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Biomedical subjects

G Simonneau

Publications and source records attributed to G Simonneau.

At least 181 records · Page 10Linked to original sources

Therapeutic approach to acute pulmonary embolism.

Many therapeutic aspects of venous thromboembolism continue to generate controversy so that the general therapeutic guidelines given below are only indicative. The first step is the diagnosis of venous thromboembolism; this is done in the vast majority of patients by visualization of blood clots using either pulmonary angiography or phlebography. The second step is to arrest the thrombotic process; the best means of doing this is to administer IV heparin. In the case of contra-indication or documented inefficacy of heparin therapy, the only therapeutic solution is to interrupt the inferior vena cava either with a clip, an umbrella or a filter. The blood clot lysis, which represents the third step, is effected by the natural fibrinolytic system. Thrombolytics , administered as a bolus of urokinase (15000 CTA U/kg), are indicated in cases of life-threatening pulmonary emboli, i.e. those with a pulmonary vascular obstruction of more than 50% and with hypotension, shock, or acute right ventricular failure. The use of thrombolytics is more questionable when they are administered to improve the quality of vascular patency. The only indication for pulmonary embolectomy is a contra-indication or inefficacy of thrombolytics . Due to the diagnostic and therapeutic difficulties, the first and most important part of the treatment of pulmonary emboli must be the broad application of prophylaxis treatment in patients with a high risk of venous thromboembolism.

Acute Disease↗

Computation of ventilation-perfusion ratio with Kr-81m in pulmonary embolism.

Diagnostic difficulties occur in pulmonary embolism (PE) during visual analysis of ventilation-perfusion images in matched defects or in chronic obstructive lung disease (COPD). In 44 patients with angiographically confirmed PE and in 40 patients with COPD, the regional ventilation-perfusion ratios (V/Q) were therefore computed using krypton-81m for each perfusion defect, and were displayed in a functional image. In patients with PE and mismatched defects, a high V/Q (1.96) was observed. A V/Q greater than 1.25 was also found in nine of 11 patients having PE and indeterminate studies (studies with perfusion abnormalities matched by radiographic abnormalities). COPD was characterized by matched defects and low V/Q. The percentage of patients correctly classified as having PE or COPD increased from 56% when considering the match or mismatched character to 88% when based on a V/Q of 1.25 in the region of the perfusion defect. This quantitative analysis, therefore, seems useful in classifying patients with scintigraphic suspicion of PE.

Adult↗

Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperative pain.

The effects of upper abdominal surgery on diaphragmatic function were studied in 5 patients. During quiet tidal breathing, the volume displacement of the abdomen within the tidal volume (Vab/Vt) and the ratio of abdominal and transdiaphragmatic pressure changes (delta Pab/delta Pdi), taken as an index of the diaphragmatic contribution to the breathing process, decreased significantly on the first postoperative day (p less than 0.001); in 2 patients, a cephalad paradoxical motion of the diaphragm during inspiration was observed. Diaphragmatic dysfunction also occurred during maximal inspiratory efforts as shown by the significant fall in maximal static transdiaphragmatic pressure (Pdimax) and cephalocaudal diaphragmatic displacement on the first (p less than 0.001) and third (p less than 0.001) postoperative days. On the first postoperative day, opiate epidural analgesia did not modify Vab/VT, delta Pab/delta Pdi, and Pdimax. These parameters spontaneously returned towards control values on the seventh postoperative day. We conclude that upper abdominal surgery induces a marked diaphragmatic dysfunction lasting about 1 wk and that it is not suppressed by postoperative pain relief. The mechanism of this dysfunction remains to be determined. It may be the main cause of the postoperative pulmonary restrictive pattern.

Abdomen↗

A comparative study of the cardiorespiratory effects of continuous positive airway pressure breathing and continuous positive pressure ventilation in acute respiratory failure.

Positive end expiratory pressure (PEEP) produces cardiopulmonary effects whether administered by controlled positive pressure ventilation (CPPV) or continuous positive airway pressure (CPAP). In eight patients with acute respiratory failure, the effects of 20 cm PEEP administered via CPPV and CPAP were compared. An esophageal balloon was used to calculate the transmural vascular pressures. The control values under mechanical ventilation with no PEEP (IPPV) for PaO2 and QS/QT (FiO2 being 1.0) were respectively 132 +/- 15 mmHg and 31 +/- 3%; CPPV gave a PaO2 of 369 +/- 27 mmHg and QS/QT fo 14 +/- 1.6%, CPAP 365 +/- 18 mmHg and 18 +/- 1.3% respectively. The two different modes of ventilation (CPPV and CPAP) gave identical blood gas improvement through the same level of end expiratory transpulmonary pressure despite marked differences between absolute mean airway and esophageal pressures. Conversely, hemodynamic tolerance was very different from one technique to the other: CPPV depressed cardiac index from 3.4 +/- 0.3 to 2.4 +/- 0.2 1/min/m2 as well as decreasing transmural filling pressures, suggesting a reduction in venous return. Conversely, filling pressures maintained at control values during CPAP and cardiac indexes were unchanged.

Acute Disease↗