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Unexplained asystole during thoracotomy irrigation: A case report MARK WELLIVER, CRNA, MS RONALD KUMOR, CRNA, MS Philadelphia,Pennsylvania This case presentationinvolves a 76-year-old man with a 60-year history of smoking one and a halfpacks of cigarettesper day, who presentedfor a transurethralresection of the prostate (TURP). A preadmission chest x-ray revealed a left upper lobe lung lesion that was suggestive of carcinoma by subsequent computerizedaxial tomography. The TURP procedurewas postponed, and the patient was advised to undergo an open thoracotomy biopsy with possible left upper lobectomy. The patient consented, and an open thoracotomy biopsy confirmed carcinoma. A left upper lobectomy was then performed. The operativeprocedure was significantfor a 12-second acute episode of atrioventricular standstill duringpost-thoracotomy thoracic irrigationwith warm saline. Return of sinus rhythm occurredspontaneously after cessation of irrigation.The operativefield was closed, and the patient's recovery was unremarkable.Postoperative evaluation was unremarkable, and the patient was discharged1 week later.Anatomic and physiologic vagal mechanisms are reviewed, and applicationto this case presentation is discussed. Key words: Asystole, baroreceptor reflex, lobectomy, parasympathetic innervation, thoracotomy, vagus. October 1998/ Vol. 66/No. 5 Case summary A 76-year-old man with a 60-year history of smoking one and a half packs of cigarettes per day presented for a transurethral resection of the prostate (TURP). On preadmission evaluation, a chest x-ray revealed a left upper lobe lesion. Computerized axial tomography further revealed a left upper lobe "ill-defined" density that was suggestive of carcinoma. No hilar, mediastinal, or para-aortic adenopathy was found. Subsequently, the patient was scheduled for a left upper lobectomy. Preoperative pulmonary function tests were performed and revealed mild restrictive lung disease with moderate impairment of gas transfer. The patient's cardiovascular assessment was significant for a fourth heart sound (S4) with a grade I/VI systolic murmur and suggested mild atherosclerotic cardiovascular disease. His electrocardiogram (ECG) revealed a normal sinus rhythm with left atrial hypertrophy. The patient denied further history of cardiovascular disease. Upon arrival to the cardiovascular/cardiothoracic operating suite, the standard routine was begun. This included ECG, pulse oximetry, intravenous access, and central venous access, and an arterial line and a thoracic epidural catheter were inserted. General anesthesia was then induced with thiopental sodium, fentanyl, and vecuronium. The patient was intubated with a 37 French doublelumen endobronchial tube. Placement was verified by fiberoptic bronchoscopy. After the patient was moved to the right lateral decubitus position, 451 proper tube placement was reconfirmed by fiberoptic bronchoscopy. General anesthesia was maintained with isoflurane and fentanyl, 9.0 pg/kg, which was titrated intravenously before incision. Muscle relaxation was maintained with vecuronium. A left upper lobe open lung biopsy was performed. Carcinoma was confirmed, and a left upper lobectomy followed without incident. After lobectomy, warm (approximately 38 0 C) normal saline irrigation of the pleural cavity by the surgeon was associated with an 8- to 12-second acute episode of asystole. The patient's baseline heart rate was a sinus bradycardia of 50 beats per minute. Irrigation was immediately discontinued, and manual compression of the pericardium was performed by the surgeon. Return of the patient's bradycardia occurred without pharmocologic intervention. Blood pressure was maintained after asystole at 140/60 mmHg without further intervention. Glycopyrrolate, 0.2 mg, was given intravenously to attenuate vagal tone. The vital signs remained stable throughout surgical closure. Before the end of closure, the patient was given a bolus of 5 mg of morphine sulfate and 100/ g of fentanyl via the epidural catheter for postoperative pain management. At the conclusion of surgery, neostigmine, 4.0 mg, and glycopyrrolate, 0.6 mg, was given intravenously over 5 minutes for muscle relaxant reversal. Before extubation, the