Canadian Journal of Anesthesia 50:67-70 (2003)
© Canadian Anesthesiologists' Society, 2003
Cardiothoracic Anesthesia, Respiration and Airway
The effect of isoflurane 0.6% on respiratory mechanics in anesthetized-paralyzed humans is not increased at concentrations of 0.9% and 1.2%
[L’effet de l’isoflurane à 0,6 % sur la mécanique respiratoire n’a pas augmenté chez l’humain anesthésie et paralysé à des concentrations de 0,9 % et 1,2 %]
Pedro Ruiz, MD, PhD and
Daniel Chartrand, MD, PhD
From the Department of Anesthesia, McGill University, Montreal, Quebec, Canada.
Address correspondence to: Dr. Pedro Ruiz, Department of Anesthesia, McGill University, Montreal General Hospital, Room D8-132, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada. Phone: 514-934-1934; E-mail: pedroruizmd{at}hotmail.com
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Abstract
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Purpose: To assess the dose-dependent effect of low concentrations of isoflurane on respiratory mechanics in normal subjects.
Methods: 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•kg-1 iv, the trachea was intubated and an esophageal balloon was placed optimally by the occlusion test. After introduction of N2O 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•kg-1, 10 breaths•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) = EVT(t) + RF(t) + K, where t is time, VT tidal volume from integration of F, and K an estimation of end-expiratory pressure. ANOVA was used for comparing the basal state with the three concentrations.
Results: E and R were statistically lower at 0.6, 0.9 and 1.2% compared to basal values for RS, L and W. Concentrations equal to or higher than 0.6% did not further change respiratory mechanics, except for EL1.2 compared to EL0.6, 12.37 ± 5.72 and 13.52 ± 5.64 cm H2O.L-1, respectively.
Conclusion: Isoflurane concentrations between 0.6–1.2% are not associated to a dose-dependent effect on respiratory mechanics.
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Introduction
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VOLATILE agents are potent bronchodilators and can be used in severe status asthmaticus. Considering the potentially therapeutic properties of those agents, we assessed the dose-dependent effect of three different concentrations of isoflurane on respiratory mechanics to define the lowest useful concentration for bronchodilation while limiting side effects.
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Methods
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After hospital Ethics Committee approval and patient informed consent, we studied 12 ASA I patients undergoing general anesthesia for lower abdominal or extremity surgery. None had previous evidence of respiratory disease and presented normal forced vital capacity and forced expiratory volume in one second preoperative values. No premedication was given and standard monitoring was used. Induction consisted of thiopental 5–7 mg•kg-1 iv and succinylcholine 1.0 mg•kg-1 iv. Anesthesia was maintained with isoflurane and a 1:1 N2O: O2 mixture. An esophageal balloon was inserted during spontaneous breathing and the esophageal pressure used for estimating pleural pressure. The patient was then paralyzed with vecuronium (0.08 mg•kg-1 iv) followed by intermittent doses according to neuromuscular monitoring. We studied the effects of 0.6, 0.9 and 1.2% isoflurane after the basal condition (no isoflurane). Data were recorded after obtaining the steady end-tidal concentration for each condition. Flow (F), and tracheal and esophageal pressures (Ptr and Pes) signals were sampled at 100 Hz and then fed into a 12-bit analogue digital converter (DT2801A, Data Translation) installed in a personal computer. Data were collected and analyzed using LABDAT and ANADAT software (RHT - InfoData USA Inc.). A 60–90 sec sample was obtained during mechanical ventilation using a tidal volume of 10 mL•kg-1, an I:E ratio of 1:2, and a respiratory rate of 10 cycles•min-1. Analysis of F, Ptr and Pes signals enabled us to estimate dynamic elastance (E) and resistance (R) of the total respiratory system (ERS, RRS), lungs (EL, RL) and chest wall (EW, RW). We estimated variables for chest wall and lung using Pes and transpulmonary pressure, obtained by subtracting Pes from Ptr. Ptr was corrected for tracheal tube resistance. We estimated respiratory system (RS), lung (L) and chest wall (W) dynamic elastance (E) and resistance (R) by P(t) = EVT(t) + RF(t) + K, where t is time, VT tidal volume from integration of F, and K an estimation of end-expiratory pressure. ANOVA test, Levene’s test for the H0 hypothesis, Bartlett’s test for homogeneity of variances and Bonferroni’s correction were used for statistical analysis. P < 0.05 was considered statistically significant.
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Results
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The Table
and Figures 1 and 2 describe the values of E and R (mean ± SD). Baseline ERS (ERS0) is statistically higher than ERS under 0.6, 0.9 and 1.2% isoflurane (ERS0.6, ERS0.9 and ERS1.2 respectively). Increasing isoflurane concentration showed no significant effect for ERS. Baseline EL was significantly higher than EL0.6, EL0.9 and EL1.2. Values for EL0.6 were higher than EL1.2, and EW0.9 was similar to EW1.2. Baseline EW was statistically higher than EW0.6, EW0.9 and EW1.2. Values of EW0.6, EW0.9 and EW1.2 were comparable.
