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

Young healthy test subjects showed adaptation to chronic hypercapnia during long-term exposure to an atmosphere containing 0.8--1.8% CO2 at normal atmospheric pressure: bradycardia, increase in vital lung capacity and chest movements, improvement of tests with breathing retention and further decrease in oxyhemoglobin. Simultaneously they exhibited an increase in the alkaline reserve of the blood and of the 2 min step-test index. This can be interpreted both as cause and effect: products of glycolysis are bound by buffer bases, thus reducing oxygen uptake per time unit. Study of adaptation to exercises of increasing workload demonstrated an earlier involvement of anaerobic mechanisms than under normal conditions: linear relationship between the workload and heart rate persisted only up to 150 beats/min. By the end of the second and the beginning of the third month of isolation the test subjects displayed deteriorated health state and work capacity in parallel with compensated acidosis.
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PMID:[Tolerance for controlled physical loading in chronic hypercapnia in man]. 64 21

Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing 133Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 +/- 19 mm Hg, and a mean arterial PCO2 of 36.2 +/- 2.9 mm Hg, mean CBF was 103 +/- 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial PCO2. CBF was measured during steady state levels of hypo- and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg. CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.
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PMID:Cerebral blood flow autoregulation in the rat. 64 8

The alveolar to arterial oxygen pressure difference (AaDO2) and pulmonary venous admixture (Qs/Qt) were measured in 32 patients with chronic obstructive pulmonary disease during right heart catheterization at inspired oxygen concentrations (FIO2) of 21, 24, 28, 35, and 40%. Patients without chronic hypercapnia (PaCO2 is less than 45 torr, group A) had Qs/Qt less than 25% while breathing room air; their AaDO2 rose at a rate of 3 torr for each percent increase in FIO2. In those with chronic hypercapnia (PaCO2 greater than 44 torr., (group B), THE Qs/Qt was always greater than 24% during air breathing and the AaDO2 rose at a rate of 5 torr for each percentage increase in FIO2. These changes should be considered in the interpretation of the AaDO2 in patients with COPD in whom the FIO2 is changed during the course of therapy. The Qs/Qt fell curvilinearly with increasing FIO2 but the rates of fall were quantitatively different in groups A and B. A physiological explanation for the changes in Qs/Qt and ADO2 which result from changes in FIO2 is presented.
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PMID:The AaDO2 and venous admixture at varying inspired oxygen concentrations in chronic obstructive pulmonary disease. 65 13

The measurement of pressure in the mouth 0.1 sec after the initiation of an occluded inspiratory effort (P0.1) has been proposed as an index of activity of medullary inspiratory neurons. If changes in FRC can be interpreted as important changes in the length-tension curve of the diaphragm or the total respiratory musculature, then changes in FRC from one occlusion pressure measurement to another can complicate such an interpretation of the P0.1 measurement. Forty-five subjects divided into three different groups were seated in a variable volume body plethysmograph. They had their FRC, P0.1, VT and VE measured while breathing air, 100% oxygen, 11% oxygen balance nitrogen, and 4% carbon dioxide in 20% oxygen balance nigrogen. All 45 showed a decrease in FRC during hyperoxia (-12%); 40 of 43 showed increases in FRC during hypoxia (14%); 42 of 43 showed an increased FRC during hypercapnia (15%). Changes in VE were small as were changes in P0.1 values. These latter changes generally followed the same pattern of changes as FRC though the magnitude of the changes showed more variability. We were unable to demonstrate a significant correlation between changes in FRC and changes in P0.1 under the conditions of our experiments.
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PMID:The effect of hyperoxia, hypoxia and hypercapnia on FRC and occlusion pressure in human subjects. 69 49

In 12 patients with heart disease, hypercarbia was induced for carotid endarterectomy. Anesthesia was maintained with nitrous oxide in oxygen and methoxyflurane. In addition to intra-arterial measurements of blood pressure, cardiac output, systolic time intervals (STI), and pressure time indices (PTI) were determined in order to assess cardiovascular responses in these patients. Internal carotid stump blood pressure was measured in five patients before and after induction of hypercarbia. Mild elevation of the Paco2 level affected systolic time intervals but not heart rate and blood pressure. When Paco2 levels reached 56 to 65 torr, systolic but not diastolic blood pressure rose significantly, heart rate and cardiac output increased, while the shortening in the preejection period (PEP), left ventricular ejection time (LVET), and the decrease in the PEP/LVET ratio signified increased mechanical cardiac activity. Hypercarbia caused intense sympathetic stimulation as demonstrated by twofold to threefold increases in plasma catecholamine levels. Stump blood pressure was elevated. Cardiac oxygen demand was significantly increased, while coronary filling time was shortened, as indicated by the increase in the tension time index and shortening in the diastolic time. This signified a relative myocardial underperfusion. Thus, while hypercarbia to levels of 66 to 70 torr increased internal carotid artery stump pressure, it also caused increased cardiac mechanical activity and concomitant unfavorable balance between myocardial oxygen consumption and supply. The measurement of STI and the computation of PTI provided early detection of alterations in cardiac function.
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PMID:Cardiac function and hypercarbia. 70 41

