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Blackwell Science, LtdOxford, UKRESRespirology1323-77992004 Blackwell Science Asia Pty LtdSeptember 200493320325Original ArticleCOPD and treadmill exercise testingM

Yazici
et al.

Respirology (2004) 9, 320–325

ORIGINAL ARTICLE

Relationship between arterial blood gas values, pulmonary


function tests and treadmill exercise testing parameters in
patients with COPD
Mehmet YAZICI,1 Peri ARBAK,2 Oner BALBAY,2 Emin MADEN,3 Mete ERBAS,2 Enver ERBILEN,1
Sinan ALBAYRAK,1 Ramazan AKDEMIR1 AND Cihangir UYAN1

Departments of 1Cardiology and 2Chest Diseases, Duzce Medical Faculty, Abant Izzet Baysal University,
Duzce, Turkey and 3Department of Chest Diseases, Sureyyapasa State Hospital, Istanbul, Turkey

Relationship between arterial blood gas values, pulmonary function tests and treadmill exercise
testing parameters in patients with COPD
YAZICI M, ARBAK P, BALBAY O, MADEN E, ERBAS M, ERBILEN E, ALBAYRAK S, AKDEMIR R, UYAN
C. Respirology 2004; 9: 320–325
Objective: There have been controversial reports regarding the relationship between exercise tol-
erance and resting pulmonary function in patients with COPD. The aim of this study was to examine
the relationship between resting pulmonary function tests (rPFT) and cardiopulmonary exercise
testing parameters (CETP) and their value in estimating exercise tolerance of patients.
Methodology: In total, 45 patients with COPD (nine females, 36 males; mean age 61.2 ± 11.2) and
21 healthy subjects (four females, 17 males; mean age 60.3 ± 9.7) as a control group were studied.
COPD patients (group I) were divided into three subgroups according to their FEV1 (mild/group II:
FEV1 60–79% of predicted; moderate/group III: FEV1 40–59%; severe/group IV: FEV1 < 40%). In con-
trols FEV1 was ≥ 80%.
Results: There were significant correlations between FEV1 and CETP in group III (maximal O2 con-
sumption (mVO2), r = 0.35, P < 0.005; total treadmill time (TTT), r = 0.31, P < 0.01; total metabolic
equivalent values (TMET), r = 0.29, P < 0.01)) and in group IV (mVO2, r = 0.49, P < 0.001; TTT, r = 0.45,
P < 0.005; TMET, r = 0.31, P < 0.01; peak heart rate (pHR), r = 0.29, P < 0.02; frequency of ventricular
extrasystole (fVES), r = -0.27, P < 0.05). Additionally, in group IV there were significant correlations
between PaO2 and CETP (mVO2, r = 0.41, P < 0.02; TTT, r = 0.38, P < 0.03; TMET, r = 0.31, P < 0.05; pHR,
r = 0.29, P < 0.05; fVES, r = -0.28, P < 0.05).
Conclusion: There are significant correlations of resting FEV1% predicted and PaO2 values with
CETP in patients with moderate and severe COPD and these parameters may also have a role as indi-
cators of exercise tolerance in these COPD patients.

Key words: COPD, treadmill exercise testing.

INTRODUCTION abnormalities, including increased dead-space ven-


tilation, a reduced ventilatory reserve, increased
COPD is characterized by dyspnoea and limited work of breathing, and mechanical problems due to
exercise capacity as a result of changes in pulmo- the position of the diaphragm, may also affect the
nary mechanics, impaired cardiac function, abnor- exercise performance of patients with COPD.3–5 Max-
mal gas exchange, respiratory muscle dysfunction, imum exercise tolerance in patients with COPD has
and nutritional factors.1,2 Additionally, ventilatory multiple determinants and is not easy to estimate
from resting pulmonary function tests (rPFT). How-
ever, it has been reported that maximum exercise
Correspondence: Mehmet Yazici, Department of tolerance during cardiopulmonary exercise testing
Cardiology, Abant Izzet Baysal University, 14450 Duzce, (CET) may be useful in evaluating the disability and
Turkey. Email: yazicimehmet@hotmail.com determining the cause of exertional dyspnoea,
Received 4 July 2003; revised 17 December 2003; establishing exercise training programmes for pul-
accepted for publication 22 February 2004. monary rehabilitation, the assessment of treatment
COPD and treadmill exercise testing 321

