Restoration of spontaneous circulation from asystole with aminophylline

350

AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 18, Number 3 • May 2000

TABLE 1. Frequency of Situs Inversus Reporting in an Acute Presentation in the Literature

Presenting System

Number of Reports

Appendix Trauma Cardiovascular Gastrointestinal Gallbladder Spleen

4 4 3 3 3 1

although the viscera are transposed, their nerve supply is the same. Although well described in appendicitis, this discrepancy in symptoms does not seem to be so pronounced with diseases affecting the billiary tract, and although atypical symptoms are not uncommon, the pain usually is localized in the left upper quadrant and radiates toward the left scapula. 25 Perhaps the greatest challenge in care of these patients is surgical, s Although the basic principles are the same, the surgical approach may be altered, particularly because of the increased incidence of polysplenia which may result in uncontrolled hemorrhage if not identified. Prior knowledge of sims can be of great help in an emergency situation. It is suggested that in cases of sims inversus the families of such patients should undergo a chest radiograph and thus affected members would be made aware of inversion if present. Physician knowledge of the presence of situs inversus will allow for the most accurate and efficient diagnosis and treatment. TIMOTHYJANCHAR,MD

Emergency Medicine Research Division Providence Hospital Washington, DC Harbor-UCIA Department of Emergency Medicine Torrance, CA DAVID MILZMAN,MD MARTINEZCLEMENT,MD

Emergency Medicine Research Division Providence Hospital Washington, DC

References 1. Varma N, Merkin R: Situs inversus: Review of the literature, report of four cases and analysis of the clinical implications. J Int Coil Surg 1960;33:131-145 2. Southam J: Left-sided gallbladder: Calculous cholecystitis with situs inversus. Ann Su rg 1975; 182:135-137 3. Aristotle: De generatione animalium, quoted by Schmutzer and Linde. 4. Nugent E, Edwards J, Plauth J, et al: The pathology, abnormal physiology, clinical recognition, and medical and surgical treatment of congenital heart disease, in Hurst J, Schlant R, Rackley C, Sonnernblick E, Wenger N (eds): The Heart (ed 7). New York, McGraw Hill, 1990, pp 759-765 5. Cockayne E: The genetics of transposition of the viscera. Q J Med 1938;7:479-483 6. Ruken G, Tempteton J, Ziegler M: Situs inversus: The complex inducing neonatal intestinal obstruction. J Pediatr Surg 1983;18:751 756 7. Fonkalsrud E, Tompkins R, Clatworthy H: Abdominal manifestations of situs inversus in infants and children. Arch Surg 1966;92:791795 8. Kulick D, Park S, Harrison B e t al: Traumatic aortic and diaphragmatic rupture in a patient with dextrocardia and situs inversus: Case report. J Trauma 1998;45:397-399

9. Engelberg M, Jedeikin R, Zager M, et al: Traumatic rupture of a left-sided liver and postoperative acute respiratory failure in a patient with Kartagener's syndrome. J Trauma 1978;18:545-547 10. Contini S, Dalla Valle R, Ainicola R: Suspected appendicitis in situs inversus totalis: an indication for a laparoscopic approach. Surg Laparoscopy Endoscopy 1998;8:393-4 11. Occhionorelli S, Navarra G, Santini M, et al: Symptomatic abdominal aortic aneurysm and "situs viscerum inversus": Diagnostic and therapeutic approach. J Cardiovasc Surg 1998;39:31-3 12. Badui E, Lepe L, Solorio S, et al: Heart block in dextrocardia with situs inversus. A case report. Angiology 1995;46:537-40 13. McFarland S: Situs inversus with choleltihiasis: A case report. Tennessee Med Assoc 1989;82:69-70 14. Hass G, Harris J, Segal L: Situs inversus totalis with calculi in a left-sided gallbladder: Report of a case. J Am Osteopathis Assoc 1984;83:718-20 15. Ringer P, Killam A, Davis B: Situs inversus viscerum associated with intermittent midgut volvulus. South Med J 1982;75:620-3 16. Carmichael K, Gayle W: Situs inversus and appendicitis. South Med J 1979;72:253-4 17. Heimann T, Sicular A: Acute cholecystitis with situs inversus. NY State J Med 1979;79:253-4 18. Moreno A, Toney M, Henry C, et al: Acute cholecystitis in a patient with situs inversus. Clin Nucl Med 1990;15:350-1 19. Liem K, ten Veen J: Inferior myocardial infarction in a patient with mirror-image dextrocardia and situs inversus totalis. Chest 1976;69:239-41 20. Holgersen L, Kuehner C, Stanley-Brown E: Acute appendicitis in a child with complete situs inversus. J Ped Surg 1970;5:379-80 21. Wike C, Caldwell B, Parrish R: A case of abdominal situs inversus with non-rotation and cholelithiasis. Am Surg 1970;36:346-8 22. Etter L: Left-sided gallbladder: Necessity for film of the entire abdomen in cholecystography. Am L Roentgenol 1953;70:987-990 23. Mayo C, Kendrick D: Anomalies of the gallbladder: Report of a case of left-sided floating gallbladder. Arch Surg 1950;60:668-673 24. Gross R: Congenital anomalies of the gallbladder: A review of 148 cases with report of a double gallbladder.Arch Su rg 1936;32:131 135 25. Wood G, Black A: Situs inversus totalis and disease of the billiary tract: Survey of the literature and report of a case. Arch Surg 1940;40:885-896

