Shinshu Med J, 66⑹：443～449, 2018

Flattening of the Interventricular Septum during One-lung
Ventilation in a Patient with Arrhythmogenic Right
Ventricular Cardiomyopathy
Satoshi Fuseya＊, Takashi Ishida, Takashi Ichino and Mikito Kawamata
Department of Anesthesiology and Resuscitology, Shinshu University School of Medicine

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by ventricular arrhythmia andright heart failure due to right ventricular (RV) fibrofatty atrophy. A 70-year-old male with ARVC underwent
elective endoscopic left upper lobectomy for treatment of lung cancer. We found that one-lung ventilation (OLV)
caused flattening of the interventricular septum (IVS) during diastole and changed the left ventricular (LV)
configuration from a circle to a “D-shape” in the patient, which was imaged with transesophageal echocardiog­
raphy (TEE). The LV “D-shape” returned to a normal circular configuration immediately after conversion from
OLV to two-lung ventilation. Since flattening of the IVS is a sign of RV overload and since continuous RV
overload may result in the development of RV dysfunction, early diagnosis is important. We recommend moni­
toring of IVS movement by TEE during OLV in patients with ARVC. Shinshu Med J 66 : 443―449, 2018
(Received for publication June 5, 2018 ; accepted in revised form July 25, 2018)
Key words : flattening of the interventricular septum, one-lung ventilation,arrhythmogenic right ventricular cardiomyopathy

Ⅰ Introduction

Ⅱ

Case Report

Arrhythmogenic right ventricular cardiomyopathy

A 70-year-old male (height, 165 cm ; weight, 66(ARVC), a heart muscle disease of unknown etiology,kg) had been suffering from sudden attacks ofis characterized by replacement of the right ventric­

unconsciousness for 13 years. An echocardiogram

ular (RV) myocardium by fibrofatty tissue and elec­

showed RV dilatation (RV end-diastolic dimension

trical instability associated with ventricular tachy­of 43.2 mm (＞28 mm)), an endomyocardial biopsy

1）
2）. The regional or diffuse fibrofatty

showed fibrofatty replacement of the myocardium,atrophy of the RV free wall causes wall thinning andand an electrocardiogram showed VT exhibiting

cardia (VT)1）

chamber dilatation, leading to right heart failure . It

left bundle-branch block morphology. ARVC was

has been reported that one-lung ventilation (OLV)

diagnosed by these findings according to the criteria

increases RV preload3） as well as afterload3）-6）, possi­

for diagnosis of ARVC/dysplasia7）. He had been

bly resulting in dysfunction of the right heart fortreated with amiodarone (100 mg/day) and had

ARVC patients. We report a case of ARVC in which

been implanted with an implantable cardioverter-

OLV caused flattening of the interventricular sep­

defibrillator (ICD). He had no familial history oftum (IVS), which is a sign of the development of RV

premature sudden death due to suspected ARVC.

dysfunction due to RV overload, revealed by transe­

He underwent abdominoperineal resection of thesophageal echocardiography (TEE).

rectum for treatment of rectal cancer three years
ago. Follow-up blood chemistry studies showed＊

Corresponding author : Satoshi Fuseya
Department of Anesthesiology and Resuscitology,
Shinshu University School of Medicine, 3-1-1 Asahi,
Matsumoto, Nagano 390-8621, Japan
E-mail : sfuseya@shinshu-u.ac.jp

No. 6, 2018

elevation of tumor makers such as carbohydrate
antigen 19-9 and carcinoembryonic antigen. Comput­
ed tomography and positron emission tomography
revealed lung cancer in the left upper lobe. The patient443

Fuseya・Ishida・Ichino et al.

