Sympathetic crashing acute pulmonary edema (SCAPE)

Background

  • 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
Pulmonary edema with small pleural effusions on both sides.

Clinical Features

  • Rales, crackles
  • SBP >180 mmHg
  • Tachycardic

Differential Diagnosis

Pulmonary Edema Types

Cardiogenic pulmonary edema

Noncardiogenic pulmonary edema

Evaluation

  • CBC (rule out anemia)
  • Chem
  • ECG
  • CXR - signs of pulmonary congestion may not show for hours after acute flash pulmonary edema, so normal CXR is frequently seen
    • Cephalization
    • Interstitial edema
    • Pulmonary venous congestion
    • Pleural effusion
    • Alveolar edema
    • Cardiomegaly
  • Troponin
  • Ultrasound
  • Consider arterial line monitoring for titration of NTG

Brain natriuretic peptide (BNP)[1]

  • Biologically active metabolite of proBNP (released from ventricles in response to increased volume/pressure)
  • Utility is controversial and may not affect patient centered outcomes[2]
  • May be trended to gauge treatment response in acute decompensated CHF
  • May have false negative with isolated diastolic dysfunction
  • 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%)
  • American College of Cardiology, American Heart Association, Heart Failure Society of America guidelines as of May 2017[3]
    • BNP should be measured in patients presenting with dyspnea to help diagnose or exclude heart failure
    • BNP or nt-pro-BNP should be measured to determine prognosis or disease severity in chronic heart failure
    • Baseline BNP, cardiac troponin, or both should be measured upon hospital admission to determine prognosis in patients with acutely decompensated heart failure

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

  • N-terminal proBNP (biologically inert metabolite of proBNP)
  • <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

Differential Diagnosis (Elevated BNP)

BNP In Obese Patients

  • Visceral fat expansion leads to increased clearance of active natriuretic peptides[7]
  • Obese patients also frequently treated for hypertension or coronary artery disease which may also contribute to lower BNP levels

Interpretation

  • In one study of 204 patients with acute CHF, an inverse relationship between BMI and BNP was noted. The standard cutoff of 100pg/mL resulted in a 20% false-negative rate[8]
  • Analysis of a subgroup of patients with documented BMI from the Breathing Not Properly study showed that a lower cutoff was more appropriate to maintain 90% sensitivity in obese and morbidly obese patients (54pg/mL)[9]

Management

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[10])
    • 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[11]
  • 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[12]
  • If intubation required, consider delayed sequence intubation

Disposition

  • Admit

See Also

External Links

References

  1. 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.
  2. Carpenter CR et al. BRAIN NATRIURETIC PEPTIDE IN THE EVALUATION OF EMERGENCY DEPARTMENT DYSPNEA: IS THERE A ROLE? J Emerg Med. 2012 Feb; 42(2): 197–205.
  3. Yancy CW et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure.
  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. Clerico A, Giannoni A, Vittorini S, Emdin M. The paradox of low BNP levels in obesity. Heart Fail Rev. 2011;17(1):81-96. doi:10.1007/s10741-011-9249-z.
  8. Krauser DG, Lloyd-Jones DM, Chae CU, et al. Effect of body mass index on natriuretic peptide levels in patients with acute congestive heart failure: A ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) substudy. Am Heart J. 2005;149(4):744-750. doi:10.1016/j.ahj.2004.07.010.
  9. Daniels LB, Clopton P, Bhalla V, et al. How obesity affects the cut-points for B-type natriuretic peptide in the diagnosis of acute heart failure. Results from the Breathing Not Properly Multinational Study. Am Heart J. 2006;151(5):999-1005. doi:10.1016/j.ahj.2005.10.011.
  10. Haber et al. Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance. J Am Coll Cardiol. 1993;22(1):251-257.
  11. Hamilton RJ, Carter WA, Gallagher JE. Rapid Improvement of acute pulmonary edema with sublingual captopril. Acad Emerg Med 1996; 3: 205-12.
  12. GlobalRPH. Nitroprusside (Nipride®). http://www.globalrph.com/nitroprusside_dilution.htm