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The work of breathing
The American VOL. XVIII
Journal JUNE,
of Medicine
1955
Editorial The Work
of Breathing
T
chronic pulmonary congestion but not in a case with mitral stenosis without chronic pulmonary congestion. The high resting oxygen consumption of patients with diffuse pulmonary fibrosis or granulomatosis is due to increased oxygen required for respiration rather than to a systemic hypermetabolic state. In considering the mechanical work of breathing, we might first take into account the resistances which are overcome during breathing. These include the elastic resistance of the lung and chest wall; non-elastic tissue resistance, due to friction of abdominal and thoracic viscera during respiration as well as tissue viscance developed in deformation of tissues during respiration; and airway resistance, the resistance offered by the bronchopulmonary tree to air flow and the resistance developed due to the viscosity and turbulence of the gas. An additional factor, the inertia of the system, has been found to be very small. Another factor, the surface tension within the bronchopulmonary tree, becomes important in pathologic conditions such as atelectasis; an opening pressure must be developed to overcome the surface tension before air flow will occur during respiration. Theoretical analysis as well as experimental observations have made possible an understanding of the factors which influence the magnitude of these resistances, and, in turn, the effect of these resistances on respiration in normal and pathologic states. The mechanical work of breathing may be estimated by several methods. Construction of pressure-volume curves for differing tidal volumes, using the Drinker respirator and passive ventilation, makes possible measurement of the total mechanical work of respiration, Pressure-volume curves
HE work of breathing, a subject of particular interest to physiologist and clinician alike, has been intensively investigated in recent years and its relation to a variety of clinical problems brought into focus. Such studies have clarified some of the pathophysiologic mechanisms involved in mitral pulmonary emphysema and other stenosis, diseases and further have helped to clarify the therapeutic requirements. Measurement of the Work of Breathing. The work of breathing has been delineated by two separate lines of investigation, (1) measurement of the total energy required for breathing as reflected in the oxygen utilized and (2) calculation of the mechanical work from the transpulmonary pressure developed for given tidal volumes. The oxygen cost of breathing may be estimated by measuring oxygen utilized for quiet breathing and for hyperventilation. In normal man increase in oxygen utilization for small increases in ventilation is minimal and gives an estimate of the oxygen consumption per liter of ventilation at rest. Data collected with careful attention to steady state measurements establish that the oxygen cost of breathing at rest is about 0.5 cc. per liter of ventilation (about 2 per cent of resting oxygen consumption in normal man). With hyperventilation, oxygen utilization increases, slowly at first, then markedly to reach values of 10 to 15 cc. of oxygen consumed per liter increase in ventilation at 60 to 90 liters of ventilation per minute. Cournand and co-workers have demonstrated that the oxygen cost of hyperpnea is greater than normal in patients with chronic pulmonary emphysema, diffuse pulmonary granulomatosis and mitral stenosis with 8jI
Editorial derived from measurement of tidal volume and of transpulmonary pressure, i.e., the difference between the mouth pressure and that in the pleural space or at a selected level in the esophagus (as a reflection of intrapleural pressure), do not include the work done against the elastic resistance Or non-elastic tissue resistance of the chest wall. The latter technic is the one most commonly employed. Pulmonary Elastance and Comfiliance. Pulmonary elastance is the pressure required for a given volume displacement of the lung from relaxation volume, and may be expressed in the formula :
P = KV where P is the pressure developed for the displaced volume, V. K is the elastance expressed in units of P/V and is estimated by measurement of the transpulmonic pressure developed at the end of inspiration when airflow has stopped. In practice, the reciprocal of the elastance is commonly used to express the “stretchability” of the lungs. Contrary to common usage, a decrease in elastance means a more stretchable, less rigid lung. The term pulmonary compliance avoids confusion. A loss in compliance is evidence of a less “compliant” (less “stretchable”), more rigid lung. Normally, compliance is about 0.22 L. per cm. of water pressure. Work done against elastic resistance is a function of the degree of distention of the lungs and is increased to values greater than normal in patients who have less compliant lungs. Pulmonary Airway Resistance. From the pressure-volume curve, pulmonary airway resistance can be calculated. Normally it is 1.7 cm. of water per L. per second. This resistance is a function not only of the diameter of the pulmonary airways but depends also on the physical properties of the gas and the nature of its flow. Pressure required for laminar airflow is dependent on the velocity of flow, and a factor related to the viscosity of the gas P = K’V where P = the pressure required the resistance due to air viscance
