Editorial Respiratory Muscle Weakness, Pattern of Breathing, and CO2 Retention in Chronic Obstructive Pulmonary Disease
Normal breathing is characterized by can be explained by passive mechanical the ease with which it is accomplished, factors alone. and by the enormous reserve capacity of COPD compromises the capacity of the respiratory muscles. In chronic ob- the respiratory muscles to sustain the venstructive pulmonary disease (COPD), the tilatory load in several ways. The combibalance between the work of breathing nation of passive and dynamic hyperinand the respiratory muscle reserve is shift- flation puts the inspiratory muscles, esed in an unfavorable direction. The work pecially the diaphragm, at a severe and energy cost of breathing are very high mechanical disadvantage (5). To some exand the capacity of the respiratory mus- tent this can be offset by the loss of sarcles to cope with the ventilatory burden comeres in the chronically shortened diis markedly attenuated (1). Thus, it is in- aphragm (6), although this mechanism tuitively attractive to hypothesize that has not yet been demonstrated concluhypercapnia is the outward clinical sively in humans with COPD (7). In any manifestation of respiratory muscle fail- case, sarcomere adaptation can restore force-generating capacity to the chroniure or fatigue. In order to examine this hypothesis cally shortened diaphragm, but it cancritically, it is helpful to review several not restore the lost capacity for shortencharacteristics of respiratory system func- ing and volume displacement. Expiratory air flow limitation prevents tion in COPD. Gas exchange is severely impaired by ventilation-perfusion im- the expiratory muscles from increasing balance (2), but the partial pressure of the VT, even if these muscles contract carbon dioxide in arterial blood (Pac02) vigorously (4). Dynamic hyperinflation can be kept normal or near normal, also may increase the burden on the inprovided that minute ventilation (VE) is spiratory muscles by imposing elastic and maintained at a sufficiently high level. threshold loads. The elastic load results Given the increase in the ratio of dead from the decrease in lung compliance at space to tidal volume (VD/VT) that is very high lung volume, and the threshcharacteristic of COPD, resting VE must old load is the result of intrinsic or autobe twice the normal level. Typically, this positive end-expiratory pressure (PEEP). is accomplished by a 50 to 100070 increase Of interest, acutely induced hyperinflain the respiratory rate, with a normal or tion in asthma did not increase inspiratory work because at high lung volume slightly increased VT (3). The problem with maintaining VE the increase in elastic work was offset by above normal is that there are significant the decrease in flow-resistive work (8). mechanical impediments to breathing. Moreover, total work per breath was deCOPD is characterized by increased re- creased by 39070 because of the marked sistance to inspiratory as well as expira- decrease in expiratory work at the high tory air flow, and passive hyperinflation lung volume. The balance between the mechanical of the lungs. These static mechanical abnormalities are not by themselves so se- impediments to breathing and the capacvere, but further mechanical limitation ity of the inspiratory muscles to cope with is caused by dynamic hyperinflation (4). them can be expressed as the ratio of the Because of the expiratory air flow limi- inspiratory pressure for a given breath tation, it takes a long time after the end (Pbreath) to maximal inspiratory presof inspiration for the lung volume to re- sure (MIP). Thus, Pbreath/MIP reflects turn to its resting level. With the increase the relative force required for inspiration. in respiratory rate, the next inspiration In like fashion, the ratio of the duration starts well before the air from the previ- of inspiration (TI) to total breath time ous breath has been expelled. As a re- (Ttot) is the fractional or relative duration sult, the lung volume increases more than of inspiration. The product of (Pbreathl AM REV RESPIR DIS 1991; 143:901-903
MIP) and (Tr/Ttot) is the pressure-time index (PTI), also referred to as the tension-time index (9). Note that Pbreath/MIP and PTI can be increased by any combination of increased resistance, decreased compliance, and inspiratory muscle weakness, and that respiratory muscle weakness consequent to metabolic and nutritional disarray is quite common in COPD (5). Note also that Pbreath is higher with large breaths and lower with small breaths. In this issue of the journal, Begin and Grassino analyze the pathophysiology of hypercapnia in relation to three physiologic characteristics of COPD: impaired gas exchange, the severity of the air flow limitation, and the force reserve of the inspiratory muscles (10). Their data were obtained from more than 300 ambulatory patients. One third of these patients were hypercapnic, but severe hypercapnia was relatively uncommon. The Pac02 was found to correlate best with (1) the increase in respiratory dead space (VD/VT); (2) air flow limitation, as