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Year : 2008  |  Volume : 52  |  Issue : 1  |  Page : 81 Table of Contents     

Asystole Following Profound Vagal Stimulation During Hepatectomy

1 Lecturer, Department of Anesthesiology, Christian Medical College, Vellore, India
2 P.G. Resident, Department of Anesthesiology, Christian Medical College, Vellore, India
3 Senior Lecturer, Department of Anesthesiology, Christian Medical College, Vellore, India

Date of Acceptance09-Dec-2007
Date of Web Publication19-Mar-2010

Correspondence Address:
Preeta John
Department of Anesthesiology, Christian Medical College, Vellore, Tamil Nadu, Pin 632004.
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Source of Support: None, Conflict of Interest: None

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Asystole in a non laparoscopic upper abdominal surgery following intense vagal stimulation is a rare event. This case report highlights the need for awareness of such a complication when a thoracic epidural anaesthetic has been given in addition to a general anaesthetic for an upper abdominal procedure. A combined thoracic epidural and general anaesthetic was given. The anterior abdominal wall was retracted forty minutes after administration of the epidural bolus. This maneuver resulted in a profound vagal response with bradycardia and asystole. The patient was resuscitated successfully with a cardiac massage, atropine and adrenaline and the surgery was resumed. Surgery lasted eleven hours and was uneventful.

Keywords: Asystole, Hepatectomy, Peritoneal stimulus

How to cite this article:
John P, Raj S, Kartikeyan, Chandy TT. Asystole Following Profound Vagal Stimulation During Hepatectomy. Indian J Anaesth 2008;52:81

How to cite this URL:
John P, Raj S, Kartikeyan, Chandy TT. Asystole Following Profound Vagal Stimulation During Hepatectomy. Indian J Anaesth [serial online] 2008 [cited 2020 Oct 25];52:81. Available from: https://www.ijaweb.org/text.asp?2008/52/1/81/60603

   Introduction Top

Central neuraxial blockade is associated with a predominance of the parasympathetic nervous system. In our case scenario a combined general as well as a mid thoracic epidural anaesthetic for an extended right hepatectomy manifested in a profound vagal response resulting in an asystole, following elevation of the ante­rior abdominal wall with a retractor.

   Case report Top

A 59-year-old gentleman, 161cm tall, weighing 60 kg, an asthmatic with a diagnosis of adenocarcinoma of the sigmoid colon involving the dome of the bladder un­derwent a hemicolectomy and a partial cystectomy in December 2003. On routine follow up he was detected to have liver metastases in the right lobe of the liver. A re­cent positron emission tomography confirmed the diagno­sis with no other secondaries. Portal vein embolisation was done a month prior to the proposed surgery to pro­mote left lobe hypertrophy as an extended right hepatec­tomy was planned. Routine investigations which included a haemogram, chest roentgenogram, ECG, bleeding pa­rameters and liver function tests were normal.

Patient was premedicated with diazepam and metoclopromide. On arrival to the operating room, in­travenous access was secured and monitors were placed. Under strict aseptic precautions a mid thoracic epidural catheter was placed at T8-T9 level, 4cm within the space. Anaesthesia was induced with midazolam 2mg, fentanyl 100mcg, thiopentone 225mg and vecuronium 6 mg. The airway was secured with an 8.5sized endotracheal tube and maintained with air-oxygen and 2%isoflurane. A total epidural bolus of 10 + 5 ml of 0.25% bupicaine was given intermittently and a continuous infusion of 0.2% bupivacaine with fentanyl 2 mcg. ml -1 at a rate of 7 ml.hr -1 was started before skin incision was made. The blood pressure was 100/70 mmHg and heart rate was 65/min with an EtCO2 of 30 mm of Hg and a central venous pressure of 4 mmHg was maintained in view of liver resection. Surgical inci­sion evoked no response from the patient, but on retract­ing lower flap of the anterior abdominal wall the patient had a sudden episode of bradycardia with a drop in heart rate followed by asystole. On removal of the retractor and simultaneous resuscitation with a cardiac massage, atropine 0.6mg and 1ml of 1:10000 adrenaline, the asys­tole reverted immediately with a momentary escalation of the heart rate to 180/min and a blood pressure to 200/ 120mmHg. The haemodynamics gradually settled to baseline in a couple of minutes. The retractor was again introduced slowly and the proposed surgery was contin­ued with no further untoward incident. The surgery spanned 11 hours at the end of which the patient was haemodynamically stable, euthermic with a blood loss of 1.2 litres. The patient was transferred to the surgical in­tensive care unit for postoperative monitoring and he was extubated the following morning.

