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

Lethal pulmonary embolism is associated with hypoxemia and hypocapnia in the vast majority of cases. The easily calculated ventilation corrected oxygen tension was a very sensitive test in patients breathing air. It yielded no normals, four percent mild hypoxemia, and 96 percent moderate to extreme hypoxemia. The alveolar-arterial oxygen tension difference and oxygen ratio were equally sensitive during air breathing. During oxygen inhalation, alveolar-arterial oxygen difference was most sensitive; oxygen ratio was second best; and oxygen saturation was the least sensitive test.
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PMID:Ventilation corrected oxygen tension in lethal pulmonary embolism. 70 44

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

Increased body temperature stimulates hyperventilation in man but little is known about its effects on ventilatory responsiveness to hypoxia. Hence this study examined the effects of hyperthermia on hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR), and oxygen consumption (VO2). Six fasting subjects had these variables measured under basal conditions and at two levels of hyperthermia. Hypoxic ventilatory response was measured as the shape paramater A of the VE/PAO2 curves. Since hyperthermia produces hyperventilation and, therefore, hypocapnia, HVR was measured at the hyperthermic (hypocapnic alveolar CO2 tension (PACO2) and at the basal (normothermic) PACO2. Hypoxic ventilatory response (A) increased when measured at basal PACO2 levels, from 113 +/- 8.8 (S.E.M.) to 189 +/- 21.8 at 0.7 degrees C. and 240 +/- 34.0 at + 1.40 degrees C. (P less than 0.005). HVR measured during hyperthermic hypocapnia also increased at each temperature level but did not reach statistical significance (P = 0.1). Hypercapnic ventilatory response, as measured by the slope S of VE/PACO2 lines, increased significantly at each temperature elevation (P less than 0.025). We conclude that raising body temperature causes a significant augmentation of ventilatory responses to hypoxia (during normothermic PACO2 conditions) and to hypercapnia.
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PMID:Effects of hyperthermia on hypoxic ventilatory response in normal man. 83 15

Previous workers have reported that ethyl methylene blue (EMB) diminishes cyanide-induced increases in blood lactate (CIL); the present study investigates the mechanism underlying this interaction. Accordingly, sodium cyanide (1.2 mg./Kg.) was infused into the abdominal aorta of anesthetized, spontaneously breathing dogs. Following cyanide infusion, arterial lactate concentration increased 5.4 +/- 1.1 mmol./L. and arterial PCO2 decreased 22 +/- 3 mm. Hg. A second group of dogs was pretreated with EMB (8 to 15 mg./Kg.); this dose of EMB elicited twofold increments in oxygen consumption and induced the formation in vivo of methemoglobin (0.8 +/- 0.1 gm./100 ml.). Following cyanide infusion, the increase in lactate in EMB animals was only 0.6 +/- 0.2 mmol./L.; the decrease in arterial PCO2 was limited to 5 +/- 1 mm. Hg. In order to clarify the relationship between cyanide-induced hypocapnia and CIL, cyanide was infused into a third group of dogs that were maintained isocapneic via mechanical ventilation; despite constancy of arterial PCO2, lactate increased 6.0 +/- 0.7 mmol./L. To determine the effect of EMB-induced tissue hypermetabolism on CIL, twofold increments in oxygen consumption were produced in a fourth group of dogs by pretreatment with sodium salicylate. Following cyanide infusion, salicylate-pretreated animals increased lactate 7.2 +/- 1.2 mmol./L. In order to assess the relationship between EMB-induced methemoglobinemia and the decrease in CIL, similar concentrations of methemoglobin were produced in two subsequent groups of dogs by two different techniques (i.e., by aniline pretreatment or by infusion of methemoglobinemic blood that had been prepared in vitro by addition of sodium nitrite). CIL in these animals was again markedly diminished (i.e., increments of only 0.6 +/- 0.3 mmol./L.) It is concluded that EMB diminishes CIL by a mechanism other than elimination of cyanide-induced hypocapnia or induction of tissue hypermetabolism. The results suggest that methemoglobin formation may completely account for the ability of EMB to effect a decrement in CIL.
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PMID:Interaction between ethyl methylene blue and cyanide-induced increases in blood lactate. 83 20

Hemodynamics and myocardial contractility were evaluated in 6 unanesthetized ponies during hypocapnic and isocapnic hypoxia and during hypocapnic hypoxia after beta adrenergic blockade with propranolol. Hypocapnic hypoxia, with a mean arterial oxygen pressure (PaO2) of 41.9 mm of Hg, produced a decrease in stroke index and an increase in heart rate, with no change of cardiac index. A moderate increase in left ventricular contractility occurred during hypocapnic hypoxia. Beta adrenergic blockade abolished changes in nearly all indices of left ventricular contractility during hypocapnic hypoxia, suggesting that the antonomic nervous system plays a definite role in the genesis of circulatory changes during acute hypoxia. Isocapnic hypoxia produced a more well-defined increase in left ventricular contractility. Changes in right ventricular contractility were not observed in any of the hypoxia periods when the concurrent effects of a significant increase in afterload was taken into consideration. The tension-time index, measured as a guide to myocardial oxygen consumption, increased during each hypoxia period in both the right and left ventricle, and was not affected by beta adrenergic blockade.
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PMID:Hemodynamics and myocardial function during acute hypoxia in the pony. 85 Dec 70

