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, often associated with accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of acutely elevated cardiac filling pressures (cardiogenic pulmonary edema) . ADHF can also present as elevated left ventricular filling pressures and dyspnea without pulmonary edema or as low cardiac output (ie, cardiogenic shock) leading to hypoperfusion of vital organs with or without pulmonary edema.
ADHF is most commonly due to left ventricular systolic and/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 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, and severe renal disease.
General considerations related to the management of ADHF in patients with and without acute myocardial infarction (MI) will be reviewed here. The components of therapy of ADHF and the pathophysiology and evaluation of patients with ADHF are presented separately. (See "Treatment of acute decompensated heart failure: Specific therapies" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".) (Related Pathway(s): Acute decompensated heart failure: Initial management of hypervolemic patients with adequate perfusion.)
Treatment of ADHF and cardiogenic shock in the setting of acute coronary syndrome are 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 "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Right ventricular myocardial infarction".)
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 . This disorder is discussed elsewhere. (See "Noncardiogenic pulmonary edema".)
SITE OF CARE — In patients with acute HF, clinical features that generally indicate need for hospital-level evaluation and care include (related Pathway(s): Heart failure: Selecting the site of care from the emergency department and Acute decompensated heart failure: Selecting the site of care from the outpatient clinic):
●New HF or change in HF: Previously undiagnosed HF with signs and symptoms of pulmonary or systemic congestion, suspected new cause of HF in a patient with prior HF, or repeated presentation with acute HF over a relatively short period of time.
●Symptoms and signs:
•Chest pain or other symptoms or signs suggestive of an acute coronary syndrome. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department" and "Treatment of acute decompensated heart failure in acute coronary syndromes".)
•Dyspnea at rest (typically reflected by resting tachypnea and less commonly reflected by oxygen desaturation). Also, paroxysmal nocturnal dyspnea; severe, progressive orthopnea; or severe, progressive dyspnea with minimal exertion, even if not dyspneic at rest.
•Hypoxemia (ie, oxygen saturation ≤90 percent), unless chronic, stable, and due to known pulmonary disease.
•Evidence of severe decompensation including:
-Relative hypotension (blood pressure substantially lower than usual pressures recorded during prior visits).
-Signs of hypoperfusion (abdominal pain, cool extremities, decline in urine output, decreased cognitive functioning).
•Symptoms or signs that suggest a concomitant acute illness such as pneumonia, pulmonary embolus, diabetic ketoacidosis, altered mental status, transient ischemic attack, or stroke.
•Repeated implantable cardioverter-defibrillator (ICD) discharges.
•Hemodynamically significant arrhythmia (including new atrial fibrillation with rapid ventricular response).
●Certain laboratory abnormalities:
•Major electrolyte disturbance.
•Elevated troponin levels in the absence of acute coronary syndrome.
Hospitalization should also be considered for patients with ADHF with risk factors for unsuccessful or unsafe outpatient treatment including:
●Risks factors for inadequate monitoring and nonadherence:
•Inability to self-monitor and report symptoms.
•History of nonadherence to therapy.
•Recent failure of outpatient HF management.
•Substance use disorder.
•Mental illness that limits self-care.
•Cognitive or functional impairment.
•Absent social supports.
•Residence far from a health care facility.
•Limited transportation or severe weather.
•Necessary supplies unavailable in an acceptable time frame (eg, home oxygen or home IV treatment).
•Visiting Nurse Association, if needed, is not available or cannot be activated in the necessary time frame.
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 Heart Failure Society of America 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, blood urea nitrogen, serum creatinine, and oxygen saturation until stable . Serum potassium and magnesium levels should be monitored at least daily, and more frequent monitoring may be required when diuresis is rapid. Routine tests include blood glucose, troponin, complete blood count, and the International Normalized Ratio if warfarin is used. Evaluation of liver function tests, and urinalysis is frequently indicated and arterial blood gas testing is occasionally indicated (eg, to detect carbon dioxide retention). Measurement of brain natriuretic peptide (BNP) or N-terminal pro BNP can be of value in clarifying the cardiac basis of respiratory distress and/or guiding therapy. Telemetry is usually continued for at least 24 to 48 hours. This may be discontinued once the patient's hemodynamics, medication regimen, and electrolytes are stable.
Documentation of effective diuresis — ADHF is associated with an exceptionally high rate of readmissions, which is due in part to inadequate fluid removal during the initial admission [4,5]. Persistent congestion may be difficult to discern, and accurate intake and output assessments are important, though often difficult to obtain.
Daily assessment of patient weight can be an effective method for documenting effective diuresis, particularly when combined with assessment of fluid intake and output . 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.
Hemodynamic monitoring — The role of invasive hemodynamic monitoring in patients with ADHF is discussed separately. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Swan-Ganz catheter' and "Management of refractory heart failure with reduced ejection fraction", section on 'Use of pulmonary artery catheter'.)
