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Oxygen Therapy in Surgical Patients
Oxygen Therapy in Surgical Patients OSCAR FEINSILVER, M.D.*
The problems of oxygen therapy in the surgical patient differ from those of medical patients insofar as they present themselves in individuals whose pulmonary and cardiovascular systems are normal. They occur after relatively minor procedures carried out under general anesthesia. Hypoxia under these circumstances may, indeed, be profound. 4 • 28 Magnitude of the Problem It has been calculated that a normal 70 kg. man possesses about 1500 mI. of oxygen. At a normal rate of consumption, this supply will be completely exhausted within a period of 5 minutes. 15 • 31 The surgeon, consequently, may be faced with the problem of providing an adequate supply of oxygen to the tissues in the face of either reduced alveolar ventilation in patients with normal lungs or ineffective exchange of gases in patients with intrathoracic disease. The following questions must be answered for each individual: 1. When is oxygen therapy indicated? 2. What is the objective of therapy in terms of Po. (partial pressure of oxygen) and oxygen saturation? 3. Does a satisfactory arterial Po. level guarantee adequate tissue oxygenation? 4. What are the optimum techniques for providing supplementary oxygen? 5. When is ventilatory assistance in the form of stimulants helpful? 6. When is mechanical assistance useful? 7. What are the indications for hyperbaric oxygen treatment? 8. Can excessive oxygen be harmful?
Each of the above will be considered separately. When Is Oxygen Therapy Indicated? The answer to this question is obviously when hypoxia exists and requires recognition of acceptable values. In eastern Massachusetts, the normal P02 value is 85 to 98 mm. Hg. In Denver, Colorado, it is about 75 mm. Hg. A glance at the oxygen saturation curve shows that hemoglobin will be more than 90 per cent saturated, if pH is normal, when P02 is 65 ·Senior Physician, St. Vincent Hospital, Worcester, Massachusetts Surgical Clinics of North America- Vol. 49, No.3, June, 1969
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Figure 1. Oxygen-hemoglobin dissociation curves. (From Physiology of Flight. Air Force Manual 160-30. Reproduced with permission.)
mm. (Fig. 1). Consequently, a P0 2 of 60 to 65 is regarded as the critical level below which the patient is in danger.38 It should be pointed out that no rigid rule can be established because a P0 2 that is adequate for patients with normal circulation may be totally inadequate for those whose circulation is compromised by disease. How Can One Recognize Hypoxia? While cyanosis suggests the presence of at least 5 gm. of reduced hemoglobin in the capillary circulation of the presenting area, it has been shown to be a very unreliable sign. 12 Furthermore, its presence may indicate a high degree of dilatation of capillaries on the venous side, such as may be present in polycythemia, while arterial P02 may be normal. Patients with anemia or carbon monoxide poisoning may be severely hypoxic but not show cyanosis. Signs of tissue hypoxia depend largely upon the organ or organs involved. One of the earliest to show evidence of reduced oxygen supply is the cerebrum. Confusion or loss of consciousness may appear. Moderate hypoxia calls for increased cardiac output, while progressive reduction of arterial P02 makes adequate myocardial performance impossible. 6 Consequently, cardiac hypoxia leads to congestive heart failure which does not respond to digitalis or diuresis but responds promptly to oxygen. 16 Frequently one observes generalized edema resembling that seen in nephrosis. This, however, disappears completely with oxygen therapy. It is assumed, therefore, that in the presence of severe anoxia the capillary endothelial barrier fails to function adequately. It is essential to watch for hypoxia after general anesthesia. Arterial blood study is the only reliable indication of its existence, and this study should be performed as often as necessary for adequate guidance.
OXYGEN THERAPY IN SURGICAL PATIENTS
659
What Is the Relationship Between Arterial P02 and Tissue Requirements? When blood and circulation are normal, adequate oxygenation of tissues is guaranteed by a normal Po2 • However, this is not true in the presence of severe anemia, poisoning by carbon monoxide or cyanide, markedly increased viscosity of blood by polycythemia, vasomotor collapse, or severe arteriosclerosis. Under these circumstances, profound tissue anoxia may accompany normal arterial Po2 • It is important to view the common practice of administering oxygen by intermittent positive pressure breathing (IPPB) as an example of a situation in which tissue hypoxia may exist while the arterial blood is fully saturated. I have seen patients, in continuous coma while receiving oxygen by IPPB, awakened by the simple expedient of allowing them to breathe air at atmospheric pressure, thereby restoring cardiac output and cerebral blood flow to normal.
