CORRESPONDENCE
225
4. Anserming JM, Blogg CE, Carrie LE. Failed tracheal intubation at Caesarean section and the laryngeal mask. British Journal of Anaesthesia 1992; 68: 118.
P. J. BUTLER
Melbourne 1. Cobley M, Vaughan RS. Recognition and management of difficult airway problems. British Journal of Anaesthesia 1992; 66: 90-97. 2. Oates JDL, Oates PD, Pearsall RJ, Howie JC, Murray GD. Comparison of two methods for predicting difficult intubation. British Journal of Anaesthesia 1991; 66: 305-309. 3. Mathew M, Hanna LS, Aldrete JA. Preoperative indices to anticipate difficult tracheal intubation. Anesthesia and Analgesia 1989; 68: S187. 4. Butler PJ, Dhara SS. Prediction of difficult laryngoscopy. An assessment of the thyromental distance and Mallampati predictive tests. Anaesthesia and Intensive Care 1992; (in press). Sir,—We thank you for the opportunity to respond to the letters received following our recent review article. Dr Calder's points are, as always, well made. He regrets that we did not quote the work of Block and Brcchner. However, we did mention the importance of temporomandibular joint movement, the degree of forward protrusion of the mandible and the mobility of the cervical spine. In everyday practice, radiology continues to be used more after encountering a difficult intubation and not during the prediction. We are grateful to Dr Calder for the helpful additional information in respect of patients with known cervical disease. The use of a fibreoptic bronchoscope is a personal choice, as we believe it is easier to use than a fibreoptic laryngoscope. Additionally, it enables the operator to see the Carina clearly and, as thefibrescopeis withdrawn, the end of the tracheal tube in the trachea. Although this may not be regarded as a routine method of confirmation of tracheal tube placement, under the circumstances of a difficult intubation it seems very appropriate. To each bis own! Dr Calder is correct that amethocaine lozenges are no longer manufactured. We are perhaps lucky that our pharmacy still has a store! Moreover, when that is depleted we intend to use benzocaine compound lozenges (Penn Pharmaceutical). We disagree that 1 % lignocaine is ineffective, but accept Dr Calder's contention that 4% lignocaine may be a better choice for "spray as you go", producing faster and perhaps better local anaesthesia. Although a dose of 400 mg is unlikely to produce a plasma concentration greater than the reported toxic plasma concentration of 5 ug ml"1 in the majority of patients, we would suggest that greater vigilance is required to avoid producing toxic plasma concentrations. We would most certainly take issue with the claim that fibreoptic intubation is associated with "stable cardiovascular variables". There are many papers in the world literature devoted to methods which reduce the tachycardia and hypertensive responses associated with intubation. While we accept that awake fibreoptic intubation need not necessarily result in hypertension and
M. COBLEY R. S. VAUGHAN Cardiff
VERAPAMIL AND CARDIOVASCULAR RESPONSES TO TRACHEAL INTUBATION Sir,—I read with interest the article by Yaku and colleagues [1] and wish to make some comments regarding the clinical implications. Their article demonstrated that verapamil 0.05— O.Imgkg"1 attenuated the increases in arterial pressure and rate-pressure product associated with laryngoscopy and tracheal intubation in normotensive patients, although they observed no significant effect on heart rate responses. These results are consistent with previous investigations [2, 3] showing little effect of either verapamil or sodium nitroprusside on heart rate increases after tracheal intubation. My previous study [2] in hypertensive patients showed that mean arterial pressure increased from baseline after tracheal intubation by 18 (9)% (mean (SD)) when verapamil 0.1 mg kg"1 was given i.v. 1 min before laryngoscopy and tracheal intubation, and by 53 (14)% after normal saline (P < 0.001). This result supports their assumption that pretreatment with i.v. verapamil may be useful in hypertensive patients undergoing txacheal intubation. Furthermore, I agree that failure of verapamil to attenuate tachycardia associated with tracheal intubation limits its usefulness in patients with ischaemic heart disease, as it is generally supposed that such patients tolerate hypertension better, and tolerate hypotension and tachycardia poorly; Lieberman and colleagues [4] have noted that myocardial ischaemia accompanied significant increases in heart rate and decreases in arterial and coronary perfusion pressure in patients undergoing coronary artery revascularizarion with halothane anaesthesia. T. NISHIKAWA