reflected in the FEV 1 or total lung resistance (RL); and (3) the balance between Pbreath and MIP, as reflected by either Pbreath/MIP or RL/MIP. Begin and Grassino showed that there was an excellent correlation between Pbreath and RL, and found RL to be the best single indicator of the mechanical impediment to breathing (10). As expected, RL/MIP was higher with greater degrees of hyperinflation (which lowers MIP) and air flow limitation (which increases RL). Although the graph relating Pac02 to RL/MIP showed a wide range of Pac02 values for any given value of RL/MIP, the probability of a patient being hypercapnic rose sharply as RL/MIP increased. Being overweight and underweight, respectively, enhanced and lowered the probability of hypercapnia at any level of RL/MIP. The impact of weight on Pac0 2 can be assessed in another way. The percentage of patients who were severely underweight (body weight < 80% predicted) 901
902
must have been approximately 10070 for all three patient groups, based on the mean values and standard deviations (SD) for weight. In contrast, the percentage of patients who were markedly overweight (body weight> 130070 predicted) increased geometrically from 8070 of eucapnic, to 15% of moderately hypercapnic and 30% of severely hypercapnic patients. Surprisingly, severe underweight does not appear to be a risk factor for hypercapnia, whereas severe overweight does. Begin and Grassino found that no single variable or combination of two variables in ratio form could explain more than 35070 of the variance in Paoo, (10). Even when they expressed Paco2 as a function of as many as five independent variables, including RL, VD/VT, body weight, dynamic elastance, and MIP, the investigators could explain only half the variance in Paco2' Thus, other factors must have been involved. It seems very likely that one of these is the rapid, shallow pattern of breathing. Is inspiratory muscle fatigue the main cause of chronic hypercapnia? Probably not. Bellemare and Grassino showed that normal subjects could develop inspiratory muscle fatigue, by breathing through inspiratory airflow resistances. In order for fatigue to occur, the subjects had to achieve a pattern of breathing that caused the PTI to exceed 0.15 and maintain the tension time level for a sufficiently long time (9). Patients with COPD have a much higher PTI than normal subjects, but their PTI does not lie in the fatiguing range unless they are made to breathe more slowly and deeply than they normally choose (11). Begin and Grassino show that the PTI was higher in hypercapnic than in eucapnic COPD patients, but even in the severely hypercapnic group the PTI did not exceed the fatigue threshold (10).Moreover, overt respiratory muscle fatigue could be identified in less than 10% of COPD patients who were hospitalized for worsening dyspnea (12). How does the pattern of breathing affect CO 2 retention? Begin and Grassino point out that the ratio RL/MIP, which has the units of lIair flow, can be thought of as the inverse of ventilatory capacity (10). In effect, Paoo, rises as ventilatory capacity falls. What causes the ventilatory capacity to fall? It has been shown repeatedly that the VT is significantly smaller in hypercapnic as compared with eucapnic patients with COPD or kyphoscoliosis (3, 13-15). Begin and
EDITORIAL
Grassino also found this to be true, especially for their severely hypercapnic patients (10). The reduction in VT is largely offset by an increase in the respiratory rate, so VE is not significantly different in hypercapnic as compared with eucapnic patients. However, rapid, shallow breathing has undesirable consequences. The increased respiratory rate aggravates dynamic hyperinflation and the small VT increases VD out of proportion to the effects of ventilation-perfusion mismatch within the lung. Why does the pattern of breathing change in such a disadvantageous way? The answer to this question lies in another consequence of the increase in Pbreath/MIP. The perception of respiratory effort and dyspnea are closely linked to Pbreath/MIP, which reflects the relative force of inspiratory muscle contraction (16). A reduction in VT lowers Pbreath as well as Pbreath/Ml P, Thus, it is thought that reducing the VT helps to minimize perceived effort, respiratory distress, and dyspnea. Supporting evidence is provided by studies in animals. It is very difficult to induce overt inspiratory muscle fatigue in spontaneously breathing animals with inspiratory flow-resistive loads, even ones that are severe enough to cause acute respiratory acidosis (17-19). As soon as the inspiratory resistance is put in place, there is an immediate large reduction in VT. This subsequently leads to hypercapnia and tachypnea. It is striking to observe that even though the inspiratory resistive load remains in place, the VT can be restored promptly to normal or even above normal by administration of naloxone (17) or by bilateral cervical vagotomy (18). In other words, the animals could inspire an adequate VT through the resistance, but would not. The small VT is not the result of ventilatory load per se or of inspiratory muscle fatigue. Instead, the reduction in VT reflects an integrated respiratory system response to a ventilatory load. This response minimizes actual and perceived ventilatory effort, but predisposes to hypercapnia. To summarize, the current working hypothesis is that inspiratory muscle fatigue plays no role in the pathogenesis of chronic hypercapnia in human COPD, whereas inspiratory muscle weakness definitely does. In order for the inspiratory muscles to become fatigued, they must remain in a fatiguing pattern of breathing. This occurs infrequently in the clinical arena because the integrated re-
