Shinshu M ed J, 64⑶ :153〜157, 2016

Eﬃcacy of Temporary Transvenous Pacing toPrevent Atropine‑resistant Bradycardia during Surgery for a Tumorin the Brainstem Region:A Case Report
Yuki YOSHIYAMA , Yuki SUGIYAMA, Susumu IDE, Satoshi FUSEYAToru MURAKAMI and Mikito KAWAMATA
Department of Anesthesiology and Resuscitology, Shinshu University School of Medicine

When surgery is performed in the brainstem region, the parasympathetic cardiac reﬂex via the vagus
nerve may occur, possibly resulting in bradycardia/asystole and hypotension. We report a case in whichtemporary cardiac pacing was useful to prevent recurrent atropine‑resistant bradycardia during surgeryin thebrainstem region.A 42‑year‑old woman underwent resection of a large ependymoma that extended from themidbrain to the medulla oblongata.She had no episodes of syncope,preoperative bradycardia,or arrhythmia.
Because the anticipated long duration of surgical manipulation in the brainstem region came with a high riskof bradycardia/asystole occurrence due to tumor removal,a transvenous pacing (TVP)wire was temporarily
implanted before surgery. Just after the beginning of tumor removal, severe bradycardia (28 bpm) andhypotension occurred. Tumor removal was paused, and 0.5 mg of atropine was administered intravenously.
The heart rate immediately increased to 57 bpm and hemodynamics were stable for 2 min ;however, severe
bradycardia (13 bpm)and hypotension recurred 1 min after the resumption of tumor removal.TVP (back‑up
VVI pacing at 40 bpm)was initiated, and bradycardia and hypotension did not occur again. The subsequent
course was uneventful and there were no neurological abnormalities. These ﬁndings suggested that atropine
was onlyinitiallyeﬀective in this patient after surgical manipulation was started,and that placement of a TVP
wire is useful even when atropine‑resistant bradycardia occurs during brainstem surgery.Shinshu Med J 64 :153 ―157, 2016
(Received for publication November 17, 2015;accepted in revised form January 27, 2016)
Key words:brainstem region surgery,vagal reﬂex,atropine‑resistant bradycardia,transvenous pacing

Introduction

which a transvenous pacing (TVP)wire was temporarily implanted before surgery because theSurgery in the brainstem region often induces

anticipated long duration of surgical manipulation

temporary hemodynamic changes, includingin the brainstem region came with a high risk ofbradycardia/asystole and hypotension . These

bradycardia/asystole occurrence due to tumor

hemodynamic changes are thought to be a result ofremoval. In this case, surgery induced bradycardia

a parasympathetic reﬂex, such as the vagal reﬂex,

was found to be atropine‑resistant and occurredalthough the precise mechanisms underlying thesefrequently;therefore TVP was eﬀective and indis-changes remain unclear. Here we report a case inpensable during surgical manipulation in the brainstem region.

Corresponding author:Yuki Yoshiyama
Department of Anesthesiologyand Resuscitology,Shinshu
University School of Medicine, 3‑1‑1 Asahi, M atsumoto,
Nagano 390‑8621, JapanE‑mail:yoshiyama＠shinshu‑u.ac.jp

No. 3, 2016

Case Report
A 42‑year‑old female,165 cm tall and weighing 41kg,presented with paroxysmal vomiting and weight153

Yoshiyama.Sugiyama.Ide et al.

loss for 2 years, and vertigo for 4 months.She wasdiagnosed by M RI with a large brain tumor, which
originated in the fourth ventricle, extending fromthe midbrain to the medulla oblongata and partiallyinvading the cerebellum (Fig. 1, 2).The patient had
not experienced any preoperative episodes ofsyncope,arrhythmia,including bradycardia,or orthostatic hypotension.Electrocardiogram showed normal sinus rhythm and a heart rate (HR)of 71 bpm.
No abnormalities,including cardiac function abnormalities, were identiﬁed by preoperative tests. The
patient was scheduled to undergo resection of thetumor, and no premedication was administered.
Anesthesia was induced with 100μg of fentanyland propofol via a target‑controlled infusion (TCI)
at an eﬀect‑site concentration of 4.0μg/ml. After

