SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST

CASE REPORT

Survival of a Neurologically Intact Patient With Subarachnoid Hemorrhage and Cardiopulmonary Arrest
ERIK P. HESS, MD; ERIC T. BOIE, MD; AND ROGER D. WHITE, MD
Subarachnoid hemorrhage (SAH) is a relatively common cause of cardiopulmonary arrest (CPA). Long-term survival with SAH and CPA is rare, and the vast majority of those who survive have moderate to severe neurologic disability. To our knowledge, there are no prior reports of patients with SAH who experience CPA and survive without neurologic deficit. We describe a patient with SAH who experienced CPA shortly after hospital admission and survived without neurologic sequelae (Cerebral Performance Category 1). Prompt defibrillation of SAH-induced ventricular fibrillation and timely neurologic intervention are essential for good neurologic outcome.

Mayo Clin Proc. 2005;80(8):1073-1076
CPA = cardiopulmonary arrest; CPC = Cerebral Performance Category; CT = computed tomography; ECG = electrocardiography; ED = emergency department; OHCA = out-of-hospital cardiac arrest; RCA = right coronary artery; ROSC = return of spontaneous circulation; SAH = subarachnoid hemorrhage; VF = ventricular fibrillation

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ubarachnoid hemorrhage (SAH) has been reported in 4% to 10% of patients who experience out-of-hospital cardiac arrest (OHCA).1-2 Long-term survival with SAH and cardiopulmonary arrest (CPA) is rare, and the prognosis for survivors is poor.1,3-5 There are no prior reports of patients with SAH who experienced CPA and survived without neurologic deficit. We describe a patient with SAH who experienced CPA shortly after admission and survived without neurologic sequelae (Cerebral Performance Category [CPC] 1).6-7 REPORT OF A CASE A 40-year-old previously healthy man with a history of heavy tobacco use presented to a local emergency department (ED) with acute-onset frontal and occipital headache. His only associated symptom was nausea. No meningismus or other focal neurologic findings were present on physical examination. A computed tomographic (CT) scan of the head was obtained and interpreted as normal. The patient declined cerebrospinal fluid evaluation and was dismissed with narcotic analgesics. Ten days later, the patient develFrom the Department of Emergency Medicine (E.P.H., E.T.B.) and Department of Anesthesiology and Department of Internal Medicine, Division of Cardiovascular Diseases (R.D.W.), Mayo Clinic College of Medicine, Rochester, Minn. Individual reprints of this article are not available. Address correspondence to Roger D. White, MD, Department of Anesthesiology, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 (e-mail: white.roger @mayo.edu). © 2005 Mayo Foundation for Medical Education and Research

oped a severe holocephalic headache during the climax of sexual intercourse. He subsequently became unresponsive with tonic posturing and shaking movements of all 4 extremities. Emergency medical services were dispatched, and on arrival, paramedics found the patient was awake, responded slowly to questions, and had a headache. The patient was transported to the local ED where electrocardiography (ECG) revealed atrial fibrillation, a heart rate of 120 beats/min, and ST-segment elevation in leads III and aVF. Associated with the headache were nausea and photophobia, but the patient denied chest pain or shortness of breath. The patient was given diltiazem, which slowed his heart rate to 60 beats/min. He subsequently developed substernal chest pressure radiating to his left arm as well as worsening nausea and vomiting. Sublingual nitroglycerin, meperidine, and ondansetron were given, and the patient was transported by air ambulance to our institution. On arrival, the patient reported only a headache. The chest and left arm discomfort had resolved before arrival. Vital signs were remarkable for blood pressure at 106/42 mm Hg and a pulse rate of 46/min. The patient was alert and oriented and appeared moderately pale. Cardiovascular and respiratory examination findings were unremarkable. Neurologic examination revealed a Glasgow Coma Scale score of 15 with an upgoing Babinski reflex on the left but was otherwise nonfocal. An ECG was obtained (Figure 1). Pertinent laboratory values included the following: potassium, 2.9 mEq/L; white blood cell count, 24.2 × 109/L; and troponin T, less than 0.01 ng/mL (normal, ≤0.03 ng/mL). The international normalized ratio and activated partial thromboplastin time were within normal limits. Given the high degree of clinical suspicion for SAH, emergent CT of the head was performed (Figure 2). After the CT images were acquired and the patient was still on the scanning table, he became unresponsive and pulseless. The monitor revealed ventricular fibrillation (VF), and return of spontaneous circulation (ROSC) was achieved with a 120-joule rectilinear biphasic waveform defibrillation shock. Mask ventilation was initiated, and the patient was transported rapidly back to the ED. Within 2 minutes of CPA, ROSC was observed, and return of spontaneous respiration occurred within about 5 minutes. Neither endotracheal intubation nor chest compressions were performed. After the patient was given a lidocaine bolus followed by continuous infusion, ECG was repeated (Figure 3). Emer• www.mayoclinicproceedings.com 1073

Mayo Clin Proc.

