Pulmonary Physiology in Surgery

Pulmonary Physiology in Surgery WATTS R. WEBB, M.D., F.A.C.S.*

An understanding of basic pulmonary physiology is of major importance to the surgeon, not only as a basis for rational therapy of respiratory insufficiency, but also for routine management of airway problems occurring in the preoperative, transoperative and postoperative ' periods. In the following presentation, the mechanics of breathing will be briefly reviewed along with more recent concepts and developments.

MECHANICS OF RESPIRATION ~echamdcalForces

The pleural surfaces of the lungs are held in intimate contact with the pleural lining of the thorax and diaphgram by a thin film of fluid. Lateral gliding motion is facilitated, but, since fluid is neither compressible nor expansible by the physiologic pressures found within the chest, the two pleural surfaces are bound together as if a single structure. Pulmonary expansion is accomplished by the direct pull of the expanding chest wall and descending diaphragm which is transmitted through the film of fluid to the lung. Atmospheric pressure then moves air into the areas of diminished pressure inside the lung. "Negative" pleural pressure measures the elastic resistance of the lung to being stretched, like the tension of a rubber band as it is stretched. Exhalation is accomplished by the elastic recoil of the lung and rib cage and, during active respiration, by contraction of the respiratory muscles. Only during more active respiration approaching levels of 40 to 60 liters per minute do the accessory muscles of inspiration and expiration become active." The diaphragm itself has no active role in expiration, but contraction of the abdominal muscles may increase intrathoracic pressure by pushing the viscera upward and elevating the diaphragm. The function

* Professor

and Chairman, Division of Cardiovascular Surgery, The University of Texas Southwestern Medical School, Dallas, Texas Supported in part by Grants NIH 1 R01-HE 08946-01 and NIH 7 R01-HE 09036-01 from the United States Public Health Service.

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of the diaphragm, with its contribution of 50 to 70 per cent of the vital capacity, is of extreme importance, particularly in coughing since a full diaphragmatic descent is necessary to "load the popgun" for the expiratory blast of the cough. The elastic recoil of the lung which provides the motive force for exhalation is furnished in part by the elastic fibers of the lung parenchyma, but more significantly by the surface tension of the fluid layer lining the alveoli. According to the LaPlace formula (P = 2Tjr), surface tension of the spherical alveolar air spaces should increase as their diameters decrease. Should this law hold in the lung, small alveoli would be difficult to inflate and would tend to empty into the larger alveoli which would have less tension. The effect would be progressive collapse and atelectasis. Von Neergaard, PattIe and Clements, and their co-workers have stressed the concept of a variable surface tension produced by the presence of a phospholipid lipoprotein substance, termed surfactant, which tends to produce the reverse effect. Thus, the surface tension is reduced as the alveoli becomes smaller and becomes greater as the alveoli are distended. During inspiration this adds to the retractive force aiding exhalation and tends to stabilize the lung to prevent atelectasis by keeping pressure within the large alveoli greater than that within the smaller alveoli. Surfactant can be extracted as a white powder from lung edema fluid or can be obtained in solution for measurement by washings from the tracheobronchial tree, or by mincing portions of the lung in saline. Surface tension can be measured on a Wilhelmi balance (Fig. 1) which records the pull of the surface film on a suspended platinum strip as the area of the surface film is altered by moving a barrier back and forth across the surface of the liquid. Surfactant is markedly diminished in hyaline membrane disease, by pulmonary emboli, by prolonged periods of cardiopulmonary bypass, and by four to five hours' exposure to hyperbaric oxygen (3 atmospheres of pressure). Hyaline membrane disease is prone to occur in premature males, infants of diabetic mothers, and in cesarean section deliveries done for fetal distress.' In addition, it is known that, at least experimentally, the condition is enhanced by high oxygen concentrations, histamine or sympathomimetic drugs, and is reduced by parasympathomimetic agents, antihistaminics and estrogen. Tooley, Finley and Gardner demonstrated that plasma from blood which had been pumped through a pump oxygenator for six hours or longer, when given to normal dogs, could unstabilize the pulmonary surfactant and produce congestive atelectasis in the living animal, thus demonstrating that the lungs can be lethally disturbed by substances liberated into the circulation.

Work of Breathing The energy requirements of breathing are very small during quiet breathing, having been estimated to cost about 0.5 mI. of oxygen per liter

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of ventilation, but this can rise tenfold at maximal levels of normal ventilation." Similarly, any abnormal state which obstructs the bronchi, reduces functioning alveoli, impairs pulmonary circulation or retards movement of the thoracic cage increases the energy expenditure for breathing. Patients with severe emphysema or after cardiopulmonary bypass procedures may utilize nearly half their total energy expenditure in the work of breathing." In patients with severe obstructive disease the increased work of breathing can produce CO 2 in excess of their maximal ventilatory excretion rate and thus exaggerate their respiratory acidosis. Even normal patients will retain carbon dioxide when they breathe against an external resistance of the same magnitude as the intrinsic resistance observed in severe emphysema. The primary therapeutic approach is to decrease the work of breathing and improve alveolar ventilation by use of bronchodilator

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SURFACE TENS I ON (dynes/em)

Figure 1. Chart of surface tension plotted on horizontal axis with relative area plotted on vertical axis as determined on a Wilhelmi balance. The surface tensions of water, saline and mucomyst mixtures are nearly identical and are not altered by area changes. The curve of lung washings (containing surfactant) is shifted only minimally to the left by mucomyst, but is much reduced in stability by cigarette smoke.

