Management of impaired respiratory function

Management

JAMES

L. WHITTENBERGER,

From tbe Department of Physiology, Public

Health,

of Impaired Function M.D.,

Harvard School of

INCE

AmericanJournalofSurgery,Volume 90,October, 1931

Boston, Massachusetts

incIude + IO or 15 per cent of the mean vaIuc based on a popuIation previousIy studied. Since a patient is his own best contro1, the patient’s symptoms may be the most sensitive guide to the adequacy of respiratory performance. The diffIcuIty in interpreting this estimate is the impossibility of measuring a subjective evaluation. Thus an athIete in the earIy stages of diffuse puImonary disease may note that dyspnea occurs at a high Ievel of physical activity which was not previousIy associated with dyspnea. AI1 puImonary function tests may give results “above normaI” yet such a patient’s symptom must obviousIy be taken seriousIy. At the same time his symptom of dyspnea cannot be quantitativeIy compared with the dyspnea sensed by a semi-invaIid. With the foregoing reservations in mind, one can propose that impaired respiratory function wiI1 be understood to mean a significant reduction of respiratory reserve, a loss which an average patient wouId recognize in the course of his usua1 activities. At Ieast one of severa types of puImonary function tests wouId be expected to be significantly beIow the “norma1 ” Iimits. Impairment can occur in one or more of the artificially separabIe components of respiration. It shouId be emphasized, however, that respiratory impairment is more profitably examined from the point of view of integrated respiratory and circuIatory activities. To keep the arterial bIood gases normaI, the air must go where the bIood is and both must have the same rate of repIenishment. To be sure, diseases attack primarily one system or the other; in uncompIicated asthma the pulmonary probIem starts as one in respiratory mechanics. In a later and extreme form of asthma, or in emphysema associated with chronic bronchitis, non-uniform aIveoIar ventiIation is combined with nonuniform aIveoIar perfusion in a system in which large forces are necessary to drive both air and bIood.

Boston, Massachusetts.

impaired respiratory function may occur in neuromuscuIar, cardiac and other diseases in which puImonic effects are not primary, it is necessary to Iimit the scope of this articIe. DiffIcuIties remain even if discussion is restricted to chronic puImonary disease of nonspecific origin. A precise definition of impaired respiratory function cannot be given without detaiIed consideration of cardiorespiratory physioIogy and the reIationship between respiratory demand and respiratory capabiIities; consequentIy onIy a working definition wiII be proposed. In spite of intense interest in the measurement of puImonary function over a period of years, it must be admitted that only crude information is provided by the usua1 battery of puImonary function tests done on a given patient. Microscopic examination, if possible, wouId revea1 many Iesions which are undetectabIe by the best standardized tests. Even radiography, vaIuabIe though it is, can be quite misIeading from a functiona point of view. Two basic causes underIie shortcomings in the interpretation of puImonary function tests; one is the Iack of suff%ientIy precise standards of reference, the other is the integration of respiratory and circuIatory function at the microscopic IeveI, with the result that disturbances in one system Iead automaticaIIy to compensatory adjustments in the other. In other words, if ventiIation of a IobuIe is impaired, circuIation is aIso reduced; with passage of time this compensation is often compIete, and functionaIIy the Iung has mereIy Iost a part of its substance. If standards of reference were suffIcientIy good, the Ioss might be detected. In general, however, a given vaIue must be compared with a “normaI” range which may

S

Respiratory

648

Impaired Since the latter type ment is probably most likely to increase in the most consideration in follows. PREVENTION

OF

Respiratory

obscured by the popuIation.

of pulmonary impaircommon today and is future, it will receive the discussion which