to overcome (K’) for vol-
ume flow (V). Pressure required for turbulent flow is proportional to the square of volume flow times a constant related to the density of the gas: P = K+
In an irregular branching system, such as the tracheobronchopulmonary tree, turbulence plays a significant role, particularly at high rates of flow. Obstruction of inflammatory, spastic, neoplastic or exudative origin increases the turbulence considerably. Optimum Respiratory Frequency for Minimum Work of Breathing. Since pressure X volume equals work, total mechanical work of breathing may be obtained cartographically from the pressure-volume loop, or from a formula incorporating the pressure equations cited. Using the intra-esophageal pressure technic, the mechanical work done during quiet breathing is about 0.3 to 0.7 kg. M/min. For a given alveolar ventilation, at slow rates of ventilation, work done against elastic resistance comprises most of this work of breathing. As frequency increases, distention of the lungs is diminished and, since the elastic work increases as the square of the increase in volume, there is a marked fall in work done against elastic resistance for more shallow tidal volumes. More rapid respiration, however, produces an increase in work done against viscous and turbulent air resistance. Summation of the work curves for the various components gives a total work of breathing curve for a given alveolar ventilation which is high at low respiratory frequencies, falls to a minimum and rises again at higher respiratory frequencies when pulmonary airway resistance increases. This minimum point is the optimum frequency for minimum work of breathing. These facts were theoretically suggested by Rohrer and formulated by Otis, Fenn and Rahn. In normal man, Marshall, McIlroy and Christie found that elastic work during quiet breathing is about 68 per cent of the total work of breathing and the optimum frequency is about 15 per minute for an alveolar ventilation of 7.6 L. per minute (with a dead space of 210 cc.). They further demonstrated that in normal man the frequency of respiration spontaneously chosen by the subject was optimal for minimum respiratory work both at rest and for the frequency chosen during exercise. In pathologic states in which the coefficient of elastic resistance is increased it would be expected that the optimum frequency of respiration at rest would be more rapid in order to minimize the work done against elastic resistance. This has been experimentally verified by Marshall, McIlroy and Christie in patients with AMERICAN
JOURNAL
OF
MEDICINE
Editorial mitral stenosis not only during rest and exercise but for the recumbent position as well. These authors suggest that analysis of the data with respect to optimum frequency for minimum for the work “offers a teleologic explanation rapid and shallow breathing of heart disease.” Such considerations probably apply to other conditions with increased rigidity of the lungs, such as interstitial fibrosis and granulomatosis, certain cases of Boeck’s sarcoid, pulmonary beryllosis, lymphangitic carcinomatosis of the lung, and so on. Studies in normal man of the oxygen cost of hyperventilation support this concept of minimum work. Analysis of oxygen utilization versus ventilation curves reveals that at low ventilation volumes more oxygen is required for breathing at a frequency of 30 per minute compared to 20 per minute, while at high ventilation volumes the reverse is true. Mechanics of Breathing in Pathologic States. Measurements in patients with mitral stenosis and pulmonary emphysema have demonstrated an increased work of breathing. Not only is more oxygen utilized (total energy requirement), as already noted, but the mechanical work done is greater (Christie et al.). Analysis of the component factors responsible for this increased work of breathing has helped elucidate some physiologic mechanisms in disease. It has been demonstrated that pulmonary compliance correlates directly with vital capacity, body height and surface area. Pulmonary resistance varies inversely with and is less significantly related to these measurements. In patients with rheumatic heart disease in whom mitral stenosis is the predominant valvular lesion the pulmonary compliance is significantly reduced. While this reduction has been noted in patients with rheumatic heart disease with or without heart failure, the reduction is much greater in those with heart failure. Reduction in compliance may be present in patients who have no significant disability and for whom conventional vrntilatory tests give normal results. Pulmonar), resistance is increased only slightly, the increase lacing more marked when congestive heart failure is present. These changes may be found with no significant abnormalities demonstrable in conventional ventilatory fests (for example, maximum breathing capacity or timed vital capacity). In pulmonary emphysema there is often a considerable increase in pulmonary resistance, compliance being altered to a lesser extent. This confirms the conclusion drawn from JUNE,
