> Table of Contents > Heart Failure, Acutely Decompensated
Heart Failure, Acutely Decompensated
Bruce L. Lovins, MD
Jennifer M. Slowik, DO, MS
Christopher J. Snyder, MD
image BASICS
DESCRIPTION
Acute decompensated heart failure (ADHF) is a heterogeneous syndrome of acute impairment in cardiac pump function resulting in inefficient perfusion to bodily tissues. This may be due to structural or functional cardiac disorders and may represent a new diagnosis or worsening of preexisting chronic HF.
EPIDEMIOLOGY
Incidence
  • Medicare spends more to diagnose and treat HF than any other medical condition. In 2012, the total cost of HF approached $30.7 billion. In the United States, there are 870,000 new cases annually. HF is the primary cause of >55,000 deaths each year and a contributing factor in >280,000 deaths.
  • 1 million hospital discharges/year and about half of people who have HF die within 5 years of diagnosis.
Prevalence
  • ~5.7 million people over the age of 20 in the United States carry an HF diagnosis; prevalence is expected to increase 46% from 2012 to 2030 resulting in more than 8 million cases.
  • Primarily a disease of the elderly; 75% of hospital admissions for HF are in persons >65 years of age.
ETIOLOGY AND PATHOPHYSIOLOGY
  • Two physiologic components explain most of the clinical findings of ADHF.
    • Systolic dysfunction: an inotropic abnormality, often due to myocardial infarction (MI) or dilated or ischemic cardiomyopathy, resulting in diminished systolic emptying (ejection fraction <45%)
    • Diastolic dysfunction: a compliance abnormality, often due to hypertensive cardiomyopathy, in which the ventricular relaxation is impaired (ejection fraction >45%).
  • Common causes of ADHF
    • Exacerbation of chronic HF caused by dietary or medication nonadherence, infection, or any of the following as cause of new HF or exacerbation
    • Coronary artery disease (CAD), MI (especially new-onset ADHF)
    • Arrhythmia: atrial fibrillation, tachyarrhythmias, high-grade heart block
    • Valvular and vascular abnormalities: aortic stenosis or regurgitation, rheumatic heart disease (mitral and aortic valvular disease)
    • Uncontrolled hypertension (HTN), pulmonary HTN
    • High-output states: hyperthyroidism, anemia
    • Medications: cardiac depressants (&bgr;-blocker overdose), chemotherapeutic agents
    • Others: infiltrative disease, Chagas disease, pericardial disease, postpartum cardiomyopathy, wet beriberi, sepsis, COPD, pulmonary embolism
Genetics
Familial cardiomyopathy predisposes to development of HF (rare).
RISK FACTORS
  • History of chronic HF
  • CAD and MI
  • HTN, systemic or pulmonary
  • Valvular heart disease
  • Diabetes mellitus
  • Cardiotoxic medications
  • Chronic kidney disease and acute kidney injury (AKI)
  • Arrhythmia
  • Infection
GENERAL PREVENTION
Control BP and other risk factors. Thiazide diuretics and ACE inhibitors are superior to other agents in preventing development of HF. Treat cardiovascular disease.
COMMONLY ASSOCIATED CONDITIONS
  • Dysrhythmia followed by pump failure is the leading cause of death in ADHF. Most patients have >5 comorbidities (especially CAD, chronic kidney disease, and diabetes) and take >5 medications.
  • Cardiogenic shock
  • Hyponatremia and altered mental status, especially in the elderly
image DIAGNOSIS
Clinical diagnosis, no gold standard: ED diagnosis of ADHF is incorrect 10-20% of the time.
PHYSICAL EXAM
  • S3 and/or jugular venous distension most useful positive finding, although no vital sign/PE finding has sensitivity >70%
  • Peripheral edema, cool extremities, cyanosis, hepatomegaly, hepatojugular reflux, cardiac murmur, hypotension, laterally displaced apical impulse
  • Lung exam: rales (crackles) and sometimes wheezing, Cheyne-Stokes respirations
DIFFERENTIAL DIAGNOSIS
Pulmonary embolism, exertional asthma, acute MI, cardiac ischemia with angina, chronic obstructive pulmonary disease (COPD), pneumonia, constrictive pericarditis, tamponade, tension pneumothorax, high-output states (anemia, sepsis, hyperthyroidism, ARDS)
DIAGNOSTIC TESTS & INTERPRETATION
Laboratory data are adjunctive and indicative of complications.
Initial Tests (lab, imaging)
  • Cardiac troponins, EKG to evaluate for ACS (1)[C]
  • Echocardiogram: Determining ejection fraction (EF) is critical to proper diagnosis and management of heart failure, but may not be necessary in the acute setting if performed recently. Formal echocardiographic study is most useful single test to determine EF and valvular abnormalities; may be repeated if change suspected in underlying cardiac status. Echocardiogram: EF <45% is HF with reduced EF, EF >45% is HF with preserved EF, valvular abnormalities, tamponade (1)[C].
