Rosen & Barkin's 5-Minute Emergency Medicine Consult (587 page)

• ECG to evaluate for cardiac ischemia and dysrhythmias.
  
• Chest x-ray to confirm the diagnosis and assessing illness severity.
  
• Labs: B-type natriuretic peptide (BNP), cardiac enzymes, and creatinine
  

• BNP:
  
  • Lab parameter for the detection and follow-up of heart failure:
    
    • <100 pg/mL: CHF unlikely
      
    • 100–500 pg/mL: Indeterminate
      
    • >500 pg/mL: Most consistent with CHF
      
  • May not be elevated in very acute CHF or ventricular inflow obstruction
    
  • May be falsely elevated in patients with renal failure undergoing dialysis due to LVH
    
• N-terminal pro-BNP:
  
  • Similar test characteristics to BNP
    
• Cardiac troponins:
  
  • May be elevated due to myocardial ischemia causing AHF or as result of AHF’s effects on cardiac myocytes
    
  • Elevated in 20% of AHF episodes
    
  • Strong negative prognostic factor
    
• Serum chemistry panel:
  
  • Creatinine elevation:
    
    • Predicts all-cause mortality in chronic heart failure
      
    • Indication of acute end-organ hypoperfusion
      
    • Indication for admission or observation
      
  • Hyponatremia: Marker of severe HF
    
  • Electrolyte abnormalities are common due to various HF treatments.
    
• Elevated alanine aminotransferase, aspartate aminotransferase, or bilirubin suggests congestive hepatopathy.
  
• Serum lipase if pancreatitis is suspected as the underlying cause
  
• Arterial blood gas: Evaluates hypoxemia, ventilation/perfusion mismatch, hypercapnia, and acidosis.
  

• CXR:
  
  • Pulmonary redistribution: Cephalization of vessels
    
  • Cardiomegaly: Cardiac silhouette >50% of thoracic width on PA exam only
    
  • Interstitial edema:
    
    • Pleural effusions
      
    • Kerley B lines
      
  • Bilateral perihilar alveolar edema producing a characteristic butterfly pattern
    
  • Noncardiogenic: Bilateral interstitial or alveolar infiltrates in a homogeneous pattern, typically without enlarged heart shadow
    
  • Radiographs are often normal in the 1st 12 hr of the disease process.
    
• ECG:
  
  • Assess for underlying cardiac disorders:
    
    • Acute dysrhythmias
      
    • Signs of acute coronary syndromes
      
    • Signs of electrolyte abnormalities
      
    • Atrial fibrillation occurs in 30–42% of patients admitted for acute heart failure.
      
    • Both tachy- and bradydysrhythmias can lead to decreased cardiac output.
      
• Echocardiography:
  
  • Evaluates left ventricle function
    
  • Assesses acute valvular or pericardial pathology
    
  • Measures cardiac output
    
• Bedside ultrasonography:
  
  • Bilateral B-lines: Comet-tail artifacts arising from pleural line extending to the far field without a decrease in intensity on both the left and the right thorax
    

• COPD exacerbation
  
• Pneumonia
  
• Asthma
  
• Pulmonary embolism
  
• Pericardial tamponade
  
• Pneumothorax
  
• Pleural effusion
  
• Anaphylaxis
  
• Acidosis
  
• Hyperventilation syndrome
  

TREATMENT

• IV access
  
• Supplemental oxygen
  
• 100% nonrebreather mask
  
• Cardiac monitor
  
• Pulse oximetry
  
• Sublingual nitrates
  
• If bag valve mask is needed, should use PEEP valve if available
  
• Endotracheal intubation in severe cases.
  

• Assess and gain control of airway, breathing, and circulation.
  
• Noninvasive ventilation or endotracheal intubation for impending respiratory failure.
  
• IV access
  
• Supplemental oxygen
  
• Cardiac monitor
  
• Pulse oximetry
  
• Place patient in an upright position.
  
• Inotropic therapy for hypotensive patient with signs of end-organ dysfunction
  

• Treatment decisions should be based on the underlying cause of pulmonary edema.
  
