Respiratory Mechanics during Xenon Anesthesia in Pigs: Comparison with Nitrous Oxide

Background: Because of its high density and viscosity, xenon (Xe) may influence respiratory mechanics when used as an inhaled anesthetic. Therefore the authors studied respiratory mechanics during xenon and nitrous oxide (N2O) anesthesia before and during methacholine-induced bronchoconstriction.

Methods: Sixteen pentobarbital-anesthetized pigs initially were ventilated with 70% nitrogen-oxygen. Then they were randomly assigned to a test period of ventilation with either 70% xenon-oxygen or 70% N2O-oxygen (n = 8 for each group). Nitrogen-oxygen ventilation was then resumed. Tidal volume and inspiratory flow rate were set equally throughout the study. During each condition the authors measured peak and mean airway pressure (Pmax and Pmean) and airway resistance (Raw) by the end-inspiratory occlusion technique. This sequence was then repeated during a methacholine infusion.

Results: Both before and during methacholine airway resistance was significantly higher with xenon-oxygen (4.0 +/- 1.7 and 10.9 +/- 3.8 cm H2O [middle dot] s-1 [middle dot] l-1, mean +/- SD) when compared to nitrogen-oxygen (2.6 +/- 1.1 and 5.8 +/- 1.4 cm H2O [middle dot] s-1 [middle dot] l-1, P < 0.01) and N2O-oxygen (2.9 +/- 0.8 and 7.0 +/- 1.9, P < 0.01). Pmax and Pmean did not differ before bronchoconstriction, regardless of the inspired gas mixture. During bronchoconstriction Pmax and Pmean both were significantly higher with xenon-oxygen (Pmax, 33.1 +/- 5.5 and Pmean, 11.9 +/- 1.6 cm H2O) when compared to N2O-oxygen (28.4 +/- 5.7 and 9.5 +/- 1.6 cm H2O, P < 0.01) and nitrogen-oxygen (28.0 +/- 4.4 and 10.6 +/- 1.3 cm H2O, P < 0.01).     

The effect of IPPV, with or without PEEP, on central venous pressure

Changes in central venous pressure (CVP) during intermittent positive pressure ventilation with a Bennett 7200 respirator were measured in 30 postoperative patients without hemodynamic abnormalities. The tidal volume was changed from 300 ml to 900 ml and the PEEP was changed from 0 cmH2O to 8 cmH2O, step by step, respectively. Mean airway pressure (Pmean), maximal airway pressure (Pmax), arterial blood pressure, and heart rate were measured simultaneously with the measurement of CVP. CVP increased linearly with increases in the tidal volume and PEEP. A linear correlation was seen between Pmean and CVP. The value of A was 7.5 +/- 6.2 cmH2O and that of B was 0.32 +/- 0.13 when the equation of the regression line was Y = A + BX, where X was Pmean and Y was CVP. The coefficient of correlation was 0.88 +/- 0.09 (n = 30, P less than 0.01). The value of CVP during intermittent positive pressure ventilation increased linearly at rate which was 32% of the increase in Pmean. The value of CVP was considered to be 7.5 +/- 6.2 cmH2O when Pmean was zero. There was no change in the arterial blood pressure and heart rate throughout the measurement. This suggests that increases in CVP might not reflect any accompanying hemodynamic change.     

Xenon inhalation increases airway pressure in ventilated patients

BACKGROUND: The inert gas xenon, known as an anaesthetic for nearly 50 years, is also used as a contrast agent during computerised tomography (CT)-scanning. As xenon has a higher density and viscosity than air, xenon inhalation may increase airway resistance. METHODS: In a retrospective study we investigated the effects of 33% xenon/67% oxygen on airway pressure and cardio-respiratory parameters in 37 long-term mechanically ventilated patients undergoing cerebral blood flow (rCBF) measurements by means of stable xenon-enhanced CT. RESULTS: Xenon administration caused a significant increase in peak airway pressure from 31.6+/-8.0 cm H2O to 42.7+/-16.9 cm H2O. This effect was reproducible, did not occur after reduction of inspiratory flow rate by 50% from 0.56+/-0.15 L x s(-1) to 0.28+/-0.08 L x s(-1), and vanished immediately after termination of xenon delivery. CONCLUSION: Due to the higher density and viscosity of this gas mixture, ventilation with xenon/oxygen produces a higher Reynolds' number than oxygen/air when given at the same flow rate. This means that during xenon ventilation the zone of transition from turbulent to laminar gas flow may be located more peripherally (in smaller airways) than during oxygen/air ventilation with a subsequent increase in airway resistance. Our results indicate that xenon inhalation may cause a clinically relevant increase of peak airway pressure in mechanically ventilated patients.     