1955
853
conventional ventilatory tests that airway obstruction is a major problem inemphysema. Caution should be used in speaking of emphy sema as a disease of “loss of elasticity of the lungs.” While the role of bronchial obstruction in this disease is very important it is not the sole cause for the increase in non-elastic resistance, as indicated by the studies of Christie and McIlroy using hydrogen in inspired gas. This gas, much less dense than ambient air, tends to reduce the turbulent resistance. The persistence of increased airway resistance under these circumstances suggests that a change in the visco-elastic properties of the lung must have taken place. It is of considerable interest that not only is pulmonary compliance altered in diseases such as mitral stenosis and congestive heart failure, in which increased lung rigidity is a familiar pathologic finding, but also in patients recovering from poliomyelitis with respiratory paralysis and in normal man under the influence of general anesthesia and neuromuscular blocking agents. This loss of compliance may limit the effectiveness of artificial ventilation in such patients. UnWork of Breathing in Relation to Dyspnea. fortunately, despite this new information the mechanisms of dyspnea are still obscure. From the studies of the oxygen cost of hyperpnea in normal man and in patients with heart and lung disease, Cournand and co-workers conclude that the increased energy required in abnormal states probably plays an important role in the development of dyspnea. McIlroy and Christie likewise suggest that the increase in the mechanical work of breathing in pulmonary emphysema “must at least be an important factor in the production of dyspnea.” An approach which is of interest in this connection is the estimation of the mechanical efficiency of respiration. This is calculated from the total energy requirement as estimated from oxygen consumption and by determining the mechanical work done for the given ventilation volume. Otis, Fenn and Rahn have calculated mechanical efficiency in normal man to be 3 to 7 per cent. Both Cournand and Comroe have suggested the importance of simultaneous determination of total energy required and mechanical work done in pathologic states. Such studies may throw some light on the_. problem of dyspnea, particularly in pulmonary emphysema and perhaps in the important problem of the dyspnea of pregnancy.
Editorial Whether or not efficiency of respiration is related to dyspnea in such lesions as pulmonary fibrosis or mitral stenosis is less predictable. Work of Breathing in Relation to Respiratory Acidosis. Analysis of the work of breathing in relation to the arterial carbon dioxide tension by Riley and by Otis has indicated that, while hyperventilation results in a fall in arterial carbon dioxide tension, there is a point beyond which further increase in alveolar ventilation results in such an increase in the work of the respiratory muscles that carbon dioxide production exceeds the rate of elimination and the arterial CO, tension will start to rise. In one normal subject this occurred at a rate of 67 L./ minute. In emphysematous patients this point (that is, the ventilation volume above which arterial CO2 tension rises instead of falls) is much lower and may account for the fact that these patients do not increase their minute volume to any extent with exercise. Galdston, using diamox@ and aminophylline as respiratory stimulants, has shown that increasing minute ventilation in patients with pulmonary emphysema caused an initial fall in the arterial CO:! tension but beyond a certain ventilation, which was not very high, the arterial CO? tension did not fall and even increased. An additional deduction derived from analysis of this problem by Riley was that the total oxygen available for non-respiratory work (in cases of hyperventilation in which patients had pulmonary emphysema) is greater at high arterial CO, tensions (for example, 60 mm. Hg) than at lower arterial CO2 tensions. From this and provocative analysis Riley interesting suggests that respiratory acidosis might be “an adaptive mechanism by which the body tolerates an increased work of breathing which would otherwise be intolerable, to the extent that breathing can be made easier.” From this point of view respiratory acidosis may be a blessing as well as a curse in patients with emphysema. It is apparent that therapeutic measures used to stimulate respiration may be disadvantageous if the work of breathing also is increased. Measures designed to reduce the work of breathand artificial ing, such as bronchodilators ventilation, and prompt treatment of pulmonary infection still offer the best therapeutic approach to the problem of pulmonary emphysema. It is clear that these investigations of the mechanics of respiration have changed some concepts derived from older conventional pul-
monary function studies, and have afforded a new understanding of other problems. Most important, they have uncovered as many problems as they have solved. MORTIMER E. BADER, M.D. RICHARD A. BADER, M.D. The Mount Sinai Hospital, New York, New York REFERENCES 1. BAYLISS, L. E. and ROBERTSON, G. W. The visco-
2.