   Discussion Top

We put forth the following reasons to substantiate our case in favour of increased vagal tone as the etiol­ogy for asystole. To begin with, we had given adequate intermittent boluses of bupivacaine amounting to a vol­ume of 15 ml at the T8-9 level, assuming to span a block between T5-12. However we were unable to confirm the level as the patient was under anaesthesia. There was a mild response to intubation in the form of hyper­tension and tachycardia. No further analgesia were given and he was maintained with 70:30 air -oxygen and 2%isoflurane. There was absolutely no haemodynamic response to surgical incision with a blood pressure of 100/60mmHg and a pulse of 64/min. The possibility of the epidural bolus resulting in a rapid ascent to block T1­4, as the cause of asystole could be ruled out since the bolus was given slowly and over an extended period of time,and the haemodynamics had reached a steady state well before surgical incision.

The main attribute to the vagal cause of asystole, was primarily due to the inhibition of the thoracic sym­pathetic outflow resulting from a midthoracic epidural blockade thus allowing the dominance of the parasym­pathetic nervous system. The intense vagal stimulation following retraction of the anterior abdominal wall with the peritoneum had resulted in an asystole. [1] [Figure 1] The other contributory factors include decreased venous re­turn to the heart following central blockade. [2] In view of liver resection the central venous pressure was kept low. This, in turn, may have activated reflexes that cause bradycardia. [3] At least three such reflexes have been proposed [4] . The first involves collapse-firing of low pres­sure baroreceptors located in the right atrium and vena cava. [5] A second reflex involves an arc located within the pacemaker cells of the myocardium, in which heart rate is proportional to the degree of stretch. Finally, a paradoxical Bezold-Jarisch response, in which mechan­oreceptors located in the inferoposterior wall of the left ventricle when stimulated, can cause bradycardia.. The effector arm in each of these mechanisms involves an increased vagal tone. In addition to these myocardial reflexes, sympathetic blockade may alter the balance of autonomic input to the heart, favoring vagal tone, and bradycardia. Secondary factors, including opioid admin­istration, hypoxaemia, sedation, hypercarbia, concurrent medical illness, and use of chronic medications, are other causative factors. However these factors were ruled out in our patient.

In conclusion, to our knowledge this is the first case report of asystole due to intense vagal stimulation fol­lowing an anterior abdominal wall retraction in a hepate­ctomy. Anaesthesiologists should be particularly vigilant toward such an intense vagal response during abdomi­nal retraction.

   References Top

1.Kinsella SM, Tuckey JP. Perioperative bradycardia and asys­tole: relationship to vasovagal syncope and the Bezold jarisch reflex. Br J Anaesth 2001;86:859-68.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Jacobson J, Sofelt S, BrocksV, Fernandes A, Warberg J, Secher NH. Reduced ventricle diameters at onset of bradycardia dur­ing epidural anaesthesia. Acta Anaesthesiol Scand 1992;36:831-­6.  Back to cited text no. 2      
3.Movillo CA, Eilenbogen KA, Pava LF. Pathophysiologic basis for vasodepressor syncope. Syncope 1997;15:233-49.  Back to cited text no. 3      
4.Stienstra.R. Mechanisms behind and treatment of sudden, un­expected circulatory collapse during central neuraxis blockade. Acta Anaesthesiol Scand 2000; 44: 965-71.  Back to cited text no. 4      
5.Dickinson C. Fainting precipitated by collapse firing of venous baroreceptors. Lancet 1993; 342:970-2.  Back to cited text no. 5      


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