Continuous Arterial PO(2) and PCO(2) Measurements in Swine during Nitrous Oxide and Xenon Elimination: Prevention of Diffusion Hypoxia

Background: During nitrous oxide (N2 O) elimination, arterial oxygen tension (PaO(2)) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination.

Methods: Nineteen anesthetized paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2 O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO(2) and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor.

Results: The PaO(2) decreased from 119 +/- 10 mmHg to 102 +/- 12 mmHg (mean +/- SD) during N2 O washout (P < 0.01) and from 116 +/- 9 mmHg to 110 +/- 8 mmHg during xenon elimination (P < 0.01), with a significant difference (P < 0.01) between baseline and minimum PaO(2) values (Delta PaO(2), 17 +/- 6 mmHg during N2 O washout and 6 +/- 3 mmHg during xenon washout). The PaCO(2) value also decreased (from 39.3 +/- 6.3 mmHg to 37.6 +/- 5.8 mmHg) during N2 O washout (P < 0.01) and during xenon elimination (from 35.4 +/- 1.6 mmHg to 34.9 +/- 1.6 mmHg; P < 0.01). The Delta PaCO(2) was 1.7 +/- 0.9 mmHg in the N2 O group and 0.5 +/- 0.3 mmHg in the xenon group (P < 0.01).     

Continuous arterial P(O2) and P(CO2) measurements in swine during nitrous oxide and xenon elimination: prevention of diffusion hypoxia

BACKGROUND: During nitrous oxide (N2O) elimination, arterial oxygen tension (PaO2) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination. METHODS: Nineteen anesthetized and paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO2 and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor. RESULTS: The PaO2 decreased from 119+/-10 mm Hg to 102+/-12 mm Hg (mean+/-SD) during N2O washout (P<0.01) and from 116+/-9 mm Hg to 110+/-8 mm Hg during xenon elimination (P<0.01), with a significant difference (P<0.01) between baseline and minimum PaO2 values (deltaPaO2, 17+/-6 mm Hg during N2O washout and 6+/-3 mm Hg during xenon washout). The PaCO2 value also decreased (from 39.3+/-6.3 mm Hg to 37.6+/-5.8 mm Hg) during N2O washout (P<0.01) and during xenon elimination (from 35.4+/-1.6 mm Hg to 34.9+/-1.6 mm Hg; P< 0.01). The deltaPaCO2 was 1.7+/-0.9 mm Hg in the N2O group and 0.5+/-0.3 mm Hg in the xenon group (P<0.01). CONCLUSION: Diffusive hypoxia is unlikely to occur during recovery from xenon anesthesia, probably because of the low blood solubility of this gas.     

Efficacy of anticholinergic and beta-adrenergic agonist treatment of maximal cholinergic bronchospasm in tracheally intubated rabbits.

Cholinergically induced bronchoconstriction is thought to be a major cause of bronchospasm during anesthesia. We used tracheally intubated rabbits (4-mm endotracheal tube) stimulated with methacholine to assess the efficacy of beta-adrenergic agonist and anticholinergic treatment in reversing the increases in respiratory system resistance. Four groups were compared: (a) inhaled metaproterenol, 20 puffs via metered dose inhaler (0.65 mg/puff); (b) inhaled ipratropium bromide, 20 puffs from a metered dose inhaler (18 micrograms/puff); (c) 2 mg of intravenous atropine; and (d) no treatment after methacholine challenge as a control group. Methacholine increased respiratory system resistance from 0.041 +/- 0.001 (mean +/- SEM) to 0.098 +/- 0.006 cm H2O.mL-1.s-1 (P < 0.001). Whereas beta-adrenergic agonist treatment was ineffective in ameliorating bronchoconstriction, inhaled ipratropium bromide and atropine were highly effective, causing an 86%-88% reversal in the methacholine-induced increase in respiratory system resistance. Both these agents were also effective in improving dynamic compliance. We conclude that inhaled ipratropium bromide is effective in treating cholinergic bronchospasm even when administered via a small endotracheal tube and that the beta-adrenergic agonist metaproterenol is ineffective in rabbits in the face of maximal cholinergic stimulation.     