3.
4.
5. 6. 7. 8. 9.
10.
il. 12.
13.
14.
15. 16. 17.
18.
elastic properties of the lungs. Quart. J. Exper. Physiol., 29: 27, 1939. CHRISTIE, R. V. Dyspnea in relation to the viscoelastic properties of the lung. Pm. Roy. SW. Med., 46: 381, 1953. COMROE, J. H., JR., FORSTER, R. E., II, DUBOIS,A. B., BRISCOE, W. A. and CARLSEN, E. The lung; clinical physiology and pulmonary function tests, pp. 110-141. Chicago, 1955. The Year Book Publishers. COURNAND,A., RICHARDS,D. W., JR., BADER, R. A., BADER, M. E. and FISHMAN,A. P. The oxygen cost of breathing. Tr. A. Am. Phylsicians, 67: 162, 1954. DEAN, R. B. and VISSCHER, M. B. The kinetics of lung ventilation. Am. J. Physiol., 134: 450, 1941. FENN, W. 0. Mechanics of respiration. Am. J. Mfd., 10: 77, 1951. GALDSTON,M. Personal communication. LILJESTRAND, G. Untersuchungen ueber Atmungsarbeit. Skandinav. Arch. f. Physiol., 35: 199, 1918. MARSHALL,R., MCILROY, M. B. and CHRISTIE, R. V. The work of breathing in mitral stenosis. Clin. SC., 13: 137, 1954. MCILROY, M. B., MARSHALL,R. and CHRISTIE, R. V. The work of breathing in normal subjects. Clin. SC., 13: 127, 1954. MCILROY, M. B. and CHRISTIE, R. V. The work of breathing in emphysema. Clin. SC., 13: 147, 1954. MEAD, J. and WHITTENBERCER, J. L. Physical properties of human lungs measured during spontaneous respiration. J. Appl. Physiol., 5: 779. 1953. MEAD, J., FRANK, N. R., LINDCREN, I., GAENSLER, A. E. and WHITTENBERGER,J. L. A technic for the measurement of pulmonary compliance and resistance; its application to normal patients and patients with mitral stenosis. Proc. Am, Federation Clin. Research (National Meeting), abst. 90, 1953. NEERGAARD, K. and WIRZ, K. Uber eine Methode zur Messung der Lungenelastizitlt am lebenden Menschen, insbesondere beim Emphysem. Ztschr. klin. Med., 105: 35, 1927. OTIS, A. B. The work of breathing. Physiol. Reo., 34: 449,1954. OTIS, A. B., FENN, W. 0. and RAHN, H. Mechanics of breathing in man. J. A@. Physiol., 2: 592, 1950. RAHN, H., OTIS, A. B., CHADWICK,L. F. and FENN, W. 0. The pressure volume diagram of the lung and thorax. Am. J. Physiol., 146: 161, 1946. ROHRER, F. Der Striimungswiderstand in den menschlichen Atemwegen und der Einfluss der unregelmksigen Verzweigung der Bronchialsysverschiedene terns auf den Atmungsverlauf Lungenbezirken. Arch. f. d. ges. Physiol., 162: 225, 1915. AMERICAN
JOURNAL
OF MEDICINE
Journal JUNE,
of Medicine
1955
Editorial The Work
of Breathing
T
chronic pulmonary congestion but not in a case with mitral stenosis without chronic pulmonary congestion. The high resting oxygen consumption of patients with diffuse pulmonary fibrosis or granulomatosis is due to increased oxygen required for respiration rather than to a systemic hypermetabolic state. In considering the mechanical work of breathing, we might first take into account the resistances which are overcome during breathing. These include the elastic resistance of the lung and chest wall; non-elastic tissue resistance, due to friction of abdominal and thoracic viscera during respiration as well as tissue viscance developed in deformation of tissues during respiration; and airway resistance, the resistance offered by the bronchopulmonary tree to air flow and the resistance developed due to the viscosity and turbulence of the gas. An additional factor, the inertia of the system, has been found to be very small. Another factor, the surface tension within the bronchopulmonary tree, becomes important in pathologic conditions such as atelectasis; an opening pressure must be developed to overcome the surface tension before air flow will occur during respiration. Theoretical analysis as well as experimental observations have made possible an understanding of the factors which influence the magnitude of these resistances, and, in turn, the effect of these resistances on respiration in normal and pathologic states. The mechanical work of breathing may be estimated by several methods. Construction of pressure-volume curves for differing tidal volumes, using the Drinker respirator and passive ventilation, makes possible measurement of the total mechanical work of respiration, Pressure-volume curves