  • B-type natriuretic peptide (BNP) and/or N-type pro-BNP (BT-BNP) may be helpful to differentiate the cause of dyspnea if diagnosis is not certain, but is not indicated in routine care of ADHF. Both tests have been shown to have similar specificities and sensitivities in identifying ADHF (2)[A].
  • BNP < 100 essentially rules out HF as a cause of dyspnea with negative predictive value of ˜99%. Most dyspneic patients with ADHF have BNP >400.
  • BNP values of 100 to 400 are more problematic, as they may indicate HF or may be due to conditions such as pulmonary embolism, AKI, ACS, atrial fibrillation, and pulmonary HTN.
  • BNP may be higher in the elderly, lower in the obese
  • NT-proBNP values >450 pg/mL for people below age 50, >900 pg/mL ages 50 to 75 years, and >1,800 pg/mL for people older than 75 years are highly suggestive of HF (sensitivity 90%, specificity of 84%) (3)[B].
  • Chest x-ray (changes lag clinical symptoms by up to 6 hours): increased heart size (cardiothoracic ratio >50%), vascular redistribution (cephalization) with “butterfly” pattern of pulmonary edema, interstitial and alveolar edema, Kerley B lines, pleural effusions
  • Other labs that may help identify the cause of the decompensation: TSH (hypothyroidism), CBC (anemia), serum creatinine (renal disease) (1)[C]
  • Respiratory alkalosis and dilutional hyponatremia (poor prognosis) may also be present.
Follow-Up Tests & Special Considerations
Please see “Heart Failure, Chronic” topic.
Diagnostic Procedures/Other
Cardiac catheterization may be considered when CAD is suspected. Pulmonary artery catheterization may be performed to guide therapy in severe cases with cardiogenic shock.
Test Interpretation
Cardiac pathology depends on the etiology of HF. Please refer to “Heart Failure, Chronic” topic.
image TREATMENT
Approach is to improve symptoms, hemodynamics, and renal function, to minimize myocardial damage and hospital length of stay, and to identify the etiology or precipitating factors. See “Heart Failure, Chronic” chapter as well.
MEDICATION
First Line
  • Loop diuretics initially for fluid-overloaded ADHF in hemodynamically stable patients (contraindicated if SBP <90 mm Hg, severe hyponatremia, acidosis) (6)[A]; be cautious of electrolyte abnormalities if kidney disease is present. Avoid if possible diagnosis of pneumonia. Continuous infusion is not better than bolus, and high dose is not significantly better than low dose (5)[B].
    • Furosemide (Lasix): 40 mg IV
    • If on Lasix chronically, initial IV dose should be equal or exceed chronic oral daily dose (max 180 mg). Monitor for appropriate urine output.
    • Metolazone (Zaroxolyn): 2.5 to 20 mg/day PO, more useful if reduced creatinine clearance
  • Thiazides in combination with loop diuretics may be useful if resistant to diuresis (HCTZ 25 mg PO).
    P.447

    Thiazides and spironolactone or eplerenone (25 to 50 mg PO) may be used in combination with loop diuretics if excessive volume overload
  • Vasodilators: no change in outcomes but may reduce dyspnea in patients with severe HTN, mitral regurgitation, or acute pulmonary edema; don't use if SBP <90 mm Hg, history of aortic stenosis, or phosphodiesterase inhibitor use (5)[A]
    • IV nitroglycerin may be of short-term benefit to decrease preload, afterload, and systemic resistance (IV 10 to 20 &mgr;g/min).
    • IV nitroprusside: Administer with caution, infusion rate 5 to 10 &mgr;g/min. Consider an arterial line.
  • Morphine: IV boluses 2.5 to 5 mg IV helps with chest pain and restlessness. Monitor respirations.
Second Line
  • Tolvaptan (an oral vasopressin antagonist), for treatment of cognitive symptoms of severe hypervolemic hyponatremia refractory to water restriction and maximum medical therapy (5)[B]
  • Inotropes: consider adding if reduced systolic function and signs of hypoperfusion. Withdraw as soon as hemodynamic parameters improve, as these may increase short- and medium-term mortality.
    • Phosphodiesterase inhibitors (milrinone, enoximone) decrease pulmonary resistance; may be used for patients on &bgr;-blockers but may increase medium-term mortality in CAD patients
    • Dobutamine infusion requires close BP monitoring; avoid in cardiogenic shock or with tachyarrhythmias.
    • Low-dose dopamine infusion may be considered.
    • Levosimendan (calcium sensitizer) improves hemodynamic parameters but not survival compared to placebo while improving hemodynamic parameters and survival compared to dobutamine
  • Nesiritide, a BNP analog, is not recommended for most hospitalized patients with ADHF; higher rates of hypotension, no benefit on death, or rehospitalization rates
ADDITIONAL THERAPIES
  • Oxygen: begin treatment early; ideally, arterial oxygen saturation >92% (90% if COPD). For acute cardiogenic pulmonary edema, noninvasive positive pressure ventilation decreases early mortality compared to standard therapy (7)[A].
  • No significant difference between continuous positive airway pressure (CPAP) and noninvasive positive pressure ventilation (NIPPV). If possible, avoid mechanical ventilation for patients with right HF (7)[A].
