Key result
Subarachnoid hemorrhage presents with rapid AF and preserved LVEF, mimicking cardiogenic pulmonary edema.
Why the study?
Neurogenic pulmonary edema is an acute pulmonary complication after severe central nervous system injury, and its diagnosis is challenging when respiratory deterioration coincides with cardiac abnormalities capable of causing pulmonary congestion.
Case Report (n=1)
No
This case highlights the diagnostic complexity of distinguishing suspected neurogenic pulmonary edema from cardiogenic pulmonary congestion after subarachnoid hemorrhage when preserved systolic function coexists with rapid atrial fibrillation, left ventricular hypertrophy, and diastolic dysfunction.
Diagnostic overlap of neurogenic and cardiogenic edema occurs in subarachnoid hemorrhage despite preserved LVEF and rapid AF; leaves open mechanistic primacy.
Background Neurogenic pulmonary edema (NPE) is an acute pulmonary complication after severe central nervous system injury. Its diagnosis is challenging when respiratory deterioration coincides with cardiac abnormalities capable of causing pulmonary congestion. Case presentation A 66-year-old man with hypertension and diabetes mellitus presented with sudden dyspnea, hypoxemia, tachypnea, bilateral fine crackles, and an irregular tachyarrhythmia. Non-contrast brain computed tomography showed focal right temporoparietal subarachnoid hemorrhage. Serial electrocardiograms demonstrated atrial fibrillation with rapid/variable ventricular response with elevated high-sensitivity troponin I. Echocardiography showed a left ventricular ejection fraction of 71%, global normokinesis, no regional wall-motion abnormality, concentric left ventricular hypertrophy, and diastolic dysfunction. Initial chest radiography showed increased bronchovascular markings without cardiomegaly or bilateral infiltrates. The patient received respiratory, cardiovascular, and neurological treatment, underwent urgent craniectomy and evacuation, and subsequently developed progressive hemodynamic deterioration with recurrent cardiac arrest and death. Conclusions The close temporal relationship between subarachnoid hemorrhage and abrupt hypoxemic respiratory distress supported a working diagnosis of suspected NPE. Preserved ventricular systolic function made severe systolic pump failure less likely, but it did not exclude a cardiogenic contribution. Atrial fibrillation, hypertension, concentric left ventricular hypertrophy, and diastolic dysfunction therefore remained clinically relevant competing explanations.
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Kasvana et al. (2026) conducted a case report in Suspected neurogenic pulmonary edema after subarachnoid hemorrhage (n=1). Multimodal respiratory, cardiovascular, and neurosurgical management (oxygen, furosemide, digoxin, norepinephrine, mannitol, nimodipine, urgent craniectomy and evacuation) was evaluated on Clinical course and in-hospital mortality. Focal subarachnoid hemorrhage presented with acute hypoxemia (SpO2 89%), rapid atrial fibrillation (180 bpm), and preserved LVEF (71%), illustrating overlap between neurogenic and cardiogenic edema.
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