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 and improve symptoms (eg, renin-angiotensin-aldosterone system 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 . Some of the cornerstones of chronic HF therapy should not be added, should be used with caution, or should be withdrawn in ADHF (eg, beta blockers), particularly during the period of initial stabilization. Such therapies may be initiated or titrated upward later in a patient's course.
The Heart Failure Society of America guidelines recommend the following treatment goals for patients admitted for ADHF :
●Improve symptoms, especially congestion and low-output symptoms.
●Restore normal oxygenation.
●Optimize volume status.
●Identify and address 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".)
●Identify patients who might benefit from device therapy. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Cardiac resynchronization therapy in heart failure: Indications and choice of system".)
●Identify risk of thromboembolism and need for anticoagulant therapy.
●Educate patients concerning medications and self-management of HF. (See "Heart failure self-management".)
●Consider and, where possible, initiate a disease-management program. (See "Systems-based strategies to reduce hospitalizations in patients with heart failure".)
SYSTOLIC VERSUS DIASTOLIC DYSFUNCTION — Among patients with chronic HF, long-term management strategies differ according to whether or not the patient has HF with reduced ejection fraction (left ventricular ejection fraction ≤40 percent; HFrEF) versus HF with preserved ejection fraction (HFpEF). (See "Treatment and prognosis of heart failure with preserved ejection fraction" and "Overview of the management of heart failure with reduced ejection fraction in adults".)
In the acute setting, however, some of the initial therapies are similar in systolic and diastolic HF, including the following:
●Supplemental oxygen and assisted ventilation, if necessary
●Vasodilator therapy 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 not be initiated or should be used with caution in the acute setting (eg, beta blockers). In contrast, for patients with primarily diastolic dysfunction, treatment of hypertension and tachycardia is particularly important. Inotropic agents are not indicated in patients with diastolic dysfunction with preserved systolic function.
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 often 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. In addition, in patients with chronic AF, decompensation may be caused by inadequate rate control. 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. Management of AF in patients with acute HF is discussed separately. (See "The management of atrial fibrillation in patients with heart failure", section on 'Acute heart failure management'.)
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, particularly with amiodarone, may be effective. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Overview of the acute management of tachyarrhythmias", section on 'Ventricular tachycardia'.)
The development of ventricular fibrillation mandates prompt resuscitation. (See "Advanced cardiac life support (ACLS) in adults".)
RENOVASCULAR HYPERTENSION — Recurrent unexplained HF decompensation and/or flash (sudden-onset) pulmonary edema occurs in some patients with renovascular hypertension, often with preserved (normal or near normal) left ventricular systolic function. Flash pulmonary edema appears to be more common in patients with bilateral renal artery stenosis as compared to those with unilateral disease (eg, 41 versus 12 percent) [7,8]. The combination of bilateral renal artery stenosis and flash pulmonary edema has been named the Pickering syndrome [9,10]. Acute treatment of acute decompensate HF in patients with this syndrome includes blood pressure control and, in some cases, diuresis. In patients who are euvolemic or dehydrated, diuresis should be avoided, as it may lead to renal insufficiency, and preload reduction with nitrates is preferable.
Only limited observational data are available on the efficacy of revascularization for this condition. A review of revascularization (percutaneous, largely with stenting, or surgery) in 87 reported cases of bilateral renal artery stenosis and flash pulmonary edema reported that renal function improved in 81 percent and 92 percent had no further episodes of flash pulmonary edema . However, these data must be viewed with caution, given the limited controls and risk of bias in these case series.
The 2005 American College of Cardiology/American Heart Association (AHA) peripheral arterial disease guidelines recommended percutaneous revascularization for patients with hemodynamically significant renal artery stenosis and recurrent, unexplained HF or sudden unexplained pulmonary edema . However, an AHA writing group later noted that treatment of atherosclerotic renal artery disease is controversial since the benefits and risks are not well defined . (See "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney" and "Treatment of unilateral atherosclerotic renal artery stenosis".)
PREDICTORS OF OUTCOME — In patients hospitalized with ADHF, probably the most important determinant of the short-term outcomes, and in particular, early readmissions, is the adequacy of diuresis prior to discharge. Several factors have been identified as predictors of better short-term outcome and likely reflect the degree of diuresis, including weight loss, clinical signs of improvement in congestion, and the rise in albumin or hemoglobin .