Tsukuba, Japan 1. Yaku H, Mikawa K, Maekawa N, Obara H. Effect of verapamil on the cardiovascular responses to tracheal intubation. British Journal of Anaesthesia 1992; 68: 85-89. 2. Nishikawa T, Namiki A. Attenuation of the pressor response to laryngoscopy and tracheal intubation with intravenous verapamil. Acta Anaesthesiologica Scandinavica
1989; 33:
232-235. 3. Stoelting RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesthesia and Analgesia 1979; 58: 116-119. 4. Lieberman RW, Orkin FK, Jobes DR, Schwartz AJ. Hemodynamic predictors of myocardial ischemia during halothane anesthesia for coronary-artery revascularizarion. Anesthesiology 1983; 59: 36-41. Sir,—Thank you for the opportunity to reply to Dr Nishikawa's letter. No data in patients with hypertension were presented, but we speculated that mean arterial pressure (MAP) increased markedly and that maximal values after intubation were more than 165 mm Hg in some of the hypertensive patients receiving normal saline. Bedford and Feinstein [1] have reported that peak MAP after intubation was mean 152 (SEM 4) mm Hg and observed
Downloaded from http://bja.oxfordjournals.org/ at Ryerson University on September 9, 2015
Sir,—The review article by Cobley and Vaughan [1] discusses several of the preoperative screening tests for the prediction of difficult intubation. Whilst recent papers such as that by Oates and colleagues [2] have shown the unreliability of the Mallampati and Wilson tests, the thyromental distance is quoted still as a predictor of difficult or impossible laryngoscopy. The paper by Mathew, Hanna and Aldrete [3] was a retrospective study of 22 easy and 22 difficult intubations in 44 patients and showed correlation between thyromental distance less than 6 cm, Mallampati class III or IV and difficulty in intubation. A prospective study of 250 patients in Singapore [4] has shown a spread of thyromental distance from 3.5 to 9 cm, with patients either side of the 6-cm distance in easy and difficult laryngoscopy groups. It was found that a thyromental distance of less than 6 cm correctly predicted 61 % of difficult laryngoscopies, but just 25 % of easy laryngoscopies. Only 10% of predicted difficult laryngoscopies actually proved to be difficult. Even a measure of 6.5 cm or more could not be taken to signify an easy laryngoscopy, which further devalues the test.
tachycardia, especially when practised by experienced operators, nevertheless, we still contend that cardiovascular instability is a possible sequela which should be given close consideration. It is pleasing that we are both of the same opinion that sedation plus local anaesthesia produces the best conditions for awake intubation. We agree with Dr Heath. Intubation through an LMA is a recognized technique in normal patients. However, until such time as sufficient patients whose tracheas are known to be difficult to intubate are investigated, we should remain circumspect in its use for these patients'. After all, the design of the LMA was based on the anatomy of normal patients, which is probably quite different from that in patients in whom intubation is difficult. Notwithstanding, this technique may represent a welcome addition to the array of methods available for accomplishing intubation in a difficult patient. Finally, we are grateful for the letter from Dr Butler. It confirms that, where the prediction of airway problems is concerned, nothing is sacrosanct!
BRITISH JOURNAL OF ANAESTHESIA
226 transient ST-T segment depression in two of 12 hypertensive patients. As hypertensive patients sustain a progressive increase in mortality and morbidity from coronary artery disease [2], hypcrdynamic responses leading possibly to myocardial ischaemia should be treated in these patients. We thank Dr Nishikawa for calling attention to the results of his study indicating the usefulness of verapamil in hypertensive patients. H. YAKU K. MlKAWA
Kobe, Japan 1. Bedford RF, Feinstein B. Hospital admission blood pressure: A predictor for hypertension following cndotrachcal intubation. Anesthesia and Analgesia 1980; 59: 367-370. 2. Castelli WP. Epidemiology of coronary heart disease: The Framingham study. American Journal of Medicine 1984; 76: 4-12.
N. T. A. CAMPKIN J. R. HOOD S. A. FELDMAN
1. Fletcher JE, Sebel PS, Mick SA, Van Duys J, Ryan K. Comparison of the train-of-four profiles produced by vecuronium and atracurium. British Journal of Anaesthesia 1992; 68: 207-208.
