[Accidental deep hypothermia and circulatory arrest. Treatment with extracorporeal circulation]. / Hypothermie profonde accidentelle et arrêt circulatoire. Traitement par circulation extracorporelle.

A 27-year old female was discovered at 4 a.m. lying in a wet field, the ambient temperature being of 4 degrees C. Her rectal temperature had fallen to 19 degrees C. She was comatose and failed to respond to noxious stimuli. Her pupils were dilated and fixed. Her respiratory rate was reduced to three to four breaths per min. Her blood pressure was not measurable and neither femoral or carotid pulse could be detected. The heart was in sinus rhythm with a rate of 40 b X min-1. During her transfer to hospital, she was ventilated with oxygen, a tidal volume of 300 ml and a rate of 10 b X min-1. On arrival in the emergency room, a short period of ventricular fibrillation preceded cardiac arrest. Cardiac massage and sodium bicarbonate infusion were continued during the transfer of the patient to the operating theatre. A femoro-femoral cardiopulmonary bypass was started with a bloodless priming, 3 mg X kg-1 heparin and a flow of 3,000 to 3,500 ml X min-1. Mean arterial pressure was maintained between 65 and 85 mmHg; cardiac massage was discontinued during the bypass. Within 50 min, ventricular fibrillation appeared, rectal temperature had increased to 33 degrees C. Electrical defibrillation (300 J) was successful. Cardiopulmonary bypass was stopped after 63 min. The postoperative course was uneventful, apart from transient pulmonary oedema. At the time of discharge, a week later, no loss of intellect or change in behaviour could be perceived.(ABSTRACT TRUNCATED AT 250 WORDS)

[Pulmonary oxygen transfer under a respirator in anesthesia and resuscitation]. / Transfert pulmonaire de l'oxygène sous respirateur en anesthésie et en réanimation.

The resistance of the passage of oxygen from air to blood is estimated in measuring P(A-a)O2. This index varies with FIO2. P(a/A)O2, the index proposed by GILBERT and KEIGHLEY [18], expresses PaO2 as a percentage of PAO2. This index would be independent of FIO2. Two groups are studied. Patients of the first group (n = 22) are artificially ventilated in intensive care for severe parenchymal lesion. Those of the second group (n = 25) have no notable history of pulmonary disease and are anaesthetized and hooked up to a respiratory for surgery. Blood gases are measured and the transfer indices calculated for increasing FIO2 (0.4, 0.6, 0.8 and 1). Under conditions of anaesthesia, the effect of thermic decrease on PaCO2 is dampened by maintaining a constant PACO2 during measurement. P(a/A)O2 does not vary significantly as a function of FIO2 in the intensive care group, whereas the results observed in the anaesthetized patients are substantially dispersed. Factors which are susceptible to affect oxygen transfer as well as the effects of FIO2 increase are discussed. P(a/A)O2 stability observed in intensive care is probably related to the predominant effect of venous admixture, which is hardly affected by variations in FIO2. In anaesthesia, resistance to the transfer of oxygen appears to be linked mainly to changes in the distribution of the ventilation/perfusion ratio (reduction in CRF; pharmacological effect of oxygen on pulmonary vascular reactivity). These phenomena lead to alveolar instability and a variable shunt effect.(ABSTRACT TRUNCATED AT 250 WORDS)