Fig. 1 Preoperative electrocardiogram. An electrocardiogram showed low voltage in extremity leads, right axis
deviation and T-wave inversions in leads V1-6 without right bundle-branch block as the minor sign of thecriteria for diagnosis of ARVC/dysplasia7）; the electrocardiogram also revealed QRS complex prolongation(＞110 msec) in leads V1-3 and epsilon waves as the two major signs of the criteria for diagnosis of ARVC/
dysplasia7）. These findings of the electrocardiogram are typical for ARVC2）.

Fig. 2 Preoperative transthoracic echocardiography. (A) and (B) are a short axis cross-sectional view and afour-chamber view at end diastole, respectively. Note the remarkable dilation of the right ventricle so thatthe volume of the right ventricle is larger than that of the left ventricle (white arrowhead) (A, B) and apex
consisting of the right ventricle (white arrow) (B). Right ventricular trabeculae carneae were also welldeveloped. RV : right ventricle, LV : left ventricle.

was thus scheduled for elective endoscopic left upper

except for creatinine of 1.23 mg/dl and forced expi­

lobectomy for treatment of lung cancer.

ratory volume ％ in one second of 67.4 ％. An elec­

Preoperative physical examination did not reveal

trocardiogram showed typical findings2） as the one

any symptoms of heart failure such as dyspnea

minor sign and the two major signs of the criteria

during daily activities, orthopnea, or pitting edema.

for diagnosis of ARVC/dysplasia (Fig. 1)7）. Preopera­

Results of hematologic and blood chemistry studies

tive transthoracic echocardiography showed remark­and results of spirometry were in normal ranges

able RV dilation (Fig. 2), tricuspid valve regurgita­

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Flattening of the interventricular septum during one-lung ventilation

tion (TR) of mild to moderate severity diagnosed by2

was started at a tidal volume of 500 ml on volume-control

a TR jet area of 4.2 cm , vena contracta width of 4ventilation and at a rate of 10 breaths/min with 12mm, and pressure gradient of 27.8 mmHg between

cmH2O of peak positive inspiratory airway pressure

the right ventricle and right atrium. RV wall motion,(PIP) (mean airway pressure of 4 cmH2O). At thisespecially at the apex, appeared to be hypokinetic.

point, the values of IAP and CVP were 98/60 mmHg

Left ventricular (LV) ejection fraction (EF) and LV

and 8 mmHg, respectively. TEE did not show any

end-diastolic dimension were 63 ％ and 43 mm,

abnormality in LV wall motion with EF of 49.7 ％ .

respectively. LV wall motion was normal, which isWhen OLV of the right lung was started, PIP in­

one of the major signs of the criteria for diagnosis ofcreased up to 18 to 20 cmH2O (mean airway pres­

7）

ARVC/dysplasia . Taken together, our patient ful­

sure of 6 cmH2O) with the same settings of ventilator

filled the three signs of the major criteria and two

parameters, and CVP also increased up to 11 mmHg.

signs of the minor criteria, being consistent with a

A TEE image of the left ventricle showed a change

7）

to a “D-shape” by flattening of the IVS during dias­

On the day of surgery, the patient did not receive

tole (Fig. 3A). Partial pressures of oxygen and car­any premedication. Routine noninvasive monitoringbon dioxide in arterial blood on 100 ％ oxygen were

including blood pressure, electrocardiogram, andmaintained at 101-157 mmHg and 45-46 mmHg, re­percutaneous oxygen saturation (SpO 2 ) was per­spectively, during OLV. Although TEE showed flat­

formed in the operating room. Before anesthesia, his

tening of the IVS during OLV, IAP and EF were

blood pressure was 140/90 mmHg, heart rate was 80

maintained at 92-125/56-76 mmHg and 46-63 ％ ,b.p.m, and SpO2 was 96 ％ on 21 ％ oxygen. An epi­

respectively, which were comparable to those during

dural catheter was inserted at T5-6. In order to

TLV. Surgery was uneventfully completed underprevent malfunction of the ICD during surgery bygeneral anesthesia with OLV. PIP and CVP were

electrocautery, we placed external defibrillator pads

decreased to 13 cmH2O and 9 mmHg, respectively,

instead of the ICD. After preoxygenation, anesthesia

and the LV “D-shape” returned to a normal circular

was induced with midazolam (5 mg i.v.) and remifen­

configuration immediately after OLV was stopped

tanil (0.2 μg/kg/min). Then rocuronium (40 mg i.v.)

