Cardiac Arrhythmias and Sudden Death in

Subarachnoid Hemorrhage
BY BRUNO V. ESTANOL, M.D., AND OSCAR S. M. MARIN, M.D.

Abstract: • Life-threatening cardiac arrhythmias can occur in patients with subarachnoid hemorrhage
Cardiac secondary to rupture of intracranial aneurysms. The arrhythmias are secondary to acute
Arrhythmias
and Sudden dysfunction of the central nervous system and possibly to sudden increase in intracranial
Death in pressure. The autonomic nervous system is the mediator in the production of these disorders.
Subarachnoid The clinical significance of these rhythm disorders is discussed, particularly in regard to the
Hemorrhage sudden, unexpected death seen in this type of patient. The possible mechanisms of production
are analyzed and their therapeutic implications are stressed.

Additional Key Words intracranial aneurysms autonomic nervous system

electrocardiographical abnormalities

D The functional relationship between heart and
brain is an ancient topic.1'2 It has been known since
19473 that primary, spontaneous subarachnoid
hemorrhage (SAH) and other acute intracranial
events can precipitate dramatic changes in the
morphology of the waves of the electrocardiogram
(ECG). A wealth of literature has been published since
that time on this subject. Distinctive electrocar-
diographical abnormalities associated with this in-
tracranial event include a prolonged QT interval (the
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and sparse collections of histiocytes in the area of
necrosis. The mechanism responsible for the
pathological myocardial changes produced by in-
tracranial lesions is not known. However, it appears
that the autonomic nervous system and its various
chemical mediators play a role in its pathogenesis.9
In contradistinction to the abundance of informa-
tion concerning ECG changes in SAH, there is hardly
any mention of disturbances of cardiac rhythm in the
neurological and cardiological literature. Scattered