Collapsibility of the Upper Airway during Anesthesia with Isoflurane

Background: The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition.

Methods: To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures.

Results: The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r2 = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H2O; at 0.4% it decreased to -0.2 +/- 3.6 cm H2O (P < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H2O (P < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth.     

Mechanisms of Bronchoprotection by Anesthetic Induction Agents: Propofol versus Ketamine

Background: Propofol and ketamine have been purported to decrease bronchoconstriction during induction of anesthesia and intubation. Whether they act on airway smooth muscle or through neural reflexes has not been determined. We compared propofol and ketamine to attenuate the direct activation of airway smooth muscle by methacholine and limit neurally mediated bronchoconstriction (vagal nerve stimulation).

Methods: After approval from the institutional review board, eight sleep were anesthetized with pentobarbital, paralyzed, and ventilated. After left thoracotomy, the bronchial artery was cannulated and perfused. In random order, 5 mg/ml concentrations of propofol, ketamine, and thiopental were infused into the bronchial artery at rates of 0.06, 0.20, and 0.60 ml/min. After 10 min, airway resistance was measured before and after vagal nerve stimulation and methacholine given via the bronchial artery. Data were expressed as a percent of baseline response before infusion of drug and analyzed by analysis of variance with significance set at P Results: Systemic blood pressure was not affected by any of the drugs (P > 0.46). Baseline airway resistance was not different among the three agents (P = 0.56) or by dose (P = 0.96). Infusion of propofol and ketamine into the bronchial artery caused a dose-dependent attenuation of the vagal nerve stimulation-induced bronchoconstriction to 26 +/- 11% and 8 +/- 2% of maximum, respectively (P < 0.0001). In addition, propofol caused a significant decrease in the methacholine-induced bronchoconstriction to 43 +/- 27% of maximum at the highest concentration (P = 0.05).     

Mechanical versus manual ventilation via a face mask during the induction of anesthesia: a prospective, randomized, crossover study

One approach to make ventilation safer in an unprotected airway has been to limit tidal volumes; another one might be to limit peak airway pressure, although it is unknown whether adequate tidal volumes can be delivered. Accordingly, the purpose of this study was to evaluate the quality of automatic pressure-controlled ventilation versus manual circle system face-mask ventilation regarding ventilatory variables in an unprotected airway. We studied 41 adults (ASA status I-II) in a prospective, randomized, crossover design with both devices during the induction of anesthesia. Respiratory variables were measured with a pulmonary monitor (CP-100). Pressure-controlled mask ventilation versus circle system ventilation resulted in lower (mean +/- SD) peak airway pressures (10.6 +/- 1.5 cm H(2)O versus 14.4 +/- 2.4 cm H(2)O; P < 0.001), delta airway pressures (8.5 +/- 1.5 cm H(2)O versus 11.9 +/- 2.3 cm H(2)O; P < 0.001), expiratory tidal volume (650 +/- 100 mL versus 680 +/- 100 mL; P = 0.001), minute ventilation (10.4 +/- 1.8 L/min versus 11.6 +/- 1.8 L/min; P < 0.001), and peak inspiratory flow rates (0.81 +/- 0.06 L/s versus 1.06 +/- 0.26 L/s; P < 0.001) but higher inspiratory time fraction (48% +/- 0.8% versus 33% +/- 7.7%; P < 0.001) and end-tidal carbon dioxide (34 +/- 3 mm Hg versus 33 +/- 4 mm Hg; not significant). We conclude that in this model of apneic patients with an unprotected airway, pressure-controlled ventilation resulted in reduced inspiratory peak flow rates and peak airway pressures when compared with circle system ventilation, thus providing an additional patient safety effect during mask ventilation. IMPLICATIONS: In this model of apneic patients with an unprotected airway, pressure-controlled ventilation resulted in reduced inspiratory peak flow rates and lower peak airway pressures when compared with circle system ventilation, thus providing an additional patient safety effect during face-mask ventilation.     