results, and for preoperative evaluation.1,6–11 Further- Spirometric measurements and arterial blood
more, whether exercise intolerance is due to cardiac gas analysis
dysfunction (unrecognized ischaemic heart disease)
or pulmonary disease can be differentiated by Inhaled medications were withheld for 3 h or longer
CET.3,12 Nevertheless, a clear-cut relationship prior to the exercise test. Before and after the exercise
between rPFT and exercise tolerance has not been test, arterial blood gas samples were obtained while
established in patients with COPD.13–16 In recent breathing room air, then arterial blood gas tensions
years, studies investigating the relationship between (PaO2, PaCO2) and pH were measured on an arterial
rPFT and exercise tolerance and the role of CET in blood gas analyzer (I-STAT Corporation, USA).
the evaluation of respiratory impairment have Spirometry was performed using a Vitalograph alpha
regained popularity.7,13–21 CET may be performed (Ennis, Ireland) 1–2 h prior to the exercise test. Spiro-
using either the treadmill or the cycle ergometer. metric values were obtained before and 30 min after
Thus, maximal O2 uptake (mVO2) indicating exer- two inhalations of salbutamol. FEV1, FVC, FEV1/FVC
cise capacity, arterial oxygen desaturation and meta- and FEF25-75% were recorded (as percentage of pre-
bolic acidosis, which are undetectable at rest, may dicted). Maximal voluntary ventilation (MVV) was
also be detected.7 measured indirectly and calculated as FEV1 ¥ 35.23
The aim of this study was to examine the relation- Spirometric measurements were repeated until three
ship between rPFT and cardiopulmonary exercise technically satisfactory and consistent values were
testing parameters (CETP) and their value in estimat- achieved, and the highest value was recorded. The
ing exercise tolerance of patients. spirometric standards of Morris et al. were used.24

METHODS Exercise testing

Study population All patients and controls fasted for at least 2 h before
exercise testing, which was performed using a tread-
The study was carried out in the Departments of mill (Nihon-Kohden, ECG 9320 K), with patients in a
Cardiology and Chest Disease, Faculty of Medicine, bronchodilated state and breathing room air. The
Abant Izzet Baysal University. In toal, 45 patients exercise test was performed according to Bruce’s mul-
with COPD (nine female and 36 male; mean age tistage maximal treadmill protocol. Every 3 min the
61.2 ± 11.2) and 21 healthy control subjects (four gradient of the treadmill was increased by 2%, starting
female and 17 male; mean age 60.3 ± 9.7) were from a 10% gradient at the first step, until the maximal
studied. The control subjects had no known car- effort that the patient could support was reached.
diac, pulmonary or other disease by history, physi- ECG and heart rate (HR) were monitored prior to and
cal examination, spirometric values, continuously during and for 5 min after the exercise
electrocardiogram (ECG), and CXR. All patients met test. CET was stopped according to previously
the following criteria: (i) a clinical diagnosis of defined reasons for termination.25 Simultaneously
COPD confirmed by history, physical examination, during exercise the subjects breathed through a
abnormal spirometric values (FEV1 £ 80% of pre- breathing mask to measure mVO2. Some exercise
dicted and FEV1/VC < 70%) and CXR; (ii) no other data, including total metabolic equivalent (TMET)
significant lung disease; (iii) clinically stable on an values, were obtained with a computer-based auto-
acceptable drug regimen (regular ipratropium bro- mated CET system (Metalyzer 3 B-CPX Systems, Scot
mide, two puffs (40 mg), four times a day, and short Medical Products, Leipzig, Germany). Metabolic
acting b2-agonists on demand); (iv) no known car- equivalent (MET) is a unit of sitting/resting oxygen
diac disease by history, physical examination, ECG uptake (one MET is 3.5 mL O2 per kilogram of body
and echocardiography; (v) no important ST seg- weight per minute (mL/kg per min)). Blood pressures
ment and T wave changes or arrhythmias possibly were taken manually before, after and at periodic
related to COPD or other disease on ECG; and (vi) intervals during the exercise test. We used the for-
no neuromuscular disease or other medical prob- mula, maximal HR = 210 – 0.65 ¥ age, to calculate the
lems that could prevent performance of a treadmill maximal predicted HR.11,26 In COPD patients, all tests
exercise test. None of the COPD patients or control were stopped because of dyspnoea.
subjects were smoking at the time of this study.
Patients with COPD were divided into three sub-
groups according to their FEV1 values, as suggested Echocardiographic assessment
by the British Thoracic Society:22 group II (mild
COPD patients had a FEV1 between 60% and 79% of M-mode, two-dimensional and pulsed-Doppler
predicted), group III (moderate COPD patients had examinations were performed in all individuals using
an FEV1 between 40% and 59% of predicted) and a commercially available system (Toshiba Diagnostic
group IV (severe COPD patients had an FEV1 < 40% Ultrasound System, Model SSA 270 A, Toshiba Corpo-
of predicted). ration 1992, Tochigiken, Japan) that used 2.5 or
All subjects gave written informed consent, and the 3.5 MHz. The measurements were carried out and
study protocol was approved by the Ethics Committee interpreted according to the recommendations of the
of the Duzce Medical Faculty, Abant Izzet Baysal American Society of Echocardiography.27 Five repre-
University. sentative consecutive or nearly consecutive cardiac
322 M Yazici et al.