and TLV was started (Fig. 3B). The durations of

was administered to facilitate tracheal intubation

anesthesia and OLV were 391 min and 278 min, re­with a 37 Fr left-sided double-lumen endotracheal

spectively. The total volume of crystalloid fluid ad­

tube. Anesthesia was maintained using sevoflurane

ministered was 1150 ml. Total amounts of blood loss

with an end-tidal concentration of 1.2-1.5 ％ in 72-

and urine were 120 ml and 215 ml, respectively.

100 ％ oxygen, remifentanil (0.05-0.1 μg/kg/min), andDuring the postoperative period, no ventricular ar­continuous epidural infusion of 0.2 ％ ropivacaine (3rhythmia or symptoms of right heart failure wereml/h). The following parameters were monitoredobserved. He was discharged on schedule.

positive diagnosis of ARVC .

intraoperatively : expired end-tidal carbon dioxide
tension, invasive arterial pressure (IAP), central

Ⅲ

Discussion

venous pressure (CVP), and cardiac function by

Previous investigators have reported sudden deathusing TEE. A pulmonary artery catheter was notin patients with ARVC during the perioperative

inserted in order to avoid induction of VT. As aperiod due to arrhythmia and/or acute heart fail­result, pulmonary arterial pressure (PAP) and pul­ure8）-11）. Therefore, it is important to monitor cardi­acmonary vascular resistance (PVR) were not evaluat­

function during and after surgery. We observed

ed in this patient.

a flat IVS during OLV and normal curvature of theFollowing anesthetic induction and maintenance,

IVS when OLV was stopped and TLV was started

the patient was placed in a right lateral decubitus

in our patient with ARVC. The LV “D-shape” re­position. First, mechanical two-lung ventilation (TLV)

turned to a normal circular configuration immediate­

No. 6, 2018445

Fuseya・Ishida・Ichino et al.

Fig. 3 Transesophageal echocardiographic short axis cross-sectional view at end diastole. (A) and (B) are aview during one-lung ventilation and a view during two-lung ventilation, respectively. (A1) and (B1) are
original photographs, and (A2) and (B2) are shown to emphasize the biventricular wall shape by tracing theoutline. Note that left ventricular wall shape was changed to a “D-shape” by flattening of the interventricular
septum (IVS) in (A1) and (A2) (black arrow). Note that the left ventricular wall “D-shape” completely
recovered to the normal circular configuration (black arrow) and that left chamber size was enlarged to theoriginal size in (B1) and (B2).

ly after conversion from OLV to TLV. These results

creases after conversion from TLV to OLV. In addition,strongly suggest that pre- and/or after-overload of

Abe et al.4） and Carlsson et al.13） reported that mean

the right ventricle due to OLV caused flattening of

PAP of 4-5 mmHg and PVR were significantly in­

the IVS in this patient.

creased after conversion from TLV to OLV at volume-

Indeed, in our patient, CVP during OLV was 3

controlled ventilation with the same settings ofmmHg higher than that during TLV, being consis­

ventilator parameters under sevoflurane or isoflu­

tent with the results of a previous study showingrane anesthesia. Wilkinson et al.3） also reported thatthat CVP during OVL is significantly higher thanboth RV end-systolic area and RV end-diastolic areathat during TLV under the condition of the same

were significantly increased during OLV compared12）

settings of ventilator parameters . These findings

to those during TLV. These findings indicate thatindicate that preload of the right ventricle in­

