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

The effects of 26 h of normoxic hypocapnia (PaCO2, 31 MMHg) vs. 26 h of hypocapnia plus hypobaric hypoxia (PaCO2 32, PaO2 57 mmHg) were compared with respect to: a) CSF acid-base status; and b) the spontaneous ventilation (at PIO2 145 mmHg) which followed the imposed (voluntary) hyperventilation. For each condition of prolonged hypocapnia, PaCO2 was held constant throughout and pHa and [HCO3-]a were constant over the final 6-10 h. We assumed that measured changes in lumbar CSF acid-base status paralleled those in cisternal CSF. Spontaneous hyperventilation followed both normoxic and hypoxic hypocapnia but was significantly greater following hypoxic hypocapnia. In the CSF, pH compensation after 26 h of hyperventilation was incomplete (similar to 45-50%), was similar to that in arterial blood, and was unaffected by a superimposed hypoxemia. These data were inconsistent with current theory which proposes the regulation of CSF [HCO2] via local mechanisms and, in turn, the mediation of ventilatory acclimatization to hypoxemia and/or hypocapnia via CSF [H+]. Alternative mediators of ventilatory acclimatization were postulated, including mechanisms both dependent on and independent of "chemoreceptor" stimuli.
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PMID:Effects of moderate hypoxemia and hypocapnia on CSF [H+] and ventilation in man. 23 66

This study has assessed the regulation of arterial blood and cerebrospinal fluid acid-base status in seven healthy men, at 250 m altitude and after 5 and 10-11 days sojourn at 4,300 m altitude (PaO2 = 39 mmHg day 1 to 48 mmHg day 11). We assumed that observed changes in lumbar spinal fluid acid-base status paralleled those in cisternal CSF, under these relatively steady-state conditions. Ventilatory acclimatization during the sojourn (-14 mmHg PaCO2 at day 11) was accompanied by: 1) reductions in [HCO3-] (-5 to -7 meq/1) which were similar in arterial blood and CSF; 2) substantial, yet incomplete, compensation (70-75%) of both CSF and blood pH; and 3) a level of CSF pH which was maintained significantly alkaline (+0.05 +/- 0.01) to normoxic control values. These data at 4,300 m confirmed and extended our previous findings for more moderate conditions of chronic hypoxia. It was postulated that the magnitude and time course of pH compensation in the CSF during chronic hypoxia and/or hypocapnia are determined by corresponding changes in plasma [HCO2-].
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PMID:Incomplete compensation of CSF [H+] in man during acclimatization to high altitude (48300 M). 23 69

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.
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PMID:Effect of hyperventilation on dynamics of cerebral energy metabolism. 23 2

Awake, intact dogs trained to wear a respiratory mask were studied in a hypobaric chamber at 140 m and at various stages of a 4-week exposure to 3,550 m. Resting ventilation, pulmonary gas exchanges, arterial blood gases and pH, acid-base status of the cisternal fluid (CSF) and ventilatory responses to transient O2 inhalation were measured. Attention is focussed on the time course of ventilatory acclimatization to altitude, characterized by hyperventilation with hypocapnia and a consequent increase of arterial Po2. (1) 75 percent of the increment in pulmonary ventilation due to hypoxia was achieved in 30 minutes; (2) the further increase, 25 percent of the total hyperventilation, was complete after 3 hr, with a corresponding Pco2 drop and pH increase in blood and CSF, and an increase in Pao2; (3) the secondary increase in ventilation, beyond the acute exposure period, was not related to return of [H+] in CSF towards control value; (4) the large transient decrease of ventilation following brief oxygen inhalation demonstrated a strong arterial chemoreflex drive in acclimatized animals. The extremely rapid ventilatory acclimatization to moderately high altitude in normal dogs appears to be mediated not by CSF hydrogen ion concentration but by a strong chemoreflex drive of ventilation.
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PMID:Blood and CSF acid-base changes, and rate of ventilatory acclimatization of awake dogs to 3,550 m. 24 Nov 5

The effects of halothane, enflurane, and methoxyflurane on hypocapnic bronchoconstriction (increased airway resistance and decreased compliance of the lung) were studied in vivo in the isolated left lower lobe of the canine lung. Hypocapnic bronchoconstriction, induced by altering the concentration of CO2 in gas ventilating the lobe, was repeated in the presence and absence of various concentrations of anesthetic gases (halothane: 0.5, 1.0, and 3.0 per cent; enflurane: 1.0, 3.0, and 5.0 per cent; methoxyflurane: 0.25, 0.50, and 1.0 per cent). In the higher concentrations, all three drugs blocked the bronchoconstrictor effect produced when the inspired CO2 was decreased from 5 to 0 per cent. In lower concentrations, halothane was the most effective blocking drug. Propranolol did not affect the ability of the three anesthetics to block hypocapnic bronchoconstriction, nor did the beta-receptor blocking drug sotalol affect the blocking effects of halothane. The ability of these anesthetics to block hypocapnic bronchoconstriction probably is mediated not through an adrenergic mechanism but by one that is nonspecific. (Key words: Lung, bronchoconstriction; Carbon dioxide, hypocarbia; Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Anesthetics, volatile, methoxyflurane.)
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PMID:Hypocapnic bronchoconstriction and inhalation anesthetics. 24 37

