moderate altitude increases right ventricular pressure and oxygen desaturation in adolescents with...

Moderate Altitude Increases Right Ventricular Pressure andOxygen Desaturation in Adolescents with Surgically ClosedSeptal Defectchd_425 556..564

Thomas Möller, MD,* Henrik Brun, MD,† Per M. Fredriksen, PT, PhD,‡

Henrik Holmstrøm, MD, PhD,† Eirik Pettersen, MD,§ and Erik Thaulow, MD, PhD†

*Pediatric Department—Vestfold Hospital Trust, Tønsberg, Norway; †Department of Pediatric Cardiology, Pulmology andAllergy, Oslo University Hospital/Rikshospitalet, Oslo, Norway; ‡Clinical Trials Unit—Oslo University Hospital, Oslo,Norway; §Department of Cardiology—Oslo University Hospital/Rikshospitalet, Oslo, Norway

A B S T R A C T

Objectives. Abnormal right ventricular systolic pressure response (RVPR) during exercise has previously beendemonstrated in patients with septal defects of the heart. Our study investigated whether moderate altitude affectsRVPR and oxygen saturation during rest and exercise in patients with surgically closed septal defects.Design. Ten patients with surgically closed heart septal defects (six secundum atrial septal defects, four ventricularseptal defects) were examined by cardiopulmonary exercise testing and by echocardiography at rest and duringsupine cycling at sea level. After 2 hours in a hypobaric chamber at 2500 m/8200 ft altitude, exercise echocardio-graphy was repeated.Results. During sea level exercise four patients showed abnormal RVPR (>50 mm Hg). Acute hypoxic exposure ledto right ventricular systolic pressure increase above 40 mm Hg in two patients. During altitude exercise sevenpatients showed abnormal RVPR. Average maximal right ventricular systolic pressure was 56.5 � 12.7 mm Hg andaverage for the lowest oxygen saturation was 80.0 � 5.7%. Two patients had simultaneous oxygen desaturation below80% and right ventricular systolic pressure above 50 mm Hg.Conclusions. Moderate altitude affects right ventricular systolic pressure and oxygen saturation in adolescents withsurgically closed ventricular or atrial septal defects. Moderate altitude may induce or aggravate abnormal RVPR andoxygen desaturation during exercise in these patients.

Key words. Congenital Heart Defects; Heart Septal Defects; Pulmonary Hypertension; Hypoxia; Exercise;Altitude

Introduction

Congenital heart septal defects with left-to-right shunt, either atrial septal defect (ASD)

or ventricular septal defect (VSD), cause pulmo-nary vascular volume overload and may therebyinduce pulmonary vasculopathy. We have recentlyshown a high prevalence of right ventricular sys-tolic pressure response (RVPR) to exercise above50 mm Hg in asymptomatic patients with isolatedheart septal defects1 which has to be interpreted asan indication of exercise-induced pulmonaryhypertension in these patients. In normally trainedhealthy individuals 50 mm Hg can be consideredthe upper normal limit of exercise-induced

RVPR.2 Whether abnormal RVPR to exerciserepresents a static/structural or dynamic/vasoconstrictive phenomenon in the pulmonarycirculation of these patients remains unclear.

RVPR during sea level exercise and RVPR dueto acute hypoxic exposure has been shown to cor-relate with susceptibility to high altitude pul-monary edema (HAPE).3–5 The prevalence ofabnormal RVPR due to acute hypoxia and suscep-tibility to HAPE in healthy individuals has beendemonstrated to be as low as 5–6%.6,7 The preva-lence of abnormal RVPR in healthy individualsduring sea level exercise is equally low.2 Patentforamen ovale with a possibility of an intracardiacleft-to-right shunt has been found to be four times