FIG. 1. Maximal twitches of the adductor pollicis muscles evoked by stimulation of the ulnar nerve at 0.1 Hz. During recovery a tetanus (50 Hz for 5 s) was interposed. The upper record shows the response to vecuronium 0.3 mg injected into an isolated arm. After release of the tourniquet, at 50% recovery from 95% block there is little tetanic fade and relatively little post-tetanic facilitation. The lower record shows 90 % block produced by cumulative i.v. vecuronium (total dose 1.5 mg). At 50 % recovery there is marked tetanic fade and greater post-tetanic facilitation.
Downloaded from http://bja.oxfordjournals.org/ at Ryerson University on September 9, 2015
FADE DURING RECOVERY FROM VECURONIUM Sir,—Fletcher and colleagues [1] have repeated the observations of Bowman [2], Pearcc, Casson and Jones [3] and others in demonstrating that greater train-of-four fade occurs during offset of the action of vecuronium than during onset. They suggest that fade results from block of prejunctional receptors at the neuromuscular junction, and that vecuronium is able to enter and leave the region of the prejunctional receptor only slowly, resulting in a slower onset and offset of prejunctional effects. Bowman and Webb [4] showed that tetanic fade in the cat soleus muscle was more pronounced when neuromuscular block had been produced by bolus i.v. injection of tubocurarine, than after the same degree of block produced by a much smaller i.a. injection. Bowman [2] postulated that " a slower rate of binding to the ' fade sites' would explain the observations that peak tension depression and fade develop and recover with different time courses. " He argued that a slower rate of binding "would also explain the absence of tetanic fade when twitch depression is produced by intra-arterial rather than intravenous injection of tubocurarine, since the relatively small bolus dose administered intra-arterially would pass through the muscle and be diluted in the general circulation before there was time for binding to the fade sites to occur". We have observed a marked difference between tetanic fade during recovery from vecuronium block in the isolated forearm and from systemic i.v. injection. In the isolated forearm technique, a small dose of vecuronium (0.3 mg diluted in saline 20 ml) is injected into a forearm isolated from the general circulation by an arterial tourniquet. This dose rapidly produces > 9 0 % twitch depression of the adductor pollicis muscle, following which the cuff is released (3 min after injection). When twitch height has
recovered to approximately 50 %, a 50-Hz tetanic stimulation for 5 s produces no perceptible fade. At a similar point of recovery following an EDW systemic dose, however, there is marked fade in response to tetanic stimulation (fig. 1). The authors of the recent article suggest that the difference in fade between onset and offset was caused by slow drug transfer both to and from the prejunctional receptor region. Whilst this explains the observations after systemic drug administration, it docs not explain the difference seen in the isolated forearm. If fade during offset was caused by slow local movement of vecuronium away from the prejunctional region, then it should be present to the same degree in the previously isolated forearm which reaches a given twitch height earlier than after a systemic ED M dose. It is possible that less prejunctional block could occur during onset of vecuronium block in the isolated forearm for the reason postulated by Bowman regarding i.a. injection—that is, that there is less time for binding to "fade sites" before the tourniquet is released, and drug is washed out into the general circulation. However, recovery in the previously isolated forearm, although more rapid than after a systemic dose, takes 15-30 min. This implies that there is a significant biophase concentration in the neuromuscular junction during the recovery period, which produces single twitch depression. Given this time span, this would be expected to allow time for access of drug to the prejunctional region. Whilst drug biophase concentration is modelled to mirror closely the slowly declining plasma concentration during the beta phase of recovery after a systemic bolus, a considerable concentration gradient exists between plasma and the biophase of a recovering previously isolated forearm, and between plasma and biophase during recovery from i.a. injection. We believe that the reduction of tetanic fade seen during offset of neuromuscular block in the isolated forearm and after i.a. injection is linked to that concentration gradient. If there is a difference in pharmacodynamic characteristics between pre- and postjunctional receptors, redistribution of drug between binding sites within the neuromuscular junction may have an important influence on receptor occupancy in these situations, leading to differences in relative degrees of pre- and postjunctional effects.
