Letters to the Editor The Genioglossus Muscle Belongs Not to InsGiratorv But to Expiratory’ MuscL? To the Editor: Respiratory muscles are basically divided into inspiratory and expiratory muscles. Respiratory muscles that discharge in the inspiratory phase belong to the inspiratory group, whereas those in the expiratory phase belong to the expiratory group. The most representative inspiratory muscle is the diaphragm, excitation of which gives a reference of inspiratory phase. Under normal conditions, most of the expiratory muscles are inactive in the expiratory phase. The silent period of the diaphragm usually serves as the expiratory phase. Ochiai et al. (1)recently reported that among the inspiratory muscles in kittens, the genioglossus, which maintains upper airway patency during inspiration, was most vulnerable to halothane anesthesia. In their article, Figure 1 shows a typical recording of an electromyogram of three inspiratory muscles (diaphragm, intercostal, and genioglossus muscles) during 1%halothane anesthesia in a kitten as a control. If we carefully evaluate each tracing of the figure, we will easily discover that the genioglossus muscle discharged completely out of phase compared with the other inspiratory muscles, the diaphragm and intercostal muscles. This means that this muscle, studied in this experiment, did not belong to the inspiratory muscles. Based on the aforementioned definition, it should belong not to the inspiratory but to the expiratory muscles. In other words, it was not the genioglossus muscle. The genioglossus muscle recorded in adult cats actually discharged in phase with other inspiratory muscle discharges (2). It must be very difficult to record the activity of a tiny muscle such as the genioglossus in kittens. Probably, expiratory muscle activity was unexpectedly recorded on some occasions. It could be said that some expiratory muscles in kittens are vulnerable to halothane anesthesia. Yoshihiro Ohta, MD, PhD Osamu Kemmotsu, MD, FhD, FCCM Department of Anesthesiology and Intensive Care H o h i d o University School of Medicine Kitaku, N15 W7 Sapporo 060, Japan
References 1. Ochiai RO, Guthrie RD, Motoyama EK. Differential sensitivity to halothane anesthesia of the genioglossus, intercostals, and diaphragm in kittens. Anesth Analg 1992;74:33&24. 2. Ochiai RO, Guthrie RD, Motoyama EK. Effects of varying concentrations of halothane on the activity of the genioglossus, intercostals, and dia-
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phragm in cats: an electromyographic study. Anesthesiology 1989;70: 812-6.
Intravenous HalothaneQuestions Remain To the Editor: Drs. Kawamoto, Suzuki, and Takasaki (1) presented a study of the pulmonary and circulatory effects of intravenous (IV) halothane in dogs. Previous studies have suggested that halothane-induced pulmonary edema is accompanied by structural damage to the pulmonary microvasculature, resulting in increased capillary permeability. In permeability edema, the oncotic pressure gradient is substantially decreased. Therefore, the most important determinant for the development of pulmonary edema is the pressure gradient across the pulmonary microcirculation. Indeed, the authors report increased mean pulmonary artery pressure and pulmonary vascular resistance in the injured lungs, with no significant change in pulmonary arterial occlusion (wedge) pressure or central venous pressure. It has been noted in numerous studies that an elevated capillary pressure can be present despite a normal or subnormal wedge pressure (2-6). The increased lung water measured after IV halothane could have resulted from either hydrostatic or permeability changes or from a combination of both factors. The contribution of the hydrostatic capillary pressure to the development of pulmonary edema and increased extravascular lung water cannot be determined by this study. Moreover, histologic studies were not a part of this study. Therefore, the conclusion reached by the authors that “pulmonary edema induced by IV liquid halothane was due to direct pulmonary vascular damage“ is not substantiated. Second, the authors state that prostaglandin El resulted in myocardial damage. It is unclear how this damage was determined. Although LV dpldt and SV decreased early in the PGE,-treated group, which is consistent with depression of myocardial contractility, no evidence was presented to substantiate a claim of myocardial “damage.” Finally, as the authors state in their study, it should be noted that the dose of IV halothane used in this study does indeed represent a massive overdose of halothane compared with customary clinical doses. The injection of 7.5 mmol represents approximately 170 mL of 100% halothane vapor, or about one tidal volume of the dogs studied. The 7% end-tidal concentration indicates that a large volume of halothane was not eliminated during first pass through the lungs. Perhaps an investigation of the cardiopulmonary effects of a smaller IV dose or dilute infusion, with a more
01992 by the International Anesthesia Research Society
ANESTH ANALG 1992;75107&5
physiologic end-tidal concentration, might have intriguing implications for the clinical setting. David A. Cross, MD Doris K. Cope, MD Departments of Anesthesiology and Physiology The University of South Alabama Medical Center Mobile, AL 36617
References 1. Kawamoto M, Suzuki N, Takasaki M. Acute pulmonary edema after intravenous liquid halothane in dogs. Anesth Analg 1992;74:747-2. 2. Cope DK, Allison RC, Parmentier JL, et al. Measurement of effective pulmonary capillary pressure using pulmonary artery pressure profiles after occlusion. Crit Care Med 1986;14:1&22. 3. DOrio V, Hallux J, Rodriquez L, et al. Effects of Escherichiu endotoxin on pulmonary vascular resistance in intact dogs. Crit Care Med 1986;14:80210. 4. Cope DK, Allison RC, Dumond ME, et al. Changes in pulmonary capillary pressure following cardiac surgery. J Cardiothorac Anesth 1988;2:866-8. 5. Cope DK, Baisden CE, Fortier-Bensen RF. Circulatory effects of gravitation rotation in oleic add-induced lung injury (abstract). Anesthesiology 1991;75:A262. 6. Isago T, Fujioka K, Traber LD, et al. Derived pulmonary capillary pressure changes after smoke inhalation in sheep. Crit Care Med 1919; 191407-13.