556

© 2010 Copyright the AuthorsCongenital Heart Disease © 2010 Wiley Periodicals, Inc.Congenit Heart Dis. 2010;5:556–564

as frequent among individuals encountering highaltitude pulmonary edema compared with thegeneral population.8 Under high altitude condi-tions pulmonary circulation and peripheral oxygensaturation (SpO2) are modulated by multiplefactors and mechanisms. Cardiac output andsmooth muscle tone in the pulmonary arteriolestogether determine pulmonary arterial pressure.The latter is influenced both by hypoxic pulmo-nary vasoconstriction and by hypocapnic pulmo-nary vasodilatation due to hyperventilation. SpO2

declines with lowered atmospheric oxygen partialpressure and alveolar oxygen pressure, and it issimultaneously increased by the hypoxic ventila-tory response. Complex adaptation thus makes itdifficult to study the isolated circulatory or venti-latory effects of altitude.9

This study aims to explore to what extentabnormal RVPR in patients with surgically closedASD or VSD is a dynamic condition, whichcan be influenced by external factors like acuteexposure to hypobaric hypoxia during simulatedmoderate altitude conditions. We wanted toinvestigate if abnormal RVPR can be evoked bymoderate altitude or if abnormal response at sealevel can be worsened by moderate altitude. Pre-vious data show higher prevalence of abnormalRVPR during sea level exercise in patients withVSD compared with those with ASD.1 We wereinterested whether altitude-induced changeslikewise would be more pronounced in patientswith VSD. We hypothesized that moderate alti-tude may induce abnormal RVPR to exercisein individuals with normal RVPR at sea level.We further hypothesized that abnormal RVPRduring sea level exercise can be worsened bymoderate altitude.

Methods

For the study we enrolled 10 patients aged 13 to25 years who had undergone surgical closure ofan ASD or VSD in early childhood with no rightventricular outflow tract obstruction. All defectswere closed by direct suture without use of a sur-gical patch. The patients were chosen from agroup of 44 patients with isolated secundum ASDor VSD who had been examined in our institu-tion during the last 12 months before inclusion.1None of the patients had known lung diseaseand all were low altitude residents. None of thepatients had undergone any major cardiovascularintervention other than defect closure. Allpatients had been examined by cardiorespiratory

exercise testing on a treadmill and by echocardio-graphy at rest and exercise echocardiography(ExE). Results from echocardiography at rest andcardiopulmonary exercise testing at sea level arebased on this examination several weeks or a fewmonths before altitude exposition. Sea level ExEresults are based on ExE performed right beforesimulated ascent.

All the 44 patients had been asked for partici-pation in an altitude study, but group selectionhad to ensure that there was approximately equalrepresentation of males/females, ASD/VSD andnormal/abnormal right ventricular pressure(RVSP) responders (Table 2). Patients withuncomplicated measurement of RVSP during thefirst examination were preferred to patients withless good assessable tricuspid regurgitation jet.None of the patients reported symptoms of exer-cise intolerance. No one had experienced any inci-dents of high altitude illness or major symptomsduring air travel.

Examination ProtocolThe selected patients were examined by ExEduring supine cycling at sea level right beforeexposition to altitude conditions. Using a hy-pobaric chamber the patients then were exposed toa simulated ascent to an altitude of 2500 m or 8200feet above sea level. During the following twohours of supine rest (acute hypoxic exposurephase) peripheral oxygen saturation (SpO2), bloodpressure, right ventricular performance and RVSPwere monitored every 15 minutes. Finally ExE wasrepeated before descent.

Cardiopulmonary Exercise TestingThe patients were examined by cardiopulmonaryexercise testing according to the Oslo protocol10

(Equipment: Jaeger Oxycon Delta, VIASYSHealthcare GmbH, Höchberg, Germany). Peakoxygen uptake (VO2peak) was corrected for bodyweight confounding11 and expressed as mL kg-0.67

min-1. The individual results were compared withreference values from healthy Norwegian adoles-cents12 and expressed by standard deviation (Zscore) from age-related mean in the referencematerial.

Echocardiography at Rest and During ExerciseEchocardiography recordings were obtained witha Vivid 7 Dimension scanner (GE Vingmed Ultra-sound, Horten, Norway). All echocardiographystudies were both videotaped and saved digitally(still frame and loops) for offline analysis. Echocar-

Congenit Heart Dis. 2010;5:556–564

Altitude Effects in Heart Septal Defects 557

diography at rest included the following measure-ments of right ventricular performance13–15:

• M-mode registration of tricuspid annular planesystolic excursion (TAPSE).16

• Peak tricuspid annular plane systolic motionvelocity (TASM) assessed by tissue Doppler.17,18

• Duration of right ventricular systole (ejectionphase) measured as the average of three subse-quent heart cycles assessed by tissue Doppler.