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drugs, expectorants, mechanical respiratory assistance, and antibiotics when needed to eradicate any infection. These patients develop dyspnea on exertion, leading to a vicious cycle of inactivity with progressive muscular atrophy and increasingly severe fatigability and dyspnea, but they can be improved if their program includes exercise training with oxygen breathing. It is important to relieve the hypoxia which aggravates bronchospasm and constricts the pulmonary vascular bed but yet stimulates faster and more oostly breathing. In these patients, adequate oxygen can be obtained at slow respiratory rates only if oxygen is provided in increased concentrations. Physical training utilizing supplementary oxygen during the period of exercise can be rewarded with increased strength, muscle tone and work capacity, and improved cardiopulmonary function." In the patient with borderline cardiac reserve, controlled ventilation in the postoperative period can almost completely eliminate the work requirements of breathing, and reduce the work load imposed upon the heart to make the difference between death and survival. This usually necessitates a mechanical respirator with an oxygen-enriched atmosphere, preferably 40 per cent, administered through an indwelling endotracheal tube or cuffed tracheostomy tube. In addition, maintaining the oxygen tension of the blood at high levels is of extreme importance in preventing cardiac arrhythmias which may further impair the efficiency of the heart and reduce cardiac output.

Compliance The ease of expansion of the lungs and thorax is expressed as compliance, which is calculated as the increase in volume of lung for each unit increase in airway pressure expressed as liters per centimeter of water pressure. Compliance of the normal lung is usually about 0.2 liters per centimeter of water and that of the chest is essentially the same so that in the intact chest compliance is about 0.1 liters per centimeter of water, both in the adult and in the child. The reciprocal of this is called "elastance" and measures the increase in airway pressure for a given increase in volume. Since the average elastance is 10 em. of water per liter of air inhaled, a normal tidal volume of 500 ml. requires about 5 em. of water pressure to overcome the total resistance. Resistance, being a measurement of dynamic rather than static forces, tends to decrease during early inspiration as the lungs and airways expand and, conversely, when the airways narrow in expiration, resistance increases as a function of the fourth or fifth power of the airway diameter. If any lung segments or airways are occluded, the resistance progressively increases as the ventilated volume decreases. During expiration-particularly forced expiration in patients with asthma or emphysema-airways tend to collapse to the point where flow cannot be increased regardless of additional effort. 6

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AmWAY PRESSURES

TRACHEAL PRESSURES. During quiet respiration without obstruction the tracheal pressure remains approximately atmospheric, but during coughing or forced respiration the pressure can be raised to over 100 mm. Hg. The maximal negative pressure that can be achieved is around - 60 mm. Hg. In some patients with wheezing, cinefluoroscopy demonstrates that the posterior membranous wall of the trachea and major bronchi approximates the anterior cartilaginous portion, and this is reflected by high pressures throughout the distal tracheobronchial tree. INTRA-ALVEOLAR PRESSURES. As the respiratory muscles expand the rib cage and the lungs during inspiration, the intra-alveolar pressure becomes negative-normally about -3 mm. Hg. Surface tension retraction during exhalation causes the intra-alveolar pressure to become about 3 mm. Hg greater than atmospheric to force air out of the lung. INTRAPLEURAL PRESSURES. Because of the retractive forces of the lung, intrapleural pressures are 4 to 6 mm. Hg lower than the intra-alveolar pressures, so that expiration proceeds even while intrapleural pressure is negative (relative to atmospheric pressure).

ABNORMAL STATES: THEm EFFECT ON RESPIRATORY MECHANICS

Airway Obstruction Any airway obstruction decreases compliance and increases the work of breathing. A partial obstruction may produce overdistention distally, while complete obstruction results in atelectasis. Blood flowing through nonventilated atelectatic lung constitutes a right-to-left shunt with a proportionate reduction of oxygen saturation and an increase in carbon dioxide concentration of the arterial blood. Where there is generalized obstruction, the high intrathoracic pressures necessary to achieve ventilation. can interfere with venous return to the heart and even result in a pleural effusion. Compression States Acute reduction of total lung volume down to 2 or 3 liters, as by pneumothorax or hemothorax, can be tolerated by the normal adult, but progressive impairment may develop from compression of small bronchioles to further reduce functioning volume and increase airway resistance. Blood flow to the atelectatic area may be reduced but since usually this is not a proportionate reduction, hypercapnea and hypoxemia may result. Flail Chest Flail chest resulting from fracture of the sternum or multiple ribs may cause little difficulty during exhalation as the work is performed primarily

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NORMAL VENTILATION VENTILATION POST TRACHEOSTOMY

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by the elastic recoil of the lung. A stable chest is necessary, however, during inspiration and, of course, during coughing or forceful respiration such as is often necessitated by partial airway obstruction from increased secretions, hemorrhage or edema. It was formerly believed that air would flow back and forth (Pendelluft) from the good lung into the lung on the flail side, but Maloney has beautifully demonstrated that such does not occur. Owing to the mobility of the mediastinum, both lungs are subjected to essentially equal pressures and the intrinsic elastic recoil of the lung further tends to stabilize the various pressures to which the lung is subjected. Stabilization can be accomplished by .either internal or external fixation. External stabilization can be provided by strapping, by traction on the flail segment, or temporarily merely by having the patient lie on the injured side. Internal stabilization is accomplished by a constant, positive pressure or preferably by intermittent positive pressure breathing with a mechanical respirator. Often the easiest means of stabilization is a tracheostomy which (1) diminishes the dead space so that a smaller tidal volume is required for each breath, (2) removes the resistance offered by the larynx and (3) perhaps equally important, facilitates removal of secretions to prevent airway obstruction (Fig. 2).

