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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of cerebral hypoxia as a causative factor in the alteration of the qEEG during hyperventilation, qEEG changes caused by progressive hypocapnia were compared with qEEG changes due to progressive normobaric hypoxia in two parallel groups of 12 and 10 healthy male subjects (age 20-27 years), respectively. In the first group, qEEG records were obtained before and during hyperventilation to pCO2 levels of 4.0, 3.0 and 2.0 kPa. In the second group, the qEEG samples were taken before and during hypoxia with hemoglobin oxygen saturations of 80, 70 and 60%. In both groups, blood flow velocity in the middle cerebral artery was also recorded. Hyperventilation caused an exponential increase in slow activity and a decrease in alpha power. No shift in the alpha mean frequency and alpha peak frequency was observed, except with the pCO2 level of 4.0 kPa, which caused an increase in both variables. Hypoxia with a hemoglobin oxygen saturation of 60% caused a much less pronounced increase in slow activity. No change in total power in the alpha band was found, but both the alpha peak frequency and alpha mean frequency decreased. Lesser degrees of hypoxia caused only minimal EEG changes. Blood flow velocity was decreased by hyperventilation but increased by hypoxia. It is concluded that the EEG changes observed during hyperventilation must mainly or totally be attributed to factors other than cerebral hypoxia.
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PMID:Quantitative EEG during progressive hypocarbia and hypoxia. Hyperventilation-induced EEG changes reconsidered. 171 5

The objectives of these experiments were 1) to describe the effect of maximum treadmill exercise on gas exchange, arterial blood gases, and arterial blood oxygenation in rats acclimated for 3 wk to simulated altitude (SA, barometric pressure 370-380 Torr) and 2) to determine the contribution of acid-base changes to the changes in arterial blood oxygenation of hypoxic exercise. Maximum O2 uptake (VO2max) was measured in four groups of rats: 1) normoxic controls run in normoxia (Nx), 2) normoxic controls run in acute hypoxia [AHx inspiratory PO2 (PIO2) approximately 70 Torr], 3) SA rats run in hypoxia (3WHx, PIO2 approximately 70 Torr), and 4) SA rats run in normoxia (ANx). VO2max (ml STPD.min-1.kg-1) was 70.8 +/- 0.9 in Nx, 46.4 +/- 1.9 in AHx, 52.6 +/- 1.1 in 3WHx, and 70.0 +/- 2.4 in ANx. Exercise resulted in acidosis, hypocapnia, and elevated blood lactate in all groups. Although blood lactate increased less in 3WHx and ANx, pH was the same or lower than in Nx and AHx, reflecting the low buffer capacity of SA. In AHx and 3WHx, arterial PO2 increased with exercise; however, O2 saturation of hemoglobin in arterial blood (SaO2) decreased. In vitro measurements of the Bohr shift suggest that SaO2 decreased as a result of a decrease in hemoglobin O2 affinity. The data indicate that several features of hypoxic exercise in this model are similar to those seen in humans, with the exception of the mechanism of decrease in SaO2, which, in humans, appears to be due to incomplete alveolar-capillary equilibration.
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PMID:Maximum oxygen uptake and arterial blood oxygenation during hypoxic exercise in rats. 175 99

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
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PMID:Myocardial protection: what the anesthesiologist does. 213 51

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.
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PMID:EEG and spectral analysis in acute hyperventilation. 241 22

Eggs laid at sea level and incubated at high altitude are subject to hypoxia, hypocapnia, and excessive water loss, resulting in retarded development and poor hatchability. The effect of altitude hypocapnia alone was studied in two series of eggs incubated at a simulated altitude of 2,800 m, PB = 542 torr; the incubator was ventilated at a low flow rate with O2-enriched air; the relative humidity was 70-74%, PH2O 34.4-36.4 torr; ambient PO2 about 130 torr at the plateau stage. In the normocapnic series, CO2 produced by the embryos increased ambient PCO2 to 14 torr at 18-19 days; altitude hypoxia, hypocapnia, and excessive water loss were practically compensated for. In the hypocapnic series, ambient CO2 was almost completely absorbed by soda lime, so that only hypocapnia was not compensated for. In 17-19-day eggs with similar sea level mass specific shell conductances [sp GH2O = 0.26-0.25 mg [g.d.torr]-1], the measured PO2 in the gas space, hematocrit, hemoglobin concentration, lengths of beak and third toe, and masses of body and brain were essentially the same in both series. The masses of heart, liver, and left wing were slightly different on day 19. Altitude hypocapnia alone, without altitude hypoxia and excessive water loss, had almost no significant effect on the embryos' development and hatchability.
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PMID:Altitude hypocapnia at 2,800 m does not affect development of the chicken embryo. 311 Mar 64