OLV increases afterload as well as preload of the446

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Flattening of the interventricular septum during one-lung ventilationright ventricle. Thus, although we did not examine

small in patients with COPD compared to that in

PAP and PVR by using a pulmonary artery catheter

patients with normal lungs. Thus, although an

in order to avoid induction of VT, RV afterload wasincrease in PIP caused an increase in RV afterload,

probably increased during OLV in our patient.

the range of increase in RV afterload might have

Although the mechanisms of OLV-induced in­crease in RV afterload and preload have not been

been small. As a result, flattening of IVS did notoccur during systole in our patient.

elucidated, increase in airway pressure and maldis­

On the other hand, flattening of IVS occurred duringtribution of pulmonary blood flow may contribute todiastole in our patient. Flattening of IVS during

it. OLV-induced increase in mean PAP was reported

diastole indicates an increase in RV preload17）. As

to be 4-5 mmHg and at least less than 10 mmHg

stated in the second paragraph in the Discussion

during sevoflurane or isoflurane anesthesia in pa­

section, RV preload actually increased during OLV

tients without heart disease4）13）, while it has beenin our patient. It has been reported that an increase

shown that flattening of the IVS could be caused by

in RV afterload raised RV contractility with un­

more than 45 mmHg of systolic PAP, more than 46

changed RV end-diastolic pressure and volume in

mmHg of systolic RV pressure, and more than 24

controls with normal cardiac function18）. However, an

mmHg of mean PAP14）15）. Therefore, OLV alone will

increase in RV afterload led to concomitant increases

not cause flattening of the IVS in patients within RV end-diastolic pressure and volume in a groupnormal cardiac function. Since we did not examinewith chronic volume overload18）. These findings sug­

the changes of TR pressure gradient throughout thegest that although chronic volume overload does

surgery, we cannot use the data of TR pressure

not impair RV contractility, the inotropic adaptation

gradients for evidence of an increase in RV afterload

to an increased RV afterload is limited and partly

during OLV. However, since OLV was reported tocompensated by the Frank-Starling mechanism. Our

3）
4）
13）

, TR pressure gradientspatient had chronic volume overload as shown by

probably increased during OLV. If TR pressure gra­TR of mild to moderate severity and remarkable RV

dients were the same in the preoperative period anddilatation diagnosed by TEE before surgery. In

during TLV under general anesthesia in our patient,addition, diffuse fibrofatty atrophy of the RV freesystolic RV pressure (≈systolic PAP)＝CVP＋TR

wall in our patient decreased tolerability of the rightpressure gradient＝8＋27.8＝35.8 mmHg. Mean PAP

ventricle to OLV-induced increase in RV afterload,increase in RV afterload

16）＝0.6×systolic PAP＋2 ＝0.6×35.8＋2＝23.5 mmHg

resulting in flattening of the IVS during diastole.

during TLV. If mean PAP increased by 4 mmHg after

Since a pulmonary artery catheter was not insert­

conversion from TLV to OLV as shown in previous

ed, we did not examine cardiac output (CO) through­reports

4）13）, mean PAP could be 27.5 mmHg during

out the surgery. However, it has been reported that

OLV. Thus, OLV-induced increase in RV afterload

total blood flow of two lungs (namely, CO) did not

could have caused flattening of IVS in our patient.

change after conversion from TLV to OLV in pa­

Since it has been reported that an increase in RV

tients with normal cardiac function13）. Although OLV

afterload caused flattening of IVS not only during

increases in RV afterload3）4）13）, an increase in RV

diastole but also mainly during systole17）, flattening

afterload did not change CO in a group with chronicof IVS could also have been caused during systole involume overload as well as with normal hearts18）.

our patient. Our patient had chronic obstructive

Thus, CO was probably maintained after conversion

pulmonary disease (COPD) with forced expiratoryfrom TLV to OLV in our patient. In addition, partial

volume ％ in one second of 67.4 ％. Since lung com­pressure of oxygen in arterial blood on 100 ％ oxygen

pliance in patients with COPD is larger than that in

and invasive arterial pressure were also maintained

patients with normal lungs, an increase in PIP

in normal ranges during OLV. These findings suggest

during OLV in volume-controlled ventilation may bethat pulmonary circulation impairment did not occur

No. 6, 2018447

Fuseya・Ishida・Ichino et al.

sidered20）. Since hypoxia and hypercapnia can increaseduring OLV in our patient.
Since flattening of the IVS is a sign of develop­
ment of RV dysfunction, early diagnosis is important.

