Rosen & Barkin's 5-Minute Emergency Medicine Consult (170 page)

• Primary care physician to coordinate care
  
• Cardiologist for diagnosis, medical management, and ongoing monitoring
  
• Cardiothoracic evaluation for surgery
  

• Plan for follow-up should be determined in consult with the pediatric cardiologist.
  
• Clear instructions for return visits, as any physiologic stress may worsen condition.
  

• Visual appearance of cyanosis requires >3–5 mg/dL deoxygenated hemoglobin.
  
• Duct-dependent lesions:
  
  • Present at 2–3 wk of age
    
  • Sudden cyanosis or cardiovascular collapse
    
  • Treat with PGE1:
    
    • Beware apnea and hypotension
      

• Apitz C, Webb GD, Redington AN. Tetralogy of Fallot.
  Lancet
  . 2009;374:1462–1471.
  
• Bonow RO, Mann DL, Zipes DP, et al., eds. Congenital heart disease.
  Braunwald’s Heart Disease
  . 98th ed. Philadelphia, PA: Saunders Elsevier; 2012:1411–1467.
  
• Dolbec K, Mick N. Congenital heart disease.
  Emerg Med Clin North Am.
  2011;29:811–827.
  
• Fleisher GR, Ludwig S, Bachur RG, et al., eds. Cardiac emergencies.
  Textbook of Pediatric Emergency Medicine
  . 6th ed. Philadelphia, PA: Lippincott Williams, & Wilkins, 2010:690–701.
  
• Yee L. Cardiac emergencies in the first year of life.
  Emerg Med Clin North Am
  . 2007;25:981–1008.
  

CODES

• 745.2 Tetralogy of fallot
  
• 745.4 Ventricular septal defect
  
• 746.89 Other specified congenital anomalies of heart
  

BASICS

• 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.
  

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
    

DIAGNOSIS

• 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
    

• 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.
  

• 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
    

• 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