Diaphragmatic O2 and lactate extraction were examined in seven healthy ponies during maximal exercise (ME) carried out without, as well as with, inspiratory resistive breathing. Arterial and diaphragmatic venous blood were sampled simultaneously at rest and at 30-s intervals during the 4 min of ME. Experiments were carried out before and after left laryngeal hemiplegia (LH) was produced. During ME, normal ponies exhibited hypocapnia, hemoconcentration, and a decrease in arterial PO2 (PaO2) with insignificant change in O2 saturation. In LH ponies, PaO2 and O2 saturation decreased well below that in normal ponies, but because of higher hemoglobin concentration, arterial O2 content exceeded that in normal ponies. Because of their high PaCO2 during ME, acidosis was more pronounced in LH animals despite similar lactate values. Diaphragmatic venous PO2 and O2 saturation decreased with ME to 15.5 +/- 0.9 Torr and 18 +/- 0.5%, respectively, at 120 s of exercise in normal ponies. In LH ponies, corresponding values were significantly less: 12.4 +/- 1.3 Torr and 15.5 +/- 0.7% at 120 s and 9.8 +/- 1.4 Torr and 14.3 +/- 0.6% at 240 s of ME. Mean phrenic O2 extraction plateaued at 81 and 83% in normal and LH animals, respectively. Significant differences in lactate concentration between arterial and phrenic-venous blood were not observed during ME. It is concluded that PO2 and O2 saturation in the phrenic-venous blood of normal ponies do not reach their lowest possible values even during ME. Also, the healthy equine diaphragm, even with the added stress of inspiratory resistive breathing, did not engage in net lactate production.
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PMID:Costal diaphragmatic O2 and lactate extraction in laryngeal hemiplegic ponies during exercise. 318 33

Sea level hen eggs, selected for their shell conductance (water vapor conductance, HH2O), were incubated at a simulated high altitude, PB = 529 Torr, ca. 2900 m, at 72% relative humidity (rh) to prevent excessive water loss due to hypobaric condition; they were transferred to 150 m 18-24 h before measurements. Control eggs were incubated at 150 m, PB = 750 Torr, rh = 60%. In 8- to 18-day embryos, total CO diffusive conductance, GCO; embyronic body mass, BM; oxygen consumption, MO2; blood hematocrit, Hct; hemoglobin concentration, [Hb]; and heart mass, HM, were measured. Total water loss was the same in both groups, 12% initial egg mass. However, the severe effects of high altitude: 72% mortality and 9% malformation, and reduced increases of BM and MO2, can be related partially to the strong hypocapnia, which resulted from the high shell conductance (GH2O = 18.1 mg X (d X Torr)-1, and was superimposed on the hypoxia. GCO was reduced, while Hct, [Hb] and HM were not significantly affected. When measurements were normalized to BM, MO2 and GCO were identical in the two groups, whereas [Hb] and HM were higher at 2900 m (differential growth). Thus, during incubation, gas diffusive conductance appeared to depend on embryo development and did not adapt to altitude hypoxia. Compared with controls, GCO in high-altitude eggs actually decreased in proportion to BM growth.
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PMID:Gas diffusive conductance of sea-level hen eggs incubated at 2900 m altitude. 392 18