• Supplemental O
  ₂
  
• Volume restriction
  
• Urine output monitoring with or without urinary catheter
  
• BiPAP/CPAP:
  
  • Improves oxygenation, reduces respiratory work, decreases left ventricular afterload
    
  • Reduces need for intubation, length of stay, and mortality
    
  • Efficacy of BiPAP = CPAP
    
• Noncardiogenic causes: Frequently require positive-pressure ventilation:
  
  • Low-volume ventilation recommended (6 mL/kg)
    
• Positive-end expiratory pressure: Most useful strategy for oxygenation
  
• Hypotensive patients:
  
  • Avoid nitrates, angiotensin-converting enzyme inhibitors (ACEIs), and morphine.
    
  • Initiate inotropes:
    
    • Dobutamine, Dopamine, Norepinephrine, or Milrinone
      
  • Direct cardioversion for new onset unstable atrial fibrillation
    
• Normotensive or hypertensive patients:
  
  • Nitrates (nitroglycerin vs. nitroprusside)
    
  • Diuretics (furosemide vs. bumetanide) may be most effective after initial stabilization
    
• Noncardiogenic: Treat underlying cause.
  

• Aspirin: 325 mg PO/PR if myocardial infarction suspected
  
• Bumetanide: 1–3 mg IV
  
• Captopril: 6.25 mg SL
  
• Dobutamine: 2–10 μg/kg/min IV, titrate. May lower BP due to vasodilatory effects.
  
• Dopamine: 2 × 20 μg/kg/min IV; titrate
  
• Enalapril: 0.625–1.25 mg IV
  
• Furosemide: 20–80 mg IV
  
• Torsemide: 10–20 mg IV
  
• Milrinone: 50 μg/kg IV; titrate; inotropic effects comparable to dobutamine
  
• Nitroglycerin: 0.4 mg SL; 1–2 in; 5–20 μg/min IV and titrate; Nitropaste is not preferred as it is more difficult to titrate and to use in diaphoretic patients.
  
• Nitroprusside: 0.25–0.3 μg/kg/min, titrate up by 0.5 μg/kg/min q2–3 min until desired effect
  
• Norepinephrine: 2–12 μg/min IV; titrate
  

FOLLOW-UP

• ICU:
  
  • Positive-pressure ventilation
    
  • Inotropic support
    
  • Acute cardiac ischemia or infarction
    
  • ARDS
    
• Monitored unit:
  
  • New-onset pulmonary edema
    
  • Electrocardiographic changes
    
  • Patients presenting with risk factors for mortality, including advanced age, renal dysfunction, hypotension, digoxin use, and anemia
    

• Most patients with pulmonary edema should be admitted or observed for 24 hr.
  
• Patients with mild underlying disease and a mild exacerbation that responds fully to ED management and have no risk factors for in-house mortality (see above) may be discharged.
  
• Ensure close outpatient follow-up.
  

• Contact patient’s primary physician and/or cardiologist to establish close follow-up.
  
• Continue diuresis.
  
• Low-salt diet
  
• Daily weights
  

• Nitrates, SL and IV, are 1st-line therapy to reduce preload.
  
• BNP can reliably differentiate between AHF syndromes and other causes of dyspnea.
  
• AHF chest radiography findings can be absent early in disease course.
  
• Aggressive, early treatment of normotensive and hypertensive patients with nitrates, diuretics, and ACEIs can rapidly reverse the clinical course.
  
• Positive-pressure ventilation is an essential intervention in noncardiogenic pulmonary edema and can reduce rates of intubation and mortality in AHF.
  

• Heart Failure Society of America, LindenfeldJ, Albert NM, et al. HFSA2010 Comprehensive Heart Failure Practice Guideline.
  J Card Fail.
  2010;16(6):e1–e194.
  
• Jois-Bilowich P, Diercks D. Emergency department stabilization of heart failure.
  Heart Fail Clin.
  2009;5(1):37–42.
  
• Wang CS, FitzGerald M, Schulzer M. Does this dyspneic patient in the emergency department have congestive heart failure?
  JAMA
  . 2005;294:1944–1956.
  
• Ware LB, MatthayMA. Clinical practice. Acute pulmonary edema.
  N Engl JMed
  .2005;353:2788–2796.
  

See Also (Topic, Algorithm, Electronic Media Element)

Congestive Heart Failure

CODES