RESPIRATORY

Function

CONTROL

OF

losses

to senescence

RESPIRATORY

in our

IMPAIRMENT

The next stage in the management of respiratory impairment is the arrest of disease and preservation of function. There is, of course, overlap between this and the earlier and Iater stages of management. For example, in cases in which evidence of industrial pneumoconiosis is present, the worker wouId be removed as effectiveIy as possible from the source of exposure. Having corrected environmentaI factors to the extent possibIe, attention shouId be directed toward the respiratory and genera1 hygiene of the patient. Respiratory infections, although not avoidabIe, shouId be treated more diIigentIy in this type of patient. In more seriously ill patients respiratory infections are notorious13 IikeIy to deveIop into respiratory failure and even death.gr lo Since tobacco smoke is an irritant, avoidance shouId be encouraged. Preservation of respiratory function requires, in addition, a consideration of respiratory demand. The norma respiratory response to muscuIar exercise is an exceIIentIy adjusted increase of respiratory minute voIume in proportion to the increased metaboIic demands of the body. In states of anxietv, fatigue or poor fitness due to lack of exercise or other factors the respiratory response is exaggerated out of proportion to the metaboIic increase, and excess respiratory effort is often associated with pronounced awareness of breathing or dyspnea. The respiratory muscles themseIves may be “ unfit,” although this would be diff&It to establish. A similar reaction may develop in patients with puImonary disease who are UnnecessariIy restricted by doctor’s orders or their own fears and lack of motivation. As in the case of physical fitness in general, activity and stress breed fitness; inactivity inevitabIy corrodes fitness. Therefore, it appears wise to encourage the habits of regular exercise and other physical activities, incIuding work, up to the limit of tolerance. General measures such as maintenance of normal or less than average weight should also be undertaken.

DISEASE

The logical beginning of the management of respirator,v impairment is the prevention of respiratory disease. Much has been accomplished in the control of industrial lung diseases, although severe probIems remain, as in coal miners’ pneumoconioses.‘v2 The extent to which chronic puImonary disease in the general population is preventabIe is not known. Some experience suggests that industrial air poIIution may contribute to the incidence and severity of chronic puImonary disease; Flint found that the most common etiologic type of heart disease in an English industria1 city was car puImonaIe;” Pemberton and GoIdberg found a significant correlation between air poIIution and deaths from bronchitis.4 Furthermore, there was a high incidence of deaths among patients with chronic puImonary diseases in the 1952 smog episode in London.5 If this relationship is established, a preventabIe type of pulmonary disease will have been uncovered; the cost of prevention has not been estimated. Circumstantial evidence suggests that the incidence of puImonary neopIasms could be substantially reduced if more people were to stop smoking.‘+* Whether other pulmonary diseases are associated with tobacco smoking has not been proved. PuImonary function tests have been quite disappointing to those who have attempted to estabIish such a reIationship. On the other hand there is IittIe doubt that some cases of chronic cough associated with chronic puruIent expectoration cIear up when the habit of smoking is terminated. U’hether this kind of chronic bronchial irritation is associated with more serious puImonary disease is not known. Despite its effective protective mechanisms, the respiratory system is basically a Iarge and delicate membrane in close contact with the atmospheric environment. Chemical, physical and microbiologic invaders of the Iungs must leave their marks in injury and repair, and these must accumuIate with age. AIso the senescent processes of elastic and coIIagenous tissues are not in abeyance in the lungs. Consrquently the gains in prevention may be

MEDICAL

This medical 649

TREATMENT

AND

REHABILITATION

articIe is not intended to deal with management of specific etiologic dis-

Whittenberger lung disease; and if puImonary hypertension is present, the distensibiIity of the lungs may in turn be inff uenced by the turgor of the vascuIar bed. Lastly, as emphysematous Iung disease progresses the over-a11 lung voIume increases, the diaphragm descends and respiratory muscles operate under poor mechanica conditions. Beset by these mechanica probIems the respiratory muscIes carry out with difficulty their function of providing adequate aIveoIar ventilation. It should cause IittIe wonder, then, that pulmonary infections cause respiratory failure by increasing metaboIic demands at the same time they further impede the respiratory muscIes by accentuating air4 ow resistance and diminishing lung distensibiIity. NevertheIess the use of externa1 aids to Iessen respiratory effort has not been promoted unti1 recentIy. Motley and his associates” found that patients were benefited by bronchodiIator aerosoIs and 0% given by means of specia1 pressure breathing devices. These devices gave adjustabIe degrees of inspiratory positive pressure in a face mask, were cycIed from one phase of respiration to the other by the patient and had a high flow capacity, thus satisfying the inspiratory demand of even dyspneic patients. Other investigators have also been impressed with the vaIue of this therapeutic regimen. However, it is not easy to separate the effects of the bronchodilator and O2 from those of the pressure breathing. In other words, couId a patient breathing deeply by effort of his own muscIes obtain the same benefit from bronchodiIator aerosols and 02? FowIer, HeImhoIz and MiIIer12 compared the effects of bronchodiIators and 02 with and without pressure breathing, in a group of patients with chronic puImonary disease. They found definite improvement with bronchodiIators and O2 but were unabIe to establish a significant effect for the pressure breathing itseIf. It appears IikeIy that if a patient is capable of moving his Iungs through a sufficient voIume range, he can obtain resuIts from 02 and bronchodiIators similar to those obtained with the aid of a pressure-breathing device. The vaIue of positive pressure wouId therefore be in assisting the patient to breathe deeply to a IeveI of Iung distention which he was unable or unwiIIing to achieve by his own efforts. Pressure-breathing devices in genera1 cause hyperventiIation, and this effect is desirabIe in a patient bordering on hypoventilation. Other Mechanical Adjuncts. In the more

