The use of a temporary pacemaker for patients who develop bradycardia during general anaesthesia is controversial. We describe two episodes of severe bradycardia in the same patient during general anaesthesia, the second of which was managed with a pacemaker. She was admitted to hospital to have direct laryngoscopy and vocal cord biopsy, because of a history of hoarseness. This was to be carried out under general anaesthesia. She gave a history of a myomectomy under general anaesthesia in , which was uneventful, and asthma for the last 25 yr.
She was given 5 mg diazepam by mouth before going to the operating theatre. Sinus rhythm was present throughout the episode. Immediately after direct laryngoscopy by the surgeon, the heart rate suddenly decreased to 28 beats min —1. Despite withdrawal of the laryngoscope, bradycardia persisted.
Atropine 0. A further dose of atropine 0. Hypotension persisted and was treated with infusion of ml of hydroxyethyl starch. Arterial blood gas and serum electrolyte measurements were normal. After 12 min the patient became cadiovascularly stable. The operation was postponed, and the patient recovered without sequelae. Subsequent cardiac examination was normal. Six months later the same patient returned for treatment of nasal polyps, by nasal endoscopy.
Her hoarseness had resolved with medical therapy. For the second operation, she was given diazepam 5 mg by mouth. After tracheal intubation, the heart rate decreased. Virtually all anesthetic agents have intrinsic myocardial depressant properties, although some may mask this with sympathetic stimulation. The vasodilatory effects of the volatile agents can result in serious hypotension when combined with this negative inotropy.
In the patient with pre-existing cardiac disease, these cardiovascular anesthetic effects become much more serious. However, the effect of propofol on parasympathetic nerve activity has not been studied well. In the present study, propofol anesthesia caused a reduction in HF but not in LF, indicating rapid sequence induction of anesthesia with propofol might reduce a cardiac parasympathetic tone more than sympathetic tone.
Similar results were observed after induction of anesthesia with propofol in humans. Therefore, the ratio of spectral power showed a shift toward LF in the HRV spectrum, suggesting sympathetic dominance. Scheffer et al. Their results clearly indicate that propofol, thiopentone, and etomidate show differences in their effects on HRV.
These findings concerning the effects of propofol on HRV are in reasonably good agreement with our present results. Anesthesia with propofol is sometimes associated with bradycardia; however, the mechanism underlying this is not known. Because the autonomic nervous system plays an important role in regulating HR, propofol might induce bradycardia by altering the relative activities of the sympathetic and parasympathetic components.
Deutshchman et al. They observed that induction of anesthesia with propofol was associated with a significant reduction in total, LF, and HF power. Maintenance of anesthesia with propofol resulted in further reductions in total and LF, but not HF, power. They speculate that propofol anesthesia reduces parasympathetic tone to a lesser degree than sympathetic tone, developing to bradycardia.
However, several points should be discussed to resolve the question. First, induction and maintenance of anesthesia with propofol did not cause a reduction in HR in their study, indicating a discrepancy between HR and autonomic tone.
Similarly, in our present results, propofol anesthesia caused a reduction in HF, but not in LF, without significant change in HR. HRV is a measure of an end-organ response to peripheral and central neural centers that both produce and respond to HR and blood pressure oscillations.
Anesthetics that may disrupt integrative processes of the central nervous system or communication between the central nervous system and the end organ or the direct effects of anesthetics on the end organ itself will obviously affect changes in how the end organ responds and the measurement of it. Therefore, interpretation of HRV data must consider 1 the ability of the end organ to respond appropriately to neural regulation, 2 the ability of the two respective neural rhythms sympathetic and vagal to arrive at the heart, and 3 the ability of the neural regulatory centers to receive and integrate information from peripheral receptors.
Such multifactors might be associated with lack of correlation between HR and autonomic tone. In addition, the fact that induction of anesthesia with propofol caused larger decreases in muscle sympathetic nerve activity and blood pressure, indicating a decrease in peripheral sympathetic nerve activity, with a small increase in HR, indicating a decrease in cardiac parasympathetic nerve activity, in humans 7,8 support our HRV data.
However, the direct negative chronotropic effect of propofol 33 may offset an increase in HR response to HRV in the present study. Second, a lack of information about the depth of anesthesia might cause misinterpretation of the results because they observed HRV at just after and after 5 min of propofol administration.
Because they administered a 2. Third, propofol may decrease HR via its direct effect on heart. In animal experiments, propofol exerts a negative inotropic and chronotropic effect. Although sevoflurane is widely used for its favorable property of low blood—gas solubility that permits more rapid induction and emergence from anesthesia and more rapid control of anesthetic depth, 25 little is known about the effects of sevoflurane on HRV.
However, it can be speculated that sevoflurane has little or no effect on HRV because of its mild cardiovascular depression. Several studies have examined the effects of sevoflurane on the autonomic nervous system by means of measuring sympathetic nerve activity or baroreflex sensitivity as an alternative to measuring HRV.
In the present study, sevoflurane attenuated the LF without any significant effects in HF and entropy, indicating sevoflurane may inhibit sympathetic nerve activity without any significant changes in parasympathetic nerve activity. Differences in autonomic nervous tone during the study period would explain the differences in the effect of sevoflurane on sympathetic or parasympathetic nerve activities.
Our results showed the direct effects of anesthetics on HRV, i. In contrast, the effects of anesthetics on the baroreflex showed the dynamic side of autonomic nervous system—mediated responses. Therefore, it is not surprising that sevoflurane showed different effects between HRV and baroreflex. In fact, sevoflurane has been reported to have different effects on spontaneous efferent renal sympathetic nerve activity and the baroreceptor-sympathetic reflex in rabbits.
We recognize several limitations of our study. First, we did not measure sympathetic and parasympathetic nerve activity per se. Although HRV is a widely used, noninvasive technique to assess autonomic indexes of neural cardiac control, the changes in HRV might not reflect the effects of anesthetics on the autonomic nervous system but on the reflex arc.
In fact, baroreflex function and the autonomic nervous system are influenced by various physiologic and pathophysiologic factors, 15 including sex, 35 age, 36 hypothermia, 37 and preexisting cardiopulmonary diseases.
Second, anesthesia-induced changes in respiratory rate and tidal volume should influence HRV. The HF component of HRV has been known to result from respiratory-related vagal modulation of HR, and the amplitude has been demonstrated to correlate with cardiac vagal tone.
In the present study, we tried to maintain steady state respiration to minimize the influences on HRV. Third, it was uncertain whether the equal depth of anesthesia was achieved at the same BIS value between propofol and sevoflurane anesthesia.
Although BIS has been found to be an effective measure of depth of sedation with propofol, midazolam, isoflurane, and sevoflurane, 19,20,43 the BIS demonstrates significant variability among the anesthetics. To date, the precise mechanism underlying these variations in BIS is not known. Moreover, there is no convincing evidence that the BIS value was independent of the depth of anesthesia in our present study.
Therefore, we believe that the gradual decreases in the BIS values correlated with the depth of anesthesia during propofol and sevoflurane anesthesia.
In summary, propofol decreased HF and entropy rather than LF in the BIS-dependent manner, indicating that cardiac parasympathetic nerve would be inhibited to a greater degree than sympathetic nerve during induction of anesthesia with propofol. Anesthesia specialists devote careful attention and use many methods to prevent this.
Freedman MD - Anesthesiology. Author: Healthwise Staff. This information does not replace the advice of a doctor. Healthwise, Incorporated, disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use.
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