Incentive Spirometry

controlled only after repeated doses of intravenous digoxin and propranolol. Ruskin and Hutter'? reported an improvement in exercise tolerance in one patient with PPH treated with oral phentolamine. Although the drug produced only minor hemodynamic changes at rest, it prevented the significant increase in pulmonary resistance with exercise which was seen during control state prior to initiation of therapy. The mechanism of action of phentolamine may be at least partially explained by its ability to block the sympathetic nervous activity and to antagonize circulating catecholamines. The drug, therefore, may be more effective during exercise when there is an augmentation of sympathetic activity accompanied by an increase in pulmonary arteriolar tone. Oral hydralazine has also been added to the list of vasodilator agents used for the treatment of PPH. Rubin and Peter!' have treated four severe PPH patients with 200 mg oral hydralazine daily and showed significant fall of pulmonary vascular resistance and enhancement of cardiac output, both at rest and during exercise. Hydralazine, which has a direct relaxing effect on smooth muscle, mainly of the systemic arteriolar circulation, appears to have a similar action on the pulmonary vessels. Our experience in one patient with severe PPH has been somewhat at variance with that of Rubin and Peter. We administered hydralazine to a 48-year-old woman with an II-year history of PPH in increasing doses up to 400 mg daily with no hemodynamic response. The administration of 5 mg of oral prazosin, however, was followed by a moderate but consistent fall in pulmonary resistance and pressure accompanied by an enhancement of cardiac output. These findings suggest that prazosin, a vasodilator whose cardiocirculatory action is mainly attributable to alpha adrenergic receptor blockade, may warrant a clinical trial in patients with PPH. In summary, vasodilator agents such as isoproterenol, phentolamine, diazoxide, hydralazine and prazosin appear to have beneficial effects on the hemodynamic profile and symptoms in some patients with PPH. More information in larger groups of patients should lead us to a re6nement of our ability to optimize the usage of this therapeutic option in patients with the progressive and fatal syndrome called PPH. Uri Elkayam, M.D.· Orange, CA • Assistant Professor of Medicine and Director, CCU, California College of Medicine, UDiversity of California Irvine Medical Center. Reprint requests: Dr. EUcayam, University of California I ",ine Medical Center, Division of Cardiology, 101 City Drive South, Orange, California 92668

254 EDITORIALS

1 Hutchins GM. The pathogenesis of the two forms of hypertensive pulmonary vascular disease. Am Heart J 1976; 92:797-803 2 Aviado DM Jr, Schmidt CF. Effects of sympathomimetic drugs on pulmonary circulation: with special reference to a new pulmonary vasodilator. J Pharmacal Exp Ther 1957; 120:512-27 3 Polli JF, Jacono A, Bendezu-Prieto J. Effect of isoproterenol on the circulation of the lung. Arch Intern Pharmacodyn Ther 1960; 124:488-94 4 Lee TO Jr, Roveti GC, Ross RS. The hemodynamic effects of isoproterenol on pulmonary hypertension in man. Am Heart J 1963; 65:361-67 5 Shettigar UR, Hultgren HN, Specter M, Martin R, Davies DH. Primary pulmonary hypertension: favorable effect of isoproterenol. N Engl J Med 1976; 295: 1414-15 6 Elkayam U, Frishman WH, Yoran C, Strom J, Sonnenblick EH, Cohen M. Unfavorable hemodynamic and clinical effects of isoproterenol therapy in primary pulmonary hypertension. Cardiovasc Med 1978; 3:1177-80 7 Daoud FS, Reeves JT, Kelly DB. Isoproterenol as a , potential pulmonary vasodilator in primary pulmonary hypertension. Am J Cardiol 1978; 42:817-22 8 Wang SWS, Pohl JEF, Rowlands DJ, Wade EG. Diazoxide in treatment of primary pulmonary hypertension. Br Heart J 1978; 40:572-74 9 Klinke P, Gilbert AL. Diazoxide in primary pulmonary hypertension. N Eng! J Med 1980; 302:91-92 10 Ruskin JM, Hutter AM Jr. Primary pulmonary hypertension treated with oral phentolamine. Ann Intern Med 1979; 90:772-74 11 Rubin LJ, Peter RH. Oral hydralazine therapy for primary pulmonary hypertension. New Engl J Med 1980; 302: 69-73

