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Work of Breathing and Abnormal Mechanics
Symposium on Pulmonary Problems in Surgery
Work of Breathing and Abnormal Mechanics
Richard M. Peters, M.D.*
Astute clinicians have always evaluated the degree of pulmonary dysfunction by assessing the respiratory effort of their patients. One need only look at an Olympic athlete immediately after a swimming or running race to recognize that he would be unable to continue indefinitely the high minute ventilation present at the end of the race. Even such a superbly conditioned individual has a limit on his ability to perform excessive respiratory work. The postoperative or injured patient has fewer reserves and also has abnormalities of his lungs and chest wall which make them inefficient. As a result, the work of breathing is increased without the hyperventilation of exercise. The elderly or debilitated patient with low physical reserves may exceed his work capacity with only moderate degrees of dysfunction of the respiratory system. On the other hand an otherwise strong young patient may tolerate quite severe derangements of pulmonary function.
DEFINITION OF RESPIRATORY WORK Work is done when a force moves an object through a distance. Work has the dimension of kilogram-meters. In a volume system such as the lungs, distance is measured by determining the change in volume of the system and has ,the dimensions of liters or cubic centimeters. Force is measured by determining the pressure acting on the system and has the dimensions of grams per square centimeter or kilograms per square meter. Change in volume multiplied by forcing pressure equals work. For example, if the forcing pressure equals 10 cm of H 2 0 or 0.01 kg, and the volume change is 500 ml or 0.5 liter, the work done would be 10 gm of H 2 0 cm
-=-:'~=--:'::2:"=c:...::.. X
500 cm 3
=
5000 gm-cm of work or 0.005 kg-m.
'Professor of Surgery and Bioengineering, University of California, San Diego, School of Medicine; Head, Division of Thomcic Surgery, University Hospital of San Diego County
Surgical Clinics of North America- Vol. 54, No.5, October 1974
955
956
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900
~
~
~
600
Figure 1. Graphic representation of elastic work. Change in force required to stretch the lung. pleural pressure, is plotted on the horizontal axis, change in lung volume on the vertical axis. The elastic work to expand the lungs for first 300 ml, equivalent to the area covered by oblique lines, is '/3 that required for the second 300 ml, the stippled area. It takes 4.5 times as much work for the third 300ml.
--P.-i~~~-¥
....I
o >
t!)
~ 300 ....I
o
2
4
6
8
PLEURAL PRESSURE Volume change in the lungs can be measured with a spirometer, or with a pneumotachograph and integration of the airflow signal. It is possible to measure the force acting on the lungs by measuring the difference between the intrapleural pressure and the pressure at the mouth or top of an artificial airway. Intrapleural pressure can be approximated by measuring intraesophageal pressure. It is not possible to measure the forces acting on the chest cage during spontaneous ventilation, since this would require measuring the forces applied by each muscle group. When a patient is being ventilated with a mechanical respirator, the pressure in the airway is the force moving the chest cage and lungs. In this manner the work done on both the chest cage and lungs can be measured. In the example cited above, it was assumed that the force of 10 cm of H 2 0 pressure was the same throughout during the 500 ml volume change. This would be the case if the lungs and chest cage were simple pistons and the only opposing force was the friction between piston and cylinder. However, the lung and chest cage are not simple pistons; they change volume by stretching elastic elements in their structure. Like all elastic structures, they require a stretching force that is directly proportional to the change in volume. As the volume increases the force must increase. The compliance of the lungs defines the force or pressure required per unit of volume change. At resting volume, forces acting on the lungs and chest cage are zero. For a respirator to pump air into a patient whose lungs and chest cage have a compliance of 0.1 liter per centimeter of water, the pressure in the airway would increase from 0 to 1 cm H 2 0 during the first 100 ml, from 1 to 2 cm of H 2 0 for the second 100 ml, and so forth (Fig. 1). The work for the second 100 ml is 21/2 times that required for the first 100 ml, the work required for the third 100 ml is 31/2 times that of the first, etc. The pressure to overcome elastic work is continually changing during inspiration. The elastic work, done to stretch the lung during inspiration, is stored as potential energy in the stretched components of the lungs. When the inflating force is removed from the airway, the stored potential energy is available to do work during expiration.