Right atrial pressure at rest was estimated byvena cava inferior index.19

Echocardiography has been shown to providereliable measurements of RVSP compared withinvasive measurement at rest20 and during exer-cise.2,21,22 In the absence of right ventricularoutflow tract obstruction, RVSP reflects, but doesnot equal pulmonary arterial systolic pressure.23

ExE was performed during supine cycling (Equip-ment: Ergoselect 1200 EL, Ergoline GmbH, Bitz,Germany). A stepwise exercise protocol was usedwith a starting load of 25 W and an increase of25 Watt every second minute until the targetheart rate of 160/min was reached. Above thatlevel, echocardiographic recordings become futilebecause of upper body movement and interposi-tion of the lungs. Systemic blood pressure wasmeasured at every exercise level, as well as themaximal velocity of tricuspid regurgitation jet.RVSP was calculated from each recorded Dopplerprofile by the modified Bernoulli’s equation andadding the right atrial pressure at rest (RAP) to thecalculated pressure gradient between right ven-tricle and right atrium. (RVSP = 4 V2 + RAP).20

Right ventricular pressure rise above 50 mm Hgduring exercise was defined as abnormal RVPR.2

Pressure measurements were made offline byanalysis of all digitally stored still images of tricus-pid regurgitation velocity. Every frame was classi-fied as a good, reasonable or poor/impossiblemeasurement. For every minute of exercise, amaximum of ten measurements were summarizedinto a conclusive pressure value (maximum of twovalues per workload level) based on the best acces-sible Doppler measurements. Obvious outliermeasurements were ignored. For approval of theentire exercise study at least the second last passedworkload level had to be evaluable.

Altitude ConditionsAll altitude tests were conducted in a hypobaricchamber (Norwegian Universal Technology AS,Haugesund, Norway). The hypobaric chamberwas located at the Norwegian School of Sports

Science at an altitude of 180 m above sea level.The temperature during sea level exercise testingoutside the chamber was 20°C. After decompres-sion atmospheric conditions were monitored everyfive minutes. During acute hypoxic exposure andaltitude exercise the air temperature was 21.5 �1.2°C. Chamber pressure after decompressionsimulated a stable altitude of 2500 m, oxygen per-centage was 20.8 � 0.04% and carbon dioxidepercentage was 0.044 � 0.013%.

StatisticsPaired Student’s t-tests were performed tocompare measurements in different conditionswhen normal distribution was found. Pearson’scorrelation coefficient and linear regression analy-sis were used to determine relations between dif-ferent variables. Parametric data are presented asmean with (�) standard deviation. P values below0.05 were considered statistically significant. Sta-tistical analysis was performed with SPSS 16(SPSS Inc., Chicago, IL, USA).

ApprovalsThe study complies with the Declaration of Hel-sinki and it was approved by the NorwegianRegional Committee for Medical Research Ethicsand all participating subjects gave informedconsent. The authors had full access to the dataand take responsibility for its integrity. All authorshave read and agree to the article as written.

Results

Ten patients could be included in the study. Forage, sex, aerobic capacity, and defect distributionsee Table 1. RVSP was within normal limits at rest(Table 1). Measurements of right ventricular per-formance were subnormal at rest as expected inpatients after surgical defect closure.1 Aerobiccapacity at sea level was lower than in healthyindividuals resulting in a mean Z score of -1.17(CI -2.13,-0.21; P = 0.022) (Table 1).

ExE at sea level (Table 2, Figure 1): MaximalRVSP during sea level exercise was significantlyhigher compared with resting RVSP (mean of dif-ference 26.8 mm Hg [CI 22.4, 31.2 P < 0.001]).Four of the patients showed abnormal RVPR >50 mm Hg. All patients had normal peripheraloxygen saturation during sea level exercise. Dura-tion of exercise necessary to achieve target heartrate was 636 � 149 seconds.

