The Adult Acute Respiratory Insufficiency Syndrome Following Nonthoracic Trauma: The Lung in Shock EDWARD
As one war has succeeded another in the present century, a syndrome of acute pulmonary insufficiency following shock or trauma has emerged and become increasingly well defined. With greater success in the general management and the improved survival of the wounded, more detailed descriptions of the clinical course and pathologic anatomy of this entity have become availab1e.l In general, there is a remarkably stereotyped presentation, characterized by a short latent period of several hours, the subsequent development of tachypnea, dyspnea, cyanosis, respiratory alkalosis and diffuse pneumonic or interstitial radiologic infiltrates; moreover, failure to relieve the cyanosis with the breathing of pure oxygen, the development of respiratory acidosis and rapid, extremely shallow breaths requiring tracheostomy and ventilatory assistance are often preterminal features. The pathologists have established that in most cases the lung is not primarily overloaded with water ; hyperemia, periarterial, capillary or interstitial edema and diffuse microatelectasis, with or without bacterial pneumonia, seem to predominate. In some cases, alveolar fluid and hyaline-like membranes reminiscent of the acute respiratory distress syndrome in the newborn are also present. In all cases the lungs at postmortem examination are inflatable only with difficulty, and in the worse cases they are not inflatable at all. These observations strongly suggest that a major physiologic counterpart of the anatomic observations would be a decrease in the compliance of the lung. Indeed, profound decreases in the stretchability have been documented by direct physiologic study as well as the clinical impressions gained from the very high inflation pressures required by an automatic ventilator to accomplish a normal tidal volume. But, therein lies the From the Departments of Physiology and Rehabilitation Medicine, School of Medicine, New York University Medical Center, New York, N.Y. Address for reprints: Edward H. Bergofsky, MD, Department of Physiology, School of Medicine, New York University Medical Center, 550 First Ave., New York, N.Y. 10016.
enigma: Is the decreased compliance due to selfevident anatomic changes easily observable in the lung, that is, the interstitial edema and engorgement and the reduction in the total number of patent alveoli which occur with alveolar exudation and atelectasis? Or, is the stiffness of the lung primarily attributable to a loss of the surface tension-lowering agent (surfactant) and the consequent exaggeration of the surface tension at the air-liquid interface of the alveoli? The difficulties encountered in assigning responsibility for the stiff lungs to either factor are compounded since alveolar exudates, capillary permeability and microatelectasis are theoretically closely related pathogenetically to a loss of surfactant; however, it remains to be determined which is the cause and which the effect. For instance, a primary lesion producing alveolar atelectasis not only can decrease the rate of synthesis of surfactant from the resulting disturbed alveolar pneumocytes, but also can interfere with the assay of the surfactant by preventing the extraction by saline washes from the lung. Conversely, it is theoretically possible that a primary reduction in surfactant could account for these anatomic changes by so heightening alveolar surface tension as to cause transudation of proteinaceous fluid from the capillary into the lung parenchyma. Because of these uncertainties, a step by step analysis of the development of the acute respiratory insufficiency syndrome is not yet possible. Nonetheless, the bulk of the evidence is beginning to shift to a working hypothesis involving 3 related variables: pulmonary blood flow, the pulmonary microcirculation and the manufacture of surfactant (Fig. 1). As Figure 1 indicates, the state of shock leading to decreased. pulmonary blood flow has been given a prime position in the constellation of this form of acute respiratory insufficiency. Although it has not been a unanimous election, a plurality of the investigative papers at a recent conference on the pulmonary effects of nonthoracic trauma1 dealt with the pulmonary circulation, and, at the
BLOOD VESSEL CLOSURE
Figure 1. Alternate pathways leading to alveolar microatelectask. Clinical and experimental evidence exists to support both pathways. A.N.S. = autonomic nervous system.