Obesity Extremely obese patients who have been described picturesquely as Pickwickian develop hypoxemia and hypercapnea with somnolence, dyspnea, cyanosis and polycythemia." Many factors conspire to produce this picture. The increased weight-itself compresses the chest cavity, elevates the diaphragm when the patient is supine, and holds the diaphragm down

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when the patient is erect. 26 Airway resistance is increased due to the decrease in airway size. Lung volume is decreased and compressed units are hypo ventilated to result in arterial hypoxemia because the perfusing blood is not adequately aerated. These problems are often magnified by muscular weakness due to inactivity and poor physical condition. The tendency for obese patients to hypoventilate increases the danger of atelectasis and pulmonary infection following trauma, sedation or operation. Many patients have mild pulmonary hypertension due to the reduced vascular bed, and intermittent positive pressure ventilation may serve to decrease pulmonary blood flow further as the tremendous weight of the chest precludes its adequate motion at physiologic pressures. This is the reverse of normal respiration in which inflation of the lungs increases the capillary volume and decreases pulmonary vascular resistance. Correction of hypoxia and hypercapnea will reduce pulmonary vascular resistance.14 These patients require all the methods of management used in chronic obstructive bronchopulmonary disease for preventing bronchial edema and bronchospasm, and removing obstructing secretions. Chronic care obviously requires weight reduction, which totally reverses the entire picture.

PULMONARY FUNCTION TESTING

By convention, the air space of the lung has been divided into four primary volumes. The easiest defined is the tidal volume which is the amount of gas inspired or expired during each respiratory cycle. The inspiratory reserve volume is the maximal amount inhaled after a normal inspiration. The expiratory reserve volume is that amount which can be exhaled after a normal expiration. The residual volume refers to the air remaining in the lungs at the end of maximal expiration. For an explanation of terms used in spirometric measurements see Table 1.

Capacities Total lung capacity refers to the amount of gas contained in the lung at the end of a maximal inspiration. The vital capacity is that amount of air which can be expelled from the lungs by forceful effort following a maximal inspiration. The next two capacities are less frequently referred to, being the inspiratory capacity, which is the maximal amount of air that can be inspired at the end of a normal exhalation, and the junctional res1'd1lal capacity, which is the volume of gas remaining in the lungs at the end of a normal exhalation. All volumes except the residual volume can be measured by an ordinary spirometer (Figs. 3 and 4). In bronchospirometry, endobronchial catheters separate the gas flows and volumes of each lung for individual measurement of the volumes, ventilation and oxygen uptake of each lung. The lung

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Table 1.

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Terms Used in Spirometric Measurements

TERM

SYMBOL

Vital Capacity

VC

Tidal Volume

TV

Inspiratory Reserve Volume

IRV

Expiratory Reserve Volume

ERV

Residual Volume

RV

Inspiratory Vital Capacity

IVC

Forced Expiratory Volume, per time interval in seconds Maximal Expiratory Flow Rate

FEVt MEFR

Maximal Mid-expiratory Flow

MMF

Maximal Voluntary Ventilation

MVV

DESCRIPTION

Maximal volume exhaled after deepest inspiration (includes TV, IRV and ERV). Volume inhaled or exhaled during steadystate respiration. Maximal gas that can be inhaled after a quiet inspiration. Maximal gas that can be exhaled after quiet exhalation. Volume remaining in lungs after full exhalation. Maximal volume inhaled after full expiration. Volume exhaled in a given time period during a complete forced expiration (FVC). Volume exhaled/second measured between the 200 ml and 1200 ml volumes of the forced expiratory spirogram. Volume of air per second exhaled during middle half of expired volume of forced expiratory spirogram. Maximum breathing capacity-liters/min. subject can breathe with maximal voluntary effort (actual measurement for 12 seconds only).

volumes may be reduced by many lesions such as pleural effusions, lung cysts, obesity, scoliosis, pulmonary congestion or fibrosis, paralysis or surgical removal of the lung. These are known as restrictive lesions and can be evaluated by the vital capacity as compared to the predicted normal vital capacity. Obstructive lesions are those such as bronchospasm or neoplasms which slow air flow through the airways. The rate of air flow can be measured on an ordinary spirometer if a rapidly moving drum is used which provides a paper speed of 20 mm. per second or greater. Obstruction is probably easiest measured by the forced vital capacity (FVC; timed vital capacity), which is performed with a single breath exhaled as forcefully and rapidly as possible. The FEVo. 5 has a normal value of approximately 60 per cent of the total FVC, while 70 per cent should be expired in the first second (FEVI.o), 80 per cent within two seconds and 90 per cent within the first three seconds. The FEVo.5 or FEVl. o is highly reproducible and bears a very close relationship to the MVV, but is not as time-consuming or fatiguing to the patient. Thus, a single-breath test which gives the forced vital capacity in relation to time affords a very useful evaluation, both of obstructive and restrictive lesions of the lung. The forced vital capacity compared with the predicted vital capacity measures the degree of restrictive element present.

