|Year : 2008 | Volume
| Issue : 1 | Page : 81
Asystole Following Profound Vagal Stimulation During Hepatectomy
Preeta John1, S Raj1, Kartikeyan2, Tony T Chandy3
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 Acceptance||09-Dec-2007|
|Date of Web Publication||19-Mar-2010|
Department of Anesthesiology, Christian Medical College, Vellore, Tamil Nadu, Pin 632004.
Source of Support: None, Conflict of Interest: None
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 The anterior abdominal wall was retracted forty minutes after administration of the epidural bolus.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 2018 Oct 18];52:81. Available from: http://www.ijaweb.org/text.asp?2008/52/1/81/60603
| Introduction|| |
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|| |
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|| |
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.  [Figure 1] The other contributory factors include decreased venous return to the heart following central blockade.  In view of liver resection the central venous pressure was kept low. This, in turn, may have activated reflexes that cause bradycardia.  At least three such reflexes have been proposed  . The first involves collapse-firing of low pressure baroreceptors located in the right atrium and vena cava.  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|| |
|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. [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. |
|3.||Movillo CA, Eilenbogen KA, Pava LF. Pathophysiologic basis for vasodepressor syncope. Syncope 1997;15:233-49. |
|4.||Stienstra.R. Mechanisms behind and treatment of sudden, unexpected circulatory collapse during central neuraxis blockade. Acta Anaesthesiol Scand 2000; 44: 965-71. |
|5.||Dickinson C. Fainting precipitated by collapse firing of venous baroreceptors. Lancet 1993; 342:970-2. |