- Email: [email protected]
Preoperative and Postoperative Inhalation Therapy
Preoperative and Postoperative Inhalation Therapy REUBEN C. BALAGOT, M.D.* VALERIE R. BANDELIN, M.D.**
PREOPERATIVE INHALATION THERAPY Although it is not the intent to treat chronic respiratory insufficiency on a permanent basis, since this does not seem possible, any attempt to improve the disease in order to optimize respiratory function for surgery must be oriented toward three big categories under this condition: 8 1. Diffuse pulmonary fibrosis and/or granuloma, e.g., scleroderma, Boeck's sarcoid, berylliosis. These patients have an "alveolar-capillary" block. 2. Chronic bronchitis and/or emphysema. Between these two extremes is a spectrum with admixtures of both conditions to varying degrees. 3. Alveolar hypoventilation. Patients with normal lungs but with damaged respiratory centers, or paralyzed respiratory muscles, skeletal deformities as in the kyphotic, and the obese-Pickwickian syndrome.
Clearly, the objectives in preoperative inhalation therapy are to improve (1) alveolar ventilation, (2) arterial oxygenation, and (3) carbon dioxide elimination. The first may be improved by diminishing or eliminating airway resistance, e.g., bronchoconstriction, and the second and third by improving ventilation-perfusion.
Diffuse Pulmonary Fibrosis Not much can be done at the moment to change or mitigate pulmonary fibrosis, although awareness of the possible presence of "stiff" lungs in conditions such as scleroderma or Boeck's sarcoid might make the surgeon and the anesthesiologist more wary of getting the patient into situations where artificial ventilation might be needed but found *Chairman, Department of Anesthesiology, Presbyterian-St. Luke's Hospital. Clinical Professor of Anesthesiology, University of Illinois College of Medicine, Chicago, Illinois **Clinical Instructor in Anesthesiology, University of Illinois College of Medicine and Research and Educational Hospitals; Assistant Attending Anesthesiologist, PresbyterianSt. Luke's Hospital
Surgical Clinics of North America- Vol. 48, No. 1, February, 1968
29
30
REUBEN
C.
BALAGOT, VALERIE
R.
BANDELIN
ineffective. Inhalation therapy in this patient may be helpful in the presence of complications such as bronchitis and bronchopneumonia. But then, under such conditions, elective surgery will not be contemplated. What about emergency surgery? If only a short period of time is available for preparing the patient, the administration of nebulized bronchodilators such as isopropylnorepinephrine might help temporarily if no more than to assuage the mental state of the medical attendants. Chronic Bronchitis and/or Emphysema Strict delineation of the two extremes of obstructive lung disease, chronic bronchitis and emphysema, is frequently difficult. One can only pick from the varied spectrum between these extremes and state categorically that a patient has more bronchitis (obstruction) than emphysema or vice versa depending upon which group of signs and symptoms predominate. Briscoe and Nash 2 considered (a) dyspnea, (b) little cough, (c) little sputum, (d) translucent lung fields in the x-ray, (e) no cor pulmonale except terminally, and (f) normal hematocrit as predominantly emphysema; whereas (a) occasional dyspnea, (b) much cough, (c) much sputum, (d) normal lucency of lung fields, (e) tendency to cor pulmonale and (f) raised hematocrit or polycythemia represented a condition that was predominantly bronchitic. They assessed the contribution of what Hickam et al. 10 called the "slow space" to arterial oxygen saturation in a group of emphysematous and bronchitic patients. The slow space by definition consists of groups of alveoli probably scattered throughout the lungs that wash out nitrogen very slowly when oxygen is breathed. When in the normal lung, nitrogen washout is maximal within five to seven minutes, it may take more than 20 minutes for the slow space to achieve this state. The slow space is somewhat greater in volume in the purely emphysematous patient than the purely bronchitic patient. With intermittent positive pressure breathing (IPPB) alone without bronchodilators, arterial oxygen saturation in an emphysematous group was shown by Briscoe and N ash 2 to be significantly better than in a bronchitic group and was probably due to improved ventilation of the slow space. Interestingly enough, Briscoe et al. 3 also found a decrease in ventilation of the slow space with voluntary hyperventilation but a marked increase with IPPB. There was increased oxygen consumption due to increased work of breathing with voluntary hyperventilation but negligible increase with IPPB. Surely, therefore, there is a decided advantage to using IPPB in the preoperative preparation of the patient who suffers from obstructive bronchitis and emphysema. The advantage is much more so in the emphysematous patient, but is also significant in the bronchitic patient. Bronchodilators increase the advantageous results effected by IPPB. Goldberg and Cherniack9 showed an equal improvement in the various pulmonary function tests utilized whether the bronchodilator was adminstered by IPPB or by a properly used hand nebulizer to hospital patients suffering from chronic bronchitis and emphysema. And, contrary to the findings of Jones et al., 11 they did not find IPPB to produce air trapping and overinfiation in patients with severe emphysema. They fur-
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
31
ther speculated that IPPB might be more effective than a hand nebulizer in those patients with severe or acute respiratory distress. Secretions are usually a great problem in the predominantly bronchitic patient. If profuse amounts are brought up by the patient they must surely add to the airway obstruction.
