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(Chest. 2001;119:811-817.)
© 2001 American College of Chest Physicians

Significance of End-Tidal PCO2 Response to Exercise and Its Relation to Functional Capacity in Patients With Chronic Heart Failure*

Yasuhiko Tanabe, MD; Yukio Hosaka, MD; Masahiro Ito, MD; Eiichi Ito, MD and Kaoru Suzuki, MD

* From the Department of Internal Medicine, Niigata Prefectural Shibata Hospital, Shibata, Japan.

Correspondence to: Yasuhiko Tanabe, MD, Niigata Prefectural Shibata Hospital, Ohtemachi 4–5-48, Shibata City, Niigata, 957-8588 Japan


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 References
 
Objectives: The value of end-tidal PCO2 monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO2 response to exercise and its relation to functional capacity in patients with chronic heart failure.

Methods and results: Maximal upright ergometer exercise with respiratory gas analysis and arterial blood gas analysis were performed in 105 patients with chronic heart failure (34 patients in New York Heart Association [NYHA] class I, 38 patients in NYHA class II, and 33 patients in NYHA class III) and 14 normal control subjects. Peak O2 uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO2 output (E-CO2), and the ratio of physiologic dead space to tidal volume (VD/VT) were determined. Cardiac output was also measured during exercise in 28 patients with chronic heart failure. Arterial PO2 or PCO2 values at rest and during exercise were not different among the four groups. However, end-tidal PCO2 was significantly lower, and arterial to end-tidal PCO2 difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO2 during exercise was significantly reduced as the severity of chronic heart failure advanced (45.7 ± 4.0 mm Hg in normal control subjects, 43.5 ± 4.8 mm Hg in NYHA class I patients, 39.7 ± 5.1 mm Hg in NYHA class II patients, and 34.9 ± 5.3 mm Hg in NYHA class III patients). The maximal end-tidal PCO2 during exercise was significantly correlated with peak O2 uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to E-CO2 (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001).

Conclusions: The decreased end-tidal PCO2 during exercise, which is caused by high ventilation/perfusion ratio mismatching, reflects both reduced cardiac output response to exercise and increased exercise ventilation due to enlarged physiologic dead space in advanced chronic heart failure. The end-tidal PCO2 during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.

Key Words: cardiac output • cardiomyopathy • exercise • heart failure • ventilation


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusions
 References
 
In normal subjects, end-tidal PCO2 is slightly lower than arterial PCO2 at rest and is slightly higher than arterial PCO2 at peak exercise.1 2 3 4 5 6 7 8 As a result, the difference between arterial and end-tidal PCO2 [P(a-ET)CO2] shows negative value at peak exercise in normal subjects.5 6 7 8 9 Previous studies10 11 have demonstrated that the end-tidal PCO2 is reduced in patients with pulmonary embolism who have large dead space ventilation. Patients with advanced chronic heart failure are characterized by reduced cardiac output and increased ventilation due to enlarged physiologic dead space during exercise.12 13 14 However, to our knowledge, the value of end-tidal PCO2 monitoring during exercise in patients with chronic heart failure has not been elucidated.

We hypothesized that patients with severe chronic heart failure who have reduced cardiac output and increased ventilation due to enlarged physiologic dead space during exercise exhibited abnormal end-tidal PCO2 response to exercise, and that the end-tidal PCO2 during exercise could be used to evaluate the functional capacity of patients with chronic heart failure. To clarify the value of end-tidal PCO2 monitoring during exercise in evaluating functional capacity of patients with chronic heart failure, maximal exercise tests with breath-by-breath respiratory gas analysis and arterial blood gas analysis, and cardiac output measurement were performed in patients with chronic heart failure.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusions
 References
 
Subjects
We studied 105 patients (58 men and 47 women; mean ± SD age, 52 ± 10 years) with chronic heart failure and 14 normal volunteer subjects (mean age, 49 ± 5 years). All patients had a history of chronic heart failure of at least 3 months’ duration before the evaluation of exercise tolerance in the present study. The etiologic basis of their chronic heart failure included dilated cardiomyopathy (40 patients), hypertrophic cardiomyopathy (5 patients), dilated cardiomyopathy after valve replacement (3 patients), old myocardial infarction (16 patients), mitral regurgitation (8 patients), aortic regurgitation (4 patients), and mitral stenosis (29 patients). Left ventricular ejection fraction determined by contrast ventriculography or echocardiography was 42 ± 15%. All patients, except those with old myocardial infarction, had normal or minimally sclerotic coronary arteries. No patients with old myocardial infarction showed scintigraphic evidence of exercise-induced myocardial ischemia. Respiratory function tests were performed in 82 patients: vital capacity was 100 ± 19%, and FEV1/forced expiratory volume was 77 ± 10%. Patients were classified into three groups according to the New York Heart Association (NYHA) functional classification: 34 patients were in NYHA class I, 38 patients were in NYHA class II, and 33 patients were in NYHA class III. Written informed consent was obtained from each subject before the study, and ethical approval was obtained.

