and in-hospital mortality [32,33], although a causal relationship has not been established. In one retrospective analysis, morphine was administered in 14 percent of 150000 ADHF hospitalizations [33]. Morphine use was associated with more frequent mechanical ventilation, longer hospitalizations, more intensive care unit admissions, and greater mortality. After risk adjustment and exclusion of ventilated patients, morphine remained an independent predictor of mortality (OR 4.8, 95% CI 4.52 to 5.18, p <0.001). Although risk adjustment in this study may not have been adequate, these results raise concern about the safety of morphine in this population.

The 2008 ESC guidelines for the treatment of acute heart failure include consideration of morphine as an ungraded recommendation noting that supporting data are limited [4]. Morphine therapy is not mentioned in the 2006 HFSA guidelines on management of ADHF or in the 2009 ACC/AHA focused update.

Given the limited evidence of benefits and potential risks of morphine, we suggest generally avoiding morphine therapy in the treatment of ADHF without acute MI.

The role of morphine sulfate in patients with ADHF who have an acute MI is discussed separately. (See "Treatment of acute decompensated heart failure in acute coronary syndromes".)Morphine sulfate).

ADDITIONAL CONSIDERATIONS — In addition to the above treatments, several additional options and considerations may be relevant to selected patients.

Arrhythmia management — Both supraventricular and ventricular arrhythmias can occur in association with pulmonary edema.

Atrial fibrillation — Atrial fibrillation (AF) is a common arrhythmia, particularly in patients with underlying heart disease. Among patients with both HF and AF, there are several possible relationships:

* Acute HF can precipitate AF due to increases in left atrial pressure and wall stress.
* AF can cause acute HF, particularly if the ventricular response is rapid. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm".)

* AF may be chronic and not directly related to the acute HF decompensation.

It is usually difficult to determine whether AF is the cause or result of ADHF. A reliable history of palpitations that clearly precede the decompensation suggests but does not prove that AF was the cause of the pulmonary edema. The treatment of AF depends upon whether or not it is associated with significant hemodynamic instability and whether or not it is believed to be the precipitant of HF decompensation.

Rate control is often the preferred initial strategy for the following reasons:

* Because acute HF can precipitate AF, cardioversion prior to the resolution of acute HF will often be followed by early recurrence of AF.
* AF is often a chronic condition that is not contributing to the acute decompensation.

However, if a rate control strategy is selected, the negative inotropic effects of beta blockers and nondihydropyridine calcium channel blockers can be problematic in patients with systolic dysfunction. For this reason, short-acting IV formulations of such drugs (eg, esmolol or diltiazem) are often used. In addition, digoxin is also potentially useful in this setting.

Amiodarone can be considered.

In some patients with AF and ADHF, effective treatment of pulmonary edema results in slowing of the ventricular rate or spontaneous reversion of the arrhythmia. If AF persists, it is treated in the same fashion as AF in other situations. (See "Overview of the evaluation and management of atrial fibrillation".)

Restoration of sinus rhythm should be considered in the following settings. (See "Restoration of sinus rhythm in atrial fibrillation: Recommendations", section on 'AF and unstable hemodynamics',:

* If AF is associated with hypotension or evidence of cardiogenic shock.
* If AF is clearly the cause for pulmonary edema.
* If the response to effective therapy of pulmonary edema is slow or suboptimal.

Patients should be begun on heparin prior to cardioversion, if possible. (See "Anticoagulation prior to and after restoration of sinus rhythm in atrial fibrillation".)

Ventricular arrhythmia — Ventricular tachycardia during pulmonary edema is usually life-threatening. As a result, prompt electrical cardioversion or defibrillation is required. If the arrhythmia recurs after reversion, antiarrhythmic therapy with amiodarone or lidocaine may be effective. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction" and "Overview of the acute management of tachyarrhythmias", section on 'Monomorphic ventricular tachycardia'.)

The development of ventricular fibrillation mandates prompt resuscitation.

Mechanical cardiac assistance — Patients with cardiogenic pulmonary edema who are also in cardiogenic shock should be considered candidates for mechanical circulatory support. These patients usually have a cardiac index less than 2.0 L/min per m2, a systolic arterial pressure below 90 mmHg, and a pulmonary capillary wedge pressure above 18 mmHg, despite adequate pharmacologic therapy.