Optimum Techniques for Administration of Oxygen Precise ventilatory standards have been set by Radford and coworkers.30 Some of the common devices for administration of oxygen have been compared by Kory and co-workers.21 Campbell prefers the Venturi mask. 9 The plastic nasal catheter is the choice of this author for several reasons. It can be used continuously with relative comfort during meals and other activities. It does not by-pass the nose. Consequently, humidification and warming of the inhaled gas is adequate. While general rules may be formulated for the normal lung with respect to the relationship between oxygen flow rate and desired arterial Po2 , this is impossible to provide for the diseased lung. Large variations of physiologic dead space, which can be as high as 70 to 80 per cent of the tidal volume, as well as large venous-to-arterial pulmonary shunts, make guidance possible only by the routine examination of arterial blood for Po2 , pH, and Pco2 , until a relationship for the individual is established, and, of course, this may change with alteration of his status. Humidification When a nasal catheter is used, or when the patient breathes through his mouth, adequate provision must be made for humidification at a temperature of 53 degrees C., and for a conducting tube which does not exceed 5 feet in length. 39 Since air, when saturated, at body temperature contains 10 times the amount of water that it does at 0 degrees C., cold inspired oxygen, even if fully saturated, must cause intense drying of the lower respiratory tract, as its temperature rises, when it has been allowed to by-pass the nose. Importance of Periodic Deep Breathing Postoperatively One of the sources of postoperative disability is failure on the part of the patient to breathe deeply because of sedation, prun, or both. Since pulmonary compliance varies directly with tidal volume, encouraging the patient to take deep breaths is frequently desirable. The mechanism by which compliance is increased following a deep breath is said to be the
660
OSCAR FEINSILVER
result of entry of stored surfactant into the expanding alveolae and consequent lowering of surface tension. l l Inhalation of Detergents and Enzymes Preparations such as Alevaire, Mucomyst, and Dornavac and trypsin and streptokinase have been in use for some time. Beneficial results are difficult to demonstrate. There are many violent reactions. Frequently chronic irritation results, and the cause may not be apparent until the use of these substances is terminated. It is the author's belief that whatever remote benefits Inight be obtained are greatly counterbalanced by potential chemical irritation. The only adjuvant that can be used safely from time to time is steam. Avoidance of CO2 Narcosis An occasional complication of oxygen therapy can occur in individuals with obstructive lung disease in whom CO 2 elimination has been impaired. It has been shown that these individuals establish a compromise with respect to elimination of CO 2 in order to miniInize the work of breathing in a system already overloaded. 2 , 10,24 Consequently, their respiratory centers fail to respond to CO2 in the same degree as respiratory centers of those whose lungs are normal. The result of oxygen adIninistration can be prompt reduction of ventilation by elimination or lessening of the anoxic stimulus and accumulation of CO2 to narcotic proportions (Fig. 2). The following steps are taken in the management of this problem. CONTROLLED OXYGEN THERAPY. The rate of oxygen administration is adjusted to provide the lowest possible P0 2 that will be helpful to the 140 rom.
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Figure 2. Influence of oxygen therapy upon an alert but anoxic patient. Reduced ventilation leads to changes indicated. Broken horizontal lines indicate nonnallevels. (Reproduced by permission from Feinsilver, 0.: An approach to the complexity of cor pulmonale. Amer. Pract. Dig. Treat., 8:1368,1957.)
OXYGEN THERAPY IN SURGICAL PATIENTS
661
patient without eliminating this anoxic stimulus in accordance with the guidelines described above. 3s RESPIRATORY STIMULANTS. If the above compromise cannot be accomplished satisfactorily, the use of respiratory stimulants, such as Coramine or Emivan, is indicated. 1s. 33 The use of respiratory stimulants is favored over the use of mechanical ventilators because the latter are associated with many undersirable disturbances. They may reduce sharply the oxygen supply to tissues by reduction of cardiac output. 7• 1S Often, air trapping is increased, and ventilation actually deteriorates. 2o Infection disseminated by this equipment is much more common than is realized. 32 Finally, mortality is actually increased by the use of these machines. 36 Treatment of Coma Due to Respiratory Failure The development of coma in respiratory insufficiency is complex in origin. The most obvious disorder is the rise in Pco2and the development of acidosis. However, there probably exists a marked reduction in cerebral blood flow. While both CO 2 and hypoxia will increase cerebral blood flow initially, sustained abnormality of one or both leads to elevation of intracranial pressure by impairment of function of the blood-fluid barrier.23 Routine spinal taps during the course of coma associated with respiratory insufficiency reveal pressures from 300 to 450 mm. H 20. If these levels are converted to mm. Hg, a level of 22 to 32 is obtained. This constitutes resistance to blood flow. Since intracapillary pressure is 15 to 35 mm. Hg,Slittle or no blood flow can take place under these conditions. Consequently, the author has adopted the routine performance of spinal taps in all of these patients, removing as much fluid as necessary to bring the pressure down to 100 mm. H 20. This is repeated as often as necessary to keep the level normal. It has been observed that the simple step of lowering the intracranial pressure to normal frequently leads to prompt restoration of consciousness and spontaneous increase in minute ventilation. When coma persists despite adequate care of the airway, decompression of the brain, and chemical stimulation, mechanical assistance becomes necessary. Use of Mechanical Assistance This author feels, as does Campbell,9 that mechanical assistance is probably never necessary when the patient is conscious. When it is used, an endotracheal tube should be utilized. Although an IPPB machine can be utilized for this purpose, a more effective device is a volume-controlled ventilator such as the one manufactured by the Emerson Company. With this apparatus any predetermined minute ventilation can be maintained without concern about changing airway resistance or pulmonary compliance. 5 When available, the use of the Drinker Tank respirator is most effective because it avoids the complications that result from the application of positive pressure to the airway. When any mechanical device is used, arterial blood must be carefully monitored in order to avoid the hazard of hyperventilation and guarantee adequate respiratory exchange.
