Biomedical subjects
Publications and source records attributed to P Dechamps.
After a retrospective study of 17 cases of caustic intoxication in the intensive care unit, the epidemiologic, pathophysiologic, clinic and therapeutic aspects are reviewed. The following procedure is suggested: early endoscopies, abstention of any gastric lavage, corticosteroids and empiric antibiotic therapy and the most early possible introduction of a parenteral nutrition.
The effect of almitrine bismesylate on hypoxic pulmonary vasoconstriction (HPV) remains controversial. We therefore investigated in a double-blind, placebo-controlled, randomized design the effects of low dose of almitrine bismesylate (4 micrograms/kg/min given intravenously) on blood gases, pulmonary hemodynamics, and ventilation-perfusion (VA/Q) distributions in normal subjects breathing a hypoxic mixture (FIO2, 0.125), room air (FIO2, 0.21), and oxygen (FIO2, 1.0) in a random sequence. In the placebo group (7 subjects), no change was recorded. In the almitrine group (10 subjects), arterial PO2 improved during hypoxia (from 42 +/- 2 to 47 +/- 1 mm Hg, p less than 0.05, mean +/- SEM) and normoxia (from 99 +/- 3 to 104 +/- 2, p less than 0.05). Pulmonary arterial mean pressure and pulmonary vascular resistance index increased with almitrine during hypoxia, respectively, from 20 +/- 1 to 23 +/- 1 mm Hg (p less than 0.01) and from 207 +/- 22 to 283 +/- 35 dyne.s.cm-5.m2 (p less than 0.01), and during normoxia, respectively, from 12 +/- 1 to 14 +/- 1 mm Hg (p less than 0.05) and from 90 +/- 11 to 137 +/- 13 dyne.s.cm-5.m2 (p less than 0.05). The VA/Q distribution improved during hypoxia, with a shift of the blood flow distribution to better oxygenated lung units with higher VA/Q ratios. We conclude that in normal humans low dose of almitrine improves gas exchange by an enhancement of HPV.
To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven patients had an arterial hypoxemia (PaO2 = 69 +/- 6 mm Hg, mean +/- SD), and three patients were normoxemic (PaO2 = 89 +/- 6 mm Hg). In each hypoxemic patient, the VA/Q distributions were characterized by the presence of low VA/Q units. A negative logarithmic correlation was found between the dispersion of the blood flow distribution and the arterial PO2. An acute inspiratory hypoxia (FIO2, 0.125) elicited an increase in pulmonary vascular resistance by 58.5% in the hypoxemic group and by 81.6% in the normoxemic one (p = NS between the two groups). The percent change in pulmonary vascular resistance induced by hypoxia was not correlated with the percent change in the dispersion of the blood flow distribution. A theoretical analysis showed that the mean arterial PO2 of 69 mm Hg of the hypoxemic group differed from a normal reference value of 96 mm Hg as a result of the combined effects of reduced hemoglobin (-4 mm Hg), increased P50 (+4 mm Hg), increased ventilation (+10 mm Hg), low VA/Q (-35 mm Hg), and true shunt (-2 mm Hg). These results show that the "hypoxemia of liver cirrhosis" is essentially caused by VA/Q mismatching, which is not explained by an abnormal hypoxic pulmonary vasoconstriction.
Pulmonary arterial hypertension represents an important parameter for the assessment of the severity of chronic bronchitis. The measurement of the pulmonary arterial pressure, however, requires invasive techniques of limited routine use because of costs and associated risks. The aim of this study is to evaluate whether the 81mKr right ventricular ejection fraction and parameters derived from equilibrium 99mTc red blood cells' right ventricular curve allow a better estimation of PAP than the 99mTc RVEF. In 41 patients with severe chronic bronchitis, the linear correlation between PAP and 99mTc RVEF was -0.61 (p less than 0.001). None of the parameters derived from the right ventricular curve was better correlated to PAP than the 99mTc RVEF. In 16 other chronic bronchitis patients, the 81mKr RVEF correlated moderately to PAP. In conclusion, the alternative isotopic methods proposed in this work do not provide a reliable estimation of pulmonary arterial pressure in patients with chronic bronchitis.
To evaluate the influence of beta 2 mimetics on ventricular contractility and pump function, radionuclide ventriculography and right heart catheterization were simultaneously performed in 10 patients with severe chronic obstructive pulmonary disease. After a 60 min constant infusion of 17 micrograms/min salbutamol, cardiac index increased by 60%, heart rate by 39%, and stroke volume index by 14%. Mean pulmonary artery pressure remained unchanged and mean arterial pressure decreased slightly but not significantly. Right ventricular (RV) function improved as attested to by an increase of RV ejection fraction (+8%), a decrease of RV end-diastolic pressure (-5 mm Hg), and RV end-systolic volume index (-18%). Simultaneously, the pulmonary vascular resistance index decreased by 33% and RV contractility, appreciated by RV dP/dtmax, RV (dP/dtmax)/P, and RV end-systolic pressure/volume ratio, increased by 44, 77, and 27%, respectively. Left ventricular (LV) function also improved. The LV ejection fraction increased by 18% and LV end-systolic volume decreased by 34%. Concomitantly, the systemic vascular resistance index decreased by 40% and the LV end-systolic pressure/volume ratio increased by 50%. Our results suggest that the infusion of salbutamol improves ventricular performance by a decrease of ventricular afterload and by a positive inotropic effect.