LETTERS TO THE EDITOR
774
3. Lockridge 0: Substance P hydrolysis by human serum cholinesterase. J Neurochem 39:106-l lo,1982 4. Nigrovic V, Auen M, Wajskol A: Enzymatic hydrolysis of atracurium in vivo. Anesthesiology 62:606-609, 1985 5. Kaplan JA: Role of ultrashort-acting beta-blockers in the postoperative period. J Cardiothorac Anesth 2:683-691, 1988 6. Savarese JJ, Ali HH, Basta SJ, et al: The clinical neuromuscular pharmacology of mivacurium chloride (BW1090U). Anesthesiology 68:723-732,198s
Bradycardia
Following
Induction
7. Ali H: Neuromuscular block and its antagonism: Clinical aspects, in Nunn JF. Uttling JE, Brown BR (eds): General Anesthesia (ed 5). 1989, pp 164-184 8. Ostergaard D. Jensen FS, Jensen E, et al: Mivacurium induced neuromuscular blockade in patients heterozygous for the atypical gene for plasma cholinesterase. Anesthesiology 71:A782, 1989 9. Baraka A, Cava L. Jaude CA: Atracurium v. suxamethonium in a case of organophosphorus poisoning. Br J Anesth 56:673, 1984
With Alfentanil
and Vecuronium
To the Editor: The association of vecuronium with some induction agents, including fentanyl,‘,’ sufentanil,” thiopental,4 and etomidate;’ has been shown to produce bradycardia, and even asystole” in some patients. We have not seen the same effect reported for the combination of alfentanil and vecuronium. Therefore, we would like to comment on two patients undergoing elective carotid endarterectomy in whom extreme bradycardia developed following induction with alfentanil and vecuronium. A 72-year-old-man’s past medical history included hypertension and hyperlipidemia. Coronary surgery had been performed 7 years before. He was currently free of angina and under treatment with propranolol, 20 mg every 8 hours. Premeditation was 0.1 mgikg of morphine. The patient was monitored with an ECG, a 20-g brachial artery catheter, pulmonary artery catheter, pulse oximetry, and end-tidal gas analyzer. Monitoring was completed before induction. Breathing 100% oxygen by mask, the patient was given (3 to 5 min) 120 kg/kg of alfentanil and 0.15 mg/kg of vecuronium. Baseline heart rate (HR) was 50 beatsimin and blood pressure (BP) 160170 mmHg. The patient was induced, his trachea intubated, and the surgical field prepared. As the drugs were injected, HR decreased gradually to a lowest value of 35 beats/min, while BP dropped concomitantly to 75/35 mmHg. At that time, the patient was mechanically ventilated with 100% 02. Atropine, 0.5 mg, ephedrine, 16 mg, and phenylephrine, 75 pg in three boluses were given IV. Heart rate and BP recovered to baseline within 3 minutes. An 84-year-old man with a medical history of severe hypertension was under treatment with nifedipine, 10 mg every 12 hours, and quinidine, 200 mg daily, for past atria1 fibrillation. Premeditation was 0.1 mg/kg of morphine. The patient was monitored with an electroencephalogram, 20-g brachial artery catheter, pulmonary artery catheter, pulse oximetry, and end-tidal gas analyzer. Baseline HR was 89 beats/min and BP 210/80 mmHg. Following induction with 120 kg/kg of alfentanil and 0.15 mgikg of vecuronium (in 3 to 5 min), and before tracheal intubation, the HR decreased to 43 beats/min and blood pressure dropped to 120/45 mmHg. Heart rate and blood pressure recovered to normal values following skin incision. No chronotropic or inotropic drugs were used in this case. Anesthesia and surgery were completed uneventfully in both cases. Bradycardia on induction has been described following administration of many drugs; in the case of opioids, this effect is probably centrally mediated. It has been attributed to rapid drug injection, use of P-blockers or calcium channel antagonists, or to a synergistic effect with other anesthetics drugs with vagotonic properties.” In these two cases, vecuronium was used; there are conflicting reports in the literature concerning an intrinsic bradycardic effect for this muscle relaxant.4-h In both cases, there was simultaneous injection of alfentanil and vecuronium, so we cannot blame any of the drugs in isolation, but possibly together. The first patient was on P-blockers and the