DESCRIPTION

• A clinical syndrome in which the heart fails to maintain adequate circulation for metabolic needs, characterized by chronic debility, acute decompensation, and high mortality.
• Acute Decompensated Heart Failure (ADHF) is a rapidly progressive failure state (hr–days)
  • Common reason for presentation to the ED
  • Usually caused by a precipitating event in which the heart does not have the reserve to compensate for the added burden
• Chronic HF is a progressive failure state (mo–yr) characterized by cardiac remodeling and neurohormonal changes, with multiple subclasses:
  • Systolic heart failure
    • Impaired contractile or pump function causing decreased ejection fraction
  • Diastolic heart failure
    • Impaired ventricular relaxation resulting in decreased cardiac filling
  • Low-output failure
    • Decreased cardiac output
  • High-output failure:
    • Normal or increased cardiac output, but insufficient to meet metabolic demands
  • Left-sided failure
    • Systolic or diastolic (or both) dysfunction of the left ventricle
    • Resultant pulmonary congestion
  • Right-sided heart failure
    • Due to either intrinsic dysfunction or secondary to left heart failure or pulmonary hypertension (cor pulmonale)
    • Hepatic enlargement, JVD, and dependent edema can occur
• CHF affects ~5.8 million Americans.
• Estimated 2012 cost of CHF is $40 billion
• ADHF is the leading Medicare diagnosis for hospitalized patients ≥65 yr old.

ETIOLOGY

Underlying causes and acute precipitants

• Decreased myocardial contractility:
  • Myocardial ischemia/infarction
  • Cardiomyopathy (including, alcoholic and pregnancy-related)
  • Myocarditis
  • Dysrhythmias
  • Decreased contractile efficiency:
    • Drug related (negative inotropes)
    • Metabolic disorders
• Pressure overload states:
  • HTN
  • Valvular abnormalities
  • Arrhythmia
  • Congenital heart disease
  • Pulmonary embolism
  • Primary pulmonary hypertension, sleep apnea syndromes (right heart failure)
• Restricted cardiac output:
  • Myocardial infiltrative disease
• Volume overload:
  • Dietary indiscretion (sodium overload)
  • Drugs leading to sodium retention (glucocorticoids, NSAIDs)
  • Overload due to transfusion or IV fluid
• High demand states:
  • Hyperthyroidism, thyrotoxicosis
  • Pregnancy
  • A-V fistula
  • Beriberi (thiamine deficiency)
  • Paget disease
  • Severe anemia
  • Aortic insufficiency
• Pediatric etiologies: Volume/pressure overload lesions vs. acquired HD:
  • 1st 6 mo: VSD and PDA
  • Older children: Subvalvular aortic stenosis, coarctation
  • Acquired dysfunction: Nonspecific age of onset, including myocarditis, valvular disease, and cardiomyopathies; cocaine/stimulant abuse in adolescents

[Outline]

• DESCRIPTION
• ETIOLOGY

SIGNS AND SYMPTOMS

• Poor perfusion:
  • Fatigue, somnolence, lightheadedness
  • Palpitations, or irregular pulse
  • Shortness of breath
  • Cool extremities
  • Worsening renal function
• Congestion
  • Dyspnea, cough
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Evidence of sleep disordered breathing
  • Decreased exercise tolerance
  • Elevated JVD or abdominojugular reflex
  • Dependent edema (poor sensitivity and specifity)
  • Rales and/or wheezing, (absent in 80% with chronically elevated filling pressure due to compensatory lymphatic drainage)
  • Pleural effusion, dullness at lung bases
  • S3 gallop and/or S4.
  • Laterally displaced apical impulse
  • Hepatic enlargement/tenderness
  • Nausea
  • Ascites
• ADHF with hemodynamic instability:
  • Confusion, anxiety, syncope
  • Tachypnea
  • Tachycardia
  • Hypotension
  • Cool, pale or cyanotic extremities
  • Narrow pulse pressure or pulsus alternans
  • Cheyne–Stokes respirations

ESSENTIAL WORKUP

• The CXR is important in confirming the diagnosis and assessing severity.
• 12-hr radiographic lag from onset of symptoms may occur.
• Radiographic findings may persist for several days despite clinical improvement.