HE work of breathing, a subject of particular interest to physiologist and clinician alike, has been intensively investigated in recent years and its relation to a variety of clinical problems brought into focus. Such studies have clarified some of the pathophysiologic mechanisms involved in mitral pulmonary emphysema and other stenosis, diseases and further have helped to clarify the therapeutic requirements. Measurement of the Work of Breathing. The work of breathing has been delineated by two separate lines of investigation, (1) measurement of the total energy required for breathing as reflected in the oxygen utilized and (2) calculation of the mechanical work from the transpulmonary pressure developed for given tidal volumes. The oxygen cost of breathing may be estimated by measuring oxygen utilized for quiet breathing and for hyperventilation. In normal man increase in oxygen utilization for small increases in ventilation is minimal and gives an estimate of the oxygen consumption per liter of ventilation at rest. Data collected with careful attention to steady state measurements establish that the oxygen cost of breathing at rest is about 0.5 cc. per liter of ventilation (about 2 per cent of resting oxygen consumption in normal man). With hyperventilation, oxygen utilization increases, slowly at first, then markedly to reach values of 10 to 15 cc. of oxygen consumed per liter increase in ventilation at 60 to 90 liters of ventilation per minute. Cournand and co-workers have demonstrated that the oxygen cost of hyperpnea is greater than normal in patients with chronic pulmonary emphysema, diffuse pulmonary granulomatosis and mitral stenosis with 8jI
Editorial derived from measurement of tidal volume and of transpulmonary pressure, i.e., the difference between the mouth pressure and that in the pleural space or at a selected level in the esophagus (as a reflection of intrapleural pressure), do not include the work done against the elastic resistance Or non-elastic tissue resistance of the chest wall. The latter technic is the one most commonly employed. Pulmonary Elastance and Comfiliance. Pulmonary elastance is the pressure required for a given volume displacement of the lung from relaxation volume, and may be expressed in the formula :
P = KV where P is the pressure developed for the displaced volume, V. K is the elastance expressed in units of P/V and is estimated by measurement of the transpulmonic pressure developed at the end of inspiration when airflow has stopped. In practice, the reciprocal of the elastance is commonly used to express the “stretchability” of the lungs. Contrary to common usage, a decrease in elastance means a more stretchable, less rigid lung. The term pulmonary compliance avoids confusion. A loss in compliance is evidence of a less “compliant” (less “stretchable”), more rigid lung. Normally, compliance is about 0.22 L. per cm. of water pressure. Work done against elastic resistance is a function of the degree of distention of the lungs and is increased to values greater than normal in patients who have less compliant lungs. Pulmonary Airway Resistance. From the pressure-volume curve, pulmonary airway resistance can be calculated. Normally it is 1.7 cm. of water per L. per second. This resistance is a function not only of the diameter of the pulmonary airways but depends also on the physical properties of the gas and the nature of its flow. Pressure required for laminar airflow is dependent on the velocity of flow, and a factor related to the viscosity of the gas P = K’V where P = the pressure required the resistance due to air viscance
to overcome (K’) for vol-
ume flow (V). Pressure required for turbulent flow is proportional to the square of volume flow times a constant related to the density of the gas: P = K+
In an irregular branching system, such as the tracheobronchopulmonary tree, turbulence plays a significant role, particularly at high rates of flow. Obstruction of inflammatory, spastic, neoplastic or exudative origin increases the turbulence considerably. Optimum Respiratory Frequency for Minimum Work of Breathing. Since pressure X volume equals work, total mechanical work of breathing may be obtained cartographically from the pressure-volume loop, or from a formula incorporating the pressure equations cited. Using the intra-esophageal pressure technic, the mechanical work done during quiet breathing is about 0.3 to 0.7 kg. M/min. For a given alveolar ventilation, at slow rates of ventilation, work done against elastic resistance comprises most of this work of breathing. As frequency increases, distention of the lungs is diminished and, since the elastic work increases as the square of the increase in volume, there is a marked fall in work done against elastic resistance for more shallow tidal volumes. More rapid respiration, however, produces an increase in work