sponse of the respiratory system that minimizes respiratory distress also minimizes the probability that fatigue will occur. The PTI is kept below the fatigue threshold, in part by the effect that lowering the VT has on Pbreath/MIP, and in part by a decrease in Tr/Ttot (10). The data of Begin and Grassino are entirely consistent with this hypothesis. The second hypothesis is that inspiratory muscle weakness contributes significantly to perception of respiratory effort and therefore to the reduction in VT volume. That is, weakness increases Pbreath/MIP, and this triggers the signal for the integrated response that leads to the change in the pattern of breathing. The price paid for this strategy is the reduction in the size of the VT. If gas exchange is essentially normal, as in neuromuscular disease, then the small VT is well tolerated. However, when VD/VT is as high as it is in COPD, hypercapnia will occur when the VT is only slightly smaller than normal. What are the practical implications? First, it should be appreciated that chronic hypercapnia is economical because the hypercapnic patient can eliminate CO 2 with far less ventilatory effort and energy expenditure than the eucapnic COPD patient (1). Second, a variety of training techniques may relieve respiratory distress, enhance inspiratory muscle strength and endurance, and increase the capacity for physical exercise and activities of daily living. Recent reports support the hope that innovative approaches to training really can benefit COPD patients. Biofeedback relaxation techniques may help to increase the VT by reducing the perceived effort, as noted in patients weaning from mechanical ventilation (20). Strengthening the inspiratory muscles may relieve perceived respiratory effort in COPD as it does in normal subjects exposed to added inspiratory loads (21). The combination of physical exercise training and inspiratory muscle training also looks promising because it enhances both inspiratory muscle strength and the distance that can be walked in 12 minutes (22). Perhaps the optimal regimen of rehabilitation and training would utilize all three of these approaches. Whether by direct or indirect mechanisms, respiratory muscle weakness contributes to disability and hypercapnia in COPD. Research in pulmonary rehabilitation should focus on finding ways to improve the pattern of breathing by increasing the VT volume, as well as optimizing
903
EDITORIAL
regimens designed to enhance respiratory muscle strength and endurance.
F. ROCHESTER, M.D. Division of Pulmonary and Critical Care Medicine Department of Internal Medicine University of Virginia Health Sciences Center Charlottesville, VA DUDLEY
References 1. Rochester DE Effects of COPD on the respiratory muscles. In: Cherniack NS, ed. Chronic obstructive pulmonary disease. Philadelphia: W. B. Saunders Co., 1991; 134-57. 2. West JB. Causes of carbon dioxide retention in lung disease. N Engl J Med 1971; 284:1232-6. 3. Loveridge B, West P, Kryger MH, Anthonisen NR. Alteration in breathing pattern with progression of chronic obstructive pulmonary disease.Am Rev Respir Dis 1986; 134:930-4. 4. Younes, M. Load responses, dyspnea and respiratory failure. Chest 1990; 97:59S-68S. 5. Rochester DF, Braun NMT. Determinants of maximal inspiratory pressure in chronic obstructive pulmonary disease. Am Rev Respir Dis 1985;
132:42-7. 6. Farkas GA, Roussos C. Diaphragm in emphysematous hamsters: sarcomere adaptability. J Appl Physiol 1983; 54:1635-40. 7. Arora NS, Rochester DE COPD and human diaphragm muscle dimensions. Chest 1987; 91: 719-24. 8. Wheatley JR, West S, Cala SJ, Engel LA. The effect of hyperinflation of respiratory muscle work in acute induced asthma. Eur Respir J 1990; 3: 625-32. 9. BellemareF, Grassino A. Effect of pressure and timing of contraction on human diaphragm fatigue. J Appl Physiol 1982; 53:1190-5. 10. Begin P, Grassino, A. Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991; 143:905-12. 11. Bellemare F, Grassino A. Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease. J Appl Physiol 1983; 55:8-15. 12. Efthimiou J, Fleming J, Spiro SG. Sternomastoid muscle function and fatigue in breathless patients with severe respiratory disease. Am Rev Respir Dis 1987: 136:1099-105. 13. Burrows B, Saksena FB, Diener CE Carbon dioxide retention and ventilatory mechanics in chronic obstructive lung disease. Ann Intern Med 1966; 65:685-700. 14. Kafer ER. Idiopathic scoliosis. Gas exchange and the age dependence of arterial blood gases.