Möller et al.558


Tab

le1.

Bas

icP

aram

eter

s

Pat

ient

no.

Sex

Age

(yea

rs)

Dia

gnos

is

Age

atD

efec

tC

losu

re(m

onth

s)

Bod

yM

ass

Inde

x

PR

Inte

rval

(ms)

QR

SD

urat

ion

(ms)

Zsc

ore

VO

2pea

k

VO

2at

Hea

rtR

ate

160

bpm

(mL/

kg/m

in)

Ve/

VC

O2

slop

eF

EV

1(L

)F

EV

1(p

erc.

pred

.)F

VC

(L)

FV

C(p

erc.

pred

.)F

EV

1/F

VC

ratio

(%)

1F

emal

e13

Clo

sed

VS

D45

18.1

126

84-2

.531

.035

2.21

802.

8888

772

Fem

ale

19C

lose

dA

SD

3321

.113

086

-1.3

26.0

283.

0995

3.42

9290

3F

emal

e17

Clo

sed

AS

D35

18.9

122

76-1

.925

.929

3.17

110

3.91

115

814

Fem

ale

24C

lose

dA

SD

125

25.2

122

94-1

.525

.723

2.59

953.

1410

083

5F

emal

e25

Clo

sed

VS

D85

23.5

143

72-1

.325

.529

2.59

743.

2180

816

Mal

e21

Clo

sed

AS

D76

20.3

142

101

-3.3

36.9

292.

7168

3.30

7082

7M

ale

14C

lose

dV

SD

2017

.813

010

40.

236

.327

2.36

893.

1298

768

Mal

e19

Clo

sed

VS

D43

20.6

160

114

-0.1

30.5

264.

3597

5.08

9386

9M

ale

17C

lose

dA

SD

6623

.913

510

71.

339

.226

4.78

124

5.26

113

9110

Fem

ale

19C

lose

dA

SD

8622

.116

810

1-1

.325

.630

4.02

123

4.31

110

93M

ean

�S

D20

.7�

2.6

138

�16

94�

14-1

.17

�1.

3330

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28.2

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295

�19

.196

�14

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5.8

Tab

le2.

Indi

vidu

alM

easu

rem

ents

Pat

ient

no.

Sea

Leve

lPre

-exe

rcis

eS

eaLe

vele

xerc

ise

Acu

teH

ypox

icE

xpos

ure

Alti

tude

Exe

rcis

e

RV

SP

TAP

SE

TAS

MR

Vsy

st.

HR

SB

PM

axR

VS

PM

inS

pO2

Max

/DS

BP

Max

RV

SP

Min

SpO

2

Min

TAP

SE

Min

TAS

MR

Vsy

st.

Max

/DS

BP

Max

RV

SP

Min

SpO

2

Max

/DS

BP

129

2411

.428

756

—67

9915

3/43

4992

218.

535

097

/10

7081

152/

202

1717

7.1

283

67—

3698

154/

3924

8716

7.7

283

109/

1539

6815

5/31

318

156.

129

368

9943

9515

4/44

3293

125.

527

011

8/21

6077

127/

94

2317

7.5

290

8412

243

9717

2/45

2390

177.

030

311

6/24

4684

177/

575

2418

9.5

267

7799

5796

183/

4834

9018

8.8

247

121/

1860

7918

4/30

618

188.

230

059

9146

9718

0/58

2685

165.

732

011

5/17

5180

174/

337

3612

8.8

263

70—

6798

134/

3356

8614

7.3

283

95/9

8289

122/

48

2117

7.7

297

6411

841

9621

9/50

2488

187.

129

312

3/15

4680

205/

429

2317

10.9

237

6514

149

9715

9/9

2889

169.

128

012

1/19

5182

149/

810

2312

6.2

307

100

—51

—20

1/68

3294

125.

730

713

7/20

60—

212/

62M

ean

�S

D23

.2�

5.7

16.7

�3.

48.

3�1.

828

2�

21.1

71�

13.0

111.

7�18

.750

.0�

10.6

97.0

�1.

