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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hemorrhagic shock on intrapulmonary right-to-left shunt and dead space ratio was investigated in spontaneously breathing dogs under barbiturate anesthesia. Intrapulmonary right-to-left shunt was reduced sufficiently to offset the marked increase in arteriovenous oxygen difference and PaO2 did not fall. Dead space ratio was increased markedly; therefore, in shock, sufficient CO2-elimination depends on severe hyperventilation. According to this empirical findings, a decrease in PaO2 in shock must not be interpreted as a consequence of the shock itself, but it implies an additional pulmonary pathology.
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PMID:Effect of hemorrhagic shock on intrapulmonary right-to-left shunt (QS/QT) and dead space (VD/VT). 93 76

The effects of halothane and enflurane anesthesia under conditions of normo-, hyper-, and hypocarbia on the autoregulation of cerebral blood flow (CBF) in the goat were evaluated. The goat was selected because of its unique arterial blood supply to the head and the development of a method by which CBF may be continuously measured. The study revealed that 1 MAC of halothane or enflurane anesthesia at normocarbia abolished cerebral autoregulation, CBF increasing or decreasing with increasing or decreasing peripheral blood pressure. Reduction of anesthesia to 0.5 MAC partially restored cerebral autoregulatory capability. The effect of 1 MAC and 0.5 MAC anesthesia on cerebral autoregulation of blood flow was potentiated by hypercarbia and antagonized by hypocarbia, indicating that the vascular response to blood CO2 fluctuations remained intact.
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PMID:Absence of autoregulation of cerebral blood flow during halothane and enflurane anesthesia. 94 20

Ventilatory responses to CO2 (delta VI/delta PCO2) were measured half, one, two and four hours after infusions of thiopentone, morphine, fentanyl and saline in healthy men in order to test the idea that variation in clinical recovery and control of breathing after anaesthetic drugs are associated with interindividual differences in control measurements of delta VI/delta PCO2. Ventilatory response to CO2 was profoundly reduced one half hour after each drug, in contrast to the observation during air breathing that ventilation and end tidal PCO2 had returned to within 10 per cent of control. Mean delta VI/delta PCO2 increased progressively at one, two, and four hours, returning to near control after thiopentone, but remaining less than 80 per cent of control four hours after morphine and fentanyl. From the regression equations of each ventilatory response, ventilation at PCO2 of 58 and 70 mmHg (VI58 and VI70) were computed to estimate displacement of the response curves by the drugs. Following thiopentone there was no significant change of V158. In contrast ther was a highly siginificant fall of VI58 one half hour after fentanyl (p less than 0.01), with progressive return towards control at one, two, and four hours; similar changes were observed after morphine. For each drug, changes of VI70 were substantially greater than corresponding changes of V158. At all times during these recovery measurements, subjects were conscious and co-operative and, by traditional clinical criteria, were judged to have recovered from the effects of the drugs. Differences between high and low responding subjects were assessed by plotting control measurements against values obtained half and one hour after drugs. No systematic differences were found. These findings suggest that delta VI/delta PCO2 is a sensitive indicator of central nervous activity, but do not support the concepts that individuals with low delta VI/delta PCO2 might be more susceptible to the ventilatory depressant effects of anaesthetic drugs, or that low delta VI/delta PCO2 might be associated with delayed return of spontaneous breathing after general anaesthesia. Plasma thiopentone levels at half, one, and four hours were highly reproducible, in contrast to the wide variation of delta VI/delta PCO2 among subjects in this study. These findings together support the notion that wide variation in clinical recovery from anaesthesia may have a primary physiological basis in addition to variation caused by interindividual differences in drug dosage, biotransformation and excretion.
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PMID:Recovery of ventilatory response to carbon dioxide after thiopentone, morphine and fentanyl in man. 94 99

The pressures generated by the inspiratory muscles as they contract isometrically during airway occlusion seem to be a measure of respiratory neuron efferent activity. The ventilatory and occlusion pressure responses to increasing levels of CO2 were studied in goats, awake and anesthetized, with and without inspiratory flow resistance. Hypercapnia was produced by rebreathing. Randomly, during rebreathing, inspiratory airflow was prevented on single breaths. Ventilation and pressures developed during the first 100, 200, 300 and 400 milliseconds of an inspiratory effort against a complete occlusion increased linearly with CO2 in both awake and anesthetized animals. Anesthesia reduced both the ventilatory and occlusion pressure responses to CO2. Inspiratory resistance increased occlusion pressure responses in awake goats but not in the same animals when anesthetized. Inspiratory airflow resistance seems to augment respiratory efferent activity as reflected in the pressure responses only in conscious goats. Thus the response to an inspiratory resistance seems to depend on the state of consciousness.
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PMID:Airway occlusion pressures in awake and anesthetized goats. 96 4

Paired cerebral blood flow measurements at two levels of arterial carbon dioxide (CO2) tension were made in 36 awake patients and 85 patients under general anesthesia to measure the percent change in flow per mm Hg change in PaCO2 (CO2 reactivity). CO2 reactivity was significantly greater in the generally anesthetized (5.96) than in the awake group (3.65). In both groups, a linear correlation was found between mean percent CO2 reactivity and conductance (the reciprocal of resistance), up to a level of conductance of 0.85 in awake and 0.95 in unconscious patients. When the CO2 reactivity of 18 awake patients and 59 unconscious patients was compared with that of respective control groups, only 11 patients were found to have abnormal CO2 reactivities for their conductance levels.
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PMID:Cerebrovascular carbon dioxide reactivity and conductance in patients awake and under general anesthesia. 98 26

