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Canadian Journal of Anesthesia 51:188-189 (2004)
© Canadian Anesthesiologists' Society, 2004


Correspondence

Clonidine attenuates the hemodynamic responses to hypercapnia during propofol anesthesia

Masayoshi Uchida, MD, Hiroki Iida, MD, Yoko Osawa, MD, Sigeaki Tanahashi, MD, Masahiko Kumazawa, MD, Kazuyuki Sumi, MD and Shuji Dohi, MD

Gifu, Japan

To the Editor:

Clonidine, an alpha2-adrenergic agonist, is widely used as an anesthetic adjuvant,1,2 and is reported to decrease sympathetic nervous activity,2,3 plasma norepinephrine concentration,2 and sympathoadrenal responses.2,3 Propofol can cause hypotension and bradycardia via a profound decrease in sympathetic tone.4 The purpose of our study was to examine the hemodynamic changes to hypercapnia during propofol and isoflurane anesthesia, and to compare them in the presence and absence of clonidine premedication.

After obtaining approval from our institutional Human Investigation Committee and informed consent from each patient, 60 adult patients (ASA physical status I) were randomly assigned to one of two groups. Thirty patients received famotidine 20 mg (control group) orally 90 min before the induction of anesthesia, whereas the remaining 30 patients received clonidine 5 µg•kg-1 and famotidine 20 mg (clonidine group). General anesthesia was induced with iv propofol 2 mg•kg-1, and tracheal intubation was facilitated with iv vecuronium 0.2 mg•kg-1. In 15 patients in each group, anesthesia was maintained with isoflurane 1% (end-tidal) in oxygen, and in the other 15 patients with iv propofol 100 µg•kg-1•min-1 during ventilation with oxygen. The baseline measurements including mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), and plasma catecholamine concentration were made during normocapnia (an 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 (FigureGo). Plasma norepinephrine concentrations (but not epinephrine concentration) were significantly lower in clonidine-propofol patients.



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FIGURE Difference from normocapnic values of mean arterial pressure (MAP), heart rate (HR) and cardiac index (CI) during hypercapnia (PaCO2 = 55 mmHg). Values are mean ± SD. *P < 0.05 vs normocapnic value. {dagger}P < 0.05 vs the other three subgroups.

 
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.

References

1 Maze M, Tranquilli W. Alpha-2 adrenoceptor agonists: defining the role in clinical anesthesia. Anesthesiology 1991; 74: 581–605.[Medline]

2 Nishikawa T, Naito H. Clonidine modulation of hemodynamic and catecholamine responses associated with hypoxia or hypercapnia in dogs. Anesthesiology 1996; 84: 672–85.[Medline]

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.[Medline]

4 Krassioukov AV, Gelb AW, Weaver LC. Action of propofol on central sympathetic mechanisms controlling blood pressure. Can J Anaesth 1993; 40: 761–9.[Abstract/Free Full Text]

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.[Medline]





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