Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test the relationship between changes in plasma potassium concentration and pH changes of respiratory origin, we produced hypercapnia (mean PaCO2 71 mmHg = 9.5 kPa) in a group of 17 patients and hypocapnia (mean PaCO2 21 mmHg = 2.8 kPa) in another 20 patients during neurolept analgesia and intraabdominal operations. A control group of 19 patients was studied under normocapnia but otherwise identical conditions. During hypercapnia, serum potassium rose, deltaK/deltapH amounting to -0.82, -1.05 and -1.34 after 30, 60 and 90 min, respectively. During hypocapnia, serum potassium decreased, deltaK/deltapH being a little more negative than during hypercapnia (mean values -1.62, -2.44 and -1.60). Red cell potassium concentration decreased in all three groups to a similar extent. Blood lactate levels during hypercapnia decreased to 75% of control and during hypocapnia rose to a maximum of 186% of control. In order to obtain reasonable values for base excess in primarily respiratory acid-base disorders, it is necessary to use nomograms based on in vivo ECF-CO2-titration curves. With this premise, hypercapnia or hypocapnia in our patients was not associated with significant changes in base excess.
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PMID:Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia. 3 56

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.
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PMID:Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog. 3 75

The maternal and neonatal influences of continuous lumbar epidural analgesia (CLEA; bupivacaine) administered during labor after amniotomy were studied. Intravenous oxytocin supplementation was employed in some cases. Analgesic blockade increased the incidence of transient uterine hypertonus. Fetal heart rate changes, primarily bradycardia, were associated with uterine hypertonus. At birth, a lower degree of maternal metabolic acidosis was observed in comparison with normal unanesthetized controls. A slight degree of hypoxia and hypercapnia was observed in the fetuses. Possible explanations for these changes are discussed. The application of CLEA in the elective induction of labor, whether accompanied by intravenous oxytocin or not, may have risks, though these are probably acceptable for the mother and fetus if they are closely observed, the amounts of bupivacaine administered are limited, and if the duration of the 2nd stage of labor is kept to a minimum. However, epidural analgesia poses greater risks to patients with placental insufficiency and very active labor.
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PMID:Elective induction of labor conducted under lumbar epidural block. I. Labor induction by amniotomy and intravenous oxytocin. 26 52

A statistical analysis of the case material at the Intensive Care Unit, Freiburg, for the years 1975 and 1976 established that 40% and 39% respectively of patients with multiple injuries had also suffered a chest trauma and that the latter was the direct cause of respiratory insufficiency in 61% (1975) and 57% (1976) of patients in need of controlled respiration, i.e. respiratory insufficiency dominated the clinical and pathophysiological picture. The causes were: restricted respiratory movements due to pain, compression of the lungs or pathological changes in the injured lung, and they affected the normal gaseous exchange in a variety of ways. Alveolar hypoventilation with disturbance of ventilation-perfusion, increase in the functional shunt volume, rise in the functional dead space combined with reduced functional residual capacity and compliance result, if left uncorrected, in a drastic increase of resistance on the part of the pulmonary vessels and finally in, often fatal, hyoxaemia and hypercapnia. Regular estimations of the arterial blood gases in air and pure oxygen, of the arterio-alveolar difference in oxygen pressure, shunt volume, dead space and effective compliance of the chest wall and lungs are, therefore, essential. Treatment in an intensive care unit comprises the relief of any acute condition, such as tension pneumothorax, haemothorax, and general measures. Means to relieve pain in patients whose chest injuries are not sufficiently severe to require artificial ventilation are: intercostal blocking, acupuncture or peridural analgesia; efficient breathing exercises are important. The indications for artificial ventilation should be interpreted generously and the decision to perform it should be made at an early stage. The technique is determined by the type of pathological changes in the gaseous exchange and should aim at restoring normal conditions as far as possible.
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PMID:[Intensive care in chest trauma (author's transl)]. 46 37