Effects of the beach chair position, positive end-expiratory pressure, and pneumoperitoneum on respiratory function in morbidly obese patients during anesthesia and paralysis

BACKGROUND: The authors studied the effects of the beach chair (BC) position, 10 cm H2O positive end-expiratory pressure (PEEP), and pneumoperitoneum on respiratory function in morbidly obese patients undergoing laparoscopic gastric banding. METHODS: The authors studied 20 patients (body mass index 42 +/- 5 kg/m2) during the supine and BC positions, before and after pneumoperitoneum was instituted (13.6 +/- 1.2 mmHg). PEEP was applied during each combination of position and pneumoperitoneum. The authors measured elastance (E,rs) of the respiratory system, end-expiratory lung volume (helium technique), and arterial oxygen tension. Pressure-volume curves were also taken (occlusion technique). Patients were paralyzed during total intravenous anesthesia. Tidal volume (10.5 +/- 1 ml/kg ideal body weight) and respiratory rate (11 +/- 1 breaths/min) were kept constant throughout. RESULTS: In the supine position, respiratory function was abnormal: E,rs was 21.71 +/- 5.26 cm H2O/l, and end-expiratory lung volume was 0.46 +/- 0.1 l. Both the BC position and PEEP improved E,rs (P < 0.01). End-expiratory lung volume almost doubled (0.83 +/- 0.3 and 0.85 +/- 0.3 l, BC and PEEP, respectively; P < 0.01 vs. supine zero end-expiratory pressure), with no evidence of lung recruitment (0.04 +/- 0.1 l in the supine and 0.07 +/- 0.2 in the BC position). PEEP was associated with higher airway pressures than the BC position (22.1 +/- 2.01 vs. 13.8 +/- 1.8 cm H2O; P < 0.01). Pneumoperitoneum further worsened E,rs (31.59 +/- 6.73; P < 0.01) and end-expiratory lung volume (0.35 +/- 0.1 l; P < 0.01). Changes of lung volume correlated with changes of oxygenation (linear regression, R2 = 0.524, P < 0.001) so that during pneumoperitoneum, only the combination of the BC position and PEEP improved oxygenation. CONCLUSIONS: The BC position and PEEP counteracted the major derangements of respiratory function produced by anesthesia and paralysis. During pneumoperitoneum, only the combination of the two maneuvers improved oxygenation.     

Minimum Alveolar Concentration-Awake of Xenon Alone and in Combination with Isoflurane or Sevoflurane

Background: The minimum alveolar concentration (MAC)-awake is a traditional index of hypnotic potency of an inhalational anesthetic. The MAC-awake of xenon, an inert gas with anesthetic properties (MAC = 71%), has not been determined. It is also unknown how xenon interacts with isoflurane or sevoflurane on the MAC-awake.

Methods: In the first part of the study, 90 female patients received xenon, nitrous oxide (N2O), isoflurane, or sevoflurane supplemented with epidural anesthesia (n = 36 for xenon and n = 18 per group for other anesthetics). In the second part, 72 additional patients received either xenon or N2O combined with the 0.5 times MAC-awake concentration of isoflurane or sevoflurane (0.2% and 0.3%, respectively, based on the results of the first part; n = 18 per group). During emergence, the concentration of an assigned anesthetic (xenon or N2O only in the second part) was decreased in 0.1 MAC decrements every 15 min from 0.8 MAC or from 70% in the case of N2O until the patient followed the command to either open her eyes or to squeeze and release the investigator's hand. The concentration midway between the value permitting the first response to command and that just preventing it was defined as the MAC-awake.

Results: The MAC-awake were as follows: xenon, 32.6 +/- 6.1% (mean +/- SD) or 0.46 +/- 0.09 MAC; N2O, 63.3 +/- 7.1% (0.61 +/- 0.07 MAC); isoflurane, 0.40 +/- 0.07% (0.35 +/- 0.06 MAC); and sevoflurane, 0.59 +/- 0.10% (0.35 +/- 0.06 MAC). Addition of the 0.5 MAC-awake concentrations of isoflurane and sevoflurane reduced the MAC-awake of xenon to 0.50 +/- 0.15 and 0.51 +/- 0.16 times its MAC-awake as a sole agent, but that of N2O to the values significantly greater than 0.5 times its MAC-awake as a sole agent (0.68 +/- 0.12 and 0.66 +/- 0.14 times MAC-awake;P < 0.01, analysis of variance and Dunnett's test).     

