Influence of 0.1 minimum alveolar concentration of sevoflurane, desflurane and isoflurane on dynamic ventilatory response to hypercapnia in humans (original) (raw)
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Hypoxic and hypercapnic ventilatory responses during isoflurane sedation and anaesthesia in women
Acta Anaesthesiologica Scandinavica, 1995
This study primarily examined the effect of three endtidal isoflurane concentrations (0.2, 1 .O and 1.4%) on the isocapnic hypoxic ventilatory response (HVR), as well as the hypercapnic ventilatory response (HCVR), in 18 women (ASA I) who were all in the follicular phase of their menstrual cycle. Capnography was used, together with pulseoximetry to indicate desired levels of hypoxia (SpO, 75-80%). This hypoxic challenge resulted, after 3-4 min, in a stable ventilation, and ventilation measurements were then taken during a 90 s period. The HCVR provocation (inhalation of 4.5% CO, in air) and measurements were conducted using a similar time frame as for HVR. Isoflurane 0.2% did not affect any ventilatory parameter. Isoflurane 1 .O and 1.4% dose-dependently increased endtidal CO, and respiratory rate, while tidal volumes decreased. Minute ventilation was not reduced. HVR, as well as HCVR, were both uninfluenced by isoflurane 0.2%. HVR was reduced by 60-70% at isoflurane 1.4% (P<O.Ol), and was parallelled by a similar depression of HCVR (P<O.Ol). The HVR during anaesthesia was accomplished by a respiratory rate response, while the increase in tidal volume, seen in the awake state, was abolished. The HCVR during anaesthesia was, on the other hand, the result of a dose-dependently depressed tidal volume response, without any increase in respiratory rate. In conclusion, isoflurane 0.2% did not affect the ventilatory response to mild isocapnic hypoxia, nor to mild hypercapnic challenge. During anaesthesia with isoflurane (1 .O and 1.4%), there was a parallel reduction of HVR and HCVR.
British Journal of Anaesthesia, 2011
Background. To investigate whether the effects of desflurane on inspiratory resistance are similar to those of isoflurane and sevoflurane during 30 min administration at 1 and 1.5 MAC in patients with healthy lungs. Methods. Seventy-one patients undergoing elective surgery were randomly assigned to receive isoflurane, sevoflurane, or desflurane. Baseline inspiratory resistance was obtained after intubation and establishment of volume control ventilation. Anaesthesia was maintained with desflurane, isoflurane, or sevoflurane at 1 MAC for 30 min followed by 1.5 MAC for another 30 min. Tidal volume, flow, and inspiratory pressures were continuously recorded with a pneumotachograph. Total inspiratory resistance (R rs), minimal resistance (R min), and effective resistance (D Rrs) were calculated every 5 min using the end-inspiratory occlusion technique. Results. No significant differences of the evaluated parameters (R rs , R min and D Rrs) were observed during administration of the three agents at 1 MAC for 30 min. At 1.5 MAC, desflurane caused a maximum increase in R rs by 26% and in R min by 30% above baseline, in contrast to isoflurane and sevoflurane which did not display a significant effect on R rs (+3.7% by isoflurane and +7.6% by sevoflurane) and R min (+4.7% by isoflurane and +9.6% by sevoflurane). All parameters returned to baseline after discontinuation of the volatile agent. Conclusions. In healthy adults, neither sevoflurane nor isoflurane produced bronchodilation at 1 and 1.5 MAC. Desflurane did not affect respiratory resistance at 1 MAC, but at 1.5 MAC caused significant increase in both total and airway resistance with return to near baseline values after discontinuation of the agent.
Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans
Acta Anaesthesiologica Scandinavica, 1995
In order to evaluate the difference between poikilo-capnic (no CO, added to inspircd gas) and iso-capnic (CO, added to keep end-tidal CO, constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal 0, tension approx. 7 kPa). In the awake state, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a Vlc that on average increased by l.4+ 1.0 (mean fs.d.) I'min-l, whereas the iso-capnic hypoxic challenges resulted in a V, increase that was 4.7 2.3 1. min I on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 f 0.8 1. min-' (88% of the awake responses, n.s.) and during iso-capnia 2.3 f 1.4 I. min. ' (49% of the awake, P < 0.02). Awake H V R was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchangcd. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 f I .7 breath. minto 20.2 2.2) and during isocapnia by a combination of increased rate (from 17. I + I .9 breath. min to 19.1 f 1.8) and tidal volume (from 496 f 80 to 560 f 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%. In addition, both poikilo-and iso-capnic HVR were accomplished by greater tidal volumes at unchanged respiratory rates in the awake state while the opposite occurred during isofluranc anaesthesia. The more dominating chronotropic HVR during hypoxic challenge under anaesthesia will have to bc further clarified in experimental studies.
