References of "Saad, G"
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See detailPressure-Flow Relationships of the Pulmonary Circulation During Endotoxin Infusion in Intact Dogs
D'Orio, Vincenzo ULg; Fatemi, M.; Marnette, J. M. et al

in Critical Care Medicine (1992), 20(7), 1005-13

BACKGROUND AND METHODS: We aimed to characterize the effects of an endotoxin insult (Escherichia coli 0127:B8) on the relationships between pulmonary vascular pressure and flow in intact dogs. To achieve ... [more ▼]

BACKGROUND AND METHODS: We aimed to characterize the effects of an endotoxin insult (Escherichia coli 0127:B8) on the relationships between pulmonary vascular pressure and flow in intact dogs. To achieve this goal, multipoint plots of total pressure gradient, arterial pressure gradient, and venous pressure gradient vs. flow were generated by graded inflation of a right atrial balloon, which was used to vary flow. The partitioning of the total pressure decrease across the pulmonary vasculature (total pressure gradient = pulmonary arterial pressure-pulmonary artery occlusion pressure [PAOP]) into gradients across pulmonary arterial (arterial pressure gradient = pulmonary arterial pressure--effective capillary pressure) and pulmonary venous (venous pressure gradient = effective capillary pressure--PAOP) regions was assessed by a waveform mathematical analysis of the pulmonary arterial pressure profile during arterial occlusion, with computation of both PAOP and effective pulmonary capillary pressures. Slopes and extrapolated pressure intercepts from linear regression fits to the pulmonary vascular pressure/flow plots were determined in seven dogs after a 2-hr endotoxic infusion interval and were compared with the corresponding values that characterized a similar group of sham-operated dogs. RESULTS: Under normal conditions, the extrapolated pressure intercept for pulmonary arterial pressure gradient was virtually 0 mm Hg; for total pulmonary arterial pressure gradient and pulmonary venous pressure gradient, the mean extrapolated pressure intercepts were substantially positive: 2.4 +/- 0.2 and 2.1 +/- 0.3 mm Hg, respectively. Endotoxin infusion at 0.25 micrograms/kg/min significantly increased the pressure intercepts from 2.4 to 8.7 and from 2.1 to 8.3 mm Hg of total pressure gradient and venous pressure gradient vs. flow, respectively. This infusion produced a minor, nonsignificant change in the intercept of arterial pressure gradient vs. flow, whereas it increased its slope significantly (p less than .05) from 0.036 to 0.081 mm Hg/mL/min/kg. CONCLUSIONS: These data suggest that endotoxin's effects on vascular resistance are exerted at two different loci such that these effects are additive. These endotoxin-induced effects consisted of increased vascular resistance of the arterial segment and appearance of a Starling resistor at the venous side of the pulmonary circulation, which acted as the relevant back-pressure to flow. [less ▲]

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See detailEffect of Positive End-Expiratory Pressure on Pulmonary Vascular Pressure-Flow Characteristics in Canine Endotoxin Shock
D'Orio, Vincenzo ULg; Fatemi, M.; Mendes, P. et al

in Circulatory Shock (1992), 37(3), 189-97

The vascular pulmonary pressure-flow (P-Q degree) relationships were studied in anesthetized dogs in order to characterize the distribution of total resistance in the pulmonary bed with respect to ... [more ▼]

The vascular pulmonary pressure-flow (P-Q degree) relationships were studied in anesthetized dogs in order to characterize the distribution of total resistance in the pulmonary bed with respect to incremental resistance and critical closure prior to and after endotoxin insult. Incremental resistance was computed as the slope of the P-Q degree relation, whereas critical closure was referred to as the extrapolated pressure intercept at zero flow. P-Q degree coordinates were obtained by varying Q degree through graded inflation of right atrial balloon. The gradients across the arterial segment (Pa = Ppa - Pc) and across the venous segment (Pv = Pc - Pw) of the pulmonary vasculature were defined by the computation of effective capillary pressure (Pc) obtained from the analysis of the transient decay of pulmonary artery pressure (Ppa) toward wedge pressure (Pw) after arterial occlusion. Six group E dogs were infused with endotoxin at a rate of 0.25 microgram/kg min, while six additional animals served as control (group C). Endotoxin induced increases in flow resistance from 0.056 to 0.096 mm Hg/ml/min/kg due to arterial vasoconstriction and increases in critical closure from 2.3 to 8.4 mm Hg due to a venous waterfall. Before and after endotoxin insult, we assessed effects of each of three levels of static lung inflation (PEEP) on P-Q degree relationships.(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