225
4. Anserming JM, Blogg CE, Carrie LE. Failed tracheal intubation at Caesarean section and the laryngeal mask. British Journal of Anaesthesia 1992; 68: 118.
P. J. BUTLER
Melbourne 1. Cobley M, Vaughan RS. Recognition and management of difficult airway problems. British Journal of Anaesthesia 1992; 66: 90-97. 2. Oates JDL, Oates PD, Pearsall RJ, Howie JC, Murray GD. Comparison of two methods for predicting difficult intubation. British Journal of Anaesthesia 1991; 66: 305-309. 3. Mathew M, Hanna LS, Aldrete JA. Preoperative indices to anticipate difficult tracheal intubation. Anesthesia and Analgesia 1989; 68: S187. 4. Butler PJ, Dhara SS. Prediction of difficult laryngoscopy. An assessment of the thyromental distance and Mallampati predictive tests. Anaesthesia and Intensive Care 1992; (in press). Sir,—We thank you for the opportunity to respond to the letters received following our recent review article. Dr Calder's points are, as always, well made. He regrets that we did not quote the work of Block and Brcchner. However, we did mention the importance of temporomandibular joint movement, the degree of forward protrusion of the mandible and the mobility of the cervical spine. In everyday practice, radiology continues to be used more after encountering a difficult intubation and not during the prediction. We are grateful to Dr Calder for the helpful additional information in respect of patients with known cervical disease. The use of a fibreoptic bronchoscope is a personal choice, as we believe it is easier to use than a fibreoptic laryngoscope. Additionally, it enables the operator to see the Carina clearly and, as thefibrescopeis withdrawn, the end of the tracheal tube in the trachea. Although this may not be regarded as a routine method of confirmation of tracheal tube placement, under the circumstances of a difficult intubation it seems very appropriate. To each bis own! Dr Calder is correct that amethocaine lozenges are no longer manufactured. We are perhaps lucky that our pharmacy still has a store! Moreover, when that is depleted we intend to use benzocaine compound lozenges (Penn Pharmaceutical). We disagree that 1 % lignocaine is ineffective, but accept Dr Calder's contention that 4% lignocaine may be a better choice for "spray as you go", producing faster and perhaps better local anaesthesia. Although a dose of 400 mg is unlikely to produce a plasma concentration greater than the reported toxic plasma concentration of 5 ug ml"1 in the majority of patients, we would suggest that greater vigilance is required to avoid producing toxic plasma concentrations. We would most certainly take issue with the claim that fibreoptic intubation is associated with "stable cardiovascular variables". There are many papers in the world literature devoted to methods which reduce the tachycardia and hypertensive responses associated with intubation. While we accept that awake fibreoptic intubation need not necessarily result in hypertension and
M. COBLEY R. S. VAUGHAN Cardiff
VERAPAMIL AND CARDIOVASCULAR RESPONSES TO TRACHEAL INTUBATION Sir,—I read with interest the article by Yaku and colleagues [1] and wish to make some comments regarding the clinical implications. Their article demonstrated that verapamil 0.05— O.Imgkg"1 attenuated the increases in arterial pressure and rate-pressure product associated with laryngoscopy and tracheal intubation in normotensive patients, although they observed no significant effect on heart rate responses. These results are consistent with previous investigations [2, 3] showing little effect of either verapamil or sodium nitroprusside on heart rate increases after tracheal intubation. My previous study [2] in hypertensive patients showed that mean arterial pressure increased from baseline after tracheal intubation by 18 (9)% (mean (SD)) when verapamil 0.1 mg kg"1 was given i.v. 1 min before laryngoscopy and tracheal intubation, and by 53 (14)% after normal saline (P < 0.001). This result supports their assumption that pretreatment with i.v. verapamil may be useful in hypertensive patients undergoing txacheal intubation. Furthermore, I agree that failure of verapamil to attenuate tachycardia associated with tracheal intubation limits its usefulness in patients with ischaemic heart disease, as it is generally supposed that such patients tolerate hypertension better, and tolerate hypotension and tachycardia poorly; Lieberman and colleagues [4] have noted that myocardial ischaemia accompanied significant increases in heart rate and decreases in arterial and coronary perfusion pressure in patients undergoing coronary artery revascularizarion with halothane anaesthesia. T. NISHIKAWA
