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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH less than 7-10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH less than 7-10 were judged to have "appropriate hypocapnia", and fifteen had "submaximal hypocapnia". Thirteen of the latter fifteen had circulatory failture and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate greater than 9 mmol/1. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.
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PMID:The ventilatory response in severe metabolic acidosis. 0 84

This study reports clinical and neuropathological findings in six premature infants dying after prolonged assisted ventilation (IPPB and CPPB) due to pulmonary insufficiency (gestational age: 26.--32. week; birth weight 820--1400 Gm; respirator therapy 41--143 days; survival 104--263 days). During the rspirator therapy the children developed marked extensor rigidity of the trunc and spasticity of the extremities. Postmortem examination revealed cor pulmonale and right ventricular failure. Signs of marked perinatal brain damage were missed. The slightly atrophic brains showed predominant damage to the telencephalic white matter of varying intensity ranging from focal necroses to gliosis and retarded myelination. Constant findings were increased vascularisation and transformation of the premyelinating glia into astrocytes in the deep and subcortical white matter. This form of telencephalic leucoencephalopathy indicates the particular vulnerability of the developing white matter in conditions with chronic hypoxia, hypercapnia, acidosis and vascular congestion. The varying intensity of the lesions suggests that, in principle, minor lesions are either reversible or may be compensated in surviving children.
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PMID:Telencephalic leucoencephalopathy in premature infants dying after prolonged artificial respiration. Report on 6 cases. 124 20

In a series of 102 patients with multiple injury including a blunt lesion of the chest treated in 1970 through 1973 the mortality rate could be reduced to 17 per cent. This compares favourably with a mortality of about 34 per cent in a similar group of patients treated in the same hospital during 1965 through 1969. The improvement is partly due to increasing experience of the surgical and anaesthesiological teams and especially to a better appreciation of the importance of ventilatory pulmonary insufficiency and acute respiratory distress syndrome which are frequent in these patients. Early respiratory assistance is indicated in all cases with an instability of the chest wall. The imminence of a respiratory distress syndrome may announce itself by the classical symptoms of an increased breathing rate with hypocarbia before hypoxia becomes manifest. In the majority of patients with a thoracic lesion however the syndrome starts with a combination of increasing dyspnoea and normo- or even hypercarbia. This should be recognized and promptly treated by artificial respiration before acidosis and hypoxia with cardiac arrest can occur.
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PMID:Blunt thoracic trauma in multiple injury. 124 43

Studies were carried out to determine the influence of the chronic level of arterial carbon dioxide tension upon the buffering response to acute changes in arterial carbon dioxide tension. After chronic adaptation to six levels of arterial CO(2) tension, ranging between 35 and 110 mm Hg, unanesthetized dogs underwent acute whole body CO(2) titrations. In each instance a linear relationship was observed between the plasma hydrogen ion concentration and the arterial carbon dioxide tension. Because of this linear relationship, it has been convenient to compare the acute buffering responses among dogs in terms of the slope, dH(+)/dPaco(2). With increasing chronic hypercapnia there was a decrease in this slope, i.e. an improvement in buffer capacity, which is expressed by the equation dH(+)/dPaco(2)=-0.005 (Paco(2))(chronic) + 0.95. In effect, the ability to defend pH during acute titration virtually doubled as chronic Paco(2) increased from 35 to 110 mm Hg. The change in slope, dH(+)/dPaco(2), was the consequence of the following two factors: the rise in plasma bicarbonate concentration which occurs with chronic hypercapnia of increasing severity, and the greater change in bicarbonate concentration which occurred during the acute CO(2) titration in the animals with more severe chronic hypercapnia. These findings demonstrate the importance of the acid-base status before acute titration in determining the character of the carbon dioxide titration curve. They also suggest that a quantitative definition of the interplay between acute and chronic hypercapnia in man should assist in the rational analysis of acid-base disorders in chronic pulmonary insufficiency.
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PMID:The influence of graded degrees of chronic hypercapnia on the acute carbon dioxide titration curve. 554 76

Young rats are thought to be more tolerant to hyperoxia. We propose that this may not be proven and depends on how tolerance is defined. We assessed oxygen tolerance in Sprague-Dawley rats from birth to maturity by comparing survival, lung water, antioxidant enzyme activity, lung morphometrics, heart weight, and arterial blood gases in newborn and 27-, 44-, 48-, and 96-day-old rats exposed to 100% O2 or room air for 22 days. Some 96-day-old rats (rest group) received only 50% O2 between 48 and 72 h. Mortality after 5 days of O2 was 0% in newborn and 27-day-old rats and 27% in 44-day-old rats but was > 80% in 48- and 96-day-old rats. Between 5 and 22 days, the death rate was 100% in newborns, 25% in 27-day-old rats, and 0% in 44- to 96-day-old rats. Death occurred when lung water was > 84% except in newborns, which tolerated high lung water for the first 7 days. In chronically exposed 44- and 96-day-old rats, lung water returned to normal. Enzyme activity increased with O2 at all ages but did not relate to survival. In 96-day-old rats, the initial increase was suppressed on day 3. All chronically O2-exposed rats had minimal nonvascular parenchymal changes but developed right ventricular hypertrophy and increased alveolar ductal artery muscularization and lost alveolar capillaries. The most mature rats were least affected. In O2, there was pulmonary insufficiency the first 3 days, followed by recovery, and later hypercarbia and decreased arterial PO2. We conclude that young rats, 0-44 days old, are more O2 tolerant for 5 days. More mature animals, surviving 5 days, are more tolerant to chronic exposure.
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PMID:Comparative age-related acute and chronic pulmonary oxygen tolerance in rats. 789 11