cycle sinus beats were measured and averaged for ues, peak heart rate (pHR)) were statistically signifi-
each measurement. All studies were performed dur- cantly different in COPD patients (group I) when
ing normal quiet respiration. All echocardiograms compared with the control group (Table 2). Similarly,
were recorded and analyzed by one of the investiga- when compared with the control group, there were
tors who had no knowledge of the patient’s clinical significant differences in group III and group IV.
status. Left ventricular end-diastolic volume, end- Additionally, in group IV the frequency of ven-
systolic volume and ejection fraction (normal 55– tricular extrasystole (fVES) was significantly increased
70%) were determined from apical two or four cham- (2.9 ± 1.4 vs. 1.7 ± 1.1, P < 0.01). In group II (mild
ber views by using the modified Simpson method. COPD), all measurements were similar to those in the
Right ventricular ejection fraction was evaluated by controls subjects (Table 2). There were significant
measuring the excursion of tricuspid annulus in sys- correlations between FEV1 and CETP in group III
tole (TAPSE) recorded in the apical four chamber (Table 2). Additionally, in group IV there were signifi-
view.28,29 The normal value of TAPSE is 24.9 ± 3.5 with cant correlations between PaO2 and CETP (Table 3).
lateral measurement. PaCO2 and pH values were similar in all groups
(Table 1). There were no correlations between PaCO2,
pH and any of the CETP (P > 0.05).
Statistical analysis

Values are presented as mean ± SD. The Mann– DISCUSSION


Whitney U-test was used to compare groups. Simple
regression analysis was used to examine correlations rPFT are used to assess patients with COPD and its
between CETP, resting spirometric measurements, progression. FEV1 and FEV1/FVC are the most com-
and blood gas analyses. A P-value less than 0.05 was monly used parameters in assessing the severity of
considered significant. The r-value was the correla- COPD. FEV1/FVC is sensitive in mild COPD while
tion coefficient. The analyses were performed using FEV1 is sensitive in moderate to severe COPD. FEV1 is
SPSS 7.5 for Windows (release 7.5; SPSS; Chicago, IL, easily measured, less variable than other measures of
USA). airway dynamics, and predicts airway changes more
accurately.30
Knox et al. reported that there was a significant
RESULTS relationship between walking distance and FEV1 and
FVC.31 Another study performed with a cycle ergom-
General characteristics, arterial blood gas analyses, eter, showed a significant correlation between mVO2
and pulmonary function test results for the study and FEV1 in 81 COPD patients. In the same study, it
populations are summarized in Table 1. CETP (maxi- was concluded that there was no significant relation-
mum oxygen consumption (mVO2), total treadmill ship between mVO2 and resting or exercise arterial
time (TTT), total metabolic equivalent (TMET) val- gas values.32 Other studies show an inconsistent rela-

Table 1 Comparison of demographic and laboratory characteristics of COPD patients and controls

Controls Group I Group II Group III Group IV


(n = 21) (n = 45) (n = 15) (n = 13) (n = 17)