The two major mechanical modalities used in this setting are intraaortic balloon counterpulsation and an internally implanted left ventricular assist device. (See "Intraaortic balloon pump counterpulsation" and "Circulatory assist devices: Cardiopulmonary assist device and short-term left ventricular assist devices".)

Ultrafiltration — Ultrafiltration is an effective method of fluid removal with advantages that include adjustable fluid removal volumes and rates, no effect on serum electrolytes, and decreased neurohormonal activity. (See "Continuous renal replacement therapies: Overview".)

Patients with ADHF accompanied by renal insufficiency or diuretic resistance may benefit from ultrafiltration. Most studies have used a peripherally inserted ultrafiltration device that does not require central access, specialized nursing, or ICU admission [2,27,34].

In the RAPID-CHF trial, 40 patients with ADHF and renal insufficiency (serum creatinine ≥1.5 mg/dL [133 µmol/L]) and/or anticipated diuretic resistance (high daily oral diuretic doses) were randomly assigned to receive usual care with or without ultrafiltration [35]. Ultrafiltration was associated with significant increases in fluid removal after 24 hours (4650 versus 2838 mL without ultrafiltration) and weight loss (2.5 versus 1.9 kg).

In the UNLOAD trial, 200 patients hospitalized for ADHF were randomly assigned to ultrafiltration or to standard care including intravenous diuretics during the admission [29]. Unlike earlier studies, renal dysfunction and/or anticipated diuretic resistance were not entry criteria. Thus, this study included a less selected group of HF patients. The following findings were noted:

* At 48 hours, patients assigned to ultrafiltration had a significantly greater fluid loss (4.6 versus 3.3 liters with standard care). This difference may in part reflect the relatively modest level of diuretic therapy used in the standard care arm.
* At 90 days, patients assigned to ultrafiltration had significantly fewer HF rehospitalizations than patients assigned to standard care (0.22 versus 0.46 admissions per patient) and fewer unscheduled clinic visits (21 versus 44 percent with standard care).
* The rates of adverse events were similar in the two groups, although there was a higher incidence of bleeding in the standard care arm. Renal function was not better with ultrafiltration, as was also found in a substudy incorporating detailed assessment of renal hemodynamics [36].

While these data suggest that ultrafiltration is an effective method for fluid volume removal, it is not clear whether it provides an advantage in patients who respond adequately to standard intravenous diuretics or those who require more aggressive diuresis. In addition, given the relatively small body of data, it is not possible to assess the safety of ultrafiltration.

At present, we reserve ultrafiltration for patients who do not achieve an adequate response to an aggressive diuretic regimen. This recommendation is consistent with the 2005 (with 2009 update) ACC/AHA, 2008 ESC and 2006 HFSA heart failure guidelines [2-4]. Consultation with a kidney specialist may be appropriate prior to opting for a mechanical strategy of fluid removal [2].

Vasopressin receptor antagonists — Vasopressin receptor antagonists have been investigated as an adjunct to diuretics and other standard therapies in patients with ADHF as a means of countering arterial vasoconstriction, hyponatremia, and water retention. However, such treatment is controversial and not included in the HFSA guidelines. The 2008 ESC guidelines suggest consideration of Tolvaptan for HF patients with hyponatremia in an ungraded recommendation [4]. Tolvaptan is the most studied agent in this setting but is not FDA-approved. (See "Possibly effective emerging therapies for heart failure".)Vasopressin receptor antagonists and (see "Hyponatremia in heart failure", section on 'Vasopressin receptor antagonists'.

Discharge from hospital — Careful in-hospital management and discharge planning is indicated to reduce the risk of post-discharge mortality and readmission. Recommended discharge criteria (table 2) include addressing exacerbating factors, achieving near optimal volume status and pharmacologic therapy, and transition to outpatient care [3]. Discharge planning should address details of medication, dietary sodium restriction, and recommended activity level; early follow-up by phone or clinic visit; compliance; monitoring of body weight, electrolytes, and renal function; and consideration of referral for formal disease management.

