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Use of a bolus injection of nicardipine to prevent severe electroconvulsive therapy–induced bradycardia
Correspondence Thomas Weissmqller, MD (Clinical Fellow) Holger K. Eltzschig, MD, PhD (Assistant Professor of Anesthesiology) Department of Anesthesiology and Intensive Care Medicine University Hospital D-72076 Tu¨bingen, Germany E-mail address: [email protected] DOI of original article 10.1016/j.jclinane.2003.02.007 doi: 10.1016/j.jclinane.2004.12.009
147 [4] van der Wouw PA, Koster RW, Delemarre BJ, de Vos R, LampeSchoenmaeckers AJ, Lie KI. Diagnostic accuracy of transesophageal echocardiography during cardiopulmonary resuscitation. J Am Coll Cardiol 1997;30:780 - 3. [5] Rosenberger P, Shernan SK, Body SC, Eltzschig HK. Utility of intraoperative transesophageal echocardiography for diagnosis of pulmonary embolism. Anesth Analg 2004;99:12 - 6. [6] Tsai SK, Chang CI, Wang MJ, et al. The assessment of the proximal left pulmonary artery by transesophageal echocardiography and computed tomography in neonates and infants: a case series. Anesth Analg 2001;93:594 - 7.
Shao-Wei Hsieh, MD Department of Anesthesiology E-DA Hospital Kaohsiung 824, Taiwan, ROC
Reply We wish to thank Rosenberger et al for their comments and for sharing their excellent experience with transesophageal echocardiography in diagnosing pulmonary embolism. In our article, we demonstrated the usefulness of perioperative TEE in determining PE as the cause of sudden cardiac arrest in a patient receiving laparoscopic hysterectomy. Although the incidence of PE after laparoscopic surgery is quite low at a rate of 0.06% [1], laparoscopy is regarded as a risk factor for pulmonary thromboembolism [2]. Laparoscopic pneumoperitoneum may lead to a reduction in femoral venous blood flow and venous stasis, implicating the potential risk of deep vein thrombosis and PE after prolonged laparoscopic surgery [3]. Because the role of TEE during cardiopulmonary resuscitation has been highlighted [4], it prompted us to use TEE to differentiate the diagnosis after cardiac arrest in our patient. We agree with Rosenberger et al that TEE can be the primary diagnosing tool for perioperative cardiovascular catastrophe because of its features. We also agree that the accuracy and sensitivity of TEE for PE could be low because of the different sizes and locations of the thromboemboli in the pulmonary circulation [5], especially in the left pulmonary artery. Yet the difficulty in viewing the proximal LPA might be lessened by a left paracarinal window with TEE [6]. As Rosenberger et al indicated, in the absence of located thrombus, a new onset of right ventricular dysfunction is strongly suggestive of PE and warrants sequential examinations. Hence, even in a low-risk patient undergoing laparoscopic hysterectomy, TEE plays a valuable role in making prompt differential diagnosis when unexpected cardiac arrest occurs perioperatively.
References [1] Lindberg F, Bergqvist D, Rasmussen I. Incidence of thromboembolic complications after laparoscopic cholecystectomy: review of the literature. Surg Laparosc Endosc 1997;7:324 - 31. [2] Kuroiwa M, Arai M, Kinoshita S, Takenaka T, Okamoto H, Hoka S. Clinical characteristics of perioperative pulmonary thromboembolism: analysis of 18 patients in Kitasato University Hospital. Masui 2002;51:977 - 82. [3] Beebe DS, McNevin MP, Crain JM, et al. Evidence of venous stasis after abdominal insufflation for laparoscopic cholecystectomy. Surg Gynecol Obstet 1993;176:443 - 7.