Age (years) 60.3 ± 9.7 61.2 ± 11.2 61.7 ± 9.8 60.6 ± 11.9 61.8 ± 10.8
Gender (female/male) 4/17 9/36 3/12 3/11 3/13
Weight (kg) 69.8 ± 8.7 67.9 ± 8.9 68.1 ± 7.2 67.3 ± 8.9 66.8 ± 9.3
Height (cm) 171 ± 14.6 168 ± 17.1 169 ± 13.4 166 ± 11.4 167 ± 15.1
BMI (kg/m2) 23.7 ± 4.7 22.4 ± 5.3 23.2 ± 3.7 22.3 ± 4.3 21.4 ± 3.9
LVEF (%) 64.5 ± 5.3 62.3 ± 6.7 64.9 ± 4.9 61.5 ± 5.3 59.8 ± 6.3
RVEF/TAPSE (mm) 24.2 ± 4.3 22.3 ± 5.3 23.7 ± 4.3 22.5 ± 3.7 21.2 ± 4.7
FVC (%) 94.7 ± 8.5 81.7 ± 8.6§ 86.2 ± 7.6¶ 82.7 ± 12.6§ 67.4 ± 4.5†
FEV1 (%) 85.9 ± 5.1 48.3 ± 7.1† 66.4 ± 6.2‡ 49.7 ± 5.9† 34.7 ± 3.9†
FEV1/FVC (%) 85.7 ± 5.6 52.7 ± 6.7† 66.7 ± 3.2‡ 51.8 ± 6.5† 37.6 ± 2.5†
FEF25-75% (%) 84.9 ± 4.3 56.3 ± 7.6† 79.8 ± 7.3 53.5 ± 6.1‡ 33.8 ± 5.1†
MVV (%) 85.3 ± 4.2 51.7 ± 11.4† 63.7 ± 6.9‡ 47.9 ± 5.7† 33.9 ± 4.3†
PaO2 (mmHg) 91.2 ± 7.3 70.2 ± 11. 7‡ 78.3 ± 8.7§ 68.7 ± 7.6‡ 61.8 ± 6.7†
PaCO2 (mmHg) 39.8 ± 3.7 38.7 ± 3.5 38.7 ± 4.3 36.3 ± 5.1 45.9 ± 6.3
pH 7.42 ± 0. 03 7.42 ± 0.06 7.43 ± 0.05 7.42 ± 0.05 7.39 ± 0.05

Values are presented as mean ± SD.



When compared to control group, P < 0.0001; ‡when compared to control group, P < 0.001; §when compared to control
group, P < 0.01; ¶when compared to control group, P < 0.05.
BMI, body mass index; LVEF, left ventricular ejection fraction; RVEF, right ventricular ejection fraction; TAPSE, tricuspid
annular plane systolic excursion.
COPD and treadmill exercise testing 323

Table 2 Comparison of cardiopulmonary exercise testing parameters in COPD and control groups and their correlations
with FEV1 values

Control group Group I Group II Group III Group IV


(n = 21) (n = 45) (n = 15) (n = 13) (n = 17)
FEV1% = 85.9 ± 5.1 FEV1% = 48.3 ± 7.1 FEV1% = 66.4 ± 6.2 FEV1% = 49.7 ± 5.9 FEV1% = 34.7 ± 3.9

mVO2 27.3 ± 5.9 19.7 ± 5.9‡ 25.9 ± 7.5 17.6 ± 4.9† 15.2 ± 5.3†
(mL/kg per min) r = 0.35, P < 0.05 r = 0.43, P < 0.005 r = 0.22, P > 0.05 r = 0.35, P < 0.005 r = 0.49, P < 0.001
TTT 7.1 ± 1.3 4.6 ± 1.5‡ 6.7 ± 1.5 3.8 ± 1.1† 3.3 ± 1.2†
(min) r = 0.34, P < 0.05 r = 0.41, P < 0.005 r = 0.23, P > 0.05 r = 0.31, P < 0.01 r = 0.45, P < 0.005
TMET 8.3 ± 2.2 5.3 ± 1.7‡ 7.6 ± 1.4 4.8 ± 1.3† 3.9 ± 1.5†
(mL/kg per min) r = 0.33, P < 0.05 r = 0.38, P < 0.01 r = 0.21, P > 0.05 r = 0.29 P < 0.01 r = 0.31, P < 0.01
pHR 137.3 ± 13.4 126.7 ± 19.4§ 134.9 ± 14.7 127.9 ± 17.3§ 114.9 ± 15.6‡
(beats/min) r = 0.23, P > 0.05 r = 0.31, P < 0.01 r = 0.19, P > 0.05 r = 0.21, P > 0.05 r = 0.29, P < 0.02
fVES 1.7 ± 1.1 2.1 ± 1.3 1.9 ± 0.9 1.6 ± 1.1 2.9 ± 1.4§
(beat/min) r = - 0.19, P > 0.05 r = - 0.21, P > 0.05 r = - 0.17, P > 0.05 r = - 0.15, P > 0.05 r = - 0.27, P < 0.05

Values are presented as mean ± SD.