importance of this change will be discussed later),
large upright or deeply inverted T waves, elevation or
depression of ST segments, prominent U waves and a
marked increase in the amplitude of the U waves in
postextrasystolic beats.3'18 The time course of these
abnormalities has not been adequately documented.10
These ECG changes may closely resemble an acute
myocardial infarction.6' n'13> 16 The most widely
accepted view is that they represent disturbances of
ventricular repolarization. It is likely that the ECG
changes are secondary to a derangement in the
autonomic control of the heart. A large body of ex-
perimental and clinical evidence exists to support this
view.10- " Many of the patients who had abnormal
ECGs and who died of central nervous system lesions
had normal hearts at autopsy.10 On the other hand,
there is experimental and clinical evidence that shows
that many of these patients have acute structural
changes in the myocardium, and furthermore that this
myocardial damage appears to be secondary to brain
lesions.1822 Connor 19 -" demonstrated structural
changes of the myocardium in patients dying with a
variety of diseases of the brain. These changes con-
sisted of focal myocytolysis, myofibrillar degenera-
tion, lipofuscin pigment deposition in the myofibrils
Department of Neurology, Baltimore City Hospitals and Johns
Hopkins University School of Medicine, Baltimore, Maryland
21224.
382
reports on this subject have been published;23'28
nevertheless, there is a dearth of information concern-
ing the incidence, time of appearance, clinical impor-
tance and methods of prevention and treatment of
these feared events. No mention of arrhythmias is
made in the standard textbooks of neurology and the
condition is merely regarded as a curiosity at best.
However, the presence of these disorders of the heart
beat is likely to have great clinical importance, par-
ticularly as it pertains to the distressingly common,
sudden and now somewhat expected death so unfor-
tunately frequent in these patients. Moreover, when
there is a concomitant impairment of consciousness
and no clinical history, the disturbance of the cardiac
rhythm may appear to be the primary illness of these
patients.23 Parizel24 described two cases of spon-
taneous SAH, both of which developed several
different arrhythmias within a short period of time:
supraventricular tachycardia, short bursts of ven-
tricular premature beats, multifocal ventricular
tachycardia, ventricular flutter and ventricular fibrilla-
tion necessitating D.C. countershock and intravenous
antiarrhythmic drugs. Both patients survived. His
comments are enlightening: "Life-threatening
arrhythmias can occur in patients with subarachnoid
hemorrhage. Our two patients would undoubtedly
have died without the prompt resuscitative measures
made possible by their admission to a coronary care
unit. Their death would have been attributed to their
Stroke, Vol. 6, July-August 1975
 CARDIAC ARRHYTHMIAS AND SUDDEN DEATH IN SAH
nervous system disease." Prior to this report the
seriousness of these events had not been emphasized.
Plum and Posner23 described a 44-year-old man who
presented with arrhythmias of various sorts: 2:1 block,
sino-atrial block, sinus arrhythmia, intermittent com-
plete atrioventricular block, supraventricular tachy-
cardia and finally ventricular tachycardia. This patient
was mistakenly diagnosed as having a myocardial in-
farction, but postmortem examination showed a
massive SAH from rupture of an aneurysm of the
anterior communicating artery. No mention was
made of the state of the heart. The transient nature of
these disorders and the fact that many of these
patients are not under careful cardiac monitoring dur-
ing the acute illness are also additional factors in the
poor documentation of these arrhythmias. A prospec-
tive study of electrocardiographical changes
associated with SAH does not mention the presence of
cardiac arrhythmias.29 We have recently seen two
cases of acute SAH secondary to rupture of in-
tracranial aneurysms in whom life-threatening cardiac
arrhythmias were present. In only one case was it
possible to obtain full documentation of the disorder.
Casel
A 61-year-old white man was brought to the emergency
room of the Baltimore City Hospitals in a stuporous state.
Cardiac examination disclosed a very fast apical rate with a
varying first sound. ECG revealed ventricular flutter at a
rate of 250 per minute (fig. 1) that spontaneously reverted to
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normal sinus rhythm in about 30 seconds. Over the next few
minutes he had multiple premature atrial contractions
(PACs), intermittent 2:1 block, multifocal premature ven-
tricular contractions (PVCs), and short episodes of
-ri 4i-4rr+rfflIfr mfiFfllrftT-r, h ; rlr
FIGURE 1
Trace A shows ventricular flutter at a rale of 250 per minute. No P
waves are discernible in this tracing. B and C show multifocal
premature ventricular contractions (PVCs).
Stroke. Vol. 6, July-August 1975
bigeminal rhythm. Fifty milligrams of intravenous xylocaine
were given with restoration of normal sinus rhythm. Follow-
ing these events the patient was lethargic, but easily
arousable, and oriented. He complained of a severe
headache. He related that he was standing on the street when
he suddenly became dizzy and then "blacked out." He did
not recall falling or having a headache prior to losing con-
sciousness. The next memory he had was that of waking up
in the ambulance with a severe headache; he remembered he
suddenly lost consciousness again upon entering the
emergency room. His past medical history was un-
remarkable except for mild hypertension of ten years' dura-
tion, for which he had been treated intermittently with 50 mg
of hydrochlorothiazide daily. An ECG taken one year prior
to his admission was within normal limits and a chest x-ray
taken at the same time was normal as well. He denied any
history of heart disease. He denied angina or symptoms of
congestive heart failure. He did not smoke or drink, and
stated that his general health prior to this incident had been
excellent.
Physical examination on admission revealed a man in
acute distress complaining of a severe headache. He was
lethargic but easily arousable and oriented. Blood pressure
when the patient was in normal sinus rhythm was 200/120
mm Hg, respiratory rate was 25 per minute and regular, and
pulse 110 per minute and regular. Rectal temperature was
101°. General physical examination showed no evidence of
jugular venous distention, the lungs were clear, the heart
sounds were normal with no gallops or murmurs, and the
heart was not enlarged. There was grade 1 hypertensive
retinal changes (Keith-Wagener classification) and normal
peripheral pulses. Neurological examination revealed slight
neck stiffness and the presence of an incomplete left third
nerve palsy, with 50% palpebral ptosis, and a left pupil which
was 2 mm larger than the right and sluggishly reactive to
light. There was paresis of left medial rectus, inferior
oblique and superior rectus. There were no hemipareses,
sensory deficits or visual field defects. A lumbar puncture
showed an opening pressure higher than 300 mm H 2 O. The
CSF was grossly bloody with a xanthochromic supernatant
and a hematocrit of 6%. The urine showed no protein or
sugar and the sediment contained no red or white cells. An
ECG taken one hour after admission revealed a sinus
rhythm of 85 per minute, first degree AV block, left axis
deviation (-15°), and a QT interval of 0.44 second. There
were no U waves but the T waves were slightly depressed
over the precordial leads. There was no evidence of a
myocardial infarction in the ECG. A blood count showed
leukocytosis with a shift to the left. Two hours after admis-
sion the electrolytes were normal, including potassium. Con-
tinuous monitoring over the next 48 hours did not reveal the
presence of a serious cardiac arrhythmia. The ECG
remained unchanged. Serial arterial blood gases were nor-
mal. An arteriogram revealed a left posterior com-
municating artery aneurysm at the point of junction with the
left internal carotid artery.
Case 2
A 29-year-old black man was admitted to the Johns
Hopkins Hospital because of sudden onset of severe,
generalized headache that developed while the patient was
having intercourse. His previous health had been good and
his family history was negative for neurological or cardiac
diseases. His general physical examination on admission
was negative. Neurological examination showed moderate
383