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Similarly, the FEVo.5 gives an excellent indication of the degree of obstruction present and can be evaluated before and after bronchodilators to appraise the degree of bronchospasm present. If the FVC O•5, expressed in percentage of the total vital capacity, is multiplied by the total vital capacity expressed as a percentage of predicted vital capacity, one obtains a fairly precise evaluation of the patient's pulmonary function which takes into account both the restrictive and obstructive elements.t? If the product of these two equals 50 or better, the patient is an excellent risk; if this is above 30 per cent, the patient can still be regarded as a satisfactory operative risk. Between 30 and 15 per cent, the patient must be considered a poor candidate, and below 15 per cent as an extreme if not prohibitive risk. Inequalities of Ventilation

Even in healthy persons there are some inequities of gas distribution throughout the lungs, and this becomes exaggerated by bronchospasm, emphysema, cysts, diaphragmatic paralysis, etc. If an entire lung is 120

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underventilated, hypoxemia, carbon dioxide retention and respiratory acidosis invariably result. Uneven ventilation may cause hypoxemia, but rarely hypercapnea since hyperventilation of the normal lung can blow off additional carbon dioxide. Hyperventilation cannot raise oxygen saturation satisfactorily since blood from normally ventilated areas is already saturated by room air. Uneven distribution is demonstrated by techniques which continuously measure the concentration of poorly soluble gases such as nitrogen or helium in the expired alveolar samples. If the distribution is normal, the gas concentration should stay relatively stable throughout expiration, rising not more than 5 per cent terminally as air is exhaled from the poorest ventilated areas. In patients with severe irregularities of distribution, the terminal nitrogen concentration may rise to as much as 16 per cent. This test is of great value in determining which cases of bullous disease should have resection. If the p02 and pC0 2 are normal but the N 2 test demonstrates inequality of ventilation and thus communication of the cyst, resection is indicated. If the major problem is generalized obstructive disease, resection of the bullae will not be beneficial.

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PERFUSION AND DIFFUSION

Perfusion Often the alveoli are unevenly perfused with capillary blood as the result of embolization, regional stasis, arteriovenous shunts or compression or kinking of the pulmonary vessels. Ideally, those alveoli which are maximally ventilated should be maximally perfused with blood. If the well ventilated areas are poorly perfused or the well perfused areas are poorly ventilated, hypoxemia and, in more severe cases, carbon dioxide retention may result. If there are poorly ventilated alveoli, prolonged oxygen breathing will usually restore arterial oxygen concentration to normal. On the other hand, if there is a large right-to-Icft shunt as occurs either anatomically in congenital heart conditions and pulmonary arteriovenous fistula, or physiologically with nonventilated segments of the lung in atelectasis or obesity, the arterial oxygen tensions will not necessarily rise to normal. ' Comparison of the alveolar CO 2 tension with that in the arterial blood is an excellent means of differentiating pulmonary emboli from simulating lesions. Ventilation of the nonperfused lung reduces the alveolar CO 2 level below that of the blood if any significant portion of tile pulmonary vascular bed is blocked.

Diffusion Not only must the alveoli be adequately ventilated and adequately perfused with blood, but adequate exchange of gases must occur between the alveoli and the pulmonary capillary blood. The rate of diffusion may be decreased by edema fluid, infiltrates of sarcoid, asbestosis or other pneumoconioses, or when the total surface area of contact between ventilated alveoli and pulmonary capillaries is severely reduced as in pulmonary emphysema, The classic picture of diffusion difficulty (alveolar capillary block) includes cyanosis, dyspnea, rapid and deep breathing and occasionally mild evidence of restrictive lung disease, but not obstruction. The carbon dioxide tension is normal or even low since the diffusion of carbon dioxide is over twenty tunes as rapid as that of oxygen. The process of diffusion can be quantitatively evaluated by determining the volume of oxygen or carbon monoxide that can be transferred per minute from the alveoli to blood. The standardized tests are reported as millimeters of oxygen or CO transferred per minute for each mm. Hg pressure differential across the alveolar membrane.

OXYGEN

It is convenient to distinguish between hypoxemia in which the arterial oxygen tension is low and hypoxia in which the arterial oxygen tension is normal but oxygen tension in tissue and venous blood is reduced. Hypox-

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emia is unusual except in heart and lung disease and at high altitudes. Primary tissue hypoxia is common during increased metabolic activity such as muscular exercise or during inadequate tissue perfusion as in shock. Hypoxemia

Hypoxemia has little effect on the lung, but stimulates respiration weakly through the chemoreceptors of the aortic and carotid bodies. It produces vasodilatation of the pulmonary artery, but an increase in its pressure due to arteriolar and venous constriction and an increased volume of blood within the lung. Most vascular beds except the skin show dilatation, as do the coronary arteries. Increased capillary permeability to fluid and protein occurs in most capillary beds when the venous p02 falls to 10 or 12 mm. Hg, and the capillaries of the lung appear to be more susceptible than systemic capillaries. CLINICAL EFFECTS. Hypoxemia does not necessarily produce disability or symptoms even with arterial blood saturations as low as 75 per cent. The earliest changes are usually psychomotor with mental confusion, restlessness and emotional lability, followed by incoordination, dimness of vision, delirium and unconsciousness. Hypoxia

Hypoxia, or inadequate perfusion of the peripheral tissues, is usually manifested as a severe mixed metabolic and respiratory acidosis with a low pH, a normal or high pC0 2 , and an elevation of organic and inorganic acids including phosphates, sulfates, and lactic, pyruvic and citric acids. Cellular acidosis results as the buffering capacity is overwhelmed, and this is manifested by myocardial insufficiency and arrhythmias, inadequate response to catecholamines and an inability to use carbohydrates in the Krebs oxidation cycle. If progressive, a shocklike state results with deteriorating cardiac function, tachycardia, hypotension, low blood flow, hypercapnea, hyponatremia, and secondary renal acidosis with hypochloruria. Proper prophylaxis requires adequate ventilation with increased oxygen, utilizing tracheostomy or intermittent positive pressure breathing (IPPB) if necessary, and adequate perfusion of the entire body. Sodium bicarbonate in repeated dosage is of value as long as the total dose of sodium is not excessive, but one of the organic buffers such as THAM is of greater value in more severe cases with pH below 7.20. THAl\1 also causes a profound sodium diuresis and markedly depresses respiration, so these adverse effects must be corrected. Chronic hypoxia stimulates a circulatory response consisting of an increased cardiac output, tachycardia, and a normal or reduced arterial pressure with a normal or increased stroke volume as oxygen requirements of the tissues are met insofar as possible by accelerated blood flow and increased oxygen extraction.! In chronic anemia with hemoglobin as low as