Relocation of a Double-Lumen Tube During Patient Positioning To the Editor: It is well known that the position of a tracheal tube during anesthesia may be altered by surgical manipulation, patient coughing, or movement of the head, neck, or the entire patient (1-3). We wish to report a case of movement of a double-lumen tube (DLT) from the left to right mainstem bronchus during patient repositioning. A 61-yr-old man (ASA physical status III) was scheduled for open thoracotomy. Anesthesia was induced with intravenous propofol, and muscle relaxation was achieved with intravenous vecuronium. A 39F left-sided Broncho-Cath (Mallinckrodt)DLT was placed during laryngoscopy. Manual ventilation commenced, and compliance seemed reduced. Auscultation of the axillae revealed right-sided breath sounds when the endobronchial (left) tube was ventilated, and no breath sounds were heard when ventilation via the tracheal lumen was attempted. The DLT was withdrawn to the vocal cords and reintroduced. Ventilation appeared normal, and a "leak test" was performed (4). With the tracheal cuff inflated and the endobronchial cuff deflated, the test indicated successful isolation of each lung. No leak was detected across the endobronchial cuff, and it was therefore left deflated. Controlled mechanical ventilation was commenced, and the DLT was firmly tied in position with a long piece of gauze. With the anesthesiologist supporting the head, the patient was then turned 90" to the left lateral position and secured by evacuation of air from a large beanbag. Peak airway pressures were then noted to be approximately 40 cm H,O. Manual ventilation was begun while a flexible fiberoptic bronchoscope was quickly passed through the tracheal lumen. However, on exit from the distal lumen, it came to rest on the tracheal wall. Right mainstem intuba-
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tion by the endobronchial tube was diagnosed. Meanwhile, the surgeon had made rapid progress and requested deflation of the right lung at this time. Ventilation of the left lung was attempted but was impossible. The bronchoscope was then passed down the endobronchial (left) lumen and the DLT withdrawn slowly. When the carina came into view, the bronchoscope was advanced into the left mainstem bronchus. The DLT was then easily advanced into its correct position. The right lung was then deflated with ease, and surgery proceeded uneventfully. For the distal end of a DLT to migrate to the contralateral side, several factors need consideration. First, it is likely that the tip of the DLT was not positioned far into the left mainstem bronchus, Flexible bronchoscopy could have been used to optimize tube position before turning. Second, some movements of the head and neck are inevitable during a patient turn, allowing distal tube movement to occur, cephalad and then caudad. Double-lumen tube movement is always possible during turning of patients, and although it has been previoulsy suggested that deflation of the endobronchial cuff should occur to reduce the possibility of mucosal damage (5), relocation of a DLT to the contralateral side has not been recorded. This report, then, describes yet another consequence of movement of a tracheal tube during the turning of patients. Richard H. Riley, MD Ivan L. Marples, MD Department of Anaesthesia Royal Perth Hospital, Box X2213 GPO Perth, Western Australia 6002
References 1. Toung TJK, Grayson R, Saklad J, Wang H. Movement of the distal end of the endotracheal tube during flexion and extension of the neck. Anesth Analg 1985;64:103C4 2. Conrady PA, Goodman LR, Lainge F, Singer MM. Alteration of endotracheal tube position. Crit Care Med 1976;48-12. 3. Stone DJ, Gal TJ. Airway management. In: Miller RD, ed. Anesthesia. 3rd ed. New York Churchill Livingstone, 1990:1289. 4. Spragg RG, Benumof JL, Alfery DD. New methods for the performance of unilateral lung lavage. Anesthesiology 1982;57535-8. 5. Benumof JL, Alfery DD. Anesthesia for thoracic surgery. In: Miller RD, ed. Anesthesia. 3rd ed. New York: Churchill Livingston, 1990:1554.