The concentration of red cell 2,3-diphosphoglycerate (2,3-DPG), hemoglobin-oxygen affinity and other oxygen transport variables were determined during first, second and third trimester of normal pregnancy as well as 3 months post partum in 18 healthy women. The median concentration of red cell 2,3-DPG increased significantly from the first to the third trimester (16.1 to 17.0 mumol/gHb, p less than 0.01), whereas 2,3-DPG decreased significantly post partum (p less than 0.01). Normal pregnancy was also associated with relative anemia, a significant increase in arterial pH, hypocapnia and hypophosphatemia. The difference in hemoglobin concentration from the first trimester to 3 months post partum was correlated inversely with the difference in red cell 2,3-DPG content (r = -0.52, p less than 0.05). In spite of the variations in red cell 2,3-DPG, hemoglobin-oxygen affinity expressed as P50 at actual pH remained unchanged during pregnancy and post partum. The study suggests that the increased level of 2,3-DPG during pregnancy may in part represent compensation for physiologic anemia and also compensate for a factor leading to increased hemoglobin-oxygen affinity during pregnancy.
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PMID:Red cell 2,3-diphosphoglycerate and hemoglobin--oxygen affinity during normal pregnancy. 649 42

Factors involved in blood oxygen transport were measured serially in the first, second and third trimester of pregnancy in 23 insulin-dependent diabetic women. Twenty-six non-pregnant diabetic patients served as a reference group. Diabetic pregnancy was associated with relative anemia, a significant increase in arterial pH, and hypocapnia. The concentration of red cell 2,3-diphosphoglycerate was significantly higher in the first trimester of diabetic pregnancy compared with non-pregnant diabetics (median value 16.4 vs. 15.0 mumol/g hemoglobin, p less than 0.02) and increased gradually from the first to the third trimester (16.4 to 17.2 mumol/g hemoglobin, p less than 0.01). The hemoglobin A1c concentration decreased simultaneously from 8.1% to 7.3% (p less than 0.01). The level of hemoglobin A1c in the first trimester was significantly lower than that in the non-pregnant diabetic patients (8.1 vs. 9.3%, p less than 0.01). In spite of the increase in red cell 2,3-diphosphoglycerate content and the decrease in hemoglobin A1c, factors known to reduce hemoglobin-oxygen affinity, the position of the oxyhemoglobin dissociation curve remained unchanged during diabetic pregnancy: P50 at actual pH in the first trimester, was 26.0 mmHg; in the second trimester, 26.9 mmHg, and in the third trimester, 26.8 mmHg (NS). These values of P50 at actual pH were identical with the value in the non-pregnant group (26.6 mmHg). Other factors influencing hemoglobin-oxygen affinity, such as hemoglobin concentration, hydrogen ion concentration and arterial oxygen saturation remained unchanged during diabetic pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Red cell 2,3-diphosphoglycerate and hemoglobin-oxygen affinity during diabetic pregnancy. 649 43

Ten splenectomized and ten nonsplenectomized conscious dogs were subjected to hemorrhage of 41% of their blood volume over a 15-minute period. Hemodynamic and metabolic variables were monitored for 4 hours after hemorrhage. Mortality (100%) occurred in the splenectomized group. Significant (P < 0.001) hemodynamic responses after hemorrhage included hypotension, tachycardia, low central venous pressure, and decreased ECG voltage of the R wave. Tachypnea was noted in the absence of hypoxia, hypercapnia, and acidosis inthe nonsplenectomized dogs. Significant (P < 0.001) hypocapnia and mean PCO2 values of 13.9 MM of Hg and 23.5 mm of Hg in splenectomized and nonssplenectomized dogs, respectively, was noted. Mean hemoglobin levels were significantly (P < 0.001) decreased after hemorrhage in the splenectomized dogs. The absence of a change in hemoglobin in thenonsplenectomized dogs was attributed to the translocationof extracellular fluid into the vascular space which diluted the high concentration of RBC from splenic contraction. Other changes noted after hemorrhage were hyperglycemia, increased blood cortisol, and increased pyruvate and lacte levels. Changes were not noted in pyruvate-to-lactate ratios.
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PMID:Experimental hemorrhage in splenectomized and nonsplenectomized dogs. 740 89


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