second patient was receiving calcium channel blockers and quinidine, so we could also attribute the decrease in HR to a combination of the effects of these drugs with opioids; however, the maintenance of the bradycardic effect and the intensity of it could be a synergistic effect of alfentanil and vecuronium. A combination of short-acting anesthetic agents with a bradycardic effect can be desirable in some cases; however, the two cases reported suggest that precautions should be taken when alfentanil and vecuronium are used in combination, such as has been suggested for the combination of other synthetic opioids and vecuronium.3
Catholic
Guillermo Lemu, MD Carla Sacco, MD Jotge U&a, MD Department of Anesthesiology University, School of Medicine Santiago Chile
LETTERS TO THE EDITOR
775
REFERENCES 1. Bailey N, Stanley T: Narcotic intravenous anesthetics, in Miller RD (ed): Anesthesia,vol 1. New York, NY, 1990, pp 281-366 2. Mirakhur RK, Ferres CJ, Clarke RSJ, et al: Clinical evaluation of Org NC 45. Br J Anaesthesia 55:119, 1983 3. Starr NJ, Sethna DH, Estafanous FG: Bradycardia and asystole following the rapid administration of sufentanil with vecuronium. Anesthesiology 64:521-523, 1986 4. Inoue K, El-Banayosy A, Stolarski L, Reichelt W: Vecuroniurn-induced bradycardia following induction of anaesthesia with
Right Ventricular
etomidate or thiopentone, with or without fentanyl. Br J Anaesth 60:10-17, 1988 5. Cozanitis DA, Erkola 0: A clinical study into the possible intrinsic bradycardia activity of vecuronium. Anaesthesia 44:648650,1989 6. Chen BB, Nythan DP, Blanck TJJ: Hemodynamic effects and onset time of increasing doses of vecuronium in patients undergoing myocardial revascularization. J Cardiothorac Vast Anesth 5569-573, 1991
Dysfunction During Cardiac Transplantation: Role for Transesophageal Echocardiography
An Essential
To the Editor: During cardiac transplantation, right ventricular (RV) dysfunction is often seen in the newly implanted graft after weaning from cardiopulmonary bypass (CPB). This is frequently the result of existing high pulmonary vascular resistance (PVR) in the recipient with which the donor right heart struggles to contend. Various pulmonary dilators such as dobutamine, isoproterenol, or prostaglandin El are frequently necessary at this time. l-3 This letter reports another cause of acute RV failure in the donor heart detected by transesophageal echocardiography (TEE). A 55-year-old man with endstage congestive cardiomyopathy presented for cardiac transplantation. He had previously undergone two mitral valve replacements. The first was 17 years prior to transplant for rheumatic valvular disease. The second was 3 years prior to transplant for replacement of his original bioprosthesis. He had frequent episodes of severe congestive heart failure (CHF) despite maximal medical therapy. Preoperative cardiac catheterization data included pulmonary artery pressures (PAP) of 33/14/22 mmHg with a pulmonary capillary wedge pressure of 15 mmHg; cardiac index (CI) of 2.6 L/min/m2; PVR 1.4 Wood units; and ejection fraction of 10% to 15%. There was a history of ventricular arrhythmias requiring treatment with amiodarone. Other medical problems included bronchial asthma with pulmonary function tests revealing a mixed obstructive and restrictive defect with significant bronchodilator response. At the time of surgery a peripheral venous catheter and a brachial arterial catheter were placed. A mixed venous oxygen saturation pulmonary artery catheter and a 14-gauge catheter were placed in the right internal jugular vein. Initial hemodynamic parameters were CI 2.2 L/min/mz, PAP 40/26 mmHg, CVP 8 mmHg, MAP 101 mmHg, and systemic vascular resistance and maintained with (SVR) of 1700 dyne set . cm-5. Anesthesia was induced with diazepam, fentanyl, and pancuronium, air, oxygen, and fentanyl. After induction and intubation, a ~-MHZ biplane TEE probe (Toshiba American Medical Systems, Inc, Carrolton, TX) was placed atraumatically. Findings on the long-axis four-chamber and short-axis views were compatible with prior descriptions of the patient’s ventricular function.