RESTORATION OF SPONTANEOUSCIRCULATIONFROM ASYSTOLE WITH AMINOPHYLLINE To the Editor:--Although difficult to estimate, bradyasystole is believed to initiate cardiac arrest in one quarter to one half of adults suffering out-of-hospital cardiac arrest. Survival from asystolic cardiac arrest is uniformly poor at approximately 1% even in settings of rapid and aggressive therapy. One of the factors implicated in atropine-resistant bradyasystolic rhythms is the accumulation of endogenous adenosine in the setting of low-flow states, hypoxia and ischemia) ,2,3 Adenosine and other endogenous nucleotides accumulate during hypoxia, ischemia and low flow states. It acts to inhibit myocardial oxygen consumption during ischemic states. In 1929, Drury and Szent-Gyoryi4 showed that adenosine dilates coronary arteries and slows heart rate. Adenosine binds to the AI subreceptors affecting adenosine-sensitive potassium channels and decreasing cyclic adenosine monophosphate (cAMP) production with resultant potassium effiux. Atrial myocytes and pacemaker cells hyperpolarize with loss of spontaneous electrical activity.5,6Additionally, adrenergic stimulation of ventricular myocytes is inhibited by adenosine resulting in indirect negative inotropy.7 The effect on conduction supression of the sinoatrial and atrioventricular nodes is similar m that produced by acetylcholine with the exception that adenosine is not antagonized by atropine. 8,9 As such, vagolytic measures are ineffective. Aminophylline is a Copyright © 2000 by W.B. Saunders Company doi:10.1053/JE.2000.3999

CORRESPONDENCE

phosphodiesterase inhibitor, which increases cAMP concentration, thereby providing an alternative mechanism to reverse cellular hyperpolarization. A 21-year-old woman with a history of asthma and peanut allergy ate a cookie at a wedding reception, which was later discovered to contain peanuts. Shortly after the ingestion the patient began to wheeze and rapidly lost consciousness. Within minutes the patient suffered cardiac arrest as assessed by bystanders. Family members immediately instituted cardiopulmonary resuscitation (CPR). Fifteen minutes later paramedics arrived on scene at which time the patient was noted to be asystolic. ACLS was initiated and the patient was transported to the ED. Prehospital measures included endotracheal intubation, 3 doses of epinephrine (l mg per dose every 3 to 5 rain × 3 doses) and 1 mg of atropine. The total prehospital time was 30 minutes. On arrival in the ED, the patient had persistent asystole refractory to standard ACLS. In light of the strong prehospital effort and the age, recuscitative efforts were continued despite her poor prognosis. As preparations were being made for pacing, 500 mg of intravenous aminophylline was administered in addition to repeat dosing of epinephrine and atropine. Subsequently, the patient developed a slow wide complex ventricular rhythm, which spontaneously became pulseless ventricular tachycardia. Sequential countershocks converted the rhythm to a sinus tachycardia with a rate of 140 beats/minute with restoration of spontaneous circulation (ROSC). ABG: pH 7.04/pCO2 75 mmHg/pO2 83 mmHg. Standard intensive care was continued including transcranial doppler confirmation of cerebral blood flow. Forty hours after admission the patient developed severe autonomic instability with severe hyperthermia (T = 108F). The patient failed to recover neurological activity and died on hospital day 5. Conventional therapy for asystole includes intravenous epinephrine, atropine, and possibly pacing in addition to CPR and artificial ventilation, s° Prognosis after asystole is poor. This is true whether as a presenting rhythm or after another rhythm. Asystole is the final common pathway of all terminal events. It represents the collapse of all cardiac mechanical and electrical activity and represents the greatest magnitude of metablic dysfunction and injury. Large amounts of endogenous catecholamines are released during cardiac arrest. I1,12Therefore, the development of bradyasystolic rhythms seems paradoxical. Variable factors including sympathetic and parasympathetic dysfunction, acidosis and hypoxia all contribute to impairment of mechanical and electrical activity, and may account for the development of bradyasystole. One of the factors is the local accumulation of adenosine. Belardinelli et al ~3 showed that adenosine attenuates the stimulatory action of catecholamines on cardiac myocytes, pacemaker cell and the release of norepinephrine from presynaptic adrenergic nerve terminals. Furthermore, he concluded that adenosine acts as an indirect negative inotrope via blockade of catecholamine stimulation. The role of adenosine as a cardiac pacemaker depressant suggests a role for its antagonism in bradyasystolic events. Viskin et all4 administered 250 mg of antinophylline to 15 patients suffering asystolic cardiac arrest refractory to standard ACLS. Despite ROSC in 11 patients only one was discharged neurologically intact. Subsequently, Mader and Gibson Is reported a pilot study in patient with asystole, refractory to standard ACLS. Half of their patients in the treatment in the treatment group had return of electrical activity versus none in the placebo group. The prototype of resuscitation from cardiac arrest is ventricular fibrillation. Early defibrillation with ROSC is the goal of therapy. CPR and artificial ventilation serve as a bridge to definitive therapy, which is defibrillation. Survival is dependent on time to ROSC. Irreversible neurological injury commonly occurs in the setting of prolonged cardiac arrest even if the heart can be successfully restarted. In each case of aminophylline use in asystole the

