I suppose it is appropriate that we come to respiratory failure at the end of a longish day. The definition of respiratory failure has an interesting history. Barcroft, 30 to 40 years ago, understood respiratory failure as a tissue phenomenon. He would have described cyanide poisoning to you as an example of respiratory failure.  Ventilatory failure  came into fashion but is not a very good term because total ventilation may be fine but gas exchange may be very poor. Europeans have invented various terms like  global insufficiency,  which sounds very impressive in German, but always sounds to me more like a term from the Pentagon than a medical or physiological definition. I prefer to use the term  respiratory failure  to mean everything related to disordered gas tensions; but if you attempt a precise definition, you run into unexpected difficulties

Bates, David V.

VCU Scholars Compass

The Modern Treatment of Respiratory Failure* DAVID V. BATES Department of Medicine, Royal Victoria Hospital McGill University, Montreal, Canada I suppose it is appropriate that we come to respiratory failure at the end of a longish day. The definition of re-spiratory failure has an interesting his-tory. Barcroft, 30 to 40 years ago, understood respiratory failure as a tissue phenomenon. He would have described cyanide poisoning to you as an example of respiratory failure. "Ventilatory failure" came into fash-ion but is not a very good term be-cause total ventilation may be fine but gas exchange may be very poor. Euro-peans have invented various terms like "global insufficiency," which sounds very impressive in German, but always sounds to me more like a term from the Pentagon than a medi-cal or physiological definition. I prefer to use the term "respiratory failure" to mean everything related to dis-ordered gas tensions; but if you at-tempt a precise definition, you run into unexpected difficulties. If you define it in terms of blood gases only, you will call patients with an arterio-venous fistula in the lung sufferers from "respiratory failure," which is nonsense. You would also conclude that a man, walking up a mountain, whose arterial oxygen tension was lowered, had "respiratory failure," which isn't strictly true. So you can invent possible definitions only to dis-card them. I do not think there is much interest in following that line of thought. I do think it is valuable to distin-guish between acute and chronic re-spiratory failure. We can recognize that there is a state of chronic mal-adjustment or inadequacy, with com-* Presented as the second of the Seven-teenth Annual Stoneburner Lectures at the Medical College of Virginia, March 12, 1964. 42 pensatory adjustments of polycythe-mia and bicarbonate retention. We can recognize not only acute and chronic, but acute on chronic; this category in-cludes many of the patients with re-spiratory failure that we commonly encounter. They have been precipi-tated into an acute dangerous situa-tion, often having lived satisfactorily for several years with a chronic form of respiratory failure. In table 1 are set out some of the common forms of acute and chronic respiratory failure. TABLE 1 Respiratory Failure A. Chronic: 1. Chronic hypoventilation with normal lungs : a. Neuromuscular disorders . b. Skeletal deformity. c. Primary alveolar hypoventi-lation syndrome. 2. Chronic hypercapnia (pC02i) and hypoxia (p02ll as conse-quence of chronic lung disease (V /Q distribution abnormal-ity). Arterial pH usually nor-mal as a result of bicarbonate retention. B. Acute: 1. Acute infection superimposed on chronic respiratory fai lure. 2. Acute respiratory depression . 3. Acute status asthmaticus . 4. Chest injury. 5. Acute paralysis. 6. Following cardiac arrest or pulmonary edema. Insidious Nature of Respiratory Failure The first point I wish to stress is that progressive hypoventilation is a dangerous condition and very difficult sometimes to spot clinically. Let us consider a patient who has just been operated on. He has an oxygen up-take of 300 ml per minute, a respira-tory quotient of 0.8, which is average, and an alveolar ventilation of 5 L per minute. His arterial oxygen tension will be 100 mm of Hg on air; his saturation 96%; the arterial C02 ten-sion will be 40 mm of Hg; and the pH 7.40. I want you to notice what happens if you just depress his al-veolar ventilation, by 1 L per minute, in steps, keeping everything else the same, and assuming that his lung has perfect gas distribution and a normal diffusing capacity. When I drop it 1 L per minute, I have dropped the ar-terial oxygen tension to 82 mm of Hg. The saturation is still high because of the shape of the dissociation curve; the pC02 has gone to 50 mm of Hg and with no bicarbonate adjustment, and the pH will have fallen to 7.32. The next stage of a further liter per minute drop in alveolar ventilation to 3 L per minute results in another fall in arterial pO, . The saturation is now 87 % , which is not detectable as cy-anosis, on air. The CO, tension will now be about 75 mm of Hg. The pa-tient, from perhaps being a little rest-less earlier if in pain, is noted by the nursing staff now to be "sleeping quietly." This is due to the anesthetic property of C02 . The pH is now 7 .2 and the patient has reached a critical situation; because if you drop alveolar ventilation another liter per minute, it is evident to everyone that disaster has occurred. The oxygen saturation will be 40%, the arterial oxygen tension is 30 mm of