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From the Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Address correspondence to: Dr. Richard J. Bjerke, Anesthesia Service, VA Pittsburgh Health Care System, University Drive C, Pittsburgh, PA 15240 USA. Phone: 412-688-6152; Fax: 412-688-6906; E-mail: bjerkerj{at}anes.upmc.edu
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Abstract |
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Clinical features: A 67-yr-old man, 11 yr post heart transplant underwent left upper lung lobectomy. He developed asystole after intravenous administration of 4 mg neostigmine with 0.8 mg glycopyrrolate for reversal of the muscle relaxant. He had no history of rate or rhythm abnormalities either prior to or subsequent to the event.
Conclusion: When administering anticholinesterase medications to heart transplant patients, despite surgical dennervation, one must be prepared for a possible profound cardiac response.
THE unique physiology of the recently transplanted heart has been well described.1 Heart rate responses to exercise and medications early after transplant have demonstrated the denervated character.2 More recently, there have been more studies of patients who are years post-transplantation showing consistent evidence of reinnervation. In most studies the clinical significance of the reinnervation is minor.3,4 Of more importance, a report of two cases of sinus arrest after neostigmine administration in heart transplant patients suggested the possibility of considerable responsiveness to the drug previously thought to have no effect on a denervated heart.5 However, both patients required permanent pacemakers because of repeated episodes of sinus pauses and severe bradycardia indicating underlying pathology. We present a case of a heart transplant recipient who developed asystole after neostigmine administration and had a history of a stable sinus rhythm both prior and subsequent to the episode.
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Case report |
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General anesthesia was induced with 250 mg thiopental and 140 mg succinylcholine was given to facilitate intubation with a double lumen tube and its position was verified by fibreoptic bronchoscopy. Anesthesia was maintained with isoflurane 0.5 – 2%, 600 µg fentanyl, and 6 mg pancuronium. Hydrocortisone, 100 mg, was given intravenously. The surgical procedure was performed uneventfully, and the patient was hemodynamically stable throughout with a heart rate ranging from 78 to 108 beat•min. At the conclusion of the procedure isoflurane was discontinued and 4 mg neostigmine and 0.8 mg glycopyrrolate iv were administered. The heart rate was 78 beat•min-1, blood pressure 125/63 mmHg and the arterial hemoglobin saturation was 100% by pulse oximetry. Within a few minutes the patient became responsive; however at the same time the heart rate began to slow. The slowing of the sinus rate progressed to asystole as the patient also became unresponsive. Atropine, 0.8 mg, iv was administered as chest compressions were initiated. Intravenous 1.0 mg epinephrine was then administered. After approximately 45 sec of asystole spontaneous sinus rhythm resumed, which rapidly progressed to a rate of 160 beat•min-1 and a blood pressure of 230/125 mmHg. The patient became responsive and cooperative. The hyperdynamic state resolved over several minutes and then the trachea was extubated and the patient was transferred to the recovery room. Further recovery was uneventful. A 12-lead ECG showed no changes. He was monitored with telemetry for 48 hr with no further rate or rhythm disturbances. After 12 months of follow-up, which included three minor surgical procedures but no pharmacological challenges, he has had no symptoms or signs of an unstable sinus rhythm.
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Discussion |
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Transplanted hearts have demonstrated a higher incidence of sinus node abnormalities.6 This has resulted in a higher rate of pacemaker implantation. Possible etiologies include surgical trauma especially with the biatrial anastomosis, organ rejection, nodal ischemia, and preservation injury. Reinnervation may be another cause of variability in donor sinus node function. When heart transplantation was first achieved it was thought that the denervation was permanent. However then reports of patients experiencing anginal symptoms appeared.7 This has been shown to correlate with significance of coronary artery disease. Studies performed assessing both the sympathetic function and parasympathetic responses have demonstrated some evidence of response. The probability of response increased with increasing time span post transplant.3,4 There have been reports by Backman et al. of heart rate responses to anti-cholinesterases in heart transplant patients in which the proposed mechanism may be direct activation of the cholinergic receptor on the ganglion producing a release of acetylcholine.8
These were the first reports suggesting caution with these drugs despite lack of evidence of reinnervation. The previously mentioned sinus arrests occurred after intravenous neostigmine in two patients — at four and eight years post-transplantation, respectively — occurred despite the concomitant use of an anti-muscarinic. Both patients continued to have episodes of significant bradycardia requiring permanent pacemakers. This suggested underlying nodal disease, but also might have been secondary to ischemia during the periods of asystole.
Our patient had not demonstrated any instability in rate before or after the event. Since oxygenation and perfusion were optimal the primary consideration for the cause of the asystole is the administration of neostigmine.
The neostigmine may have acted through the pathway of blocking cholinesterase activity in the presence of acetylcholine from a reinnervated ganglion. The other possible mechanism suggested by Backman et al. would have involved a pathway of stimulation of release of acetylcholine from the still denervated ganglion that then acts on the cardiac receptor.
The paucity of reports of any clinically important effect of anti-cholinesterases through the parasympathetic pathway in heart transplant patients indicates that the risk of a profound response such as occurred in our patient is extremely low. Normal patients may have a profound response to anti-cholinesterases but this is also rare however they have the benefit of the counterbalancing efferent sympathetic response that is lacking in our patient.
Our case suggests that for optimum safety the heart transplant patient requiring reversal of muscle relaxation should be managed as if the heart rate response to the anti-cholinesterase and vagolytic combination could require further intervention. The standard practice of reversal using the concurrent administration of a vagolytic with the anticholinesterase along with maintaining the means available, e.g., potent beta agonist, to rescue the patient if a profound effect occurs is the safest approach.
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Footnotes |
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Accepted for publication November 11, 2000.
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References |
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2
Cheng DCH, Ong DD. Anaesthesia for non-cardiac surgery in heart-transplanted patients. Can J Anaesth 1993; 40: 981–6.
3 Tio RA, Reyners AKL, van Veldhuisen DJ, et al. Evidence for differential sympathetic and parasympathetic reinnervation after heart transplantation in humans. J Auton Nerv Syst 1997; 67: 176–83.[Medline]
4 Wesche J, Orning O, Eriksen M, Walløe L. Electrophysiological evidence of reinnervation of the transplanted human heart. Cardiology 1998; 89: 73–5.[Medline]
5
Beebe DS, Shumway SJ, Maddock R. Sinus arrest after intravenous neostigmine in two heart transplant recipients. Anesth Analg 1994; 78: 779–82.
6 Rothman SA, Jeevanandam V, Combs WG, et al. Eliminating bradyarrythmias after orthotopic heart transplantation. Circulation 1996; 94(SupplII): 278–82.
7 Stark RP, McGinn AL, Wilson RF. Chest pain in cardiac-transplant recipients. Evidence of sensory reinnervation after cardiac transplantation. N Engl J Med 1991; 324: 1791–4.[Medline]
8 Backman SB, Ralley FE, Fox GS. Neostigmine produces bradycardia in a heart transplant patient. Anesthesiology 1993; 78: 777–9.[Medline]
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