An anaesthetic circle system without a carbon dioxide absorber is described. The efficiency of the circle, i.e., the fraction of alveolar gas in the outflow from the circle, was measured in 15 patients during halothane anaesthesia or neurolept analgesia. The fraction ranged from 0.88 to 0.95 (mean 0.91), while the ratio between the alveolar ventilation and the fresh gas inflow ranged from 0.97 to 1.71. The efficiency was not correlated to this ratio. There was no need for hyperventilation if the fresh gas inflow was 10% higher than the alveolar ventilation required to maintain normal PaCO2. The circle was used in 50 patients manually ventilated by nurse anaesthetists. Mean fresh gas inflow was 60 ml/kg. Mean PaCO2 was 5.47 kPa (41 mmHg). In a similar group of 50 other patients, in which the standard circle used in the department was employed, the mean PaCO2 was 4.80 kPa (36 mmHg). The frequency of hypercapnia was equal in the two groups, but hypocapnia was not seen when the circle without absorber was used.
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PMID:A circle system without carbon dioxide absorption. 67 46

The ventilatory changes during the course of high spinal anesthesia and the effect of hypotension on ventilation during high spinal anesthesia were studied. Spinal anesthesia with hyperbaric tetracaine was applied to 30 patients scheduled for elective surgery. Patients breathed by mask for ten minutes at rest before and after receiving spinal anesthesia. Respiratory parameters were measured in supine position during (1) pre-anesthetic period under resting condition, (2) anesthetic period when analgesia with pin prick extended to T4 level and (3) anesthetic period when analgesia extended to T1 level. The patients were divided into two groups; those with and without hypotension. In hypotension group, tidal volume and minute ventilation decreased significantly for 30% compared with the control values after spinal anesthesia. PaO2 decreased and PaCO2 increased. In non-hypotension group, tidal volume and minute ventilation after spinal anesthesia increased for 10% compared with the control values. In conclusion, hyperventilation tended to occur in patients with high spinal anesthesia unless hypotension was severe enough. Once severe hypotension had occurred, obvious hypoventilation and respiratory irregularity were observed. Decrease of tidal volume and minute ventilation, hypoxia, hypercarbia and increase in VD/VT were significant during hypotension. The results suggest that during high spinal anesthesia severe hypotension causes hypoventilation and if not treated respiratory arrest ensues.
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PMID:[Ventilation under high spinal anesthesia--the effect of hypotension]. 143 30

A study of the duration of analgesia and of the respiratory response to hypercapnia was carried out in 14 children who had had a caudal block with either bupivacaine alone (group B) or combined with fentanyl (Group B+F). Fourteen ASA I or II 5 to 10-year-old children undergoing genital and urinary surgery were included. They were not premedicated. At first, general anaesthesia was induced with halothane and nitrous oxide in oxygen. Thereafter, caudal anaesthesia was then carried out with 1 ml.kg-1 of 0.25% bupivacaine with adrenaline 1 in 200,000. Group B+F patients were also given 1 microgram.kg-1 of fentanyl in 1 ml of normal saline, and those in Group B 1 ml of normal saline. The level of sensory loss on leaving the operating theatre as well as the duration of motor paralysis were monitored. Postoperative pain was scored with Hannalah and Broadman's score (0 to 10) 2, 4, 8 and 24 h after the caudal block. Respiratory rate (fR), tidal volume (VT) and minute ventilation (VE) were assessed 10 min before induction of general anaesthesia, and 30, 60 and 120 min after the caudal anaesthesia. Petco2 was also measured before induction of general anaesthesia, and 60 and 120 min after caudal anaesthesia; at the same times, the ventilatory response to hypercapnia was assessed using Read's method with a Douglas bag containing 7% CO2 and 93% O2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Caudal block in children: analgesia and respiratory effect of the combination bupivacaine-fentanyl]. 150 85