When compared to control group: P < 0.0001; ‡when compared to control group: P < 0.001; §when compared to control
group: P < 0.01.
mVO2, maximal O2 consumption; TTT, total treadmill time; TMET, total metabolic equivalents values; pHR, peak heart rate;
fVES, frequency of ventricular extrasystole; r, correlation coefficient.

Table 3 Comparison of cardiopulmonary exercise testing parameters in COPD patients and control subjects and their cor-
relations with PaO2 values

Controls Group I Group II Group III Group IV


(n = 21) (n = 45) (n = 15) (n = 13) (n = 17)
PaO2 = 91.2 ± 7.3 PaO2 = 70.2 ± 11.7 PaO2 = 78.3 ± 8.7 PaO2 = 68.7 ± 7.6 PaO2 = 61.8 ± 6.7

mVO2 27.3 ± 5.9 19.7 ± 5.9 25.9 ± 7.5 17.6 ± 4.9 15.2 ± 5.9
(mL/kg per min) r = 0.23, P > 0.05 r = 0.35, P < 0.01 r = 0.17, P > 0.05 r = 0.23, P > 0.05 r = 0.41, P < 0.02
TTT 7.1 ± 1.3 4.6 ± 1.5 6.7 ± 1.5 3.8 ± 1.1 3.3 ± 1.2
(min) r = 0.23, P > 0.05 r = 0.31, P < 0.05 r = 0.13, P > 0.05 r = 0.19, P > 0.05 r = 0.38, P < 0.03
TMET 8.3 ± 2.2 5.3 ± 1.7 7.6 ± 1.4 4.8 ± 1.3 3.9 ± 1.5
(mL/kg per min) r = 0.21, P > 0.05 r = 0.31, P < 0.05 r = 0.12, P > 0.05 r = 0.21 P > 0.05 r = 0.31, P < 0.05
pHR 137.3 ± 13.4 126.7 ± 19.4 134.9 ± 14.7 127.9 ± 17.3 114.9 ± 15.6
(beats/min) r = 0.23, P > 0.05 r = 0.31, P < 0.01 r = 0.19, P > 0.05 r = 0.21, P > 0.05 r = 0.29, P < 0.05
fVES 1.7 ± 1.1 2.1 ± 1.3 1.9 ± 0.9 1.6 ± 1.1 2.9 ± 1.4
(beats/min) r = - 0.18, P > 0.05 r = - 0.21, P > 0.05 r = - 0.13, P > 0.05 r = - 0.09, P > 0.05 r = - 0.28, P < 0.05

Values are presented as mean ± SD.


mVO2, maximal O2 consumption; TTT, total treadmill time; TMET, total metabolic equivalents values; pHR, peak heart rate;
fVES, frequency of ventricular extrasystole; r, correlation coefficient.

tionship between rPFT values and parameters of their patients were younger than our patients.16 In our
symptom-limited cardiopulmonary exercise testing study, mVO2, TTT, TMET and pHR were significantly
to a maximum tolerable level on a treadmill.15–17,21 decreased in those with moderate to severe airflow
Dillard et al. have reported a significant correlation obstruction compared with the normal and mildly
between mVO2 obtained by treadmill exercise testing obstructed groups. These results can be explained by
and DLCO and FEV1 in patients with less severe COPD respiratory muscle weakness produced by the pres-
than the patients in our study.21 In addition, Carlson ence of increased airway resistance, hyperinflation,
et al. showed a strong correlation between mVO2 and severe limitation in airflow rate, and serious dec-
DLCO and FEV1 in 119 COPD patients, but they have onditioning in advanced COPD.17,33 Furthermore,
stressed that this correlation was not valid in individ- functional deterioration in pulmonary vessels in
ual cases.15 Ortega et al. performed spirometry in 78 advanced COPD affects respiratory muscle oxygen-
COPD patients, then evaluated their exercise perfor- ation, resulting in a decrease in the exercise capacity
mance on a treadmill ergometer. Only a weak corre- of COPD patients.7 Moderate to severe COPD patients
lation was observed between mVO2 and FEV1. Thus, could not walk sufficiently far to increase their HR
they suggest that resting PFT, PaO2 and PaCO2 are not to their predicted level during exercise, therefore,
predictive of exercise performance in patients with decreased pHR was observed in these groups. How-
COPD. In their study there was no control group and ever, HR increases earlier during submaximal work in
324 M Yazici et al.

