The Tidal Volume Response to Incremental Exercise in COPD

The Tidal Volume Response to Incremental Exercise in COPO* Carlos A. Vaz Fragoso, M.D., F.C.C.R; Trudy Clark, R.N.; and Arthur Kotch, M.D., F.C.C.R Patients with severe COPD often exhibit a ventilatory limit to exercise. This is associated with a shallow breathing pattern when compared with normal control subjects. It is unclear, however, what factors affect differences in breathing patterns within this patient population. To further investigate the tidal volume (VT) response to exercise in severe COPD, nine patients were recruited to undergo a maximal incremental exercise test. Pulmonary function tests, collection of expired gases, and continuous pulse oximetry were performed. As a group, the results were as follows (mean±SD): The FEV. was 31±7 percent of predicted, the FRC was 143± 18 percent of predicted, and the Dco was 47 ± 15 percent of predicted. Exercise testing showed an oxygen consumption at peak exercise of only 44±9 percent predicted, a dyspnea index of 101±19 percent predicted, a heart rate at peak exercise of 75 ± 12 percent predicted, a tidal volume at peak exercise (PKVT) of 1.23 ± .35, a respiratory rate at peak exercise (PKlb) of 26 ± 6, and an oxygen saturation at peak exercise (PKossat) of96±4 percent. An anaerobic threshold (AT)occurred in seven of the nine patients at a mean of 31 ± 8 percent predicted maximal oxygen consumption. Regression analysis showed the PKVT to be inversely correlated with the

with advanced COPD demonstrate severe P atients impairments in exercise performance. One major

factor is a critical reduction in the maximum breathing capacity (MBC) leading to an abnormally low ventilatory reserve at peak exercise.' Such a pulmonary mechanical limitation is associated with a shallow breathing pattern when compared with normal control subjects," This is presumably due to factors imposed by the morphology of the How-volume loop, ie, a compensatory shift to higher lung volumes to generate higher expiratory How rates. 2 We have previously reported" that during a maximal incremental exercise test, the inspiratory How rate develops an abnormal plateau phase, in part related to the severity of the COPD. This phenomenon, however, is associated with a breathing pattern favoring lower respiratory rate (fb) and higher tidal volume (VT). Given these findings and the potentially contradictory effects of hyperinHation (lower VT) and obstruction (lower fb) on the breathing pattern response to incremental exercise, we sought to further explore the variables affecting the tidal volume response

FEV. (r= -0.76; p=O.OI) and the PKfb (r= -0.85; p = 0.003), while positively correlating with the FRC (r= +0.80; p=O.OI) and the PKossat (r= +0.69; p=O.04). Additionally, there was a trend for the PKVTto be inversely related with the AT (r= -0.72; p=O.(6). In COPD, the more severe the obstruction and hyperin8ation, the larger the VT response to exercise. This may serve to avoid a deleterious increase in autoPEEP by promoting a lengthening of the expiratory time. Furthermore, given the association of an earlier AT and a higher PKo.sat with a larger PKVT, this would suggest that such a response may minimize the effects of dead space and/or autoPEEP on Os delivery (early AT). (Chest 1993; 103:1438-41) AT=anaerobic threshold; DI=dyspnea index=VE at peak exercise/(FEV.X35); fb = respiratory rate in breaths/min; MVol = oxygen consumption at peak exercise as percent of predicted maximum 0 1 consumption; PKt'b = tb at peak exercise; PKrc = heart rate at peak exercise as percent o(predicted; PKolsat = oxygen saturation at peak exercise; .,PVolm = percent of predicted maximal oxygen consumption; PK percent TLC = PKVT + FRC/TLC; PKVT = VT at peak exercise; VAT= ventilatory AT by V-slope method as percent of predicted maximum 0 1 consumption; VONT = dead space volume to tidal volume ratio