Alveolar Hypoventilation The third large category of respiratory insufficiency is primary alveolar hypoventilation. Patients in this group who have either a damaged respiratory center or poorly functioning peripheral respiratory apparatus are usually already under good respiratory care, aided by ventilators, and do not need any extra preoperative inhalation therapy. One only makes sure that this excellent respiratory care they are getting is not diminished during anesthesia and postoperatively. Again in these patients the added complications of acute bronchitis and/or bronchopneumonia with its increased airway resistance caused by bronchial spasm and secretions will augment the extant alveolar hypoventilation. Some special problems in this group that are frequently encountered should be emphasized. The severe kyphoscoliotic patient has a distorted thoracic cage that severely limits the excursions of the lungs. This makes for a greater effort to ventilate and results in rapid shallow respirations. Alveolar hypoventilation frequently develops with its attendant hypoxia and hypercapnea. The same unphysiologic findings are encountered in the very obese patient-the Pickwickian syndrome. The massive chest and abdominal wall offer a tremendous resistance to respiratory effort. Cherniack, 4 in a study of a group of obese individuals, observed both hypoxia and hypercapnia in a third, and hypoxia but no hypercapnia in another third, suggesting alveolar hypoventilation in the first instance and possible altered ventilation-perfusion in the second group. Hypoxia and Hypercapnia. Any form of respiratory insufficiency eventually results in various degrees of hypoxia and hypercapnia. All signs and symptoms of any disease causing respiratory insufficiency may be related directly or indirectly to either or both conditions. Both hypoxia and hypercapnia provoke pulmonary vasoconstriction and with the added erythropoiesis of chronic hypoxia contribute greatly to cor pulmonale in these patients.
Summary of Therapy To optimize the patient with respiratory insufficiency for surgery, one hopes to decrease air-flow resistance by use of bronchodilators such as isopropylnorepinephrine or epinephrine and agents that will tend to thin or lyse bronchial secretions, examples of which are detergent aerosols such as Alevaire, Tergemist, and just plain normal saline. Mucolytic drugs like pancreatic dornase or acetylcysteine may help in this respect. They may be irritating to bronchial mucosa. The administration of a bronchodilator such as epinephrine or isoproterenol concurrently or before the mucolytic drugs may obviate bronchoconstriction from the irritation they cause.
32
REUBEN
C.
BALAGOT, VALERIE R. BANDELIN
Mechanical devices may then be employed to improve ventilation, i.e., use of IPPB units. By improving ventilation of the slow space, and assullling that improved ventilation also reflexly improves perfusion, arterial oxygen saturation is greatly augmented. One great advantage of IPPB of course over volitional hyperventilation is that the work of respiration is very much less than with hyperventilation and thus results in less oxygen consumption. Apparently, ventilation of the slow space is decreased instead of augmented with hyperventilation. 3 Caution must be observed in the vigorous treatment of severe respiratory insufficiency. Sudden marked changes in the extant hypercapnia and hypoxia can quickly lead to cardiovascular collapse and death.
POSTOPERATIVE INHALATION THERAPY It is now common knowledge that the respiration of a patient who has been subjected to a general anesthetic remains quite depressed for variable periods of time. In fact, it is not uncommon to find a Po 2 of 60 mm. Hg and rarely going above 85 mm. Hg unless respiration is augmented with IPPB or oxygen given by nasal catheter, by mask, or by face tent. This implies alveolar hypoventilation to a relative degree. Nevertheless, patients with normal respiratory function tend to do well. It becomes obvious, however, that the patient with chronic respiratory insufficiency in the immediate postoperative period may be in severe respiratory distress if the attendant postanesthetic depression is superimposed on the chronic alveolar insufficiency. Visual assessment of a patient's respiratory status in the immediate postoperative period is at best a wild, educated guess. The low arterial oxygen tensions found in these patients attest to this. It may be assumed that the overall depressive action of general anesthetic agents prevents the chemoreceptor bodies from augmenting respiratory ventilation in response to the low oxygen tensions. Since the carotid body and/or the aortic body will normally be activated by oxygen tensions below 60 mm. Hg, one may surmise that their reflex ability to respond may be frightfully diminished under the waning influence of anesthetic agents or that the respiratory center through which these bodies exert their augmentative action on ventilation is markedly depressed and will not respond to the weak chemoreceptor stimuli. Weakened or absent ciliary action and a diminished or absent cough reflex whether due to the anesthetic or premedicant narcotic undoubtedly contribute to formation of postoperative atelectasis which further augments the ventilatory insufficiency. Without doubt, therefore, some form of inhalation therapy will be beneficial in the immediate postoperative period.