2M

ax:

170.

9�

25.4

D:43

.7�

15.6

32.8

�11

.289

.4�

3.0

16.0

�2.

87.

2�

1.3

294

�28

.5M

ax:

115.

2�

12.4

D:16

.8�

4.7

56.5

�12

.780

.0�

5.7

Max

:16

5.7

�30

.2D:

29.6

�20

.0

HR

,he

art

rate

pre-

exer

cise

(bea

tspe

rm

inut

e);

RV

SP,

right

vent

ricul

arpe

aksy

stol

icpr

essu

re(m

mH

g);

RV

syst

.,du

ratio

nof

RV

ejec

tion

time

afte

rtw

oho

urs

(ms)

;S

BP,

syst

olic

bloo

dpr

essu

re(D

=in

crea

sedu

ring

exer

cise

orac

ute

hypo

xic

expo

sure

)(m

mH

g);

TAP

SE

,tr

icus

pid

annu

lar

syst

olic

excu

rsio

n(m

m);

TAS

M,

peak

tric

uspi

dan

nula

rsy

stol

icm

otio

nve

loci

ty(c

m/s

);S

pO2,

perip

hera

loxy

gen

satu

ratio

n(%

).



Altitude-Induced Cardiovascular ChangesRight Ventricular PerformanceThere was a significant reduction of right ven-tricular performance during acute hypoxic expo-sure measured by TASM (sea level 8.3 � 1.8 vs.lowest during acute hypoxic exposure 7.2 � 1.3[CI 0.34, 1.86, P = 0.01]), whereas lowest TAPSEand duration of right ventricular systole after twohours of hypoxic exposure showed no statisticalsignificant change (Table 2).

Right Ventricular PressureDuring acute hypoxic exposure RVSP curvesshowed a tendency of continuous increase duringthe entire period of 2 hours (Figure 2). MaximalRVSP during this period was higher than restingvalues at sea level (means 32.8 � 11.2 mm Hg and23.2 � 5.7 mm Hg respectively, mean difference9.6 mm Hg [CI 4.8, 14.4 P = 0.001]) (Figure 3).

Two patients showed RVSP increase above40 mm Hg during acute hypoxic exposure. Both ofthem had also shown abnormal RVPR during sealevel exercise.

During altitude exercise the mean of maximalRVSP was higher than during sea level exercise(mean difference 6.5 mm Hg [CI 2.6, 10.4 P =0.004]), seven patients showed abnormal RVPR.Three patients with normal pressure responseduring sea level exercise had abnormal pressureresponse during altitude exercise. The altitude-induced relative increase of maximal RVSP duringexercise was 13.2 � 11.0% above sea level values.

As compared with the ASD patients the VSDpatients had significantly higher maximal RVSPduring sea level exercise (mean difference13.3 mm Hg [CI 0.5, 26.2 P = 0.043]). A similartendency during acute hypoxic exposure (meandifference 13.3 [CI -0.7, 27.2 P = 0.06]) and

Figure 1. Right ventricular systolic pressure (RVSP) and oxygen saturation (SpO2) during exercise at sea level andmoderate altitude (patient no. as shown in Tables 1 and 2).

Möller et al.560


during altitude exercise (mean difference13.3 mm Hg [CI -3.6, 30.2 P = 0.106]) was found.

Oxygen SaturationDuring acute hypoxic exposure oxygen saturationshowed an initial decrease to 89.4 � 3.0 followedby an increase during the second hour of hypoxia(Figure 2, Table 2). SpO2 decreased from theinitial 98.6 � 0.5% to 94.1 � 3.0% after 2 hours(mean difference 4.5 percentage points [CI 2.2, 6.8P = 0.002]). The mean of the lowest SpO2 duringaltitude exercise was 80.0 � 5.7% which was sig-nificantly lower compared with lowest SpO2

during sea level exercise (mean difference 17.0percentage points [CI 12.7, 21.3 P < 0.001])(Figure 3).

In three patients SpO2 decreased below 80%without major symptoms. Two of these threepatients simultaneously had hypoxia and RVSP

increase above 50 mm Hg. There was, however,no significant correlation between maximal RVSPand desaturation during exercise for the wholestudy group.

