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* From the Department of Anesthesiology and Section of Cardiology, Ton Yen General Hospital, Hsin Chu, Taiwan.
Address correspondence to:Dr. Chih-Long Shen, 69, Second Shen-Chen Rd, Department of Anesthesiology, Ton Yen General Hospital, Chu Pei, Hsin Chu, 302-42 Taiwan. Phone: 886-3-5527000 Ext 1201; Fax: 886-3-5516585; E-mail: yuchun51{at}ms22.hinet.net
| Abstract |
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Methods: We studied 254 healthy women undergoing Cesarean section under spinal anesthesia prospectively. Spinal anesthesia with 10 mg bupivacaine mixed with 0.2 mg morphine was performed at the L3-4 interspace. Intraoperative arrhythmias were recorded and verified later by a cardiologist.
Results: First degree atrioventricular block developed in nine patients (3.5%), second degree atrioventricular block in nine (3.5%), severe bradycardia (heart rate < 50 beatsmin1) in seventeen (6.7%), multiple VPC in three (1.2%). The height and weight of patients with severe bradycardia, multiple VPCs, or atrioventricular block were not different from those of the other patients. However, the age of patients in the potentially dangerous arrhythmias group was greater than that in the other group (P = 0.006).
Conclusion: The incidence of arrhythmias as well as hypotension during spinal anesthesia for Cesarean section was higher than expected. Although most of these arrhythmias were transient and recovered spontaneously, they might unexpectedly occur and sometimes need immediate and prompt treatment. It is necessary to remain vigilant during spinal anesthesia for Cesarean section and careful monitoring of these patients is warranted, especially in older parturients.
| Introduction |
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| Methods |
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No premedication was given. In the operating room, automatic noninvasive blood pressure at two minute intervals, and pulse oximeter were applied. The ECG, lead II, was continuously monitored (Hewlett Packard, CMS 24 OmniCare). Patients received nasal oxygen supplementation at 2 Lmin1 and a rapid infusion of 20 mLkg1 lactated Ringer's prior to anesthesia. Then, with the patients in the right lateral decubitus position, spinal puncture was performed at the L3-4 interspace and 10 mg hyperbaric bupivacaine 0.5% mixed with 0.2 mg morphine were administered. The patients were immediately turned supine and the operating table was positioned in a left lateral tilt to achieve left uterine displacement. The levels of the block to pinprick were measured at five minute intervals. If systolic blood pressure was < 100 mmHg or 80% of baseline, intermittent 8 mg boluses of ephedrine iv were given. All parturients with severe bradycardia (heart rate < 50 min1) received 0.5 - 1 mg atropine iv.
The ECG was closely observed by the anesthesiologist. When arrhythmias occurred, the ECG was recorded and the unit allowed the recording to commence five seconds before the trigger (Hewlett Packard, REC M1116B). The ECG records were verified later by a cardiologist. Outpatient department follow-up and 24-hr Holter study were suggested to all parturients with second degree AV block. The condition of the neonatal was evaluated by Apgar scores at one and five minutes.
To identify the most important individual risk factors associated with potentially dangerous arrhythmias,8 patients with severe bradycardia, multiple VPCs, or AV block were compared with the other patients.
Statistical analysis
Statistical analysis was performed using: 1) Spearman's rank correlation coefficient to correlate spread of blockade with age, body height and weight.9,10 Dermatomal levels, age, body weight and height were changed to rank scales before statistical analysis. 2) Unpaired Student's t test to evaluate the risk factors for AV block, severe bradycardia and multiple VPC. Differences were considered to be statistically significant when P < 0.05 and data were presented as mean ± SD.
| Results |
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7 at one and five minutes.
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The body height, and weight of parturients with severe bradycardia, multiple VPCs, or AV block were not different from those of the other parturients. However, the age of patients in the potentially dangerous arrhythmias group was greater than that in the other group (31.3 ± 4.4 vs 29.0 ± 4.4 yr, P = 0.006).
| Discussion |
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The distinction between Mobitz type I and type II block is descriptive. Mobitz type I is diagnosed by the presence of blocked atrial depolarization preceded by prolongation of the PR interval. Mobitz type II AV block manifests with several consecutive impulses that are conducted with a constant conduction time and that are followed by a block of conduction.11 In our study, there were four cases in whom the PR intervals increased or decreased haphazardly. It was not necessarily the longest PR interval that was followed by the blocked impulse. Denes12 called such episodes "atypical Wenckebach periods", although some authors refer to them as Mobitz type II,13 "Mobitz type II-like",14,15 "pseudo mobitz type II"16,17 or "apparent Mobitz type II".14 However, the site of block is probably a more important determinant of prognosis and the need for pacemaker therapy than the type of block.