neck stiffness and a Kernig sign, but was otherwise negative.
While he was being examined by the house staff he suddenly
developed multifocal PVCs and runs of ventricular
tachycardia each lasting a few seconds. These arrhythmias
were directly observed on the cardiac monitor. They sub-
sided spontaneously after a few minutes and no therapy was
given. At no time was there evidence of shock or decreased
cerebral perfusion. Electrolytes, arterial blood gases, chest
x-ray and an ECG taken one hour after this episode were
within normal limits. Lumbar puncture showed an opening
pressure of 400 mm of CSF and was grossly bloody with a
xanthochromic supernatant. Cerebral angiography proved
the presence of a right posterior communicating artery
aneurysm, again at the point of junction with the internal
carotid artery.
Discussion
PATHOPHYSIOLOGY
The neural mechanisms by which these arrhythmias
are produced are not clearly understood. However,
in recent years some physiological information has
accumulated which sheds some light upon this
subject.30"36 An excellent review of this somewhat con-
fusing topic was made recently by Mauck.32 In the ex-
perimental animal, cardiac arrhythmias can be in-
duced by electrical stimulation of several cortical and
subcortical areas. These include the frontal lobes, the
limbic system, the amygdaloid nuclei, the hypo-
thalamus, the mesencephalon and other areas in the
brain stem.30 These arrhythmias are in all likelihood
mediated through the autonomic nervous system.32 In
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another study, Hockman et al.34 induced a spectrum of
ectopic ventricular rhythms by electrical stimula-
tion of some areas of the mesencephalon and
diencephalon. Observed in sequence were ventricular
tachycardia, both unifocal and multifocal, ventricular
premature contractions in bigeminal pattern, and final
return to sinus rhythm. Bilateral vagotomy had no
effect on the response; however, it was completely
abolished by beta-adrenergic blockage with pro-
pranolol. They concluded that the type of arrhythmia
observed was directly related to the intensity of the
sympathetic discharge and that all abnormal ven-
tricular complexes observed in the clinic could be
elicited experimentally. On the other hand, Smith and
Ray33 were able to provoke various cardiac
arrhythmias in anesthetized dogs by rapid increase in
intracranial pressure or by instantaneous release of
previously elevated intracranial pressure. Both the ad-
ministration of atropine and vagotomy eliminated or
prevented the arrhythmias. These animals also
developed cardiac arrhythmias after injections of
isoproterenol. More recently it has been shown35 that
if hypoxia is present the frequency of these problems is
increased. Thus, the experimental evidence appears to
indicate that both the sympathetic and the parasym-
pathetic systems are implicated in the production of
these rhythm disturbances. That sudden increase of
intracranial pressure can precipitate cardiac
arrhythmias is of particular clinical interest. Wong
384
ESTANOL, MARIN
and Cooper27 published a case of SAH with atrial
fibrillation and ventricular slowing in which a lumbar
puncture, presumably by decreasing the increased in-
tracranial pressure, abolished the cardiac arrhythmia.
Also, the prolongation of the QT interval so fre-
quently seen in these patients has been associated with
sudden death.36 According to James,36 "Prolongation
of the QT interval represents delayed ventricular
repolarization and an increase in the duration of the
vulnerable period with greater susceptibility to the
development of a ventricular dysrhythmia. In a
patient with a prolonged QT interval, therefore, it is
particularly important to prevent the occurrence of
premature ventricular beats or supraventricular
dysrhythmias." Smith25 published a case of SAH
associated with a prolonged QT interval and ven-
tricular bigeminy and quadrigeminy. He stated that
the cardiac arrhythmias were clearly related to a
prolonged QT interval. The prolonged QT interval
appears to be secondary to a non-uniformity in the
rate of repolarization of these cells.37'38
Intracellular studies of the sino-auricular node39
(SA node) have shown that the firing rate of the SA
node is modified by both sympathetic and parasym-
pathetic nervous systems. It is well established that the
rate of depolarization of the SA node is greatly in-
fluenced by neural mechanisms.39 For example, vagal
discharges depress the pacemaker by slowing the rate
of depolarization; on the other hand, an increase in
sympathetic discharge increases the slope of