J Clin Invest 1976; 58:825-33. 15. Parot S, Miara B, Milic-Emili J, Gautier H. Hypoxemia, hypercapnia, and breathing pattern in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1982; 126:882-6. 16. KillianKJ, Jones NL. Respiratorymusclesand dyspnea. Clin Chest Med 1988; 9:237-48. 17. Scardella AT,Parisi RA, Phair DK, Santiago TV, Edelman NH. The role of endogenous opioids in the ventilatory response to acute flow-resistive loads. Am Rev Respir Dis 1986; 133:26-31. 18. Adams JM, Farkas GA, Rochester DE Vagal afferents, diaphragm fatigue and inspiratory resistance in the anesthetized dog. J Appl Physiol1988; 64:2279-86. 19. Ferguson GT, Irvin CG, Cherniack RM. Relationship of diaphragmatic glycogen, lactate, and function in respiratory failure. Am Rev Respir Dis 1990; 141:926-32. 20. Holliday JE, Hyers TM. The reduction of weaning time from mechanical ventilation using tidal volume and relaxation feedback. Am Rev Respir Dis 1990; 141:1214-20. 21. Redline S, Gottfried SB, Altose MD. Effects of changes in inspiratory muscle strength on the sensation of respiratory force. J Appl Physioll991; 70:240-5. 22. Zack MB, Palange AV. Oxygen supplemental exerciseof ventilatory and nonventilatory muscles in pulmonary rehabilitation. Chest 1985; 88:669-75.
Normal breathing is characterized by can be explained by passive mechanical the ease with which it is accomplished, factors alone. and by the enormous reserve capacity of COPD compromises the capacity of the respiratory muscles. In chronic ob- the respiratory muscles to sustain the venstructive pulmonary disease (COPD), the tilatory load in several ways. The combibalance between the work of breathing nation of passive and dynamic hyperinand the respiratory muscle reserve is shift- flation puts the inspiratory muscles, esed in an unfavorable direction. The work pecially the diaphragm, at a severe and energy cost of breathing are very high mechanical disadvantage (5). To some exand the capacity of the respiratory mus- tent this can be offset by the loss of sarcles to cope with the ventilatory burden comeres in the chronically shortened diis markedly attenuated (1). Thus, it is in- aphragm (6), although this mechanism tuitively attractive to hypothesize that has not yet been demonstrated concluhypercapnia is the outward clinical sively in humans with COPD (7). In any manifestation of respiratory muscle fail- case, sarcomere adaptation can restore force-generating capacity to the chroniure or fatigue. In order to examine this hypothesis cally shortened diaphragm, but it cancritically, it is helpful to review several not restore the lost capacity for shortencharacteristics of respiratory system func- ing and volume displacement. Expiratory air flow limitation prevents tion in COPD. Gas exchange is severely impaired by ventilation-perfusion im- the expiratory muscles from increasing balance (2), but the partial pressure of the VT, even if these muscles contract carbon dioxide in arterial blood (Pac02) vigorously (4). Dynamic hyperinflation can be kept normal or near normal, also may increase the burden on the inprovided that minute ventilation (VE) is spiratory muscles by imposing elastic and maintained at a sufficiently high level. threshold loads. The elastic load results Given the increase in the ratio of dead from the decrease in lung compliance at space to tidal volume (VD/VT) that is very high lung volume, and the threshcharacteristic of COPD, resting VE must old load is the result of intrinsic or autobe twice the normal level. Typically, this positive end-expiratory pressure (PEEP). is accomplished by a 50 to 100070 increase Of interest, acutely induced hyperinflain the respiratory rate, with a normal or tion in asthma did not increase inspiratory work because at high lung volume slightly increased VT (3). The problem with maintaining VE the increase in elastic work was offset by above normal is that there are significant the decrease in flow-resistive work (8). mechanical impediments to breathing. Moreover, total work per breath was deCOPD is characterized by increased re- creased by 39070 because of the marked sistance to inspiratory as well as expira- decrease in expiratory work at the high tory air flow, and passive hyperinflation lung volume. The balance between the mechanical of the lungs. These static mechanical abnormalities are not by themselves so se- impediments to breathing and the capacvere, but further mechanical limitation ity of the inspiratory muscles to cope with is caused by dynamic hyperinflation (4). them can be expressed as the ratio of the Because of the expiratory air flow limi- inspiratory pressure for a given breath tation, it takes a long time after the end (Pbreath) to maximal inspiratory presof inspiration for the lung volume to re- sure (MIP). Thus, Pbreath/MIP reflects turn to its resting level. With the increase the relative force required for inspiration. in respiratory rate, the next inspiration In like fashion, the ratio of the duration starts well before the air from the previ- of inspiration (TI) to total breath time ous breath has been expelled. As a re- (Ttot) is the fractional or relative duration sult, the lung volume increases more than of inspiration. The product of (Pbreathl AM REV RESPIR DIS 1991; 143:901-903