Fig.1 Preoperative contrast‑enhanced T1‑weighted MRI scans,showing a large ependymoma (whitearrowheads) in the fourth ventricle located on thedorsal medulla oblongata (white arrow).

loss of consciousness, 40 mg of rocuronium wasadministered for intubation. Anesthesia wasmaintained by TCI of propofol at an eﬀect‑siteconcentration of 2.5‑3.0μg/ml and remifentanil0.15‑0.20μg/kg/min. After the induction of anesthesia,a TVP catheter (Eledyn EB 10, B. Braun Medical
Inc., Berlin, Germany) was inserted via the rightinternal jugular vein under ﬂuoroscopic guidance,
and the tip of the catheter was placed on the apicalregion of the right ventricle at a distance of 20 cm.
VVI pacing was conﬁrmed by a pacing rate of 100
bpm when the HR of the patient was 65 bpm (Fig.
3A, B), and the stimulation threshold was 1 mA.
Following conﬁrmation, pacing was suspended.
During surgery, a direct current deﬁbrillator withtranscutaneous pacing (TCP) function was madeavailable. Surgery was performed in the prone

Fig. 2 Preoperative T2‑weighted M RI scans,showing a large tumor (white arrowheads) locatedon the dorsal medulla oblongata (white arrow).

position.
Intraoperative neurophysiological monitoring

removal and administration of 0.5 mg atropine

was performed, including use of motor evoked

resulted in immediate return of HR and SBP to 57

potentials (MEP), somatosensory evoked potentials

bpm and 94 mmHg,respectively,and hemodynamics(SEP),and auditory brainstem response (ABR).HR

were stable for 2min;however,1min afterresumption

and systolic blood pressure(SBP)of the patient wasof tumor removal,severe bradycardia (13 bpm)due

64‑81 bpm and 95‑118 mmHg,respectively,from theto sinus arrest and second degree atrioventricular

start of surgery to the beginning of tumor removal.

block (Wenckebach block)recurred despite prophy-

Severe bradycardia (28 bpm) and decrease of SBP

lactic atropine administration (Fig. 3C). Therefore,

from 110 to 55 mmHg occurred immediately after

we initiated TVP (back‑up VVI pacing at 40 bpm)

the start of tumor resection. Pausing of tumor(Fig. 3D).

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Transvenous pacing for bradycardia during brainstem region surgery

Fig. 3 Perioperative electrocardiograms before surgery (A)and during VVI pacing at 100 bpm (B).
Atropine‑resistant bradycardia (13 bpm) due to surgical manipulation was seen (black arrow) (C).
Back‑up pacing (black arrowheads)was started (D). No bradycardia was seen after surgery (E).

No signiﬁcant changes were observed in neurophysiological parameters, such as 10% increase inlatency and 50% decrease in amplitude in MEP andcharged 89 days postoperatively.
Discussion

SEP, and 1 msec increase in latency and 50%

Acute changes in hemodynamics induced bysurgi-decrease in amplitude of v wave in ABR during

cal manipulation occasionally occur during neur-surgery. The surgery and anesthesia duration wasosurgery, especially in surgeries in the brainstem

683 min and 863 min, respectively. Total intraoper-region. It has been reported that surgical compres-ative blood loss was 600 g and total urine volume

sion of the medulla oblongata causes acutewas 2,350 ml. Total infusion volume was 3,700 ml

bradycardia and hypotension , as was seen in the(crystalloid ﬂuid 2,200 ml; colloid ﬂuid 1,500 ml).

present patient. Mechanisms underlying bradycar-

Although TVP was required 36 times through thedia induced by compression of the medulla oblon-

duration of the tumor removal, bradycardia/arr-gata are thought to be as follows. The excitatory

hythmia did not occur after the end of tumor

nerve ﬁbers extending from the nucleus tractus

removal (Fig. 3E);therefore, the pacing wire wassolitarius (nTS),which is located on the dorsal side

removed before the patient left the operating room.

of the medulla oblongata, activate the caudal

After surgery, the patient was referred to the ICU

ventrolateral medulla (CVLM)of the medulla oblon-for post‑operative follow‑up ; the postoperativegata.From the CVLM,GABAergic inhibitorynerve

course was uneventful, and no neurological abnor-

ﬁbers then inhibit the activity of the rostralmalities were noted. The trachea was extubated,ventrolateral medulla (RVLM ).Because the RVLM

and the patient was transferred to the general wardcontrols the sympathetic nervous system,its inhibi-on the second postoperative day.Radiation therapytion leads to suppression of sympathetic activity,

was initiated 19 days postoperatively,and the subse-and results in bradycardia.Additionally,excitatory

quent course was uneventful. The patient was dis-nerve pathways from the nTS to the nucleus am-No. 3, 2016

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Yoshiyama.Sugiyama.Ide et al.

