[Effect of cardiopulmonary bypass on respiratory function. Clinical contribution].
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Biomedical subjects
Publications and source records attributed to A Zanoni.
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In our experiments on 5 pigs of weight between 40-50 kg we've noticed changes of the parameters occurring precociously during the initial stage of the shock. Particularly we observed a sudden reduction of diuresis reaching total anuria in 15 min and persistence of this anuria for the entire time of the shock (120 min). Immediately after introduction of the removed blood the arterial pressure and the diuresis return to normal value. Concerning the blood flow in renal artery it was observed a gradual decreasing to 10-30 ml/min (normal value = 120-180 ml/min). After the restoration of the blood volume we did'nt notice a clean resumption of the flow although arterial pressure reached normal levels (flow value = 70% of the basal value). The hematic level of K+ undergoes a sudden increase that reaches. Maximal level compatible with animal's life. Within 45-60 min from the beginning of the shock and than decrease with restarting of the diuresis. Creatinine reaches 2 mg/ml in 60 min and remain constant during the following 120 min. The value of the plasma renin were precociously raised, reaching values particularly elevated after 90-120 min from the beginning of the shock and decreasing rapidly with the introduction of the removed blood (parallel behaviour of the arterial pressure).
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High incidence of postoperative arterial hypertension, confined to the first 24-48 hours and independent of the preoperative pressure situation, has been noted in patients following vascular surgery. The phenomenon is more frequent in patients whose angiosclerotic symptomatology goes back more than 2 years, and in those in whom preoperative investigation showed high daily variability in measured values, always however within non-pathological limits. Analysis of possible intraoperative pathogenetic factors in postoperative hypertension reveals a significant relationship between this phenomenon and inhalatory anesthesia, particularly with fluothane and curarization with D-tubocurarine. Co-responsibility of respiratory factors, particularly hypercapnia, has never been documented by haemogasanalysis. As for the pathogenetic mechanisms responsible for this type of hypertension, measurement of urinary catecholamines has revealed a close relationship between the two phenomena. The same investigation, extended to a wider group of patients, showed that by comparison with patients submitted to balanced anaesthesia, those who had received inhalatory anaesthesia with fluothane show, with much greater frequency, increased urinary elimination of catecholamines during the operation and for 24-48 hours afterwards. Catecholaminic hyperincretion, more frequent in fluothane anaesthesia, thus seems to be an important pathogenetic factor in these hypertensive manifestations in which the angiosclerotic medium presumably acts as an amplifier.
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