MIP) and (Tr/Ttot) is the pressure-time index (PTI), also referred to as the tension-time index (9). Note that Pbreath/MIP and PTI can be increased by any combination of increased resistance, decreased compliance, and inspiratory muscle weakness, and that respiratory muscle weakness consequent to metabolic and nutritional disarray is quite common in COPD (5). Note also that Pbreath is higher with large breaths and lower with small breaths. In this issue of the journal, Begin and Grassino analyze the pathophysiology of hypercapnia in relation to three physiologic characteristics of COPD: impaired gas exchange, the severity of the air flow limitation, and the force reserve of the inspiratory muscles (10). Their data were obtained from more than 300 ambulatory patients. One third of these patients were hypercapnic, but severe hypercapnia was relatively uncommon. The Pac02 was found to correlate best with (1) the increase in respiratory dead space (VD/VT); (2) air flow limitation, as reflected in the FEV 1 or total lung resistance (RL); and (3) the balance between Pbreath and MIP, as reflected by either Pbreath/MIP or RL/MIP. Begin and Grassino showed that there was an excellent correlation between Pbreath and RL, and found RL to be the best single indicator of the mechanical impediment to breathing (10). As expected, RL/MIP was higher with greater degrees of hyperinflation (which lowers MIP) and air flow limitation (which increases RL). Although the graph relating Pac02 to RL/MIP showed a wide range of Pac02 values for any given value of RL/MIP, the probability of a patient being hypercapnic rose sharply as RL/MIP increased. Being overweight and underweight, respectively, enhanced and lowered the probability of hypercapnia at any level of RL/MIP. The impact of weight on Pac0 2 can be assessed in another way. The percentage of patients who were severely underweight (body weight < 80% predicted) 901
902
must have been approximately 10070 for all three patient groups, based on the mean values and standard deviations (SD) for weight. In contrast, the percentage of patients who were markedly overweight (body weight> 130070 predicted) increased geometrically from 8070 of eucapnic, to 15% of moderately hypercapnic and 30% of severely hypercapnic patients. Surprisingly, severe underweight does not appear to be a risk factor for hypercapnia, whereas severe overweight does. Begin and Grassino found that no single variable or combination of two variables in ratio form could explain more than 35070 of the variance in Paoo, (10). Even when they expressed Paco2 as a function of as many as five independent variables, including RL, VD/VT, body weight, dynamic elastance, and MIP, the investigators could explain only half the variance in Paco2' Thus, other factors must have been involved. It seems very likely that one of these is the rapid, shallow pattern of breathing. Is inspiratory muscle fatigue the main cause of chronic hypercapnia? Probably not. Bellemare and Grassino showed that normal subjects could develop inspiratory muscle fatigue, by breathing through inspiratory airflow resistances. In order for fatigue to occur, the subjects had to achieve a pattern of breathing that caused the PTI to exceed 0.15 and maintain the tension time level for a sufficiently long time (9). Patients with COPD have a much higher PTI than normal subjects, but their PTI does not lie in the fatiguing range unless they are made to breathe more slowly and deeply than they normally choose (11). Begin and Grassino show that the PTI was higher in hypercapnic than in eucapnic COPD patients, but even in the severely hypercapnic group the PTI did not exceed the fatigue threshold (10).Moreover, overt respiratory muscle fatigue could be identified in less than 10% of COPD patients who were hospitalized for worsening dyspnea (12). How does the pattern of breathing affect CO 2 retention? Begin and Grassino point out that the ratio RL/MIP, which has the units of lIair flow, can be thought of as the inverse of ventilatory capacity (10). In effect, Paoo, rises as ventilatory capacity falls. What causes the ventilatory capacity to fall? It has been shown repeatedly that the VT is significantly smaller in hypercapnic as compared with eucapnic patients with COPD or kyphoscoliosis (3, 13-15). Begin and
EDITORIAL
