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)

To investigate the effects of several endoscopic procedures like introduction of the bronchoscope, removal of the instrument, catheter suction, bronchoalveolar lavage and transbronchial biopsy on heart rate, systemic blood pressure, and transcutaneously measured blood gases 77 consecutive patients (age, 20-83 years) were studied. All patients received 101 O2/min via face mask during bronchoscopy. Sedation was performed with midazolam or diazepam. The different characteristics of each patient, e.g. age, sex, smoking habits, baseline values of heart rate and systemic blood pressure, underlying pulmonary disease and kind of premedication were examined separately to analyse their special effects on the course of bronchoscopy. During the fiberoptic bronchoscopy neither a slight decrease in transcutaneous pO2 nor a small increase in transcutaneous pCO2 led to a critical situation. Nevertheless it should be stressed that the time after removal of the instrument and finishing supplemental oxygen may be critical regarding hypoxia and hypercapnia especially in older patients with hypoxia being already present before starting the endoscopy. The hemodynamic indices did not change significantly. There was no difference between midazolam or diazepam concerning the parameters under study. If supplemental oxygen is given and adequate premedication is performed, monitoring of hemodynamics and blood gases during fiberoptic bronchoscopy is not necessary in patients without cardiovascular or respiratory risk.
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PMID:Effects of diagnostic procedures during fiberoptic bronchoscopy on heart rate, blood pressure, and blood gases. 250 May 57

To assess the effects of isoflurane on chemical regulation of ventilation, we studied the ventilatory responses to (1) hyperoxic hypercarbia, (2) isocapnic hypoxaemia, and (3) a single half vital capacity breath of carbon dioxide 20 per cent in oxygen in 12 human subjects, awake and sedated or anaesthetized with isoflurane, 0.1 or 1.1 MAC. Sedation did not alter ventilation nor the ventilatory response to hypercarbia but reduced the responses to hypoxaemia and to the half vital capacity breath of CO2. Anaesthesia reduced ventilation and the response to hypercarbia and nearly abolished the responses to hypoxaemia and to the breath of CO2. The results indicate that isoflurane reduces ventilatory responses to several chemical drives and that it selectively impairs those responses mediated by peripheral chemoreceptors. In these respects, isoflurane is similar to halothane and enflurane.
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PMID:Chemical regulation of ventilation during isoflurane sedation and anaesthesia in humans. 641 54

Sedation elicited by some centrally acting antihypertensive agents may interfere with respiratory control, and by selectively inhibiting upper airway dilating muscle activity it may facilitate obstructive sleep apnea. Autoradiographic studies with [125I]p-iodoclonidine in the presence of 10 microM epinephrine to block alpha 2-adrenergic sites or 100 nM moxonidine to mask I1-imidazoline sites show that both I1- as well as alpha 2-sites are localized in putative chemosensory areas of the rostral ventrolateral medulla in the cat. We sought to determine the effect of activating I1 and alpha 2-receptors on central chemosensitivity by using moxonidine as a selective I1 agonist, clonidine as a mixed I1/alpha 2 agonist, SK&F-86466 as a specific alpha 2-antagonist, and efaroxan as a mixed I1/alpha 2 antagonist. We recorded responses of phrenic, hypoglossal, and cervical sympathetic nerve activities to progressive hypercapnia after hyperventilation to apnea. Moxonidine (3-100 micrograms/kg i.v.) caused dose-dependent decreases in tonic cervical sympathetic nerve activity and blood pressure, but had no effect on the CO2 threshold (after 30 or 100 micrograms/kg moxonidine, phrenic nerve activity reappeared at 5.8 +/- 0.2% CO2 versus 5.6 +/- 0.3% CO2 in control). Following moxonidine, the slope of the steep portion of the CO2 response tended to increase (10.3 +/- 1.8 versus 7.3 +/- 0.9). Peak phrenic nerve activity was comparable to control at 7.5% CO2 (20 +/- 2 U in control) and at 9.5% CO2 (30 +/- 3 versus 27. +/- 2 U). Similarly, the response of hypoglossal and inspiratory phasic cervical sympathetic nerve activity to a progressive CO2 rise was not affected by moxonidine. By contrast, clonidine in the same doses decreased CO2 sensitivity, because the CO2 threshold was elevated from 5.3 +/- 0.5% to 6.7 +/- 0.4% (p < 0.001). The slope of the CO2 response was decreased from 9.7 +/- 1.9 to 7.4 +/- 1.3 (p = 0.05). Peak phrenic nerve activity was reduced at 7.5% CO2 (11 +/- 5 versus 25 +/- 2 U; p < 0.05) and at 9.5% CO2 (21 +/- 4 versus 33 +/- 2 U; p = 0.06). Clonidine selectively inhibited the response of hypoglossal nerve activity to CO2. The depressive effects of clonidine were reversed by alpha 2-blockade with SK&F-86466 (0.5 or 1 mg/kg). Inspiratory phasic cervical sympathetic nerve activity increased after SK&F-86466 in parallel with phrenic and hypoglossal nerve activity, but the tonic component of cervical sympathetic nerve activity and blood pressure increased only transiently.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of I1-imidazoline receptor activation on responses of hypoglossal and phrenic nerve to chemical stimulation. 767 59