depolarization. By reciprocal effects on the rate of
depolarization in the transmitter tissue, conduction
through the atrioventricular node (AV node) is either
increased or decreased. Sudden changes in discharges
of either vagal or sympathetic systems could produce
a number of cardiac arrhythmias. In addition to the
aforementioned neural factors, pre-existent heart dis-
ease, changes in electrolytes, and pH of the blood or
Pao, may be of significance in the production of these
arrhythmias. However, neither abnormalities in the
above-mentioned factors nor an increase in circulating
catecholamines has been found to be consistently
associated with the electrocardiographical abnor-
malities of SAH.40 The role of the myocardial lesions
secondary to acute brain lesions in the genesis of these
problems is not known.41
RELATION OF ARRHYTHMIAS TO THE SUDDEN UNEXPECTED DEATH
SYNDROME
An important point that naturally arises is the possible
relationship between the cardiac arrhythmias and the
sudden unexpected death of some patients with
primary SAH. It has been estimated that as many as
15% of the patients with spontaneous SAH die before
reaching the nearest hospital.42 Twenty percent more
will die within 48 hours after the onset of symptoms.42
Hamman43 found that 8% of all patients who died
suddenly had some sort of cerebral hemorrhage.
Others44 have found SAH to be responsible for 4.7%
Stroke, Vol. 6, July-August 1975
 CARDIAC ARRHYTHMIAS AND SUDDEN DEATH IN SAH
of all sudden deaths. In a remarkable study Secher-
Hansen39 analyzed 115 cases of autopsy-proved spon-
taneous subarachnoid hemorrhage, all of which
fulfilled the criterion for sudden unexpected death (all
deaths ranging from "instantaneous" to the first 24
hours) and found that 75% of his cases had died in-
stantaneously!
The mechanisms of death in these patients are not
entirely clear and are doubtless multiple. Acute
destruction or compression of vital centers operates in
some cases.45-te According to Helpern et al.44 the most
common postmortem finding is a diffuse subarachnoid
hemorrhage covering the base of the brain. Also,
Crompton47 has shown that blood may rapidly distend
the basal cisterns, stretching perforating arteries
which pass into the brain, causing spasm of these
vessels and resultant diencephalic ischemia. This can
bring as a consequence impairment of vegetative func-
tions. It is entirely possible that the incidence of car-
diac arrhythmias is greater when an aneurysm rup-
tures in the base of the brain, but there is not enough
clinical information to decide upon this point.
There is no satisfactory explanation for the initial
loss of consciousness that usually accompanies SAH.
There is no evidence that extravasation of blood in the
subarachnoid space can, by itself, cause un-
consciousness.48 Hemorrhage into the brain, infarc-
tion or arterial spasm have been incriminated, but the
clinical fact that many patients recover consciousness
with intact nervous system function militates against
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this thesis. Some of these patients may have seizures,
albeit the incidence of seizures at the time the
aneurysm ruptures is not known. It should be stressed
that patients with SAH should have cardiac monitor-
ing in a place in which proper treatment is available.
In regard to the treatment of these disorders, the few
arrhythmias reported in the literature responded well
to the standard methods of treatment for arrhythmias
of other causes.24 However, chemical blockage of the
sympathetic and parasympathetic systems with
atropine and propranolol has been advocated for the
prevention of myocardial damage in patients with in-
tracranial hemorrhage.22'49> 50 It is probably signifi-
cant that these patients and three others reported in
the literature2325 had bizarre atrial and ventricular
arrhythmias similar to those reported in the ex-
perimental animal by Hockman et al.34 Also, from the
cases isolated from the literature in which the location
of the aneurysm was known, two cases23'27 had
aneurysms of the anterior communicating artery, and
at least three cases23 (and those reported here) had
aneurysms of the posterior communicating in the
junction with the internal carotid. The fact that these
aneurysms were located in the base of the brain may
imply an important relationship between the location
of an intracranial hemorrhage and its potential
pathogenicity; however, more studies are needed to
clarify this point and many others in this important
medical problem.
Stroke, Vol. 6. July-August 1975
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