Dextropropoxyphene (DP) is a commonly used medicament for suicide attempts in Denmark. Death may occur from respiratory depression or cardiac arrest. Mechanical hyperventilation which induces hypocapnia seems to reduce the occurrence of cardiac complications. In an attempt to relate the clinical events to the plasma concentrations of DP and the major metabolite norpropoxyphene (NP) we studied patients with acute poisoning treated either for 48 h with induced hypocapnia by hyperventilation or under a conservative regime. Hypocapnia was found to lead to a significant increase in the plasma half-life of DP. Under conservative treatment the plasma half-life was 17.9 +/- 6.7 (S.D.) h (n = 6), while under induced hypocapnia the mean of values from 5 patients was 30.5 +/- 6.9 (S.D.) h. Maximum serum levels of DP and NP were, however, significantly higher in the intensively treated patients (n = 7) than in those treated conservatively (n = 9), though less marked for NP compared to DP (DP: 4.9 +/- 2.1/2.4 +/- 1.0 mumol/l, NP: 6.3 +/- 2.4/4.1 +/- 1.7 mumol/l). A concentration dependent renal clearance of NP was not demonstrable. Possible explanations are the following: 1) A change in disposition pattern blood/tissue of DP during hypocapnia. 2) A reduced metabolism DP to NP during hypocapnia. 3) A reduction in other routes of elimination.
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PMID:Pharmacokinetics of dextropropoxyphene in acute poisoning. 27 28

From this analysis we may conclude that the most important factors influencing the outcome of coma due to injury are age, vegetative state, level of coma, decerebration, and hypocapnia. In all cases where a combination of four or more of any of the above-mentioned factors was present the patient died. EEG seems less predictive in the early period, but may give some information for late prognosis.
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PMID:Factors influencing the outcome of coma in severely injured patients. 29 Jan 39

Pentobarbital-anesthetized greyhounds were passively hyperventilated using intermittent positive-pressure breathing (IPPV) and the effects of raised airway pressure, accompanied by hypocapnia and then by normocapnia, on liver blood flow and oxygen consumption were studied. Electromagnetic flowmeters were used to measure hepatic arterial, portal venous, and splenic venous blood flow. Studies were carried out at three levels of raised airway pressure, both at normocapnia and hypocapnia. It was found that hypocapnic hyperventilation produced a decrease in portal venous and hepatic arterial blood flow. Normocapnic hyperventilation resulted in a restoration of portal venous blood flow but with a further decrease in hepatic arterial blood flow. A decrease in oxygen consumption with hypocapnia, returning to control values with normocapnia, was seen. It is suggested that the reduction in liver blood flow and oxygen consumption seen with passive hyperventilation is chiefly an effect of hypocapnia and is largely reversed by restoration of normocapnia.
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PMID:Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound. 38 Dec 63

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.
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PMID:Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates. 40 43

The Asthma Symptom Checklist (ASC), describing the subjective symptoms reported to occur during asthmatic attacks, has been developed previously. In the present study, the ASC key cluster solution was replicated and refined within a sample of 374 asthmatic inpatients. All of the original symptom categories were reporduced, including two mood categories, Panic-Fear and Irritability, a Fatigue category, and two somatic categories. Hyperventilation-Hypocapnia and Airway Obstruction. Two refinements were notable: (1) The Airway Obstruction category was empirically divided into two conceptually clear components, Dyspnea anc Congestion, and (2) three secondary mood categories, Worry, Loneliness, and Anger, were identified, which describe a continuum of mood between the polar extremes of panic and irritability. Of the symptom categories, only Panic-Fear was related to the intensity of the discharge drug regimens recommended 2 to 6 mouths after ASC administration. Panic-Fear scores were independent of pulmonary function measurements. A combined index based on pulmonary functions and panic-fear yielded the best prediction of discharge steroid regiments. Finally, those physicians rated highest in "sensitivity" to their patients by their supervisors prescribed less steroids overall, but most frequently prescribed discharge steriod regimens in relation to their patients' Panic-Fear scores. In contrast, physicians rated lower on sensitivity prescribed higher steroid regimens overall, but based these drug recommendations more cleary on objective pulmonary functioning, and not in relation to their patients' Panic-Fear scores. The results strongly suggest that the ASC Panic-Fear scale is associated with coping behaviors that importantly affect the patient's overall clinical picture by increasing the apparent severity of the asthma, thereby leading to intensified treatment. The findings stress the need to evaluate independently the objective medical condition and subjective symptomatology with its related coping behavior, in order to direct appropriate modes of therapy to each.
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PMID:Obervations on subjective symptomatology, coping behavior, and medical decisions is asthma. 40 66


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