Sedation may be used in intensive care and emergency medicine to improve the oxygen demand/delivery ratio. The influence of sedation has most frequently been investigated in a dose-related manner. The aim of the present study was to determine the effect-related influence of different sedatives on oxygen uptake (VO2) in relation to defined resting conditions. METHODS. Forty ASA I patients who had to undergo a minor surgical procedure were investigated 1.5 h before surgery at basal energy-expenditure measurement conditions. One of the following substances was given with a preset bolus rate in a double-blind, randomised order until a defined level of sleep or side effects was encountered: propofol (n = 8), midazolam (n = 8), thiopentone (n = 8), sodium chloride (n = 8), and fentanyl (n = 8). The sleep level was defined as sluggish response to a loud voice or tapping on the forearm. The variables VO2, carbon dioxide elimination (VCO2), end tidal CO2 (p(et)CO2), oxygen saturation (SaO2), heart rate, systemic blood pressure, skin temperature, and skin resistance on the sole of the foot were documented on-line on a computer. All variables were compared using differences of averages from 10-min periods before and after sedation during which the VO2 was minimal. RESULTS. The mean VO2 before sedation was 264 +/- 60 ml/min, and the measured energy expenditure did differ by -0.2% (+/- 14%) from mean predicted values using the Harris-Benedict equation. The VO2 was reduced by 15 +/- 2% with propofol, by 12 +/- 8% with midazolam, and by 10 +/- 5% with thiopentone. This was statistically significant compared to placebo treatment, as was the difference between propofol and thiopentone effects. All patients in these groups reached the defined sleep level, which was not achieved by the placebo and fentanyl groups. Placebo treatment changed the VO2 by 0.1% (+/- 2%). Fentanyl increased the VO2 by 5% (+/- 8%), which did not reach significance. In the fentanyl group the bolus application had to be stopped at a p(et)CO2 of 50 mm Hg in all patients. In the propofol, midazolam, and thiopentone groups the phasic changes of skin resistance were reduced to zero and the skin temperature increased from 27 +/- 2 degrees C to 32 +/- 2 degrees C. The fentanyl group showed an increase in changes of skin resistance without changes in temperature. CONCLUSIONS. Sleep induced by propofol, midazolam, or thiopentone to a clinically maximal desirable level in spontaneously breathing patients reduced VO2 by 10% to 15%. This level of sedation did not induce a relevant change in P(et)CO2 or SaO2. The effect of propofol appeared to be the most pronounced and least variable. This may be attributable to a more pronounced reduction in single-organ VO2 or to an undetected difference in level of sedation. Fentanyl did, in contrast to most publications on opioid effects, seem to increase VO2. Underlying mechanisms may be sought in an increased rate-pressure product and sympathetic activity on the basis of hypercapnia and changes in muscle tension.
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PMID:[The effect of sedation on oxygen uptake during spontaneous breathing]. 834 51

