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PODCAST: Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

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We discuss the diagnosis and management of SCAPE in the ED.

Hosts:

Naz Sarpoulaki, MD, MPH
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/SCAPEv2.mp3

Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care

Show Notes Core EM Modular CME CourseMaximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.

Course Highlights:

  • Credit: 12.5 AMA PRA Category 1 Credits
  • Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.
  • Cost:
    • Free for NYU Learners
    • $250 for Non-NYU Learners

      • Click Here to Register and Begin Module 1 The Clinical Case

      • Presentation: 60-year-old male with a history of HTN and asthma.
      • EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180.
      • Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing.
      • Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis).

        • Differential Diagnosis for the Hypoxic/Tachypneic Patient

        • Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis.
        • Cardiac: CHF, ACS, Tamponade.
        • Systemic: Anemia, Acidosis.
        • Neuro: Neuromuscular weakness.

          • What is SCAPE?Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload.

          • Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload.

            • Bedside Diagnosis: POCUS vs. CXRPOCUS is the gold standard for rapid bedside diagnosis.

            • Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones).
            • Cardiac: Assess LV function and check for pericardial effusion.
            • Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR.

              • Management Strategy 1. NIPPV (CPAP or BiPAP)Start NIPPV immediately to reduce preload/afterload and recruit alveoli.

              • Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation.
              • Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13).

                • 2. High-Dose NitroglycerinThe goal is to drop SBP to < 140–160 mmHg within minutes.

                • No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously.
                • IV Bolus: 500–1000 mcg over 2 minutes.
                • IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required).
                • Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues.

                  • 3. Refractory HypertensionIf SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator:

                  • Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid).
                  • Nicardipine: Effective alternative for rapid BP control.
                  • Enalaprilat: Consider if the above are unavailable.

                    • Troubleshooting & Pitfalls The “Mask Intolerant” PatientHypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV).

                    • AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam).

                      • The Role of DiureticsIn SCAPE, diuretics are not first-line.

                      • The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient.
                      • Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed.

                        • Disposition

                        • Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions.
                        • Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered.

                          • Take-Home Points

                          1. Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR.
                          2. NIPPV Immediately: Don’t wait. It saves lives and prevents tubes.
                          3. High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose.
                          4. Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask.
                          5. Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase.

                            6. The post PODCAST: Sympathetic Crashing Acute Pulmonary Edema (SCAPE) first appeared on האיגוד הישראלי לרפואה דחופה.

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