J Cardiol 2007 Aug; 50（2）: 135 – 139

Incessant Monomorphic Ventricular
Tachycardia Associated With
Pneumococcal Meningitis : A Case
ReportYoung Soo LEE, MD
Seong WookKee Sik

HAN, MD＊1
KIM, MD

Yoon Nyun

KIM, MD＊1

Yong Won

CHO, MD＊2

Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────A 22-year-old man with incessant ventricular tachycardia（VT）
associated with pneumococcal meningitis
without obvious heart disease manifesting as febrile sensation and severe headache visited our emergency
department. Initial electrocardiography showed ventricular premature couplets, but the rhythm grew more
serious and developed into incessant monomorphic VT resulting in an electrical storm. After examining
the cerebrospinal fluid, bacterial meningitis was suspected. The electrical storm ended 21 hr after he hadreceived conservative treatment for meningitis. Streptococcus pneumonia was cultured from the cerebrospinal fluid. No VT was observed during the remainder of the hospital stay and could not be induced in
the electrophysiological study.
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Key Words■ Tachycardia（monomorphic ventricular）

INTRODUCTION
The interconnection between the central nervoussystem（CNS）and heart was first described in1903.1）Electrocardiographic（ ECG）changes andarrhythmias are frequent complications in patientswith cerebral injury.2）Increased plasma concentrations of catecholamines may result in tachyarrhythmias, whereas enhanced vagal activity can cause
sinus bradycardia and atrioventricular block.
Among the cardiac arrhythmias, ventricular tachycardia（VT）accounts for 2% of the rhythm disturbances in patients with a subarachnoid
hemorrhage.3）The vasocardiac reflexes from thecircle of Willis and diffuse cerebral dysfunction
may be possible factors causing ECG changes inpatients with pyogenic meningitis.4）We report a■ Infectious disease（pneumococcal meningitis）

case of an incessant monomorphic VT in a patientwith pneumococcal meningitis associated with amarked increase in the intracranial pressure.
CASE REPORT
A 22-year-old man visited the emergency room
because of a fever and severe headache lasting for 6
hr. He had no cardiovascular risk factors. His vital
signs were blood pressure of 130/80 mmHg, respiratory rate of 30/min, pulse rate of 100 beats/min,and body temperature of 39.0 °C. The initial ECG
showed frequent couplets of ventricular prematurebeats（Fig. 1）. The initial laboratory findings wereas follows : white blood cell count 25,980/mm 3（neutrophil count 93%）
, serum potassium level 3.7
mEq/l, serum calcium level 9.3 mg/dl, and the others were within normal limits. Transthoracic──────────────────────────────────────────────Deparment of Cardiology, Catholic University of Daegu, Daegu, Korea ; Departments of ＊ 1Cardiology and ＊ 2Neurology, Keimyung
University, Daegu, Korea
Address for correspondence : HAN SW, MD, Department of Cardiology, Keimyung University, 194 Dongsan-dong, Jung-gu, Daegu,Korea ; E-mail : swhan@dsmc.or.kr
Manuscript received March 12, 2007 ; revised May 10, 2007 ; accepted May 10, 2007

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Lee, Han, Kim et al

Fig. 1 Initial 12-lead electrocardiogram showing couplets of ventricular premature beats with rightbundle branch block morphology and superior axis

echocardiography revealed normal systolic function
and chamber size.
Two hr later, monomorphic VT spontaneously
developed with a right bundle branch block morphology and superior axis（Fig. 2−A）
, and was terminated by electrical cardioversion. Continuous
infusion of amiodarone was started. After 12 hr, acerebrospinal fluid study was performed, which
revealed that the intracranial pressure was
550 mmH2O, red blood cell 1,400/high power field（HPF）, white blood cell 18,000/HPF（neutrophil90%）, protein 269 mg/dl, and glucose 10 mg/dl.
Following that, intravenous antibiotics（vancomycinand ceftria-xone）
were started as an empirical treatment for a suspected bacterial meningitis. After 16hr, monomorphic VT with the same morphology as
the previous event occurred（Fig. 2−B）. However,his blood pressure was stable. Attempts were madeto terminate the VT with electrical cardioversion
and continuous infusions of anti-arrhythmic agents
such as amiodarone, lidocaine, procainamide, andesmolol, were administered, but none worked andthe VT continued. The potassium level decreased to3.0 mEq/l even with a continuous infusion of potassium（Fig. 3）. Fortunately, the VT spontaneously

ended 10 hr after the continuous administration oflarge amounts of potassium, and agents used tolower the intracranial pressure such as mannitol andcorticosteroids. Streptococcus pneumoniae was cultured from the cerebrospinal fluid several days later.
An electrophysiologic study was performed 2weeks later. No ventricular tachyarrhythmia could
be induced by the programmed electrical stimulation. The patient was discharged without sequelae.
DISCUSSION
Subarachnoid hemorrhages and strokes are themost common CNS causes related to ventriculartachyarrhythmias. The present case is a unique
report of incessant VT associated with a CNS
infection.
Incessant VT is an uncommon arrhythmia and isrefractory to anti-arrhythmic drugs and repeatedelectrical cardioversions.5）Incessant monomorphic
VT has been reported in a variety of clinical settings, including coronary artery disease,6）Brugadasyndrome,7）and dilated cardiomyopathy.8）
Morphological electrocardiographic changes
have mostly been reported in patients with subarachnoid and intracerebral hemorrhages, but could
J Cardiol 2007 Aug; 50（2）: 135 – 139

Incessant Monomorphic Ventricular Tachycardia

Fig. 2 Twelve-lead electrocardiograms showing monomorphic ventricular tachycardia with rightbundle branch block morphology and superior axis
Panel A shows the initial monomorphic ventricular tachycardia.
Panel B shows the second monomorphic ventricular tachycardia which was the incessant type and occurred
16 hr later.

