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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 clinical effects of a propofol-alfentanil association were studied in fifteen patients ASA II (mean age 50.1 +/- 14.1) anaesthetized for E.N.T. endoscopy after informed consent. All the patients received an intramuscular premedication with 0.10 to 0.15 mg.kg-1 midazolam. Propofol 2.5 mg.kg-1 was injected in a peripheral venous line with alfentanil 10 micrograms.kg-1, followed by continuous automatic injection of propofol at a dose of 5 to 10 mg.kg.h-1 and alfentanil 5 micrograms.kg-1 given just before suspension. After induction and during maintenance of anaesthesia, the patients were allowed to breathe oxygen spontaneously O2 assisted when apneic. The following variables were studied before induction (to), after induction (t1), during suspension (t2) and when stopping the infusion (t3): haemodynamic parameters using an invasive method and blood gases. Statistical analysis was performed using the Student's test for paired samples. Surgical conditions and anaesthetic quality were good with early recovery of consciousness and return of all reflexes. After an initial period of cardio vascular depression, the haemodynamic parameters did not vary much during the anaesthesia and propofol-alfentanil appeared to limit considerably the hypertension due to laryngoscopy. However, there was a moderate degree of hypercapnia (p less than 0.001) in most patients, giving evidence of some respiratory depression and possibly a greater depth of anaesthesia than desirable. Indeed, the doses of alfentanil required seemed to be more important with propofol because of a probably interference between the two drugs; the doses of these drugs should therefore be modified according to the length of surgery.
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PMID:[Circulatory and respiratory repercussions to direct suspension laryngoscopy in the adult: value of a propofol-alfentanil combination]. 249 72

Propofol like thiopental and etomidate, suppresses cortical electrical activity in a dose-related manner, which leads to a 36% decrease in cerebral oxygen uptake and a 51% decrease in cerebral blood flow after an induction dose of 2 mg/kg followed by a maintenance dose of 0.2 mg/kg per min. In this study, the effects of propofol and varying paCO2 values on cerebral energy and amino acid metabolism were examined. METHODS. Eleven male patients between 49 and 63 years of age who were about to undergo coronary artery bypass surgery were studied. Measurements were performed with the patient awake (I), during steady-state maintenance anesthesia after propofol 2 mg/kg as an induction dose with 0.2 mg/kg per min by infusion with normocapnia (paCO2 39.9 +/- 3.1 mm Hg) (II), during hypocapnia (paCO2 29.9 +/- 2.6 mmHg) (III), and during hypercapnia (paCO2 50.6 +/- 3.3 mmHg) (IV). Cerebral blood flow was measured using the argon wash-in technique. A catheter was advanced into the superior bulb of the right internal jugular vein for measurement of cerebral oxygen, glucose, lactate, and amino acid uptake and release, which were calculated by multiplying the arterial-cerebral venous oxygen and substrate difference by the cerebral blood flow. Lactate/glucose index was calculated from the equation. Formula: see text. where a-vD lactate and a-vD glucose represent the arterial-cerebral venous substrate differences in mmol/l. Cerebral electrical activity was recorded by Fourier analysis of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Energy and amino acid metabolism in the human brain under Disoprivan anesthesia with various paCO2 values]. 289 87

Patients in the ICU who require intubation and mechanical ventilation benefit from adequate sedation and analgesia. Traditionally, this has been achieved using benzodiazepines and opioids. Alternatively, propofol is being administered for sedation of patients in the ICU with increasing frequency. Propofol has a number of properties that make it a potentially superior choice for sedation of intubated ICU patients. The rapid onset and offset of sedation with propofol, even after prolonged administration, allow for greater control over the level of sedation and more rapid weaning from mechanical ventilation. In addition, long-term administration of propofol does not appear to be associated with the development of tolerance, addiction, or withdrawal following discontinuation. Propofol suppresses cellular oxygen consumption and carbon dioxide production without increasing anaerobic metabolism. This may be beneficial in patients with severe hypoxemia, hypercarbia, or myocardial ischemia. Finally, the use of propofol may reduce or eliminate the need for other medications in these patients such as muscle relaxants, antihypertensives, lipid nutritional supplements, and analgesics, thereby simplifying their medication regimens and reducing the overall cost of their care while in the ICU. Propofol can be administered to critically ill patients for sedation with a high degree of safety and efficacy. Propofol causes systemic vasodilatation which may result in unwanted hypotension, especially in patients who are already hemodynamically compromised. Propofol also causes ventilatory depression, so its use should be restricted in the ICU to patients whose airway is protected by an endotracheal tube and whose ventilation is closely monitored. Finally, continuous administration of propofol may cause clinically significant hypertriglyceridemia in patients with disordered triglyceride metabolism, or in patients receiving excessive doses of propofol or parenteral lipid supplements. Although propofol is more expensive than equipotent doses of other sedative agents, the additional cost of using propofol for sedation of critically ill patients in the ICU may be more than offset by the savings accrued from faster times to extubation, shorter ICU stays, and the use of fewer medications to manage these patients. Further research needs to be done to determine the potential clinical and cost benefits of using propofol for sedation of patients in the ICU.
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PMID:Propofol: a new drug for sedation in the intensive care unit. 763 54