Hsiang-Ning Luk, MD Bruno Jawan, MD First Department of Anesthesiology Chang Gung Memorial Hospital Kaohsiung 833, Taiwan, ROC E-mail address: [email protected] doi: 10.1016/j.jclinane.2004.12.010
Letter to the editor Use of a bolus injection of nicardipine to prevent severe electroconvulsive therapy–induced bradycardia To the Editor: Electroconvulsive therapy (ECT) is associated with profound changes in both heart rate (HR) and blood pressure immediately after application of the electrical stimulus [1]. Nicardipine 1.25 to 5 mg given intravenously (IV) has previously been evaluated for the prevention of the acute hyperdynamic response to ECT [2]. However, when nicardipine was administered before induction of anesthesia, its use was associated with hypotension and tachycardia. Saito et al [3] reported that nicardipine 0.02 mg/kg IV bolus prevented acute hemodynamic changes after ECT when administered immediately before application of the ECT stimulus. In a severely depressed 52-year-old 100-kg patient, who developed profound bradycardia (b10 beats per minute) after his initial 2 ECT treatments, the use of nicardipine (0.025 mg/kg IV) immediately before the ECT stimulus facilitated control of the ECT-induced increase in BP without enhancing the associated bradycardia. Using an anesthetic regimen consisting of glycopyrrolate 0.2 mg IV, labetalol 10 mg IV, thiopental sodium 200 mg IV, and succinylcholine 100 mg IV, we found that the addition of nicardipine 2.5 mg IV approximately 30 seconds before application of the electrical stimulus minimized the hypertensive response to the ECT stimulus, and the HR never decreased below 80 beats per minute.
148 Nicardipine, which is a parenterally active calciumchannel blocker, has previously been used for pretreatment of patients undergoing ECT procedures [2]. In the management of this patient’s ECT-related hypertension and bradycardia, the administration of nicardipine immediately before applying the ECT stimulus minimized the risk of nicardipineinduced hypotension after induction of anesthesia. In addition, the reflex increase in HR after the bolus injection of nicardipine provided protection against the ECT-induced bradycardia. The dose of nicardipine used to treat this patient (2.5 mg IV) was based on the findings of earlier studies using IV boluses of nicardipine to prevent the acute hypertensive responses to ECT [3,4]. Although a dose of 0.025 mg/kg IV was successful in this patient, a proper dose-finding study is needed to determine the optimal IV bolus dose of the calcium-channel blocker when it is administered immediately before the ECT stimulus [4]. We conclude that nicardipine 2.5 mg IV would appear to be a useful adjuvant to other antihypertensive therapies for ECT patients who develop severe hypertension and bradycardia after the electrical stimulus is applied.
References [1] Ding Z, White PF. Anesthesia for electroconvulsive therapy. Anesth Analg 2002;13:51 - 64. [2] Avramov MN, Stool LA, White PF, Husain MM. Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy. J Clin Anesth 1998;10:394 - 400. [3] Saito S, Kadoi Y, Iriuchijima N, et al. Reduction of cerebral hyperemia with antihypertensive medication after electroconvulsive therapy. Can J Anaesth 2000;47:767 - 74. [4] Zhang V, White PF, Thorton L, et al: The use of nicardipine for electro convulsive therapy: A dose-ranging study. Anesth Analg 2005;100: 378 - 81.
Paul F. White, PhD, MD, FANZCA (Professor and Holder, Distinguished Chair) Department of Anesthesiology and Pain Management University of Texas Southwestern Medical Center at Dallas Dallas, TX 75390-9068, USA E-mail address: [email protected] Lisa Perdue, MD (Associate Professor) Michael Downing, MD (Associate Professor) Larry Thornton, MD (Associate Professor) Department of Psychiatry University of Texas Southwestern Medical Center at Dallas Dallas, TX 75390-9068, USA doi: 10.1016/j.jclinane.2005.01.001 Air bubbles produced during blood warming for transfusion at slow rate: their composition and a device (reservoir with a filter) to eliminate them To the Editor: Warming of blood for transfusion produces air bubbles. The composition of those bubbles has not been thoroughly