PVR, arterial blood gas should also be checked.
One of the weaknesses of the present study is

TEE enables real-time and noninvasive monitoringthat evidence for an increase in RV afterload includ­of IVS movement during surgery. Therefore, we

ing systolic PAP calculated by TR pressure gradi­

recommend monitoring of IVS movement by TEE

ents or mean PAP calculated by early-diastolicduring OLV in patients with ARVC. While positive

pulmonary regurgitation velocity was not obtained.

end-expiratory pressure (PEEP) is commonly used

These parameters and CO calculated by velocity-

to improve hypoxia during OLV, PEEP can increasetime integral and diameter of the RV outflow tract

RV afterload. It has been shown that PEEP of more

could be useful for estimating PVR. If these parame­

than 20 cmH 2 O causes flattening of the IVS inters had been investigated after conversion from19）

patients without heart disease during TLV . Since

TLV to OLV and from OLV to TLV, we could havediffuse fibrofatty atrophy of the RV free wall as

directly shown that OLV-induced increase in RV

observed in our patient decreases tolerability ofafterload caused flattening of IVS. In addition, we

the right ventricle to OLV-induced increase in RV

were not able to use 3D echocardiography in our

afterload, when PEEP is applied in patients withpatient because the equipment was outdated. If we

ARVC during OLV, PEEP should be set up withhad examined the configuration of the heart by 3D

observation of IVS movement by TEE.

echocardiography, we could have shown evidence

In our patient, since blood pressure and EF werethat OLV changed the configuration of the tricuspid

not changed when flattening of the IVS occurred,valve complex, resulting in impairment of tricuspid

we carefully monitored hemodynamic status without

valve coaptation, which deteriorates TR and leads totreatment. If hemodynamics deteriorate with flatten­

an increase in RV preload.

ing of the IVS after starting OLV, administration of

In conclusion, we experienced OLV-induced patho­

inotropic agents such as dobutamine, vasopressors,

logic IVS movement (flattening) in a patient with ARVC.

pulmonary vasodilators such as phosphodiesterase-3

We recommend monitoring of IVS movement by TEE

inhibitors, or nitroglycerin or inhalation of nitricduring OLV in patients with ARVC.

oxide in addition to cessation of OLV should be con­
References
1） Kiès P, Bootsma M, Bax J, Schalij MJ, Wall EE : Arrhythmogenic right ventricular dysplasia/cardiomyopa­
thy : screening, diagnosis, and treatment. Heart Rhythm 3 : 225-234, 2006
2） McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstorm-Lundqvist C, Fontaine G, Camerini F : Diagnosis ofarrhythmogenic right ventricular dysplasia/ cardiomyopathy. Task Force of the Working Group Myocardial and
Pericardial Diseases of the European Society of Cardiology and the Scientific Council on Cardiomyopathies of theInternational Society and Federation of Cardiology. Br Heart J 71 : 215-218, 1994
3） Wilkinson JN, Scanlan M, Skinner H, Malik M : Right heart function during one-lung ventilation-observations usingtransoesophageal echocardiography. Anaesthesia 64 : 1387-1388, 20094） Abe K, Mashimo T, Yoshida I : Arterial oxygenation and shunt fraction during one-lung ventilation : a comparisonof isoflurane and sevoflurane. Anesth Analg 86 : 1266-1270, 1998
5） Mcmahon CC, Irvine T, Conacher ID : Transoesophageal echocardiography in the management of whole lunglavage. Br J Anaesth 81 : 262-264, 1998
6） Pagel PS, Fu JL, Damask MC, Davis RF, Samuelson PN, Howie MB, Warltier DC : Desflurane and isoflurane produce
similar alterations in systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing onelung ventilation during thoracotomy. Anesth Analg 87 : 800-807, 1998
448