same conference, a feature of every clinical case report was a period of profound shock with unobtainable readings of systemic blood pressure and, presumably, minimal levels of pulmonary blood flow. In Figure 1, alternative pathways are shown, each of which alone or in combination could theoretically lead to alveolar microatelectasis. The first route, labeled 1, involves direct damage to the pulmonary vasculature by both low levels of blood flow and some toxic agents. Among the agents mentioned have been vasoactive polypeptides, serotonin, endotoxins, fatty acids and other unidentified debris from blood- and tissue-formed elements, along with the direct and intensive pulmonary vasoconstrictor effects of the autonomic nervous system. At present there is considerable disagreement on the type of pulmonary blood vessel that suffers the major damage. The histologic evidence of Veith et al.” points to injury to the small pulmonary artery, whereas Sugg et al.3 interpret their observations of hemodynamic wedge pressure as an indication of prolonged venoconstriction. Our own data-*,” in recent experiments in shock models in animals indicate such marked reduction in pulmonary-capillary blood volume, even after total blood volume and pulmonary arterial pressure are fully restored, as to implicate direct capillary damage as a major determinant in this form of respiratory failure. The second possible pathway, labeled 2, also has
a substantial body of supportive evidence. In experimental shock in animals, inflation studies with air-filled lungs reveal marked decreases in lung compliance, but these same lungs become completely normal when they are filled with saline; such data suggest the loss of pulmonary surfactant and increased surface tension at the air-liquid interface in the lung in experimental shock.” These data are supported by isotopic studies showing decreased phospholipid synthesis and decreased incorporation of fatty acids, presumably in the alveolar pneumocytes manufacturing surfactant. Direct measurements of surfactant levels in lungs in either experimental or clinical shock have been much less consistent and convincing because of the difficulties encountered in extracting the material from partly collapsed lungs by the saline wash technique or in dispassionately choosing a representative sample of an unevenly affected lung for the mincing technique. However, the end result from either pathway is the same ; widespread alveolar microatelectasis with or without alveolar fluid, stiff lungs and a ventilation-perfusion imbalance with venous admixture predominating. And, as with many other clinical syndromes, a therapeutic approach to the acute respiratory insufficiency syndrome has emerged before the identification of the causative factors. Therapy : The major premise to this approach is the recent lesson that even the stiffest of lungs tends to remain inflated if it is maintained in an inspiratory position. Moreover, lungs with apparent widespread atelectasis can be mechanically inflated by the use of brief high pressure inflation efforts, either manually with resuscitation bags or by mechanical ventilators. And, once inflated, the lungs become less stiff and are far more easily ventilated. It appears that the most important component of this approach is not so much the type of automatic ventilation system used, that is volume-cycled versus pressure-cycled ventilators, but rather the maintenance of continuous positive pressure throughout the respiratory cycle.7,By this technique, endotracheal pressures at the end of expiration are set at about 6 cm of water either by a mechanical expiratory retard or by immersing the expiratory limb of the breathing system below water; the latter method gives an overall lower intrathoracic pressure and is perhaps more desirable from the standpoint of facilitating venous return. Studies such as that of Ayres et al.8 in this issue are of considerable value in documenting in such patients during continuous positive pressure ventilation a significant improvement in the balance between ventilation and perfusion, a consequent decrease in the physiologic shunting and an increase in the arterial oxygen tension. Several other considerations regarding this syndrome await resolution. The role of overinfusion
of noncolloidal replacement fluid during shock in perpetuating the transudate from capillary to lung has been repeatedly emphasized, but whether this represents an initiating factor in the production of respiratory distress or merely an aggravating factor is still unclear. The degree to which oxygen concentrations of greater than 60 percent in the inspired air are capable of superimposing their documented toxic effects on the preexisting respiratory insufficiency is also uncertain ; however, this factor is unlikely to have been important in the majority of clinical instances, since abnormally high arterial oxygen tensions are required to elicit the oxygen toxicity effect; and, in the future, continuous positive pressure breathing, along with other procedures, is likely to minimize the need for inspired oxygen concentrations greater than 50 percent. Of all the variables, the contributions of fat emboli to this syndrome, especially during severe trauma, are the most obscure, and further. investigation is needed along these lines. Finally, some reassurance may be passed to the clinician that we have reached the point where our knowledge of lung mechanics permits a hopeful therapeutic approach to a stiff and collapsed lung, an approach that may maintain respiration until
the acute respiratory distress syndrome spontaneously resolves, even though the initiating factors and intimate mechanisms of the syndrome have not been definitively determined. REFERENCES 1. Pulmonary effects of nonthoracic trauma symposium. J Trauma 8:625-648, 1968 A pattern of 2. Veith FJ, Panossian A, Nehlsen SL, et al: pulmonary vascular reactivity and its importance in the pathogenesis of postoperative and posttraumatic pulmonary insufficiency. J Trauma 8:788-792, 1968 Congestive atelecta3. Sugg WL, Webb WR, Nohoe S, et al: sis: an experimental study. Ann Surg 168:234-242, 1968 4. Porcelli RJ,. Bergofsky EH, Foster WM, et al: A model for shock lung in dogs and monkeys. Submitted for publication 5. Foster WM, Reich T, Porcelli RJ, et al: Prediction of shock lung by pulmonary vascular hemodynamics. Submitted for publication A study of the 6. Henry JN, McArdle AH, Scott HJ, et al: acute and chronic respiratory pathophysiology of hemorrhagic shock. J Thorac Cardiovasc Surg 54:666-681, 1967 Acute respira7. Ashbaugh DG, Bigelow DB, Petty TL, et al: tory distress in adults. Lancet 2:319-323, 1967 The lung in 8. Ayres SM, Mueller H, Gianelli S Jr, et al: shock. Alveolar-capillary gas exchange in the shock syndrome. Amer J Cardiol 26:588-594, 1970