Grassino also found this to be true, especially for their severely hypercapnic patients (10). The reduction in VT is largely offset by an increase in the respiratory rate, so VE is not significantly different in hypercapnic as compared with eucapnic patients. However, rapid, shallow breathing has undesirable consequences. The increased respiratory rate aggravates dynamic hyperinflation and the small VT increases VD out of proportion to the effects of ventilation-perfusion mismatch within the lung. Why does the pattern of breathing change in such a disadvantageous way? The answer to this question lies in another consequence of the increase in Pbreath/MIP. The perception of respiratory effort and dyspnea are closely linked to Pbreath/MIP, which reflects the relative force of inspiratory muscle contraction (16). A reduction in VT lowers Pbreath as well as Pbreath/Ml P, Thus, it is thought that reducing the VT helps to minimize perceived effort, respiratory distress, and dyspnea. Supporting evidence is provided by studies in animals. It is very difficult to induce overt inspiratory muscle fatigue in spontaneously breathing animals with inspiratory flow-resistive loads, even ones that are severe enough to cause acute respiratory acidosis (17-19). As soon as the inspiratory resistance is put in place, there is an immediate large reduction in VT. This subsequently leads to hypercapnia and tachypnea. It is striking to observe that even though the inspiratory resistive load remains in place, the VT can be restored promptly to normal or even above normal by administration of naloxone (17) or by bilateral cervical vagotomy (18). In other words, the animals could inspire an adequate VT through the resistance, but would not. The small VT is not the result of ventilatory load per se or of inspiratory muscle fatigue. Instead, the reduction in VT reflects an integrated respiratory system response to a ventilatory load. This response minimizes actual and perceived ventilatory effort, but predisposes to hypercapnia. To summarize, the current working hypothesis is that inspiratory muscle fatigue plays no role in the pathogenesis of chronic hypercapnia in human COPD, whereas inspiratory muscle weakness definitely does. In order for the inspiratory muscles to become fatigued, they must remain in a fatiguing pattern of breathing. This occurs infrequently in the clinical arena because the integrated re-
sponse of the respiratory system that minimizes respiratory distress also minimizes the probability that fatigue will occur. The PTI is kept below the fatigue threshold, in part by the effect that lowering the VT has on Pbreath/MIP, and in part by a decrease in Tr/Ttot (10). The data of Begin and Grassino are entirely consistent with this hypothesis. The second hypothesis is that inspiratory muscle weakness contributes significantly to perception of respiratory effort and therefore to the reduction in VT volume. That is, weakness increases Pbreath/MIP, and this triggers the signal for the integrated response that leads to the change in the pattern of breathing. The price paid for this strategy is the reduction in the size of the VT. If gas exchange is essentially normal, as in neuromuscular disease, then the small VT is well tolerated. However, when VD/VT is as high as it is in COPD, hypercapnia will occur when the VT is only slightly smaller than normal. What are the practical implications? First, it should be appreciated that chronic hypercapnia is economical because the hypercapnic patient can eliminate CO 2 with far less ventilatory effort and energy expenditure than the eucapnic COPD patient (1). Second, a variety of training techniques may relieve respiratory distress, enhance inspiratory muscle strength and endurance, and increase the capacity for physical exercise and activities of daily living. Recent reports support the hope that innovative approaches to training really can benefit COPD patients. Biofeedback relaxation techniques may help to increase the VT by reducing the perceived effort, as noted in patients weaning from mechanical ventilation (20). Strengthening the inspiratory muscles may relieve perceived respiratory effort in COPD as it does in normal subjects exposed to added inspiratory loads (21). The combination of physical exercise training and inspiratory muscle training also looks promising because it enhances both inspiratory muscle strength and the distance that can be walked in 12 minutes (22). Perhaps the optimal regimen of rehabilitation and training would utilize all three of these approaches. Whether by direct or indirect mechanisms, respiratory muscle weakness contributes to disability and hypercapnia in COPD. Research in pulmonary rehabilitation should focus on finding ways to improve the pattern of breathing by increasing the VT volume, as well as optimizing
903
EDITORIAL
regimens designed to enhance respiratory muscle strength and endurance.