Postanesthetic H ypoventilation Postanesthetic hypoventilation frequently goes unrecognized un· less arterial Po 2 and Pco 2 are monitored during this period. Our experience has shown that venous values, as well, will also reflect alveolar hypoventilation provided one is aware that Po 2 is lower and Pco2 higher in venous blood. The difference may be around 10 mm. Hg (higher) for
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
33
Pco 2 and 10 to 20 mm. Hg (lower) for 0 2 • Once hypoventilation is recognized, however, oxygen therapy, as has been routinely administered for years, is not the corrective method of choice. The use of IPPB to augment ventilation is the proper therapeutic approach. The pressurecycled ventilators have worked well for this purpose, e.g., the Bennett or the Bird IPPB units. It is always a temptation to administer 100 per cent oxygen with the reasoning that if 20 per cent in ambient air works well under normal conditions, more of it under abnormal conditions will by the same token work wonders. This of course is a perfect example of of too much of a good thing causing more harm than good. The use of 40 or 50 per cent oxygen with the IPPB is more than sufficient. In fact, nebulization of water or saline with oxygen to humidify the inhaled atmosphere frequently increased oxygen concentration to 93 per cent. s, 13 Oxygen toxicity and a few other unphysiologic effects of oxygen might offset all the advantages therapy offers. Atelectasis Atelectasis is a very frequent postsurgical complication that is most often ignored or missed until it becomes extensive and presents the classical findings of elevated temperature, pulse rate, and respiratory rate, and probably the other findings of segmental or regional lung density such as absence of breath sounds, dullness to percussion, and changes in radiolucency. The classic explanation for this syndrome is obstruction of a bronchus with thickened secretions and subsequent absorption of the gases beyond the obstruction, leading to alveolar collapse. Although atelectasis will develop with complete bronchial obstruction, there is really no correlation between atelectasis and partial obstruction with thickened secretions. Part of this erroneous conclusion may have been based on a study by Coryllos and Birnbaum6 in 1932 showing that it takes 16 hours for low solubility gases such as helium, nitrogen, and air to be absorbed from a lung whose bronchus is totally occluded whereas oxygen will be absorbed in a matter of minutes. These authors were not then aware of the role of surfactants in maintaining alveolar stability and possibly even gas transport. The current thinking is that atelectasis is caused by inspiratory insufficiency. This conclusion is based on studies by Mead and Collier12 and by Bendixen et al. 1 that spontaneous or artificial ventilation at constant tidal volumes will usually result in (1) decreased compliance, (2) decreased lung volume, and (3) increased shunting (venous admixture). These changes are conducive to atelectasis. They have been found to be preventable by sighing and/or occasional deep breathing. Clement et al. 5 postulates that deep breathing will mobilize surfactant from within the alveolar cell to augment or replace aging surfactant on the alveolar surface, maintaining alveolar stability and preventing atelectasis. From a therapeutic standpoint, some volume ventilators like the Emerson are capable of instituting the "sigh" or deep breathing at regularly designated intervals by means of a timing mechanism. The usual IPPB units in common use do not have this mechanism. In our Intensive Therapy Unit, this function is frequently performed by manual hyperinflation with an Ambu bag.
34
REUBEN
C.
BALAGOT, VALERIE
R. BANDELIN
The use of high humidity to soften or loosen or dissolve hard or desiccated secretions, as frequently practiced in the past, is probably of some value, not because of this particular action but because of its effect on ciliary activity. Inhaled air with a relative humidity lower than 70 per cent will inhibit ciliary activity; and it is ciliary activity that will usually break up secretions. Nebulization which serves to provide the humidity also functions as a vehicle for detergent solutions (Alevaire and Tergimist) to thin secretions, for mucolytic agents like Dornavac (deoxyribonuclease) or Mucomyst (acetylcysteine), and for bronchodilator agents such as epinephrine (levo or racemic) and isoproterenol. Deoxyribonuclease attacks pus and cellular debris whereas acetylcysteine acts on the polysaccharide bond of mucin. These mucolytic agents may be irritating to the mucosa and cause bronchoconstriction. 7 Previous or concomitant administration of isoproterenol might be helpful in preventing the bronchoconstriction. In view of changing concepts in regard to causation of atelectasis, i.e., inspiratory insufficiency instead of the classical "block" caused by mucous plugs, the value of agents that act primarily on secretions becomes somewhat limited, not to say conjectural to a degree. The occasional or even frequent augmentation of inspiration ("sigh") may be more helpful in preventing atelectasis than all the paraphernalia and accessories which make inhalation therapy impressive and expensive. There are other methods of treating a full-blown atelectasis. The relief of pain in upper abdominal area operations frequently eliminates "splinting" and enables the patient to take deep breaths-improving the atelectasis. The inhalation of carbon dioxide for a very brief period of time to the point of hyperpnea has worked well in our hands. Carbon dioxide gas is allowed to flow from a tank through a piece of tubing gently onto a patient's face, the tip of the tube being held 3 to 6 inches above his nose. The heavier-than-air gas will very quickly be inhaled by the patient causing rapid and deep respirations. This is allowed to continue for six to ten breaths, then stopped. This may be repeated every two to three hours until signs of atelectasis diminish or disappear. The same effects may be accomplished by inhalation of 5 per cent carbon dioxide in oxygen through a face mask and a bag. The temptation to administer the treatment for a longer period of time than necessary is very great with this technique, which in unfamiliar hands has been observed to provoke C0 2 convulsions and as serious a complication as a cerebrovascular accident. Another simple method is to increase the dead space by making the patient breathe into a long piece of corrugated anesthetic tubing. The rebreathing of a C0 2-enriched atmosphere again provokes hyperpnea. Schwartz et al. 16 have modified this by adding a face mask to one end of the tube to facilitate administration. In passing, pneumonia, which is probably an infected atelectasis, and pulmonary embolism should be mentioned as complications. Inhalation therapy serves as an excellent adjunct in the management of these conditions, but the infection has to be treated in pneumonia, and the perfusion improved in embolism. Both aspects are outside the scope of this paper.
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
35
Pulmonary Edema Pulmonary edema is not uncommon. The easy access to blood, plasma expanders, and other fluids during surgery increases this predilection. The inhalation of ether, ethyl alcohol (5 to 20 per cent), or a tertiary alcohol supposedly destroys the stabile foam formed which interferes with oxygen alveolar transport. The stability of the foam, however, was shown by Pattle 14 to be due to alveolar surfactant material which lined the foam formed from edema fluid and was quite resistant to the effects of ether or alcohol. From a chemical standpoint, however, sufficient amounts of the ether or alcohol will tend to disrupt the lipid lining of the foam. The beneficial effect of IPPB derives from its pressure effect of decreasing venous retum and probably from the forcible distention of alveoli, mobilization of alveolar cell surfactant, and diminishing surface tension, thus improving oxygenation.
