Sympathetic Crashing Acute Pulmonary Edema (SCAPE) – An Anesthesia Perspective

Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is a rapidly progressive form of decompensated heart failure triggered by a neurohormonal surge. Unlike volume-overload heart failure, SCAPE is primarily an afterload mismatch syndrome, characterized by preserved or elevated cardiac output, sudden pulmonary edema, and hypertensive crisis.

Key Clinical Features

• Acute dyspnea and hypoxia
• Systolic blood pressure typically >180 mmHg
• Bilateral rales on auscultation
• Often absent peripheral edema or hypotension

Clinical Insight: SCAPE represents a high systemic vascular resistance (SVR) emergency, not a volume-overload state.

References:

Movahed MR. The Movahed protocol for management of SCAPE. Am J Emerg Med. 2017;35(12):1984.e5-7.

Marik PE. Pulmonary edema due to negative pressure and SCAPE: What the anesthesiologist needs to know. Crit Care Med. 2013;41(7):e158-9.

Levy P, Compton S, Welch R, et al. Treatment strategies in acute decompensated heart failure. Emerg Med Clin North Am. 2005;23(4):927-47.

Clinical Case Vignette

A 68-year-old female with chronic kidney disease and long-standing hypertension presents for urgent laparoscopic cholecystectomy. In the preoperative area, she suddenly develops acute dyspnea, oxygen saturation of 88%, systolic blood pressure of 220 mmHg, bilateral pulmonary rales, and agitation. She is known to have heart failure with preserved ejection fraction (HFpEF). A chest X-ray shows pulmonary congestion. The anesthesiologist is faced with immediate decision-making for stabilization.

High-Risk Groups for SCAPE and Intubation Collapse

• Chronic Hypertension: Reduced vascular compliance increases sensitivity to afterload surges.
• HFpEF: Diastolic dysfunction impairs left ventricular filling under pressure load.
• Chronic Kidney Disease: Renin–angiotensin–aldosterone system activation and endothelial dysfunction contribute to afterload mismatch.
• Aortic Stenosis: Fixed cardiac output worsens under sudden vasoconstriction.
• Elderly Patients: Blunted baroreflex and increased sympathetic tone.
• Rebound from Clonidine or Beta-Blockers: Sudden catecholamine surge.
• Acute Neurological Injury: Central autonomic dysregulation.

References:

Delerme S, Ray P. Acute decompensated heart failure. N Engl J Med. 2007;357(5):502-11.

Gheorghiade M, Pang PS. Acute heart failure syndromes. J Am Coll Cardiol. 2009;53(7):557-73.

Packer M. Pathophysiology of acute heart failure syndromes. Am J Cardiol. 2005;96(6A):3G-7G.

Mechanisms and PathophysiologyNeurohormonal Surge

• Norepinephrine: Sympathetic nerve terminals
• Epinephrine: Adrenal medulla
• Angiotensin II: RAAS activation
• Arginine vasopressin: Posterior pituitary
• Endothelin-1: Vascular endothelium

These mediators cause acute systemic vasoconstriction, raising afterload, left ventricular end-diastolic pressure, and pulmonary capillary pressures.

Flash Pulmonary Edema

A stiff left ventricle with impaired relaxation leads to sudden elevation in left atrial pressure, precipitating pulmonary congestion.

References:

Guyton AC, Hall JE. Textbook of Medical Physiology. 13th ed. Philadelphia: Elsevier; 2016.

Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science. 5th ed. New York: McGraw-Hill; 2013.

Gheorghiade M, Filippatos G, Felker GM. Neurohormonal mechanisms in acute heart failure. Am J Cardiol. 2005;96(6A):3G-7G.

Monitoring in SCAPE

• Arterial Line: Allows real-time titration of nitroglycerin infusion.
• Capnography: Verifies endotracheal tube placement and monitors ventilation.
• Transthoracic Echocardiography (TTE): Assesses volume status, ejection fraction, and wall motion.
• Lung Ultrasound: Detects B-lines as a marker of interstitial edema and evaluates ventilation.
• Central Venous Access: Considered if vasopressor support becomes necessary.

