Severe Hypocapnia Research Articles

Lymphangitic Carcinomatosis of the Lungs with Normal Appearing Chest X-Ray Films

A 48-year-old woman with severe dyspnea, cough, cyanosis and normal appearing chest x-ray films nine months after radical mastectomy for carcinoma is described. Pulmonary function tests suggested restrictive ventilatory impairment. Arterial blood gas measurement showed severe hypoxemia and hypocapnia. Postmortem microscopic examination revealed neoplastic cells within the pulmonary lymphatics.

Lactate production in blood circulating in a pump oxygenator: effect of carbon dioxide

Blood gas tensions, pH, and glucose, lactate, and pyruvate concentrations were determined in whole blood circulated through a pump-oxygenator, ventilating the oxygenator with 100% O 2 and 93% O 2-7% CO 2 in random order. Blood to which insulin or glucose had been added also was studied in a similar fashion. A high P O 2 was maintained throughout the study, thus eliminating any element of cellular hypoxia. Blood utilized glucose and produced lactate at a constant rate during conditions of cucapnia, and at an accelerated rate during conditions of severe hypocapnia and respiratory alkalosis. Eucapnia after hypocapnia slowed the rate of lactate production and glucose utilization but did not stop them, nor did it decrease the level of lactate in the blood. Pyruvate concentrations decreased then stabilized with hypocapnia and increased with eucapnia. Blood alone, however, seems to account for only a small fraction of the hyperlactatemia of hyperventilation in vivo. The mechanism of lactate production in blood alone with adequate oxygen levels is due to red blood cell metabolism being primarily anaerobic through the Embden-Meyerhof pathway. Whether this is accentuated by hyperoxia is not known. Also, why lactate is not decreased with hypercapnia in blood alone as occurs in vivo is not understood.

Effect of low maternal carbon dioxide tension on placental gas exchange

The effect on the fetus of spontaneous and induced maternal hyperventilation has been assessed in 58 patients. A decrease in maternal pCO 2 was accompanied by a corresponding decrease in fetal pCO 2 . Severe maternal hypocapnia with a maternal venous blood pCO 2 below 22 to 23mm. Hg was associated with a small but significant decrease in umbilical vein and artery oxygen tension; however, in the current study this was not accompanied by evidence of oxygen debt or metabolic acidosis. Maternal hyperventilation, with hypocapnia and respiratory alkalosis, was associated with increased maternal and fetal lactate and pyruvate concentration.

Disturbances of Gas Metabolism in Patients with Occlusive Cerebrovascular Disease

The physiological details of brain circulation and gas metabolism have been widely studied both in experimental animals and men; the results of those investigations have been exhaustively reviewed. Considerably less work has been devoted to the investigation of gas metabolism of the brain tissue and of lung gas exchange in the conditions of cerebrovascular disease. Nevertheless, the general changes in lung ventilation, in cerebral blood flow and, accordingly, in cerebral oxygen metabolism, which take place in patients with occlusive cerebrovascular disease, have been determined rather well. This paper is a review of some of the studies performed at Tartu State University on the pulmonary ventilation, general and cerebral gas exchange in patients with occlusive cerbrovascular disease. That equilibrium is disturbed when brain infarction develops. In cases with secondary involvement of the upper brain stem a marked central neurogenic hyperventilation occurs. Severe respiratory hypocapnia follows which in its turn causes secondary restriction of the brain oxygen supply. Both arterial hypoxemia and hypocapnia are in close correlation with mortality and most of the stroke patients with an unfavorable outcome of the disease “breathe themselves to death.” Timely surgical restoration of the blood flow via the occluded artery normalizes the brain gas metabolism. The inhalation of the gas mixture containing 7 % CO 2 permits temporary normalization of cerebral gas metabolism, but most likely only in the unaffected region of the brain.

Discussion and Comments to Section IV on Effect of Severe Hypocapnia on Cerebral Oxygenation

Discussion and Comments to Section IV on Effect of Severe Hypocapnia on Cerebral Oxygenation