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

Arterial blood gases were measured during 7 hours of sleep in 15 patients with severe stable chronic obstructive pulmonary discrease (COPD); 6 awake patients with COPD studies in recumbency for an average of 5 hours served as controls. Mean maximal decrease in arterial oxygen partial pressure (PaO2) (plus or minus SD) was 13.5 plus or minus 3.9 mm Hg for sleeping patients (p less than 0.005) and 5.5 plus or minus 1.7 mm Hg for controls (p less than 0.1), respectively. Changes in pH during sleep were of the magnitude expected with acute changes in arterial carbon dioxide partial pressure (PaCO2) in patients with chronic hypercapnia. Consistent changes in heart rate, respiratory frequency or cardiac rhythm were not observed during sleep. Nocturnal worsening of hypoxemia could be explained by alveolar hypoventilation in six sleeping patients and in five controls; in nine sleeping patients, further impariment of ventilation-perfusion mismatch also contributed to worsening of hypoxemia. There was no relationship between the decrease in PaO2 during sleep and the degree of airways obstruction or the PaO2 level when awake. Because of low PaO2, when awake, a fall in PaO2 during sleep brings values into the steep part of the oxyhemoglobin dissociation curve where slight changes in PaO2 result in marked changes in oxygen content. All patients with COPD whose waking PaO2 was below 60 mm Hg had PaO2 below 50 mm Hg during sleep; nocturnal oxygen therapy should be considered in such patients, particularly in the presence of polycythemia or troublesome right-sided heart failure.
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PMID:Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease. 23 52

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by "conventional" airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite "sensitivity" when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.
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PMID:Regulation of arterial PCO2 during intravenous CO2 loading. 23 64

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.
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PMID:Effect of liver failure on the response of ventilation and cerebral criculation to carbon dioxide in man and in the goat. 23 83

In resting conscious dogs physiological dead space was calculated using the Bohr equation and measurements of arterial and mixed expired carbon dioxide tension. Whenever dogs inhaled carbon dioxide mixtures (5-10%) that had normal or low oxygen concentrations, the calculated dead space became negative. This paradox was based on the fact that the mixed expired carbon dioxide tension in resting hypercapnic dogs. Under these circumstances carbon dioxide was produced from the lung as measured by gas analyses and blood analyses. By the lung as measured by gas analyses and blood analyses. By reasoning this implies that "alveolar" carbon dioxide tension was higher than pulmonary venous carbon dioxide tension. The negative carbon dioxide gradient persisted at 14 days of chronic hypercapnia and reverted to normal within 10 min of breathing air after chronic hypercapnia. These findings suggest that the exchange of carbon dioxide in the lung cannot be explained solely on the basis of passive diffusion.
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PMID:Negative arterial-mixed expired PC02 gradient during acute and chronic hypercapnia. 23 27

1. The purpose of this investigation was to determine the effects of maternal hyperoxaemia and hypercapnia on the uterine vascular bed and foetal oxygenation in the large white sow at 80-90 days gestation. 2. When maternal hyperoxaemia was induced with 100% oxygen, there was a highly significant rise in the maternal arterial oxygen tension, but no other significant blood gas or vascular changes were observed. 3. When mild maternal hypercapnia was superimposed on maternal hyperoxaemia (oxygen plus 6% carbon dioxide), the oxygen tension and saturation of both the maternal uterine venous and foetal umbilical venous bloods were found when severe hypercapnia was induced (oxygen plus 50% carbon dioxide) but in this case all blood samples showed dramatic changes in PCO2 and pH. These changes were accompanied by an increase in the systemic blood pressure and uterine blood flow, and a decrease in uterine vascular resistance. 4. When mild hypercapnia was induced without hyperoxaemia (air plus 5% carbon dioxide) significant increases were recorded in the oxygen tension and saturation of uterine venous and foetal umbilical venous bloods. Systemic and uterine vascular resistance fell. 5. It was concluded that the increased foetal oxygen tension during maternal hypercapnia was the result of the increased uterine blood flow and greater mass delivery of oxygen to the placenta, so that once the oxygen requirements of the placental tissues themselves were exceeded there would be an increased oxygen gradient at the site of gas exchange. 6. Carbon dioxide concentration in arterial blood plays an important role in determining blood flow through the pregnant uterus in the sow.
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PMID:The effects of maternal hypercapnia on foetal oxygenation and uterine blood flow in the pig. 23 26