Canadian journal of anaesthesia = Journal canadien d'anesthésie, 2003
To assess the dose-dependent effect of low concentrations of isoflurane on respiratory mechanics in normal subjects. We studied 12 non-premedicated ASA I patients scheduled for lower abdominal or extremity surgery. After thiopental 5-7 mg*kg(-1) iv and succinylcholine 1 mg x kg(-1) iv, the trachea was intubated and an esophageal balloon was placed optimally by the occlusion test. After introduction of N(2)O and muscle paralysis with vecuronium, we studied 0, 0.6, 0.9 and 1.2% isoflurane. We recorded flow (F), airway opening and esophageal pressures. Signals were amplified, filtered, sampled at 100 Hz, and then fed in a 12-bit analogue-digital converter in a personal computer. Data were collected and analyzed using LABDAT and ANADAT software. Signals were acquired for 60-90 sec during mechanical ventilation (10 mL x kg(-1), 10 breaths x min(-1), I:E ratio 1:2). We estimated respiratory system (RS), lung (L) and chest wall (W) dynamic elastance (E) and resistance (R) by P(t) = EV(T)(t...
Pulmonary mechanics during isoflurane, sevoflurane and desflurane anaesthesia
Anaesthesia, 2003
This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n ¼ 22), sevoflurane (n ¼ 23), or desflurane (n ¼ 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.
2021
Background: Intensive care unit (ICU) physicians have extended the minimum alveolar concentration (MAC) to deliver and monitor long-term volatile sedation in critically ill patients. There is limited evidence of MAC’s reliability in controlling sedation depth in this setting. We hypothesized that sedation depth, measured by the electroencephalography (EEG)-derived Narcotrend-Index (burst-suppression N_Index 0 – awake N_Index 100), might drift downward over time despite constant MAC values.Methods: This prospective single-centre randomized clinical study was conducted at a University Hospital Surgical Intensive Care Unit and included consecutive, postoperative ICU patients fulfilling the inclusion criteria. Patients were randomly assigned to receive uninterrupted inhalational sedation with isoflurane, sevoflurane, or desflurane. The end-expiratory concentration of the anaesthetics and the EEG-derived index were measured continuously in time-stamped pairs. Sedation depth was also moni...
The Effect of Sevoflurane and Desflurane on Upper Airway Reactivity
Anesthesiology, 2001
Background: Although bronchial reactivity can be assessed by changes in airway resistance, there is no well-accepted measure of upper airway reactivity during anesthesia. The authors used the stimulus of endotracheal tube cuff inflation and deflation to assess changes in airway reactivity in patients anesthetized with sevoflurane and desflurane.
Clinical Evalualtion in Isoflurane and Sevoflurane Anesthesia in Rat
Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca. Veterinary Medicine, 2016
The present study focused on evaluation of induction, maintenance and emergence of inhaled anesthesia and comparison of these anesthetic times for isoflurane and sevoflurane. The biological material consisted of 12 Wistar rats divided into 2 groups, each containing a number of 6 rats. One group was anesthetized with isoflurane and the other with sevoflurane. We monitorized the rats during all stages of anesthesia, observing how the induction established, the state of the rats throughout the anestesia and the moment of the first recovery signs, the moment the rats became active as well as the moment of full recovery from anesthesia. Both isoflurane and sevoflurane rapidly induced the anesthesia, without excitation signs and the emergence was significantly faster in sevoflurane group in comparison to the isoflurane group, being accompanied by horripilation in both anesthetics.
Anesthesia & Analgesia, 1995
The spinal cord is an important site where inhaled anesthetics suppress movement in response to noxious stimuli. Inhaled anesthetics also act in peripheral tissues, although it is unclear whether these actions influence anesthetic requirements. In six isoflurane-anesthetized mongrel dogs, we placed Y cannulas in the lower aorta and vena cava, allowing us to divert blood to, and infuse blood from, a bubble oxygenator/roller pump system or to maintain normal blood flow. This technique permits a greatly diminished isoflurane concentration at the site of the noxious stimulus (tail), while maintaining isoflurane in the remainder of the body. After baseline minimum alveolar anesthetic concentration (MAGI) was determined, venous blood from the lower body was diverted to the bubble oxygenator and reinfused into the lower body via the aortic cannula; MAC2 was determined with isoflurane in the lower body at-0.2%, and MAC3 was determined with isoflurane in the lower body matched to the end-tidal isoflurane. Bypass was terminated, the native circulation established, and MAC4 determined. MACl, 2, 3, and 4 were (mean ? SD) 1.3 2 0.3%, 1.2 ? O.l%, 1.2-C 0.2%, and 1.1-C 0.2%, respectively (P > 0.05). We conclude that the peripheral effects of isoflurane do not influence the response to a noxious stimulus.