Acute cardiogenic pulmonary edema — the failing pump floods the lungs
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Acute cardiogenic pulmonary edema = left-ventricular failure → back-pressure floods the alveoli.
↓LV output raises filling pressure; it backs up the pulmonary circuit until hydrostatic pressure > oncotic and fluid pours into the air sacs.
SCAPE = Sympathetic Crashing Acute Pulmonary Edema — the hypertensive flash: minutes, not days. Usually fluid MALDISTRIBUTION, not overload.
1Pathophysiologythe vicious cycle
1↓ LV function — ischemia, HTN crisis, arrhythmia or valve → the ventricle can't eject → forward output falls.
Distinct from "dry" dyspnea: wet lungs, sudden onset, hypertensive, sits bolt upright — responds to nitrates + NIV, not bronchodilators.
SSeverityread the BP · pick the pathway
PATTERN
BP
ONSET
THE FIX
SCAPE
SBP>180
minutes
NIV + high-dose nitro
Decomp. HF
normal/↑
days
nitro + diurese (real overload)
Cardiogenic shock
SBP low
hours
pressor/inotrope — NOT nitrates
SCAPE is the hypertensive crash — hypoxic, panicked, flooding fast. Treat the blood pressure; it is usually maldistribution, not litres of extra fluid.
Hydrostatic beats oncotic → transudate fills the sac.
Hypoxia
Fluid widens the diffusion path → V/Q shunt.
4Diagnosticsit's clinical — confirm the pattern
Bedside: clinical dx first — monitor, IV, SpO₂. Lung ultrasound: diffuse bilateral B-lines (>3/field) — fast, sensitive for interstitial edema.
ECG: hunt the trigger — STEMI / ischemia, AF with RVR, arrhythmia. Troponin for ACS.
CXR: cephalization, Kerley-B lines, perihilar "bat-wing", effusions — don't wait for it. BNP supports HF when the diagnosis is unclear (context, not the acute driver); echo for EF, valve, wall motion.
Nitroglycerin — the workhorse. SL 0.4 mg q3–5 min → IV infusion, high-dose in the hypertensive crash. Venodilation → preload↓; higher doses → afterload↓.