Removal of a Tenacious Epidural Catheter To the Editor: Quite a lot has been written lately about removal of epidural catheters that seem to have become firmly lodged in patients' backs. So, I thought I would offer my words of wisdom on the subject. I'm sure all of us who perform many epidurals have at some time encountered varying degrees of difficulty in extracting epidural catheters. Of note in the recent literature is a case report by Drs. Sia-Kho and Kudlak in Anesthesia & Analgesia (l),advocating extreme flexion of the patient in the lateral decubitus position. This case report reemphasizes Dr. Blackshear's report (2) that more tension is needed to remove epidural catheters with patients sitting versus lying.
References 1. Ochiai RO, Guthrie RD, Motoyama EK. Differential sensitivity to halothane anesthesia of the genioglossus, intercostals, and diaphragm in kittens. Anesth Analg 1992;74:33&24. 2. Ochiai RO, Guthrie RD, Motoyama EK. Effects of varying concentrations of halothane on the activity of the genioglossus, intercostals, and dia-
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Anesth Analg 1992;75:1070-5
phragm in cats: an electromyographic study. Anesthesiology 1989;70: 812-6.
Intravenous HalothaneQuestions Remain To the Editor: Drs. Kawamoto, Suzuki, and Takasaki (1) presented a study of the pulmonary and circulatory effects of intravenous (IV) halothane in dogs. Previous studies have suggested that halothane-induced pulmonary edema is accompanied by structural damage to the pulmonary microvasculature, resulting in increased capillary permeability. In permeability edema, the oncotic pressure gradient is substantially decreased. Therefore, the most important determinant for the development of pulmonary edema is the pressure gradient across the pulmonary microcirculation. Indeed, the authors report increased mean pulmonary artery pressure and pulmonary vascular resistance in the injured lungs, with no significant change in pulmonary arterial occlusion (wedge) pressure or central venous pressure. It has been noted in numerous studies that an elevated capillary pressure can be present despite a normal or subnormal wedge pressure (2-6). The increased lung water measured after IV halothane could have resulted from either hydrostatic or permeability changes or from a combination of both factors. The contribution of the hydrostatic capillary pressure to the development of pulmonary edema and increased extravascular lung water cannot be determined by this study. Moreover, histologic studies were not a part of this study. Therefore, the conclusion reached by the authors that “pulmonary edema induced by IV liquid halothane was due to direct pulmonary vascular damage“ is not substantiated. Second, the authors state that prostaglandin El resulted in myocardial damage. It is unclear how this damage was determined. Although LV dpldt and SV decreased early in the PGE,-treated group, which is consistent with depression of myocardial contractility, no evidence was presented to substantiate a claim of myocardial “damage.” Finally, as the authors state in their study, it should be noted that the dose of IV halothane used in this study does indeed represent a massive overdose of halothane compared with customary clinical doses. The injection of 7.5 mmol represents approximately 170 mL of 100% halothane vapor, or about one tidal volume of the dogs studied. The 7% end-tidal concentration indicates that a large volume of halothane was not eliminated during first pass through the lungs. Perhaps an investigation of the cardiopulmonary effects of a smaller IV dose or dilute infusion, with a more
01992 by the International Anesthesia Research Society
ANESTH ANALG 1992;75107&5
physiologic end-tidal concentration, might have intriguing implications for the clinical setting. David A. Cross, MD Doris K. Cope, MD Departments of Anesthesiology and Physiology The University of South Alabama Medical Center Mobile, AL 36617
References 1. Kawamoto M, Suzuki N, Takasaki M. Acute pulmonary edema after intravenous liquid halothane in dogs. Anesth Analg 1992;74:747-2. 2. Cope DK, Allison RC, Parmentier JL, et al. Measurement of effective pulmonary capillary pressure using pulmonary artery pressure profiles after occlusion. Crit Care Med 1986;14:1&22. 3. DOrio V, Hallux J, Rodriquez L, et al. Effects of Escherichiu endotoxin on pulmonary vascular resistance in intact dogs. Crit Care Med 1986;14:80210. 4. Cope DK, Allison RC, Dumond ME, et al. Changes in pulmonary capillary pressure following cardiac surgery. J Cardiothorac Anesth 1988;2:866-8. 5. Cope DK, Baisden CE, Fortier-Bensen RF. Circulatory effects of gravitation rotation in oleic add-induced lung injury (abstract). Anesthesiology 1991;75:A262. 6. Isago T, Fujioka K, Traber LD, et al. Derived pulmonary capillary pressure changes after smoke inhalation in sheep. Crit Care Med 1919; 191407-13.