Fig 1. Transesophageal echocardiograph strating echogenic material in left ventricle.
demon-
774
3. Lockridge 0: Substance P hydrolysis by human serum cholinesterase. J Neurochem 39:106-l lo,1982 4. Nigrovic V, Auen M, Wajskol A: Enzymatic hydrolysis of atracurium in vivo. Anesthesiology 62:606-609, 1985 5. Kaplan JA: Role of ultrashort-acting beta-blockers in the postoperative period. J Cardiothorac Anesth 2:683-691, 1988 6. Savarese JJ, Ali HH, Basta SJ, et al: The clinical neuromuscular pharmacology of mivacurium chloride (BW1090U). Anesthesiology 68:723-732,198s
Bradycardia
Following
Induction
7. Ali H: Neuromuscular block and its antagonism: Clinical aspects, in Nunn JF. Uttling JE, Brown BR (eds): General Anesthesia (ed 5). 1989, pp 164-184 8. Ostergaard D. Jensen FS, Jensen E, et al: Mivacurium induced neuromuscular blockade in patients heterozygous for the atypical gene for plasma cholinesterase. Anesthesiology 71:A782, 1989 9. Baraka A, Cava L. Jaude CA: Atracurium v. suxamethonium in a case of organophosphorus poisoning. Br J Anesth 56:673, 1984
With Alfentanil
and Vecuronium
To the Editor: The association of vecuronium with some induction agents, including fentanyl,‘,’ sufentanil,” thiopental,4 and etomidate;’ has been shown to produce bradycardia, and even asystole” in some patients. We have not seen the same effect reported for the combination of alfentanil and vecuronium. Therefore, we would like to comment on two patients undergoing elective carotid endarterectomy in whom extreme bradycardia developed following induction with alfentanil and vecuronium. A 72-year-old-man’s past medical history included hypertension and hyperlipidemia. Coronary surgery had been performed 7 years before. He was currently free of angina and under treatment with propranolol, 20 mg every 8 hours. Premeditation was 0.1 mgikg of morphine. The patient was monitored with an ECG, a 20-g brachial artery catheter, pulmonary artery catheter, pulse oximetry, and end-tidal gas analyzer. Monitoring was completed before induction. Breathing 100% oxygen by mask, the patient was given (3 to 5 min) 120 kg/kg of alfentanil and 0.15 mg/kg of vecuronium. Baseline heart rate (HR) was 50 beatsimin and blood pressure (BP) 160170 mmHg. The patient was induced, his trachea intubated, and the surgical field prepared. As the drugs were injected, HR decreased gradually to a lowest value of 35 beats/min, while BP dropped concomitantly to 75/35 mmHg. At that time, the patient was mechanically ventilated with 100% 02. Atropine, 0.5 mg, ephedrine, 16 mg, and phenylephrine, 75 pg in three boluses were given IV. Heart rate and BP recovered to baseline within 3 minutes. An 84-year-old man with a medical history of severe hypertension was under treatment with nifedipine, 10 mg every 12 hours, and quinidine, 200 mg daily, for past atria1 fibrillation. Premeditation was 0.1 mg/kg of morphine. The patient was monitored with an electroencephalogram, 20-g brachial artery catheter, pulmonary artery catheter, pulse oximetry, and end-tidal gas analyzer. Baseline HR was 89 beats/min and BP 210/80 mmHg. Following induction with 120 kg/kg of alfentanil and 0.15 mgikg of vecuronium (in 3 to 5 min), and before tracheal intubation, the HR decreased to 43 beats/min and blood pressure dropped to 120/45 mmHg. Heart rate and blood pressure recovered to normal values following skin incision. No chronotropic or inotropic drugs were used in this case. Anesthesia and surgery were completed uneventfully in both cases. Bradycardia on induction has been described following administration of many drugs; in the case of opioids, this effect is probably centrally mediated. It has been attributed to rapid drug injection, use of P-blockers or calcium channel antagonists, or to a synergistic effect with other anesthetics drugs with vagotonic properties.” In these two cases, vecuronium was used; there are conflicting reports in the literature concerning an intrinsic bradycardic effect for this muscle relaxant.4-h In both cases, there was simultaneous injection of alfentanil and vecuronium, so we cannot blame any of the drugs in isolation, but possibly together. The first patient was on P-blockers and the second patient was receiving calcium channel blockers and quinidine, so we could also attribute the decrease in HR to a combination of the effects of these drugs with opioids; however, the maintenance of the bradycardic effect and the intensity of it could be a synergistic effect of alfentanil and vecuronium. A combination of short-acting anesthetic agents with a bradycardic effect can be desirable in some cases; however, the two cases reported suggest that precautions should be taken when alfentanil and vecuronium are used in combination, such as has been suggested for the combination of other synthetic opioids and vecuronium.3