Ketamine-fentanyl-propofol and ketamine-fentanyl-etomidate combinations were administered intravenously to four groups of rabbits. Each group received ketamine (30 mg/kg of body weight) and fentanyl (0.025 mg/kg) for anesthesia induction. Either propofol or etomidate was administered by an infusion pump to maintain anesthesia. The rabbit's responses to noxious stimuli were determined before anesthesia was induced and at 10-min intervals thereafter until the rabbit recovered. The effects of the anesthetic combinations on the cardiopulmonary system were measured by monitoring respiratory and heart rates, blood pressure, and arterial blood gas tensions. Etomidate infused at the rate of 0.2 or 0.1 mg/kg/min could maintain surgical anesthesia with fewer effects on the cardiopulmonary system for 40 and 30 min respectively. However, the high mortality and side effects such as hemolysis in these two groups preclude the clinical use of etomidate for anesthesia maintenance. Propofol administered intravenously at rates of 0.8 and 0.4 mg/kg/min could maintain surgical anesthesia for 40 and 30 min respectively. However, relatively severe hypotension, hypercapnia, and respiratory acidosis were associated with this drug. Recovery from the propofol infusion was very rapid. Ketamine-fentanyl-etomidate combination is not recommended for clinical anesthesia in rabbits. Ketamine-fentanyl-propofol combination at a dosage of 30-0.025-0.4 mg/kg/min can be safely used for short-term surgery.
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PMID:Comparison of anesthesia induced by ketamine-fentanyl combination and maintained by propofol or etomidate in New Zealand white rabbits. 765 Aug 97

Early mental and psychomotor recovery was studied in 67 patients undergoing colorectal surgery under continuous epidural anaesthesia and light general anaesthesia using propofol, halothane, and midazolam/fentanyl. The study was approved by the local ethics committee. All patients received epidural anaesthesia with 0.25% bupivacaine and were then randomly allocated to one of three groups. In group I (halothane), light general anaesthesia was induced with thiopental 3-5 mg/kg and maintained with halothane. The propofol group (II) received 2 mg/kg for induction and a mean continuous infusion of 1.7 mg/kg.h. In group III (Mi/Fe), midazolam and fentanyl were used for induction and maintenance. All patients were intubated, received non-depolarising muscle relaxants, and were manually ventilated with nitrous oxide-oxygen (2:1.2). For postoperative analgesia, 0.05 mg/kg morphine was administrated epidurally 30 min before the end of the operation; 30, 60, 90, and 120 min after arriving in the recovery room, vigilance was assessed using a modified Steward score, the Trieger test, the ability to recall a column of numbers (KAI test), and symbol counting (CI test). Heart rate, blood pressure, arterial oxygen saturation, and blood gases were recorded. RESULTS. The three groups were comparable with regard to age, sex, ASA classification, and duration of anaesthesia and operation (Table 3). There was no difference between the groups in performance of the recovery tests (Figs. 2-5), blood pressure, heart rate, arterial blood gas analysis (Fig. 6), or oxygen saturation. Comparing pre- and postoperative values, we found severe psychomotor and mental impairment in all groups. pCO2 was slightly elevated in all groups, but only 3 patients in the propofol group and 6 in the midazolam/fentanyl group developed hypercapnia above 50 mm Hg. Patients receiving propofol or midazolam/fentanyl had significantly less postoperative nausea and vomiting than those receiving halothane (Table 5). CONCLUSION. It is concluded that propofol offers no advantage over halothane or midazolam/fentanyl where early postoperative recovery is concerned. Intraoperatively, all three techniques provided good anaesthesia. Propofol and midazolam/fentanyl caused less postoperative nausea and vomiting than halothane anaesthesia.
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PMID:[No better vigilance after general anesthesia with propofol in colonic surgery. A comparison of three procedures for general anesthesia (propofol, halothane and midazolam/fentanyl) in combination with catheter epidural anesthesia]. 817 65