662
OSCAR FEINSILVER
Tracheostomy adds considerably to complications of mechanical ventilatory assistance and is probably never necessary except for laryngeal obstruction or esophageal obstruction. 9. 36. 37 Indications for Hyperbaric Oxygen Recent reviews by Saltzman3. 34 describe the indications and the technical problems of hyperbaric oxygen treatment. The most important indications may be listed as follows: carbon monoxide poisoning, decompression sickness, certain malignant tumors in conjunction with radiotherapy, gas gangrene, and clostridial infections. What Is the Consequence of Excessive Oxygenation of Arterial Blood? Since the normal P0 2 of 90 to 100 gives rise to almost 100 per cent saturation of arterial blood by virtue of the characteristics of the oxygen saturation curve, nothing is gained by exceeding a P02 of 100. Additional oxygen can be dissolved in the plasma, however, at the rate of 0.003 mI. per mm. Hg of oxygen. Consequently, if the P0 2 is 200 instead of 100, the oxygen in solution becomes 0.6 m!. instead of 0.3 mi., and if the P02 is 600 as a result of administration of 100 per cent oxygen, 1.8 mi. of oxygen would be dissolved. The consequences of this situation is manifold and will be discussed briefly. INFLUENCE ON ACID-BASE BALANCE OF TISSUES. Normally, after removal of oxygen, 4 to 5 gm. of reduced hemoglobin is available to the body tissues for combination with carbon dioxide. It is the hemoglobin that is responsible initially for carriage of most of the CO 2.13 If a significant portion of the oxygen is made available to the tissues by that which is dissolved in plasma, there is correspondingly less reduced hemoglobin available for removal of CO 2, The result is increasing tissue acidosis in the presence of highly oxygenated blood and arterial alkalemia. 22 INFLUENCE ON ENZYME ACTION. Ever since Pasteur called attention to the inhibitory effect of oxygen on fermentation, evidence has been accumulating that shows it has a similar effect when it is present in concentrations only little beyond normal for only a short time. These effects have been recently summarized by Haugaard. 19 Davies and Davies 14 present a list of 38 enzymes whose action is reduced or inhibited by oxygen tension above normal levels. DIRECT EFFECT UPON LUNG STRUCTURE. Direct damage to pulmonary structure by elevated P0 2 has been described both in animals and in humans. Pulmonary changes described by Pratt in human lungs exposed to 50 per cent oxygen, in some instances for less than 24 hours, consist of capillary proliferation, irregular thickening of alveolar septae, and increased amount of reticulum. 29 Pulmonary hemorrhage has been described by several sources.\' 26. 35 Nash and associates 26 studied 70 patients after prolonged oxygen therapy. They described early exudative changes with congestion, edema, intra-alveolar hemorrhage, and fibrinous exudate, followed by a late proliferative stage with hyperplasia of alveolar cells. Similar changes have been described in infants.27 AI-
OXYGEN THERAPY IN SURGICAL PATIENTS
teration in atelectasis.
663
pulmonary surfactant takes place,25 predisposing to
INVOLVEMENT OF OTHER ORGANS. Toxic effects upon most other organs have been reported. 22 The most prominent are those of the nervous system and the eyes, in which the development of retrolental fibroplasia takes place. 1
SUMMARY Supplementary oxygen treatment must be considered in every surgical patient who has been subjected to general anesthesia. This should be provided by the simplest technique available with proper humidification. The indication for oxygen treatment is a level of arterial blood below 65 mm. Hg. When simple techniques are inadequate, the use of respiratory stimulants should be tried. Finally, ventilatory assistance should be provided when no other approach will provide an adequate P02. However, under these circumstances we must be concerned about the adequacy of cardiac output, the tissue oxygen supply, the endotracheal connection, and increased intratracheal secretion. A discussion of the hazards of providing a P02 in excess of 100 is presented.
REFERENCES 1. Balentine, J. D.: Pathologic effects of exposure to high oxygen tensions. New Eng. J. . Med., 275:1038, 1966. 2. Barnett, T. B., and Peters, R. M.: Studies on the mechanism of oxygen-induced hypoventilation. An experiment approach. J. Clin. Invest., 41 :335, 1962. 3. Behnke, A. R., and Saltzman, H. A.: Hyperbaric oxygenation. New Eng. J. Med., 276: 1423, 1967. 4. Bendixen, H. H., Hedley-Whyte, J., and Laver, M. B.: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. New Eng. J. Med., 269:991, 1963. 5. Bendixen, H. H., Egbert, L. D., Hedley-Whyte, J., Laver, M. D., and Pontoppidan, H.: Respiratory Care. St. Louis, The C. v. Mosby Co., 1955. 6. Bing, R. J., Hammond, M. M., Handelsman, J. C., Powers, S. R., Spencer, F. C., Echenkoff, J. E., Goodale, W. T., Hafkenschiel, J. H., and Kety, S. S.: Measurement of coronary blood flow, oxygen consumption, and ventricular efficiency of the left ventricle in man. Amer. Heart J., 38:1,1949. 7. Brecher, G. A., and Mixter, G., Jr.: Effect of respiratory movement of superior cava flow under normal and abnormal conditions. Amer. J. Phys., 172:457, 1953. 8. Burton, A. C.: Physiology and Biophysics of the Circulation. Chicago, Year Book Medical Publishers, Inc., 1965. 9. Campbell, E. J. M.: The J. Burns Amberson Lecture. The management of acute respiratory failure in chronic bronchitis and emphysema. Amer. Rev. Resp. Dis., 96:626,1967. 10. Cherniak, R. M., and Snidel, D. P.: The effect of obstruction to breathing on the ventilatory response to CO2 , J. Clin. Invest., 35:1286,1956. 11. Clements,.J. A.: Surface active materials in the lungs. In The Lung. Baltimore, The Williams & Wilkins Co., 1968. 12. Comroe, J. H., and Dripps, R. D.: The Physiological Basis for Oxygen Therapy. Springfield, Illinois, Charles C Thomas, Publisher, 1950. 13. Davenport, H. W.: The ABC of Acid-Base Chemistry. Chicago, University of Chicago Press, 1950. 14. Davies, H. C. and Davies, R. E.: Biochemical aspects of oxygen poisoning. In Respiration. Vol. 2. Baltimore, The Williams & Wilkins Co., 1965. 15. Fahri, L. E.: Gas stores of the body. In Respiration. Vol. 1. Baltimore, The Williams & Wilkins Co., 1964. 16. Feinsilver, 0.: An approach to the complexity of cor pulmonale. Amer. Pract. Dig. Treat., 8:1368,1957. 17. Feinsilver, 0.: Circulatory changes associated with intermittent positive pressure treatment. Dis. Chest, 37:87, 1958.