A comparison of the laryngeal mask airway ProSeal and the laryngeal tube airway in paralyzed anesthetized adult patients undergoing pressure-controlled ventilation

We compared the laryngeal mask airway ProSeal (PLMA) and the laryngeal tube airway (LTA), two new extraglottic airway devices, with respect to: 1) insertion success rates and times, 2) efficacy of seal, 3) ventilatory variables during pressure-controlled ventilation, 4) tidal volume in different head/neck positions, and 5) airway interventional requirements. One-hundred-twenty paralyzed anesthetized ASA physical status I and II adult patients were randomly allocated to the PLMA or LTA for airway management. A standardized anesthesia protocol was followed by two anesthesiologists experienced with both devices. The criteria for an effective airway included a minimal expired tidal volume of 6 mL/kg during pressure-controlled ventilation at 17 cm H(2)O with no oropharyngeal leak or gastric insufflation. First attempt success rates at achieving an effective airway were similar (PLMA: 85%; LTA: 87%), but after 3 attempts, success was more frequent for the PLMA (100% versus 92%, P = 0.02). Effective airway time was similar. Oropharyngeal leak pressure was larger for PLMA at 50% maximal recommended cuff volume (29 +/- 7 versus 21 +/- 6 cm H(2)O, P < 0.0001), but was similar at the maximal recommended cuff volume (33 +/- 7 versus 31 +/- 8 cm H(2)O). Tidal volumes (614 +/- 173 versus 456 +/- 207 mL, P < 0.0001) were larger and ETCO(2) (33 +/- 9 versus 40 +/- 11 mm Hg, P = 0.0001) lower for the PLMA. The number of airway interventions was significantly less frequent for the PLMA. Airway obstruction was more common with the LTA. When comparing mean tidal volumes in different head/neck positions, the quality of airway was unchanged in 56 of 60 patients (93%) with the PLMA and 42 of 55 (76%) with the LTA (P = 0.01). The PLMA offers advantages over the LTA in most technical aspects of airway management in paralyzed patients undergoing pressure-controlled ventilation. IMPLICATIONS: The laryngeal mask airway ProSeal offers advantages over the laryngeal tube airway in most technical aspects of airway management in paralyzed patients undergoing pressure-controlled ventilation.     

Constant positive airway pressure reduces hypoventilation induced by inhalation anesthesia

STUDY OBJECTIVE: To discover if reducing respiratory system impedance would increase tidal volume and improve ventilation during inhalation anesthesia. DESIGN: Prospective, randomized cross-over study. SUBJECTS: Nine ASA physical status I and II adult female oncology patients undergoing breast operations with or without lymph node dissection and general anesthesia while breathing spontaneously. INTERVENTIONS AND MEASUREMENTS: Patients underwent alternating trials of constant positive airway pressure, with or without pressure support. Constant positive airway pressure and pressure support were titrated to maximize respiratory system compliance and equal inspiratory pressure gradient across tracheal tube, respectively. Variables reflecting cardiovascular function, pulmonary mechanics and lung gas exchange, and respired gases and isoflurane concentrations were measured. MAIN RESULTS: End-tidal concentration of isoflurane (1.3 +/- 0.2%), Fio(2) (0.43 +/- 0.09 ), and CO(2) elimination (209 +/- 42 mL min(-1)) was unchanged throughout study in patients aged 63 +/- 12 years, weighing 72 +/- 12 kg. Constant positive airway pressure (12 +/- 2 cm H(2)O) increased respiratory system compliance from 52 +/- 8 to 80 +/- 9 mL cm H(2)O(-1) (P < .001), tidal volume from 156 +/- 32 to 325 +/- 52 mL (P < .001), and minute ventilation from 4.37 +/- 0.86 to 6.18 +/- 0.92 L min(-1) (P < .001). Respiratory rate decreased from 29 +/- 7 to 19 +/- 2 min(-1) (P < .001), Paco(2) decreased from 54 +/- 8 to 44 +/- 6 mm Hg (P < .001), and Pao(2) increased from 137 +/- 37 to 160 +/- 64 mm Hg (P < .001). Pressure support (3.1 +/- 0.3 cm H(2)O) did not alter ventilation or gas exchange. CONCLUSION: We conclude that constant positive airway pressure titrated to optimal respiratory system compliance will increase efficiency of inspiratory muscles and improve ventilation. Constant positive airway pressure facilitates a pattern of breathing that minimizes some of the adverse pulmonary effects of inhalation anesthesia.     