Usually, Mobitz type I AV block is due to excess vagotonia and the site of the block is within the AV node. The likelihood of the development of complete AV block may be very low. Usually, Mobitz type II is associated with a wide QRS complex and is due to disease of the His-Purkinje system.18 It is more likely associated with a high mortality rate and requires a pacemaker to prevent more advanced AV block or cardiac arrest. However, electrophysiologic studies in Mobitz type II block with narrow QRS complexes (absence of bundle-branch block) sometimes localized the block at the AV node or proximal His-bundle.13,1921 Some studies demonstrated that vagal activity could modify AV conduction to produce first degree to complete heart block including Mobitz type II.13,2025 For vagally mediated AV block, the decision regarding the use of pacemakers is not based on the type of block or on QRS duration but on the underlying clinical settings and the correlation of symptoms.26 For all our patients with second degree AV block, the prognosis was benign, because they had narrow QRS complexes and only occurred transiently during spinal anesthesia without significant ventricular pause.
There were 17 cases (6.7%) of severe bradycardia during spinal anesthesia in our patients. There are no studies of the relation between neonatal outcome and maternal bradycardia during anesthesia. However, maternal bradycardia might reduce uterine blood flow. To protect both the fetus and the parturient, all of the parturients with severe bradycardia received 0.5 - 1 mg atropine iv. One case suddenly developed severe bradycardia and loss of consciousness without warning Thus, we emphasize the importance of careful monitoring of patients and early management of side effects. These may be the keys in preventing more dangerous conditions, such as asystole.
There are many mechanisms to explain the high incidence of intraoperative arrhythmias. First, the cephalic spread of spinal block induced a relative increase in parasympathetic activity by blockade of cardiac sympathetic stimulation or vasovagal attack through decreased venous return.6 The differences in latency and duration of various cardiac tissues in response to this unstable autonomic tone22 might encourage arrhythmias. Second, nausea, vomiting and surgical manipulation during Cesarean section might also increase vagal tone. The relative increase in parasympathetic activity was not associated only with hypotension, but also with bradycardia and AV block in our study. Third, there were four cases of second degree AV block occurring immediately after intravenous ephedrine for hypotension or atropine for bradycardia. Though AV nodal conduction was enhanced and intranodal block tended to decrease after administration of atropine,27 some studies have shown that atropine that only minimally improved conduction in the AV node, but markedly increased the sinus rate. This could increase the degree of block as a result of the increasing atrial rate.19,20 Spear et al. demonstrated differences in the latency, duration and threshold of the SA node and the AV conduction in response to the sympathetic effect.22 This mechanism was like "tachycardia-dependent conduction disturbance", AV block might occur after increased vagal tone stopped, due to the relatively prolonged AV nodal refractoriness.26 Fourth, hemodynamic, hormonal, autonomic, and emotional changes related to pregnancy might be associated with arrhythmias.28,29
Body height has been considered an important determinant of the dose of spinal anesthesia although some evidence suggested no correlation between body height or weight of parturients and spread of spinal block.30,31 In our study, all parturients were given the same dose of spinal anesthetic agent. There was no difference between age, body height, weight and spread of the blockade. Thus, it is not necessary to vary the dose of hyperbaric bupivacaine according to parturient's age, body height or weight.
In summary, our study showed that the incidence of arrhythmias as well as hypotension during spinal anesthesia for Cesarean section was higher than we expected. Although most of these arrhythmias were transient and recovered spontaneously, they might occur unexpectedly and, sometimes, require immediate treatment. It is necessary to remain vigilant and careful monitoring of patients during spinal anesthesia for Cesarean section is warranted, especially in older parturients.
| Footnotes |
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Accepted for publication January 7, 2000.
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