Correspondence investigated; it was assumed to be carbon dioxide [1] or nitrogen [2]. The aim of the present study was to determine the composition and the volume of those bubbles and to demonstrate the newly fabricated reservoir attached to a warming coil (BLT-500F; Toray Co Ltd, Tokyo, Japan), which is efficient in trapping the bubbles. A new reservoir is a columnar container made of polyvinyl chloride (30 mL) with a tent-shaped filter inside (Fig. 1). The reservoir was combined with an ordinary warming coil (3.4 5500 mm, 50 mL). This new coil-and-reservoir was connected to a transfusion set that has a dripping chamber. The coiland-reservoir was put in the hot water (378C). One unit (~400 mL) of 2-week-old whole blood stored at 48C was transfused in about an hour. Six samples of trapped bubbles were obtained from 6 units of the whole blood and analyzed by a mass spectrometer (GCMS-QP 1000EX; Shimadzu, Kyoto, Japan). The volume of bubbles in the reservoir was roughly calculated from the diameter of the reservoir and the height of the air layer. In another setting of the experiment, the volume of bubbles produced by the warming of the blood from 48C to 378C also was measured. The bubbles were efficiently trapped by buoyancy and by the mesh filter, accumulated at the upper end of the reservoir, and did not move to the patient’s side beyond the mesh filter. The composition of the bubbles was 84.6% F 1.2% of nitrogen, 4.0% F 1.0% of oxygen, 10.4% F 0.9% of carbon dioxide, and 1.1% F 0.1% of argon (mean F SD, n = 6). The volume of the bubbles in the reservoir was about 4.0 F 0.5 mL per 400 mL of whole blood (n = 6). But the volume of bubbles produced by simple warming was 0.6 F 0.3 mL per 400 mL of whole blood (n = 4). Warming the transfusing blood through the coil immersed in the hot water is still widely used in certain countries including Japan, and the bubbles produced are sometimes overlooked or ignored. The mechanism of air trapping is the buoyancy and the surface tension [3] of the bubble at the mesh filter. Air-trapping devices for transfusion have been reported [4] or in commercial use, but some of those devices are very small in capacity, some lacks the filter, and almost all of them are put outside the warming part. The high concentration of nitrogen and the existence of argon in the bubbles suggest that a large part of those bubbles came from the air. These bubbles might arise from the solubility difference at different temperatures [2]. Or the bubbles might have been formed by the dripping of blood in the dripping chamber. The volume was 4 F 0.5 mL per 400 mL of blood from the reservoir, and 0.6 F 0.3 mL per 400 mL of blood from simple warming without dripping. The amount of the bubbles is small compared to the lethal volume of 200 mL in human being [5], but it might cause some serious problems in those who have silent foramen ovale [6,7] or obvious rightto-left shunting. Further, the air bubble is reported to cause The blood warming device (warming coil-and-reservoirs BLT-500F) was manufactured and provided by Toray Medical, Co Ltd, Tokyo, Japan.
147 [4] van der Wouw PA, Koster RW, Delemarre BJ, de Vos R, LampeSchoenmaeckers AJ, Lie KI. Diagnostic accuracy of transesophageal echocardiography during cardiopulmonary resuscitation. J Am Coll Cardiol 1997;30:780 - 3. [5] Rosenberger P, Shernan SK, Body SC, Eltzschig HK. Utility of intraoperative transesophageal echocardiography for diagnosis of pulmonary embolism. Anesth Analg 2004;99:12 - 6. [6] Tsai SK, Chang CI, Wang MJ, et al. The assessment of the proximal left pulmonary artery by transesophageal echocardiography and computed tomography in neonates and infants: a case series. Anesth Analg 2001;93:594 - 7.
Shao-Wei Hsieh, MD Department of Anesthesiology E-DA Hospital Kaohsiung 824, Taiwan, ROC
Reply We wish to thank Rosenberger et al for their comments and for sharing their excellent experience with transesophageal echocardiography in diagnosing pulmonary embolism. In our article, we demonstrated the usefulness of perioperative TEE in determining PE as the cause of sudden cardiac arrest in a patient receiving laparoscopic hysterectomy. Although the incidence of PE after laparoscopic surgery is quite low at a rate of 0.06% [1], laparoscopy is regarded as a risk factor for pulmonary thromboembolism [2]. Laparoscopic pneumoperitoneum may lead to a reduction in femoral venous blood flow and venous stasis, implicating the potential risk of deep vein thrombosis and PE after prolonged laparoscopic surgery [3]. Because the role of TEE during cardiopulmonary resuscitation has been highlighted [4], it prompted us to use TEE to differentiate the diagnosis after cardiac arrest in our patient. We agree with Rosenberger et al that TEE can be the primary diagnosing tool for perioperative cardiovascular catastrophe because of its features. We also agree that the accuracy and sensitivity of TEE for PE could be low because of the different sizes and locations of the thromboemboli in the pulmonary circulation [5], especially in the left pulmonary artery. Yet the difficulty in viewing the proximal LPA might be lessened by a left paracarinal window with TEE [6]. As Rosenberger et al indicated, in the absence of located thrombus, a new onset of right ventricular dysfunction is strongly suggestive of PE and warrants sequential examinations. Hence, even in a low-risk patient undergoing laparoscopic hysterectomy, TEE plays a valuable role in making prompt differential diagnosis when unexpected cardiac arrest occurs perioperatively.