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TABLE Mean ± SD values of total respiratory system elastance (ERS), lung elastance (EL), chest wall elastance (EW), total respiratory system resistance (RRS), lung resistance (RL) and chest wall resistance (RW) at baseline, 0.6%, 0.9% and 1.2% conditions in cm H2O.L-1 cm H2O.L-1•sec-1, respectively
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FIGURE 1 Mean ± SD values of total respiratory system elastance (ERS), lung elastance (EL), chest wall elastance (EW) at baseline, 0.6%, 0.9% and 1.2% conditions in cm H2O.L-1.
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FIGURE 2 Mean ± SD values of total respiratory system resistance (RRS), lung resistance (RL) and chest wall resistance (RW) at baseline, 0.6%, 0.9% and 1.2% conditions in cm H2O.L-1•sec-1.
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Baseline RRS, RL and RW were significantly higher than those obtained under 0.6, 0.9 and 1.2% isoflurane, although no effect was showed for a higher concentration of isoflurane.
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Discussion
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As expected, isoflurane at 0.6% reduced RRS, RL and RW. Nonetheless, increasing isoflurane concentration to 0.9 and 1.2% had no further effect on these variables. Wu et al. observed no bronchodilation potentialization when a ß2-adrenergic agonist was administered simultaneously to 1.3% isoflurane.1 The mechanisms controlling bronchomotor tonus could present a "ceiling effect", or once a maximum effect on smooth muscle has been reached, it does not change regardless of the association of pathway-acting drugs. Rooke et al. compared the effects of 1.1 MAC of halothane, sevoflurane and isoflurane on RRS to thiopental 0.25 mg•kg-1•min-1 iv infusion.2 While RRS increased under thiopental, equipotent doses of halothane and sevoflurane reduced RRS by 31% and 42%, respectively. Isoflurane (1.1 MAC) reduced RRS by 25%, similar to our results. We observed a decrease of ERS after isoflurane, although concentrations above 0.6% did not cause further decrease of ERS. Others, using 0.5 and 0.6% isoflurane also observed a significant decrease of ERS compared to baseline.3 Similarly, Canet et al. observed that increasing the dose of isoflurane from 1.2 to 2.0 MAC does not produce a significant effect on respiratory mechanics.4 We observed that 0.6% isoflurane also reduced EL but there was no difference between 0.6 and 0.9% isoflurane. Compared to 0.6% however, EL at 1.2% is statistically lower. Although the lower airway resistance during 1.2% isoflurane was not enough to change ERS statistically it might be sufficient to change EL. Barnas et al. studied EL during mechanical ventilation at 0.5% and 0.6% isoflurane, reporting a similar effect on pulmonary elastance.3 Few studies draw attention to the effects of inhalation anesthesia on the elastic properties of the chest wall, probably due to technical difficulties associated to accurate recording of pleural pressure. Our EW values are similar to those reported by others using 1–2% isoflurane.3,5,6 The chest wall anatomical configuration is important for its elastic properties, and concentrations above 0.6% do not seem to affect its structure enough to change it.
Inhalation agents can have at least two potentially antagonistic effects over airway resistance. First, they can relax airway smooth muscles either by inhibiting the parasympathetic neural pathway or by a direct effect on muscle fibres and receptors.7,8 But volatile agents can also change thoracic configuration reducing functional residual capacity (FRC). As airway resistance increases with the decrease in lung volume, decreasing FRC is followed by an increase in airway resistance. Thus, the final effect of volatile agents will depend on the interaction between both factors. However, the relationship between pulmonary volume and respiratory resistance has been stated to depend on airway muscle tonus: the tonus relaxation decreases the dependence of the resistance regarding lung volume.9 We may say that by relaxing smooth muscle tonus, volatile agents make the changes of FRC play a smaller role on pulmonary resistance. Anticipated changes of airway resistance associated with anesthesia are still complicated by another factor. Although the majority of in vivo studies assessing the airway muscle tonus use lung resistance as an index of the airway diameter, the parameter is a sum of two resistances. The first depends on airflow resistive properties and the other is associated to the elastic properties of the pulmonary tissue. Like the first resistance, tissue resistance also depends on lung volume and on bronchial tonus.10 However, differently from the first, tissue resistance decreases as lung volume decreases, putting another variable in the equation describing the respiratory resistance behaviour. In conclusion, we observed that the effect of isoflurane 0.6% on the resistance and elastance of the respiratory system and its subcomponents was not increased with concentrations of 0.9% and 1.2%.
Revision received October 18, 2002.
Accepted for publication May 23, 2002.
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References
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1 Wu RSC, Wu KC, Wong TKM, et al. Isoflurane anesthesia does not add to the bronchodilating effect of a ß2-adrenergic agonist after tracheal intubation. Anesth Analg 1996; 83: 238–41.[Abstract]
2 Rooke GA, Choi JH, Bishop MJ. The effect of isoflurane, halothane, sevoflurane, and thiopental/nitrous oxide on respiratory system resistance after tracheal intubation. Anesthesiology 1997; 86: 1294–9.[Medline]
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5 Dechman GS, Chartrand DA, Ruiz-Neto PP, Bates JHT. The effect of changing end-expiratory pressure on respiratory system mechanics in open- and closed-chest anesthetized, paralyzed patients. Anesth Analg 1995; 81, 279–86.[Abstract]
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8 Warner DO, Vettermann J, Brichant JF, Rehder K. Direct and neurally mediated effects of halothane on pulmonary resistance in vivo. Anesthesiology 1990; 72: 1057–63.[Medline]
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Abstract
Introduction