patients with moderate to severe COPD than in level in those patients.16,45 In our study, all patients
healthy individuals. It is most likely that different fac- stopped the test due to dyspnoea. No cardiovascular
tors are responsible for exercise limitation in different complication or primary cardiac reason for termina-
patients. Thus, some patients may have attained a tion were observed during the exercise test.
true ventilatory limitation based on mechanical fac- We concluded that especially in severe and moder-
tors, some may reach a true cardiac limitation based ate COPD patients, resting FEV1 and PaO2 values are
on occult left ventricular disease or right ventricular significantly correlated with CETP, but FEV1 is more
dysfunction, and others by deconditioning. However, strongly correlated with CETP than resting PaO2. FEV1
in other studies, the possibility of left ventricular dis- and PaO2 values may have a modest role in estimating
ease or right ventricular dysfunction was not assessed exercise performance and predicting exercise
by echocardiography, as occurred in our study. Both induced arrhythmias in moderate and severe COPD.
left and right ventricular ejection fraction were Maximal exercise testing could be performed safely in
slightly, but not significantly, decreased in the moder- mild and moderate COPD and in severe COPD, with
ate and severe COPD patients. caution due to larger fVES values. Prospective studies
Rasche et al. using a cycle ergometer in 64 patients that include large patient populations are required to
with COPD, concluded that rPFT and blood gas values reach a definitive conclusion in this area.
were predictors of gas exchange during exercise. In
that study, abnormal PaO2 values were observed in
21.9% of patients with COPD and a negative correla-
tion was observed between exercise PaCO2 values and
REFERENCES
resting FEV1.34 Conversely, Ortega et al. showed no 1 Epstein SK, Celli BR. Cardiopulmonary exercise testing
correlation between exercise mVCO2, mVO2, and PaO2 in patients with chronic obstructive pulmonary disease.
or PaCO2. They suggested that resting blood gas anal- Cleve. Clin. J. Med. 1993; 60: 119–28.
ysis was not predictive of exercise performance in 2 Owens GR, Rogers RM, Pennock BE, Levin D. The diffus-
patients with COPD.16 These differences in results ing capacity as a predictor of arterial oxygen desatura-
may be related to differences in patient characteris- tion during exercise in patients with chronic obstructive
tics, including age, gender and severity of disease. We pulmonary disease. N. Engl. J. Med. 1984; 310: 1218–21.
applied strict rules in the selection of patients with 3 Wasserman K, Whipp BJ. Exercise physiology in health
stable COPD, excluding patients with confounding and disease. Am. Rev. Respir. Dis. 1975; 112: 219–49.
factors, such as accompanying heart or other lung 4 Brown HV, Wasserman K. Exercise performance in
diseases and especially factors affecting the cardio- chronic obstructive pulmonary diseases. Med. Clin.
pulmonary system. North Am. 1981; 65: 525–47.
In COPD of mild to moderate severity, hypoxaemia 5 Loke J, Mahler DA, Man SFB, Wiedemann HP, Matthay