Exercise Tests
All subjects performed a preliminary exercise test with respiratory gas analysis 2 to 14 days before the study to become familiarized with the procedure. All subjects underwent maximal upright exercise testing using an electronically braked ergometer. After a 3-min rest period sitting on the ergometer, exercise began with a 3-min warm-up period at 10 W, followed by a continuous ramp protocol corresponding to increments of 10 to 20 W/min (1 W/6 s or 1 W/3 s) until the subjects could no longer continue. The end point of the exercise tests was leg fatigue with various degrees of breathlessness in all subjects. The ECG was monitored throughout exercise in all subjects, and the 12-lead ECG was recorded at 1-min intervals in all patients. Cuff BP was measured at 1-min intervals.

Respiratory gas analysis was performed on a breath-by-breath basis (Aero Monitor AE-280; Minato Medical Science; Osaka, Japan); this system consists of a hot-wire spirometer, a zirconium solid O2 analyzer, and an infrared CO2 analyzer. The apparatus was calibrated before each study was performed. Data were processed using an on-line computer system, and the following parameters were calculated: expired minute ventilation (E), O2 uptake (O2), CO2 output (CO2), end-tidal PO2, end-tidal PCO2, and respiratory exchange ratio (CO2/O2). End-tidal PCO2 gradually increases during incremental exercise and reaches its maximal value at the beginning of the respiratory compensation for the lactic acidosis; thereafter, it slightly decreases until maximal exercise. Examples of end-tidal PCO2 response to exercise are shown in Figure 1 . Maximal end-tidal PCO2 during exercise was determined in each subject. If end-tidal PCO2 continues to increase until stopping exercise, the maximal end-tidal PCO2 is equal to end-tidal PCO2 at peak exercise. Before exercise, a catheter (Surflo; Terumo; Tokyo, Japan) was introduced into a radial or brachial artery. Arterial blood was sampled at rest, during the warm-up period, and at 1-min intervals throughout the exercise. Arterial PO2 and arterial PCO2 were measured (ABL-2; Radiometer; Copenhagen, Denmark), and the P(a-ET)CO2 was calculated.



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  		Figure 1.. Examples of end-tidal PCO2 response to exercise in a normal subject and in a patient with chronic heart failure. End-tidal PCO2 gradually increases during incremental exercise and reaches its maximal value at the beginning of respiratory compensation for lactic acidosis, and then slightly decreases until maximal exercise. CHF = chronic heart failure.

 
Exercise capacity was assessed by peak O2 and anaerobic threshold. Peak O2 was determined as the average of values obtained during the final 15 s of exercise. The anaerobic threshold was determined by two experienced reviewers using the V-slope method.15 During exercise, E increases with CO2 so as to keep arterial PCO2 relatively unchanged. Therefore, exercise ventilation was assessed by correlating E with CO2 from the start of exercise to peak exercise using linear regression analysis. The slope of the regression line between VE and CO2 during exercise (E-CO2) was used as a marker of excessive exercise ventilation.14 16 17 Physiologic dead space to tidal volume ratio (VD/VT) was calculated from the modified alveolar gas equation:

In the calculation of VD/VT, it is necessary to subtract mechanical dead space. We determined this to be 100 mL.

In 28 patients with chronic heart failure, exercise cardiac output was also measured. Before exercise, a 7F Swan-Ganz catheter was inserted into the pulmonary artery via an internal jugular vein. Pulmonary arterial blood was sampled simultaneously with arterial blood sampling at rest, during the warm-up period, and at 1-min intervals throughout the exercise. The blood samples were used to measure oxygen saturation and hemoglobin concentration. Cardiac output was determined by the Fick principle.

Statistical Analysis
All data were expressed as mean ± SD. Multiple comparisons among groups were performed by one-way analysis of variance combined with Scheffe’s test. Linear regression analysis was used to assess the relation between maximal end-tidal PCO2 during exercise and E-CO2, VD/VT, peak O2, or peak cardiac index. A value of p < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusions
 References
 
Table 1 shows characteristics of the subjects and the results of exercise testing. Heart rate at rest or at peak exercise was not different among groups. Systolic BP at peak exercise was significantly lower in NYHA class III patients than other groups. Exercise capacity determined by peak O2 or anaerobic threshold significantly reduced as the severity of chronic heart failure advanced. Excessive exercise ventilation assessed by E-CO2 was significantly greater in NYHA class III than other groups.