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18. Feinsilver, O. The role of nikethamide as a respiratory stimulant in the management of pulmonary insufficiency. Curro Ther. Res., 4: 165, 1962. 19. Haugaard, N.: Cellular mechanisms of oxygen toxicity. Physiol. Rev., 48:311, 1968. 20. Jones, R H., Macnamara, J., and Gaensler, E. A.: Effects of intermittent positive pressure breathing in simulated pulmonary obstruction. Amer. Rev. Resp. Dis., 82:164,1960. 21. Kory, R C., Bergmann, J. C., Sweet, R D., and Smith, J. R: Comparative evaluation of oxygen therapy techniques. J.A.M.A., 179:767, 1962. 22. Lambertson, C. J.: Effect of oxygen at high partial pressure. In Respiration. Vol. 2. Baltimore, The Williams & Wilkins Co., 1965. 23. Lending, M.: Effect of hyperoxia, hypercapnia, and hypoxia on blood-cerebrospinal fluid barrier. Amer. J. Physiol., 200:959, 1961. 24. Laurenco, R V., and Miranda, J. M.: Drive and performance of ventilatory apparatus in chronic obstructive lung disease. New Eng. J. Med., 279:53,1968. 25. Morgan, T. E., Finley, T. N., Huber, G. L., and Fialkow, H.: Alterations in pulmonary surface active lipids during exposure to increased oxygen tension. J. Clin. Invest., 44:1737,1965. 26. Nash, G., Blennerhassett, J. B., and Pontoppidan, H.: Pulmonary lesions associated with oxygen therapy and artificial ventilation. New Eng. J. Med., 276:368, 1967. 27. Northway, W. H., Jr., Rosan, R C., and Porter, D. Y.: Pulmonary disease following respiration therapy of hyaline-membrane disease. New Eng. J. Med., 276:357, 1967. 28. Nunn, J. F., and Payne, J. P.: Hypoxaemia after general anaesthesia. Lancet, 2:631, 1962. 29. Pratt, P. C.: The reaction of human lung to enriched oxygen atmosphere. Ann. N.Y. Acad. Med., 121 :809,1965. 30. Radford, E. P., Jr., Ferris, B. G., Jr., and Kriete, B. C.: Clinical use of a nomogram to estimate proper ventilation during artificial ventilation. New Eng. J. Med., 251 :877, 1954. 31. Rahn, H.: Oxygen stores of man. In Oxygen in the Animal Organism. I.V.B.Symposium, 31 :609, 1963. 32. Reinarz, J. A., Pierce, A. K., Mays, B. B., and Sanford, J. P.: Potential role of inhalation therapy equipment in nosocomial pulmonary infection. J. Clin. Invest., 44:831,1965. 33. Said, I. S., and Banerjee, C. M.: Effects of a newer respiratory stimulant (vanillic diethylamide) in respiratory acidosis due to obstructive pulmonary insufficiency. Amer. J. Med., 33:845,1962. 34. Saltzman, H. A.: Rational normobaric and hyperbaric oxygen therapy. Ann. Int. Med., 67:845, 1967. 35. Shanklin, D. R, and Wolfson, S. L.: Therapeutic oxygen as a possible cause of pulmonary hemorrhage in premature infants. New Eng. J. Med., 277:833, 1967. 36. Smith, J. P., Stone, R W., and Muschenheim, C.: Acute respiratory failure in chronic lung disease. Amer. Rev. Resp. Dis., 97:791, 1968. 37. Stone, D. J., Keltz, H., and Kaplan, S.: A controlled study of assist ventilation in the therapy of acute pulmonary insufficiency. Trans. 25th Res. Conf. Pulm. Dis., VAArmed Forces, 1966. 38. Therapy of acute respiratory failure - Statement of committee on therapy of the American Thoracic Society. Amer. Rev. Resp. Dis., 93:475,1966. 39. Wells, R E., Jr., Perera, R D., and Kinney, J. M.: Humidification of oxygen during inhalation therapy. New Eng. J. Med., 268:644,1963. 390 Main Street Worcester, Massachusetts 01608
The problems of oxygen therapy in the surgical patient differ from those of medical patients insofar as they present themselves in individuals whose pulmonary and cardiovascular systems are normal. They occur after relatively minor procedures carried out under general anesthesia. Hypoxia under these circumstances may, indeed, be profound. 4 • 28 Magnitude of the Problem It has been calculated that a normal 70 kg. man possesses about 1500 mI. of oxygen. At a normal rate of consumption, this supply will be completely exhausted within a period of 5 minutes. 15 • 31 The surgeon, consequently, may be faced with the problem of providing an adequate supply of oxygen to the tissues in the face of either reduced alveolar ventilation in patients with normal lungs or ineffective exchange of gases in patients with intrathoracic disease. The following questions must be answered for each individual: 1. When is oxygen therapy indicated? 2. What is the objective of therapy in terms of Po. (partial pressure of oxygen) and oxygen saturation? 3. Does a satisfactory arterial Po. level guarantee adequate tissue oxygenation? 4. What are the optimum techniques for providing supplementary oxygen? 5. When is ventilatory assistance in the form of stimulants helpful? 6. When is mechanical assistance useful? 7. What are the indications for hyperbaric oxygen treatment? 8. Can excessive oxygen be harmful?