References [1] Lindberg F, Bergqvist D, Rasmussen I. Incidence of thromboembolic complications after laparoscopic cholecystectomy: review of the literature. Surg Laparosc Endosc 1997;7:324 - 31. [2] Kuroiwa M, Arai M, Kinoshita S, Takenaka T, Okamoto H, Hoka S. Clinical characteristics of perioperative pulmonary thromboembolism: analysis of 18 patients in Kitasato University Hospital. Masui 2002;51:977 - 82. [3] Beebe DS, McNevin MP, Crain JM, et al. Evidence of venous stasis after abdominal insufflation for laparoscopic cholecystectomy. Surg Gynecol Obstet 1993;176:443 - 7.
Hsiang-Ning Luk, MD Bruno Jawan, MD First Department of Anesthesiology Chang Gung Memorial Hospital Kaohsiung 833, Taiwan, ROC E-mail address: [email protected] doi: 10.1016/j.jclinane.2004.12.010
Letter to the editor Use of a bolus injection of nicardipine to prevent severe electroconvulsive therapy–induced bradycardia To the Editor: Electroconvulsive therapy (ECT) is associated with profound changes in both heart rate (HR) and blood pressure immediately after application of the electrical stimulus [1]. Nicardipine 1.25 to 5 mg given intravenously (IV) has previously been evaluated for the prevention of the acute hyperdynamic response to ECT [2]. However, when nicardipine was administered before induction of anesthesia, its use was associated with hypotension and tachycardia. Saito et al [3] reported that nicardipine 0.02 mg/kg IV bolus prevented acute hemodynamic changes after ECT when administered immediately before application of the ECT stimulus. In a severely depressed 52-year-old 100-kg patient, who developed profound bradycardia (b10 beats per minute) after his initial 2 ECT treatments, the use of nicardipine (0.025 mg/kg IV) immediately before the ECT stimulus facilitated control of the ECT-induced increase in BP without enhancing the associated bradycardia. Using an anesthetic regimen consisting of glycopyrrolate 0.2 mg IV, labetalol 10 mg IV, thiopental sodium 200 mg IV, and succinylcholine 100 mg IV, we found that the addition of nicardipine 2.5 mg IV approximately 30 seconds before application of the electrical stimulus minimized the hypertensive response to the ECT stimulus, and the HR never decreased below 80 beats per minute.
148 Nicardipine, which is a parenterally active calciumchannel blocker, has previously been used for pretreatment of patients undergoing ECT procedures [2]. In the management of this patient’s ECT-related hypertension and bradycardia, the administration of nicardipine immediately before applying the ECT stimulus minimized the risk of nicardipineinduced hypotension after induction of anesthesia. In addition, the reflex increase in HR after the bolus injection of nicardipine provided protection against the ECT-induced bradycardia. The dose of nicardipine used to treat this patient (2.5 mg IV) was based on the findings of earlier studies using IV boluses of nicardipine to prevent the acute hypertensive responses to ECT [3,4]. Although a dose of 0.025 mg/kg IV was successful in this patient, a proper dose-finding study is needed to determine the optimal IV bolus dose of the calcium-channel blocker when it is administered immediately before the ECT stimulus [4]. We conclude that nicardipine 2.5 mg IV would appear to be a useful adjuvant to other antihypertensive therapies for ECT patients who develop severe hypertension and bradycardia after the electrical stimulus is applied.