Comprehensive written discharge instructions are recommended for all patients hospitalized for HF and their caregivers with special emphasis on the following issues [2,3]:

* Diet (including dietary sodium restriction)
* Discharge medications (with special focus on compliance and uptitration to recommended doses of ACE inhibitor, ARB and beta blocker medication) (see "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use" and "Angiotensin II receptor blockers in heart failure due to systolic dysfunction: Therapeutic use" and "Use of beta blockers in heart failure due to systolic dysfunction")

* Activity level
* Follow-up including monitoring of electrolytes and renal function, early follow-up by phone or clinic visit, and postdischarge systems of care including consideration of referral for formal disease management
* Daily weight monitoring, and
* What to do if HF symptoms worsen

SUMMARY AND RECOMMENDATIONS — The following summary and recommendations apply to the management of patients with ADHF. They are generally in agreement with those published in the 2005 ACC/AHA HF guidelines with 2009 focused update, the 2006 HFSA ADHF guidelines [3] and the 2004 ACC/AHA STEMI guidelines with 2007 focused update and the 2002 ACC/AHA NSTEMI guidelines [2,37-39].

* Initial therapy includes the following:

- Supplemental oxygen and assisted ventilation if necessary

- Diuresis with an intravenous loop diuretic

- Vasodilator therapy in patients without hypotension (eg, intravenous nitroglycerin)

* In selected patients with severe or refractory symptoms, the following additional therapies may be indicated:

- Intravenous positive inotropic agents

- Mechanical cardiac assistance

- Ultrafiltration

Oxygen and ventilatory support — Patients with ADHF and a decreased oxygen saturation should be treated with supplemental oxygen.

* Patients with significant hypoxia or respiratory distress are generally treated with 100 percent oxygen via a nonrebreather facemask, and later titrated to patient comfort and an oxygen saturation of at least 90 percent.
* For patients with ADHF and respiratory failure, we recommend a trial of noninvasive positive pressure ventilation (NPPV) if emergent intubation is not indicated, no contraindications to NPPV exist (table 1), and personnel with experience in NPPV are available (Grade 1A). (See 'Supplemental oxygen and assisted ventilation' above and "Noninvasive positive pressure ventilation in acute respiratory failure in adults", section on 'Cardiogenic pulmonary edema'.)

* Patients with respiratory failure due to ADHF who fail NPPV, do not tolerate NPPV, or have contraindications to NPPV (table 1), require endotracheal intubation for conventional mechanical ventilation. (See "Overview of mechanical ventilation".)

Fluid removal — Patients with ADHF and pulmonary edema have symptomatic relief and improved oxygenation with fluid removal. Diuretics are recommended except in patients with severe hypotension or cardiogenic shock.

* In patients with ADHF and fluid overload, we recommend that initial therapy include an intravenous loop diuretic (Grade 1B). (See 'Diuretics' above.) Dosing is individualized, determined largely by the patient's renal function and prior diuretic exposure. (See 'Diuretic dosing' above.)

Bolus dosing with intravenous loop diuretics achieves adequate diuresis in most patients. Determination of effective diuretic dosing should be confirmed by demonstration of a negative fluid balance. For patients who do not have adequate fluid removal with this approach, options include:

* Continuous infusion of loop diuretic
* Addition of a thiazide diuretic

In addition, many HF patients are treated with a thiazide diuretic and/or an aldosterone antagonist as part of their chronic medical regimen. In most patients, these medications can be continued during an episode of acute decompensation, with appropriate monitoring of blood pressure, renal function, and electrolytes.

Ultrafiltration is an option for patients refractory to diuretic therapy. (See 'Ultrafiltration' above.)

Vasodilators — Vasodilators, including nesiritide, nitroglycerin, and nitroprusside, can reduce filling pressures, improve symptoms, and facilitate diuresis. (See 'Vasodilator therapy' above.)

