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end-tidal carbon dioxide partial pressure of 30–35 mmHg). CI was estimated by dye dilution method using 10 mg of indocyanine green as an indicator (DDG1001; Nihon Koden Inc., Tokyo, Japan). Subsequently, carbon dioxide was added to the inspiratory gases, so that PaCO2 rose to approximately 55 mmHg. The same set of measurements was repeated in each patient. MAP, CI and HR responses to hypercapnia in the clonidine-propofol subgroup were significantly attenuated compared with those in the other three subgroups (Figure). Plasma norepinephrine concentrations (but not epinephrine concentration) were significantly lower in clonidine-propofol patients. The cardiovascular effects of hypercapnia are suppressed in patients given clonidine prior to propofol anesthesia, perhaps due to the profound suppression of sympathetic nervous system activity. The hemodynamic response to hypercapnia depends on the level and extent of any sympathetic blockade.5 The interaction between the basal anesthetic agent and clonidine (given as a premedicant) can apparently modify the hemodynamic response to hypercapnia to a significant extent. Masayoshi Uchida MD Hiroki Iida MD Yoko Osawa MD Sigeaki Tanahashi MD Masahiko Kumazawa MD Kazuyuki Sumi MD Shuji Dohi MD Gifu, Japan

References 1 Maze M, Tranquilli W. Alpha-2 adrenoceptor agonists: defining the role in clinical anesthesia. Anesthesiology 1991; 74: 581–605. 2 Nishikawa T, Naito H. Clonidine modulation of hemodynamic and catecholamine responses associated with hypoxia or hypercapnia in dogs. Anesthesiology 1996; 84: 672–85. 3 Muzi M, Goff DR, Kampine JP, Roerig DL, Ebert TJ. Clonidine reduces sympathetic activity but maintains baroreflex responses in normotensive humans. Anesthesiology 1992; 77: 864–71. 4 Krassioukov AV, Gelb AW, Weaver LC. Action of propofol on central sympathetic mechanisms controlling blood pressure. Can J Anaesth 1993; 40: 761–9. 5 Shibata K, Futagami A, Taki Y, Kobayashi T. Epidural anesthesia modifies the cardiovascular response to marked hypercapnia in dogs. Anesthesiology 1994; 81: 1454–60.

The early detection of bupivacaine toxicity in dogs To the Editor: We read with interest the article of Kim et al.1 «Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs». In 1988, we conducted similar work,2 also showing that cardiac output appeared to be the first and the most affected hemodynamic variable, whereas mean systemic blood pressure remained unchanged because of the compensatory increase in systemic vascular resistance. In fact, bupivacaine iv primarily impairs cardiac intraventricular conduction3,4 enhancing QRS duration, as noted in Kim et al.’s Table and Figure 2.1 Contractile deficiency occurs only later. Marc Freysz MD PhD François Lenfant MD Dijon, France

PhD

References 1 Kim JT, Rhee KY, Bahk JH, et al. Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs. Can J Anesth 2003; 50: 376–81. 2 Beal JL, Freysz M, Timour Q, Bertrix L, Lang J, Faucon G. Haemodynamic effects of high plasma concentrations of bupivacaine in the dog. Eur J Anaesthesiol 1988; 5: 251–60. 3 Freysz M, Timour Q, Mazze RI, et al. Potentiation by mild hypothermia of ventricular conduction disturbances and reentrant arrhythmias induced by bupivacaine in dogs. Anesthesiology 1989; 70: 799–804. 4 de La Coussaye JE, Brugada J, Allessie MA. Electrophysiologic and arrhythmogenic effects of bupivacaine. A study with high-resolution ventricular epicardial mapping in rabbit hearts. Anesthesiology 1992; 77: 132–41.