Each of the above will be considered separately. When Is Oxygen Therapy Indicated? The answer to this question is obviously when hypoxia exists and requires recognition of acceptable values. In eastern Massachusetts, the normal P02 value is 85 to 98 mm. Hg. In Denver, Colorado, it is about 75 mm. Hg. A glance at the oxygen saturation curve shows that hemoglobin will be more than 90 per cent saturated, if pH is normal, when P02 is 65 ·Senior Physician, St. Vincent Hospital, Worcester, Massachusetts Surgical Clinics of North America- Vol. 49, No.3, June, 1969
657
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Figure 1. Oxygen-hemoglobin dissociation curves. (From Physiology of Flight. Air Force Manual 160-30. Reproduced with permission.)
mm. (Fig. 1). Consequently, a P0 2 of 60 to 65 is regarded as the critical level below which the patient is in danger.38 It should be pointed out that no rigid rule can be established because a P0 2 that is adequate for patients with normal circulation may be totally inadequate for those whose circulation is compromised by disease. How Can One Recognize Hypoxia? While cyanosis suggests the presence of at least 5 gm. of reduced hemoglobin in the capillary circulation of the presenting area, it has been shown to be a very unreliable sign. 12 Furthermore, its presence may indicate a high degree of dilatation of capillaries on the venous side, such as may be present in polycythemia, while arterial P02 may be normal. Patients with anemia or carbon monoxide poisoning may be severely hypoxic but not show cyanosis. Signs of tissue hypoxia depend largely upon the organ or organs involved. One of the earliest to show evidence of reduced oxygen supply is the cerebrum. Confusion or loss of consciousness may appear. Moderate hypoxia calls for increased cardiac output, while progressive reduction of arterial P02 makes adequate myocardial performance impossible. 6 Consequently, cardiac hypoxia leads to congestive heart failure which does not respond to digitalis or diuresis but responds promptly to oxygen. 16 Frequently one observes generalized edema resembling that seen in nephrosis. This, however, disappears completely with oxygen therapy. It is assumed, therefore, that in the presence of severe anoxia the capillary endothelial barrier fails to function adequately. It is essential to watch for hypoxia after general anesthesia. Arterial blood study is the only reliable indication of its existence, and this study should be performed as often as necessary for adequate guidance.
OXYGEN THERAPY IN SURGICAL PATIENTS
659
What Is the Relationship Between Arterial P02 and Tissue Requirements? When blood and circulation are normal, adequate oxygenation of tissues is guaranteed by a normal Po2 • However, this is not true in the presence of severe anemia, poisoning by carbon monoxide or cyanide, markedly increased viscosity of blood by polycythemia, vasomotor collapse, or severe arteriosclerosis. Under these circumstances, profound tissue anoxia may accompany normal arterial Po2 • It is important to view the common practice of administering oxygen by intermittent positive pressure breathing (IPPB) as an example of a situation in which tissue hypoxia may exist while the arterial blood is fully saturated. I have seen patients, in continuous coma while receiving oxygen by IPPB, awakened by the simple expedient of allowing them to breathe air at atmospheric pressure, thereby restoring cardiac output and cerebral blood flow to normal.
