Flash pulmonary edema

(Redirected from Acute pulmonary edema)

Background

  • Also known as "sympathetic crashing acute pulmonary edema" (SCAPE)
  • Different from acute CHF exacerbation or hypotensive cardiogenic shock, which do not have sympathetic overdrive
  • Patients can decompensate rapidly, so rapid intervention required
  • Patients are generally more fluid depleted despite "wet" lungs, so do not give diuretics
  • Usually history of poorly controlled hypertension
    • Acute afterload increase causes pulmonary edema and poor peripheral perfusion
    • Sympathetic surge occurs as a result of decreased systemic perfusion
    • Afterload further increases and patient rapidly decompensates

Clinical Features

Marked jugular venous distension (arrow).
Pitting pedal edema

Differential Diagnosis

Pulmonary Edema Types

Pulmonary capillary wedge pressure <18 mmHg differentiates noncardiogenic from cardiogenic pulmonary edema[1]

Evaluation

Pulmonary edema with small pleural effusions on both sides.
Kerley B lines in acute cardiac decompensation. The short, horizontal lines can be found everywhere in the right lung.

Workup

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%)
    • Combination of BNP with clinician judgment 94% sensitive 70% specific (compared to 49% sn and 96% spec clinical judgement alone) [3]

NT-proBNP[4][5][6]

  • <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

Goal in heart failure management is to reduce preload (EDV), to reach higher SV on Frank Starling curve.

Vasodilate arterial side, while maintaining oxygenation

  • BiPAP with PEEP of 8 mmHg
    • Titrate PEEP quickly to 12
  • High dose nitroglycerin over 2 min (at these doses, nitroglycerin has vasodilation > venodilation[7])
    • Goal BP at the patient's norm
    • Load 800 mcg over 2 min (may start at 100 mcg/min, then titrate rapidly to 400 mcg/min for 2 min)
    • Then start maintenance at 100 mcg/min, titrate up as needed
    • NOTE: it takes time to set up nitroglycerin drip, so consider SL nitroglycerin in interim
      • 0.4mg tab during 5 min = ~80 mcg/min (2 tabs = ~160 mcg/min, etc.)
      • Difficult to titrate if giving more than 1-2 tabs
  • Patients are likely more dehydrated that overloaded but should be recurrently volume assessed
  • Consider captopril 12.5 - 25mg SL for continuation of afterload reduction[8]
  • Wean CPAP after sustained BP at patient's baseline
    • Decrease FiO2 to 40%
    • Wean PEEP down 2 cm H2O q10 min
    • At 5 cmH2O, trial of NC

Other Interventions

  • Furosemide
    • Targets kidneys which are poorly perfused in BOTH hypotension and catecholamine surge
    • Consider waiting until BiPAP and nitroglycerin control hypertension first
  • Nitroprusside, alternative when insufficient response to NTG
    • Start 0.5 mcg/kg/min, titrate to blood pressure
    • Max 10 mcg/kg/min for x10 min
    • Cyanide toxicity risk increases proportionately with infusion rate as well as length of time[9]
  • If intubation required, consider delayed sequence intubation

Disposition

  • Admit

See Also

External Links

References

  1. ↑ Clark SB, Soos MP. Noncardiogenic Pulmonary Edema. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 1, 2020.
  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. ↑ McCullough et al. B-Type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from breathing not properly (BNP) multinational study. Circulation. 2002:DOI: 10.1161/01.CIR.0000025242.79963.4
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ Haber et al. Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance. J Am Coll Cardiol. 1993;22(1):251-257.
  8. ↑ Hamilton RJ, Carter WA, Gallagher JE. Rapid Improvement of acute pulmonary edema with sublingual captopril. Acad Emerg Med 1996; 3: 205-12.
  9. ↑ GlobalRPH. Nitroprusside (Nipride®). http://www.globalrph.com/nitroprusside_dilution.htm
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