patient was awake and met all extubation criteria. Naloxone hydrochloride, 60.0 pg intravenously, was given to increase the respiratory rate from 12 per minute to 16 per minute, and the patient was successfully extubated. He was transferred and maintained on full monitoring in the recovery room and intensive care without incident. Postoperative evaluation found no pathological irregularities of cardiac function. Physiological considerations A review of thoracic parasympathetic innervation is helpful in understanding possible causes of this intraoperative asystole. The vagus nerve is the most extensive of all cranial nerves, and it is the primary nerve of the parasympathetic system. The origin of the vagus nerve is the nucleus tractus solitarius in the medulla located at the base of the fourth ventricle. As the vagus nerve descends between the jugular vein and the carotid artery, it begins to branch (Table). The heart is innervated by parasympathetic and sympathetic nerve fibers. The parasympathetic innervation to the heart is via the vagus nerve which sends branches to the conduction system, especially the sinoatrial (SA) and atrioventricular (AV) nodes and, to a lesser extent, the myocardium 452 Table Branches of the vagus nerve' Anatomic location of vagus nerve v Branches Jugular fossa Meningeal Auricular Neck Pharyngeal Superior laryngeal Recurrent laryngeal Cervical cardiac Thoracic cardiac Anterior pulmonary Posterior pulmonary Esophageal Gastric Thorax Abdomen itself. Parasympathetic innervation to the myocardium is primarily in the atrial tissue with very few fibers in the ventricular muscle. The parasympathetic nervous system harbors the ability to set the : 24 ' tone for cardiac function.'(P Afferent impulses are carried centrally primarily by the glossopharyngeal and vagus nerves, and cranial nerves IX and X, respectively. Stimulation of the cardiac vagal nerve fibers causes the release of acetylcholine (Ach). Among the effects of Ach release is an increase in the permeability of the cardiac conductive cell membranes to potassium. The increase in permeability allows potassium to flow more easily out of the cell causing the cell to become more electronegative. The lower membrane potential will require a greater stimuli to propagate an action potential or a longer period for spontaneous depolarization to occur. The net result is a slower heart rate. In addition, stimulating cardiac muscarinic receptors inhibits norepinephrine release from adrenergic receptors, preventing normal sympathetic derived cardiac tone and, thus, furthering the vagotonic effects.3 It is well known that vagal stimulation can cause severe bradycardia and, in rare .rcumstances, asystole. The Valsalva maneuver, carotid sinus massage, diving reflex, occulocardiac reflex, and visceral traction all cause vagally medicated bradycardia. Berk et al tested several vag.ly mediated reflexes: diving reflex, Valsalva maneuver, carotid massage, ocular compression, and Muller maneuver (inspiration against a closed glottis) and found the diving reflex produces the greatest slowing of heart rate. Cervical and thoracic cardiac branches terminate as a cardiac plexus surrounding the aorta. Specific receptors of the cardiac plexus along the aortic arch respond to longitudinal and circumferential stretch of the vessel and send afferent vagal Journalof the American Association of Nurse Anesthetists impulses to the vasomotor center (nucleus tractus solitarius) in the medulla." Efferent vagal impulses .travel back from the vasomotor center to the heart to slow firing of the SA and AV nodes and also cause vasodilatation. This is known as the baroreceptor reflex. If these baroreceptors, found in abundance in the aortic arch and carotid arteries, receive strong enough stimulation, complete cessation of heart rate can occur. The cardiac vagal plexus tissue itself may be stimulated mechanically. An impulse can be generated with a stimulus anywhere along a nerve fiber: at the dendrite, cell body, or axon. Direct nerve stimulation could mimic massive baroreceptor discharge by utilizing the same nerve pathway but with an axonal or cell body origin. Vagally mediated asystole, even with strong continued stimulation, is not sustainable due to the little vagal and high sympathetic