Esmolol
Procainamide
Lidocaine
Drug

Amiodarone
K
Mannitol& steroid
Antibiotics

K level
3.7（mEq/l）

3.3

3.0
CSF study
ICP 550 mmH2O

VTTime ofhospital stay

24

68

10

1214Hour161820222426Fig. 3 Time course of the ventricular tachycardia attack, potassium level and administration of various types of medications
VT ＝ ventricular tachycardia ; CSF ＝ cerebrospinal fluid ; ICP ＝ intracranial pressure.

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Lee, Han, Kim et aloccur in a variety of CNS injuries including infections, tumors or neurosurgical procedures.9）The
most commonly reported cause of ventriculararrhythmias associated with CNS disease such assustained VT and torsade de pointes is subarachnoid hemorrhage. Other causes have rarely beenreported.
Several studies have suggested possible mechanisms of the ECG alterations in patients with cerebral injuries. First, a sympathetic storm which causes inhomogeneity in the ventricular repolarization.
The level of the norepinephrine metabolism is correlated with the prolongation of the QTc interval,
predisposing to substrate to ventricular tachyarrhythmias. Cerebral injury causes a stressresponse resulting in increased concentrations ofplasma catecholamines. However, increased
intracranial pressure（ ICP）can cause a marked
reflex sympathetic discharge. The increased ICP
may be important in mediating the observed ECGchanges.10）Second, hypokalemia may precipitate
ventricular arrhythmias by prolonging the action
potential duration. Vomiting, which increases thecirculating catecholamines and rennin, or hypercortisolism are obvious causative factors.11）In particular, excessive activation of the renin-angiotensinsystem（RAS）can lead to hypokalemia. It is unclear
whether the activation of the RAS results from thedirect effect of hypothalamus stimulation or an
overactivity of the sympathetic system.12）Third,
stimulation of the hypothalamus has been shown tocause frequent ventricular arrhythmias as well aschanges in the ECG morphology.
In this case, the initial ICP was 550 mmH2O andwas sufficient to cause a sympathetic overflow, but
was not confirmed by the blood test. The potassium
References1）Cushing H : The blood pressure reaction of acute cerebral
compression illustrated by cases of intracranial hemorrhage. Am J Med Sci 1903 ; 125 : 1017−10442）Andreoli A, di Pasquale G, Pinelli G, Grazi P, Tognetti F,Testa C : Subarachnoid hemorrhage : Frequency and severity of cardiac arrhythmias : A survey of 70 cases studied inthe acute phase. Stroke 1987 ; 18 : 558−5643）Sakr YL, Ghosn I, Vincent JL : Cardiac manifestations
after subarachnoid hemorrhage : A systematic review of theliterature. Prog Cardiovasc Dis 2002 ; 45 : 67−804）Hersch C : Electrocardiographic changes in subarachnoid
hemorrhage, meningitis, and intracranial space-occupying
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level was 3.7 mEq/l. Even though the potassium
levels continued to decrease whether this was theeffect of using the steroids or an overactive state of
the RAS remained unclear. Because the initial
potassium level could have predisposed the patient
to ventricular arrhythmias, it can be assumed thatthe effect of the hypokalemia on the VT was aresult of the meningitis. Antibiotics including
macrolides, quinolones, and amphotericin B can
induce fatal cardiac arrhythmias.13,14）In this case,
we gave vancomycin and ceftriaxone, which have a
low possibility of causing cardiac arrhythmias. The
QT interval was 320 msec at the time of the initial
ECG. The proarrhythmic effect of amiodarone isassociated with QT interval prolongation.15）Even
though we infused amiodarone continuously after
the termination of the VT, no arrhythmias werenoted, but a mild prolongation of the QT interval to
480 msec was observed.
In the case of intracranial or subarachnoid hemorrhage, cardiac arrhythmias could be directly
induced by space-occupying lesions such as hemorrhage-associated transtentorial herniations, which
could cause autonomic stimulation over a wide
area. On the other hand, cardiac arrhythmias associated with meningitis are caused only by secondarychanges such as an elevated ICP or excessive activation of the RAS. Vasocardiac reflexes in the circle of Willis and diffuse cerebral dysfunction may
be factors causing ECG changes in patients withpyogenic meningitis.4）
The main cause of the VT in this case appeared
to be a marked increase in the ICP which was facilitated by the hypokalemia. The tachycardia was terminated by decreasing the elevated ICP and correcting the hypokalemia.
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