DISCHARGE FROM HOSPITAL — Careful in-hospital management and discharge planning is indicated to reduce the risk of postdischarge mortality and readmission. Recommended discharge criteria (table 1) include addressing precipitating or exacerbating factors, achieving near optimal volume status and pharmacologic therapy, documentation of left ventricular ejection fraction (generally by echocardiogram), referral to an electrophysiologist if indicated (eg, if evaluation for implantable cardioverter-defibrillator or cardiac resynchronization therapy is appropriate), and transition to outpatient care. Discharge planning should address patient and caregiver education (including details of medication, monitoring of symptoms and body weight, dietary sodium restriction, compliance, and recommended activity level), communication with clinicians involved with postdischarge follow-up, follow-up appointments with clinicians, monitoring of electrolytes and renal function, and consideration of referral for formal disease management. (See "Heart failure self-management" and "Systems-based strategies to reduce hospitalizations in patients with heart failure" and "Overview of the management of heart failure with reduced ejection fraction in adults".) (Related Pathway(s): Acute decompensated heart failure: Discharge checklist and Acute decompensated heart failure: Determining if a hospitalized adult is ready for discharge.)
Although most patients respond well to therapy for ADHF in the hospital where diuretics are generally administered intravenously and dietary sodium/fluid intake are regulated, it is often difficult to predict an effective outpatient diuretic regimen. One way of improving the selection of an effective outpatient diuretic regimen is to convert from intravenous to oral diuretics two or more days prior to discharge. Even when this is done, further dose adjustment is often needed after the patient returns to the home environment where salt and fluid intake is less well regulated.
The importance of early outpatient follow-up after hospital discharge was illustrated by a study of 30,136 Medicare beneficiaries hospitalized for HF at 225 hospitals . The rate of 30-day hospital readmission was slightly but significantly higher (23.3 versus 20.5 percent) in the quartile of hospitals with the lowest rates of early (within seven days) follow-up than in the next quartile (early follow-up rate <32.4 percent versus 32.4 to 37.9 percent). The difference in readmission rates remained significant after adjustment for baseline patient characteristics.
Comprehensive written discharge instructions are recommended for all patients hospitalized for HF and their caregivers with special emphasis on the following issues  (see "Heart failure self-management"):
●Diet (including dietary sodium restriction). (See "Use of diuretics in patients with heart failure", section on 'Sodium and fluid restriction'.)
●Discharge medications (with a focus on safe and appropriate dosing of recommended medications as well as adherence). (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)
●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.
●What to do if HF symptoms worsen. (See "Heart failure self-management".)
Evidence on the efficacy of discharge support is discussed separately. The available evidence suggests that discharge support must go well beyond a simple discharge instruction sheet to be effective. (See "Systems-based strategies to reduce hospitalizations in patients with heart failure", section on 'Inpatient and transitional care strategies'.)
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: Arrhythmias in adults" and "Society guideline links: Heart failure in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topics (see "Patient education: When your lungs fill with fluid (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Site of care – Hospital admission is recommended for patients with acute decompensated heart failure (ADHF) with evidence of severe decompensation (including hypotension, worsening renal function, or altered mentation), dyspnea at rest, hemodynamically significant arrhythmia including new onset atrial fibrillation (AF), or acute coronary syndrome. (See 'Site of care' above.)
Hospitalization should be considered for other patients with ADHF, including those with signs or symptoms of pulmonary or systemic congestion (with or without weight gain), major electrolyte disturbance, or associated comorbid conditions.
●Inpatient monitoring – High hospital readmission rates are partly due to ineffective fluid removal prior to discharge. Daily assessment of patient weight may be the most effective method for documenting effective diuresis. 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. (See 'Inpatient monitoring' above and 'Documentation of effective diuresis' above.)
●Treatment goals – Treatment goals for patients admitted with ADHF include improving symptoms, optimizing volume status, identifying etiology and precipitating factors (particularly ischemia or arrhythmias), initiating and optimizing oral therapy, minimizing side effects, educating patients, and considering a disease management program. (See 'Treatment goals for acute versus chronic HF' above.)
●General treatment – The following initial therapies are similar in systolic and diastolic HF: diuresis, supplemental oxygen and assisted ventilation, and vasodilator therapy in selected patients. (Related Pathway(s): Acute decompensated heart failure: Initial management of hypervolemic patients with adequate perfusion.)
Outpatient medications should be avoided, withdrawn, or used with caution in the acute setting (eg, beta blockers) in patients with systolic dysfunction. In patients on renin-angiotensin-aldosterone system inhibitors and beta blockers, the medications can be continued if the patient is relatively stable (eg, just needs diuresis). (See 'Systolic versus diastolic dysfunction' above.)
●Rhythm management – Restoration of sinus rhythm should be considered if AF is associated with hypotension or cardiogenic shock, if AF is the cause for pulmonary edema, or if the response to therapy of pulmonary edema is suboptimal. (See 'Atrial fibrillation' above.)
Ventricular tachycardia during pulmonary edema generally requires prompt electrical cardioversion or defibrillation. (See 'Ventricular arrhythmia' above.)
●Transition from the inpatient to outpatient setting – Careful discharge planning and transition to outpatient care is indicated to reduce the risk of postdischarge mortality and readmission. (See 'Discharge from hospital' above.)
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