351

intervention was performed late in the course of resuscitation. As such, one would expect a high incidence of neurological injury. Optimizing survival from cardiac arrest requires rapid ROSC. CPR serves as a bridge to definitive therapy, especially defibrillation of ventricular fibrillation. If aminophylline proves to definitively reverse asystole, it will have to be used earlier in the course of resuscitation. As in this case, neurological injury limits the success of resuscitation despite restoration of cardiovascular ruction. Cerebral preservation measures in the setting of prolonged cardiac arrest are under investigation. If this devastating complication of cardiac arrest can be mitigated, aminophylline or other adenosine antagonists may play an important role in resuscitation from cardiac arrest complicated by asystole. CHRISTOPHERC. LEE, MD CURTE. DmL, MD WALLACEA. CARTER,MD

Bellevue Hospital Center New York University Medical Center Department of Emergency Medicine New York, NY

References 1. Ornato JP, PeberdyMA: Etiology, electrophysiology and myocardial mechanics of bradyasystolic states in Paradis NA, Halperin HR, Nowak RM (eds): Cardiac Arrest: The science and Practice of Resuscitation Medicine. Baltimore, Williams & Wilkins, 1996, pp 338-352 2. Manning JE, Zoll PM: Therapy of bradyasystolic arrest in Paradis NA, Halperin HR, Nowak RM (eds): Cardiac Arrest: The Science and Practice of Resuscitation Medicine. Baltimore, Williams & Wilkins, 1996 pp 621-640 3. Omato J, Perberdy M: The mystery of bradyasystole during cardiac arrest. Ann Emerg Med 27:576-587 4. DruryAN, Szent-Gyorgi A: The physiologic activity of adenosine compounds with special reference to their action upon the mammalian heart. J Physio 1929;293:23-49 5. Berne BM: The role of adenosine in the regulation of coronary blood flow. Circ Res 1980;47:807-813 6. Wesley RC, Boykin MT, Belardinelli L: Role of adenosine as mediator of bradyarythmias during hypoxia in isolated guinea pig hearts. Cardiovasc Res 1986;20:752-759 7. Belardinelli L, Linden J, Berne RM: The cardiac effects of adenosine. Prog Cardiovasc Res 1989;32:73-97 8. Belardinelli L, Giles WR, West A: Ionic mechanisms of adenosine actions in pacemaker cells from rabbit heart. J Physiol 1988;405: 615-633 9. Belardinelli L, Isenberg G: Isolated atrial myocytes: Adenosine and acetylchoiine increase potasiium conductance. Am J Physiol 1983;244:H734-H737 10. American Heart Association Emergency Cardiac Care Committee and Subcommittees: Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1992;268:2171-2302 11. Lang GS, Kummar PS, Fraya KN, et al: Cardiac arrest and plasma catecholamines. J R Soc Med 1983;76:1080-1081 12. Little RA, Frayn KN, Randall PE, et al: Plasma catecholamines in patients with myocardial infarction and in cardiac arrest. Quart J Med 1985;54:133-140 13. Belardinelli L, Fenton RA, West A, et al: Extracellular action of adenosine and the antagonism by aminophylline on the atriventricular conduction of isolated perfused guinea pig and rat hearts. Circ Res 1982;51:569-579 14. Viskin S, Belhassen B, Roth A, et al: Aminophylline for bradyasystolic cardiac arrest refractory to atropine and epinephrine. Ann Intern Med 1993;118:279-281 15. Mader TJ, Gibson P: Adenosine receptor antagonism in refractory asystolic cardiac arrest: Results of a human pilot study. Resuscitation 1997;35:3-7