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Biomedical subjects

Charles Her

Publications and source records attributed to Charles Her.

5 recordsLinked to original sources
PubMed2006

Right ventricular systolic function is not depressed in morbid obesity.

BACKGROUND: The increased pulmonary blood volume associated with the increased total blood volume in morbidly obese patients increases pulmonary artery pressure and pulmonary vascular resistance, resulting in increased right ventricular (RV) afterload. Thus, the morbidly obese may develop RV dysfunction owing to the increased RV afterload. We examined this possibility by assessing RV contractile function in morbidly obese patients, using RV end-systolic pressure-volume relationship and RV systolic time intervals. METHODS: Included were 25 morbidly obese patients undergoing gastric bypass surgery under general anesthesia. Pulmonary artery pressure and RV end-systolic volume were measured with a thermodilution pulmonary artery catheter. Pulmonary arterial dicrotic notch pressure was used as an estimate of RV end-systolic pressure. Two data points were used to define RV end-systolic pressure-volume relationship. RV systolic time intervals were determined by simultaneous graphic display of the electrocardiograph, phonocardiograph, and pulmonary artery pressure curve, and were expressed as a pre-ejection period/RV ejection time ratio. RESULTS: The mean slope of right ventricular end-systolic pressure-volume relationship line was 0.54 +/- 0.13 and mean pulmonary vascular resistance 274 +/- 80 dyne.sec.cm(-5).m(-2). The mean pre-ejection period/RV ejection time ratio was 0.4 +/- 0.11. There was an inverse correlation between the pre-ejection/RV ejection time ratio and the slope of RV end-systolic pressure-volume relationship line (R(2)=0.658, P<0.0001). CONCLUSION: Our data indicate that RV function is not depressed in morbid obesity despite increased RV afterload.

Adult↗
PubMed2005

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↗
PubMed2004

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↗
PubMed2004

Deadspace ratio.

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Humans↗