Hg, and the C02 is up to 105 mm of Hg. It is this stage that is critical in the postoperative period. In other words, everything may be going well until the patient, perhaps awaken· ing with a lot of pain, is hit with a moderate dose of Demerol. His ven-tilation is depressed and he now sleeps quietly. What happens next depends on a number of circumstances, e.g., whether he collapses a lobe of his Jung, which is a very serious complication at this stage, or whether he gets a slight degree of pulmonary edema, which increases the work of breathing and drops venti-lation still further. Thus, the first im-portant concept I want to present to you is the insidious nature of respira-tory failure. It is insidious particularly in the postoperative situation. It is so difficult to diagnose early in cases of chest injury that you would be well ad-vised to distrust your own or anyone else's estimates of ventilation. In these cases, a patient may come to the brink of disaster with every observer con-vinced, until 20 minutes before, when the blood pressure disappeared, that there really hadn't been "too much of a problem." It has been the great con-tribution of the last 15 years, with the common availability of laboratory methods, that we are getting a much better idea really of what a dangerous enemy respiratory failure may be. And we also are beginning to under-stand the entity which was very com-monly taught about 20 years ago, namely peripheral circulatory failure. The urgency of teaching about re-spiratory failure consists in recogniz-ing that you can usually reverse it, at least in part, and that by the time the patient has moved into the next stage of severe tissue hypoxia, or of circula-tory failure, it may be too late. Sieker and Hickam (Medicine 35: 389-423 , 1956), who I think intro-duced the term "C02 narcosis" for the first time, made the point that, as se-vere respiratory acidosis is treated prop-erly, and the C02 has fallen from 100 to 50 (or so) mm of Hg, the patient may still be confused and drowsy. So, just as in the treatment of diabetic coma the return of consciousness does not follow precisely the curve of the blood sugar, the same is true in treating C02 narcosis. This occasionally can give rise to anxiety. In one or two people we have treated, we have been fairly con-vinced the patient must have suffered irreversible cerebral damage, or pos-sibly a cerebral thrombosis, because we have had the pC02 at 40 or 50 for 1 hour or so and there has been little return of consciousness; yet full re-covery has occurred. Circulatory Changes in Respiratory Failure One of the important physiological contributions to this area was the dem-onstration by Nahas and Cavert (Am. J. Physiol. 190: 483-491, 1957) that in the intact dog, giving C02 and reducing the pH from normal levels to 7 .1, caused a progressive fall in cardiac output, which fell almost linearly with the pH change. This was mainly due to a fall in stroke volume. Patterson (Proc. Roy. Soc. (London), Ser. B 88: 371-396, 1915) had dem-onstrated as early as 1915 that CO,, regardless of its pH effect, had a de-pressant effect on the isolated dog heart. It has also been shown that the body has a protection against this which is the secretion of catecholamines, which goes some way toward counter-acting this effect. So my second point is to emphasize that there is, almost at the beginning, an inevitable interaction between respiratory failure and the state of the circulation. 43 Superimposed Metabolic Acidosis There is another very important way in which these manifestations in-teract. When tissue perfusion is re-duced below proper levels, even in the presence of a normal arterial oxygen tension, you get a brisk peripheral tis-sue hypoxia with accumulation of lac-tic acid. I think we really learned this from early experiments of perfusing dogs with cardiac bypass circuits in which total cardiac output was inade-quate, and watching the metabolic aci-dosis develop. The point was also brought home strongly when we began to restart hearts that had been stopped. We found that after a few moments of cardiac arrest the pH will be down at 6.9. Simply taking patients who have high pC02 values or respiratory fail-ure and plotting, to start with, the plasma bicarbonate against the lac-tate, (and I do not have many obser-vations here as this is work we have in progress), the higher the lactate, the lower the bicarbonate, which is to be expected. And the lactic acidosis, often reaching quite high levels in these patients, is responsible for a considerable part of the "total" acido-sis. So this is the second interaction. Failure of the circulation gives rise to problems at the tissue level. When these are severe enough to cause lactic acidosis, you immediately add a meta-bolic acidosis to the respiratory one. Table 2 summarizes these events se-quentially. Thus the physician's task is obvi-ously 3-fold. The first problem is to ensure oxygenation. The second is to make sure that this is not causing more hypercapnea. If the patient can-not get rid of CO, , his ventilation · must be assisted and the pC02 re-44 TABLE 2 Sequence of Events in Acute Res-piratory Failure 1. Acute elevation of pCO, . l 2. Acute respiratory acidosis (pH low). l 3. Secondary circulatory depression with fall in cardiac output and later cardiac arrest . l 4. Secondary superimposed metabo-lic acidosis . l 5. Final severe combined metabolic and respiratory acidosis . l 6. Cardiac arrest/ cerebral