Tsukuba, Japan 1. Yaku H, Mikawa K, Maekawa N, Obara H. Effect of verapamil on the cardiovascular responses to tracheal intubation. British Journal of Anaesthesia 1992; 68: 85-89. 2. Nishikawa T, Namiki A. Attenuation of the pressor response to laryngoscopy and tracheal intubation with intravenous verapamil. Acta Anaesthesiologica Scandinavica
1989; 33:
232-235. 3. Stoelting RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesthesia and Analgesia 1979; 58: 116-119. 4. Lieberman RW, Orkin FK, Jobes DR, Schwartz AJ. Hemodynamic predictors of myocardial ischemia during halothane anesthesia for coronary-artery revascularizarion. Anesthesiology 1983; 59: 36-41. Sir,—Thank you for the opportunity to reply to Dr Nishikawa's letter. No data in patients with hypertension were presented, but we speculated that mean arterial pressure (MAP) increased markedly and that maximal values after intubation were more than 165 mm Hg in some of the hypertensive patients receiving normal saline. Bedford and Feinstein [1] have reported that peak MAP after intubation was mean 152 (SEM 4) mm Hg and observed
Downloaded from http://bja.oxfordjournals.org/ at Ryerson University on September 9, 2015
Sir,—The review article by Cobley and Vaughan [1] discusses several of the preoperative screening tests for the prediction of difficult intubation. Whilst recent papers such as that by Oates and colleagues [2] have shown the unreliability of the Mallampati and Wilson tests, the thyromental distance is quoted still as a predictor of difficult or impossible laryngoscopy. The paper by Mathew, Hanna and Aldrete [3] was a retrospective study of 22 easy and 22 difficult intubations in 44 patients and showed correlation between thyromental distance less than 6 cm, Mallampati class III or IV and difficulty in intubation. A prospective study of 250 patients in Singapore [4] has shown a spread of thyromental distance from 3.5 to 9 cm, with patients either side of the 6-cm distance in easy and difficult laryngoscopy groups. It was found that a thyromental distance of less than 6 cm correctly predicted 61 % of difficult laryngoscopies, but just 25 % of easy laryngoscopies. Only 10% of predicted difficult laryngoscopies actually proved to be difficult. Even a measure of 6.5 cm or more could not be taken to signify an easy laryngoscopy, which further devalues the test.
tachycardia, especially when practised by experienced operators, nevertheless, we still contend that cardiovascular instability is a possible sequela which should be given close consideration. It is pleasing that we are both of the same opinion that sedation plus local anaesthesia produces the best conditions for awake intubation. We agree with Dr Heath. Intubation through an LMA is a recognized technique in normal patients. However, until such time as sufficient patients whose tracheas are known to be difficult to intubate are investigated, we should remain circumspect in its use for these patients'. After all, the design of the LMA was based on the anatomy of normal patients, which is probably quite different from that in patients in whom intubation is difficult. Notwithstanding, this technique may represent a welcome addition to the array of methods available for accomplishing intubation in a difficult patient. Finally, we are grateful for the letter from Dr Butler. It confirms that, where the prediction of airway problems is concerned, nothing is sacrosanct!
BRITISH JOURNAL OF ANAESTHESIA
226 transient ST-T segment depression in two of 12 hypertensive patients. As hypertensive patients sustain a progressive increase in mortality and morbidity from coronary artery disease [2], hypcrdynamic responses leading possibly to myocardial ischaemia should be treated in these patients. We thank Dr Nishikawa for calling attention to the results of his study indicating the usefulness of verapamil in hypertensive patients. H. YAKU K. MlKAWA
Kobe, Japan 1. Bedford RF, Feinstein B. Hospital admission blood pressure: A predictor for hypertension following cndotrachcal intubation. Anesthesia and Analgesia 1980; 59: 367-370. 2. Castelli WP. Epidemiology of coronary heart disease: The Framingham study. American Journal of Medicine 1984; 76: 4-12.
N. T. A. CAMPKIN J. R. HOOD S. A. FELDMAN
1. Fletcher JE, Sebel PS, Mick SA, Van Duys J, Ryan K. Comparison of the train-of-four profiles produced by vecuronium and atracurium. British Journal of Anaesthesia 1992; 68: 207-208.
