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CASE REPORT
Year : 2009  |  Volume : 3  |  Issue : 1  |  Page : 35-38

Reflex bradycardia and asystole during anaesthesia


St Michael's Hospital, Southwell Street, Bristol, BS2 8EG, United Kingdom

Correspondence Address:
Stephen Michael Kinsella
St Michael's Hospital, Southwell Street, Bristol, BS2 8EG
United Kingdom
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1658-354X.51833

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Date of Web Publication18-Jul-2009
 

   Abstract 

Neurogenically mediated bradycardia that may result in cardiac arrest is a rare but well-recognised complication during anaesthesia. Three cases are described that illustrate certain features. In the first, hidden haemorrhage during laparoscopy under general anaesthesia was revealed during reinsufflation of gas into the peritoneum at the end of the operation. The second case developed asystole when positioned supine with tilt after spinal anaesthesia for caesarean section. This occurred on two occasions separated by ten years. In the third case, asystole developed 95 minutes after a spinal when the patients legs were lowered down from the lithotomy position. All patients were resuscitated with drug treatment and, in the first case, intravenous fluids.


How to cite this article:
Kinsella SM. Reflex bradycardia and asystole during anaesthesia. Saudi J Anaesth 2009;3:35-8

How to cite this URL:
Kinsella SM. Reflex bradycardia and asystole during anaesthesia. Saudi J Anaesth [serial online] 2009 [cited 2019 Jun 16];3:35-8. Available from: http://www.saudija.org/text.asp?2009/3/1/35/51833


   Introduction Top


DECREASED HEART RATE may occur during anaesthesia from many causes, including cardiac pathology, pre-operative or anaesthetic drugs and hypoxia. Sudden bradycardia may also be produced through 'paradoxical' cardiovascular reflexes [1]. These are activated especially during periods of reduced venous return to the heart, over-riding the effect of baroreflex suppression which acts to maintain blood pressure in this situation by increasing heart rate and vasoconstriction. We present three cases of perioperative bradycardia or asystole and highlight pertinent issues.

Case 1

A 46 year old ASA 1 woman had a laparoscopically-assisted vaginal hysterectomy. She had a premedication of paracetamol and metoclopramide, and general anaesthesia was induced with propofol, alfentanil and vecuronium and maintained with desflurane. She was also given 1,500 ml Hartmann's solution (Ringer lactate), morphine, cyclizine, dexamethasone and diclofenac during surgery. The laparoscopic portion of surgery took 45 minutes with steep head down tilt (Trendelenberg) followed by rapid completion vaginally with reduced head down tilt. Minimal bleeding was noted during surgery and the cardiovascular observations were stable.

The peritoneum was then re-inflated with CO 2 in order to check the dissection site and head down tilt was increased again. This was followed by a bradycardia of 35-40 beats min -1 , blood pressure of 60/- mmHg and a sudden fall in end tidal CO 2 from 35 mmHg to 20 mmHg. At the same time bleeding was identified internally at the left port site. Ephedrine, 500 ml crystalloid and 500 ml colloid were given rapidly and the left inferior epigastric artery was sutured. The cardiovascular system stabilised rapidly.

As the patient was being woken up and started to cough, there was a significant blood loss through the umbilical port site. A large drain was inserted through this. It was presumed that this blood loss was not fresh but had occurred during the operation and retained in the upper abdomen because of the head-down tilt, and so the patient was extubated. A total of 2000 ml blood collected in the drain over the next hour, and she was transfused three units of blood. She was kept on the High Dependency Unit but had no further problems.

Case 2

A 34 year old woman presented for anaesthetic assessment prior to elective caesarean section for previous caesarean section. She gave a history of cardiac arrest during an elective caesarean for breech 10 years previously. Her old case notes were reviewed. After intravenous preloading with 1000 ml Hartmann's solution, she had a spinal anaesthetic inserted in the left lateral position using 2.25 ml hyperbaric bupivacaine 0.5% following which she was turned to the supine position with lateral table tilt. 90 seconds after the spinal she developed asystole which lasted for 15 seconds but responded to 600 µg atropine and commencing an ephedrine infusion. Following this she had a tachycardia of 140 beats min -1 , blood pressure of 190 / 120 mmHg and vomited. Her block was noted to be T5/6. The rest of the anaesthesia was uneventful. An initial post­operative electrocardiogram showed first degree heart block but repeat electrocardiogram, 24-hour electrocardiographic monitoring and echocardiography were normal.

