Definition

• Neurogenic pulmonary edema (NPE) is characterized by the sudden development of lung edema minutes to hours after damage to the CNS.

Pathology

• Contraction band necrosis (myofibrillar degeneration, or coagulative myocytolysis) is the likely pathologic substrate of cardiac injury. This distinctive form of myocardial injury is frequently noted on autopsy in SAH patients.

• Generally regarded as non-cardiogenic. A view supported by the consistent finding of high protein-content edema fluid, and normal wedge pressures. Increased vascular permeability may result from barotrauma related to transient pulmonary hypertension as well as neurogenic mechanisms.

• Blast theory, as proposed by Theodore and Robin, suggests that NPE results primarily from an insult to the pulmonary circulation. In this view increased systemic and pulmonary vascular resistance is associated with a shift of blood from the systemic to the more compliant pulmonary vessels, resulting in markedly elevated pulmonary vascular pressures and the egress of fluid into the lung. Although pressures may rapidly normalize, loss of pulmonary capillary integrity from barotrauma or neurogenic mechanisms leads to persistent edema with a high protein content.

• Thus, cardiac dysfunction in patients with NPE is unexpected and infrequently recognized; this paper describes 5 cases of SAH and NPE with evidence of myocaridal injury and reduced LV systolic function.

• This paper shows that a neurogenically mediated form of cardiac injury, characterized by sudden decompensation of the LV, may lead to hemodynamic instability and the formation of lung edema; in this view cardiac injury may be regarded as a consequence of massive sympathetic discharge and increase in peripheral vascular resistance.

Clinical Features

• Hypotension (systolic BP <110 torr) developed within 6 hours of SAH in all patients in this study (6)

• Metabolic acido sis occurred in all patients. This was maximal shortly after the onset of SAH and generally cleared within hours.

• Elevated CK levels with borderline MB fraction occurred in all patients.

• ECG findings were variable; all developed QT prolongation; flattened or inverted T waves in all; T wave inversions gradually normalized after a few days but always persisted to some extent for at least a week.

• Echo in the first 4 days showed left ventricle segmental wall motion abnormalities and reduced ejection fractions in all patients.

• Wedge pressures were normal or only slightly elevated.

• Depressed LV funciton was evident by reduced stroke volume and cardiac output and elevated systemic vascular resistance.

References

Updated 081301