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  		Table 1.. Patient Characteristics and the Results of Exercise Testing*

 
Table 2 shows arterial PO2, arterial PCO2, end-tidal PCO2, P(a-ET)CO2, and VD/VT during exercise. Arterial PO2 was controlled within the normal range in each group and was not different among the four groups. Although arterial PCO2 was not different among the four groups at rest and during exercise, end-tidal PCO2 during exercise was significantly reduced in NYHA class III patients than other groups. As a result, P(a-ET)CO2 during exercise was significantly higher in NYHA class III patients than in normal subjects or patients in NYHA class I or NYHA class II. In normal subjects, P(a-ET)CO2 was positive (2.4 ± 2.3 mm Hg) at rest, and it became increasingly negative with exercise (- 5.3 ± 3.3 mm Hg at peak exercise). P(a-ET)CO2 remained positive even at peak exercise in NYHA class III patients (3.4 ± 3.2 mm Hg). VD/VT gradually decreased during exercise. VD/VT at peak exercise was significantly increased as the severity of chronic heart failure advanced. VD/VT at peak exercise was < 0.30 in all normal subjects, but it was < 0.30 in only 3 of 33 patients in NYHA class III. Maximal end-tidal PCO2 during exercise was significantly reduced as the NYHA functional class advanced (45.7 ± 4.0 mm Hg in normal control subjects, 43.5 ± 4.8 mm Hg in NYHA class I patients, 39.7 ± 5.1 mm Hg in NYHA class II patients, and 34.9 ± 5.3 mm Hg in NYHA class III patients).


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  		Table 2.. Arterial Blood Gas, End-Tidal PCO2, P(a - ET)CO2, and VD/VT During Exercise*

 
Figure 2 shows the relation between maximal end-tidal PCO2 during exercise and VD/VT at peak exercise (top) and exercise ventilation assessed by E-CO2 (bottom). Maximal end-tidal PCO2 was inversely correlated with VD/VT at peak exercise and E-CO2. Figure 3 shows the relation between maximal end-tidal PCO2 during exercise and peak O2 (top) and cardiac index at peak exercise (bottom). Maximal end-tidal PCO2 was significantly correlated with peak O2 and cardiac index at peak exercise.



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  		Figure 2.. Scatterplots showing the relation between maximal end-tidal PCO2 during exercise and VD/VT at peak exercise (top) or excessive exercise ventilation assessed by E-CO2 (bottom). See Figure 1 for abbreviation.

 


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  		Figure 3.. Scatterplots showing the relation between maximal end-tidal PCO2 during exercise and peak O2 (top) or cardiac index at peak exercise (bottom). See Figure 1 for abbreviation.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusions
 References
 
The present study showed that end-tidal PCO2 during exercise was significantly reduced in severe chronic heart failure. Maximal end-tidal PCO2 during exercise was correlated with peak O2 and cardiac index at peak exercise, and was inversely related to excessive ventilation due to increased VD/VT.

End-Tidal PCO2 in Normal Subjects or Patients With Pulmonary Diseases
The alveolar PCO2 of the lung units, at which perfusion and ventilation are uniformly distributed, is very close to arterial PCO2. Since the distribution of blood flow to apices is relatively low compared with the basal segments at rest in the upright position, alveolar PCO2 in the apices at rest in the upright position is lower than arterial PCO2. As a result, end-tidal PCO2 is slightly lower than arterial PCO2 at rest.1 2 3 4 During exercise, the pulmonary blood flow to apices increases relatively more than ventilation. Hence, the distribution of ventilation and perfusion becomes more even; subsequently, end-tidal PCO2 increases. Also, the increased rate of CO2 delivery to the lung during exercise creates an increase in slope of the alveolar phase of the CO2 expiratory curve, and end-tidal PCO2 increases during exercise.6 It has been shown that P(a-ET)CO2 goes from + 2.5 mm Hg at rest to - 4 mm Hg during heavy exercise in normal subjects.6 The result of the present study, which shows that P(a-ET)CO2 goes from + 2.4 ± 2.3 mm Hg at rest to - 5.3 ± 3.3 mm Hg at peak exercise in control subjects, is comparable to previous studies.

In contrast to normal subjects whose lung units were nearly uniformly perfused and ventilated during exercise, patients with pulmonary diseases have uneven distribution of ventilation and perfusion at rest and during exercise. In patients with pulmonary embolism who have large dead space, end-tidal PCO2 value is significantly reduced.10 11 Almost all patients with moderate or massive pulmonary emboli have a P(a-ET)CO2 value of > 5 mm Hg at rest.10 In patients with COPD or other lung diseases, physiologic dead space can be large and the P(a-ET)CO2 is correspondingly large at rest and during exercise.18 19 Patients with unevenly distributed ventilation and perfusion have lung units in which the amount of ventilation is high relative to the amount of blood flow. Gas coming from these units has a PCO2 less than arterial PCO2. Therefore, end-tidal PCO2 cannot be used as an index of arterial PCO2 in these patients with pulmonary abnormalities.10 11 18 19

End-Tidal PCO2 During Exercise in Chronic Heart Failure
Sullivan et al13 have shown that the increased exercise ventilation in patients with chronic heart failure is caused by increased VD/VT. They indicated that attenuated perfusion to lungs during exercise is the major cause of excessive exercise ventilation, by producing unevenly poorly perfused alveoli.13 Other studies14 16 17 20 21 have also shown that abnormally increased exercise ventilation is primarily caused by increased physiologic dead space. However, the role of measurements of end-tidal PCO2 in the evaluation of increased dead space during exercise in patients with chronic heart failure has not been fully elucidated.