It was decided to use spinal anaesthesia again on this occasion. An intravenous preload with 1000 ml Hartmann's solution was started. The spinal was inserted in the right lateral position using 2.5 ml hyperbaric bupivacaine 0.5% with 300 µg diamorphine and she was turned into the full left lateral position. This produced a bilateral T4 block to cold sensation after 15 minutes and she was turned supine with lateral table tilt. She was prepared for surgery, and at this point the anaesthetist commented "It seems that lightning doesn't strike twice in the same place". Within a minute, following skin incision, she developed a bradycardia of 35 beats min -1 . She was given 600 µg atropine but the heart rhythm progressed to ventricular asystole with P waves only. This lasted for 10 seconds but resolved following a second dose of 600 µg atropine. The next observations were heart rate 150 beats min -1 and blood pressure of 190 / 95 mmHg. This settled and there were no problems during the rest of the surgery.

Case 3

An 88 year old ASA 2 patient was due for vaginal hysterectomy and repair. She had hypertension treated with acebutolol. She was premedicated with 1g paracetamol and 7.5 mg meloxicam. Baseline cardiovascular readings were BP 210 / 110 mmHg, heart rate 68 beats min -1 , SpO2 94%. A spinal was inserted in the right lateral position at the L3/4 interspace using 1.8 ml hyperbanic bupivacaine 0.5% with 300 µg diamorphine. She was turned supine and once the upper level of block had reached T10 to cold sensation, the surgical team was called. Surgery was carried out in the lithotomy position, and lasted approximately 75 minutes. During surgery her systolic BP varied from 125-175 mmHg, diastolic BP 60-90 mmHg, heart rate 55-65 beats min -1 and SpO2 92-94%. As she was calm, no sedation was given.

At the end of the operation, her legs were placed flat and then the monitors were detached. Two minutes later, and 95 minutes after the spinal, she complained of feeling strange and then lost consciousness and developed marked pallor. A peripheral pulse could not be felt. The monitors were reattached and the electrocardiogram showed asystole. She was given 9 mg ephedrine and external cardiac massage was started. After 5 compressions, a heart rate of 60 beats min-1 developed. She was given a further dose of 3 mg ephedrine as well as 200 µg glycopyrronium, bringing her heart rate up to 80 beats min -1 and BP of 150/80 mmHg on first measurement. On regaining consciousness, she vomited profusely. She was given oxygen using a Hudson mask. In the recovery ward (PACU) she remained drowsy but her cardiovascular system was stable.


   Discussion Top


There are a number of terms that are applied to bradycardia caused by neurogenic mechanisms. These vary from relatively 'normal' reflexes, that is they occur in a significant number of subjects with particular stimuli, to the pathological and life threatening. Vasovagal syncope may occur from psychological stress such as fear or injections, or orthostatic stress (for example prolonged standing). Malignant vasovagal syncope is sufficiently prolonged so as to risk harm. A further term in use is neurocardiogenic syncope, which besides vasovagal syncope includes micturition syncope as well as carotid sinus syndrome. None of these patients had a history of syncope in daily life, although one had previously had the same reaction to a similar anaesthetic.

