HYPERLACTATEMIA DUE TO HYPERVENTILATION: USE OF CO₂ INHALATION

Abstract

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.

Subacute Necrotizing Encephalomyelopathy (Leigh's Disease): a Consideration of Clinical Features and Etiology

“…When hypocapnea was sustained, loss of bicarbonate continued and metabolic acidosis resulted due to accumulation of lactic and pyruvic acids. Such a sequence of events has not been well documented in human beings (whereby respiratory alkalosis progressed to lactic acidosis), though marked lactic acidemia has been seen in two patients with prolonged hyperventilation caused by brainstem lesions in Wernicke's encephalopathy (Dossetor et al 1965). Montpetit et al (1971) have suggested that this is the basic mechanism for occasional elevations of lactate and pyruvate in SNE, and 1 am inclined to agree.…”