Pulmonary edema

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Background

Pulmonary Edema Types

Cardiogenic pulmonary edema

Noncardiogenic pulmonary edema

Clinical Features

Differential Diagnosis

Acute dyspnea

Emergent

Pediatric-specific

Non-Emergent

Evaluation

Pitting pedal edema
Pulmonary edema with small pleural effusions on both sides.
POCUS shows B lines[1]

Brain natriuretic peptide (BNP)[2]

  • Measurement
    • <100 pg/mL: Negative for acute CHF (Sn 90%, NPV 89%)
    • 100-500 pg/mL: Indeterminate (Consider differential diagnosis and pre-test probability)
    • >500 pg/mL: Positive for acute CHF (Sp 87%, PPV 90%)

NT-proBNP[3][4][5]

  • <300 pg/mL → CHF unlikely
  • CHF likely in:
    • >450 pg/mL in age < 50 years old
    • >900 pg/mL in 50-75 years old
    • >1800 pg/mL in > 75 years old

Lung ultrasound of pulmonary edema

Lung ultrasound showing pulmonary edema.
  • A lines and B lines
    • A lines:
      • Appear as horizontal lines
      • Indicate dry interlobular septa.
      • Predominance of A lines has 90% sensitivity, 67% specificity for pulmonary artery wedge pressure <= 13mm Hg
      • A line predominance suggests that intravenous fluids may be safely given without concern for pulmonary edema
    • B lines ("comets"):
      • White lines from the pleura to the bottom of the screen
      • Highly sensitive for pulmonary edema, but can be present at low wedge pressures

Management

  • CPAP/BiPAP with PEEP 6-8; titrate up to PEEP of 10-12
  • Nitroglycerin
    • Dosing Options
      • Sublingual 0.4mg q5min
      • Nitropaste (better bioavailability than oral Nitroglycerin)
      • Intravenous: 0.1mcg/kg/min - 5mcg/kg/min
        • Generally start IV nitroglycerin 50mcg/min and titrate rapidly (150mcg/min or higher) to symptom relief as long as patient's blood pressure tolerates
  • If nitroglycerin fails to reduce work of breathing, consider nitroprusside (reduces both preload and afterload) or ACE-inhibitiors (preload reducer)
  • After patient improves, titrate down nitroglycerin as enalaprilat (0.625 - 1.25mg IV) or captopril are started
  • Morphine is no longer recommended do to increased morbidity[6][7]

Disposition

  • Depends on underlying cause, hemodynamic stability, and response to treatment

See Also

References

  1. http://www.thepocusatlas.com/pulmonary/
  2. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167. doi:10.1056/NEJMoa020233.
  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 Feb. 27(3):330-7.
  4. Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med. 2005 Feb 17. 352(7):666-75.
  5. Moe GW, Howlett J, Januzzi JL, Zowall H,. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation. 2007 Jun 19. 115(24):3103-10.
  6. Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J. 2008 Apr;25(4):205-9.
  7. Ellingsrud C, Agewall S. Morphine in the treatment of acute pulmonary oedema--Why? Int J Cardiol. 2016 Jan 1;202:870-3.

Authors:

Ross Donaldson