[Cerebral hemodynamic disorders in patients with chronic decompensated respiratory insufficiency. Physiopathogenetic...

The present paper reports on 12 patients (8 males, 4 females) suffering from chronic decompensated respiratory failure, who presented concomitant transient haemodynamic disturbances in the carotid and vertebrobasilary systems, manifested by hemisphere or brain stem symptoms. Owing to the adaptive capacity of these patients there exists a certain tolerance threshold to hypercapnic hypoxemia, but following accentuated or rapid aggravation of acid-base hypercapnic hypoxemia, the biological balance is abruptly perturbed leading to cerebral haemodynamic disturbances. The pathophysiological mechanism of production appears to be the accumulation of acid ions caused by pH acidification of the cerebrospinal fluid. Increase in the cerebral arterial output with decrease in the rate of circulation and vascular resistance take place especially in the vessels with atheromatous or hyaline lesions. Under conditions of severe acidosic hypercapnic hypoxemia this, nevertheless, insures a minimum of 10--20% oxygen required by the metabolism of the nerve cell, sufficient for maintaining the structure of the cell (vita minima). These vasculometabolic mechanisms explain why with improvement of haematosis, following remission of the decompensated disease and fall in acidotic hypercapnic hypoxemia values, the cerebral haemodynamic disturbances also show a more or less evident remission because the nerve cells having maintained their structure are able to take up their function again.