Problems facing a patient with severe dyspnea secondary to diaphragmatic herniation are hypoxia, hypercarbia and respiratory acidosis, and cardiovascular instability. It is easy to precipitate a crisis in these patients during anesthetic induction as a result of stress, bad positioning, induction of pneumothorax, or inappropriate anesthetic technique. These patients require a smooth, stress-free perianesthetic period with preoxygenation, positioning with the affected side down, rapid intravenous induction, endotracheal intubation, and mechanical ventilation. Maintenance with isoflurane is preferred, and nitrous oxide should be avoided. Close monitoring of the cardiovascular and pulmonary systems is essential. Recovery from anesthesia should include oxygen supplementation, pleural drainage, and local analgesia if required.
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PMID:Anesthesia for patients with diaphragmatic hernia and severe dyspnea. 158 3

Clonidine, an alpha 2-adrenergic agonist, can potentiate opioid-induced analgesia. In a double-blind placebo-controlled study in human volunteers, we sought to determine whether clonidine also potentiates opioid-induced respiratory depression. Hypercapnic ventilatory responses (minute ventilation, mean inspiratory flow rate, and mouth occlusion pressure) were measured in five healthy male volunteers on two separate occasions (with or without clonidine, approximately 3.5 micrograms.kg-1 orally) under the following conditions: baseline, 2 h after clonidine/placebo (alfentanil concentration of 0), and during computer-controlled alfentanil infusions to approximate plasma concentrations of 5, 10, 20, 40, and 80 ng.ml-1. Plasma alfentanil concentrations were measured before and after each rebreathing test, and clonidine concentrations were measured after each rebreathing test. The end-tidal CO2 (PET(CO2)) was measured continuously. Data were analyzed by repeated-measures analysis of variance. The PET(CO2) and measured concentrations of alfentanil were included as covariates, and a compound symmetry error analysis was assumed. Statistical significance was achieved when P less than 0.05. For minute ventilation, mean inspiratory flow rate, and mouth occlusion pressure there was a statistically significant relationship to the covariates of PET(CO2) and plasma alfentanil concentration. Clonidine, when compared to placebo, caused a small but significant depression of mean inspiratory flow rate. There was similarly a small, but statistically insignificant, depression of minute ventilation by clonidine. The mouth occlusion pressure was not affected by clonidine treatment. Clonidine treatment did not potentiate alfentanil-induced respiratory depression. Although the combination of an opioid and an alpha 2-adrenergic agonist may act synergistically for the analgesic response, there is no synergistic effect by this drug combination on respiratory depression.
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PMID:Ventilatory effects of clonidine alone and in the presence of alfentanil, in human volunteers. 159 10

Thirty elderly patients undergoing major hip surgery under spinal analgesia were randomly allocated in a double-blind manner into three groups. The aim was to evaluate the influence of intrathecal morphine and postoperative naloxone infusion on the regulation of ventilation. The Bupivacaine Group received spinal analgesia with 20 mg bupivacaine intrathecally. The Morphine Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally. The Naloxone Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally + postoperative naloxone infusion intravenously (1 microgram/kg/h over 12 h, 0.25 micrograms/kg/h over the next 12 h). Evaluation of resting ventilation and the ventilatory responses to hypercarbia and hypoxaemia was made on three occasions: before surgery, and 8, and 24 h after the intrathecal injection. Intrathecal morphine had no significant effect on ventilatory regulation in elderly patients undergoing major hip surgery performed under bupivacaine spinal analgesia. Postoperative administration of opioids or sedatives after intrathecal morphine as well as postoperative blood loss associated with a fall in blood pressure appeared to increase the risk of developing respiratory depression. Naloxone infusion seemed to reduce the risk of developing respiratory depression. Furthermore, one third of the elderly had a poor response to hypoxaemia before surgery.
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PMID:Influence of intrathecal morphine and naloxone intervention on postoperative ventilatory regulation in elderly patients. 163 66


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