Mechanisms of bronchoprotection by anesthetic induction agents: propofol versus ketamine

BACKGROUND: Propofol and ketamine have been purported to decrease bronchoconstriction during induction of anesthesia and intubation. Whether they act on airway smooth muscle or through neural reflexes has not been determined. We compared propofol and ketamine to attenuate the direct activation of airway smooth muscle by methacholine and limit neurally mediated bronchoconstriction (vagal nerve stimulation). METHODS: After approval from the institutional review board, eight sheep were anesthetized with pentobarbital, paralyzed, and ventilated. After left thoracotomy, the bronchial artery was cannulated and perfused. In random order, 5 mg/ml concentrations of propofol, ketamine, and thiopental were infused into the bronchial artery at rates of 0.06, 0.20, and 0.60 ml/min. After 10 min, airway resistance was measured before and after vagal nerve stimulation and methacholine given via the bronchial artery. Data were expressed as a percent of baseline response before infusion of drug and analyzed by analysis of variance with significance set at P< or =0.05. RESULTS: Systemic blood pressure was not affected by any of the drugs (P>0.46). Baseline airway resistance was not different among the three agents (P = 0.56) or by dose (P = 0.96). Infusion of propofol and ketamine into the bronchial artery caused a dose-dependent attenuation of the vagal nerve stimulation-induced bronchoconstriction to 26+/-11% and 8+/-2% of maximum, respectively (P<0.0001). In addition, propofol caused a significant decrease in the methacholine-induced bronchoconstriction to 43+/-27% of maximum at the highest concentration (P = 0.05) CONCLUSIONS: The local bronchoprotective effects of ketamine and propofol on airways is through neurally mediated mechanisms. Although the direct effects on airway smooth muscle occur at high concentrations, these are unlikely to be of primary clinical relevance.     

Positive end-expiratory pressure during induction of general anesthesia increases duration of nonhypoxic apnea in morbidly obese patients

Positive end-expiratory pressure (PEEP) applied during induction of anesthesia prevents atelectasis formation and increases the duration of nonhypoxic apnea in nonobese patients. PEEP also prevents atelectasis formation in morbidly obese patients. Because morbidly obese patients have difficult airway management more often and because arterial desaturation develops rapidly, we studied the clinical benefit of PEEP applied during anesthesia induction. Thirty morbidly obese patients were randomly allocated to one of two groups. In the PEEP group, patients breathed 100% O(2) through a continuous positive airway pressure device (10 cm H(2)O) for 5 min. After induction of anesthesia, they were mechanically ventilated with PEEP (10 cm H(2)O) for another 5 min until tracheal intubation. In the control group, the sequence was the same but without any continuous positive airway pressure or PEEP. We measured apnea duration until Spo(2) reached 90% and we performed arterial blood gases analyses just before apnea and at 92% Spo(2). Nonhypoxic apnea duration was longer in the PEEP group compared with the control group (188 +/- 46 versus 127 +/- 43 s; P = 0.002). Pao(2) was higher before apnea in the PEEP group (P = 0.038). Application of positive airway pressure during induction of general anesthesia in morbidly obese patients increases nonhypoxic apnea duration by 50%.     

Minimum alveolar concentration-awake of Xenon alone and in combination with isoflurane or sevoflurane