ease types such as puImonary tubercuIosis, neopIasms, ahergic asthma, etc. Some of the measures recommended for treatment of impaired respiratory function wiI1 naturaIIy, however, appIy to certain stages of such diseases. As in most diseases the importance of psychoIogic factors should not be underestimated. Strong motivation is effective compensation for even severe physica handicaps in respiratory function. Confidence in the physician and the power of suggestion can benefit the patient when medications and physica therapy are of no objectiveIy determinabIe merit whatever. This fact makes the evaIuation of a therapeutic agent or method a diffrcuIt one indeed. BroncrSodilators. The abnorma1 distribution of ventiIation and increased air-flow resistance which characterize emphysematous changes in the Iungs often appear to have a functional component. The administration of bronchodiIator agents frequentIy has the effect of diminishing air-flow resistance and improving respiratory function. Ephedrine, epinephrine, and other sympathomimetic drugs are effective. Agents such as isupreI@ (I-3’4’-dihydroxyphenyI-2-isopropyIaminoethano1 hydrochIoride, I : 200) can be administered as aerosols either aIone or in conjunction with 02 therapy. By diminishing bronchospasm these drugs provide the accomplishment of two objectives: the distribution of puImonary ventiIation is improved by reduction of the number of high resistance pathways; the respiratory muscIes need deveIop Iess force to provide a given rate of air flow-respiratory effort and work are diminished. of disPressure Breathing. The mechanics eased Iungs are very compIex. Not onIy are the primary eIements of mechanica behaviour abnormaI, but aIso the degree of invoIvement is highly variable throughout the Iungs. The IocaI nature of blebs and cysts and the patchy character of emphysema, ateIectasis and hbrosis make functiona evahlation of the lungs as a whole quite diffrcuIt. As mentioned previousIy resistance to air how is increased. This resuIts in an increase of the work of breathing and, if high resistance is not uniform, a distortion of ventiIation distribution. DistensibiIity of the Iungs is aIso reduced, in part because of Ioss of Iung substance and in part because the high resistance pathways effectiveIy bIock some portions of the Iungs from ventiIation. The circuIation through the Iungs may be affected by the 650

Impaired

Respiratory

severe phases of chronic emphysema, severa measures can be undertaken to improve puImonary ventilation, none of which alters the basic disturbances in the lung parenchyma but which permit the respiratory muscIes to work more effectively. Breathing exercises promote the effectiveness of both diaphragmatic and intercostal muscles; abdomina1 beIts and pneumoperitoneum elevate the diaphragm to a more favorable position. Without training, one is usually unaware of the extent to which diaphragm, abdominal, intercostal, and accessory muscIes participate in the respiratory movements. With conscious effort these muscIes can be controlled and more effective use can be made of them in cases of emphysema. Furthermore, trunk movements such as spinal extension are known to cause ventiIation of the lungs in apneic individuaIs.ra Changes of posture, arm and trunk movements, and respiratory muscle re-education may a11 be used to advantage in breathing exercises for patients with emphysema.10~14~15 Elastic and pneumatic abdomina1 beIts tend to compress the abdomen and force the diaphragm upward. Although the mechanica advantage of the diaphragm is thereby increased, the work which has to be done on inspiration is at the same time increased, and the difficulty of distending the abdomen becomes progressively greater as inspiration proceeds. IdeaIIy the abdomina1 waI1 shouId be relaxed on inspiration and compressed only on expiration. That abdominal beIts are not a complete solution to the problem of disturbed mechanics is suggested by the fact that some patients appear to be greatly benefited; others are not helped at all. Pneumoperitoneum has been advocated for the same purpose as abdomina1 beIts.16-18 Beneficial results are diffrcuIt to predict in a given patient. The increase of tracheobronchia1 secretions bvhich may accompany infections, chemical irritant exposure or autonomic nervous activity suggests the importance of tracheobronchia1 drainage. Most of the therapeutic measures mentioned have been said to promote bronchial drainage. Similar claims are made for the use of detergent and proteoIytic enzyme aerosoIs, expectorant and other cough mixtures. AI1 of these observations may be valid, but it is disappointing that there have been few efforts to make an objective and quantitative comparison of different therapeutic methods.