Optimum Techniques for Administration of Oxygen Precise ventilatory standards have been set by Radford and coworkers.30 Some of the common devices for administration of oxygen have been compared by Kory and co-workers.21 Campbell prefers the Venturi mask. 9 The plastic nasal catheter is the choice of this author for several reasons. It can be used continuously with relative comfort during meals and other activities. It does not by-pass the nose. Consequently, humidification and warming of the inhaled gas is adequate. While general rules may be formulated for the normal lung with respect to the relationship between oxygen flow rate and desired arterial Po2 , this is impossible to provide for the diseased lung. Large variations of physiologic dead space, which can be as high as 70 to 80 per cent of the tidal volume, as well as large venous-to-arterial pulmonary shunts, make guidance possible only by the routine examination of arterial blood for Po2 , pH, and Pco2 , until a relationship for the individual is established, and, of course, this may change with alteration of his status. Humidification When a nasal catheter is used, or when the patient breathes through his mouth, adequate provision must be made for humidification at a temperature of 53 degrees C., and for a conducting tube which does not exceed 5 feet in length. 39 Since air, when saturated, at body temperature contains 10 times the amount of water that it does at 0 degrees C., cold inspired oxygen, even if fully saturated, must cause intense drying of the lower respiratory tract, as its temperature rises, when it has been allowed to by-pass the nose. Importance of Periodic Deep Breathing Postoperatively One of the sources of postoperative disability is failure on the part of the patient to breathe deeply because of sedation, prun, or both. Since pulmonary compliance varies directly with tidal volume, encouraging the patient to take deep breaths is frequently desirable. The mechanism by which compliance is increased following a deep breath is said to be the
660
OSCAR FEINSILVER
result of entry of stored surfactant into the expanding alveolae and consequent lowering of surface tension. l l Inhalation of Detergents and Enzymes Preparations such as Alevaire, Mucomyst, and Dornavac and trypsin and streptokinase have been in use for some time. Beneficial results are difficult to demonstrate. There are many violent reactions. Frequently chronic irritation results, and the cause may not be apparent until the use of these substances is terminated. It is the author's belief that whatever remote benefits Inight be obtained are greatly counterbalanced by potential chemical irritation. The only adjuvant that can be used safely from time to time is steam. Avoidance of CO2 Narcosis An occasional complication of oxygen therapy can occur in individuals with obstructive lung disease in whom CO 2 elimination has been impaired. It has been shown that these individuals establish a compromise with respect to elimination of CO 2 in order to miniInize the work of breathing in a system already overloaded. 2 , 10,24 Consequently, their respiratory centers fail to respond to CO2 in the same degree as respiratory centers of those whose lungs are normal. The result of oxygen adIninistration can be prompt reduction of ventilation by elimination or lessening of the anoxic stimulus and accumulation of CO2 to narcotic proportions (Fig. 2). The following steps are taken in the management of this problem. CONTROLLED OXYGEN THERAPY. The rate of oxygen administration is adjusted to provide the lowest possible P0 2 that will be helpful to the 140 rom.
lOOmn-...
PCO
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Oxygen Saturation
Admission Levels
.
Oxygen Administered
Patient Comatose
Figure 2. Influence of oxygen therapy upon an alert but anoxic patient. Reduced ventilation leads to changes indicated. Broken horizontal lines indicate nonnallevels. (Reproduced by permission from Feinsilver, 0.: An approach to the complexity of cor pulmonale. Amer. Pract. Dig. Treat., 8:1368,1957.)
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patient without eliminating this anoxic stimulus in accordance with the guidelines described above. 3s RESPIRATORY STIMULANTS. If the above compromise cannot be accomplished satisfactorily, the use of respiratory stimulants, such as Coramine or Emivan, is indicated. 1s. 33 The use of respiratory stimulants is favored over the use of mechanical ventilators because the latter are associated with many undersirable disturbances. They may reduce sharply the oxygen supply to tissues by reduction of cardiac output. 7• 1S Often, air trapping is increased, and ventilation actually deteriorates. 2o Infection disseminated by this equipment is much more common than is realized. 32 Finally, mortality is actually increased by the use of these machines. 36 Treatment of Coma Due to Respiratory Failure The development of coma in respiratory insufficiency is complex in origin. The most obvious disorder is the rise in Pco2and the development of acidosis. However, there probably exists a marked reduction in cerebral blood flow. While both CO 2 and hypoxia will increase cerebral blood flow initially, sustained abnormality of one or both leads to elevation of intracranial pressure by impairment of function of the blood-fluid barrier.23 Routine spinal taps during the course of coma associated with respiratory insufficiency reveal pressures from 300 to 450 mm. H 20. If these levels are converted to mm. Hg, a level of 22 to 32 is obtained. This constitutes resistance to blood flow. Since intracapillary pressure is 15 to 35 mm. Hg,Slittle or no blood flow can take place under these conditions. Consequently, the author has adopted the routine performance of spinal taps in all of these patients, removing as much fluid as necessary to bring the pressure down to 100 mm. H 20. This is repeated as often as necessary to keep the level normal. It has been observed that the simple step of lowering the intracranial pressure to normal frequently leads to prompt restoration of consciousness and spontaneous increase in minute ventilation. When coma persists despite adequate care of the airway, decompression of the brain, and chemical stimulation, mechanical assistance becomes necessary. Use of Mechanical Assistance This author feels, as does Campbell,9 that mechanical assistance is probably never necessary when the patient is conscious. When it is used, an endotracheal tube should be utilized. Although an IPPB machine can be utilized for this purpose, a more effective device is a volume-controlled ventilator such as the one manufactured by the Emerson Company. With this apparatus any predetermined minute ventilation can be maintained without concern about changing airway resistance or pulmonary compliance. 5 When available, the use of the Drinker Tank respirator is most effective because it avoids the complications that result from the application of positive pressure to the airway. When any mechanical device is used, arterial blood must be carefully monitored in order to avoid the hazard of hyperventilation and guarantee adequate respiratory exchange.