Recent reports have described methods of controlling the level of CO2 during anesthesia with a N2O-relaxant sequence and controlled ventilation. This paper describes a method of predicting and controlling the PaCO2, using body weight for determination of the fresh gas flow from the anesthetic machine, removing the absorbent from the canister while leaving the canister in the circuit, and controlling ventilation at 12 ml/kg and at 12/min.
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PMID:Relation of PaCO2 to fresh gas flow in a circle system. 98 28

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2-16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100-200 mg/kg. Mean fetal arterial Pco2 increased from 49.5 to 63.4 mmHg but no significant changes in umbilical blood flow occurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. No dignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despite an increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistance did not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor in normal physiological regulation of the uteroplacental circulation in this species.
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PMID:Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep. 99 46

The respiratory depressant actions of pethidine and tilidine during anaesthesia were compared in 18 surgical patients anaesthetized with N2O + O2 after thiopental induction. Five minutes after thiopental, 0.5 mg/kg pethidine or 1.5 mg/kg tilidine were each given intravenously to six patients, the remaining six patients serving as controls. Minute ventilation, respiratory rate, end-tidal CO2 and PCO2 from arterialized venous blood were measured up to 30 min. Pethidine caused the following maximal changes: V -0.98 +/- 0.24 (s.e. mean) 1/min, rate -5.5 +/- 0.7/min, CO2ET + 0.7 +/- 0.1 vol % and PCO2 + 5.7 +/- 1.1 mm Hg. These changes occurred within 10 min of the injection.
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PMID:Respiratory depressant action of tilidine during N2O + O2 anaesthesia. 99 57

Cardiopulmonary variables were measured in 3 groups of halothane-oxygen anesthetized cats. The groups, each containing 6 animals, were treated similarly except for maintenance anesthetic systems, and system variation was the basis for comparison. Groups were maintained, using a pediatric circle CO2 absorption system with an O2 flow of 0.5 L/minute, an Ayre's T-piece system with an O2 flow of 3 L/minute, and an adult circle CO2 absorption system with an O2 flow of 0.5 L/minute. Anesthesia was induced by mask, endotracheal intubation was done, and end-expired halothane was maintained at 1.4%. Measurements of cardiopulmonary variables were reported at 30-minute intervals for 135 minutes, the first measurements being made 15 minutes after induction. Control data were similar for all groups. Measured variables were not statistically or clinically different among groups, and change from control within groups was related to halothane anesthesia. The 3 systems produced similar cardiovascular and respiratory effects. Consequently, none of the systems proved superior to the other 2 on the basis of measured variables. Halothane anesthesia produced cardiopulmonary changes comparable to changes reported in other species anesthetized and maintained by similar techniques.
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PMID:Cardiopulmonary effects of rebreathing and nonrebreathing systems during halothane anesthesia in the cat. 99 70

Autoregulation of the cerebral blood flow is a wellknown fact. In normal man the arterial pressure can vary from 80 mm Hg to 150 mm Hg without a change in the normal cerebral blood flow of 50 ml/100 g/min. The mechanism which is responsible for this autoregulation is not clearly understood. Several theories were proposed to explain this phenomenon. 1. The tissue pressure increases with an increase of the arterial pressure. A mechanical process should neutralize an increase of the cerebral blood flow. 2. The metabolic theory says that a decrease of the blood pressure, without a change of metabolism, involves an increase of the PaCO2, and a decrease of the PaO2. Those two factors provoke a decrease of the vascular tone. 3. The myogenic theory explains autoregulation by the fact that a change of the transmural pressure in the small vessels, involves a change in the activity of the smooth muscles of the vessels. 4. The exact mechanism of the autonomic nervous system in the autoregulation of the cerebral blood flow is still obscure. In some pathological conditions autoregulation is completely lost or is functioning not optimal: hypoxia, hypercapnia and brain contusion. We have measured the cerebral blood flow before and after an intravenous injection of 5 mg thiopental (Pentothal) on occasion of a carotid angiography in man. We noticed a decrease of the cerebral blood flow and at the same moment a decrease of the arterial pressure. We thought that maybe barbiturates could influence autoregulation. Our results could not prove this hypothesis. For ethical reasons we could not make the necessary measurements to prove or to reject this hypothesis (i.e. intracranial pressure, deep controlled hypotension). In the literature there are arguments which support this hypothesis although most workers found an intact autoregulation after a barbiturate anesthesia. Some workers saw that the increase of the cerebral blood flow by increasing the PaCO2 was depressed by barbiturates and exhausted by halothane and cyclopropane. As autoregulation is a more vulnerable mechanism than CO2 reactivity as seen in clinical situations, it could be true that anesthetics do influence autoregulation.
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PMID:Influence of anesthesia on autoregulation of the cerebral blood flow. 102 Jun 37


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