Function

Recently Barach and his associates have deveIoped methods for imitating certain features of a cough. lg If the method is found to be suf&cientIy safe, it might be of significant vaIue in preventing postoperative puImonary complications in post-thoracotomy patients who are incapabIe of coughing effectiveIy. The machine is connected to the patient by a face mask or mouthpiece; a high-flow capacity vacuum bIower is arranged with valves so that a sIowIy rising inspiratory mask pressure is converted instantIy to a subatmospheric expiratory phase. Thus a high rate of air flow is made to occur at the beginning of expiration. The Iungs must be we11 distended on inspiration. This is accomphshed by raising the airway pressure to 30 or 40 mm. Hg. Since this IeveI of static intrapuImonary pressure has been found to produce emphysema in experimenta animaIszO its use should be undertaken with caution in postsurgica1 patients. Oxygen Therapy. Reduction of alveolar ventilation by progressive disease and the continuation of blood flow to poorIy ventilated alveoli lead eventuahy to the inadequacy of arterial O2 tension and the need for 02 enrichment of the inspired air. This is particularly IikeIy to occur during exacerbations of bronchopuImonary infections. Administration of 02 in these circumstances often is known to be unsatisfactory and sometimes dangerous.21 Basically the probIem is one of respiratory control mechanisms in which the patient’s ventiIatory drive has become blunted to CO2 concentration and is dependent on the presence of anoxemia. Administration of 0s in severe cases of this type removes the stimulus to breathe just as sureIy as if morphine or other respiratory depressants were administered in the presence of a depressed respiratorv center. Although minimal O2 administration has been recommended for these cases, it appears wise to direct attention first to other measures which will improve ventilation of the lungs. These measures include vigorous use of bronchodilators, antibiotics (for pulmonary infections which are often inapparent), postural drainage and mechanical aids to ventilation, if avaiIabIe. If adequate puImonary ventilation is assured by a mechanical apparatus or is known to occur by measurement of the patient’s unassisted ventilation, then 02 can be given in the concentration required to relieve anoxia. Otber Forms of Therapy. When respiratory impairment is sufficient to cause retention of

Whittenberger 5. Lotinq

W. I’. D. Mortality in the L.ondon fog incident, 1952. Luncel, I : 336, 1953. 6. DOLL, R. and HILL, A. B. A study of the aetiology of carcinoma of the lung. Brit. M. J., 2: 1271,

CO2 the patient is not only subject to the hazard of further respiratory depression but is also the victim of symptoms associated with CO2 itseIf. The latter reIate particularly to functions of the central nervous system. Such patients are improved by measures which lower the body levels of CO,. A chemica1 means for promoting CO? elimination is avaiIable in the form of a carbonic anhydrase inhibitor (diamox@) (2 acetvlamino-r,-3,4-thiadiazoIe-psulfonamide). This drug affects renal function, Ieading to excess excretion of sodium and CO2 (as bicarbonate).?? The Iowering of bIood CO2 and metabolic acidosis which result are accompanied by a sIight elevation of alveoIar ventiIation and Iowering of arteria1 CO, tension. The drug has given encouraging resuIts in the contro1 of chronic emphvsema with CO2 retention. Cortisonk and adrenocorticotropic hormone have demonstrated their vaIue in the control of bronchial asthma and bronchospastic crises of emphysema. 23 However, the genera1 metaboIic and endocrine effects of these drugs are such that they shouId be used CircumspectIy, infrequentIy and only when simpler bronchodiIators have failed.