Severe haemorrhage can cause vasovagal syncope, with an incidence that varies from 4% after 440 ml loss up to 50% after 1000 - 1200 ml loss [1]. In cases where haemorrhage presents with relative bradycardia, transfusion increases the heart rate [2]. Cases of transient asystole were described at induction or maintenance of general anaesthesia in the 1980's. At this time cardiostable anaesthetic drugs and neuromuscular blockers were being introduced into clinical practice and routine vagolytic premedication was being abandoned. Such drug induced asystole was easily reversed. However, a combination of general anaesthesia and hypovolaemia is likely to require more extensive drug treatment as well as blood volume replacement. Retroperitoneal blood vessel damage during instrument insertion is the most dramatic complication of laparoscopy, and will usually be recognised immediately. In Case 1 the bleeding occurred from the epigastric artery damaged during port insertion, but was hidden in the upper abdomen because of the Trendelenberg position. Alterations in patient positioning change venous return and can precipitate or reverse vasovagal responses [3]. Other factors include lower body negative or positive pressure, inferior vena cava compression and pneumoperitoneum. Case 1 demonstrates the complex interactions that may occur during laparoscopic surgery. The increased head down tilt applied at the start of the second laparoscopic session would normally improve venous return, but this was outweighed by the effect of the pneumoperitoneum.

Vasovagal syncope may manifest to a variable degree depending on the stimulus, timing, and prior events. However, the aystolic reaction in Case 2 was very similar on both occasions, although the timing was different. On the first occasion asystole followed very soon after the spinal, when the patient was supine. The second time the patient was stable after the spinal in the left lateral position but asystole followed supine positioning. Lateral table tilt does not reliably prevent inferior vena cava compression by the term pregnant uterus in the supine position [4]. When women were managed in the full left lateral position immediately after spinal for caesarean section, hypotension was sometimes delayed until they were positioned supine for the operation [5]. Therefore in Case 2 the trigger for the asystole was not the spinal anaesthetic, but the effect of supine vena cava compression augmented by the spinal. Furthermore although on the second occasion asystole followed skin incision, this was not a 'vagal' response to incision as there was an effective regional anaesthetic blocking afferent input.

In the event of severe bradycardia or asystole with hypotension occurring in the supine tilted position in an obstetric patient, especially after regional anaesthesia, an element of inferior vena cava compression must be assumed. There are cases of resistant cardiovascular collapse, even resulted in death, where there was apparently a reliance on the initial lateral tilt [6],[7],[8]. The management of bradycardia or asystole must include increasing the tilt, the full lateral position or rapid delivery of the fetus if drug treatment does not provide immediate relief. Case 2 responded to drug treatment before delivery, but the team was in a position to perform delivery had it been necessary. With hindsight the patient should probably have been given small prophylactic doses of ephedrine or glycopyrronium at the times of greatest circulatory stress, that is on spinal insertion and on positioning supine.

Prolonged PR interval has been found to be an independent risk factor for the development of bradycardia during spinal anaesthesia [9], and spinal anaesthesia may unmask permanent cardiac conduction abnormalities [10]. On the other hand a perioperative bradycardia may be followed by transient ECG abnormalities as happened on the first occasion in Case 2.

Case 3 again demonstrates the importance of change of position, with a decrease in venous return when the patient's legs were laid flat. A number of papers have insisted on a treatment sequence of atropine-ephedrine-adrenaline to treat bradycardia or asystole [11],[12]. Strict adherence to this may not be as important as prompt treatment with what is to hand. Early external cardiac massage will also ensure the circulation of the drug to the site of action.

Asystole occurred 95 minutes after the spinal in Case 3.. Asystole after epidural or spinal has been described up to 120 minutes after the induction of anaesthesia, occurring sometimes in the recovery ward [13],[14],[15]. The period of physical and professional transfer of the patient at the end of the operation is usually a time of reduced vigilance with cessation of intraoperative monitoring, and position changes that may include putting the legs and patient flat, or even moving to a semirecumbent position [16]. We would caution the anaesthetist to continue close attention to the patient's conscious level and maintain venous return by gradual elevation of the heart above the lower body. Bradycardia in the recovery period was found to be least frequent with elevation of head and legs by 30 o compared to the supine or Trendelenberg positions [17].

Bradycardia with hypotension occurs in 5% of spinal anaesthetics [18], but the precise incidence of sudden severe bradycardia is not available. In a large survey, Kopp et al noted a frequency of cardiac arrest during regional anaesthesia of 1.8 per 10,000 cases, with the rate being higher with spinals compared to epidurals (2.9 versus 0.9 per 10,000 cases) [19]. About half of arrests were associated with anaesthetic factors and the rest with surgical factors. The risk of dying after cardiac arrest was greater with general compared to regional anaesthesia.