done against viscous and turbulent air resistance. Summation of the work curves for the various components gives a total work of breathing curve for a given alveolar ventilation which is high at low respiratory frequencies, falls to a minimum and rises again at higher respiratory frequencies when pulmonary airway resistance increases. This minimum point is the optimum frequency for minimum work of breathing. These facts were theoretically suggested by Rohrer and formulated by Otis, Fenn and Rahn. In normal man, Marshall, McIlroy and Christie found that elastic work during quiet breathing is about 68 per cent of the total work of breathing and the optimum frequency is about 15 per minute for an alveolar ventilation of 7.6 L. per minute (with a dead space of 210 cc.). They further demonstrated that in normal man the frequency of respiration spontaneously chosen by the subject was optimal for minimum respiratory work both at rest and for the frequency chosen during exercise. In pathologic states in which the coefficient of elastic resistance is increased it would be expected that the optimum frequency of respiration at rest would be more rapid in order to minimize the work done against elastic resistance. This has been experimentally verified by Marshall, McIlroy and Christie in patients with AMERICAN
JOURNAL
OF
MEDICINE
Editorial mitral stenosis not only during rest and exercise but for the recumbent position as well. These authors suggest that analysis of the data with respect to optimum frequency for minimum for the work “offers a teleologic explanation rapid and shallow breathing of heart disease.” Such considerations probably apply to other conditions with increased rigidity of the lungs, such as interstitial fibrosis and granulomatosis, certain cases of Boeck’s sarcoid, pulmonary beryllosis, lymphangitic carcinomatosis of the lung, and so on. Studies in normal man of the oxygen cost of hyperventilation support this concept of minimum work. Analysis of oxygen utilization versus ventilation curves reveals that at low ventilation volumes more oxygen is required for breathing at a frequency of 30 per minute compared to 20 per minute, while at high ventilation volumes the reverse is true. Mechanics of Breathing in Pathologic States. Measurements in patients with mitral stenosis and pulmonary emphysema have demonstrated an increased work of breathing. Not only is more oxygen utilized (total energy requirement), as already noted, but the mechanical work done is greater (Christie et al.). Analysis of the component factors responsible for this increased work of breathing has helped elucidate some physiologic mechanisms in disease. It has been demonstrated that pulmonary compliance correlates directly with vital capacity, body height and surface area. Pulmonary resistance varies inversely with and is less significantly related to these measurements. In patients with rheumatic heart disease in whom mitral stenosis is the predominant valvular lesion the pulmonary compliance is significantly reduced. While this reduction has been noted in patients with rheumatic heart disease with or without heart failure, the reduction is much greater in those with heart failure. Reduction in compliance may be present in patients who have no significant disability and for whom conventional vrntilatory tests give normal results. Pulmonar), resistance is increased only slightly, the increase lacing more marked when congestive heart failure is present. These changes may be found with no significant abnormalities demonstrable in conventional ventilatory fests (for example, maximum breathing capacity or timed vital capacity). In pulmonary emphysema there is often a considerable increase in pulmonary resistance, compliance being altered to a lesser extent. This confirms the conclusion drawn from JUNE,
1955
853
conventional ventilatory tests that airway obstruction is a major problem inemphysema. Caution should be used in speaking of emphy sema as a disease of “loss of elasticity of the lungs.” While the role of bronchial obstruction in this disease is very important it is not the sole cause for the increase in non-elastic resistance, as indicated by the studies of Christie and McIlroy using hydrogen in inspired gas. This gas, much less dense than ambient air, tends to reduce the turbulent resistance. The persistence of increased airway resistance under these circumstances suggests that a change in the visco-elastic properties of the lung must have taken place. It is of considerable