Systolic Blood PressureThere was no significant change in systolic bloodpressure during decompression or acute hypoxicexposure and no difference in maximal blood pres-sure or blood pressure rise during exercisebetween altitude conditions and sea level.

Exercise DurationThe mean of exercise duration necessary toachieve target heart rate decreased significantly by13.2 � 8.5% (mean difference 73 seconds [CI 39,107 P = 0.001]). Linear regression analysis showedno significant relationship between the change inexercise duration at moderate altitude and either

Figure 2. Oxygen saturation (SpO2) and right ventricular systolic pressure (RVSP) during acute hypoxic exposure (patientno. as shown in Tables 1 and 2).

Figure 3. Lowest oxygen saturation (SpO2) and highest right ventricular systolic pressure (RVSP) during different studyphases (patient no. as shown in Tables 1 and 2).



the relative increase of maximal exercise RVSPor exercise related oxygen desaturation. Similaranalysis could not explain either the altitude-induced increase of maximal RVSP or the decreaseof lowest SpO2 during exercise by aerobic exercisecapacity at sea level.

Apart from dizziness during acute hypoxicexposure and early fatigue during altitude exerciseno patient experienced any adverse reactions tothe test.

Discussion

Our study demonstrates remarkable altitude-induced effects. Oxygen desaturation during alti-tude exercise is more pronounced as comparedwith data from studies in healthy individuals.24–26

RVSP may increase by exposure to moderate alti-tude alone. Abnormal RVPR to exercise can beevoked by moderate altitude in individuals withnormal RVPR at sea level. Abnormal RVPR toexercise at sea level can be aggravated by moderatealtitude.

Effects on Oxygen SaturationChanges in SpO2 after exposure to 2438 m alti-tude have been studied in 502 healthy individu-als.24,25 An ascent from sea level to this altitude hasbeen shown to decrease oxygen saturation by 4–7percentage points in average. Thus, the presentedaltitude effects on resting oxygen saturationduring acute hypoxic exposure in our patientgroup are equivalent to healthy individuals. Lightexercise in moderate altitude has been shown todecrease SpO2 by 1.3 percentage points comparedwith resting values.24 As our patient group per-formed a submaximal exercise test oxygen desatu-ration during altitude exercise could not bedirectly related to data from the literature24 even ifdesaturation seemed unexpectedly distinct.

Effects on Right Ventricular Pressureand PerformanceIn acute hypoxia equivalent to 3200 m altitudemean pulmonary artery pressure has been demon-strated to increase from 14 to 19 mm Hg inhealthy individuals.27 Mean pulmonary arterialpressure (mPAP) can be mathematically convertedinto peak systolic pulmonary arterial pressure(sPAP) using a previous published formula (mPAP= 0.61 sPAP + 2 mm Hg).28 Thus, systolic pulmo-nary arterial pressure can be expected to increasefrom 20 to 28 mm Hg in moderate altitude. Themean increase in our patients was slightly higher

due to two patients with altitude-induced abnor-mal increase of RVSP at rest above 40 mm Hg(patient no.1 and no.7). RVPR to altitude both atrest and during exercise may be explained by theability of hypoxic pulmonary vasoconstriction.RVSP was still increasing as acclimatization pro-cesses have previously been shown to continue formany hours after ascent.29 Three individuals withnormal RVSP at sea level show abnormal RVPRduring altitude exercise. All individuals showingabnormal RVPR at sea level reached even higherRVSP levels when exercise is performed at mod-erate altitude.

The inconsistent changes in right ventricularperformance due to altitude do not allow conclu-sions about increase of right ventricular workloador performance due to acute hypoxia.

Effects on Exercise DurationMaximal exercise duration have been shown to bereduced by 6.7% in healthy individuals exposed tomoderate altitude.30 In our patients time needed toreach the target heart rate declined more thanexpected from these data. However, no explana-tory relationship to abnormal RVSP response oroxygen desaturation could be found. Thus the lim-iting factor of altitude exercise duration in ourpatient group is unclear. Altitude-induced reduc-tion of right ventricular performance, in our studydemonstrated by lower myocardial contractionvelocity with preserved shortening, may be sus-pected as a possible mechanism.