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3 gm. per cent, there may be no significant change in ventilation, respiratory rate, or even total oxygen consumption at rest." Blood flow is increased to the brain, heart, kidney, muscle and viscera, but decreased to the skin. THERAPY. In patients whose ventilatory drive is dependent upon a mild degree of anoxia due to existing carbon dioxide narcosis, ventilation may be decreased or even totally stopped by breathing oxygen. The subsequent cerebral complications of stupor, coma and increasing cerebral spinal fluid pressure (pseudotumor cerebri) are manifestations of an increasing carbon dioxide tension rather than of oxygen, and can be relieved by effective ventilation to remove the carbon dioxide. This situation is never a contraindication for oxygen, but an indication for providing both oxygen and the required ventilatory assistance to assure adequate alveolar gas exchange. High oxygen tensions cause arteriolar spasm in the retina of premature infants. The retinal ischemia is followed by retinal fibrosis, known as' retrolental fibroplasia, which can be prevented by keeping the inspired oxygen concentrations less than 40 per cent and limiting its use to a maximum of seven days. This assumes that the oxygen in the inspired atmosphere can equilibrate with the blood flowing through the alveolar capillaries. In the presence of a diffusion defect as in hyaline membrane disease or pulmonary edema, the concentration of inspired oxygen must be as high as is required to raise arterial oxygen saturation to at least low normal.

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In recent years the use of oxygen under increased pressure has been studied with renewed interest, though with less than exciting new knowledge or applications. Hyperbaric oxygen offers some intriguing possibilities as a potentiator of irradiation, as a stimulator of drug action-particularly the cancer chemotherapeutic agents, as therapy in carbon monoxide poisoning, shock and anaerobic infections, and as an ancillary technique in cardiac surgery for the cyanotic infant. Each gram of hemoglobin is capable of combining chemically with 1.34 ml. oxygen but this is achieved by a partial pressure of 100 mm. Hg, and little additional can be added by increasing partial pressure further. On the other hand, each 100 ml. of plasma can dissolve only 0.3 ml. of oxygen at normal alveolar pressures. If exposed to pure oxygen at one atmosphere of pressure, each 100 ml. of plasma can dissolve approximately 2.4 ml. of oxygen, and at three atmospheres of partial pressure the dissolved oxygen is over six volumes per cent, which is sufficient to supply the needs of man at rest. In addition, reducing the temperature of plasma further increases oxygen solubility. Hyperbaric oxygen presents a considerable hazard, not only to the patient but to the personnel as well, as all are subject to the same dangers of

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explosion, toxicity, decompression, air embolism and nitrogen narcosis as are caisson workers. Exposure to oxygen at three atmospheres pressure for as brief a time as one-half hour can lead to generalized convulsions and coma though these effects are completely reversible by prompt decompression. Prolonged exposure can lead to irreversible damage, permanent paralysis or death, apparently due to direct toxic chemical effect of oxygen on cerebral tissues. Oxygen at high pressures inhibits a number of enzymes and co-enzymes including dehydrogenases, catalases, hydrogenases, urease, arginase, succino-oxidases and succinodehydrogenase. It also suppresses the anaerobic metabolic processes which normally take place." In addition, one of the greatest limiting factors is the Lorrain Smith effect of oxygen on alveolar cells leading to pulmonary edema, atelectasis, progressive reduction of pulmonary function and ultimate death. Experimental studies in our laboratory demonstrate a progressive loss of surfactant in the guinea pig or rat after five to. seven days at one atmosphere, but in four to five hours of exposure to oxygen at three atmospheres. Due to loss of the surfactant, surface tension in the alveoli increases and alveoli tend to collapse in progressive atelectasis with engorgement of capillaries, pulmonary edema and inadequate oxygenation of the blood. There are, in addition, difficulties of compression and decompression. Rapid pressurization is well tolerated if pressures in the sinus cavities and middle ear are well equalized. Rapid decompression is more hazardous and arterial aeroembolism may occur due to rapid expansion of alveolar air if the subject does not exhale during decompression. The absorption of gases from any cavity is much more rapid when it is filled with oxygen than when it is filled with the usual nitrogen-oxygen mixture, and this may lead to pulmonary atelectasis, retraction of the ear drum or intense pain from the gas space beneath a filling in a tooth. If the negative pressure in the space exceeds the plasma osmotic pressure, fluid and plasma protein will transude into the closed space. Thus, to date, the use of hyperbaric oxygen must be regarded as experimental with very few areas of undisputed value. Many questions remain regarding acute and chronic toxicity, problems of toxicity recognition and prevention, and the long-term effects on the central and sympathetic nervous systems.

CARBON DIOXIDE

Carbon dioxide is the most important end acid product of metabolism. The lungs excrete some 13,000 milliequivalents of carbonic acid daily, while the kidney excretes less than 100 mEq. per day of sulfates, phosphates and other fixed acids. Since the average man exhales 200 cc. of carbon dioxide a minute, the lungs excrete some 300 liters of carbon dioxide daily. Carbon dioxide diffuses some twenty times as rapidly as oxygen and is

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never increased in the blood stream by an impairment of diffusion. However, since the alveoli contain only five volumes per cent of carbon dioxide, a decrease in effective alveolar ventilation will rapidly lead to an increase in the arterial blood pC0 2 which always indicates that the entire lung or major portions are hypoventilated. Whenever pulmonary insufficiency for carbon dioxide is demonstrated, there is always pulmonary insufficiency also for oxygen though this latter can be overcome by higher concentrations of oxygen in the inspired air. An acute increase in the arterial pC0 2 causes hypertension, tachycardia, palpitation and sweating with vasodilatation of the cerebral and visceral arteries, but little change in the coronary artery. Chronic changes may be well tolerated and patients with emphysema may be quite alert mentally with an arterial pC0 2 well over 70 mm./Hg.