within a study population with severe COPD. METHODS

Subsequent to obtaining written informed consent, nine patients with severe COPD (FEV.<50 percent predicted) performed an upright maximal incremental exercise test before initiation of a rehabilitation program. Pulmonary function tests (PITs) including spirometry, lung volumes (nitrogen washout technique), and Dco were performed on the day of testing prior to the exercise test (SensorMedics System 2200; SensorMedics Corporation, Yorba Linda, Calif). Patients were then exercised on an electronically braked and linearly ramped cycle ergometer to a symptomatic limit (ErgolinelSMC model BOOS). Breath-by-breath collection of expired gases was accomplished through a two-way, nonrebreathing valve, pneumotachograph, O2 and CO 2 analyzers (SensorMedics 2900 Metabolic Measurement Cart). Continuous pulse oximetry (Nellcor 200; Nellcor Corporation; Hayward, Calif) and electrocardiography (SensorMedics 12-lead stress system) were likewise monitored throughout exercise. Simple regression analysis was performed to evaluate the correlation between the above-listed variables and the achieved VT at peak exercise. Significance was determined at a p value SO.OS. Predicted values for lung volumes and Bow rates were derived from Crapo et al4 and exercise performance from Hansen et al." The AT was determined by the V-slope method (VAT). 6 RESULTS

*From the Section of Pulmonary and Critical Care Medicine, Danbury Hospital, Danbury, Conn. Manuscript received June 5; revision accepted September 14. Reprint requests: Dr. \flz Fragoso, Danbury Hospital, Danbury, CT06810

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Study Population Table 1 details the lung mechanics of our study population. There is severe obstruction that is associTidal VolumeResponseto Incremental Exercise (Vaz Fragoso, Clark, Kotch)

Table I-Study Population· Patient 1 2 3 4 5 6 7 8 9 Mean±SD

FEV.

FRC

Dro

MVo l

PKfc

23

152 112 145 170 165 128 142 138 137 143± 18%

42

30

79 100 67 79 73 73 72 80 54 75±12

36

27 28

22

39

42

36

29 31±7%

46

36

56 51

60

54 64

15 47±15%

44 50 35 39 49 58 45 50 44±9%

AT

DJ

PKVT

PIC%TLC

PKfb

PICo.Sat

24

lOB 90 94

1.45 0.64 1.51 1.8 0.94 1.01 1.35 1.1 1.23± .35

21 36 21 33 17 30 29 21 24 26±6

98

116 76 100 81 137 101±19%

78 73 106 92

35

23 None 25 38 None

28

44 31±8%

107

1.28

83 87 81 96

99

88±11%

92 97 99

100 97 95 100 90 96±4%

*All as percent predicted other than AT (%PVo 2m), peak VT (liters), Fb (breaths per minute), and O.Sat. Dyspnea index =VEmax/(FEV.X35); PK percent TLC = (PKVT+ FRC)/fLC. Please see text for abbreviations.

ated with hyperinflation and involvement of the alveolar-capillary unit (reduced Dco), A representative How-volume loop is shown in Figure 1. It illustrates an expiratory plateau defect suggesting significant dynamic airway collapse and a prolonged expiratory phase.

Exercise Performance Table 1 demonstrates that the study group as a

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Tulal Volume Response The VTat peak exercise (PKVT) correlated inversely with the FEV1 (Fig 2) and the respiratory rate at peak exercise (PKfb) (Fig 3), while positively correlating with the FRC (Fig 4) and the oxygen saturation at peak exercise (PKo 2sat). In addition, there was a trend for the PKVTto correlate positively with the VAT (Fig 5). None of the other variables listed in Table 1 correlated with the PKVT response. Of interest was the total lung capacity at peak exercise (PK percent TLC). Table 1 demonstrates that at peak exercise the total lung volume at end-inspiration may approach 90 percent of the TLC (ie, PK percent TLC).

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whole had a very poor peak exercise performance (low oxygen consumption at peak exercise [MVo2 ] ) characterized by a low ventilatory reserve (high dyspnea index [DI]). This occurred in the setting of an early VAT in seven of the nine patients but in the absence of any clinically significant oxygen desaturation (all ~90 percent at peak exercise as measured by pulse oximetry).