Catholic
Guillermo Lemu, MD Carla Sacco, MD Jotge U&a, MD Department of Anesthesiology University, School of Medicine Santiago Chile
LETTERS TO THE EDITOR
775
REFERENCES 1. Bailey N, Stanley T: Narcotic intravenous anesthetics, in Miller RD (ed): Anesthesia,vol 1. New York, NY, 1990, pp 281-366 2. Mirakhur RK, Ferres CJ, Clarke RSJ, et al: Clinical evaluation of Org NC 45. Br J Anaesthesia 55:119, 1983 3. Starr NJ, Sethna DH, Estafanous FG: Bradycardia and asystole following the rapid administration of sufentanil with vecuronium. Anesthesiology 64:521-523, 1986 4. Inoue K, El-Banayosy A, Stolarski L, Reichelt W: Vecuroniurn-induced bradycardia following induction of anaesthesia with
Right Ventricular
etomidate or thiopentone, with or without fentanyl. Br J Anaesth 60:10-17, 1988 5. Cozanitis DA, Erkola 0: A clinical study into the possible intrinsic bradycardia activity of vecuronium. Anaesthesia 44:648650,1989 6. Chen BB, Nythan DP, Blanck TJJ: Hemodynamic effects and onset time of increasing doses of vecuronium in patients undergoing myocardial revascularization. J Cardiothorac Vast Anesth 5569-573, 1991
Dysfunction During Cardiac Transplantation: Role for Transesophageal Echocardiography
An Essential
To the Editor: During cardiac transplantation, right ventricular (RV) dysfunction is often seen in the newly implanted graft after weaning from cardiopulmonary bypass (CPB). This is frequently the result of existing high pulmonary vascular resistance (PVR) in the recipient with which the donor right heart struggles to contend. Various pulmonary dilators such as dobutamine, isoproterenol, or prostaglandin El are frequently necessary at this time. l-3 This letter reports another cause of acute RV failure in the donor heart detected by transesophageal echocardiography (TEE). A 55-year-old man with endstage congestive cardiomyopathy presented for cardiac transplantation. He had previously undergone two mitral valve replacements. The first was 17 years prior to transplant for rheumatic valvular disease. The second was 3 years prior to transplant for replacement of his original bioprosthesis. He had frequent episodes of severe congestive heart failure (CHF) despite maximal medical therapy. Preoperative cardiac catheterization data included pulmonary artery pressures (PAP) of 33/14/22 mmHg with a pulmonary capillary wedge pressure of 15 mmHg; cardiac index (CI) of 2.6 L/min/m2; PVR 1.4 Wood units; and ejection fraction of 10% to 15%. There was a history of ventricular arrhythmias requiring treatment with amiodarone. Other medical problems included bronchial asthma with pulmonary function tests revealing a mixed obstructive and restrictive defect with significant bronchodilator response. At the time of surgery a peripheral venous catheter and a brachial arterial catheter were placed. A mixed venous oxygen saturation pulmonary artery catheter and a 14-gauge catheter were placed in the right internal jugular vein. Initial hemodynamic parameters were CI 2.2 L/min/mz, PAP 40/26 mmHg, CVP 8 mmHg, MAP 101 mmHg, and systemic vascular resistance and maintained with (SVR) of 1700 dyne set . cm-5. Anesthesia was induced with diazepam, fentanyl, and pancuronium, air, oxygen, and fentanyl. After induction and intubation, a ~-MHZ biplane TEE probe (Toshiba American Medical Systems, Inc, Carrolton, TX) was placed atraumatically. Findings on the long-axis four-chamber and short-axis views were compatible with prior descriptions of the patient’s ventricular function.
Fig 1. Transesophageal echocardiograph strating echogenic material in left ventricle.
demon-