Artificial Ventilation- Benefits and Cautions With development of radical surgical techniques particularly upon the cardiovascular system, we have found it beneficial and very helpful to take over the work of respiration immediately and for the first two or three days after surgery. The work of breathing which can, in patients with poor cardiovascular and respiratory function, take as much as 50 per cent of the oxygen consumption may be a great strain on a heart or a vascular system that has just been subjected to surgery. In taking over ventilatory function, the use of artificial ventilation with high oxygen concentrations gives rise to what was described under atelectasis, i.e., reduced compliance, reduced vital capacity, and poor oxygenation with concomitant hypoxia. This has been called the "respirator lung syndrome." Nash, Blennerhassett, and Pontoppidan 13 showed a correlation between the pathologic changes seen in the above syndrome and high oxygen tensions during ventilator therapy. These changes occurred in two phases- an exudative phase with an alveolar fibrinous exudate (hyaline membrane lining alveolar walls) and a proliferative phase with fibroblastic proliferation and hyperplasia of alveolar lining cells. Pratt, 15 on the other hand, found capillary congestion and increased alveolar septal thickness. He considers these to be a physiologic response to oxygen, i.e., increased oxygen supply to alveoli results reflexly in vasodilation of pulmonary arteries and arterioles with a consequent drop in pulmonary artery pressure. The opposite occurs with reduced oxygen supply. In a quick survey of 28 cases of "open-heart" surgery done at this institution in which the acid-base status and arterial oxygen tensions of the patients were monitored postoperatively until recovery or death, 3 out of 17 in the group who survived showed the typical decreased compliance ("stiff lungs") after more than 24 to 48 hours ventilator therapy on a pressure-cycled IPPB unit. In the group that died, 2 of 11 showed this syndrome. There were certain interesting observations made in this survey. A change from a pressure-cycled ventilator to a volume ventilator frequently resulted in a consistently lower arterial
36
REUBEN
C.
BALAGOT, VALERIE R. BANDELIN
Po 2 ; 8 out of the total demonstrated this observation (2 died). A majority of the patients who died showed a normal or alkalotic pH with normal or slightly decreased (negative) base excess. A number of these patients also showed an elevated or normal Po 2 - at least 5 showed a Po 2 of 88 to 170 mm. Hg. The significance of these preliminary observations cannot as yet be jelled into meaningful conclusions. Further studies are being done. One thing may be certain, and this is that oxygen toxicity in prolonged ventilator therapy may be contributory to morbidity or perhaps mortality. REFERENCES 1. Bendizen, H. H., Hedley-Whyte, J., and Laver, M. B.: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation-A concept of atelectasis. New Eng. J. Med., 269:991, 1963. 2. Briscoe, W. A., and Nash, E. S.: The slow space in chronia obstructive pulmonary disease. Ann. New York Acad. Sci., 121:706, 1965. 3. Briscoe, W. A., Emmanuel, G., Smith, W. M., and Cournand, A.: Effects of voluntary hyperventilation and intermittent pressure breathing on the distribution of ventilation and the distribution of perfusion. Fed. Proc., 20:421, 1964. 4. Cherniack, R. M.: Respiratory effects of obesity. Canad. Med. Assoc. J., 80:613, 1959. 5. Clements, J. A., and Tierney, D. F.: Alveolar instability associated with altered surface tension. Handbook of Physiology, Sec. 3, Respiration, Vol. II, 1565 pp., W. P. Fenn and H. Rann, (Eds.). Amer. Physiol. Soc., 1965. 6. Coryllos, P. N., and Birnbaum, G. L.: Studies in pulmonary gas absorption in bronchial obstruction. Amer. J. Med. Sc., 183:317, 1932. 7. Dalhamn, T.: Mucous flow and ciliary activity in the trachea of healthy rats and rats exposed to respiratory irritant gases. Acta Physiol. Scand., 36:Suppl. 123, 1956. 8. Fishman, A. P.: Roads to respiratory insufficiency. Ann. New York Acad. Sci. 121:657, 1965. 9. Goldberg, 1., and Cherniack, R. M.: Effects of nebulized bronchodilator delivered with and without IPPB on ventilatory function in chronic obstructive emphysema. Amer. Rev. Resp. Dis., 91:13, 1965. 10. Hickam, J. B., Blair, E., and Frayser, R.: An open circuit helium method for measuring functional residual capacity and defective intrapulmonary gas exchange. J. Clin. Invest., 33:1277, 1954. 11. Jones, R. H., MacNamara, J., and Gaensler, E. A.: Effects of IPPB on simulated pulmonary obstruction. Amer. Rev. Resp. Dis., 82:164, 1960. 12. Mead, J., and Collier, C.> Relation of volume history of lungs to respiratory mechanics in anesthetized dogs. J. Appl. Physiol., 14:669, 1959. 13. Nash, G., Blennerhassett, J. B., and Pontoppidan, H.: Pulmonary lesions associated with oxygen therapy and artificial ventilation. New Eng. J. Med., 276:369, 1967. 14. Pattie, R. E., and Burgess, F.: The lung lining film in some pathological conditions. J. Pathol. Bacterial., 82:315, 1961. 15. Pratt, P. C.: Reaction of the human lung to enriched oxygen atmosphere. Ann. New York Acad. Sci., 121:809, 1965. 16. Schwartz, S. 1., Dale, W. A., and Rahn, H.: Dead space rebreathing tube for prevention of atelectasis. ].A.M.A., 163:1248, 1957. 1753 West Congress Parkway Chicago, Illinois 60612
PREOPERATIVE INHALATION THERAPY Although it is not the intent to treat chronic respiratory insufficiency on a permanent basis, since this does not seem possible, any attempt to improve the disease in order to optimize respiratory function for surgery must be oriented toward three big categories under this condition: 8 1. Diffuse pulmonary fibrosis and/or granuloma, e.g., scleroderma, Boeck's sarcoid, berylliosis. These patients have an "alveolar-capillary" block. 2. Chronic bronchitis and/or emphysema. Between these two extremes is a spectrum with admixtures of both conditions to varying degrees. 3. Alveolar hypoventilation. Patients with normal lungs but with damaged respiratory centers, or paralyzed respiratory muscles, skeletal deformities as in the kyphotic, and the obese-Pickwickian syndrome.