damage and central respiratory failure. l Death stored to near normal values. Third, and only 1 or 2 minutes later, the physician should worry about the problem of acidosis-not only the re-spiratory acidosis but the possibility of a quite severe metabolic acidosis. If you face every problem of respira-tory failure with these three thoughts in your mind, and add a fourth, that you should worry continuously about cardiac output and renal blood flow as these often will take the patient away from you when you really deserved success, you will realize that the treat-ment of respiratory failure is not an isolated phenomenon; nor can it be reduced solely to discussion of whether to do a tracheostomy, or which par-ticular tube to use, or what kind of mechanical respirator to prefer. The physician who treats respira-tory and circulatory failure well is not one man usually, but at least two and sometimes three, who are accustomed to think together when faced with these problems, so that no aspect of the total care is ignored. The best management of such patients requires a group of people accustomed to working together without treading on each other's toes, and accustomed to thinking in terms of several systems in the body at once. This is particularly true after cardiac surgery, when the management of some of these patients certainly requires a team effort of the kind I am sketching. In table 3, I have summarized the sequence of decisions the physician may make in managing respiratory failure. I deliberately chose this topic not only because it is something I am in-volved in and feel strongly about, but because I wanted to concentrate on a field in which I believe there have been rather striking practical ad-vances. The reasons for these are his-torically interesting. But, I do not think anyone would deny or doubt that the ready availability of arterial blood gas analysis, which must be available in an intensive care unit, at least, 24 hours a day, has really played a major part. I cannot imagine how you can deal with many of these pa-tients without knowing what you are doing. The more centers there are using routine blood gas analysis, the more people have learned that there really is no substitute for this particu-lar kind of analysis in particular cases. This whole field is at a stage when many people are involved in it, some willingly and some unwillingly. I think we are all learning of the situa-tions in which we do very well and those in which, for some reason or another, we do very poorly. I have concentrated on it because I am quite firmly convinced that this is properly the province of the chest physician, which I am. Although I have been on occasion accused of being a patholo-gist, and described as a physiologist, I am really a physician. If the modern chest physician does not accept re-sponsibility and take an interest, and I would add, a devoted interest, in this kind of management, he is going to find that it is taken over by others. Of course there are some people, anes-thesiologists usually, who feel this ought to be exclusively their province. But I think, in the kind of patient I have been showing you, that these are often problems for the chest physi-cian, who will certainly need help, and assistance, and guidance from others. We found it very useful in our inten-sive care unit to have the cardiac group and ourselves side by side. Our nurses are as competent to deal with pacemaker-monitor problems and coronary thrombosis patients as they are with respirators. The chest physi-cian must work very closely with car-diologists, certainly with surgeons, and certainly with anesthesiologists. But I would not welcome a situation in which the essential problem of con-trolling breathing over long periods of time, and of treating people in these categories I have been showing you, is turned over exclusively to people other than the chest physician. With the de-cline of tuberculosis and the shift of in-terest to emphysema, the chest physi-cian has to re-evaluate what he is doing. And he has to make up his mind, I be-lieve, to do at least two things: to be able to apply simple physiological tests of function to assist other physicians and himself in the diagnosis and man-agement of lung disease, and to become an expert in managing respiratory problems. The thought I leave with you is that if he does not do both of these things, he will find that his specialty has disappeared. TABLE 3 Sequence of Decisions in Manage-ment of Respiratory Failure A. Accurate diagnosis: usually ne-cessitating arterial blood gas analysis, x-rays, ECG, etc. B. Re-establish ventilation plus 0 2 administration. C. Sequence of decisions on assisted ventilation. 1. Simple assistance via mask plus respirator, plus possibly stimu-lants. Use of 403 02 . 2. Endotracheal tube if a. Prognosis probably hope-less . b. Need of assistance probably of short duration. 3. Cuffed tracheostomy tube a. If secretions are a problem. b. If long term assistance (more than 4 days) likely. c. If pC02 is higher than 75 mm for 3 hours or so in spite of simpler measures . 4. Assisted ventilation plus mus-cle relaxants a. In status asthmaticus . b. In tetanus. c. In lung injury. D . Treatment of metabolic acidosis (immediate if cardiac arrest has occurred). 45 

The Modern Treatment of Respiratory Failure

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The Modern Treatment of Respiratory Failure

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