Acute decompensated heart failure
Acute heart failure, Decompensated heart failure, Acute systolic heart failure
Congestive heart failure
Systolic heart failure
1. Description of the problem
Acute heart failure is a complex clinical syndrome that results from the inability of the heart to meet the metabolic demands of the body. This disease is quite prevalent: over 5 million people have heart failure in the United States alone. There are nearly 300,000 deaths from heart failure annually, and well over 1 million hospitalizations for heart failure each year.Patients often present to their clinician with a variety of signs and symptoms. Most of these are related either to vascular congestion or impaired perfusion. Common signs and symptoms include dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), peripheral edema, nausea/vomiting, weight gain or weight loss, elevated jugular venous pressure, hepatomegaly, pulmonary rales, cardiac gallops (S3 or S4), and pleural effusions, to name a few.The goal for managing a patient with acute decompensated heart failure is several-fold: 1) Identify an etiology for the decompensation, 2) Decongest the patient (i.e. promote diuresis), 3) Ensure adequate perfusion to vital organs, and 4) Preserve hemodynamic stability.
2. Emergency Management
It is important to get appropriate vital signs for all patients who present with acute decompensated heart failure; for patients with hemodynamic compromise, pharmacologic and mechanical circulatory support may be necessary, intensive care admission is required, and ventilatory support should be considered.
Once hemodynamic stability is achieved, the primary goal is to reduce the cardiac filling pressures and decrease circulating volume through prompt and aggressive diuresis. In patients with normal renal function, this is usually achieved by intravenous administration of bolus-dose or continuous loop diuretic therapy. For patients with compromised renal function or with end-stage renal disease, dialysis may be required.
Management points not to be missed
Obtain vital signs – Consider pharmacologic or mechanical circulatory support for patients in shock, in order to improve perfusion pressures.
Monitor respiratory status – Consider invasive or non-invasive ventilation strategies for patients with compromised respiratory function.
Initiate intravenous diuresis, usually with loop diuretics (e.g. furosemide) administered by bolus or with a continuous infusion.
Patients who present with acute decompensated heart failure will often have a number of typical signs and symptoms. The modified Framingham criteria include several “major” and “minor” diagnostic criteria. Major criteria include PND, elevated JVP, orthopnea, pulmonary rales, 3rd heart sound (S3), cardiomegaly, pulmonary edema on chest x-ray, and recent diuresis. Minor criteria include bilateral leg edema, nocturnal cough, dyspnea with exertion, hepatomegaly, pleural effusion, tachycardia, and recent weight loss. Classically, diagnosis requires 2 major or 1 major criterion AND 2 minor criteria.
More importantly, acute decompensated heart failure is a clinical diagnosis. A number of ancillary studies and laboratory tests can help provide additional diagnostic clues.
Electrocardiograms may include q-waves (suggesting prior myocardial infarction and persistent scar), left ventricular hypertrophy (as a manifestation of cardiomegaly), heart block, or tachyarrhythmias.
Chest x-ray may reveal pulmonary edema, or may provide evidence suggesting an alternative cause of dyspnea (other than acute heart failure); other radiographic findings suggestive of heart failure include Kerley B-lines, pulmonary vascular redistribution, pleural effusions, prominent pulmonary arteries.
Serum electrolytes should be evaluated. Findings seen, particularly with advanced acute heart failure, include hyponatremia, elevated serum BUN and/or creatinine, low serum bicarbonate.
Elevated liver function tests may suggest passive hepatic congestion, seen most commonly with decompensated right heart failure.
BNP (brain natriuretic peptide) or pro-BNP levels are often elevated due to increased cardiac pressure/volume and increased myocardial wall stress. These laboratory values are highly sensitive, with a high negative predictive value for acute decompensated heart failure.
A transthoracic echocardiogram can evaluate contractile function, determine if there is concomitant valvular disease, and provide clues to cardiac and central venous pressures.
Cardiac catheterization may be performed to evaluate for the presence or absence of obstructive coronary artery disease. Right heart catheterization may be useful for evaluating intracardiac pressures, pulmonary pressures and cardiac output.
Symptoms and physical examination are the primary diagnostic tools available to help physicians determine if their patient has acute decompensated heart failure. A normal or low BNP and/or pro-BNP level argues strongly against this as a diagnosis. Echocardiography and/or invasive cardiac catheterization can provide additional clues as necessary.
Other clinical conditions that can present similarly include acute pulmonary embolism, pneumonia, pericardial effusion/cardiac tamponade, acute coronary syndrome, cirrhosis, nephrotic syndrome.
The BNP and/or pro-BNP are useful tests to assist in the evaluation of patients with acute decompensated heart failure. They have high sensitivity and negative predictive values; hence, a normal or low value would commonly exclude a diagnosis of acute heart failure.
4. Specific Treatment
Following stabilization of hemodynamics, first-line therapy includes the use of intravenous loop diuretics. Patients should receive enough diuretic therapy to promote a prompt and robust increase in urine output, and this therapy should continue until the patient is decongested and the cardiac filling pressures are normalized. Urine output should constantly be monitored to assess the need for changes in diuretic dosing.
For patients with evidence of severely symptomatic fluid overload, in the absence of systemic hypotension, vasodilator therapy can be employed. Vasodilators include intravenous nitroglycerin and intravenous nitroprusside. Oral vasodilator therapies, used to reduce left ventricular afterload, can also be used for less severe cases; most commonly, this includes the ACE inhibitors or angiotensin receptor blockers.