The effects on hemoglobin oxygen transport of acute respiratory acidosis have been studied in dogs inhaling a gaseous mixture with 12% CO2 (O2 21%) for two to five hours. In a first series of experiments, it was shown that the shape of the oxyhemoglobin dissociation curve (ODC) was not modified by severe acidosis (pH congruent to 7) lasting for two and a half hours. The Hill number (N equals 2.6) did not change significantly. The aim of the second experimental series was to stuey the Bohr effect and the hemoglobin oxygen affinity (P50). The control value for the respiratory Bohr coefficient (B) was --0.54; neither after two hours (--0.52), nor after five hours of hypercapnia (--0.55) was it significantly modified. The P50 expressed at arterial pH was much increased in acidosis (congruent to 45 torr); when expressed at standard p/ 7.4, it was slightly but significantly decreased (congruent to 1 torr) at the fifth hour. At the same time there was a decrease (p smaller than 0.05) in the erythrocyte 2,3-DPG approaching 15 p. cent; on the other hand the ATP concentration did not change significantly. No significant individual correlation was found between P50(7.4), 2,3-DPG and mean hemoglobin corpuscular concentration. These results suggest that during severe respiratory acidosis neither a change in the shape of ODC, nor a change in Bohr effect do affect the hemoglobin oxygen transport. The main characteristic remains the decrease in oxygen affinity of hemoglobin, due to the erythrocyte [H+] increase induced by hypercapnia ; this phenomenon is observed as long as the 2,3-DPG decrease stays moderate.
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PMID:[Hemoglobin oxygen transport during experimental acute hypercapnia (author's transl)]. 23 80

Twelve patients with severe chronic obstructive lung disease undergoing 15 operations were assessed with preoperative lung function tests and blood gas estimations. Their operative and postoperative course was followed. There were no deaths or serious complications. Patients fell into three groups: those with low respiratory capacity but normal blood gases, who required no special respiratory treatment apart from physiotherapy and antibiotics; those with hypoxaemia but normal arterial carbon dioxide pressure, who needed more prolonged oxygen treatment after operation; and those with hypoxaemia and hypercapnia, who needed postoperative ventilatory support. While forced expiratory volume in one second (FEV) is a good screening test in preoperative assessment it should be supplemented by arterial blood gas estimations in patients with an FEV of less than 1 litre.
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PMID:Criteria of fitness for anaesthesia in patients with chronic obstructive lung disease. 24 Apr 80

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
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PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

Rats were exposed 24 hours a day to carbon dioxide, 8 +/- 1%, during 2 and 4 weeks under normoxic conditions (21% oxygen). On the last day, blood was taken from the abdominal aorta under anesthesia. Leukocyte and erythrocyte counts, hemoglobin concentration, and mean cell volume were electronically measured. Hematocit and Wintrobe indexes were calculated. Leukocyte differential counts and peroxidase activity were determined on blood smears. After 4 weeks of hypercapnia, a slight decrease of neutrophilic granulocytes was observed. In mature polymorphs, peroxidase activity (cytochemically demonstrated) simultaneously decreased. Erythrocyte counts and mean cell volume remained unchanged. The most important hematological disturbance was an hemoglobin concentration drop. Consequently, it was concluded that an hypochromic anemia characterized the permanent normoxic hypercapnia in rats.
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PMID:Blood effects of permanent normoxic hypercapnia in conventional rats. 28 61

An earlier study has demonstrated that indomethacin, a prostaglandin synthesis inhibitor, blocks the cerebrovascular response to hypercapnia. This response is believed to be mediated by a lowering of pH in the cerebral interstitial fluid. Should autoregulation of cerebral blood flow (CBF) to changing perfusion pressure also be mediated by a changing interstitial pH (the "metabolic" theory), then indomethacin should impair autoregulation. This hypothesis was tested in anesthetized baboons. CBF was measured by the intracarotid 133Xe clearance technique; the preparation and the indomethacin protocol were identical to those of our previous investigation. Arterial pressure was increased by the intravenous infusion of angiotensin and decreased by controlled hemorrhage. Indomethacin was given by continuous infusion into the internal carotid artery. Although it reduced resting CBF, the cerebrovascular response to changing perfusion pressure was unchanged. Because indomethacin affects the response to changing CO2 but not that to changing perfusion pressure, the mechanisms for these two reactions presumably are different and it is improbable that changing interstitial pH is responsible for autoregulation in the cerebral circulation.
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PMID:Response of the cerebral circulation in baboons to changing perfusion pressure after indomethacin. 40 29


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