Clearly, the objectives in preoperative inhalation therapy are to improve (1) alveolar ventilation, (2) arterial oxygenation, and (3) carbon dioxide elimination. The first may be improved by diminishing or eliminating airway resistance, e.g., bronchoconstriction, and the second and third by improving ventilation-perfusion.
Diffuse Pulmonary Fibrosis Not much can be done at the moment to change or mitigate pulmonary fibrosis, although awareness of the possible presence of "stiff" lungs in conditions such as scleroderma or Boeck's sarcoid might make the surgeon and the anesthesiologist more wary of getting the patient into situations where artificial ventilation might be needed but found *Chairman, Department of Anesthesiology, Presbyterian-St. Luke's Hospital. Clinical Professor of Anesthesiology, University of Illinois College of Medicine, Chicago, Illinois **Clinical Instructor in Anesthesiology, University of Illinois College of Medicine and Research and Educational Hospitals; Assistant Attending Anesthesiologist, PresbyterianSt. Luke's Hospital
Surgical Clinics of North America- Vol. 48, No. 1, February, 1968
29
30
REUBEN
C.
BALAGOT, VALERIE
R.
BANDELIN
ineffective. Inhalation therapy in this patient may be helpful in the presence of complications such as bronchitis and bronchopneumonia. But then, under such conditions, elective surgery will not be contemplated. What about emergency surgery? If only a short period of time is available for preparing the patient, the administration of nebulized bronchodilators such as isopropylnorepinephrine might help temporarily if no more than to assuage the mental state of the medical attendants. Chronic Bronchitis and/or Emphysema Strict delineation of the two extremes of obstructive lung disease, chronic bronchitis and emphysema, is frequently difficult. One can only pick from the varied spectrum between these extremes and state categorically that a patient has more bronchitis (obstruction) than emphysema or vice versa depending upon which group of signs and symptoms predominate. Briscoe and Nash 2 considered (a) dyspnea, (b) little cough, (c) little sputum, (d) translucent lung fields in the x-ray, (e) no cor pulmonale except terminally, and (f) normal hematocrit as predominantly emphysema; whereas (a) occasional dyspnea, (b) much cough, (c) much sputum, (d) normal lucency of lung fields, (e) tendency to cor pulmonale and (f) raised hematocrit or polycythemia represented a condition that was predominantly bronchitic. They assessed the contribution of what Hickam et al. 10 called the "slow space" to arterial oxygen saturation in a group of emphysematous and bronchitic patients. The slow space by definition consists of groups of alveoli probably scattered throughout the lungs that wash out nitrogen very slowly when oxygen is breathed. When in the normal lung, nitrogen washout is maximal within five to seven minutes, it may take more than 20 minutes for the slow space to achieve this state. The slow space is somewhat greater in volume in the purely emphysematous patient than the purely bronchitic patient. With intermittent positive pressure breathing (IPPB) alone without bronchodilators, arterial oxygen saturation in an emphysematous group was shown by Briscoe and N ash 2 to be significantly better than in a bronchitic group and was probably due to improved ventilation of the slow space. Interestingly enough, Briscoe et al. 3 also found a decrease in ventilation of the slow space with voluntary hyperventilation but a marked increase with IPPB. There was increased oxygen consumption due to increased work of breathing with voluntary hyperventilation but negligible increase with IPPB. Surely, therefore, there is a decided advantage to using IPPB in the preoperative preparation of the patient who suffers from obstructive bronchitis and emphysema. The advantage is much more so in the emphysematous patient, but is also significant in the bronchitic patient. Bronchodilators increase the advantageous results effected by IPPB. Goldberg and Cherniack9 showed an equal improvement in the various pulmonary function tests utilized whether the bronchodilator was adminstered by IPPB or by a properly used hand nebulizer to hospital patients suffering from chronic bronchitis and emphysema. And, contrary to the findings of Jones et al., 11 they did not find IPPB to produce air trapping and overinfiation in patients with severe emphysema. They fur-
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
31
ther speculated that IPPB might be more effective than a hand nebulizer in those patients with severe or acute respiratory distress. Secretions are usually a great problem in the predominantly bronchitic patient. If profuse amounts are brought up by the patient they must surely add to the airway obstruction.