Pathophysiological ConsiderationsOur results may support the theory of abnormalpulmonary arterial pressure elevation as a dynamicvasoconstrictive process rather than a stable struc-tural phenomenon. If abnormal RVPR can beevoked or worsened by moderate altitude the pul-monary vascular endothelium and smooth musclecells thus must have the ability to increase theirabnormal reaction due to external factors. If mildhypobaric conditions may cause abnormal pulmo-nary vascular changes the potential susceptibilityto high altitude pulmonary edema in these patientsmight be considered.

Previous data have shown differences in RVPRto exercise between patients born with VSD andASD respectively in terms of higher incidences ofabnormal RVPR in VSD patients.1 In our studygroup the differences in altitude-induced changesbetween ASD and VSD were not statisticallysignificant.

Möller et al.562


Whether the mechanism of major desatura-tion is intrapulmonal left-to-right shunting, asdescribed by others,31 or altered alveolar diffusioncapacity could be confirmed by our study design.Normal respiratory equivalents (Ve/VCO2,Table 1) � 30 in 9/10 patients may indicatenormal diffusion capacity and no V/Q-mismatch.Systolic blood pressure does not seem to play arole in the described altitude-related effects as itwas unchanged by altitude in our study.

LimitationsAs the patient group was small and selected nostatement about general prevalence or magnitudeof abnormal reactions in VSD and ASD patientscan be made. However, the occurrence of circula-tory changes due to altitude can be confirmed.The investigation of a healthy control group couldhave given our conclusions more strength.However, the low prevalence of abnormal hypoxicRVPR in the normal population would havedemanded a very large number of control indi-viduals beyond practical limitations. Thus, as ourstudy did not include a healthy control groupexpectations of normal reactions to moderate alti-tude had to be derived from the literature. Forinvestigation of the character and stability of thephenomenon of excessive right ventricular pres-sure response to exercise in patients with septaldefects we planned to use the patients’ reactions atsea level as their own controls compared to RVPRunder acute hypoxic conditions.

ConclusionsModerate altitude increases oxygen desaturationduring exercise and right ventricular systolic pres-sure at rest and during exercise in adolescents withventricular or ASDs. Moderate altitude mayinduce or aggravate abnormal RVPR. Our studydid not demonstrate any relationship betweenaerobic exercise capacity and changes in RVPR oroxygen desaturation. The oxygen desaturationduring altitude exercise in these patients is aninteresting field for further exploration.

Acknowledgements

Professor Jostein Hallén from the Norwegian School ofSports Sciences kindly permitted the use of the hypobaricchamber and gave advice with the manuscript. Cand.scient. Erlend Hem operated the hypobaric chamber. AreHugo Pripp PhD, Biostatistics Unit, Rikshospitalet Uni-versity Hospital, gave advice with the statistical analysis.

Funding SourcesThis project has been financed with the aid from the fol-lowing funds, EXTRA funds from the Norwegian Foun-dation for Health and Rehabilitation, Research funding bythe South-Eastern Norway Regional Health Authority,and Private research funds located at Vestfold HospitalTrust.

Equipment was partly financed by the National ParentsAssociation; “Foreningen For Hjertesyke Barn” (FFHB)and the Hospital’s Friends Foundation in Vestfold (“Syke-husets Venner”).

Corresponding Author: Thomas Möller, MD, Pedi-atric Department, Vestfold Hospital Trust, Postboks2168 Postterminalen, Tonsberg, 3103, Norway. Tel:(+47) 33342000; Fax: (+47) 33343975; E-mail:[email protected]

Conflicts of interests: None.

Accepted in final form: May 9, 2010.

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3 Vachiery JL, McDonagh T, Moraine JJ, et al.Doppler assessment of hypoxic pulmonary vasocon-striction and susceptibility to high altitude pulmo-nary oedema. Thorax. 1995;50:22–27.

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moderate altitude increases right ventricular pressure and oxygen desaturation in adolescents with...

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