Incidence and clinical significance of cardiopulmonary complications o
f acute cerebral lesions are still unclear. Neurogenic pulmonary edema
(NPE) is characterized as an acute, protein-rich lung edema occurring
shortly after cerebral lesions associated with an acute rise of intra
cranial pressure. NPE is infrequently diagnosed, usually in associatio
n with head trauma. Pathophysiological mechanisms include a rise of th
e pulmonary vascular hydrostatic pressure either due to sympathetic in
nervation with pulmonary vasoconstriction or increased left-atrial pre
ssure following systemic arterial hypertension or an increase in pulmo
nary capillary permeability. In contrast to NPE, cardiac complications
are frequently observed, most consistently in patients with subaracho
id hemorrhage. Typical ECG changes are repolarization abnormalities, s
imilar to those observed in coronary heart disease, and cardiac arrhyt
hmias. The CK-MB may be slightly elevated; echocardiographic findings
show a depressed left-ventricular function. Pathological examination r
eveals myofibrillar necrosis. Cardiac complications are explained with
overactivity of the sympathetic innervation and high levels of circul
ating catecholamines. For adequate treatment, close cardiac monitoring
is required in all patients with acute cerebral lesions.