BACKGROUND: The minimum alveolar concentration (MAC)-awake is a traditional index of hypnotic potency of an inhalational anesthetic. The MAC-awake of xenon, an inert gas with anesthetic properties (MAC = 71%), has not been determined. It is also unknown how xenon interacts with isoflurane or sevoflurane on the MAC-awake. METHODS: In the first part of the study, 90 female patients received xenon, nitrous oxide (N2O), isoflurane, or sevoflurane supplemented with epidural anesthesia (n = 36 for xenon and n = 18 per group for other anesthetics). In the second part, 72 additional patients received either xenon or N2O combined with the 0.5 times MAC-awake concentration of isoflurane or sevoflurane (0.2% and 0.3%, respectively, based on the results of the first part; n = 18 per group). During emergence, the concentration of an assigned anesthetic (xenon or N2O only in the second part) was decreased in 0. 1 MAC decrements every 15 min from 0.8 MAC or from 70% in the case of N2O until the patient followed the command to either open her eyes or to squeeze and release the investigator's hand. The concentration midway between the value permitting the first response to command and that just preventing it was defined as the MAC-awake. RESULTS: The MAC-awake were as follows: xenon, 32.6 +/- 6.1% (mean +/- SD) or 0.46 +/- 0.09 MAC; N2O, 63.3 +/- 7.1% (0.61 +/- 0.07 MAC); isoflurane, 0.40 +/- 0.07% (0.35 +/- 0.06 MAC); and sevoflurane, 0.59 +/- 0.10% (0.35 +/- 0.06 MAC). Addition of the 0.5 MAC-awake concentrations of isoflurane and sevoflurane reduced the MAC-awake of xenon to 0.50 +/- 0.15 and 0.51 +/- 0.16 times its MAC-awake as a sole agent, but that of N2O to the values significantly greater than 0.5 times its MAC-awake as a sole agent (0.68 +/- 0.12 and 0.66 +/- 0.14 times MAC-awake; P < 0.01, analysis of variance and Dunnett's test). CONCLUSIONS: The MAC-awake of xenon is 33% or 0.46 times its MAC. In terms of the MAC-fraction, this is smaller than that for N2O but greater than those for isoflurane and sevoflurane. Unlike N2O, xenon interacts additively with isoflurane and sevoflurane on MAC-awake.     

Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis.

BACKGROUND: Morbidly obese patients, during anesthesia and paralysis, experience more severe impairment of respiratory mechanics and gas exchange than normal subjects. The authors hypothesized that positive end-expiratory pressure (PEEP) induces different responses in normal subjects (n = 9; body mass index < 25 kg/m2) versus obese patients (n = 9; body mass index > 40 kg/m2). METHODS: The authors measured lung volumes (helium technique), the elastances of the respiratory system, lung, and chest wall, the pressure-volume curves (occlusion technique and esophageal balloon), and the intraabdominal pressure (intrabladder catheter) at PEEP 0 and 10 cm H2O in paralyzed, anesthetized postoperative patients in the intensive care unit or operating room after abdominal surgery. RESULTS: At PEEP 0 cm H2O, obese patients had lower lung volume (0.59 +/- 0.17 vs. 2.15 +/- 0.58 l [mean +/- SD], P < 0.01); higher elastances of the respiratory system (26.8 +/- 4.2 vs. 16.4 +/- 3.6 cm H2O/l, P < 0.01), lung (17.4 +/- 4.5 vs. 10.3 +/- 3.2 cm H2O/l, P < 0.01), and chest wall (9.4 +/- 3.0 vs. 6.1 +/- 1.4 cm H2O/l, P < 0.01); and higher intraabdominal pressure (18.8 +/-7.8 vs. 9.0 +/- 2.4 cm H2O, P < 0.01) than normal subjects. The arterial oxygen tension was significantly lower (110 +/- 30 vs. 218 +/- 47 mmHg, P < 0.01; inspired oxygen fraction = 50%), and the arterial carbon dioxide tension significantly higher (37.8 +/- 6.8 vs. 28.4 +/- 3.1, P < 0.01) in obese patients compared with normal subjects. Increasing PEEP to 10 cm H2O significantly reduced elastances of the respiratory system, lung, and chest wall in obese patients but not in normal subjects. The pressure-volume curves were shifted upward and to the left in obese patients but were unchanged in normal subjects. The oxygenation increased with PEEP in obese patients (from 110 +/-30 to 130 +/- 28 mmHg, P < 0.01) but was unchanged in normal subjects. The oxygenation changes were significantly correlated with alveolar recruitment (r = 0.81, P < 0.01). CONCLUSIONS: During anesthesia and paralysis, PEEP improves respiratory function in morbidly obese patients but not in normal subjects.     