References:

Lichtenstein DA. Lung ultrasound in the critically ill. Ann Intensive Care. 2014;4:1.

Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-91.

Medical Stabilization: The Movahed Protocol

• Vasodilation: Intravenous nitroglycerin 800–1000 µg bolus, followed by infusion at 200–400 µg/min.
• Noninvasive Ventilation: BiPAP with inspiratory positive airway pressure (IPAP) 10–15 cm H₂O and expiratory positive airway pressure (EPAP) 5–10 cm H₂O.
• Delay in Diuresis: Diuretics should be withheld until blood pressure is controlled, as premature preload reduction can trigger hypotension in an afterload-driven syndrome.

References:

Movahed MR. The Movahed protocol for SCAPE. Am J Emerg Med. 2017;35(12):1984.e5-7.

Levy P, Compton S, Welch R, et al. Nitrates in acute heart failure. Ann Emerg Med. 2007;49(1):67-74.

Felker GM, Lee KL, Bull DA, et al. Diuretics in acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805.

Induction and Ventilation StrategySafe Induction Drugs

• Sedative: Etomidate (0.2–0.3 mg/kg) for cardiovascular stability
• Opioid: Fentanyl (0.5–1 µg/kg) for reflex control with minimal vasodilation
• Paralysis: Rocuronium (1.2 mg/kg) for rapid onset
• Vasodilator: Continue nitroglycerin infusion to maintain afterload control
• Vasopressor: Keep phenylephrine bolus ready to counteract post-induction hypotension

Post-Intubation Ventilation

• Mode: Volume or pressure control
• Tidal volume: 6 mL/kg (ideal body weight)
• PEEP: 5–8 cm H₂O initially, titrated cautiously
• Monitor for hypotension or right ventricular strain

References:

Marik PE, Varon J. Hemodynamic effects of tracheal intubation and positive pressure ventilation. Crit Care Clin. 2007;23(3):421-30.

McCarthy FH, McDermott KM, Kini V, et al. Etomidate use and cardiovascular stability. J Cardiothorac Vasc Anesth. 2013;27(3):434-9.

ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes. N Engl J Med. 2000;342(18):1301-8.

Postoperative and ICU Management

• Continue nitroglycerin until systolic blood pressure is <140 mmHg and pulmonary congestion resolves.
• Initiate furosemide only after blood pressure and intravascular status have stabilized.
• Monitor closely for recurrence of pulmonary edema, arrhythmia, or hypotension.
• Investigate precipitating factors such as acute coronary syndrome, hypertensive crisis, or missed antihypertensive medications.

References:

Peacock WF, Braunwald E, Abraham WT. Management of acute heart failure. J Am Coll Cardiol. 2010;56(5):343-51.

Felker GM, Lee KL, Bull DA, et al. Diuretics in acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805.

Stepwise SCAPE Management Algorithm

1. Identify SCAPE: Acute dyspnea, rales, systolic BP >180 mmHg, preserved EF.
2. Assess Mental Status:

• GCS ≥ 8 → BiPAP and nitroglycerin bolus.
• GCS < 8 → Controlled intubation.

1. BiPAP Settings: IPAP 10–15, EPAP 5–10.
2. Nitroglycerin Infusion: Initiate at 200–400 µg/min following bolus.
3. Monitor Response:

• If improved, continue BiPAP and nitroglycerin.
• If not, prepare for intubation.

1. Induction: Etomidate + fentanyl + rocuronium, with ongoing nitroglycerin and phenylephrine ready.
2. Ventilation Strategy: Tidal volume 6 mL/kg, PEEP 5–8 cm H₂O.
3. Post-Intubation Care: ICU admission, titrate nitroglycerin, introduce diuretics after stabilization.

Summary for Anesthesia Residents

• Do not intubate reflexively. Stabilize initially with BiPAP and nitrates.
• If intubation is required, perform under nitrate cover to prevent vasoconstrictive collapse.
• Use sympathetic-sparing agents such as etomidate and fentanyl.
• Anticipate hypotension with nitroglycerin titration and vasopressors on standby.
• ICU care is mandatory for gradual afterload and volume correction.