interest that not only is pulmonary compliance altered in diseases such as mitral stenosis and congestive heart failure, in which increased lung rigidity is a familiar pathologic finding, but also in patients recovering from poliomyelitis with respiratory paralysis and in normal man under the influence of general anesthesia and neuromuscular blocking agents. This loss of compliance may limit the effectiveness of artificial ventilation in such patients. UnWork of Breathing in Relation to Dyspnea. fortunately, despite this new information the mechanisms of dyspnea are still obscure. From the studies of the oxygen cost of hyperpnea in normal man and in patients with heart and lung disease, Cournand and co-workers conclude that the increased energy required in abnormal states probably plays an important role in the development of dyspnea. McIlroy and Christie likewise suggest that the increase in the mechanical work of breathing in pulmonary emphysema “must at least be an important factor in the production of dyspnea.” An approach which is of interest in this connection is the estimation of the mechanical efficiency of respiration. This is calculated from the total energy requirement as estimated from oxygen consumption and by determining the mechanical work done for the given ventilation volume. Otis, Fenn and Rahn have calculated mechanical efficiency in normal man to be 3 to 7 per cent. Both Cournand and Comroe have suggested the importance of simultaneous determination of total energy required and mechanical work done in pathologic states. Such studies may throw some light on the_. problem of dyspnea, particularly in pulmonary emphysema and perhaps in the important problem of the dyspnea of pregnancy.
Editorial Whether or not efficiency of respiration is related to dyspnea in such lesions as pulmonary fibrosis or mitral stenosis is less predictable. Work of Breathing in Relation to Respiratory Acidosis. Analysis of the work of breathing in relation to the arterial carbon dioxide tension by Riley and by Otis has indicated that, while hyperventilation results in a fall in arterial carbon dioxide tension, there is a point beyond which further increase in alveolar ventilation results in such an increase in the work of the respiratory muscles that carbon dioxide production exceeds the rate of elimination and the arterial CO, tension will start to rise. In one normal subject this occurred at a rate of 67 L./ minute. In emphysematous patients this point (that is, the ventilation volume above which arterial CO2 tension rises instead of falls) is much lower and may account for the fact that these patients do not increase their minute volume to any extent with exercise. Galdston, using diamox@ and aminophylline as respiratory stimulants, has shown that increasing minute ventilation in patients with pulmonary emphysema caused an initial fall in the arterial CO:! tension but beyond a certain ventilation, which was not very high, the arterial CO? tension did not fall and even increased. An additional deduction derived from analysis of this problem by Riley was that the total oxygen available for non-respiratory work (in cases of hyperventilation in which patients had pulmonary emphysema) is greater at high arterial CO, tensions (for example, 60 mm. Hg) than at lower arterial CO2 tensions. From this and provocative analysis Riley interesting suggests that respiratory acidosis might be “an adaptive mechanism by which the body tolerates an increased work of breathing which would otherwise be intolerable, to the extent that breathing can be made easier.” From this point of view respiratory acidosis may be a blessing as well as a curse in patients with emphysema. It is apparent that therapeutic measures used to stimulate respiration may be disadvantageous if the work of breathing also is increased. Measures designed to reduce the work of breathand artificial ing, such as bronchodilators ventilation, and prompt treatment of pulmonary infection still offer the best therapeutic approach to the problem of pulmonary emphysema. It is clear that these investigations of the mechanics of respiration have changed some concepts derived from older conventional pul-
monary function studies, and have afforded a new understanding of other problems. Most important, they have uncovered as many problems as they have solved. MORTIMER E. BADER, M.D. RICHARD A. BADER, M.D. The Mount Sinai Hospital, New York, New York REFERENCES 1. BAYLISS, L. E. and ROBERTSON, G. W. The visco-
2.