Many anaesthetists will only rarely deal with a case of cardiac arrest during anaesthesia. The importance of having the knowledge, vigilance, equipment and skills to deal rapidly with such a case will be crucial for the patient's survival.

Acknowledgements. I would like to thank Dr Mark Scrutton for the details of Case 1.

 
   References Top

1.Kinsella SM, Tuckey JP. Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold Jarisch reflex. Br J Anaesth 2001; 86: 859-868.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Sander-Jensen K, Secher NH, Bie P, Warberg J, Schwartz TW. Vagal slowing of the heart during haemorrhage: observations from 20 consecutive hypotensive patients. Br Med J 1986; 292: 364-366.  Back to cited text no. 2    
3.Nishikawa T, Anzai Y, Namiki A. Asystole during spinal anaesthesia after change from Trendelenburg to horizontal position. Can J Anaesth 1988; 35: 406-408.  Back to cited text no. 3  [PUBMED]  
4.Kinsella SM. Lateral tilt for pregnant women: why 15 degrees? Anaesthesia 2003; 58: 833-837.  Back to cited text no. 4    
5.Mendonca C, Griffiths J, Ateleanu B, Collis RE. Hypotension following combined spinal-epidural anaesthesia for Caesarean section: left lateral position vs. tilted supine position. Anaesthesia 2003; 58: 428-431.  Back to cited text no. 5    
6.Watkins EJ, Dresner M, Calow CE. Severe vasovagal attack during regional anaesthesia for Caesarean section. Br J Anaesth 2000; 84: 118-120.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Why mothers die; report on confidential enquiries into maternal deaths in the United Kingdom 1994-1996. London: HMSO 1998.  Back to cited text no. 7    
8.Why mothers die 1997-1999. The confidential enquiries into maternal deaths in the United Kingdom. London: RCOG press 2001.  Back to cited text no. 8    
9.Paul GE, Carpenter RL, Stephenson C, Wu R. Prolonged PR interval associated with increased incidence of bradycardia during spinal anesthesia. Anesthesiol 1993; 79; A1086.  Back to cited text no. 9    
10.Underwood SM, Glynn CJ. Sick sinus syndrome manifest after spinal anaesthesia. Anaesthesia 1988; 43: 307-309.  Back to cited text no. 10  [PUBMED]  
11.Pollard JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001; 92: 252-256.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Wahl A, Eberli FR, Thomson DA, Luginbuhl M. Coronary artery spasm and non-Q-wave myocardial infarction following intravenous ephedrine in two healthy women under spinal anaesthesia. Br J Anaesth 2002; 89: 519-523.  Back to cited text no. 12    
13.Liguori GA, Kahn, Gordon J, Gordon MA, Urban MK. The Use of Metoprolol and Glycopyrrolate to Prevent Hypotensive/Bradycardic Events During Shoulder Arthroscopy in the Sitting Position Under Interscalene Block. Anesth Analg 1998; 87: 1320-1325.  Back to cited text no. 13    
14.Geffin B, Shapiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: a report of 13 cases. J Clin Anesth 1998; 10: 278-285.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Lovstad RZ, Granhus G, Hetland S. Bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases. Acta Anaesthesiol Scand 2000; 44: 48-52.  Back to cited text no. 15    
16.Scull TJ, Carli F. Cardiac arrest after caesarean section under subarachnoid block. Br J Anaesth 1996; 77: 274-276.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Ponhold H. Vicenzi MN. Incidence of bradycardia during recovery from spinal anaesthesia: influence of patient position. Br J Anaesth 1998; 81: 723-726.  Back to cited text no. 17    
18.Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R. Incidence and risk factors for side effects of spinal anesthesia. Anesthesiol 1992; 76: 906-916.  Back to cited text no. 18    
19.Kopp SL, Horlocker TT, Warner ME, et al. Cardiac arrest during neuraxial anesthesia: frequency and predisposing factors associated with survival. Anesth Analg 2005; 100: 855-865.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]



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