WORK OF BREATHING AND ABNORMAL MECHANICS
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Work must also be done to overcome the resistance to airflow in the airways and the small frictional resistance of the tissues. The resistance to airflow also varies throughout the respiratory cycle. During inspiration the pressure in the lumen of the airways is higher than pressure in the surrounding lung. This force tends to stretch the airways during inspiration, increasing their cross-sectional area and lowering resistance. During expiration, pressure in the lumen is less than pressure surrounding the airways, so they tend to collapse and resistance is greater. In normal quiet breathing, the potential energy stored in the stretched tissues by the work done during inspiration provides adequate force to overcome airway resistance during expiration. If the airway resistance is high or there is marked hyperventilation, the stored potential energy in the stretched lungs and chest cage will not be adequate to push the air out of the lungs, and positive muscular effort will be required. This muscular effort raises the pleural pressure above atmospheric and so increases the difference between the pressures around and within the airways. This results in greater compression of the airways, which decreases their cross-sectional area and increases resistance. Even in normal individuals, hyperventilation increases the work per unit of ventilation or work per liter as well as the work per minute. 7 The ventilatory apparatus is similar to the reciprocating engine; it becomes less efficient as it increases its speed. The physiologic highway patrolman is dyspnea, which signals the individual that the speed of ventilation is excessive and the work must be decreased or the system will fail. The clinician's radar is to measure the amount of respiratory work being done.
MEASUREMENT OF MECHANICAL WORK OF RESPIRATION To measure the driving force ventilating the lungs, it is necessary to know the distance or volume change that occurs at each different forcing pressure, in other words, the rate of change of volume with respect to forcing pressure. Flow rate into or out of the mouth or artificial airway is the rate of change of volume and can be measured with a pneumotachograph. Multiplying flow at any instant by forcing pressure at the same instant gives the instantaneous work or power. Power is the rate of doing work (kg-m per sec). The work per minute is equal to the sum of all of the power units applied to the system during a minute. In mathematical terms, work per minute is the integral of power during one minute. Because this forcing pressure and flow rate are constantly changing, flow and pressure must be recorded, multiplied by one another, and the products assumed at least 25 times per second. The work should be measured for a period of 2 minu tes to get a sample of data large enough to be indicative of the patient's clinical state. Such calculations are impossible without some form of automation but are relatively simple with it. Systems for this type of measurement are becoming available. Simple analog devices are commercially available, although these require skilled operators at this stage of development. ,; There are also systems using *Medical Electronics Division of Hewlett-Packard, Waltham, Mass.
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digital computers.4-fi Clinical instruments for these determinations will be more effective and easier to use in the near future. Integrated circuit technology that has made pocket caculators generally available will be applied to these types of measurements with the same success. The only deterrent at present is the medical question of what type of instruments will be most useful so industry can be assured of recovering engineering investment in instrument development. Useful information can also be gained by calculating resistance and compliance. Airflow and trans pulmonary pressure provide the signals necessary for such calculations, and either a digital or analog processor can be used for these calculations. Like all objective determinations in medical practice, quantitation will increase the precision of treatment of 'patients with respiratory disease. AutOInation also permits collection of an adequate sample of data to diminish errors due to the unsteady state of sick patients. The value of quantitation or work can best be illustrated by discussing the effect of the mechanical derangements of the lungs and chest wall on the work of breathing.