We investigated analgesia and the adverse effects of epidural sufentanil infusion in a double-blind randomized study of 37 patients undergoing thoracic surgery. Sufentanil 1 microgram/mL was administered at a thoracic (Ts, n = 12) or lumbar level (Ls, n = 11), or combined with bupivacaine 1 mg/mL at a thoracic level (Tsb, n = 14). Postoperatively, the epidural infusion rate was titrated (4-20 mL/h) according to the visual analog pain scale when assessed during function (VAS-F) or the occurrence of side effects. When epidural analgesia failed, nonsteroidal antiinflammatory drugs (NSAIDs) were given. VAS-F was lowest in the Tsb group (Tsb < Ts = Ls) despite its having both the lowest rate of epidural infusion (Tsb < Ts < Ls) and need of additional NSAIDs (Tsb < Ts = Ls). Sedation (Tsb < Ts < Ls) and hypercapnia (Tsb = Ts < Ls) occurred most frequently in the Ls group. Vital capacity (VC) was reduced in all groups by 43%-58% (Ls > Ts) and had recovered only partially at 24 h after discontinuation of the epidural infusion. The slopes of the ventilatory response (minute ventilation [VE], inspiratory flow, and mouth occlusion pressure at 0.1 s [P0.1]) to 7% CO2 decreased during treatment in Ls, Ts, and Tsb groups at the most by 73%, 55%, and 52% (not significant [NS] between groups), 59%, 45%, and 38% (NS between groups), and 81%, 43%, and 18% (Ls > Tsb), respectively. Twenty-four hours after discontinuation of the epidural infusion, there was a complete recovery of the VE, inspiratory flow, and P0.1 response to CO2 in the Tsb group only. The study shows that, after thoracotomy, epidural sufentanil analgesia is optimal when tailored to the site of nociceptive input and combined with bupivacaine.
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PMID:The analgesic efficacy and adverse effects of continuous epidural sufentanil and bupivacaine infusion after thoracotomy. 869 25

Sedation is often needed for obtaining nuclear magnetic resonance (NMR) images in children. The aim of this study was to evaluate the efficacy of propofol administered by continuous infusion to non-intubated children for whom our hospital's usual method of sedation (oral chlorohydrate 75 mg/kg at a maximum dose of 2 g plus 4 hours sleep privation the night before) had failed. Deep sedation was induced in 37 ASA I-II children aged 4 and 14 year old, with 2.5 mg/kg propofol followed by 6 mg/kg/h in continuous infusion. An additional dose of 1 mg/kg was administered if the child moved, and the perfusion was reduced to 4 mg/kg if SpO2 fell below 95%. Apnea occurred after induction in 24% (n = 9), 29% (n = 11) required additional doses of propofol, and a tendency to hypercapnia was observed as the imaging procedure progressed. Sedation failed in one child, who required general anesthesia when opisthotonos presented after the induction dose. Awakening was early and satisfactory in all patients, with a score of 2 on the Ramsay scale 15 minutes after NMR. Deep sedation with propofol is a safe and effective method of performing NMR in a child for whom other methods of sedation have failed, provided the child is ASA I-II, monitoring is exhaustive and procedure is carried out by an anesthesiologist.
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PMID:[Propofol in continuous infusion for performing nuclear magnetic resonance in children: an effective alternative to sedation with other drugs]. 956 39

Advanced prehospital emergency medical care of patients with a severe head injury must essentially focus on the impact of secondary cerebral insults of systemic origin on the outcome. The first objective of prehospital care is to prevent hypoxaemia and hypercapnia. Therefore, all patients with a Glasgow Coma Scale score equal to or lower than 8 must be treated with endotracheal intubation and controlled ventilation under continuous monitoring of SpO2 and PETCO2. Treatment is similar in head-injured patients with significant deterioration of consciousness level, seizures, respiratory distress, or severe facial and thoracoabdominal injuries. The endotracheal tube is inserted by the orotracheal route under direct laryngoscopy, after a rapid induction sequence of anaesthesia and immobilization of the cervical spine in neutral position. For the induction of anaesthesia in these high-risk patients (full stomach, unknown medical history, deteriorated haemodynamic status), etomidate and suxamethonium are the preferred agents. Sedation is maintained with an hypnoticopioid association (fentanyl). Simultaneously, the main goal is the maintenance of an optimal cerebral perfusion pressure, as arterial hypotension severely worsens cerebral ischaemia. Volume loading is accomplished with 0.9% saline and hydroxyethyl starch.
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PMID:[Prehospital management of patients with severe head injuries]. 1083 14