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See detailEffect of endotoxin insult on critical closure in the canine pulmonary vasculature
D'Orio, Vincenzo ULg; FATEMI, M; MENDES, P et al

in Applied Cardiopulmonary Pathophysiology [=ACP] (1992), 4

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See detailPulmonary arterial impedance and right ventricular function in a canine model of septic shock
D'Orio, Vincenzo ULg; MARTINEZ, Christophe ULg; SAAD, G et al

in Intensive Care Medicine (1992), 18-S2

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See detailPulmonary artery pressure-flow plots in septic shock dogs : effects of PGE 1 and nitroprusside
D'Orio, Vincenzo ULg; MARTINEZ, Christophe ULg; SAAD, G et al

in Intensive Care Medicine (1992), 18-S2

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See detailUse of Peep in Management of Life-Threatening Status Asthmaticus: A Method for the Recovery of Appropriate Ventilation-Perfusion Ratio
Broux, R.; Foidart, G.; Mendes, P. et al

in Applied Cardiopulmonary Pathophysiology [=ACP] (1991), 4(1), 79-83

In 15 patients with asthma attack, evidence of the uneven distribution of air flow during controlled ventilation was obtained by detection of ventilatory asynchronism expressed by the incurvated profile ... [more ▼]

In 15 patients with asthma attack, evidence of the uneven distribution of air flow during controlled ventilation was obtained by detection of ventilatory asynchronism expressed by the incurvated profile of tracheal pressure waves associated with the repetitive interruptions of air flow. It was observed that low values of PEEP (mean: 5 +/- 2.5 cm H 2O) induced an increase in transbronchial pressure able to overcome ventilatory asynchronism. In these conditions, an appropriate ventilation-perfusion ratio was restored and improved gas exchanges as indicated by the mean increase of arterial PO 2 from 66.3 mmHg (+/- 2.57) to 96.89 mmHg (+/- 4.41) (p = 0.0005) associated with a mean decrease in arterial PCO 2 from 53.66 mmHg (+/- 2.71) to 42.07 mmHg (+/- 1.64) (p = 0.0005). Simultaneously hemoglobin oxygen saturation rose from 82.31% (+/- 1.97%) to 95.74% (+/- 0.5%). In our patients, such values of PEEP were not high enough to influence the pulmonary arterial circulation. The means of the pulmonary arterial pressures obtained before (syst.: 32.3; diast.: 15.1; mean: 22.00 mmHg) were quite the same (p greater than 0.2) as with PEEP (syst.: 32.00; diast.: 14.00; mean: 21.1 mmHg). The mean of the wedge pressure was found to be 8.3 (+/- 74 mmHg) prior to and 8.4 (+/- 0.68 mmHg) after PEEP (p greater than 0.3). Mean cardiac output rose slightly from 5.27 l/min (+/- 0.24) to 5.77 l/min (+/- 0.38) during PEEP (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

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See detailAccuracy in Early Prediction of Prognosis of Patients with Septic Shock by Analysis of Simple Indices: Prospective Study
D'Orio, Vincenzo ULg; Mendes, P.; Saad, G. et al

in Critical Care Medicine (1990), 18(12), 1339-45

In 26 consecutive septic shock patients, we analyzed the clinical, hemodynamic, and metabolic data before and during volume infusion to test their circulatory reserve in response to fluid repletion. These ... [more ▼]

In 26 consecutive septic shock patients, we analyzed the clinical, hemodynamic, and metabolic data before and during volume infusion to test their circulatory reserve in response to fluid repletion. These patients were investigated to identify early variables that could predict outcome. There were 15 survivors (group A) and 11 nonsurvivors (group B). As a mean, group A patients were hemodynamically evaluated 2.3 h after onset of the sepsis syndrome, whereas group B patients underwent cardiac catheterization after a 12-h interval. At the initial evaluation, both groups demonstrated similarly decreased mean arterial pressure, mean heart rate, and mean cardiac filling pressure. Only group A patients evidenced elevated cardiac index (CI) (greater than 4 L/min.m2) associated with low systemic vascular resistance index (less than 7400 dyne.sec/cm5.m2), which is generally recognized as hyperdynamic cardiac state. However, none of the initial cardiovascular variables could serve as a predictor for survival. Fluid challenge increased left ventricular preload from 6 to 12.4 and from 7.8 to 12.7 mm Hg in group A and group B, respectively. The increases were associated with significant increases in CI from 4.4 to 6.9 and from 3 to 3.8 L/min.m2. However, at the end of fluid challenge, only group A patients exhibited normal cardiac response, as evidenced by the change in left ventricular stroke work index (LVSWI) for a given increase in the pulmonary capillary wedge pressure (WP) that was referred to as left cardiac preload.(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

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See detailPathogenesis and management of acute pulmonary embolism
D'Orio, Vincenzo ULg; MENDES, P; SAAD, G et al

in Acta Clinica Belgica (1989), 44

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