Relocation of a Double-Lumen Tube During Patient Positioning To the Editor: It is well known that the position of a tracheal tube during anesthesia may be altered by surgical manipulation, patient coughing, or movement of the head, neck, or the entire patient (1-3). We wish to report a case of movement of a double-lumen tube (DLT) from the left to right mainstem bronchus during patient repositioning. A 61-yr-old man (ASA physical status III) was scheduled for open thoracotomy. Anesthesia was induced with intravenous propofol, and muscle relaxation was achieved with intravenous vecuronium. A 39F left-sided Broncho-Cath (Mallinckrodt)DLT was placed during laryngoscopy. Manual ventilation commenced, and compliance seemed reduced. Auscultation of the axillae revealed right-sided breath sounds when the endobronchial (left) tube was ventilated, and no breath sounds were heard when ventilation via the tracheal lumen was attempted. The DLT was withdrawn to the vocal cords and reintroduced. Ventilation appeared normal, and a "leak test" was performed (4). With the tracheal cuff inflated and the endobronchial cuff deflated, the test indicated successful isolation of each lung. No leak was detected across the endobronchial cuff, and it was therefore left deflated. Controlled mechanical ventilation was commenced, and the DLT was firmly tied in position with a long piece of gauze. With the anesthesiologist supporting the head, the patient was then turned 90" to the left lateral position and secured by evacuation of air from a large beanbag. Peak airway pressures were then noted to be approximately 40 cm H,O. Manual ventilation was begun while a flexible fiberoptic bronchoscope was quickly passed through the tracheal lumen. However, on exit from the distal lumen, it came to rest on the tracheal wall. Right mainstem intuba-
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tion by the endobronchial tube was diagnosed. Meanwhile, the surgeon had made rapid progress and requested deflation of the right lung at this time. Ventilation of the left lung was attempted but was impossible. The bronchoscope was then passed down the endobronchial (left) lumen and the DLT withdrawn slowly. When the carina came into view, the bronchoscope was advanced into the left mainstem bronchus. The DLT was then easily advanced into its correct position. The right lung was then deflated with ease, and surgery proceeded uneventfully. For the distal end of a DLT to migrate to the contralateral side, several factors need consideration. First, it is likely that the tip of the DLT was not positioned far into the left mainstem bronchus, Flexible bronchoscopy could have been used to optimize tube position before turning. Second, some movements of the head and neck are inevitable during a patient turn, allowing distal tube movement to occur, cephalad and then caudad. Double-lumen tube movement is always possible during turning of patients, and although it has been previoulsy suggested that deflation of the endobronchial cuff should occur to reduce the possibility of mucosal damage (5), relocation of a DLT to the contralateral side has not been recorded. This report, then, describes yet another consequence of movement of a tracheal tube during the turning of patients. Richard H. Riley, MD Ivan L. Marples, MD Department of Anaesthesia Royal Perth Hospital, Box X2213 GPO Perth, Western Australia 6002
References 1. Toung TJK, Grayson R, Saklad J, Wang H. Movement of the distal end of the endotracheal tube during flexion and extension of the neck. Anesth Analg 1985;64:103C4 2. Conrady PA, Goodman LR, Lainge F, Singer MM. Alteration of endotracheal tube position. Crit Care Med 1976;48-12. 3. Stone DJ, Gal TJ. Airway management. In: Miller RD, ed. Anesthesia. 3rd ed. New York Churchill Livingstone, 1990:1289. 4. Spragg RG, Benumof JL, Alfery DD. New methods for the performance of unilateral lung lavage. Anesthesiology 1982;57535-8. 5. Benumof JL, Alfery DD. Anesthesia for thoracic surgery. In: Miller RD, ed. Anesthesia. 3rd ed. New York: Churchill Livingston, 1990:1554.
Removal of a Tenacious Epidural Catheter To the Editor: Quite a lot has been written lately about removal of epidural catheters that seem to have become firmly lodged in patients' backs. So, I thought I would offer my words of wisdom on the subject. I'm sure all of us who perform many epidurals have at some time encountered varying degrees of difficulty in extracting epidural catheters. Of note in the recent literature is a case report by Drs. Sia-Kho and Kudlak in Anesthesia & Analgesia (l),advocating extreme flexion of the patient in the lateral decubitus position. This case report reemphasizes Dr. Blackshear's report (2) that more tension is needed to remove epidural catheters with patients sitting versus lying.