innervation of the ventricles.; The asystole usually lasts 5 to 20 seconds until ventricular escape beats or a higher pacemaker takes over. There are two main types of pulmonary vagal nerve receptors: stretch and irritant. The HeringBreuer reflex is a stretch receptor reflex carried by the vagus nerve centrally that causes a reflex to end inspiration. Irritant receptor stimulation also travels centrally to the medulla, and vagal efferent impulses cause coughing.t It is possible for stimulation of vagal nerve fibers in the respiratory tract to cause reflex bradycardia and hypotension. Visceral traction and rectal distention may also elicit '1 the celiac reflex. nia Discussion In this case study, we have discussed several likely mechanisms of the bradycardia: the celiac or baroreceptor reflex and direct cardiac vagal plexus stimulation. Pulmonary vagal afferent impulses may cause cardiac asystole. This mechanism is not likely as the irrigant was poured into a pleural space devoid of the upper lobe lung tissue and its innervation. Ligated tissues or the lower lobe may have been stimulated by the irrigant, but the direction of the irrigant flow was downward onto the October 1998/ Vol. 66/No. 5 mediastinal pleura. We have postulated that the mechanical stimulation of the falling irrigant onto the arotic arch, immediately inferior to the exposed pleura, caused massive baroreceptor discharge or direct nerve tissue stimulation and resulted in the asystole. The pressure, caused by the falling irrigant from approximately 5 inches above the open chest cavity, is suggested to be enough to cause direct nerve stimulation and likely baroreceptor firing. The asystole is not felt to be related to the temperature of the irrigation fluid as the temperature was approximately 38 0 C. Lingaraju et al found that mean heart rate actually increased with pericardial warm irrigation (44 0 C ± 5°C) in postcardiopulmonary bypass patients." Questions left unanswered include the following: Does narcoticinduced bradycardia accentuate vagotonic effects thus predisposing patients to heightened vagal reflexes? Was this asystole mediated by an unidentified reflex similar to the celiac, baroreceptor, and other reflexes? In the light of this case experience, we believe gentle irrigation of the thoracic cavity may decrease the likelihood of asystole from occurring. Thoracic irrigation-induced asystole needs to be investigated further to identify a definitive cause. We are unable to offer any specific suggestions for preventing another occurrence of this event until a definitive cause is identified. REFERENCES (1) ;ray H. Gray sAnatomy. 15th ed. New York: Bounty Books. 1995: 1252. (2) Barasch PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 2nd ed. Philadelphia: JB Lippincott. 1990. (3) (;uyton AC, Hall JE. 7extbook of Medical lPhsiology. 9th ed. Philadelphia: WB Saunders. 1996:126. (4) Berk WA, Shea MJ, Crevey MI). Bradvcardic responses to vagally mediated bedside maneuvers in healthy volunteers. Am / Med. 1991;90:725-728. (5) Assef SJ. Carotid sinus and carotid body physiology. In: Faust Rj. ed. Anesthesiology Review. New York: Churchill Livingstone. 1994:214-216. (6) Lingaraju N, Horrow JC, Colonna-Romano P, Strong MI). Haemodynamic consequences of warm cardiac irrigation during cardiac surgery. Can J Anaesth. 1994;41:384-386. AUTHOR Mark Welliver, CRNA, MS, is a stall nurse anesthetist at 'Thomas Jefferson University IHosp)ital. Philadelphia, Pennsylvania. 453 " do op jb 400 .. ate, i"o Ae. , 7 1 sa{ _ Fl r flat rFl Introducing the first fluid warmer that changes from routine to trauma in the blink of an eye. (But don't tell Lois.) Things change fast in the OR. Fortunately, the new Bair Hugger® Rangerâ„¢ blood/fluid warmer is engineered to change even faster. Brought to you by the people who invented forced air warming therapy, the Ranger can transform itself from a mild-mannered routine fluid warmer to a 30-liter/hour J^ S M **^B ^ rS BloodI'yarmIng trauma machine at superhuman speed. The Ranger unit is compact, lightweight and simple to use and maintain. 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Park Ridge, Illinois 60068-4001 Telephone: (847) 692-7050 Fax: (847) 692-3224 e-mail: [email protected] http://www.aana.com chicago ~ illinois usa -