F. ROCHESTER, M.D. Division of Pulmonary and Critical Care Medicine Department of Internal Medicine University of Virginia Health Sciences Center Charlottesville, VA DUDLEY
References 1. Rochester DE Effects of COPD on the respiratory muscles. In: Cherniack NS, ed. Chronic obstructive pulmonary disease. Philadelphia: W. B. Saunders Co., 1991; 134-57. 2. West JB. Causes of carbon dioxide retention in lung disease. N Engl J Med 1971; 284:1232-6. 3. Loveridge B, West P, Kryger MH, Anthonisen NR. Alteration in breathing pattern with progression of chronic obstructive pulmonary disease.Am Rev Respir Dis 1986; 134:930-4. 4. Younes, M. Load responses, dyspnea and respiratory failure. Chest 1990; 97:59S-68S. 5. Rochester DF, Braun NMT. Determinants of maximal inspiratory pressure in chronic obstructive pulmonary disease. Am Rev Respir Dis 1985;
132:42-7. 6. Farkas GA, Roussos C. Diaphragm in emphysematous hamsters: sarcomere adaptability. J Appl Physiol 1983; 54:1635-40. 7. Arora NS, Rochester DE COPD and human diaphragm muscle dimensions. Chest 1987; 91: 719-24. 8. Wheatley JR, West S, Cala SJ, Engel LA. The effect of hyperinflation of respiratory muscle work in acute induced asthma. Eur Respir J 1990; 3: 625-32. 9. BellemareF, Grassino A. Effect of pressure and timing of contraction on human diaphragm fatigue. J Appl Physiol 1982; 53:1190-5. 10. Begin P, Grassino, A. Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 1991; 143:905-12. 11. Bellemare F, Grassino A. Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease. J Appl Physiol 1983; 55:8-15. 12. Efthimiou J, Fleming J, Spiro SG. Sternomastoid muscle function and fatigue in breathless patients with severe respiratory disease. Am Rev Respir Dis 1987: 136:1099-105. 13. Burrows B, Saksena FB, Diener CE Carbon dioxide retention and ventilatory mechanics in chronic obstructive lung disease. Ann Intern Med 1966; 65:685-700. 14. Kafer ER. Idiopathic scoliosis. Gas exchange and the age dependence of arterial blood gases.
J Clin Invest 1976; 58:825-33. 15. Parot S, Miara B, Milic-Emili J, Gautier H. Hypoxemia, hypercapnia, and breathing pattern in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1982; 126:882-6. 16. KillianKJ, Jones NL. Respiratorymusclesand dyspnea. Clin Chest Med 1988; 9:237-48. 17. Scardella AT,Parisi RA, Phair DK, Santiago TV, Edelman NH. The role of endogenous opioids in the ventilatory response to acute flow-resistive loads. Am Rev Respir Dis 1986; 133:26-31. 18. Adams JM, Farkas GA, Rochester DE Vagal afferents, diaphragm fatigue and inspiratory resistance in the anesthetized dog. J Appl Physiol1988; 64:2279-86. 19. Ferguson GT, Irvin CG, Cherniack RM. Relationship of diaphragmatic glycogen, lactate, and function in respiratory failure. Am Rev Respir Dis 1990; 141:926-32. 20. Holliday JE, Hyers TM. The reduction of weaning time from mechanical ventilation using tidal volume and relaxation feedback. Am Rev Respir Dis 1990; 141:1214-20. 21. Redline S, Gottfried SB, Altose MD. Effects of changes in inspiratory muscle strength on the sensation of respiratory force. J Appl Physioll991; 70:240-5. 22. Zack MB, Palange AV. Oxygen supplemental exerciseof ventilatory and nonventilatory muscles in pulmonary rehabilitation. Chest 1985; 88:669-75.