Incentive Spirometry TheAnswer Is Blowing inthe Wind

Soon

after the call was raised to banish the IPPB machine to the storeroom, their place at the bedside of the postoperative patient was taken by the incentive spirometer. It may be premature to denounce the incentive spirometer, but clearly its widespread current use is disproportionate to the scanty evidence supporting its efficacy in preventing postoperative complications. Early papers by Bartlett et al l -3 showed that its use encouraged large tidal volumes and improved arterial oxygenation. These studies implied but did not demonstrate that use of the incentive spirometer would minimize postoperative atelectasis. Jung and colleagues (Chest 1980; 78:31-35) confirm earlier disappointing reports.s" incentive spirometry is no better than IPPB or blow bottles in preventing postoperative atelectasis. In one study where there was overall superiority of the incentive spirometer over physiotherapy, this difference did CHEST, 79: 3, MARCH, 1981

not exist in the high risk patients with obesity or obstructive lung disease.' Pulmonary physicians must supervise the use of these and other devices by respiratory therapists, must justify their use to various third-party payers, and must provide consultations for our surgical colleagues. We find ourselves in a difficult situation. The evidence against the efficacy of incentive spirometry is convincing. Yet, the experimental basis for expecting that this approach will be effective is no less convincing. Breathing at monotonously regular tidal volumes produced a fall in compliance in the lungs of patients" and this was reversed by lung hyperinHation. This pattern of breathing also produces areas of microatelectasis within the lungs," Mter surgery there are dramatic decreases in lung volumes including TLC and FRC.lO This effect is exaggerated in those who undergo thoracic or upper abdominal surgery. A decreased FRC will predispose to airway collapse in those patients with elevated closing volumes. This places the elderly and smokers at increased risk.I! Jung et ai, in concluding their article, may provide the resolution of this dilemma. "... sustained maximal inhalation is only one of several maneuvers which may be necessary in any given patient to prevent postoperative respiratory complications. Thus, an individual with very thick, tenacious secretions should receive therapy to decrease their tenacity, the patient should be frequently reminded and encouraged to cough, etc." We should also add to the list of possible treatments smoking cessation, weight reduction, bronchodilating aerosols, chest physiotherapy and antibiotics. Certainly, when multiple measures are used, encouraging results are obtained. The oft-quoted study by Stein et al,12 demonstrated that multifaceted therapy can reduce the complication rate in high risk patients to that seen in a group of surgical patients with normal lung function. For the present, it seems appropriate to tailor a postoperative regimen to each patient and to the availability of staff and equipment within the hospital. The use of lung hyperinflation needs to be supplemented with other measures as necessary. As Jung et al point out, "Further investigations on combinations of therapy need to be performed." Resolution of these questions is extremely important

CHEST, 79: 3, MARCH, 1981

in view of the large number of patients at risk of postoperative complications, the increase in their number as the population ages and the many manhours devoted to the prevention and treatment of this problem. M. Belman, M.D., F.C.C.P., and Charles Mittman, M.D., F.C.C.P. Duarte, California City of Hope National Medical Center. Reprint requesta: Dr. Belman, RespIratory Diseases Department, City of Hope Medical Cetue« 1S00 Duarte Road, Duarte, Califomia 91010

1 Barlett RH, Gazzaniga AB, Geraghty TR. Respiratory maneuvers to prevent postoperative pulmonary complications. A critical review. JAMA 1973; 224:1017 2 Bartlett RH, Gazzaniga AB, Geraghty TR. The yawn maneuver: prevention and treatment of postoperative pulmonary complications. Surg Forum 1971; 22:196 3 Bartlett RH, Hansen EL, Moore RD. Physiology of yawning and its application to postoperative care. Surg Forum 1970; 22:222 4 Craven JL, Evans GA, Davenport JL, Williams RHP. The evaluation of the incentive spirometer in the management of postoperative pulmonary complications. Br J Surg 1974; 61:793 5 Iverson LIG, Ecker RR, Fox HE, May IA. A comparative study of IPPB, the incentive spirometer and blow bottles: the prevention of atelectasis following cardiac surgery. Ann Thor Surg 1978; 25: 197 6 Pfenninger J, Roth F. Intermittent positive pressure breathing ( IPPB ) versus incentive spirometer ( IS ) therapy in the postoperative period. Intens Care Med 1977; 3:279 7 Van de Water JM, Watring WG, Linton LA, Murphy M, Byron RL. Prevention of postoperative pulmonary complications. Surg Gynecol Obstet 1972; 135:320 8 Ferris BG, Pollard DS. Effect of deep and quiet breathing on pulmonary compliance in man. J Coo Invest 1969; 31:143 9 Mead J, Collier C. Relation of volume history of lungs to respiratory mechanics in anesthetized dogs. J Appl Physiol1959; 14:669 10 Latimer RG, Dickman M, Day WC, Gunn ML, Schmidt C duW. Ventilatory patterns and pulmonary complications after upper abdominal surgery determined by preoperative and postoperative computerized spirometry and blood gas analysis. Am J Surg 1971; 122:622 11 Editorial: The postoperative chest. Br Med J 1968; 153 12 Stein M, Cassera EL. Preoperative pulmonary evaluation and therapy for surgery patients. JAMA 1970; 211:787

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