Wasserman et al22 have shown that end-tidal PCO2 at peak exercise is correlated with peak O2 in patients with chronic heart failure, but the relation between end-tidal PCO2 and peak O2 is not close (r = 0.355). We showed that maximal end-tidal PCO2 during incremental exercise was closely correlated with peak O2 (r = 0.68) or peak cardiac index (r = 0.73), and it was inversely correlated with excessive exercise ventilation assessed by E-CO2 (r = - 0.84). End-tidal PCO2 gradually increases during incremental exercise and reaches its maximal value at the beginning of respiratory compensation for lactic acidosis; thereafter, it decreases until maximal exercise. The decrease in end-tidal PCO2 from its maximal value to peak exercise value is smaller in severe chronic heart failure, because the patients with lowest exercise capacity have the least end-exercise metabolic acidosis.22 Therefore, the difference between maximal end-tidal PCO2 during exercise and end-tidal PCO2 at peak exercise is greater in normal subjects or patients with mild chronic heart failure than in patients with severe chronic heart failure. The maximal end-tidal PCO2 during exercise is more significant than end-tidal PCO2 at peak exercise in the evaluation of functional capacity of chronic heart failure patients.

The results of the present study show that both arterial PO2 and arterial PCO2 were controlled within normal range even in patients with severe chronic heart failure. Therefore, the neurohumoral ventilatory control mechanisms are intact even in patients with chronic heart failure, and the significantly reduced end-tidal PCO2 at rest and throughout the exercise in severe chronic heart failure did not result from hyperventilation that induces decreased arterial PCO2 value. Wasserman et al22 suggested that the decreased end-tidal PCO2 and increased P(a-ET)CO2 in chronic heart failure is caused by high ventilation/perfusion (/) ratio mismatching without low / ratio mismatching.22 They speculated that the development of high / ratio mismatching is due to pulmonary vasoconstriction and greater reduction in perfusion to lung unit with higher venous pressure.22 Our findings, that the decrease in maximal end-tidal PCO2 during exercise was closely related to the reduced cardiac output response to exercise, support the mechanisms proposed by Wasserman et al.22 The reduced end-tidal PCO2 during exercise in chronic heart failure seems to be primarily caused by uneven perfusion of the lung accompanying the reduced cardiac output response to exercise. Reduced pulmonary perfusion during exercise may produce poorly perfused alveoli (ie, lungs develop high / ratio mismatching), thereby inducing excessive exercise ventilation with larger physiologic dead space and lower end-tidal PCO2.

Limitations
This study included various causes of chronic heart failure. However, all patients were in the pathophysiologic state of decreased maximal cardiac output response to exercise. There is no reason to consider that the etiology of chronic heart failure influences the end-tidal PCO2 during exercise. We classified the subjects by NYHA functional class, which is relatively crude. However, it is unlikely that we would reach substantially different conclusions by another more quantitative classification, such as by peak O2.

End-tidal PCO2 gradually increases during incremental exercise and reaches its maximal value at the beginning of respiratory compensation for lactic acidosis, and then it slightly decreases until maximal exercise. In some patients, end-tidal PCO2 continued to increase until stopping exercise, and the maximal end-tidal PCO2 was equal to the end-tidal PCO2 at peak exercise. However, these subjects showed adequately elevated respiratory exchange ratio at peak exercise, which suggested that near maximal effort was achieved in each subject. It is unlikely that the maximal end-tidal PCO2 values in these subjects would be underestimated.


   Conclusions
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
References
 
The maximal end-tidal PCO2 during exercise, which was significantly reduced as the severity of chronic heart failure advanced, was closely correlated with peak O2 and cardiac index at peak exercise and was inversely related with increased ventilation due to enlarged VD/VT. The end-tidal PCO2 during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.


   Footnotes
 
Abbreviations: NYHA = New York Heart Association; P(a-ET)CO2 = difference between arterial and end-tidal PCO2; CO2 = CO2 output; VD/VT = physiologic dead space to tidal volume ratio; E = expired minute ventilation; E-CO2 = slope of the regression line between expired minute ventilation and CO2 output; O2 = O2 uptake; / = ventilation/perfusion

Received for publication November 10, 1999. Accepted for publication September 11, 2000.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusions
 References
 

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