DIAGNOSIS TESTS & INTERPRETATION

Lab

• Chemistry/electrolytes:
  • Establish baseline renal function when initiating diuretics, or ACE inhibitors
  • Hyperkalemia possible with low output
  • Hyponatremia associated with poor prognosis
• CBC:
  • Anemia can cause or exacerbate failure
  • Infection can cause or exacerbate failure
• Liver function tests:
  • Increase suggests hepatic congestion, or ischemia.
• Thyroid function tests:
  • Specifically in patients > 65 yr old or in a-fib
• Cardiac enzymes:
  • Evaluate for ischemia or infarction
• ANA and rheumatoid factor: Suspected lupus
• Viral panel: Suspected myocarditis
• BNP:
  • Useful for distinguishing cardiac vs. pulmonary cause of dyspnea
    • BNP > 500 pg/mL, HF likely (ppv 90%)
    • BNP < 100 pg/mL, HF unlikely, (npv 90%)
    • BNP 100–500 pg/mL, consider PE, cor pulmonale, renal failure, or stable underlying HF.
  • REDHOT II Study: BNP levels are better than physicians at predicting which patients are more likely to have bad outcomes
    • EPs were blinded to BNP values. 78% of patients discharged from ED had BNP > 400.
    • Of those discharged with a BNP > 400, 90-day mortality was 9%
  • BNP levels rise with age and are affected by gender, comorbidity, and drug therapy and should not be used in isolation
  • BNP levels may be low in acute pulmonary edema (< 1–2 hr) and obesity (BMI > 30).
• NT-proBNP: Cleavage product of prohormone.
  • NT-proBNP > 1,000 pg/mL predictive of HF
  • NT-proBNP < 300 pg/mL unlikely to be HF

Imaging

• CXR:
  • Cardiomegaly (sensitive)
  • Specific signs of CHF:
    • Cephalization (vascular prominence in the upper lungs due to fluid overload)
    • Interstitial edema/Kerley B lines
    • Alveolar edema
  • Effusions (usually right sided)
  • Bilateral confluent perihilar infiltrates leading to classic butterfly pattern:
    • May be asymmetric and mistaken for pneumonia
• EKG:
  • Underlying cardiac ischemia
  • Presence of dysrhythmias
  • Left-ventricular hypertrophy
  • Heart block
  • Normal EKG has high negative predictive value for systolic dysfunction.
• 2-D Cardiac Echo:
  • Ejection fraction
  • Acute valvular pathology
  • Pericardial tamponade
  • Pericardial thickening in constrictive pericarditis
  • Ventricle dilation, or hypertrophy
  • Regional wall motion abnormalities

DIFFERENTIAL DIAGNOSIS

• Left-sided CHF:
  • Acute exacerbation of COPD
  • Asthma exacerbation
  • Acute respiratory distress syndrome
  • Pneumonia, bronchitis
  • Constrictive pericarditis
  • Anemia, malnutrition
  • Pericardial tamponade
  • Coarctation of aorta
• Right-sided HF:
  • Nephrotic syndrome, chronic renal failure
  • Cirrhosis
  • Left-side heart failure
  • Pulmonary embolism
  • Sleep disordered breathing
  • Venous stasis

[Outline]

• SIGNS AND SYMPTOMS
• ESSENTIAL WORKUP
• DIAGNOSIS TESTS & INTERPRETATION
• DIFFERENTIAL DIAGNOSIS

PRE-HOSPITAL

• IV access
• Supplemental oxygen
• Cardiac monitor and pulse oximetry
• EKG
• Sublingual nitrates for active chest pain without hypotension
• Furosemide
• Endotracheal intubation may be required.

INITIAL STABILIZATION/THERAPY

• IV access
• Supplemental oxygen
• Cardiac monitor and pulse oximetry
• EKG
• Elevate head of bed to reduce venous return.
• Control airway as needed:
  • Noninvasive positive pressure ventilation
    • CPAP vs. BiPAP
    • Reduce work of breathing, improve oxygenation, decrease need for intubation, possible mortality benefit
    • Some studies report higher incidence of MI with BiPAP over CPAP in acute CHF; studies not conclusive
  • Intubation for impending respiratory failure