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Tracheostomy adds considerably to complications of mechanical ventilatory assistance and is probably never necessary except for laryngeal obstruction or esophageal obstruction. 9. 36. 37 Indications for Hyperbaric Oxygen Recent reviews by Saltzman3. 34 describe the indications and the technical problems of hyperbaric oxygen treatment. The most important indications may be listed as follows: carbon monoxide poisoning, decompression sickness, certain malignant tumors in conjunction with radiotherapy, gas gangrene, and clostridial infections. What Is the Consequence of Excessive Oxygenation of Arterial Blood? Since the normal P0 2 of 90 to 100 gives rise to almost 100 per cent saturation of arterial blood by virtue of the characteristics of the oxygen saturation curve, nothing is gained by exceeding a P02 of 100. Additional oxygen can be dissolved in the plasma, however, at the rate of 0.003 mI. per mm. Hg of oxygen. Consequently, if the P0 2 is 200 instead of 100, the oxygen in solution becomes 0.6 m!. instead of 0.3 mi., and if the P02 is 600 as a result of administration of 100 per cent oxygen, 1.8 mi. of oxygen would be dissolved. The consequences of this situation is manifold and will be discussed briefly. INFLUENCE ON ACID-BASE BALANCE OF TISSUES. Normally, after removal of oxygen, 4 to 5 gm. of reduced hemoglobin is available to the body tissues for combination with carbon dioxide. It is the hemoglobin that is responsible initially for carriage of most of the CO 2.13 If a significant portion of the oxygen is made available to the tissues by that which is dissolved in plasma, there is correspondingly less reduced hemoglobin available for removal of CO 2, The result is increasing tissue acidosis in the presence of highly oxygenated blood and arterial alkalemia. 22 INFLUENCE ON ENZYME ACTION. Ever since Pasteur called attention to the inhibitory effect of oxygen on fermentation, evidence has been accumulating that shows it has a similar effect when it is present in concentrations only little beyond normal for only a short time. These effects have been recently summarized by Haugaard. 19 Davies and Davies 14 present a list of 38 enzymes whose action is reduced or inhibited by oxygen tension above normal levels. DIRECT EFFECT UPON LUNG STRUCTURE. Direct damage to pulmonary structure by elevated P0 2 has been described both in animals and in humans. Pulmonary changes described by Pratt in human lungs exposed to 50 per cent oxygen, in some instances for less than 24 hours, consist of capillary proliferation, irregular thickening of alveolar septae, and increased amount of reticulum. 29 Pulmonary hemorrhage has been described by several sources.\' 26. 35 Nash and associates 26 studied 70 patients after prolonged oxygen therapy. They described early exudative changes with congestion, edema, intra-alveolar hemorrhage, and fibrinous exudate, followed by a late proliferative stage with hyperplasia of alveolar cells. Similar changes have been described in infants.27 AI-
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pulmonary surfactant takes place,25 predisposing to
INVOLVEMENT OF OTHER ORGANS. Toxic effects upon most other organs have been reported. 22 The most prominent are those of the nervous system and the eyes, in which the development of retrolental fibroplasia takes place. 1
SUMMARY Supplementary oxygen treatment must be considered in every surgical patient who has been subjected to general anesthesia. This should be provided by the simplest technique available with proper humidification. The indication for oxygen treatment is a level of arterial blood below 65 mm. Hg. When simple techniques are inadequate, the use of respiratory stimulants should be tried. Finally, ventilatory assistance should be provided when no other approach will provide an adequate P02. However, under these circumstances we must be concerned about the adequacy of cardiac output, the tissue oxygen supply, the endotracheal connection, and increased intratracheal secretion. A discussion of the hazards of providing a P02 in excess of 100 is presented.
REFERENCES 1. Balentine, J. D.: Pathologic effects of exposure to high oxygen tensions. New Eng. J. . Med., 275:1038, 1966. 2. Barnett, T. B., and Peters, R. M.: Studies on the mechanism of oxygen-induced hypoventilation. An experiment approach. J. Clin. Invest., 41 :335, 1962. 3. Behnke, A. R., and Saltzman, H. A.: Hyperbaric oxygenation. New Eng. J. Med., 276: 1423, 1967. 4. Bendixen, H. H., Hedley-Whyte, J., and Laver, M. B.: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. New Eng. J. Med., 269:991, 1963. 5. Bendixen, H. H., Egbert, L. D., Hedley-Whyte, J., Laver, M. D., and Pontoppidan, H.: Respiratory Care. St. Louis, The C. v. Mosby Co., 1955. 6. Bing, R. J., Hammond, M. M., Handelsman, J. C., Powers, S. R., Spencer, F. C., Echenkoff, J. E., Goodale, W. T., Hafkenschiel, J. H., and Kety, S. S.: Measurement of coronary blood flow, oxygen consumption, and ventricular efficiency of the left ventricle in man. Amer. Heart J., 38:1,1949. 7. Brecher, G. A., and Mixter, G., Jr.: Effect of respiratory movement of superior cava flow under normal and abnormal conditions. Amer. J. Phys., 172:457, 1953. 8. Burton, A. C.: Physiology and Biophysics of the Circulation. Chicago, Year Book Medical Publishers, Inc., 1965. 9. Campbell, E. J. M.: The J. Burns Amberson Lecture. The management of acute respiratory failure in chronic bronchitis and emphysema. Amer. Rev. Resp. Dis., 96:626,1967. 10. Cherniak, R. M., and Snidel, D. P.: The effect of obstruction to breathing on the ventilatory response to CO2 , J. Clin. Invest., 35:1286,1956. 11. Clements,.J. A.: Surface active materials in the lungs. In The Lung. Baltimore, The Williams & Wilkins Co., 1968. 12. Comroe, J. H., and Dripps, R. D.: The Physiological Basis for Oxygen Therapy. Springfield, Illinois, Charles C Thomas, Publisher, 1950. 13. Davenport, H. W.: The ABC of Acid-Base Chemistry. Chicago, University of Chicago Press, 1950. 14. Davies, H. C. and Davies, R. E.: Biochemical aspects of oxygen poisoning. In Respiration. Vol. 2. Baltimore, The Williams & Wilkins Co., 1965. 15. Fahri, L. E.: Gas stores of the body. In Respiration. Vol. 1. Baltimore, The Williams & Wilkins Co., 1964. 16. Feinsilver, 0.: An approach to the complexity of cor pulmonale. Amer. Pract. Dig. Treat., 8:1368,1957. 17. Feinsilver, 0.: Circulatory changes associated with intermittent positive pressure treatment. Dis. Chest, 37:87, 1958.
