(Circulation. 1998;98:1043-1044.)
© 1998 American Heart Association, Inc.
Lung Function and Exercise Gas Exchange in Chronic Heart Failure
Bernard Aguilaniu, MD;
; Eric Page, MD
Unité de diagnostic cardio-pulmonaire à
l'exercice,
Laboratoire de physiopathologie de l'exercice,
Grenoble, France
François Peronnet, PhD
Unité de formation et de recherche, activité physique
et sparkine Université Joseph Fourier,
Grenoble, France,
Université de Montréal,
Montréal, Canada
Hélène Perrault, PhD
Unité de formation et de recherche, activité physique
et sparkine,
Université Joseph Fourier,
Grenoble, France,
McGill University,
Montréal, Canada
To the Editor:
This letter follows the report from a multicenter study of
exercise ventilatory and gas exchange responses in 130 patients with
heart failure (HF).1 Average exercise
PaO2 and
PAO2 were observed to be normal in
spite of a relatively high VD/VT, which was
compensated for by a marked hyperventilation
(
E/O2 close
to 40 even at comparatively low workloads). The authors thus suggest
that patients with HF present a condition of reduced perfusion in a
well-ventilated lung with no disturbance in gas exchange. The
mean P(A-a)O2 was indeed found to be normal at
20 mm Hg. However, PaO2,
P(A-a)O2, and, to a lesser extent,
PAO2 were widely dispersed around
average values. In a large number of patients, supranormal values,
seldom observed in clinical practice, were observed for
PaO2 (>110 mm Hg in 30
patients), PAO2 (>130 mm Hg in
15 patients), and P(A-a)O2 (<10 mm Hg
in 30 patients). These values at the upper range of the
distributions correctly fit the description of a "reduced perfusion
in a well-ventilated lung." In contrast, at the lower range of the
distribution, 30 patients exhibited P(A-a)O2
values >30 mm Hg, and this was independent of the achieved peak
O2. It should be remembered
that in 77 subjects with normal lung function and gas exchange, Hansen
et al2 observed exercise
P(A-a)O2 >35 mm Hg in only 3. We thus
believe that the simple and attractive "high VA/Q" model due to a
high VD/VT proposed to explain the exaggerated
ventilatory response in patients with HF only fits a limited number of
these patients, namely, those with normal or supranormal
P(A-a)O2 values. However, the large prevalence
of a wide exercise P(A-a)O2 in these patients
suggests that additional factors can contribute to the marked
hyperventilation observed, such as ventilation-perfusion mismatch due
to poor alveolar ventilation and/or diffusion limitation. These and
other possible disturbances in lung function and gas exchange
in patients with HF should not be overlooked in clinical practice.
References
-
Wasserman K, Zhang Y-Y, Gitt A, Belardinelli R, Koike A,
Lubarsky L, Agostoni PG. Lung function and exercise gas exchange in
chronic heart failure. Circulation. 1997;96:2221–2227.[Abstract/Free Full Text]
-
Hansen JE, Sue DY, Wasserman K. Predicted values for
clinical exercise testing. Am Rev Respir Dis.
1984;129(suppl):S49–S55.
Response
K. Wasserman, MD, PhD;
Y-Y. Zhang, MD;
; L. Lubarsky, MD
Harbor–UCLA Medical Center,
UCLA School of Medicine,
Torrance, Calif
A. Gitt, MD
Herzzentrum Ludwigshafen Department of Cardiology
and Pneumonology,
Ludwigshafen, Germany
R. Belardinelli, MD
Ospedale Cardiologico G.M. Lancisi Ancona, Italy
A Koike, MD
2nd Department of Internal Medicine Tokyo Medical and Dental
University,
Tokyo, Japan
P.G. Agostoni, MD
Istituto di Cardiologia dell'Universita degli Studi Centro di
Studio per le Richerche Cardiovascolari del Consiglio Nazionale delle
Richerche,
Milan, Italy
In response to the letter of Aguilaniu and colleagues, we
must point out that their letter incorrectly describes our
findings.1 They state that we "suggest that
patients with HF" have "no disturbance in gas exchange."
We did find a disturbance in gas exchange in our patients with
chronic HF, the nature of which was the primary message of our article.
We found that the dead space/tidal volume ratio
(VD/VT) and arterial-end tidal
PCO2 difference
[P(a-ET)CO2] increased systematically as peak
exercise performance decreased. These findings indicate that
high ventilation-perfusion (A/
) ratio lung
units developed as exercise tolerance worsened, findings expected with
regional reduction in pulmonary blood flow relative to
ventilation. In contrast, the average arterial
PO2
(PaO2) and
alveolar-arterial PO2
difference [P(A-a)O2] values remained normal
at peak exercise and were uninfluenced by the severity of the exercise.
These observations suggest that there is no systematic development of
low A/ lung units as exercise tolerance
worsens.
The letter of Aguilaniu et al has as its main concern the values
of PaO2 and
P(A-a)O2 in our HF patients. They used the study
of Hansen et al2 as the reference for normal
values (adult men with average age of 54 years). These values in our HF
population have a greater dispersion than reported by Hansen et
al2
(PaO2=98.1±15.3 versus 100.6±9.9
for the HF and normal populations, respectively, and
P(A-a)O2=20.5±13.7 versus 19.0±8.8 for the HF
and normal populations, respectively, mean±SD. These values are not
significantly different. Nine of our 83 patients had a
PaO2 value ranging from 61 to 79 at
peak exercise, values that we regard to be abnormal. However, these low
values were not systematically related to the extent of exercise
limitation. Aguilaniu et al state that a
PaO2 of >110 at maximal exercise is
seldom seen in clinical practice at peak exercise. I am not sure
of the altitude of the laboratory at which Dr Aguilaniu et al work
(critically important), but at sea level, these values, while not
usual, are not uncommon at peak exercise. Given the data of Hansen
et al,2 10 (13.5%) of 74 normal subjects had a
PaO2 value >110 at peak
exercise compared with 17 (20.5%) of 83 in our HF population. The high
values at peak exercise could be accounted for by a combination of
hyperventilation and high respiratory exchange ratio (RER). Thus, the
alveolar PO2 will become 130 when
PaCO2=27 and RER=1.5 (only 3 of our
83 patients had PAO2 values in the
range of 130).
The increased dispersion in our HF population might have been due
to chronic changes resulting from repeated episodes of
pulmonary edema or the ravages of chronic cigarette smoking. We
did not prescreen our HF patients for subtle pulmonary disease,
as was done by Hansen et al.2 We also cannot
exclude the possibility that random technical errors might have
occurred in this multicenter study to account for the increased
dispersion of our data compared with that reported by Hansen et
al.2
The major finding described in our report is that patients with
chronic HF have unique lung pathophysiology. They develop high
A/ ratio lung units as exercise capacity
worsens, without development of low A/ ratio
lung units. This impairment-related abnormality in lung function, along
with the increased VCO2 relative to
O2 that our study describes,
may account for the high frequency of dyspnea reported by HF
patients.
References
-
Wasserman K, Zhang Y-Y, Gitt A, Belardinelli R, Koike A,
Lubarsky L, Agostoni PG. Lung function and exercise gas exchange in
chronic heart failure. Circulation. 1997;96:2221–2227.
-
Hansen JE, Sue DY, Wasserman K. Predicted values for
clinical exercise testing. Am Rev Respir Dis.
1984;129(suppl)S49–S55.