R E P LY : We thank Freysz et al. for their comments. Though there is a some similarity in the experimental design between the two studies,1,2 we think the point of the articles is different. In our article,1 we intended to show that continuous mixed venous oxygen saturation correlated well with cardiac output in the early and late phases of bupivacaine intoxication. Mean blood pressure (MBP) was maintained in the early phase of bupivacaine-induced cardiotoxicity. MBP decreased abruptly and correlated

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well with cardiac output (CO) with impending cardiovascular collapse or at the late period of bupivacaineinduced cardiotoxicity. The article by Beal et al.2 showed the changes of hemodynamics (CO decreased and mean systolic blood pressure remained unchanged) in the early period of bupivacaine (cardiac) intoxication. The concept of early and late bupivacaine cardiotoxicity is based on the results of Cho et al.3 and its definition can be found in our article.1 An earlier study showed that a plasma bupivacaine concentration of 1 to 2 µg·mL–1 increased BP and decreased CO.4 CO does not always decrease with bupivacaine administration. After convulsive doses (1 mg·kg–1), CO increases.5 In addition, the bupivacaine concentration in our study was much higher than in Beal et al.’s. We appreciate Drs. Freysz and Lenfant’s comments but, in our view, both studies were quite different. Jin-Tae Kim MD Kook-Hyun Lee Seoul, Korea

MD

References 1 Kim JT, Rhee KY, Bahk JH, et al. Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs. Can J Anesth 2003; 50: 376–81. 2 Beal JL, Freysz M, Timour Q, Bertrix L, Lang J, Faucon G. Haemodynamic effects of high plasma concentrations of bupivacaine in the dog. Eur J Anaesthesiol 1988; 5: 251–60. 3 Cho HS, Lee JJ, Chung IS, Shin BS, Kim JA, Lee KH. Insulin reverses bupivacaine-induced cardiac depression in dogs. Anesth Analg 2000; 91: 1096–102. 4 Hasselstrom LJ, Mogensen T, Kehlet H, Christensen NJ. Effects of intravenous bupivacaine on cardiovascular function and plasma catecholamine levels in humans. Anesth Analg 1984; 63: 1053–8. 5 Rutten AJ, Nancarrow C, Mather LE, Ilsley AH, Runciman WB, Upton RN. Hemodynamic and central nervous system effects of intravenous bolus doses of lidocaine, bupivacaine, and ropivacaine in sheep. Anesth Analg 1989; 69: 291–9.

Intrathecal morphine vs psoas compartment block for hip surgery To the Editor: Souron et al. point out that the innervation to the hip joint arises from the lumbar as well as the sacral plexus and that analgesia will be incomplete with a psoas

compartment block alone.1 The lateral cutaneous nerve of the thigh (LCNT) can still be missed in about 5% of cases.2 Cross innervation from the gluteal nerves into the LCNT territory and the relatively low volume of local anesthetic used in this study may equally have contributed to a reduced success rate. A single shot psoas block is also known to have a shorter duration of action compared with intrathecal morphine. A central neuraxial technique will always be more reliable. In our view the authors are comparing apples with oranges. We use a continuous psoas compartment block, combined with a single shot parasacral block, as described by Mansour.3 The psoas block is initiated with 40 mL of prilocaine 1% and 10 mL of bupivacaine 0.5%. For the parasacral block we use 20 mL of bupivacaine 0.5%. In conjunction with general anesthesia no further analgesia is required intraoperatively. A further bolus of 20 mL of bupivacaine 0.25% is required after about six hours. Postoperative analgesia is provided with a continuous infusion of bupivacaine 0.125% at 10 mL·hr–1 until 12 hr before mobilization. Using this technique our patients often complain about pain in the back and other joints unrelated to their surgery. Souron et al. do not refer to the site of pain in their patients, making pain scores on their own unreliable in comparing the effectiveness of these two techniques. Kate Paterson Joerg Kuehne Surrey, UK

BSc MBCHB FRCA FRCA

References 1 Souron V, Delaunay L, Schifrine P. Intrathecal morphine provides better postoperative analgesia than psoas compartment block after primary hip arthroplasty. Can J Anesth 2003; 50: 574–9. 2 Tokat O, Turker YG, Uckunkaya N, Yilmazlar A. A clinical comparison of psoas compartment and inguinal paravascular blocks combined with sciatic nerve block. J Int Med Res 2002; 30: 161–7. 3 Mansour NY. Reevaluating the sciatic nerve block: another landmark for consideration. Reg Anesth 1993; 18: 322–3.

R E P LY : I thank Drs. Paterson and Kuehne for their comments on our article.1 Unfortunately, I radically disagree with their comments. First, the comparison between analgesia techniques is a very common research subject in the anesthesia literature, even when these techniques appear to be different in