Controlled oxygen therapy may aggravate carbon dioxide retention during acute exacerbations of chronic obstructive pulmonary disease (COPD). Of 50 consecutive patients with COPD and acute respiratory failure, 13 required intubation because of carbon dioxide narcosis. With discriminant analysis of their arterial oxygen tension (PaO2) and pH on admission, a diagram separated patients into those at high risk and those at low risk for carbon dioxide narcosis. This diagram was then used to predict carbon dioxide narcosis in 73 patients with COPD and acute respiratory failure who were treated with controlled oxygen. In 16 of these patients carbon dioxide narcosis developed. Thirteen (81 per cent) were predicted by the diagram to be at high risk for this complication. Only two (4 per cent) patients judged by the diagram to be at low risk for carbon dioxide narcosis required mechanical ventilation. Utilizing an oxygen tension (PO2), carbon dioxide tension (PCO2) diagram a patient's ventilatory response was compared to that of ambulatory patients with COPD. These data suggest that hypoxemia and acidosis are more discriminatory for "carbon dioxide narcosis" than hypercapnia.
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PMID:Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: a reappraisal. 74 28

The comparative ventilatory responsiveness to CO2 was studied in 13 chronic bronchitics and 14 emphysematous patients, all exhibiting respiratory insufficiency and with FEV1 less than 1,500 ml. The gas inhaled was enriched with oxygen (F1O2 =0.6) and contained 6% CO2, and measurements were taken when the patients had reached a stable state. The ratio delta VE/deltaPaCO2, which represents the ventilatory responsiveness to CO2, was higher in the emphysematous patients (1.18+/-0.51 liters-min-1. Torr-1) than in the bronchitics (0.76+/-0.34, p less than 0.025), but the deviation on either side of the mean was large in each group. The ventilatory responsiveness to CO2 was proportional to the initial PaCO2, FEV1, total airways resistance, total pulmonary work and especially to inspiratory mechanical work done on the lung ( r=-0.73, p less than 0.001). The difference in ventilatory responsiveness to CO2 between the bronchitic and emphysematous patients may be explained by the difference in energy expended in breathing. It was not possible to exclude an effect due to a difference in sensitivity within the respiratory centers, since inspiratory mechanical work was not measured during CO2 inhalation. It was thought likely that mechanical factors play a triggering role, in that they cause a fall in ventilatory responsiveness to CO2 and hypercapnia, the latter causing the central hyposensitivity which maintains the retention of CO2.
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PMID:Comparative study of the ventilatory responsiveness to CO2 in bronchitic and emphysematous patients with chronic respiratory failure. 77 61

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95

The influence of continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP) on mortality and complication rates in severe hyaline membrane disease (HMD) was evaluated in a randomized, prospective study. Patients were admitted to the study if the Po2 was less than 50 mm Hg with FiO2 greater than 0.6. Twenty-four patients in each of three weight groups were equally divided between treatment and control groups. The treatment regimen included CPAP (6 to 14 cm H2O) for spontaneously breathing patients and PEEP for patients requiring mechanical ventilation for apnea or hypercapnia (Pco2 greater than 65 mm Hg). Control patients received oxygen and were mechanically ventilated if they had apnea, hypercapnia, or Po2 less than 50 mm Hg with FiO2 greater than 0.8. Oxygenation improved after the start of CPAP or PEEP; however, Pco2 rose after CPAP was initiated. There was no significant difference between treatment and control groups in mortality, requirement for mechanical ventilation, or incidence of pulmonary sequelae. The incidence of pulmonary air-leak was increased with Peep. the findings suggest that CPAP and PEEP have not significantly altered the outcome of HMD.
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PMID:Is continuous transpulmonary pressure better than conventional respiratory management of hyaline membrane disease? A controlled study. 79 89

Effects of intravertebral, intracarotid, and intravenous infusion of acetylcholine on cerebral blood flow (CBF) and metabolism was studied in 17 baboons anesthetized with pentobarbital. We measured CBF by the bilateral jugular venous outflow technique using two electromagnetic flowmeters. Effect of acetylcholine infusion on cerebral vascular response to hypercapnia was also assessed. Intravertebral infusion of acetylcholine (0.01 mg/kg/min) increased CBF by 27% and cerebral metabolic rate for oxygen by 19% and decreased cerebral vascular resistance by 25%. On intracarotid injection of acetylcholine, only an 8% increase in CBF was observed, and intravenous infusion produced no change in the parameters observed. Acetylcholine administered by any of the three routes did not enhance the CBF response to hypercapnia. Increase in CBF on intravertebral administration of acetylcholine is associated with an arousal effect and an increase in cerebral metabolism.
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PMID:Effect of acetylcholine on cerebral circulation. 82 37


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