3.
4.
5. 6. 7. 8. 9.
10.
il. 12.
13.
14.
15. 16. 17.
18.
elastic properties of the lungs. Quart. J. Exper. Physiol., 29: 27, 1939. CHRISTIE, R. V. Dyspnea in relation to the viscoelastic properties of the lung. Pm. Roy. SW. Med., 46: 381, 1953. COMROE, J. H., JR., FORSTER, R. E., II, DUBOIS,A. B., BRISCOE, W. A. and CARLSEN, E. The lung; clinical physiology and pulmonary function tests, pp. 110-141. Chicago, 1955. The Year Book Publishers. COURNAND,A., RICHARDS,D. W., JR., BADER, R. A., BADER, M. E. and FISHMAN,A. P. The oxygen cost of breathing. Tr. A. Am. Phylsicians, 67: 162, 1954. DEAN, R. B. and VISSCHER, M. B. The kinetics of lung ventilation. Am. J. Physiol., 134: 450, 1941. FENN, W. 0. Mechanics of respiration. Am. J. Mfd., 10: 77, 1951. GALDSTON,M. Personal communication. LILJESTRAND, G. Untersuchungen ueber Atmungsarbeit. Skandinav. Arch. f. Physiol., 35: 199, 1918. MARSHALL,R., MCILROY, M. B. and CHRISTIE, R. V. The work of breathing in mitral stenosis. Clin. SC., 13: 137, 1954. MCILROY, M. B., MARSHALL,R. and CHRISTIE, R. V. The work of breathing in normal subjects. Clin. SC., 13: 127, 1954. MCILROY, M. B. and CHRISTIE, R. V. The work of breathing in emphysema. Clin. SC., 13: 147, 1954. MEAD, J. and WHITTENBERCER, J. L. Physical properties of human lungs measured during spontaneous respiration. J. Appl. Physiol., 5: 779. 1953. MEAD, J., FRANK, N. R., LINDCREN, I., GAENSLER, A. E. and WHITTENBERGER,J. L. A technic for the measurement of pulmonary compliance and resistance; its application to normal patients and patients with mitral stenosis. Proc. Am, Federation Clin. Research (National Meeting), abst. 90, 1953. NEERGAARD, K. and WIRZ, K. Uber eine Methode zur Messung der Lungenelastizitlt am lebenden Menschen, insbesondere beim Emphysem. Ztschr. klin. Med., 105: 35, 1927. OTIS, A. B. The work of breathing. Physiol. Reo., 34: 449,1954. OTIS, A. B., FENN, W. 0. and RAHN, H. Mechanics of breathing in man. J. A@. Physiol., 2: 592, 1950. RAHN, H., OTIS, A. B., CHADWICK,L. F. and FENN, W. 0. The pressure volume diagram of the lung and thorax. Am. J. Physiol., 146: 161, 1946. ROHRER, F. Der Striimungswiderstand in den menschlichen Atemwegen und der Einfluss der unregelmksigen Verzweigung der Bronchialsysverschiedene terns auf den Atmungsverlauf Lungenbezirken. Arch. f. d. ges. Physiol., 162: 225, 1915. AMERICAN
JOURNAL
OF MEDICINE