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Charles Her

Publications and source records attributed to Charles Her.

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Increased pulmonary venous resistance contributes to increased pulmonary artery diastolic-pulmonary wedge pressure gradient in acute respiratory distress syndrome.

BACKGROUND: Pulmonary artery diastolic (PAD)-pulmonary wedge pressure (PWP) gradient has been shown to be increased in sepsis and acute respiratory distress syndrome (ARDS). Because pulmonary venous vasoconstriction induced by endotoxemia in sepsis or postcapillary leukocyte aggregation in ARDS or both can increase pulmonary venous resistance (Rpv), it is possible that the elevated Rpv increases PAD-PWP. The authors examined this possibility by assessing the correlation between Rpv and PAD-PWP gradient in patients with ARDS. METHODS: Included were 20 patients with ARDS who required surgical procedures during general anesthesia. Rpv was calculated as the difference between mean pulmonary artery (PA) output pressure and PWP divided by cardiac index. Mean PA output pressure was computed from harmonic form of the recorded PA pressure by applying an attenuating factor to its phasic components, for which Fourier analysis was used. Total pulmonary vascular resistance (TPVR) was calculated as the difference between mean PA input pressure and PWP divided by cardiac index. To avoid the effect of PA resistance on TPVR and Rpv, the relative pulmonary venous resistance (Rpv/TPVR) was used. RESULTS: There was a good correlation between Rpv/TPVR and PAD-PWP gradient (R = 0.698, P < 0.0001). When patients were classified into two groups based on PAD-PWP gradient, the Rpv/TPVR was 0.66 +/- 0.06 in the group with a PAD-PWP gradient of 6 mmHg or greater and 0.46 +/- 0.08 in the other group (P < 0.0001). CONCLUSION: A strong correlation between Rpv/TPVR and PAD-PWP gradient suggests that the increased Rpv contributes to increased PAD-PWP gradient in patients with ARDS.

Adult↗

Acute respiratory distress syndrome of the contralateral lung after reexpansion pulmonary edema of a collapsed lung.

STUDY OBJECTIVE: To report that leukocyte-mediated acute injury may develop in a nonhypoxic lung after hypoxia-reoxygenation injury of the hypoxic lung and in other systemic organs in patients with reexpansion pulmonary edema. DESIGN: Case report analysis with examination of the literature. SETTING: Intensive care unit of a university hospital. PATIENTS: Three patients who developed leukocyte-mediated acute lung injury in the contralateral lung and systemic organ injury after ipsilateral reexpansion pulmonary edema of a collapsed lung. MEASUREMENTS: To rule out the possibility that the acute lung injury in the contralateral lung was an extension of the hypoxia-reoxygenation injury, we analyzed changes in leukocyte and platelet count in the peripheral blood in relation to the development of pulmonary edema in each lung. Changes in liver enzymes were also analyzed to detect hepatic dysfunction as evidence of systemic organ injury. MAIN RESULTS: Both leukocyte and platelet counts decreased when reexpansion pulmonary edema developed, and decreased further when acute lung injury developed in the contralateral lung (F = 8.42, p = 0.037 for leukocytes, and F = 17.66, p = 0.01 for platelets). Significant hepatic dysfunction developed, as evidenced by increases in both serum bilirubin (p = 0.001) and lactic dehydrogenase, indicating the presence of systemic organ injury. CONCLUSIONS: The hypoxia-reoxygenation injury of one lung can induce acute lung injury in the other lung and systemic organ injury.

Adult↗

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