Sameridine is a new compound with both local anesthetic and opioid properties (partial micro -opioid receptor agonist). It was intended for intrathecal administration to provide anesthesia for surgery and extended postoperative analgesia. In this double-blinded pharmacodynamic study with a two-parallel-group design, we investigated, during a 24-h period, the effects of intrathecal sameridine and bupivacaine on ventilation at rest and at ventilatory challenges during hypercarbia and hypoxia. Twenty-four healthy volunteers received either 25 mg of sameridine or 15 mg of bupivacaine intrathecally. Ventilation was measured by pneumotachography and in-line capnography. Sedation was rated by a visual analog scale. Segmental spread and development of motor and sensory block were similar in both groups. There was a decrease in tidal volume 2.5 to 6 h after injection in the bupivacaine group. This was seen only at 4 h in the sameridine group. There were no other major ventilatory differences between sameridine and bupivacaine during resting ventilation. Hypercarbic (tidal volume, mean inspiratory flow) and hypoxic (mean inspiratory flow) ventilatory responses were slightly decreased in the sameridine group, but not in the bupivacaine group. We conclude that intrathecal administration of sameridine or bupivacaine in healthy volunteers produces similar, minor effects on ventilatory responses over a 24-h observation period.
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PMID:Hypercarbic and hypoxic ventilatory responses after intrathecal administration of bupivacaine and sameridine. 1253 14

Bronchiolitis is a prevalent viral disease in infants. Many of these infants require hospital admission and mechanical ventilation due to respiratory failure or apnea. The clinical and pathophysiological spectrum of this disease can range from two extremes, obstructive and restrictive disease, on which the indication for mechanical ventilation and the modality used should be based. Non-invasive ventilation is especially indicated in both obstructive and hypoxemic restrictive patterns and a pressure-controlled modality is recommended. In obstructive patterns, air trapping must be monitored, while in restrictive patterns the addition of positive end-expiratory pressure (PEEP) is indicated. High-frequency oscillatory ventilation is indicated in restrictive patterns with sever hypoxemia despite conventional ventilatory support or in cases of significant air leak syndromes. In all cases, a permissive hypercapnia strategy is recommended to prevent barotrauma. Sedation and muscle relaxation should be considered to facilitate adaptation to the ventilator and to try to limit the risks of air trapping, air leak, and barotrauma.
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PMID:[Ventilation in special situations. Mechanical ventilation in bronchiolitis]. 1464 22

We present a series of three children with trisomy 21 and obstructive sleep apnea who required sedation during magnetic resonance imaging of the upper airway. In an effort to provide effective sedation with limited effects on cardiovascular and ventilatory function, sedation was provided by a combination of ketamine and dexmedetomidine. Sedation was initiated with a bolus dose of ketamine (1 mg x kg(-1)) and dexmedetomidine (1 microg x kg(-1)) and maintained by a continuous infusion of dexmedetomidine (1 microg x kg(-1) x h(-1)). One patient required a repeat of the bolus doses of ketamine and dexmedetomidine and an increase of the dexmedetomidine infusion to 2 microg x kg(-1) x h(-1). Effective sedation was provided for all three patients. We noted no clinically significant hemodynamic or respiratory effects. No central apnea was noted although there was a brief episode of upper airway obstruction in one patient which responded to repositioning of the airway. All three patients developed some degree of hypercarbia with maximum P(E)(CO2) values of 6.4, 6.9, and 6.8 kPa (49, 53, and 52 mmHg), respectively. To date, this is the first report regarding the use of this combination in pediatric patients. Given the preliminary success noted in our three patients, prospective trials evaluating the efficacy of a dexmedetomidine-ketamine combination appears warranted.
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PMID:Monitored anesthesia care with a combination of ketamine and dexmedetomidine during magnetic resonance imaging in three children with trisomy 21 and obstructive sleep apnea. 1687 22


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