August 2005;80(8):1073-1076

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.

Electrocardiogram obtained on patient’s arrival at our emergency department reveals atrial fibrillation with a junctional rhythm and ST-segment elevation in leads II.14 ng/mL by hospital day 3 and then began to trend downward. aVL.2 Of patients with known SAH. III. . and V2-V6.80(8):1073-1076 For personal use. Death from SAH can be due to cardiac or respiratory arrest. While in the coronary care unit.8 Patients with SAH complicated by CPA rarely survive. Troponin T increased initially to a maximum of 2. and aVF with reciprocal depression in leads I. with the latter being more common. 1074 Mayo Clin Proc.94 ng/mL on hospital day 6. No intervention was performed. suggestive of chronic RCA occlusion. gent neurology and cardiology consultations were obtained.5 × 4 mm) with a 3-mm neck along the left anterior communicating artery. It showed 100% occlusion of the proximal right coronary artery (RCA) with well-developed collaterals from the middle and distal left anterior descending coronary artery. and he was dismissed as neurologically intact (CPC 1) on hospital day 9. and coiling was performed (Figure 4). suggestive of inferior ST-segment elevation myocardial infarction. The patient was transferred to the neurologic intensive care unit in stable condition. The patient’s condition stabilized over the next several days.9 Respiratory arrest has been attributed to brainstem herniation from a sudden increase • www. Serial transcranial Doppler ultrasonography revealed no evidence of cerebral vasospasm. which showed a ruptured aneurysm (5 × 4. Head computed tomography reveals acute subarachnoid blood in the interpeduncular cistern (arrow) and cerebral edema with sulcal effacement.1.1 ng/mL. • August 2005. and coronary angiography was performed. The troponin T level unexpectedly increased to 2. The next morning a cerebral angiogram was obtained. 12% experience sudden death outside the hospital setting. Nimodipine and phenytoin were initiated shortly after admission.SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST FIGURE 1. Mass reproduce only with permission from Mayo Clinic Proceedings. consistent with inferolateral and posterior myocardial infarction.mayoclinicproceedings. DISCUSSION Subarachnoid hemorrhage reportedly occurs in 4% to 10% of patients with OHCA. cardiac catheterization was not performed. Given that anticoagulation was contraindicated because of the SAH. Transthoracic echocardiography showed a left ventricular ejection fraction of 60% with severe hypokinesis of the basilar and apical segments of the lateral and posterior walls of the right ventricle. and the prognosis of those who have ROSC is poor. the patient spontaneously converted to normal sinus rhythm. The patient was admitted to the coronary care unit for monitoring overnight before transfer to the neurologic intensive care unit. The maximum creatine kinase–MB level was 87.com FIGURE 2.

Cerebral angiogram shows an aneurysm (5 × 4. regional wall motion abnormalities were present on transthoracic echocardiography on hospital day 3 and did not resolve on repeated echocardiography 14 days later. right) coiling. In patients without known coronary artery disease.20 However.5 × 4 mm) with a 3-mm neck along the left anterior communicating artery before (arrow. SAH- FIGURE 4. Although well-developed collaterals to the RCA from the middle and distal left anterior descending coronary artery suggestive of chronic occlusion also were seen. in intracranial pressure due to local mass effect. and others. Mass reproduce only with permission from Mayo Clinic Proceedings. Nearly every ECG change has been reported in the setting of SAH.10. return of spontaneous circulation. Cardiac arrest has been attributed to arrhythmias induced by a catecholamine surge and the accompanying autonomic imbalance. including atrioventricular block.com 1075 For personal use.8-10 According to the World Federation of Neurological Surgeons Subarachnoid Hemorrhage Grading Scale. 100% occlusion of the RCA on coronary angiography was observed in our patient. our patient’s condition would be classified as grade 1.mayoclinicproceedings.12-14 Several reports indicate that ECG changes in SAH can mimic ST-segment elevation myocardial infarction.80(8):1073-1076 • www.11 Given the mild severity of SAH and the occurrence of VF.SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST FIGURE 3. Electrocardiogram obtained after ventricular fibrillation.15-19 ST-segment elevation in the setting of SAH can be accompanied by elevated levels of troponin I and creatine kinase–MB. aVL.1. and V2-V6 is more pronounced. which is associated with good outcome.17. CPA likely occurred secondary to the toxic effect of catecholamines on the myocardium. VF. • August 2005. . left) and after (arrow. torsades de pointes. ST-segment elevation. ST-segment depres- sion. and return from the computed tomographic scanner reveals a junctional rhythm with no evidence of atrial activity. Mayo Clin Proc. The ST-segment elevation in leads III and aVF with reciprocal depression in leads I.