Hypocapnia A decrease in the arterial blood CO 2 occurs only with hyperventilation. ' Even in patients with pulmonary emboli, pulmonary vascular disease or uneven distribution of ventilation, pC0 2 may be kept normal by hyperventilation even though the work of breathing makes the patient dyspneic and disabled. Low CO 2 levels increase cerebral arterial resistance and diminish blood flow to cause light headedness and confusion, Numbness and tingling in the face and extremities, tachycardia and tetany may be produced if hyperventilation alkalosis is severe.

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Nitrogen constitutes approximately 79 per cent of our atmosphere and has many useful roles even though it is not actively metabolized." Convincing evidence, however, indicates that both man and laboratory animals can live and function in environments with little or no nitrogen. Nitrogen at high pressures, usually starting at 4 atmospheres or more, causes symptoms of decreased ability to work, euphoria, impaired mental abilities such as reasoning and memorizing, and impaired motor performance. The symptomatology of nitrogen narcosis matches acute alcoholic intoxication and has been quantitated by Lanphier as Martini's law: "Each 50 feet of depth has the effects of one additional dry martini, assuming the stomach to be empty." Sea creatures are not aware of these effects because the water to which they are exposed equilibrates with nitrogen only at the surface and hence the pressure of nitrogen in sea water is never greater than 0.8 atmospheres. For man, however, carrying air with him, each additional 33 feet below the surface adds one atmosphere to the pressure of the inspired gas. The primary role of nitrogen is mechanical as a space filler. The human body contains several gas-filled spaces including the lungs, nasal sinuses and middle ear in which gas is in equilibrium with surrounding tissues. Diffusion

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of nitrogen is only about 10 per cent as rapid as that of oxygen and thus the rate of collapse with occlusion of any airway, whether bronchial or eustachian tube, is ten times slower than when 100 per cent oxygen is breathed. The fact that nitrogen does retard reabsorption of gas pockets is one of the major problems leading to decompression sickness. The tissues, after exposure to high pressure nitrogen, become supersaturated. On sudden return to lower pressures the excess nitrogen comes out of solution as a multitude of 'bubbles within the tissues. Since these bubbles behave like air pockets and absorb only very slowly, the effective treatment lies in recompressing the patient, driving the nitrogen back in solution, and then more slowly decompressing the subject.

HUMIDITY

All air that is inhaled is humidified in the lungs to at least 98 per cent saturation at body temperature, representing a water vapor partial pressure of 47 mm. Hg. Since the inspired air is usually at a much lower temperature and often incompletely saturated, the lungs of a normal man must add some 700 cc. of water each day which is lost as insensible water loss. Air which is fully saturated at 70° F. will be only 40 per cent saturated when its temperature is raised to 98.6° F. On the other hand, in a hot, humid environment such as a temperature above 86° with a relative humidity approaching 100 per cent, large quantities of water may be absorbed through the respiratory tract to put an unbearable stress on the cardiovascular system of the cardiac patient. In addition, at this temperature and humidity, the lungs which ordinarily dissipate about 10 per cent of the body heat cannot perform this function. High humidity in respiratory tract infections has long been recognized as beneficial, and the recent development of adequate nebulizers has allowed the provision of a high moisture content at controlled temperatures. "Relative humidity" describes the invisible moisture in the air, whereas "absolute humidity" includes the visible droplets existing as a fog. Visible fog may contain droplets from a fraction of a micron to 40 or even 100 microns in size. The larger particles usually drop out of the atmosphere because of their weight and do not enter the lower respiratory tract. Particles of 30 microns in diameter are baffled out in the trachea, while those from 10 to 30 microns reach the terminal bronchioles. Those of 10 microns usually are stopped in the alveolar ducts, and only those of 0.5 to 5 microns penetrate into the air sacs themselves. Droplets less than 0.5 microns usually follow only Brownian movement and are exhaled. Recently aerosols have been used extensively for liquefying secretions and for stimulating a productive cough to obtain sputum specimens. A supersaturated aerosol at temperatures at or above that of the body will deposit large amounts of water in the tracheobronchial tree to provide in

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essence "bronchial washings." In the treatment of patients with emphysema, tracheobronchitis or other respiratory infections, this method is. extremely valuable in liquefying secretions and preventing their encrustation." In the use of the mechanical respirators it is extremely important that the inhaled atmosphere be at least 60 per cent saturated at body temperature and this can be achieved only by a heated aerosol with a "main stream" nebulizer in which all the inhaled atmosphere passes through the nebulizer.

VENTILATORY ASSISTANCE

In respiratory insufficiency the guiding principle is to achieve adequate alveolar ventilation which will maintain the arterial pC0 2 between 35, and 45 mm. Hg and the arterial oxygen saturation normal without reducing cardiac output or systemic blood pressure. None of the manual chest methods of artificial respiration are adequate even with an airway in place to avoid obstruction by the tongue. Mouth-to-mouth respiration can supply more than an adequate volume, and expired air is an acceptable medium since it contains at least 16.5 volumes per cent of oxygen and, including dead space, less than 4 per cent carbon dioxide. When the tidal volume is doubled the exhaled oxygen content will rise to 18.5 volumes per cent and the CO 2 will fall to 2 per cent. An adult patient should receive a volume twice his usual tidal volume at a rate between 12 and 20 per minute, while smaller patients require faster rates. A tight mask or cuffed endotracheal tube with an anesthetic rebreathing bag, or one of the self-expanding bags of the Ambu type, will allow for comfortable, prolonged, adequate ventilation.

