Two cases will be presented in which hyperlactatemia occurred without acidosis and the degree of lactatemia decreased significantly when CO, was administered as therapy.H~c k a b e e , ' .~ Eichenholz and collaborators,' and others' have shown that lactatemia occurs with hyperventilation, both in man and in dogs. Huckabee states that this is a form of lactatemia in which "excess lactate" does not occur, i.e., the lactate/pyruvate ratio would remain normal. I t is inferred that the condition in man is usually benign and passes off when the cause of hyperventilation is controlled. We would not disagree with the latter part of this statement but have evidence that the benign nature of these states leaves something to be desired. Whether this form of lactatemia should be considered as "a compensatory mechanism" or not is a matter of opinion. Eichenholz et al.' have shown that the primary respiratory alkalosis may lead, through secondary lactatemia, to an eventual acidosis. This suggests that the mechanism is not truly compensatory.Primary hyperventilation giving rise to an initial respiratory alkalosis occurs in man in a number of diseased states: (1) voluntary or hysterical hyperventilation; (2) CNS lesions, e.g., cerebrovascular accidents; (3) anoxemia, especially a t altitude6 and possibly also in pneumonic stiffness of lung (in these instances the lactatemia may be partly due to the effects of anoxemia as well as hyperventilation, i.e., mixed cases); (4) hepatic coma;' (5) salicylate poisoning; and (6) excessive ventilation by artificial means on a respirator or under anesthesia. We believe that acute Wernicke's encephalopathy (as will be described in one of the patients below) may also be associated with a pathological disorder of acid base homeostasis on the basis of hyperventilation.Eichenholz' has emphasized an important facet of lactatemia that occurs with primary hyperventilation, namely, that if five per cent CO, in air or oxygen is used as the respiratory gas, hyperlactatemia is prevented and will not occur despite continuation of hyperventilation. Further, if the gas mixture is changed from air to the Con mixture after hyperlactatemia has been induced by either salicylate or passive hyperventilation, the level of lactate will fall and the serum bicarbonate concentration will rise, concomitantly.The fact that several observers have noticed that hyperlactatemia occurs with hyperventilation of the passive type refutes the theory that this mechanism is due to the work involved in hyperventilation itself.
Studies by the stop–flow technique were carried out in dogs in which diuresis had been induced with water, with and without the addition of bicarbonate. Urine samples from the collecting duct had greater maximal CO2 tension than was recorded simultaneously in arterial blood, and this peak occurred during infusion of carbonic anhydrase as well as during its inhibition by acetazolamide. With the former procedure, curves of CO2 tension were almost identical with those in standard control experiments. After administration of acetazolamide the values were greater, even when CO2 tension in arterial blood was > 60 mm Hg; otherwise, the curves were of similar shape. Lowest values for O2 tension in urine were recorded from the collecting duct region, and they persisted when urine flow was increased by the administration of acetazolamide or when the dog breathed 100% oxygen. The curves were of similar shape but values were slightly greater during oxygen breathing. The results obtained reflect the operation of hemodynamic mechanisms in the renal medulla, during application of the stop–flow technique.
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