Subarachnoid hemorrhage mimicking acute myocardial infarction [letter]. Saito R. Zaroff JG. Kurkciyan et al2 identified SAH as the cause of CPA in 27 (4%) of 765 patients with OHCA. Snyder BD. CONCLUSIONS Subarachnoid hemorrhage is a relatively common cause of CPA. Barzilai B. Deibert E. 51:27-32. Watanabe G. Tabbaa MA. et al. Senior R. Resuscitation. Bailey WB. 7.84:960-975. the European Resuscitation Council. Ramirez-Lassepas M. Lancet. We describe the first case of a patient who experienced inhospital CPA and survived without neurologic sequelae (CPC 1). Asplin BR. Wittstein IS. White RD. 2003. Circulation. Inamasu et al5 described 5 patients with SAH and CPA who survived. J Neurosurg.95:361-362. 13. 15. Jo N. The etiology of sudden cardiopulmonary arrest in subarachnoid hemorrhage [in Japanese].35(suppl):257-262. 1994. 6.SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST associated myocardial dysfunction is typically reversible. Chamberlain DA.86:340. 2. 1987. Hirsch GA. van de Loosdrecht AA. Tognetti F. 11. 1988. Galasko GI.16:270-271. • August 2005. Heldman AW. Parisi JE. Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. 3.108. Cummins RO. J Electrocardiol. Manini G. 1975. Whisnant JP. All 5 patients experienced at least moderate long-term disability. Schulman SP. The sole survivor had good neurologic outcome (CPC 2). the Heart and Stroke Foundation of Canada. Pittaluga JM. Banki N. Henselmans JM. 2001. Am J Emerg Med. Circulation. van der Kleij FG. Most long-term survivors have moderate to severe neurologic disability. Isayama K. 2003. . 14. Resuscitation. 18.51(suppl):359-364. Cardiac arrhythmia as initial presentation of aneurysmal subarachnoid hemorrhage. 2002. 10. only 1 (4%) survived. Cathet Cardiovasc Diagn. Wijdicks EF. et al. 21:781-786.349:561.20 These data suggest that the patient’s severe underlying coronary artery disease may have predisposed his myocardium to ischemia and VF when stressed from catecholamine toxicity. 147:1661-1662. Sommargren CE. Mass reproduce only with permission from Mayo Clinic Proceedings. N Engl J Med. Masuda T. Images in clinical medicine: electrocardiographic changes in intracranial hemorrhage mimicking myocardial infarction. 1996. 19.98:741-746.80(8):1073-1076 • www. 9. Prompt defibrillation of SAH-induced VF and timely neurologic intervention are essential for good neurologic outcome. 1999. 2003. Andreoli A.com For personal use. REFERENCES 1. In SAH. Int J Cardiol. et al.e165-e166. et al. Heart. Dubowitz M. Schievink WI. to our knowledge there are no reports of patients with SAH who had CPA and survived without neurologic deficit. Hayashi N. Braverman AC. Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest.45: 871-874. Aneurysmal subarachnoid hemorrhage presenting as cardiorespiratory arrest. 12. Sterz F. Am J Cardiol. Assessment of outcome after severe brain damage. Cheng TO. Of these 27 patients. 1991. Kinoshita K. 20. Meron G. Neth J Med. Neurology. 16. Gerstenblith G. Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage. Pinelli G. 1996. 1995. Ferreira AC. Jennett B. Chaitman BR. Subarachnoid hemorrhage: atypical presentation associated with rapidly changing cardiac arrhythmias. Romanelli R. 2004. Kitahara T. Ikeda Y. 1995.59:596-600. and the Australian Resuscitation Council. Kobayashi S. Abramson NS. Although all 6 of these patients with SAH experienced OHCA. Kanto J Jpn Assoc Acute Med.51:207-211. 8. 1993. CPA represents a broad spectrum of both neurologic and cardiac disease severity. 4. Sudden death from aneurysmal subarachnoid hemorrhage.68: 985-986. and survival is rare. No Shinkei Geka. Lowery M. 17. 12:370-373. Subarachnoid haemorrhage presenting as acute myocardial infarction with electromechanical dissociation arrest. Nakamura Y. Subarachnoid hemorrhage simulating myocardial infarction. Nakazawa S. Soma S. de Marchena E. Utagawa S. Inamasu J. Arch Intern Med. 2001.37:170-173. 5.55:242-246. 1987.mayoclinicproceedings. Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: the Utstein Style: a statement for health professionals from a task force of the American Heart Association.1:480-484. Clinical significance of elevated troponin I levels in patients with nontraumatic subarachnoid hemorrhage. Morales A. Images in cardiovascular medicine: ST-segment elevation in an unresponsive patient. 2001. Fatal subarachnoid hemorrhage: patients with cardiac and respiratory arrest on arrival [in Japanese]. Drew BJ. A case of subarachnoid hemorrhage resuscitated from cardiopulmonary arrest with mild hypothermia [in Japanese]. J Neurosurg. 1076 Mayo Clin Proc. Grazi P. Piepgras DG. Bond M. Nippon Rinsho. Kurkciyan I. Report of the World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. Survival of a subarachnoid hemorrhage patient who presented with prehospital cardiopulmonary arrest: case report and review of the literature. di Pasquale G.