In patients with advanced heart failure and shock, intropes and vasopressor agents may be necessary. Inotropes increase the contractility of the heart through various mechanisms, while vasopressors more commonly increase systemic perfusion through vasoconstriction. Clinical evidence suggestive of low perfusion includes altered mental status, cool extremities, elevated serum creatinine, elevated liver function tests, low blood pressure, and narrowed pulse pressure.
Drugs and dosages
Loop diuretics – furosemide (Lasix), bumetadine (Bumex), torsemide – variable dosages, should be delivered intravenously for hospitalized patients
Nitroglycerin – 10-20 mcg/min, titrate to clinical effect up to 400 mcg/min
Nitroprusside – 0.5-0.8 mcg/kg/min, increased by 0.5 mcg/kg/min to a maximum of 8-10 mcg/kg/min; ideally titrated to systemic vascular resistance (SVR) and cardiac output (CO) goal with the use of a Swan-Ganz catheter
Dobutamine – 1-30 mcg/kg/min titrated to clinical effect
Milrinone – 0.125-0.25 mcg/kg/min; dose can be gradually titrated up to 0.5-0.75 mcg/kg/min for clinical effect
Dopamine – 2-5 mcg/kg/min, titrated to clinical effect
For patients with refractory heart failure, consider intensifying the diuretic regimen using higher doses of loop diuretics, the addition of a second diuretic (e.g. metolazone, spironolactone, chlorothiazide), or the continuous IV infusion of loop diuretic therapy. Consider the addition of inotropic or vasopressor therapy as needed. In cases with marginal renal function, consider the use of either peripheral ultrafiltration or conventional dialysis/ultrafiltration for effective volume removal.
For acute decompensated heart failure with severe volume overload and impaired systemic perfusion, the use of mechanical circulatory support may be required. This includes the percutaneous insertion of an intra-aortic balloon pump (IABP), percutaneous left ventricular assist device (LVAD), or permanent ventricular assist device.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
Most patients will have improvement in their symptoms rapidly following diuresis. Patients will also have resolution of their dyspnea, orthopnea and peripheral edema. For patients in cardiogenic shock, extremities will also get warmer, renal function may improve, alterations in mental status will resolve, and hemodynamics can considerably rebound with the introduction of inotropic therapy.
If symptoms fail to improve with adequate diuresis, particularly in the setting of increasingly compromised renal function, an alternative diagnosis should be considered. If the BNP or pro-BNP values are normal, an alternative diagnosis should be considered.
Once decongestion has been achieved, patients should be followed by a cardiologist who is comfortable managing patients with heart failure. Careful titration of evidence-based pharmacotherapies should be performed for all chronic heart failure patients seen in the outpatient arena, with the goal of improving morbidity and mortality as well as improving the systolic function of the heart. For patients at high risk for arrhythmia and sudden cardiac death, an implantable cardioverter-defibrillator should be considered. Serial echocardiographic examinations should be performed as heart failure therapies are titrated in the outpatient setting.
Many factors contribute to the pathophysiology of acute decompensated heart failure. There are a number of etiologies to heart failure that must be carefully considered. By far the majority of patients with systolic heart failure have a history of coronary artery disease. Prior myocardial infarction with scar formation, along with continued myocardial ischemia, can all put the heart at a mechanical disadvantage, leading to heart failure. For those without coronary artery disease as the cause of heart failure, other etiologies include myocarditis, infiltrative diseases, prolonged hypertension, connective tissue disease, toxins, chemotherapeutic agents, congenital disorders, and endocrinopathies, to name a few. Nearly 50% of patients with initially unexplained cardiomyopathies will never have an identifiable cause.As heart failure progresses, neurohormonal activation becomes a key contributor to its pathogenesis. Activation of the renin-angiotensin-aldosterone system leads to water and salt retention, myocardial fibrosis, vasoconstriction, and further alterations in cardiomyocyte morphology and function. Likewise, the sympathetic nervous system gets activated during progressive heart failure, leading to further vasoconstriction, sodium retention, arrhythmia development, and renin release.
Over 5 million people in the United States alone have heart failure, accounting for nearly 300,000 annual deaths, and over 1 million hospitalizations. It is most commonly the result of obstructive coronary artery disease, with resulting infarction/scar and ischemia, but can also be non-ischemic in etiology.
Heart failure is a progressive disease. Each hospitalization associated with acute decompensated heart failure substantially increases a patient’s morbidity and mortality. In-hospital mortality for a patient with acute decompensated heart failure ranges from 3-4%, increasing to 10% at 90 days. As a result, patients must be closely managed and monitored to avoid decompensation. Even with close clinical monitoring, some patients will eventually progress to end-stage disease, necessitating advanced heart failure therapies or palliative care.
Special considerations for nursing and allied health professionals.
What's the evidence?
Jessup, M. “Focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines”. Circulation. vol. 119. 2009. pp. 1977-2016. Published management guidelines for patients with acute decompensated heart failure.
McKee, PA. NEJM. vol. 85. 1971. pp. 1443Modified Framingham clinical criteria for the diagnosis of heart failure.
Nohria, A. J Cardiac Failure. vol. 6. 2000. pp. 64Conceptual guideline for risk stratification of the patient with acute decompensated heart failure.
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- Special considerations for nursing and allied health professionals.
- What's the evidence?