Alveolar Hypoventilation The third large category of respiratory insufficiency is primary alveolar hypoventilation. Patients in this group who have either a damaged respiratory center or poorly functioning peripheral respiratory apparatus are usually already under good respiratory care, aided by ventilators, and do not need any extra preoperative inhalation therapy. One only makes sure that this excellent respiratory care they are getting is not diminished during anesthesia and postoperatively. Again in these patients the added complications of acute bronchitis and/or bronchopneumonia with its increased airway resistance caused by bronchial spasm and secretions will augment the extant alveolar hypoventilation. Some special problems in this group that are frequently encountered should be emphasized. The severe kyphoscoliotic patient has a distorted thoracic cage that severely limits the excursions of the lungs. This makes for a greater effort to ventilate and results in rapid shallow respirations. Alveolar hypoventilation frequently develops with its attendant hypoxia and hypercapnea. The same unphysiologic findings are encountered in the very obese patient-the Pickwickian syndrome. The massive chest and abdominal wall offer a tremendous resistance to respiratory effort. Cherniack, 4 in a study of a group of obese individuals, observed both hypoxia and hypercapnia in a third, and hypoxia but no hypercapnia in another third, suggesting alveolar hypoventilation in the first instance and possible altered ventilation-perfusion in the second group. Hypoxia and Hypercapnia. Any form of respiratory insufficiency eventually results in various degrees of hypoxia and hypercapnia. All signs and symptoms of any disease causing respiratory insufficiency may be related directly or indirectly to either or both conditions. Both hypoxia and hypercapnia provoke pulmonary vasoconstriction and with the added erythropoiesis of chronic hypoxia contribute greatly to cor pulmonale in these patients.
Summary of Therapy To optimize the patient with respiratory insufficiency for surgery, one hopes to decrease air-flow resistance by use of bronchodilators such as isopropylnorepinephrine or epinephrine and agents that will tend to thin or lyse bronchial secretions, examples of which are detergent aerosols such as Alevaire, Tergemist, and just plain normal saline. Mucolytic drugs like pancreatic dornase or acetylcysteine may help in this respect. They may be irritating to bronchial mucosa. The administration of a bronchodilator such as epinephrine or isoproterenol concurrently or before the mucolytic drugs may obviate bronchoconstriction from the irritation they cause.
32
REUBEN
C.
BALAGOT, VALERIE R. BANDELIN
Mechanical devices may then be employed to improve ventilation, i.e., use of IPPB units. By improving ventilation of the slow space, and assullling that improved ventilation also reflexly improves perfusion, arterial oxygen saturation is greatly augmented. One great advantage of IPPB of course over volitional hyperventilation is that the work of respiration is very much less than with hyperventilation and thus results in less oxygen consumption. Apparently, ventilation of the slow space is decreased instead of augmented with hyperventilation. 3 Caution must be observed in the vigorous treatment of severe respiratory insufficiency. Sudden marked changes in the extant hypercapnia and hypoxia can quickly lead to cardiovascular collapse and death.
POSTOPERATIVE INHALATION THERAPY It is now common knowledge that the respiration of a patient who has been subjected to a general anesthetic remains quite depressed for variable periods of time. In fact, it is not uncommon to find a Po 2 of 60 mm. Hg and rarely going above 85 mm. Hg unless respiration is augmented with IPPB or oxygen given by nasal catheter, by mask, or by face tent. This implies alveolar hypoventilation to a relative degree. Nevertheless, patients with normal respiratory function tend to do well. It becomes obvious, however, that the patient with chronic respiratory insufficiency in the immediate postoperative period may be in severe respiratory distress if the attendant postanesthetic depression is superimposed on the chronic alveolar insufficiency. Visual assessment of a patient's respiratory status in the immediate postoperative period is at best a wild, educated guess. The low arterial oxygen tensions found in these patients attest to this. It may be assumed that the overall depressive action of general anesthetic agents prevents the chemoreceptor bodies from augmenting respiratory ventilation in response to the low oxygen tensions. Since the carotid body and/or the aortic body will normally be activated by oxygen tensions below 60 mm. Hg, one may surmise that their reflex ability to respond may be frightfully diminished under the waning influence of anesthetic agents or that the respiratory center through which these bodies exert their augmentative action on ventilation is markedly depressed and will not respond to the weak chemoreceptor stimuli. Weakened or absent ciliary action and a diminished or absent cough reflex whether due to the anesthetic or premedicant narcotic undoubtedly contribute to formation of postoperative atelectasis which further augments the ventilatory insufficiency. Without doubt, therefore, some form of inhalation therapy will be beneficial in the immediate postoperative period.
