CASE REPORT
SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST
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 sur-
vived without neurologic sequelae (Cerebral Performance Cat-
egory 1). Prompt defibrillation of SAH-induced ventricular fibrilla-
tion 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 = emer-
gency department; OHCA = out-of-hospital cardiac arrest; RCA = right
coronary artery; ROSC = return of spontaneous circulation;
SAH = subarachnoid hemorrhage; VF = ventricular fibrillation
S 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 neuro-
logic 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 depart-
ment (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 devel-
From the Department of Emergency Medicine (E.P.H., E.T.B.) and Department
of Anesthesiology and Department of Internal Medicine, Division of Cardiovas-
cular 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
Mayo Clin Proc. • August 2005;80(8):1073-1076
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oped a severe holocephalic headache during the climax of
sexual intercourse. He subsequently became unresponsive
with tonic posturing and shaking movements of all 4 ex-
tremities. 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 electrocar-
diography (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 photo-
phobia, 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: potas-
sium, 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 re-
turn 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 res-
piration occurred within about 5 minutes. Neither endotra-
cheal intubation nor chest compressions were performed.
After the patient was given a lidocaine bolus followed by
continuous infusion, ECG was repeated (Figure 3). Emer-
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SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST

FIGURE 1. Electrocardiogram obtained on patient’s arrival at our emergency department reveals

atrial fibrillation with a junctional rhythm and ST-segment elevation in leads II, III, and aVF with
reciprocal depression in leads I, aVL, and V2-V6, suggestive of inferior ST-segment elevation
myocardial infarction.

gent neurology and cardiology consultations were ob-
tained. Given that anticoagulation was contraindicated
because of the SAH, cardiac catheterization was not per-
formed. The patient was admitted to the coronary care unit
for monitoring overnight before transfer to the neurologic
intensive care unit. Nimodipine and phenytoin were initi-
ated shortly after admission.
While in the coronary care unit, the patient spontane-
ously converted to normal sinus rhythm. The next morning
a cerebral angiogram was obtained, which showed a rup-
tured aneurysm (5 × 4.5 × 4 mm) with a 3-mm neck along
the left anterior communicating artery, and coiling was
performed (Figure 4). The patient was transferred to the
neurologic intensive care unit in stable condition. Troponin
T increased initially to a maximum of 2.14 ng/mL by
hospital day 3 and then began to trend downward. The
maximum creatine kinase–MB level was 87.1 ng/mL.
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, consistent with inferolateral
and posterior myocardial infarction. The troponin T level
unexpectedly increased to 2.94 ng/mL on hospital day 6,
and coronary angiography was performed. 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, suggestive of chronic
RCA occlusion. No intervention was performed. Serial
transcranial Doppler ultrasonography revealed no evidence
of cerebral vasospasm. The patient’s condition stabilized
over the next several days, and he was dismissed as neuro-
logically intact (CPC 1) on hospital day 9.

FIGURE 2. Head computed tomography reveals acute subarachnoid
blood in the interpeduncular cistern (arrow) and cerebral edema with
sulcal effacement.
DISCUSSION
Subarachnoid hemorrhage reportedly occurs in 4% to 10%
of patients with OHCA.1,2 Of patients with known SAH,
12% experience sudden death outside the hospital setting.8
Patients with SAH complicated by CPA rarely survive, and
the prognosis of those who have ROSC is poor. Death from
SAH can be due to cardiac or respiratory arrest, with the
latter being more common.9 Respiratory arrest has been
attributed to brainstem herniation from a sudden increase

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 SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST

FIGURE 3. Electrocardiogram obtained after ventricular fibrillation, return of spontaneous circula-

tion, and return from the computed tomographic scanner reveals a junctional rhythm with no
evidence of atrial activity. The ST-segment elevation in leads III and aVF with reciprocal depression
in leads I, aVL, and V2-V6 is more pronounced.

in intracranial pressure due to local mass effect. Cardiac
arrest has been attributed to arrhythmias induced by a
catecholamine surge and the accompanying autonomic im-
balance.1,8-10 According to the World Federation of Neuro-
logical Surgeons Subarachnoid Hemorrhage Grading
Scale, our patient’s condition would be classified as grade
1, which is associated with good outcome.11 Given the mild
severity of SAH and the occurrence of VF, CPA likely
occurred secondary to the toxic effect of catecholamines on
the myocardium.
Nearly every ECG change has been reported in the
setting of SAH, including atrioventricular block, torsades
de pointes, VF, ST-segment elevation, ST-segment depres-
sion, and others.10,12-14 Several reports indicate that ECG
changes in SAH can mimic ST-segment elevation myocar-
dial infarction.15-19 ST-segment elevation in the setting of
SAH can be accompanied by elevated levels of troponin I
and creatine kinase–MB.17,20 However, 100% occlusion of
the RCA on coronary angiography was observed in our
patient. Although well-developed collaterals to the RCA
from the middle and distal left anterior descending coro-
nary artery suggestive of chronic occlusion also were seen,
regional wall motion abnormalities were present on trans-
thoracic echocardiography on hospital day 3 and did not
resolve on repeated echocardiography 14 days later. In
patients without known coronary artery disease, SAH-

FIGURE 4. Cerebral angiogram shows an aneurysm (5 × 4.5 × 4 mm) with a 3-mm neck along the left anterior
communicating artery before (arrow, left) and after (arrow, right) coiling.

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SUBARACHNOID HEMORRHAGE AND CARDIOPULMONARY ARREST
associated myocardial dysfunction is typically reversible.20
These data suggest that the patient’s severe underlying
coronary artery disease may have predisposed his myocar-
dium to ischemia and VF when stressed from catechola-
mine toxicity.
Kurkciyan et al2 identified SAH as the cause of CPA in
27 (4%) of 765 patients with OHCA. Of these 27 patients,
only 1 (4%) survived. The sole survivor had good neuro-
logic outcome (CPC 2). Inamasu et al5 described 5 patients
with SAH and CPA who survived. All 5 patients experi-
enced at least moderate long-term disability. Although all 6
of these patients with SAH experienced OHCA, to our
knowledge there are no reports of patients with SAH who
had CPA and survived without neurologic deficit. We
describe the first case of a patient who experienced in-
hospital CPA and survived without neurologic sequelae
(CPC 1).
CONCLUSIONS
Subarachnoid hemorrhage is a relatively common cause of
CPA, and survival is rare. Most long-term survivors have
moderate to severe neurologic disability. In SAH, CPA
represents a broad spectrum of both neurologic and cardiac
disease severity. Prompt defibrillation of SAH-induced VF
and timely neurologic intervention are essential for good
neurologic outcome.
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