  • Treat anemia with transfusion: conservative trigger Hgb <8; target Hgb 10.
  • For patients with new-onset arrhythmias, consider pacing and/or antiarrhythmics.
  • For patients with HF with preserved EF, achieve BP control; no mortality benefit demonstrated with any specific class of medications
  • For severe cardiogenic shock, consider intra-aortic balloon pump or percutaneous or surgically implanted ventricular assist devices (VADs).
  • Please refer to “Heart Failure, Chronic” for maintenance treatments.
SURGERY/OTHER PROCEDURES
  • Heart valve surgery if defective heart valve is responsible
  • PCI/CABG for patients with CAD/MI if applicable
  • Cardiac transplantation considered in patients <55 years of age and without other disqualifying medical problems who are developing chronic decompensated HF unresponsive to other therapeutic maneuvers and who are considered to have a life expectancy of >1 year.
INPATIENT CONSIDERATIONS
Postdischarge appointment, left ventricular EF assessment, and start on ACE inhibitor (or ARB) and &bgr;-blocker if left ventricular systolic dysfunction present
Admission Criteria/Initial Stabilization
See earlier discussion.
  • Acute change in HF, with pulmonary edema accompanied by decreased oxygenation, change in mental status, AKI, or significant hyponatremia
  • Consider observation unit stay for hemodynamically stable patients with preexisting HF and the following:
    • No acute interventions needed for comorbid condition
    • SBP > 120 mm Hg, BUN <40, creatinine <3.0, absence of elevated troponins/ischemic EKG changes
    • Respiratory rate <32 breaths/min without needing noninvasive ventilation
    • No actively titrated vasoactive IV infusions
    • Partial improvement in vital signs and/or increased urine output with initial treatment
    • Clinical impression that patient could be discharged in the next 24 hours and rapid outpatient follow-up is available.
IV Fluids
1.5 to 2 L/day fluid restriction may be useful to reduce congestive symptoms, especially in the case of hyponatremia (5)[C].
Discharge Criteria
Subjective improvement, resting heart rate (HR) <100 bpm, systolic BP >80 mm Hg, HF outpatient education
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient education performed at all outpatient and inpatient visits. Please see “Heart Failure, Chronic” topic.
Patient Monitoring
Rapid office follow-up after hospitalization and home health monitoring by specially trained nurses have both been shown to decrease frequency of hospitalizations.
DIET
Reduce sodium (2 g); maintain cardiac or diabetic diet if these comorbidities are present.
PATIENT EDUCATION
  • Definition and etiology: Understand the cause of HF and why symptoms occur.
  • Prognosis: Understand important prognostic factors and make realistic decisions.
  • Symptom monitoring and self-care: recognize signs/symptoms, record daily weight, know how and when to contact a health care provider; may increase diuretic dose with >1 kg in a day, >2 kg weight gain in 5 days or dyspnea/contact health care provider
  • Pharmacologic treatment: Understand indications, dosing, effects, and side effects of drugs.
  • Adherence: Understand the importance of maintaining the treatment plan.
  • Alcohol, smoking, and drugs: Abstinence is recommended in patients with alcohol-induced cardiomyopathy. Otherwise, normal alcohol guidelines apply. Smoking and illicit drug cessation.
  • Exercise: Understand the benefits of exercise.
PROGNOSIS
  • The ADHERE risk tree stratifies ADHF patients for inpatient mortality using systolic blood pressure, BUN, and creatinine.
  • S3 on physical exam correlates with poor prognosis.
  • After diagnosis, 1-year survival ˜75%, 5-year survival <50%, 10-year survival <25%
REFERENCES
1. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2012;33(14):1787-1847.
2. Worster A, Balion CM, Hill SA, et al. Diagnostic accuracy of BNP and NT-proBNP in patients presenting to acute care settings with dyspnea: a systematic review. Clin Biochem. 2008;41(4-5):250-259.
3. Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. Eur Heart J. 2006;27(3):330-337.
4. Wakai A, McCabe A, Kidney R, et al. Nitrates for acute heart failure syndromes. Cochrane Database Syst Rev. 2013;(8): CD005151.
5. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013;128(16):1810-1852.
6. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805.
7. Mariani J, Macchia A, Belziti C, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema: a meta-analysis of randomized controlled trials. J Card Fail. 2011;17(10):850-859.
Additional Reading
&NA;
Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29-e322.
Codes
&NA;
ICD10
  • I50.9 Heart failure, unspecified
  • I50.21 Acute systolic (congestive) heart failure
  • I50.31 Acute diastolic (congestive) heart failure
Clinical Pearls
&NA;
  • BNP is overused diagnostically and is best reserved for situations in which diagnosis of ADHF is unclear.
  • Look for underlying cause of each episode of ADHF.
  • IV diuretics are used initially in fluid-overload acute HF, with nitrates added if needed.
  • Using early noninvasive ventilation for the treatment of pulmonary edema can bridge care while awaiting the effects of diuretics, and can decrease morbidity and mortality associated with intubation.