Postanesthetic H ypoventilation Postanesthetic hypoventilation frequently goes unrecognized un· less arterial Po 2 and Pco 2 are monitored during this period. Our experience has shown that venous values, as well, will also reflect alveolar hypoventilation provided one is aware that Po 2 is lower and Pco2 higher in venous blood. The difference may be around 10 mm. Hg (higher) for
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
33
Pco 2 and 10 to 20 mm. Hg (lower) for 0 2 • Once hypoventilation is recognized, however, oxygen therapy, as has been routinely administered for years, is not the corrective method of choice. The use of IPPB to augment ventilation is the proper therapeutic approach. The pressurecycled ventilators have worked well for this purpose, e.g., the Bennett or the Bird IPPB units. It is always a temptation to administer 100 per cent oxygen with the reasoning that if 20 per cent in ambient air works well under normal conditions, more of it under abnormal conditions will by the same token work wonders. This of course is a perfect example of of too much of a good thing causing more harm than good. The use of 40 or 50 per cent oxygen with the IPPB is more than sufficient. In fact, nebulization of water or saline with oxygen to humidify the inhaled atmosphere frequently increased oxygen concentration to 93 per cent. s, 13 Oxygen toxicity and a few other unphysiologic effects of oxygen might offset all the advantages therapy offers. Atelectasis Atelectasis is a very frequent postsurgical complication that is most often ignored or missed until it becomes extensive and presents the classical findings of elevated temperature, pulse rate, and respiratory rate, and probably the other findings of segmental or regional lung density such as absence of breath sounds, dullness to percussion, and changes in radiolucency. The classic explanation for this syndrome is obstruction of a bronchus with thickened secretions and subsequent absorption of the gases beyond the obstruction, leading to alveolar collapse. Although atelectasis will develop with complete bronchial obstruction, there is really no correlation between atelectasis and partial obstruction with thickened secretions. Part of this erroneous conclusion may have been based on a study by Coryllos and Birnbaum6 in 1932 showing that it takes 16 hours for low solubility gases such as helium, nitrogen, and air to be absorbed from a lung whose bronchus is totally occluded whereas oxygen will be absorbed in a matter of minutes. These authors were not then aware of the role of surfactants in maintaining alveolar stability and possibly even gas transport. The current thinking is that atelectasis is caused by inspiratory insufficiency. This conclusion is based on studies by Mead and Collier12 and by Bendixen et al. 1 that spontaneous or artificial ventilation at constant tidal volumes will usually result in (1) decreased compliance, (2) decreased lung volume, and (3) increased shunting (venous admixture). These changes are conducive to atelectasis. They have been found to be preventable by sighing and/or occasional deep breathing. Clement et al. 5 postulates that deep breathing will mobilize surfactant from within the alveolar cell to augment or replace aging surfactant on the alveolar surface, maintaining alveolar stability and preventing atelectasis. From a therapeutic standpoint, some volume ventilators like the Emerson are capable of instituting the "sigh" or deep breathing at regularly designated intervals by means of a timing mechanism. The usual IPPB units in common use do not have this mechanism. In our Intensive Therapy Unit, this function is frequently performed by manual hyperinflation with an Ambu bag.
34
REUBEN
C.
BALAGOT, VALERIE
R. BANDELIN
The use of high humidity to soften or loosen or dissolve hard or desiccated secretions, as frequently practiced in the past, is probably of some value, not because of this particular action but because of its effect on ciliary activity. Inhaled air with a relative humidity lower than 70 per cent will inhibit ciliary activity; and it is ciliary activity that will usually break up secretions. Nebulization which serves to provide the humidity also functions as a vehicle for detergent solutions (Alevaire and Tergimist) to thin secretions, for mucolytic agents like Dornavac (deoxyribonuclease) or Mucomyst (acetylcysteine), and for bronchodilator agents such as epinephrine (levo or racemic) and isoproterenol. Deoxyribonuclease attacks pus and cellular debris whereas acetylcysteine acts on the polysaccharide bond of mucin. These mucolytic agents may be irritating to the mucosa and cause bronchoconstriction. 7 Previous or concomitant administration of isoproterenol might be helpful in preventing the bronchoconstriction. In view of changing concepts in regard to causation of atelectasis, i.e., inspiratory insufficiency instead of the classical "block" caused by mucous plugs, the value of agents that act primarily on secretions becomes somewhat limited, not to say conjectural to a degree. The occasional or even frequent augmentation of inspiration ("sigh") may be more helpful in preventing atelectasis than all the paraphernalia and accessories which make inhalation therapy impressive and expensive. There are other methods of treating a full-blown atelectasis. The relief of pain in upper abdominal area operations frequently eliminates "splinting" and enables the patient to take deep breaths-improving the atelectasis. The inhalation of carbon dioxide for a very brief period of time to the point of hyperpnea has worked well in our hands. Carbon dioxide gas is allowed to flow from a tank through a piece of tubing gently onto a patient's face, the tip of the tube being held 3 to 6 inches above his nose. The heavier-than-air gas will very quickly be inhaled by the patient causing rapid and deep respirations. This is allowed to continue for six to ten breaths, then stopped. This may be repeated every two to three hours until signs of atelectasis diminish or disappear. The same effects may be accomplished by inhalation of 5 per cent carbon dioxide in oxygen through a face mask and a bag. The temptation to administer the treatment for a longer period of time than necessary is very great with this technique, which in unfamiliar hands has been observed to provoke C0 2 convulsions and as serious a complication as a cerebrovascular accident. Another simple method is to increase the dead space by making the patient breathe into a long piece of corrugated anesthetic tubing. The rebreathing of a C0 2-enriched atmosphere again provokes hyperpnea. Schwartz et al. 16 have modified this by adding a face mask to one end of the tube to facilitate administration. In passing, pneumonia, which is probably an infected atelectasis, and pulmonary embolism should be mentioned as complications. Inhalation therapy serves as an excellent adjunct in the management of these conditions, but the infection has to be treated in pneumonia, and the perfusion improved in embolism. Both aspects are outside the scope of this paper.
PREOPERATIVE AND POSTOPERATIVE INHALATION THERAPY
35
Pulmonary Edema Pulmonary edema is not uncommon. The easy access to blood, plasma expanders, and other fluids during surgery increases this predilection. The inhalation of ether, ethyl alcohol (5 to 20 per cent), or a tertiary alcohol supposedly destroys the stabile foam formed which interferes with oxygen alveolar transport. The stability of the foam, however, was shown by Pattle 14 to be due to alveolar surfactant material which lined the foam formed from edema fluid and was quite resistant to the effects of ether or alcohol. From a chemical standpoint, however, sufficient amounts of the ether or alcohol will tend to disrupt the lipid lining of the foam. The beneficial effect of IPPB derives from its pressure effect of decreasing venous retum and probably from the forcible distention of alveoli, mobilization of alveolar cell surfactant, and diminishing surface tension, thus improving oxygenation.