ED TREATMENT/PROCEDURES

• General: Oxygenate, ventilate, treat underlying condition when possible
• Congestion with adequate perfusion: Reduce preload, consider fluid restriction
  • Rapidly reduce preload in acute pulmonary edema:
    • Sublingual or IV nitroglycerin
    • Nitro paste
    • IV diuretics (less rapid/effective in patients with poor renal perfusion)
  • Avoid preload reduction in ADHF when suspected etiology is aortic stenosis, HOCM, or pulmonary hypertension.
  • Cautious afterload reduction in ADHF: Avoid ACEi and ARBs in cases of hypotension, acute renal failure, and hyperkalemia.
    • Nesiritide
  • Limited benefit, may cause hypotension
• Poor perfusion with hypotension:
  • Agents that increase contractility:
    • Dobutamine
    • Dopamine
    • Milrinone
  • Avoid vasodilators (nitrates, morphine)
  • Initiate diuretics after inotropes.
• Initiate venous thromboembolism prophylaxis in those with ADHF without contraindications

Pediatric Considerations

• Neonates (1st weeks of life):
  • Suspect ductal-dependent cardiac lesions if clinical CHF and no improvement with O₂:
    • PGE1 to maintain patent ductus
• Children:
  • IV furosemide, and dopamine or milrinone
  • IV nitroglycerin for pulmonary edema

MEDICATION

• Aspirin: 325 mg PO/PR if AMI is suspected
• Bumetanide (Bumex): 1–3 mg IV, max. 10 mg/day
• Dobutamine: 2–10 µg/kg/min IV, max. of 40 µg/kg/min
• Dopamine: 2–20 µg/kg/min IV, max. of 50 µg/kg/min
• Enalapril: 0.625–1.25 mg IV; 2.5–20 mg/d PO
• Furosemide (Lasix): No prior use: 40 mg IVP; prior use: Double 24-hr dose (80–180 mg IV); no effect in 30 min: Redouble dose
• Milrinone: 50 µg/kg IV load; 0.375–0.75 µg/kg/min IV
• Nesiritide: 2 µg/kg bolus, then infusion of 0.01 µg/kg/min
• Nitroglycerin: 0.4 mg sublingual; 1–2 in of nitro paste; 5–20 µg/min IV, max. of 100–200 µg/min IV. USE NON-PVC tubing.
• Nitroprusside: 0.3–10 µg/kg/min IV (starting dose), max. of 10 µg/kg/min

Pregnancy Considerations

ACEi and ARBs are associated with multiple fetal abnormalities and should be held

• Oxygen
• Nitroglycerin
• Furosemide

[Outline]

• PRE-HOSPITAL
• INITIAL STABILIZATION/THERAPY
• ED TREATMENT/PROCEDURES
• MEDICATION

DISPOSITION

Admission Criteria

• ICU:
  • Pulmonary edema
  • Cardiogenic shock
  • Concomitant MI or ischemia
• Medical wards:
  • New-onset CHF
  • Symptoms not relieved by ED therapy

Discharge Criteria

• Mild exacerbation of chronic CHF:
  • Responds to ED treatment
  • No other cardiac and pulmonary findings
• Close follow-up should be arranged with continuation of diuretic, vasodilator, or ACE inhibitor therapy and patient lifestyle education.

Issues for Referral

Consider ICD and/or BV pacer in advanced HF

• Shown to decrease mortality and hospitalization rates in select patient groups

FOLLOW-UP RECOMMENDATIONS

• Close follow-up within 1 wk of discharge
• Medication and dietary compliance
• Frequent home monitoring of body weight
• Monitor electrolytes and renal function during chronic diuretic therapy

[Outline]

• DISPOSITION
• FOLLOW-UP RECOMMENDATIONS

• BNP may be useful if CHF diagnosis uncertain.
• In severe CHF, NIPPV can improve impending respiratory compromise.
• Be vigilant in searching for and treating the underlying cause of the heart failure exacerbation (e.g., MI, PE, valvular pathology).

ICD9

• 428.0 Congestive heart failure, unspecified
• 428.20 Systolic heart failure, unspecified
• 428.30 Diastolic heart failure, unspecified

ICD10

• I50.9 Heart failure, unspecified
• I50.20 Unspecified systolic (congestive) heart failure
• I50.30 Unspecified diastolic (congestive) heart failure

[Outline]

• ICD9
• ICD10

• Heart Failure Society of America. Executive summary: HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010;16(6):475–535.
• Singer AJ, Birkhahn RH, Guss D, et al. Rapid Emergency Department Heart Failure Outpatients Trial (REDHOTII): A randomized controlled trial of the effect of serial B-type natriuretic peptide testing on patient management. Circ Heart Failure. 2009;2:287–293.
• Silvers SM, Howell JM, Kosowsky JM, et al. ACEP Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med. 2007;49(5):627–669.

Naomi George

Robert A. Partridge