[Central venous pressure].
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Biomedical subjects
Publications and source records attributed to F Lemaire.
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Study of ventilatory mechanics implies collection of input variables (stresses estimated by pressures) and output variables (strains), from which the parameters (compliance, resistance, etc.) of a model reproducing the functioning system can be computed. From this point of view, patients under artificial ventilation show a twofold difficulty: the one is the collection of variables, very difficult in consideration of the patients' precarious state, the other the type of the model: the first order linear model, used for lack of better solution, can be criticized, on the one hand by severe pulmonary changes in these patients, and by the special mode of applying constraints during artificial ventilation on the other. All these facts explain the methodologic and theoretical difficulties encountered in ventilatory mechanics analysis in resuscitation, which actually leads to the expression of one parameter as representative of the pulmonary parenchymal elasticity: the static compliance, and to the determination of the balancing point of the system: the functional residual capacity.
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Non cardiogenic pulmonary edema is caused by an increase of alveolocapillary permeability, due to different etiologies: fat embolism, multiple trauma, septic shock, influenza pneumonia, aspiration syndrome... Chest radiographs exhibit interstitial and/or alveolar pattern, severity of injury is assessed by the magnitude of intra-pulmonary shunting. Pulmonary wedge pressure is normal, and increased pulmonary vascular resistance is sometimes evidence in prolonged evolutions, especially in fatal cases. Treatment consists in the suppression of hypervolemia, and ventilation with positive and expiratory pressure (PEEP). Extra-corporeal membrane lung oxygenation remains since now rather unsuccessful.
Urgent cardiac transplantation in very unstable patients, kept alive in intensive care unit, is a significant (34 percent) part of the Henri-Mondor's transplantation program. Nineteen patients received a donor graft from january 1986 to october 1988. Sixteen were bridged pharmacologically as 5 received a mechanical bridge. Time on waiting list ranged from 12 to 21 days. Six patients died in the first post-operative month. Death was due to uncontrolled preoperative problems in 5, donor graft failure in one. The survival rate at one year was 52 percent, to be opposed to 76 percent in stable patients. These figures must be considered when selecting the priority of the transplantation candidates.
Increase of shunt has been demonstrated during short periods of pure oxygen breathing, mostly in patients with mild acute respiratory failure (ARF). Twenty patients with a large range of venous admixture (12 to 63%) were studied when FIO2 was increased from maintenance to one. Intrapulmonary shunt was measured with both the conventional oxygen method [QS/QT (O2)] and the multiple inert gas elimination technique [QS/QT (IG)]. Mean venous admixture decreased from 29 to 24% when FIO2 was increased and QS/QT (IG) remained unaltered. The pattern of blood flow distribution remained similar in both conditions, even in the eleven patients with ARF secondary to bacterial pneumonia and who had a low V/Q mode, highly liable to collapse with 100% oxygen. As no increase in shunt was documented in these patients, reluctance to measure shunt during 100% oxygen breathing should be re-evaluated.
A case of a right-to-left intracardiac shunt caused by a right atrial myxoma is reported. Sudden hypoxaemia was the unique symptom. Measurement of Pao2 while the patient breathed pure oxygen demonstrated the presence of a shunt. Right heart catheterization showed a patent foramen ovale and a pressure gradient between the right atrium and the right ventricle, and between the right and the left atria, explaining the shunt. Cineangiography demonstrated a right atrial myxoma, which was surgically removed. This case report illustrates how a step-by-step diagnostic procedure, based on pathophysiology, may lead to such unexpected findings.
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Acutely ill patients often show rapid and sometimes concomitant changes in haemodynamics, pulmonary exchange and O2-uptake. PaO2 reflects the interrelationships between these three factors. The Qs/Qt shunt is computed by taking two simultaneous blood samples, one systemic arterial, the other mixed venous, with the patient inhaling pure O2 for twenty minutes. In estimating the fraction of total cardiac output unsaturated in pulmonary transit, Qs/Qt is practically used as a selective test for pulmonary gas exchange. We propose a nomogram, showing in terms of Qs/Qt shunt the variations of PaO2, of haemoglobin O2 saturation and of arterial-venous difference of O2 concentrations. Blood gas changes during treatment of shock or of acute respiratory insufficiency are explained by use of this nomogram.