* In patients with ADHF who are not hypotensive, we suggest the use of a vasodilator in addition to diuretic therapy with close hemodynamic monitoring (Grade 2C). (See 'Vasodilator therapy' above.) When using vasodilators in patients with ADHF, we favor the following approach:

* - Intravenous nitroglycerin is generally recommended. Nitrate administration is contraindicated after use of PDE-5 inhibitors such as sildenafil.
* - In selected cases when there is a need for significant afterload reduction (eg, hypertensive emergency, acute aortic or mitral regurgitation), we recommend nitroprusside, although the risk of cyanide or thiocyanate toxicity limit its use.
* - Nesiritide is suggested as an alternative vasodilator therapy in patients with ADHF without hypotension with volume overload who remain dyspneic despite intravenous loop diuretics. Nesiritide has a longer effective half-life than the nitrate vasodilators so it may induce more persistent hypotension.

Inotropes and mechanical cardiac support — Patients with ADHF and systolic dysfunction who are hypotensive or who remain in pulmonary edema despite oxygen, diuresis, and, if tolerated, vasodilators, may benefit from intravenous inotropic support and may require mechanical cardiac support. (See 'Inotropic agents' above and "Inotropic agents in heart failure due to systolic dysfunction" and 'Mechanical cardiac assistance' above.)

ACE inhibitors/ARBs and beta blockers — ACE inhibitors, ARBs, and beta blockers require special consideration in patients with decompensated heart failure. The approach to their use depends upon whether the patient has primarily systolic or diastolic dysfunction. (See 'Systolic versus diastolic dysfunction' above.)

Systolic dysfunction — In patients with chronic HF due to systolic dysfunction the long-term use ACE inhibitors/ARBs and beta blockers reduces mortality, but there are short-term risks to the use of these medications in the setting of acute HF. (See 'ACE inhibitors and ARBs' above and 'Beta blockers' above.)

We approach the use of these medications in this setting in the following manner:

* For patients who are not already taking an ACE inhibitor or ARB, we suggest that they NOT be initiated at the time of presentation with an episode of ADHF (Grade 2C). An oral ACE inhibitor or ARB can usually be started within 24 to 48 hours, once the patient is hemodynamically stable.
* For patients who are not already taking a beta blocker, we suggest that they NOT be initiated at the time of presentation with an episode of ADHF (Grade 2B). Beta blockers are generally started later than ACE inhibitors or ARBs, when the patient is euvolemic, usually shortly before discharge.

A detailed discussion of the initiation of these medications, including dosing and sequence of initiation, is presented separately. (See "Overview of the therapy of heart failure due to systolic dysfunction", section on Pharmacologic therapy.)

* For patients who are already taking an ACE inhibitor or ARB, we suggest that maintenance oral therapy be cautiously continued (Grade 2C). However, the dose should be decreased or the drug discontinued if hypotension, acute renal failure, or hyperkalemia is present. (See 'Continued therapy' above.)

* For patients who are already taking a beta blocker, management depends upon the severity of HF decompensation and hemodynamic instability (see 'Beta blockers' above:

- For patients with severe decompensation (eg, severe volume overload and/or requiring inotropic support), we recommend withholding beta blockers. For patients with moderate-to-severe decompensation, we recommend decreasing or holding beta blocker therapy.

- For patients with mild decompensation without hypotension or evidence of hypoperfusion, we recommend continuation of beta blocker as tolerated.

Diastolic dysfunction — As noted above, patients with ADHF are treated similarly whether they have primarily systolic or diastolic dysfunction. However, in patients with diastolic dysfunction, long-term use of ACE inhibitors/ARBs and beta blockers does not provide the same benefit as in patients with HF due to systolic dysfunction. On the other hand, the short term risks of beta blockers are less concerning and treatment of hypertension and tachycardia are particularly important. Thus, antihypertensive agents and beta blockers may be useful in acute as well as chronic HF in patients with primarily diastolic dysfunction. (See "Treatment and prognosis of diastolic heart failure".)

Morphine — There is limited evidence of benefit (eg, reduced patient anxiety and decreased worked of breathing) from morphine sulfate and there is potential risk (eg, increased need for ventilatory support), so we suggest avoiding morphine therapy in patients with ADHF without acute myocardial infarction.

Management of ADHF in MI — Specific considerations apply to treatment of ADHF during acute MI, particularly the importance of revascularization. (See "Treatment of acute decompensated heart failure in acute coronary syndromes".)

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