FIG. 1. Maximal twitches of the adductor pollicis muscles evoked by stimulation of the ulnar nerve at 0.1 Hz. During recovery a tetanus (50 Hz for 5 s) was interposed. The upper record shows the response to vecuronium 0.3 mg injected into an isolated arm. After release of the tourniquet, at 50% recovery from 95% block there is little tetanic fade and relatively little post-tetanic facilitation. The lower record shows 90 % block produced by cumulative i.v. vecuronium (total dose 1.5 mg). At 50 % recovery there is marked tetanic fade and greater post-tetanic facilitation.
Downloaded from http://bja.oxfordjournals.org/ at Ryerson University on September 9, 2015
FADE DURING RECOVERY FROM VECURONIUM Sir,—Fletcher and colleagues [1] have repeated the observations of Bowman [2], Pearcc, Casson and Jones [3] and others in demonstrating that greater train-of-four fade occurs during offset of the action of vecuronium than during onset. They suggest that fade results from block of prejunctional receptors at the neuromuscular junction, and that vecuronium is able to enter and leave the region of the prejunctional receptor only slowly, resulting in a slower onset and offset of prejunctional effects. Bowman and Webb [4] showed that tetanic fade in the cat soleus muscle was more pronounced when neuromuscular block had been produced by bolus i.v. injection of tubocurarine, than after the same degree of block produced by a much smaller i.a. injection. Bowman [2] postulated that " a slower rate of binding to the ' fade sites' would explain the observations that peak tension depression and fade develop and recover with different time courses. " He argued that a slower rate of binding "would also explain the absence of tetanic fade when twitch depression is produced by intra-arterial rather than intravenous injection of tubocurarine, since the relatively small bolus dose administered intra-arterially would pass through the muscle and be diluted in the general circulation before there was time for binding to the fade sites to occur". We have observed a marked difference between tetanic fade during recovery from vecuronium block in the isolated forearm and from systemic i.v. injection. In the isolated forearm technique, a small dose of vecuronium (0.3 mg diluted in saline 20 ml) is injected into a forearm isolated from the general circulation by an arterial tourniquet. This dose rapidly produces > 9 0 % twitch depression of the adductor pollicis muscle, following which the cuff is released (3 min after injection). When twitch height has
recovered to approximately 50 %, a 50-Hz tetanic stimulation for 5 s produces no perceptible fade. At a similar point of recovery following an EDW systemic dose, however, there is marked fade in response to tetanic stimulation (fig. 1). The authors of the recent article suggest that the difference in fade between onset and offset was caused by slow drug transfer both to and from the prejunctional receptor region. Whilst this explains the observations after systemic drug administration, it docs not explain the difference seen in the isolated forearm. If fade during offset was caused by slow local movement of vecuronium away from the prejunctional region, then it should be present to the same degree in the previously isolated forearm which reaches a given twitch height earlier than after a systemic ED M dose. It is possible that less prejunctional block could occur during onset of vecuronium block in the isolated forearm for the reason postulated by Bowman regarding i.a. injection—that is, that there is less time for binding to "fade sites" before the tourniquet is released, and drug is washed out into the general circulation. However, recovery in the previously isolated forearm, although more rapid than after a systemic dose, takes 15-30 min. This implies that there is a significant biophase concentration in the neuromuscular junction during the recovery period, which produces single twitch depression. Given this time span, this would be expected to allow time for access of drug to the prejunctional region. Whilst drug biophase concentration is modelled to mirror closely the slowly declining plasma concentration during the beta phase of recovery after a systemic bolus, a considerable concentration gradient exists between plasma and the biophase of a recovering previously isolated forearm, and between plasma and biophase during recovery from i.a. injection. We believe that the reduction of tetanic fade seen during offset of neuromuscular block in the isolated forearm and after i.a. injection is linked to that concentration gradient. If there is a difference in pharmacodynamic characteristics between pre- and postjunctional receptors, redistribution of drug between binding sites within the neuromuscular junction may have an important influence on receptor occupancy in these situations, leading to differences in relative degrees of pre- and postjunctional effects.