can exist without hypercapnia. When COPD becomes RA. Exercise impairment in chronic obstructive pulmo-
severe, carbon dioxide retention occurs as total nary disease. Clin. Chest Med. 1984; 5: 121–43.
alveolar ventilation decreases. Mild hypoxaemia and 6 Gallagher CG. Exercise limitation and clinical exercise
hypercapnia is a terminal finding in COPD predomi- testing in chronic obstructive pulmonary disease. Clin.
nantly with emphysema. In contrast, hypoxaemia and Chest Med. 1994; 15: 305–26.
hypercapnia are observed in the earlier stages of 7 Marciniuk DD, Gallagher CG. Clinical exercise testing in
COPD, predominantly with bronchitis.35 Chronic chronic airflow limitation. Med. Clin. North Am. 1996;
hypercapnia and acidosis seem to be significant 80: 565–87.
factors in determining the prognosis of COPD.36 8 American Thoracic Society. Evaluation of impairment/
An increased incidence of arrhythmias (20–86%) has disability secondary to respiratory disorders. Am. Rev.
been observed in COPD37–40 and is related to multiple Respir. Dis 1986; 133: 1205–9.
factors, such as hypoxaemia, hypercapnia, acid-base 9 Ries AL. The role of exercise testing in pulmonary diag-
disturbance, cor pulmonale, and medications used nosis. Clin. Chest Med. 1987; 8: 81–9.
for treatment.37,39–44 It has been supposed that, espe- 10 Olsen GN. The evolving role of exercise testing prior to
cially during exercise, hypoxaemia affects left ven- lung resection. Chest 1989; 95: 218–25.
tricle performance directly or by increasing the 11 Wasserman K, Hansen JE, Sue DY, Whipp BJ. Principles
sympathetic activity, and increases the risk of tach- of Exercise Testing and Interpretation. Lea-Febiger,
yarrhythmias, especially in severe COPD.38 Similarly, Philadelphia, 1999; 72–86.
we also found weak positive correlations between 12 Wasserman K. Dyspnea on exertion: is it the heart or the
PaO2 and TTT and between pHR and mVO2 in the lungs? JAMA 1982; 248: 2039–43.
severe COPD group. In addition, there was a weak 13 Jones NL, Jones G, Edwards RHT. Exercise tolerance in
negative correlation between PaO2 and fVES (but not chronic airway obstruction. Am. Rev. Respir. Dis. 1971;
with PaCO2) in the severe COPD group, while no cor- 103: 477–91.
relation was observed between pH, PaCO2 and CETP. 14 Cotes JE, Zejda J, King B. Lung function impairment as a
The differences between our findings and the results guide to exercise limitation in work-related lung disor-
of other studies might be explained by the relatively ders. Am. Rev. Respir. Dis. 1988; 137: 1089–93.
small number of patients and the apparent lack of 15 Carlson DJ, Ries AL, Kaplan RM. Prediction of maximum
hypercapnia. Some authors have proposed that respi- exercise tolerance in patients with COPD. Chest 1991;
ratory factors were more responsible than cardiovas- 100: 307–11.
cular factors in exercise limitation in COPD, and so 16 Ortega F, Montemayor T, Sanchez A, Cabello F, Castillo J.
exercise testing should be performed to the maximal Role of cardiopulmonary exercise testing and the criteria
COPD and treadmill exercise testing 325