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In patients with advanced COPD, breathing patterns during a maximal incremental exercise test favor larger VT and lower fb, This is associated with the

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1993

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1440

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severity of obstruction and hyperinflation, and, perhaps, with factors related to oxygen delivery (ie, early AT). These results do not necessarily contradict the work of Matthews et al. 2 Their findings of a shallow breathing pattern are relative to a normal control population. Our study; in contrast, focused on differences in breathing patterns within a group of patients with severe COPD. Thus, it would appear that it is the severity of the obstruction that is the primary determinant of the VT response to exercise in this patient population. A combination of dynamic airway collapse and actual histopathologic airway changes serves to increase airway resistance progressively The latter would preclude significant reductions in the expiratory time and, thus, blunt the rise in the fb. This leaves the VT as the major means to augment flow rates and, consequently, minute ventilation. The cost of such a response may be an increase in the elastic work of breathing as the PKVT+ FRC sum may be approaching the TLC (PK percent TLC; Table 1). It would appear on first glance that the PKVTin the patients tested appears to be disproportionate to that suggested by their respective FEV r- This "discrepancy" may be reconciled by an understanding of the effects of an FVC maneuver on dynamic airway

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collapse. Specifically, a maximal forced expiratory effort may increase intrathoracic pressures to levels that accentuate collapse of the airways during exhalation. In contrast, an exercise breathing pattern that favors higher VT and low fb would not generate as high a pressure change. The consequence would be delayed collapse of the airways and an improved VT relative to that predicted by the FEV 1. Such a scenario, although feasible, remains to be proven. Clinically, the AT is used to assess the appropriateness of O2 delivery and/or extraction. 1 It reflects cardiovascular fitness in terms of central (inotropy/ chronotropy) and peripheral components (02 distribution to or extraction in the exercising muscles).' In severe COPD, the reliance on a VT response may benefit O2 delivery This may be secondary to cardiopulmonary interactions. A scenario of longer expiratory times leading to less air trapping and, therefore, less autoPEEP may be postulated. The ultimate consequence would be improved venous return and lower intrathoracic pressures relative to the cardiac fossa and pulmonary vasculature. A subsequent improvement in stroke volume and cardiac output would be anticipated. In addition, a larger VT may result in a lower VDNT, which could lead to a more effective alveolar ventilation relative to the total minute ventilation. This would diminish alveolar hypoventilation as a cause of diminished arterial O 2 content and, consequently, O2 delivery. Why there should be a trend for an inverse correlation between the PKVT and the ATis unclear. It may be that with a preexisting impairment in O2 delivery/extraction (eg, cor pulmonale with or without ventricular interdependence, primary left ventricular dysfunction, or deconditioning), a compensatory mechanism would include responses that minimize the deleterious effects of autoPEEP or dead space ventilation. Breathing patterns with a predominant VT may be such a mechanism. Perhaps the association of the PKo2sat with the PKVT reflects the end result of such a compensation. One must be cautious, however, as this may be a chance Tidal VolumeResponseto IncrementaJExercise (Vaz Fragoso, Clark, Kotch)

association given the many factors that potentially affect arterial oxygenation. This investigation is limited somewhat by the small study population and its relatively noninvasive design. However, one cannot dismiss the associations of the PKVT response with the severity of obstruction and its possible relationship to O2 delivery. Further work is needed to confirm this association and whether it represents a cause and effect relationship. We are currently embarked on a study that applies external positive end-expiratory pressure as a pneumatic splint to evaluate if there is a change in the flow-volume loop, exercise performance, or breathing patterns in patients with severe capo. If the desired response is achieved, this may lend more credence to the above discussion.

REFERENCES 1 Wasserman K, Hansen JE, Sue DY, Whipp BJ. Principles of exerci se testing and interpretation. Philadelphia: Lea & Febiger, 1987 2 Matthews Jl, Bush BA, Ewald FW Exercise responses during incr emental and high intensity and low intensity steady state exercise in patients with obstructive lung disease and normal control subjects, Chest 1989; 96:11-7 3 Fragoso C , Systrom D, Kanarek D . Breathing patterns during incr emental exercise in COPD. Am Rev Respir Dis 1989; 139:A595 4 Crapo RO, Moris AH, Gardner RM. Reference spirometric values using techniques and equipment that meets ATS recommendstions . Am Rev Respir Dis 1981; 123:185-90 5 Hansen JE, Sue DY, Wasserman K. Predicted values for clinical exerci se testing. Am Rev Respir Dis 1984; 129:S49-S55 6 Beaver WL, Wasserman K, Whipp BJ. A new method for detecting the anaerobic threshold by gas exchange . J Appl Physiol 1986; 60:2020-27

AMERICAN COLLEGE OF CHEST PHYSICIANS

59th ANNUAL SCIENTIFIC ASSEMBLY October 24 - 28, 1993 • Orlando

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