Shinshu Med J

Vol. 66

Flattening of the interventricular septum during one-lung ventilation
7） Thiene G, Corrado D, Basso C : Arrhythmogenic right ventricular cardiomyopathy/dysplasia. Orphanet J Rare Dis
2 : 45, 2007
8） Bonnet F, Samain E, Bocquet R, Corre FL, Marty J : Perioperative management of severe head injury in a patientwith arrhythmogenic right ventricular dysplasia. Anesthesiology 95 : 255-256, 20019） Houfani B, Meyer P, Merckx J, Roure P, Padovani JP, Fontaine G, Carli P : Postoperative sudden death in twoadolescents with myelomeningocele and unrecognized arrhythmogenic right ventricular dysplasia. Anesthesiology
95 : 257-259, 2001
10） Toh KW, Nadesan K, Sie MY, Vijeyasingam R, Tan PSK : Postoperative death in a patient with unrecognizedarrhythmogenic right ventricular dysplasia syndrome. Anesth Analg 99 : 350-352, 2004
11） Bastien O, Guerin JM, Artru F, Lehot JJ : Arrhythmogenic right ventricular dysplasia : an underestimated cause of
perioperative death? J Cardiothorac Vasc Anesth 16 : 357-358, 2002
12） Lee SH, Kim N, Kim HI, Oh YJ : Echocardiographic evaluation of pulmonary venous blood flow and cardiac functionchanges during one-lung ventilation. Int J Clin Exp Med 8 : 13099-13108, 201513） Carlsson AJ, Bindslev L, Hedenstierna G : Hypoxia-induced pulmonary vasoconstriction in the human lung. The
effect of isoflurane anesthesia. Anesthesiology 66 : 312-316, 1987
14） Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstrong WF : An echocardiographic index for
separation of right ventricular volume and pressure overload. J Am Coll Cardiol 5 : 918-924, 1985
15） Shimada R, Takeshita A, Nakamura M : Noninvasive assessment of right ventricular systolic pressure in atrial
septal defect : analysis of the end-systolic configuration of the ventricular septum by two-dimensional echo­
cardiography. Am J Cardiol 53 : 1117-1123, 1984
16） Chemla D, Castelain V, Humbert M, Hébert JL, Simonneau G, Lecarpentier Y, Hervé P : New formula for predicting
mean pulmonary artery pressure using systolic pulmonary artery pressure. Chest 126 : 1313-1317, 2004
17） Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, Solomon SD, Louie EK, Schiller
NB : Guidelines for the echocardiographic assessment of the right heart in adults : a report from the American
Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of
the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr
23 : 685-713, 201018） Szabó G, Soós P, Bährle S, Radovits T, Weigang E, Kékesi V, Merkely B, Hagl S : Adaptation of the right ventricle toan increased afterload in the chronically volume overloaded heart. Ann Thorac Surg 82 : 989-995, 200619） Jardin F, Farcot JC, Boisante L, Curien N, Margairaz A, Bourdarais JP : Influence of positive end-expiratory
pressure on left ventricular performance. N Engl J Med 304 : 387-392, 1981
20） Lahm T, McCaslin CA, Wozniak TC, Ghumman W, Fadl YY, Obeidat OS, Schwab K, Meldrum DR : Medical andsurgical treatment of acute right ventricular failure. J Am Coll Cardiol 56 : 1435-1446, 2010（2018. 6. 5 received；2018. 7. 25 accepted）

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