used to determine disability in patients with severe Official Statement of the European Respiratory Society.
chronic obstructive pulmonary disease. Am. J. Respir. Eur. Respir. J. 1993; 16 (Suppl. 16): 5–40.
Crit. Care Med. 1994; 150: 747–51. 31 Knox AJ, Morrison JF, Muers MF. Reproducibility of
17 Matthews JI, Bush BA, Ewald FW. Exercise responses walking test results in chronic obstructive airways dis-
during incremental and high intensity and low intensity ease. Thorax 1988; 43: 388–92.
steady state exercise in patients with obstructive lung 32 Czernicka-Cierpisz E. Exercise tolerance in patients with
disease and normal control subjects. Chest 1989; 96: 11– chronic obstructive pulmonary disease in various stages
7. of advanced disease. Pneumonol. Alergol. Pol. 1996; 64:
18 Becklake MR, Rodarte JR, Kalica AR. NHLBI workshop 604–14 (in Polish).
summary. Scientific issues in the assessment of respira- 33 Bye PT, Esau SA, Levy RD et al. Ventilatory muscle func-
tory impairment. Am. Rev. Respir. Dis. 1988; 137: 1505– tion during exercise in air and oxygen in patients with
10. chronic air-flow limitation. Am. Rev. Respir. Dis. 1985;
19 Killian KJ, Summers E, Jones NL, Campbell EJM. Exercise 132: 236–40.
capacity and the ATS criteria of severe impairment/dis- 34 Rasche K, Bauer TT, Neumeister W et al. Stress test blood
ability (Abstract). Am. Rev. Respir. Dis. 1990; 141: 830. gas analysis in chronic obstructive lung diseases.
20 Pineda H, Haas F, Axen K, Haas A. Accuracy of pulmo- Pnuemologie 1997; 51: 640–6 (in German).
nary function tests in predicting exercise tolerance in 35 Wagner PD. Effects of COPD on gas exchange. In: Cher-
chronic obstructive pulmonary disease. Chest 1984; 86: niac NS (ed). Chronic Obstructive Pulmonary Disease.
564–7. W.B. Saunders Company, Philadelphia, 1991; 73–9.
21 Dillard TA, Piantadosi S, Rajagopal KR. Determinants of 36 Jeffrey AA, Warren PM, Flenley DC. Acute hypercapnic
maximum exercise capacity in patients with chronic air- respiratory failure in patients with chronic obstructive
flow obstruction. Chest 1989; 96: 267–71. lung disease: risk factors and use of guidelines for man-
22 Standards of Care Committee of the BTS. BTS guidelines agement. Thorax 1992; 47: 34–40.
for the management of chronic obstructive pulmonary 37 Levine PA, Klein MD. Mechanisms of arrhythmias in
disease: the COPD Guidelines Group of the Standards of chronic obstructive lung disease. Geriatrics 1976; 31: 47–
Care Committee of the BTS. Thorax 1997; 52 (Suppl. 5): 56.
S1–S28. 38 Y¢ ncalzi RA, Pistelli R, Fuso L, Cocchi A, Bonetti MG,
23 Hansen JE, Sue DY, Wasserman K. Predicted values for Giordano A. Cardiac arrhythmias and left ventricular
clinical exercise testing. Am. Rev. Respir. Dis. 1984; 129: function in respiratory failure from chronic obstructive
S49–S55. pulmonary disease. Chest 1990; 97: 1092–7.
24 Morris JF, Koski A, Johnson LC. Spirometric standarts for 39 Tirlapur VG, Mir MA. Nocturnal hypoxemia and associ-
healthy nonsmoking adults. Am. Rev. Respir. Dis. 1971; ated electrocardiographic changes in patients with
103: 57–67. chronic obstructive airways disease. N. Engl. J. Med.
25 Jones NL, Campbell EJM. Clinical Exercise Testing, 2nd 1982; 306: 125–30.
edn. W.B. Saunders Company, Philadelphia, 1982; 94– 40 Shih HT, Webb CR, Conway WA, Peterson E, Tilley B,
249. Goldstein S. Frequency and significance of cardiac
26 Fletcher GF, Balady G, Froelicher VF, Hartley LH, arrhythmias in chronic obstructive lung disease. Chest
Haskell WL, Pollock ML. Exercise standards: A state- 1988; 94: 44–8.
ment for healthcare professionals from the American 41 Biggs FD, Lefrak SS, Kleiger RE, Senior RM, Oliver GC.
Heart Association. Writing Group. Circulation 1995; 91: Disturbances of rhythm in chronic lung disease. Heart
580–615. Lung 1977; 6: 256–61.
27 Henry WL, DeMaria A, Gramiak R et al. Report of the 42 Green LH, Smith TW. The use of digitalis in patients
American Society of Echocardiography Committee on with pulmonary disease. Ann. Intern. Med. 1977; 87:
Nomenclature and Standards in two-dimensional imag- 459–65.
ing. Circulation 1980; 62: 212–7. 43 Bittar G, Friedman HS. The arrhythmogenicity of theo-
28 Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right phylline. A multivariate analysis of clinical determi-
ventricular function using two-dimensional echocardio- nants. Chest 1991; 99: 1415–20.
graphy. Am. Heart J. 1984; 107: 526–31. 44 Pierson DJ, Hudson LD, Stark K, Hedgecock M. Cardiop-
29 Hammarstrom E, Wranne B, Pinto FJ, Puryear J, Popp ulmonary effects of terbutaline and a bronchodilator
RL. Tricuspid annular motion. J. Am. Soc. Echocardiogr. combination in chronic obstructive pulmonary disease.
1991; 4: 131–9. Chest 1980; 77: 176–82.
30 Quanjer PH, Tammeling GJ, Cotes JE, Pedersen OF, Pes- 45 Simmons DN, Berry MJ, Hayes SI, Walschlager SA. The
lin R, Yernault JC. Lung Volumes and forced ventilatory relationship between %HR peak and %VO2 peak in
flows. Report Working Party Standardization of Lung patients with chronic obstructive pulmonary disease.
Function Tests, European Community for Steel and Coal. Med. Sci. Sports Exerc. 2000; 32: 881–6.

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