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18. Feinsilver, O. The role of nikethamide as a respiratory stimulant in the management of pulmonary insufficiency. Curro Ther. Res., 4: 165, 1962. 19. Haugaard, N.: Cellular mechanisms of oxygen toxicity. Physiol. Rev., 48:311, 1968. 20. Jones, R H., Macnamara, J., and Gaensler, E. A.: Effects of intermittent positive pressure breathing in simulated pulmonary obstruction. Amer. Rev. Resp. Dis., 82:164,1960. 21. Kory, R C., Bergmann, J. C., Sweet, R D., and Smith, J. R: Comparative evaluation of oxygen therapy techniques. J.A.M.A., 179:767, 1962. 22. Lambertson, C. J.: Effect of oxygen at high partial pressure. In Respiration. Vol. 2. Baltimore, The Williams & Wilkins Co., 1965. 23. Lending, M.: Effect of hyperoxia, hypercapnia, and hypoxia on blood-cerebrospinal fluid barrier. Amer. J. Physiol., 200:959, 1961. 24. Laurenco, R V., and Miranda, J. M.: Drive and performance of ventilatory apparatus in chronic obstructive lung disease. New Eng. J. Med., 279:53,1968. 25. Morgan, T. E., Finley, T. N., Huber, G. L., and Fialkow, H.: Alterations in pulmonary surface active lipids during exposure to increased oxygen tension. J. Clin. Invest., 44:1737,1965. 26. Nash, G., Blennerhassett, J. B., and Pontoppidan, H.: Pulmonary lesions associated with oxygen therapy and artificial ventilation. New Eng. J. Med., 276:368, 1967. 27. Northway, W. H., Jr., Rosan, R C., and Porter, D. Y.: Pulmonary disease following respiration therapy of hyaline-membrane disease. New Eng. J. Med., 276:357, 1967. 28. Nunn, J. F., and Payne, J. P.: Hypoxaemia after general anaesthesia. Lancet, 2:631, 1962. 29. Pratt, P. C.: The reaction of human lung to enriched oxygen atmosphere. Ann. N.Y. Acad. Med., 121 :809,1965. 30. Radford, E. P., Jr., Ferris, B. G., Jr., and Kriete, B. C.: Clinical use of a nomogram to estimate proper ventilation during artificial ventilation. New Eng. J. Med., 251 :877, 1954. 31. Rahn, H.: Oxygen stores of man. In Oxygen in the Animal Organism. I.V.B.Symposium, 31 :609, 1963. 32. Reinarz, J. A., Pierce, A. K., Mays, B. B., and Sanford, J. P.: Potential role of inhalation therapy equipment in nosocomial pulmonary infection. J. Clin. Invest., 44:831,1965. 33. Said, I. S., and Banerjee, C. M.: Effects of a newer respiratory stimulant (vanillic diethylamide) in respiratory acidosis due to obstructive pulmonary insufficiency. Amer. J. Med., 33:845,1962. 34. Saltzman, H. A.: Rational normobaric and hyperbaric oxygen therapy. Ann. Int. Med., 67:845, 1967. 35. Shanklin, D. R, and Wolfson, S. L.: Therapeutic oxygen as a possible cause of pulmonary hemorrhage in premature infants. New Eng. J. Med., 277:833, 1967. 36. Smith, J. P., Stone, R W., and Muschenheim, C.: Acute respiratory failure in chronic lung disease. Amer. Rev. Resp. Dis., 97:791, 1968. 37. Stone, D. J., Keltz, H., and Kaplan, S.: A controlled study of assist ventilation in the therapy of acute pulmonary insufficiency. Trans. 25th Res. Conf. Pulm. Dis., VAArmed Forces, 1966. 38. Therapy of acute respiratory failure - Statement of committee on therapy of the American Thoracic Society. Amer. Rev. Resp. Dis., 93:475,1966. 39. Wells, R E., Jr., Perera, R D., and Kinney, J. M.: Humidification of oxygen during inhalation therapy. New Eng. J. Med., 268:644,1963. 390 Main Street Worcester, Massachusetts 01608