Intermittent Positive Pressure Breathing (IPPB) Intermittent positive pressure breathing has become almost routine during anesthesia either on an assisted or a controlled basis. Controlled IPPB results in essentially the same relative pressures as normal breathing with a reversal in phase, in that the inspiratory pressure is higher than the expiratory pressure which remains the same as in normal breathing. Since IPPB raises the mean endotracheal and intrapleural pressures, it also tends to retard the flow of blood into the chest and thereby reduces cardiac output." Peripheral vasoconstriction, particularly venoconstriction, may compensate until the mean endothoracic pressure becomes excessive. If expiratory time is at least twice the length of the inspiratory time, cardiac output can be maintained by compensatory flow during the longer period of expiration." However, in pathologic states such as heart failure, sympathetic blockade or shock from hemorrhage, IPPB can further reduce cardiac output and lower the blood pressure even to produce a lethal

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effect. The addition of negative pressure during expiration will lower the mean intrathoracic pressure to augment venous return and cardiac output." Use of the negative phase during expiration increases pulmonary ventilation by more complete deflation of the lungs during the allotted time, but in patients with extreme obstructive emphysema the elastic support of the minor airways is so weak that even minimal use of negative pressure can cause collapse of the respiratory bronchioles and actually obstruct expiration. The volume of air moved into the lungs is dependent on their compliance, which in the normal man is 0.1 liter per centimeter of water pressure. Values of compliance vary considerably and in asthma, for example, the compliance may be reduced to less than 30 ml. per centimeter of water and thus require over 15 em. of water to provide a normal tidal volume. The compliance or airway resistance changes from moment to moment depending upon body position, drug effects, secretions, and many other factors. CLASSIFICATION. Most IPPB devices can be classified as flow regulated or pressure regulated though some combine both characteristics. Flow generators have either a constant flow rate or a preset flow rate pattern during inspiration to deliver a selected volume of air, and in these the volume and pressure in the lungs increase continuously throughout inspiration. With pressure generators, the end of the inspiratory cycle is determined by a maximum preset level of pressure in the airway which allows the volume to be quite variable. Since all volume-regulated machines have a maximal pressure regulation, this difference is actually minimized. In controlled respiration the rate of breathing is determined by the machine; while in assisted respiration the apparatus is cycled by the patient's own respiration, as a sensitive valve responds to augment air flow in response to the patient's first inspiratory effort. It is important that the rate of air flow of the machine be greater than the patient's own inspiratory rate or it will act as an obstruction rather than an aid to ventilation (Fig. 5). PUACTICAL GUIDES. The adequacy of ventilation during respiratory assistance cannot be judged by pressure readings, as increased resistance increases the pressure differential between the apparatus and the alveoli and reduces ventilation. A cuffed endotracheal or tracheostomy tube is necessary to insure a patent, gas-tight airway and to facilitate removal of secretions. Any gas leak between the machine and the alveoli will usually result in inadequate ventilation. While the adequacy of ventilation can be crudely estimated by observation of chest wall movement, actual measurement of the tidal VOlUlTIe is preferable. Measurement of the arterial pH, pC0 2 and p02 constitutes the best method of assaying the effectiveness and adequacy of alveolar ventilation. Repeated determinations are simplified by the use of "arterialized" venous blood. Venous blood obtained

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from an arm or hand warmed to 370 C. for at least 15 minutes by external heat will have values essentially identical to those in the arterial blood. Patients receiving high oxygen concentrations but inadequate ventilation still develop respiratory acidosis and hypercapnea. In general, much less difficulty will be encountered by hyperventilation lowering the arterial pC0 2 than by allowing CO2 to accumulate because of inadequate ventilation. Undoubtedly, the greatest requisite to successful long-term respiratory resuscitation is someone in constant attendance who has an understanding of artificial respiration and particularly of the apparatus being used. An inflated cuff should be deflated periodically, at least every three to four hours, and at this time the trachea should be suctioned to remove any secretions which have accumulated above the cuff. The cuff should be reinflated only to the minimal pressure required to prevent airway leaks. Crusting of secretions is a real problem unless the inspired air is adequately , humidified. In addition, frequent installation of a mucolytic agent such as acetylcysteine may be of tremendous value in preventing airway obstruction." One of the most important and commonly overlooked facets in maintaining thin secretions that are easily coughed out or aspirated is

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Figure 5. Pressure tracing showing poorly regulated intermittent positive pressure breathing (IPPB) that was unable to keep up with the inspiratory flow rate of the patient. Note that the esophageal and bronchial wedge pressures are negative during inspiration and become positive only during expiration-the reverse of that desired. Tracheal pressure likewise remained positive throughout expiration. In this instance, the IPPB apparatus is actually interfering with both inspiration and expiration.

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keeping the patient extremely well hydrated. Very frequently patients in respiratory insufficiency are mentally obtunded and have been on inadequate fluid intake for a prolonged period prior to the episode of frank respiratory failure.

PULMONARY METABOLISM

No discussion of lung function would be complete without mentioning the role of the lung in the metabolism of nongaseous substances. The metabolic activity of the lung has been long suspected but only recently confirmed. Eiseman and his co-workers have demonstrated that serotonin is promptly converted in the lung to 5-HlAA. Norepinephrine likewise is rapidly degraded, but histamine is not metabolized by the lung. Our own studies suggest that a major effect of amyl nitrite inhalation is to accelerate pulmonary destruction of the circulating catecholamines, norephinephrine and epinephrine and thus prevent their angina-stimulating effects on the heart.