The effects of hypercapnia and hypocapnia on haemodynamics, coronary blood flow, and lactate metabolism were evaluated in anaesthetized closed chest dogs. Coronary flow increased with increased pCO2 and oxygen consumption and left ventricular performance were well maintained. Hypocapnia reduced coronary flow, oxygen consumption, and left ventricular functional performance.
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PMID:Effect of hypercapnia and hypocapnia on myocardial blood flow and performance in anaesthetized dogs. 95 18

A hypoxia test for placental sufficiency was performed on 24 healthy pregnant women nearing term and 23 high-risk pregnant women in advanced stages of gestation. Hypoxia was induced by inhalation of a breathing mixture containing 7% oxygen through a semi-open system which permitted partial rebreathing, thus preventing hypocapnia. The changes in fetal heart rate (FHR) resulting from maternal hypoxia were recorded continuously by external or internal monitoring. The changes observed in FHR were more marked in high-risk cases. Maternal blood gases were tested before and after 10 min of hypoxia in 10 normal and 10 high-risk patients. In no case was maternal acidosis observed. All pregnant patients regarded as high-risk because of hypertensive disorders or chronic renal disease manifested metabolic alkalosis. This finding cannot be explained. It is regarded as being responsible for the more severe FHR changes through a negative Bohr effect, which reduces the dynamic exchange of oxygen in the placenta. Metabolic alkalosis does not appear in high-risk pregnant women exposed to milder hypoxia by breathing 12% oxygen. The changes in FHR observed during severe maternal hypoxia, i.e., 7% oxygen, are probably due more to maternal metabolic alkalosis than to placental insufficiency. Consequently, the "severe hypoxia test" cannot be used as a test for placental insufficiency.
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PMID:Metabolic aspects of a hypoxia test for placental sufficiency. 95 67

The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial PCO2 was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. Each PCO2 change was made at a constant coronary flow, and CVR was calculated from the ratio of perfusion pressure to flow. Coronary sinus (CS) PCO2 and PO2 were recorded continuously from blood withdrawn through a CS catheter. Normocapnia (PCO2 = 42.3 +/- 2.8 mm Hg) was obtained with a membrane oxygenator gas composition of 95% O2-5% CO2, and hypocapnia was produced with 100% O2-0% CO2. In addition to physiology normal coronary flow (determined by a CS PO2 of 20-30 mm Hg) relatively high and low flow states were studied. At a normal control CS PO2, a decrease in coronary arterial PCO2 from 42.3 +/- 2.8 to 23.8 +/- 1.3 mm Hg caused CVR to increase by 84.2%, from 1.27 +/- 0.06 to 2.30 +/- 0.04 units. Since pH was inversely related to PCO2, the effect on CVR may have been mediated through a pH change. CS PCO2 decreased from 65.2 +/- 1.9 to 39.4 +/- 1.3 mm Hg. myocardial oxygen consumption was unchanged. Increases in CVR of 74.5, 119.5, and 69.3% occurred during hypocapnia in three additional experiments in which control arterial PO2 was maintained at 52-90 mm Hg. When CS PO2 was greater than 30 mm Hg, the normocapnic CVR was high, and was only minimally increased by hypocapnia. When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial PCO2 can have an important effect on CVR independent of changes in O2 consumption. Myocardial PCO2, derived from metabolically produced CO2 and contributed to by arterial CO2, may be a major factor in normal control of coronary flow.
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PMID:The response of canine coronary vascular resistance to local alterations in coronary arterial P CO2. 96 40

The sign of a traumatically caused alveolar hyperventilation in severe cranio-cerebral injury is a respiratory alcalosis as well as hypoxia and hypoxemia in the arterial as well in the cerebral veneous blood. The combination of decreased oxygen tension or saturation and hypocapnia can exist for several days and in a lethal course transform into a combined metabolic respiratory acidosis with increasing carbonic acid tension and so initiate the prefinal state. The extremely pathological blood gases are usually the first sign of shock-specific changes of the lung. The most impressing changes of the cerebrospinal fluid are the metabolic acidosis in combination with a diminished oxygen tension and tissue hypoxia of the brain. The acidosis of cerebrospinal fluid in severe brain injury is not only of prognostic but also of therapeutical importance. The treatment of the acidosis of cerebrospinal fluid by intrathecal administration of buffering substances in severe brain injuries and its sequelae can have a favourable influence on the cerebral circulation and brain metabolism.
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PMID:[Cerebrospinal fluid changes in severe craniocerebral injury and their therapy]. 101 May 21

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).
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PMID:Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia. 109 15


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