1952. 7. WYNDER, E. L. and GRAHAM, E. A. Tobacco smoking as possibIe etioIogic factor in bronchiogenie carcinoma; a study of 684 proved cases. J. A. M. A., 143: 329, 195”. 8. DOLL, R. and HILL, A. B. The mortaIity of doctors in relation to their smoking habits. Brit. M. J., 1: 1451, 1954; 2: 240, 1954. 9. STONE, D. J., SCHWARTZ, A., NEWMAN, W., FELTMAN, J. A. and LOVELOCK,F. J. Precipitation by pulmonary infection of acute anoxia, cardiac failure and respiratory acidosis in chronic pulmonary disease. Am. J. Med., 14: 14, 1953. I o. SIMPSON, T. Acute respiratory infections in emphysema. An accnunt of r18 cases. Bril. M. J., I: 297, 1954. I I. MOTLEY, H. L., LAX, L. P. and GOKDON, B. USC of intermittent positive pressure breathing combined with nebuIization in pulmonary disease. Am. J. Med., 5: 853, 1948. 12. FOWLEK, W. S., HELMHOLZ, 1\1. F. and MILLER, R. D. Treatment of pulmonary emphysema with aerosolized bronchodiIator drugs and intermittent positive pressure breathing. Proc. Sta,f] Meet. Mayo Clin., 28: 743, 1953. 13. KAKPOVICH,P. V. Adventures in Artificial Respiration. New York, 1953. Association Press. 14. SEGAL, M. S., SALOMON,A. and HERSCHFUS, J. A. Treatment of chronic puImonary emphysema. Am. Rev. Tuberc., 69: 915, 1954. 15. BARACH, A. L., BICKERMAN, H. A. and BECK, G. Advances in the treatment of non-tuberculous pulmonary disease. Bull. New York Acad. Med., 28: 353, 1952. 16. GAENSLER, E. A. and CARTEK, M. G. Ventilation measurements in puImonary emphysema treated with pneumoperitoneum. J. Lab. ti Clin. Med.,

CONCLUSIONS

UntiI asthma and chronic bronchitis can be prevented, chronic pulmonary emphysema wiI1 be a common disease and a distressing therapeutic probIem. AIthough anatomic damage in the Iungs is cumuIative and IargeIy irreversible, there is usuaIIy a significant component of functiona bronchospasm which can be treated. The episodes of acute respiratory faiIure. often associated with infections. -, are aIso amenable to treatment, directed mainlv at diminishing respiratory effort and increaiing alveolar ventiIation. Between such episodes the patient is often abIe to maintain satisfactory, if not normal, activities; the degree of improvement mav be remarkable in view of the desperate condition of the patient in a respiratory crisis.

35: 945. 1950. S. and D~LI;ANO. M. J. Chronic PuImonary Emphysema, p. 139. New York, 1953. Grune & Stratton, Inc. 18. BKACKENKIDGE,R. D. C. and JONES, A. T. PuImonary emphysema treated by pneumoperitoneum. Brit. M. J., I: I 135, 1953. 19. BARACH, A. L., BECK, G. J. and SMITH, W. H. Mechanica production of expiratory flow rates surpassing the capacity of human coughing. Am. J. M. SC., 226: 241, 1953. 20. MARCOTTE, R. J., PHILLIPS, F. J., ADAMS, W. E. and LIVINGSTONE,H. DifferentiaI intrabronchial emphysema. J. pressures and mediastinal Tboracic Surg., g: 346, 1940. 21. COMROE, J. H., JR. and DRIPPS, R. D. The PhysioIogicaI Basis for 02 Therapy. Springfield, III., 1950. CharIes C Thomas. 22. NADELL, J. The effects of the carbonic anhydrase inhibitor “6063” on eIectroIytes and acid-base balance in two normal subjects and two patients with respiratory acidosis. J. Clin. Investigation, 32: 622, 1953. 23. SEGAL, M. S. and DULPANO, M. J. Chronic PuImonary Emphysema, p. 107. New York, 1953. Grune & Stratton, Inc. 17. SEGAL. M.

REFERENCES

1. FLETCHEK, C. M. Pneumoconiosis of coal-miners. Brit. M. J., I: ror5-1065, 1948. 2. MOTLEY, H. L., LANG, L. P. and GOHDON, B. Studies on the respiratory gas exchange in one hundred anthracite coal miners with pulmonary complaints. Am. Rev. Tuberc., 61: 201, ,910. 3. FLINT, F. J. Cor puImonaIe-incidence and aetiology in an industrial city. Lancet, 2: 5 I, Ig++. 4. PEMBEKTON, J. and GOLDBERG, C. Air poIIution and bronchitis.

Brit.

M. J., 2: 567, ,954.

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