Fig.4 Schematic drawing of the mechanism of heart rate control.Nucleus tractus solitarius(nTS)induces both inhibition of sympathetic nerve and activation of parasympathetic nerve,
therefore compression of nTS causes severe bradycardia. RVLM ＝rostral ventrolateral
medulla, CVLM ＝caudal ventrolateral medulla, nA＝nucleus ambiguus.

biguus and vagus nerve can activate parasympa-

activity by atropine, and this imbalance resulted inthetic nerves and thus induce bradycardia (Fig. 4).

atropine‑resistant bradycardia.

Some reports pointed out the usefulness of TVP

Some studies have reported atropine‑resistantin neurosurgery .In the present case,we predicted

bradycardia in patients with spinal cord injury .

that severe and recurrent bradycardia,which is life‑

Cervical spinal cord injury‑induced bradycardia isthreatening during microsurgery in the prone posi-thought to be due to the disruption of cardiac sym-tion,might occur multiple times throughout the long

pathetic activity. Although reducing parasympa-

duration of surgery. Therefore, we inserted a TVP

thetic activity may indirectly, yet weakly, aﬀect

catheter prior to surgery and conﬁrmed that tempo-

sympathetic activity, atropine may possibly berary pacing operated correctly after the positional

ineﬀective in increasing heart rate in such cases.

change to avoid malposition of the TVP catheter .

If atropine is ineﬀective against these types ofIndeed, bradycardia ﬁrst occurred at the start ofbradycardia, temporary cardiac pacing should bebrain stem tumor removal.Although administration

required. There are two choices for temporaryof atropine was eﬀective for the ﬁrst incident ofpacing, TCP and TVP. It has been reported thatbradycardia,it was insuﬃcient to inhibit the second

there are no diﬀerences in hemodynamics between

incident induced by resumption of surgery. Whenthe use of TCP and TVP , and that TCP is a safe

the second incident occurred, we thought that theand eﬀective alternative method to prophylactic

initial administration of atropine was still in eﬀect,

TVP . In the present case, TVP was used to avoid

because the duration of atropine action is normallythe potential risk of TCP‑induced body movement,

1‑2 hr. Therefore, we speculate that predominant

which may lead to interruption of microsurgery andparasympathetic activity induced by general anes-

severe complications, such as neuronal injury. The

thesia and/or activation of parasympathetic activ-

incidence of complications related to TVP insertion,

ity induced by surgical manipulation may have beensuch as arterial puncture, pneumothorax, hemoper-

stronger than the inhibition of parasympathetic

icardium, infection, and displacement of the pacing

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Transvenous pacing for bradycardia during brainstem region surgery

wire, has been reported to be 15.0‑28.8%.

positional change.

We inserted the TVP wire just prior to the opera-

In conclusion, intraoperative TVP was eﬀectivetion to avoid TVP wire malposition. It has been

for treating intractable atropine‑resistant bradycar-shown that 17% of TVP pacing wires required

dia during surgery for a tumor in the brainstem

repositioning in the ﬁrst 12 hr after insertion , andregion. The present ﬁndings suggest that atropine

the median time to TVP wire displacement was 1

was only initially eﬀective against bradycardia in-day (range, 0.04‑8) . Therefore, TCP was also

duced by surgical manipulation during brainstem

made available in case of intraoperative TVP fail-surgery, and TVP should be inserted prior to sur-ure due to wire malposition or other TVP malfunc-

gery for prevention of recurrent atropine‑resistanttions during surgery .Although no studyhas repor-bradycardia in such cases, even if the patient has

ted a change in TVP wire position when the patient

had no preoperative episode of syncope,arrhythmia

is moved to the prone position,in the present study,

including bradycardia, or orthostatic hypotension.

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（2015.11.17 received ; 2016. 1.27 accepted）

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