There were no Group V-L patients in whom SAP or DAP increased more than 20% over baseline (i.e., at the end of surgery) (Table 2). The number of patients in whom HR increased more than 20% over baseline was smaller in the two verapamil-treated groups (Groups V and V-L) than in the lidocaine-alone group (Group L). Similar number of patients in Groups S and L experienced more than 20% increases in hemodynamics.
No patients suffered from laryngeal spasm after extubation. The numbers of patients who had coughed or strained were 25, 25, 14, and 16 in Groups S, V, L, and V-L, respectively (P = 0.0001 for Group S versus Groups L and V-L, and P = 0.0008 for Group V vs Groups L and V-L). The extubation quality scores [median (range)] were 3 (2-5), 3 (2-5), 2 (1-4), and 2 (1-3) in Groups S, V, L, and V-L, respectively (P = 0.0009, 00012, 0.0003, and 0.0002 for Group S versus Group L, Group S versus Group V-L, Group V versus Group L, and Group V versus Group V-L, respectively). The administration of lidocaine (in Groups L and V-L) significantly suppressed coughing and strain compared with the other nontreatment regimens. The number of patients with pruritus, nausea, vomiting, diarrhea, or laryngeal irritation, including sore throat and hoarseness, was similar among the four groups.
Although one patient in the control group had transient bigeminy lasting approximately 10 s, no ventricular arrhythmia was observed in the other treatment groups. None of the patients who received verapamil (alone or plus lidocaine) developed profound hypotension [SAP <80 mm Hg ], bradycardia (HR <50 bpm), or sinoatrial or atrioventricular block severe enough to require pressor or sympathomimetic drugs during or after tracheal extubation or in the ward.
In the current study, we have confirmed that the cardiovascular changes during tracheal extubation were blunted by verapamil 0.1 mg/kg and by lidocaine 1 mg/kg. We have also found that the combination of verapamil and lidocaine at these doses attenuated the hemodynamic events more effectively than did either medication alone.
Although the precise mechanism responsible for the cardiovascular changes during tracheal extubation remains to be elucidated, multifactorial stimuli during tracheal extubation, including wound pain, emergence from anesthesia, and tracheal irritation, are involved in the events. The beneficial effect of lidocaine on the hemodynamic sequences may be due, in part, to direct cardiac depression and peripheral vasodilation. Extubation irritates airways and causes cough, which is known to produce hypertension and tachycardia. IV lidocaine suppresses the cough reflex [11,12]. As in previous reports, the number of patients in the current study who experienced coughs was less in the lidocaine-treated groups than in the group treated with verapamil alone. Attenuation of the activity in afferent C fibers from the larynx may contribute to this successful intervention . Verapamil, which has a potent local anesthetic activity, failed to attenuate laryngeal irritation. This calcium channel blocker is thought to control hypertension and tachycardia by its direct vasodilatory and negative chronotropic and dromotropic properties . Because verapamil is highly protein-bound (90%), concomitant use of lidocaine is likely to increase the pharmacologically active unbound portion of verapamil , resulting in an elevation of free concentrations of verapamil. Lidocaine may have enhanced the suppressive effect of verapamil on the hemodynamic complications during tracheal extubation through this mechanism. Plasma concentrations of adrenaline and noradrenaline increase during this stressful period . The IV infusion of lidocaine inhibits hypertensive and tachycardic responses to tracheal extubation . However, the lidocaine infusion reportedly failed to inhibit the general sympathetic response to extubation as assessed by increased plasma catecholamine concentrations . At doses used in the clinical setting (0.1-0.3 micro g/mL), verapamil is also unlikely to suppress catecholamine release, inconsistent with an in vitro study .
Myocardial ischemia may occur during tracheal extubation in patients with coronary arterial disease [19,20]. The occurrence of perioperative myocardial ischemia during anesthesia is associated with postoperative myocardial infarction [21,22]. Because HR is a major controllable determinant of myocardial oxygen balance , satisfactory suppression of tachycardic response to tracheal extubation with verapamillidocaine combination may be beneficial to patients with coronary arterial disease.
The administration of an atropine-neostigmine mixture for the reversal of residual muscle blockade increases HR within one minute, with the peak effect (20% increase) occurring one to two minutes after injection. The HR returns to baseline values three minutes after injection . These phenomena are probably caused by a more rapid onset of atropine compared with neostigmine. Verapamil plus lidocaine given three minutes after the atropine-neostigmine mixture in the current study probably had no effect on the reversal-induced tachycardia. A further study with differing timings, doses, and/or modes of the administration of verapamil and lidocaine should be conducted. The HR continues to decrease below the baseline until six minutes after the administration of the atropine-neostigmine mixture and subsequently shows a 20% decrease from the baseline for more than 30 minutes . A single IV injection of verapamil decreases the mean AP 20 seconds after administration, with a return toward basal values by four minutes . Thus, neostigmine may intensify the effects of the verapamil/lidocaine combination on hemodynamics during the extubation period. In the current study, none of the patients who received the combination of verapamil and lidocaine sustained bradycardia or hypotension sufficient to require pressor or sympathomimetic drugs after extubation. However, this possibly enhanced hypotensive action of neostigmine, verapamil, and lidocaine may be disadvantageous to patients in whom cardiac depression is undesirable (e.g., those with congestive heart failure because of hypertension). In this setting, administering verapamil or lidocaine alone may be more suitable than the combination. The benefit to risk ratio of the combined method for these patients warrants further study.
In conclusion, we have shown that a combination of verapamil 0.1 mg/kg and lidocaine 1 mg/kg injected IV two minutes before extubation is a simple, effective, and practical prophylactic method for suppressing the hypertensive and tachycardic responses to tracheal extubation, and this beneficial effect is superior to that of each drug alone.
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© 1997 International Anesthesia Research Society
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