The effects of continuous infusions of propofol on baroreceptor reflex regulation of cardiac rate and peripheral sympathetic nerve activity were evaluated in seven healthy, normotensive, young (19-26 yr), male volunteers. Heart rate, radial artery pressure, and continuous recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 micrograms) followed 60 s later by phenylephrine (150 micrograms). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 micrograms.kg-1 x min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 micrograms.kg-1 x min-1) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Propofol and autonomic reflex function in humans. 831 Dec 93

Propofol is a commonly used anesthetic agent, and it attenuates hypoxic ventilatory response in humans. Propofol reduce in vivo and in vitro carotid body responses to hypoxia as well as to nicotine in experimental animals. In the present study we examined the effects of propofol on carotid body responses to hypercapnia and K(+)-induced carotid body activation and compared these effects with hypoxia in an in vitro rabbit carotid body preparation. Hypoxia, hypercapnia and potassium increased the carotid sinus nerve activity and propofol attenuated the chemoreceptor responses to all three stimuli. However, the magnitude of propofol-induced attenuation was greater for hypercapnic and K(+)-induced carotid body activation compared to the hypoxic response. These observations suggest that propofol-induced attenuation of the hypoxic response is partly secondary to depression of chemoreceptor response to hypercapnia inhibiting the synergistic interactions between O(2) and CO(2) and may involve CO(2)/H(+) sensitive K(+) channels.
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PMID:Pronounced depression by propofol on carotid body response to CO2 and K+-induced carotid body activation. 1805 27

The hypnotic agent propofol has pharmacokinetic characteristics that allow for rapid onset and offset of drug effect and fast elimination from the body. Elderly patients show a greater sensitivity to the hypnotic effect of propofol. The drug is extensively metabolized in the liver through the cytochrome P450 system and glucuronidation, with potential for drug interaction. Propofol does not cause significant inotropic depression at clinically relevant concentrations. But in vitro, propofol impairs isotonic relaxation of the heart and decreases free cytosolic Ca(2+) concentrations in myocardial cells. In animal models, the cardioprotective effects of propofol derive in part from its antioxidant and free radical scavenging properties. Propofol decreases cerebral blood flow and cerebral metabolic rate dose-dependently. The neuroprotective effect of propofol in animal models is attributed to its antioxidant property, the potentiation of gamma-aminobutyric acid type A (GABA(A))-mediated inhibition of synaptic transmission, and the inhibition of glutamate release. Subhypnotic doses of propofol induce sedative, amnestic, and anxiolytic effects in a dose-dependent fashion. Propofol impairs ventilation with a considerable effect on the control of ventilation and central chemoreceptor sensitivity. Propofol reduces the ventilatory response to hypercapnia and the ventilatory adaptation to hypoxia, even at subanesthetic doses. The drug potentiates hypoxic pulmonary vasoconstriction, an effect caused by inhibition of K(+) (ATP)-mediated pulmonary vasodilatation. Most of the pharmacological actions of propofol result from interaction with the GABA(A) receptor or with calcium channels. Propofol prolongs inhibitory postsynaptic currents mediated by GABA(A) receptors, indicating that its effects are associated with enhanced inhibitory synaptic transmission, but propofol also influences presynaptic mechanisms of GABAergic transmission. Propofol modulates various aspects of the host's inflammatory response. It decreases secretion of proinflammatory cytokines, alters the expression of nitric oxide, impairs monocyte and neutrophil functions, and has potent, dose-dependent radical scavenging activity similar to the endogenous antioxidant vitamin E.
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PMID:Propofol. 1817 94

An anesthetic combination of medetomidine-midazolam-atropine and propofol was investigated in twenty New Zealand White rabbits. Each rabbit received combined medetomidine at a dosage of 0.2 mg/kg (b.w.), midazolam (0.5 mg/kg b.w.) and atropine (0.5 mg/kg b.w.) intramuscularly for induction of anesthesia. Propofol was administered intravenously - given to effect, and after that by an infusion pump to maintain anesthesia. The influence of the anesthetic combination on the cardiopulmonary system was evaluated by monitoring respiratory and heart rates, blood pressure, and arterial blood gas tensions. The results obtained showed that propofol infusion at a rate of 0.5 mg/kg b.w./min maintained general anesthesia effectively with few side effects on the cardiopulmonary system during 30 minutes. However, slight hypotension, hypercapnia, and respiratory acidosis were associated with infusion of this anesthetic. The recovery of the rabbits from the anesthesia was smooth. Two rabbits died 20 to 24 hours after anesthesia. In conclusion, an anesthetic combination with medetomidine-midazolam-atropine and propofol at the investigated doses was shown to be a safe method to induce and maintain general anesthesia enabling short-term surgical procedures in healthy animals.
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PMID:Evaluation of medetomidine-midazolam-atropine (MeMiA) anesthesia maintained with propofol infusion in New Zealand White rabbits. 1964 51


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