References [1] Ding Z, White PF. Anesthesia for electroconvulsive therapy. Anesth Analg 2002;13:51 - 64. [2] Avramov MN, Stool LA, White PF, Husain MM. Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy. J Clin Anesth 1998;10:394 - 400. [3] Saito S, Kadoi Y, Iriuchijima N, et al. Reduction of cerebral hyperemia with antihypertensive medication after electroconvulsive therapy. Can J Anaesth 2000;47:767 - 74. [4] Zhang V, White PF, Thorton L, et al: The use of nicardipine for electro convulsive therapy: A dose-ranging study. Anesth Analg 2005;100: 378 - 81.
Paul F. White, PhD, MD, FANZCA (Professor and Holder, Distinguished Chair) Department of Anesthesiology and Pain Management University of Texas Southwestern Medical Center at Dallas Dallas, TX 75390-9068, USA E-mail address: [email protected] Lisa Perdue, MD (Associate Professor) Michael Downing, MD (Associate Professor) Larry Thornton, MD (Associate Professor) Department of Psychiatry University of Texas Southwestern Medical Center at Dallas Dallas, TX 75390-9068, USA doi: 10.1016/j.jclinane.2005.01.001 Air bubbles produced during blood warming for transfusion at slow rate: their composition and a device (reservoir with a filter) to eliminate them To the Editor: Warming of blood for transfusion produces air bubbles. The composition of those bubbles has not been thoroughly
Correspondence investigated; it was assumed to be carbon dioxide [1] or nitrogen [2]. The aim of the present study was to determine the composition and the volume of those bubbles and to demonstrate the newly fabricated reservoir attached to a warming coil (BLT-500F; Toray Co Ltd, Tokyo, Japan), which is efficient in trapping the bubbles. A new reservoir is a columnar container made of polyvinyl chloride (30 mL) with a tent-shaped filter inside (Fig. 1). The reservoir was combined with an ordinary warming coil (3.4 5500 mm, 50 mL). This new coil-and-reservoir was connected to a transfusion set that has a dripping chamber. The coiland-reservoir was put in the hot water (378C). One unit (~400 mL) of 2-week-old whole blood stored at 48C was transfused in about an hour. Six samples of trapped bubbles were obtained from 6 units of the whole blood and analyzed by a mass spectrometer (GCMS-QP 1000EX; Shimadzu, Kyoto, Japan). The volume of bubbles in the reservoir was roughly calculated from the diameter of the reservoir and the height of the air layer. In another setting of the experiment, the volume of bubbles produced by the warming of the blood from 48C to 378C also was measured. The bubbles were efficiently trapped by buoyancy and by the mesh filter, accumulated at the upper end of the reservoir, and did not move to the patient’s side beyond the mesh filter. The composition of the bubbles was 84.6% F 1.2% of nitrogen, 4.0% F 1.0% of oxygen, 10.4% F 0.9% of carbon dioxide, and 1.1% F 0.1% of argon (mean F SD, n = 6). The volume of the bubbles in the reservoir was about 4.0 F 0.5 mL per 400 mL of whole blood (n = 6). But the volume of bubbles produced by simple warming was 0.6 F 0.3 mL per 400 mL of whole blood (n = 4). Warming the transfusing blood through the coil immersed in the hot water is still widely used in certain countries including Japan, and the bubbles produced are sometimes overlooked or ignored. The mechanism of air trapping is the buoyancy and the surface tension [3] of the bubble at the mesh filter. Air-trapping devices for transfusion have been reported [4] or in commercial use, but some of those devices are very small in capacity, some lacks the filter, and almost all of them are put outside the warming part. The high concentration of nitrogen and the existence of argon in the bubbles suggest that a large part of those bubbles came from the air. These bubbles might arise from the solubility difference at different temperatures [2]. Or the bubbles might have been formed by the dripping of blood in the dripping chamber. The volume was 4 F 0.5 mL per 400 mL of blood from the reservoir, and 0.6 F 0.3 mL per 400 mL of blood from simple warming without dripping. The amount of the bubbles is small compared to the lethal volume of 200 mL in human being [5], but it might cause some serious problems in those who have silent foramen ovale [6,7] or obvious rightto-left shunting. Further, the air bubble is reported to cause The blood warming device (warming coil-and-reservoirs BLT-500F) was manufactured and provided by Toray Medical, Co Ltd, Tokyo, Japan.