Cardiorespiratory effects of automatic tube compensation during airway pressure release ventilation in patients with acute lung injury

BACKGROUND: Spontaneous breaths during airway pressure release ventilation (APRV) have to overcome the resistance of the artificial airway. Automatic tube compensation provides ventilatory assistance by increasing airway pressure during inspiration and lowering airway pressure during expiration, thereby compensating for resistance of the artificial airway. The authors studied if APRV with automatic tube compensation reduces the inspiratory effort without compromising cardiovascular function, end-expiratory lung volume, and gas exchange in patients with acute lung injury. METHODS: Fourteen patients with acute lung injury were breathing spontaneously during APRV with or without automatic tube compensation in random order. Airway pressure, esophageal and abdominal pressure, and gas flow were continuously measured, and tracheal pressure was estimated. Transdiaphragmatic pressure time product was calculated. End-expiratory lung volume was determined by nitrogen washout. The validity of the tracheal pressure calculation was investigated in seven healthy ventilated pigs. RESULTS: Automatic tube compensation during APRV increased airway pressure amplitude from 7.7+/-1.9 to 11.3+/-3.1 cm H2O (mean +/- SD; P < 0.05) while decreasing trans-diaphragmatic pressure time product from 45+/-27 to 27+/-15 cm H2O x s(-1) x min(-1) (P < 0.05), whereas tracheal pressure amplitude remained essentially unchanged (10.3+/-3.5 vs. 10.1+/-3.5 cm H2O). Minute ventilation increased from 10.4+/-1.6 to 11.4+/-1.5 l/min (P < 0.001), decreasing arterial carbon dioxide tension from 52+/-9 to 47+/-6 mmHg (P < 0.05) without affecting arterial blood oxygenation or cardiovascular function. End-expiratory lung volume increased from 2,806+/-991 to 3,009+/-994 ml (P < 0.05). Analysis of tracheal pressure-time curves indicated nonideal regulation of the dynamic pressure support during automatic tube compensation as provided by a standard ventilator. CONCLUSION: In the studied patients with acute lung injury, automatic tube compensation markedly unloaded the inspiratory muscles and increased alveolar ventilation without compromising cardiorespiratory function and end-expiratory lung volume.     

Upper airway collapsibility in anesthetized children

We sought to establish the feasibility of measuring upper airway narrowing in spontaneously breathing, anesthetized children using dynamic application of negative airway pressure. A secondary aim was to compare differences in upper airway collapsibility after the administration of sevoflurane or halothane. Subjects were randomized to either drug for inhaled anesthetic induction. Each was adjusted to their 1 MAC value (0.9% for halothane and 2.5% for sevoflurane) and a blinded anesthesia provider held the facemask without performing manual airway opening maneuvers but with inclusion of an oral airway device. Inspiratory flows were measured during partial upper airway obstruction created by an adjustable negative pressure-generating vacuum motor inserted into the anesthesia circuit. Critical closing pressure of the pharynx (Pcrit) was obtained by plotting the peak inspiratory flow of the obstructed breaths against the corresponding negative pressure in the facemask and extrapolating to zero airflow using linear correlation. Fourteen children were enrolled, seven in each anesthetic group. Two children in the halothane group did not develop flow-limited airway obstruction despite negative pressures as low as -9 cm H2O. Pcrit for sevoflurane ranged from -6.7 to -11.6 (mean +/- sd, -9.8 +/- 1.9) cm H2O. Pcrit for halothane ranged from -8.1 to -33 (mean +/- sd, -19.4 +/- 9.3) cm H2O (sevoflurane versus halothane, P = 0.048). We conclude that when using dynamic application of negative airway pressure, halothane appears to cause less upper airway obstruction than sevoflurane at equipotent concentrations.     

Diffusion of Xenon and Nitrous Oxide into the Bowel

Background: Nitrous oxide diffuses easily from blood into air filled spaces. Xenon is also a relatively insoluble gas, like nitrous oxide. Therefore, the authors measured xenon diffusion into obstructed bowel segments during xenon anesthesia and compared this with nitrous oxide and nitrogen diffusion.

Methods: Twenty-one pentobarbital-anesthetized pigs were randomly assigned to three groups to receive either xenon-oxygen, nitrous oxide-oxygen, or nitrogen-oxygen (75%-25%), respectively. In each animal, four bowel segments of 15-cm length were isolated. A pressure-measuring catheter was inserted into the lumen, and 30 ml of room air was injected into the segments. Anesthesia with the selected gas mixture was performed for 4 h. Pressure in the segments was measured continuously. The volume of gaseous bowel content was measured on completion of the study.

Results: The median volume of bowel gas in animals breathing nitrous oxide was 88.0 ml as compared with 39.0 ml with xenon anesthesia and 21.5 ml in the nitrogen-oxygen group. After 4 h of anesthesia, the intraluminal pressures in the nitrous oxide group were found to be significantly greater than in the control group and in the xenon group.