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)

Sufentanil, a synthetic opioid that is 5-10 times as potent as fentanyl, has been suggested for use during neurosurgical procedures because it maintains cardiovascular stability and produces hypnosis without the use of additional anesthetic agents. Doses as low as 2.5 micrograms.kg-1 are reported to create deep levels of anesthesia as demonstrated by EEG changes to high-amplitude delta-waves. However, there are no reports concerning the effects of sufentanil on blood flow and metabolism in the human brain. The present study was designed to investigate the influence of high-dose sufentanil-O2 anesthesia on the cerebral circulation, metabolism, and the cerebrovascular response to CO2 in man. METHODS. Nine male and 2 female patients between 41 and 60 years of age who were scheduled for coronary artery bypass surgery were studied. Premedication consisted of flunitrazepam 2 mg orally and piritramide 15 mg and promethazine 50 mg i.m. 1 h before arrival in the induction room. Measurements were performed with the patients awake (I), after sufentanil 10 micrograms.kg-1 as an induction dose followed by 0.15 micrograms.kg-1.min-1 as an infusion with normocapnia (pa CO2 42.1 +/- 2 mmHg) (II), during hypercapnia (pa CO2 53.7 +/- 3.5 mmHg) (III), and during hypocapnia (pa CO2 31.7 +/- 2 mmHg) (IV). Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral metabolic rates of oxygen (CMRO2) glucose (Mgluc) lactate (CMlac) were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. The Anaerobic Index was calculated from the equation avD lactate x 100/2 x avD glucose = ANI (%) Cerebral electrical activity was recorded by aperiodic analysis of the EEG (Lifescan). RESULTS AND DISCUSSION. In the EEG sufentanil anesthesia was characterized by a decrease in the number of high-frequency waves and an increase in the number and amplitude of delta-waves, a pattern that did not change throughout the study period. Concomitantly, under normocapnic conditions high-dose sufentanil led to the significant decrease in CBF by 29% accompanied by an 18% increase in cerebral vascular resistance (CVR). CMRO2 decreased by 22% while CMRgluc and CMRlac changed only insignificantly such that the ANI, which represents the percentage of anaerobically metabolized glucose, essentially remained unchanged. Mean perfusion pressure declined by 18% but stayed within the range of autoregulation. Hypoventilation (III) was followed by an 82% increase in CBF as a result of a 55% reduction in CVR, whereas cerebral metabolic parameters did not show important changes when compared to measurement II. Hyperventilation (IV), on the other hand, produced a distinct fall in CBF by 56% to a value that was 21% below the one obtained under normocapnia. This was due to an increase in CVR of the same magnitude. There was a 31% rise in CMRO2, resulting in a decrease in cerebral venous oxygen tension, but in no case did it fall below the critical value of 20 mmHg at which tissue hypoxia becomes severe. Although CMRlac increased and CMRgluc did not significantly change, the ANI remained essentially unchanged, which suggests a predominantly aerobic metabolism. The increase in metabolic activity with sufentanil during hypocapnia might be caused by an alkalosis-induced stimulation of glycolysis. It might also be related to a reduction in the depth of anesthesia, although neither the EEG nor the hemodynamic parameters indicated this. This study shows that the coupling between CBF and metabolism is well maintained and that the cerebrovascular response to CO2 is unimpaired during high-dose sufentanil anesthesia.
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PMID:[The effect of sufentanil on cerebral blood flow, cerebral metabolism and the CO2 reactivity of the cerebral vessels in man]. 182 62

The effect of a high epidural block on the catecholamine response to hypoventilation was studied in six unanesthetized dogs given intravenous sufentanil (15 micrograms.kg-1). Sufentanil alone resulted in a increase of norepinephrine (NE) concentration from 108 +/- 73 pg.ml-1 to 843 +/- 399 pg.ml-1 and epinephrine (E) from 279 +/- 80 pg.ml-1 to 2010 +/- 1416 pg.ml-1. At least one week later, an epidural block to T1 was achieved using 8-10 ml, two per cent lidocaine. Plasma NE and E decreased after EA to about 50 per cent of resting baseline measurements. The addition of sufentanil increased NE and E levels to reach approximately the resting base-line levels. In all dogs intravenous sufentanil resulted in bradypnoea, bradycardia, hypoxaemia, and hypercarbia. Intravenous lidocaine infusions had no significant effect on plasma catecholamine levels when plasma lidocaine levels ranged from 1.7 micrograms.ml-1 to 5.3 micrograms.ml-1. We conclude that a high two per cent lidocaine epidural block attenuates the catecholamine response to hypoventilation in dogs, but the persistence of baseline plasma levels of NE and E suggests that the efferent sympathetic block by high EA is incomplete.
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PMID:Epidural anaesthesia attenuates the catecholamine response to hypoventilation. 214 94

Microsurgical operations on the larynx require sufficient space for the surgeon in order to achieve the best surgical result. After preliminary experimental studies we integrated two jets of a specific size into the Kleinsasser tube. Simultaneously, we developed a "superimposed jet-ventilation system", which consists of a low-frequency jet ventilation and superimposed high-frequency jet ventilation. Respiration was maintained with a mixture of oxygen and air, whereby an additional increase in air and volume via the Kleinsasser tube, which is open on the outside, can be sustained on account of the Venturi effect. We tested this tubeless translaryngeal superimposed jet-ventilation system in 48 patients. Anesthesia was carried out by continuous intravenous administration of Propofol and intermittent doses of Sufentanil and Vecuronium as required. The clinical results showed optimal ventilation without hypercapnia. The arterial pC0(2) levels were below 42 mmHg. The arterial p0(2) levels were above 120 mmHg with a FIO2 of 40%. No complications were observed with regard to respiration during any of the operations. The surgeon had optimal conditions to carry out the operation. Because of the absence of a plastic tube, inhalation anesthetics and nitrous oxide, laryngeal laser surgery is another field of application for which this form of tubeless jet ventilation is excellently suited. We tested it with 12 patients, and no complications due to laser anesthesia were observed. We consider this form of a tubeless superimposed translaryngeal jet ventilation to be a great improvement in microlaryngeal surgery.
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PMID:[Tube-free translaryngeal superposed jet ventilation]. 227 68

The ventilatory and hemodynamic responses to hypoxia, hyperoxia, and hypercapnia before and during sufentanil infusion were studied in 16 chronically tracheostomized dogs anesthetized with two concentrations, 1 and 0.5 minimal alveolar concentration (MAC) of isoflurane. Sufentanil was infused at a rate to obtain a constant end-tidal carbon dioxide (PETCO2) of approximately 50 mm Hg for each isoflurane level. Before the sufentanil infusion, the PETCO2 was increased to 50 mm Hg by adding CO2 to the inspired gas, to allow comparisons at isocapnic conditions. Sufentanil caused only minor hemodynamic changes but significantly reduced ventilation during both levels of isoflurane. The ventilatory response to hypercapnia decreased substantially, but there were no significant alterations in the ventilatory response to hypoxia. After sufentanil infusion, hyperoxia caused a larger decrease in minute ventilation and caused apnea in four dogs. These results suggest that administering sufentanil during isoflurane anesthesia causes a reduction in the contribution of the central chemoreflexes to ventilatory drive and, consequently, a relative increase in the contribution from the peripheral chemoreflexes.
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PMID:Ventilatory and cardiovascular responses to sufentanil infusion in dogs anesthetized with isoflurane. 252 4

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