Artificial Ventilation- Benefits and Cautions With development of radical surgical techniques particularly upon the cardiovascular system, we have found it beneficial and very helpful to take over the work of respiration immediately and for the first two or three days after surgery. The work of breathing which can, in patients with poor cardiovascular and respiratory function, take as much as 50 per cent of the oxygen consumption may be a great strain on a heart or a vascular system that has just been subjected to surgery. In taking over ventilatory function, the use of artificial ventilation with high oxygen concentrations gives rise to what was described under atelectasis, i.e., reduced compliance, reduced vital capacity, and poor oxygenation with concomitant hypoxia. This has been called the "respirator lung syndrome." Nash, Blennerhassett, and Pontoppidan 13 showed a correlation between the pathologic changes seen in the above syndrome and high oxygen tensions during ventilator therapy. These changes occurred in two phases- an exudative phase with an alveolar fibrinous exudate (hyaline membrane lining alveolar walls) and a proliferative phase with fibroblastic proliferation and hyperplasia of alveolar lining cells. Pratt, 15 on the other hand, found capillary congestion and increased alveolar septal thickness. He considers these to be a physiologic response to oxygen, i.e., increased oxygen supply to alveoli results reflexly in vasodilation of pulmonary arteries and arterioles with a consequent drop in pulmonary artery pressure. The opposite occurs with reduced oxygen supply. In a quick survey of 28 cases of "open-heart" surgery done at this institution in which the acid-base status and arterial oxygen tensions of the patients were monitored postoperatively until recovery or death, 3 out of 17 in the group who survived showed the typical decreased compliance ("stiff lungs") after more than 24 to 48 hours ventilator therapy on a pressure-cycled IPPB unit. In the group that died, 2 of 11 showed this syndrome. There were certain interesting observations made in this survey. A change from a pressure-cycled ventilator to a volume ventilator frequently resulted in a consistently lower arterial
36
REUBEN
C.
BALAGOT, VALERIE R. BANDELIN
Po 2 ; 8 out of the total demonstrated this observation (2 died). A majority of the patients who died showed a normal or alkalotic pH with normal or slightly decreased (negative) base excess. A number of these patients also showed an elevated or normal Po 2 - at least 5 showed a Po 2 of 88 to 170 mm. Hg. The significance of these preliminary observations cannot as yet be jelled into meaningful conclusions. Further studies are being done. One thing may be certain, and this is that oxygen toxicity in prolonged ventilator therapy may be contributory to morbidity or perhaps mortality. REFERENCES 1. Bendizen, H. H., Hedley-Whyte, J., and Laver, M. B.: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation-A concept of atelectasis. New Eng. J. Med., 269:991, 1963. 2. Briscoe, W. A., and Nash, E. S.: The slow space in chronia obstructive pulmonary disease. Ann. New York Acad. Sci., 121:706, 1965. 3. Briscoe, W. A., Emmanuel, G., Smith, W. M., and Cournand, A.: Effects of voluntary hyperventilation and intermittent pressure breathing on the distribution of ventilation and the distribution of perfusion. Fed. Proc., 20:421, 1964. 4. Cherniack, R. M.: Respiratory effects of obesity. Canad. Med. Assoc. J., 80:613, 1959. 5. Clements, J. A., and Tierney, D. F.: Alveolar instability associated with altered surface tension. Handbook of Physiology, Sec. 3, Respiration, Vol. II, 1565 pp., W. P. Fenn and H. Rann, (Eds.). Amer. Physiol. Soc., 1965. 6. Coryllos, P. N., and Birnbaum, G. L.: Studies in pulmonary gas absorption in bronchial obstruction. Amer. J. Med. Sc., 183:317, 1932. 7. Dalhamn, T.: Mucous flow and ciliary activity in the trachea of healthy rats and rats exposed to respiratory irritant gases. Acta Physiol. Scand., 36:Suppl. 123, 1956. 8. Fishman, A. P.: Roads to respiratory insufficiency. Ann. New York Acad. Sci. 121:657, 1965. 9. Goldberg, 1., and Cherniack, R. M.: Effects of nebulized bronchodilator delivered with and without IPPB on ventilatory function in chronic obstructive emphysema. Amer. Rev. Resp. Dis., 91:13, 1965. 10. Hickam, J. B., Blair, E., and Frayser, R.: An open circuit helium method for measuring functional residual capacity and defective intrapulmonary gas exchange. J. Clin. Invest., 33:1277, 1954. 11. Jones, R. H., MacNamara, J., and Gaensler, E. A.: Effects of IPPB on simulated pulmonary obstruction. Amer. Rev. Resp. Dis., 82:164, 1960. 12. Mead, J., and Collier, C.> Relation of volume history of lungs to respiratory mechanics in anesthetized dogs. J. Appl. Physiol., 14:669, 1959. 13. Nash, G., Blennerhassett, J. B., and Pontoppidan, H.: Pulmonary lesions associated with oxygen therapy and artificial ventilation. New Eng. J. Med., 276:369, 1967. 14. Pattie, R. E., and Burgess, F.: The lung lining film in some pathological conditions. J. Pathol. Bacterial., 82:315, 1961. 15. Pratt, P. C.: Reaction of the human lung to enriched oxygen atmosphere. Ann. New York Acad. Sci., 121:809, 1965. 16. Schwartz, S. 1., Dale, W. A., and Rahn, H.: Dead space rebreathing tube for prevention of atelectasis. ].A.M.A., 163:1248, 1957. 1753 West Congress Parkway Chicago, Illinois 60612