REFERENCES 1. Alexander, J. K. and Dennis, E. W.: Circulatory dynamics in extreme obesity. Circulation 20: 662 (Oct.) 1959. 2. Bing, R. J. and Daley, R.: Behavior of the myocardium in health and disease as studied by coronary sinus catheterization. Am. J. Med. 10: 711 (June) 1951. 3. Blalock, A. and Harrison, T. R.: The regulation of circulation. V. The effect of anemia and hemorrhage in cardiac output of dogs. Am. J. Physiol, 80: 157-179 (March) 1929. 4. Buckingham, Sue and Sommers, S. C.: Pulmonary hyaline membranes. A.M.A. J. Dis. Child. 99: 216-227 (Feb.) 1960. 5. Campbell, E. J. M.: The Respiratory Muscles and the Mechanics of Breathing. Chicago, Year Book Publishers, 1958. 6. Campbell, E. J. M., Martin, H. B. and Riley, R. L.: Mechanics of airway obstruction. Bull. Johns Hopkins Hosp. 101: 329-343 (Dec.) 1957. 7. Cathcart, R. T., Nealon, T. F., r-, Fraimow, W., Hampton, L. J. and Gibbon, J. H., Jr.: Cardiac output under general anesthesia. Ann. Surge 148: 488-497 (Sept.) 1958. 8. Cherniack, R. M. and Snidal, D. P.: Effect of obstruction to breathing on the ventilatory response to CO 2 , J. Olin, Invest. 35: 1286-1290 (Nov.) 1956. 9. Clements, J. A.: Surface tension of lung extracts. Proc. Soc. Exper. Biol, & Med. 95: 170-172 (May) 1957. 10. Cournand, A., Motley, H. L., Werko, L. and Richards, D. W., Jr.: Physiological studies of the effects of intermittent positive pressure breathing on cardiac output in man. Am. J. Physiol. 152: 162-174 (Jan.) 1948. 11. DuBois, A. B.: Oxygen toxicity. Anesthesiology 23: 473-477 (July-Aug.) 1962. 12. Eiseman, B., Bryant, L. and Waltuch, T.: Metabolism of vasomotor agents by the isolated perfused lung. J. Thoracic & Cardiovasc. Surge 48: 798-806 (Nov.) 1964. 1'3. Farhi, L. E.: Atmospheric nitrogen and its role in modern medicine. J.A.M.A.188: 984-933 (June 15) 1964. 14. Hackney, J. D., Crane, M. G., Collier, C. C., Rokaw, S. and Griggs, D. E.:Syndrome

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15. 16. 17. 18. 19. 20. 21. 22. 23.

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of extreme obesity and hypoventilation: Studies of etiology. Ann. Int. Med. 51: 541-552 (Sept.) 1959. Hewlett, A. W., Barnett, G. D. and Lewis, J. K.: Effect of breathing oxygenenriched air during exercise upon pulmonary ventilation and upon the lactic acid content of blood and urine. J. Clin. Invest. 3: 317-322 (Dec.) 1926. Lanphier, E. H.: New Science of Skin and Scuba Diving. Conference for National Cooperation in Aquatics, N ew York, Association Press, 1962. Maloney, J. V., r-, Elam, J. 0., Handford, S. W., Balla, G. A., Eastwood, D. W., Brown, E. S. and TenPas, R. H.: Importance of negative pressure phase in mechanical respirators. J.A.M.A. 152: 212-216 (May) 1953. Maloney, J. V., Jr., Schmutzer, K. J. and Raschke, E.: Paradoxical respiration and "Pendelluft." J. Thoracic & Cardiovas. Surge 41: 291-298 (March) 1961. McKerrow, C. B. and Otis, A. B.: Oxygen cost of hyperventilation. J. Appl. Physiol. 9: 375-379 (Nov.) 1956. Miller, W. F., we, N. and Johnson, R. L.: Convenient method of evaluating pulmonary ventilatory function with a single breath test. Anesthesiology 17: 480493 (May) 1956. Miller, W. F. and Taylor, H. F.: Exercise training in the rehabilitation of patients with severe respiratory insufficiency due to pulmonary emphysema: The role of oxygen breathing. South. M. J. 55: 1216-1221 (Nov.) 1962. Pattle, R. E.: Properties, function and origin of the alveolar lining layer. Nature 175: 1125-1126 (June) 1955. Thung, N., Damman, J. F., r-, Diaz-Peres, R., Thompson, W. M., Jr., Sanmarco, M. and Mehegan, C.: Hypoxia as the cause of hemorrhage into the cardiac conduction system, arrhythmia, and sudden death. J. Thoracic & Cardiovasc, Surge 44: 687-698 (Nov.) 1962. Tooley, W. H., Finley, T. N. and Gardner, R.: Some effects on the lungs of blood from a pump oxygenator. Physiologist 4: 124 (Aug.) 1961. Tovell, R. M. and D'Ambruoso, D. C.: Humidity and inhalational therapy. Anesthesiology 23: 452-459 (July-Aug.) 1962. Tucker, D. H. and Sieker, H. 0.: Effect of change in body position on lung volumes and intrapulmonary gas mixing in patients with obesity, heart failure, and emphysema. Am. Rev. Respiratory Dis. 82: 787-791 (Dec.) 1960. von Neergaard, K.: Neve Auffassungen tiber einen Grundbegriff der Atemmechanik. Ztschr. ges. expo Med. 66: 373-394, 1929. Webb, W. R.: Clinical evaluation of a new mucolytic agent, acetylcysteine. J. Thoracic & Cardiovasc. Surge #: 330-343 (Sept.) 1962.

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