FACTORS INCREASING RESPIRATORY WORK The amount of work required of the respiratory muscles is determined by (1) oxygen consumption and carbon dioxide output, i.e., the amount of gas exchange needed; (2) the mechanical efficiency of the chest cage; (3) the mechanical properties of the lungs; and (4) the coordination of ventilation and perfusion-the efficiency of the lungs in gas exchange. Gas Exchange Oxygen consumption and carbon dioxide output are moderately increased in the uncomplicated postoperative and postinjury patient. In the severely injured or septic patient, or in patients with bums, the oxygen uptake and carbon dioxide output can be markedly elevated. 2 • 3 This elevation in demand for gas exchange increases work of respiration because the patient must hyperventilate. The postoperative hyperventilation would therefore increase work per minute and per liter. Postoperative and postinjury patients have alterations in the chest cage. s This may range in degree from splinting due to pain, to severe disruption resulting from multiple rub fractures. Splinting of the chest cage which results in fast shallow respirations significantly increases respiratory work. To decrease pain, the patient increases rate and decreases tidal volume. One hundred and fifty ml of each breath are wasted to ventilate the dead space regardless of the size of the tidal volume. To maintain the same amount of alveolar ventilation fast shallow respiration requires higher minute ventilation than a normal pattern of ventilation. The rise in minute ventilation required to maintain alveolar ventilation increases respiratory work per minute. Shallow fast respirations also lead to a decrease in lung compliance. To remain open, alveoli must be periodically hyperinflated by deep
959
WORK OF BREATHING AND ABNORMAL MECHANICS
3900 3700
Work/min.
3500 3300 3100 2900 2700 2500 f - - - - - 2300 2100 1900
o
2
4
6
8
10 12 14 16
Figure 2. The increased work required when breathing is fast and shallow. On the left side the work per breath is smaller for shallow respiration but the proportion of work wasted in dead space ventilation results in increased work per minute and per ml of alveolar ventilation. The difference is shown in the bar graph on the right.
breaths. Pain also inhibits the patient's ability to change position. As a result, areas of lung remain dependent and tend to develop interstitial edema which makes .them stiffer and results in a fall in compliance. Cough is also inhibited, causing retention of secretions and an increase in airway resistance. All of these factors interact to impair the matching of ventilation and perfusion. Dependent areas of lung that are edematous are stiffer and get less ventilation than more compliant areas, while maintaining their blood flow. The same is true of regions of lung distal to bronchi with retained secretions. To maintain normal blood gases, well ventilated areas of lung must be hyperventilated enough to compensate for the poorly ventilated areas. As a result, the total amount of ventilation required for a given amount of gas exchange is increased. The failure to control pain adequately can set a chain reaction of alterations in lung and chest wall mechanics which increases the amount of respiratory work per minute and per liter (Fig. 2). Chest Cage If there is serious injury to the chest cage such as with crushing chest injury, the disruption of lung and chest wall function further compromises the system in addition to inefficiency of ventilation due to pain. When ribs are crushed, the chest cage loses its stability and paradoxical motion of the chest cage occurs. Portions of the chest cage which should be expanding during muscular effort are pulled inward. A large amount of muscular effort is wasted and work is thereby increased. The amount of paradoxical motion of the chest cage depends on two factors, the degree of disruption of the chest cage and the amount of force needed to ventilate the lungs. The degree of chest cage disruption is a finite result of the injury. The amount of force needed to ventilate the lungs will depend on the mechanical properties of the lungs. Hemor-
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RESPIRATORY RATE 12!MIN. CO 2 OUTPUT 192cc /MIN. 02 CONSUMPTION 240 cc /MIN. DEAD SPACE 150cC 6000 5000 DEAD SPACE VENTILATION 1800
4000
DEAD SPACE 3000
VENTILATION 1800 ALVEOLAR
2000
VENTILATION 3600
1000
ALVEOLAR VENTILATION 2400
=40 mm. Hg =100 mm Hg 02 Sat. =97.5'1·,
=60 mm Hg =69 mm Hg O2 Sat. =9lY.,
pC0 2
pC0 2
p02
p02
02 ACQUISITION CO2 EXCRETION PER 100ee OF ALVEOLAR VENTILATION
Figure 3. The effect of rise in Pco, on the alveolar ventilation needed to exchange cMbon dioxide and oxygen. Top shows the effect of decreasing alveolar ventilation from 3600 to 2400 ml when carbon dioxide output is 192 ml per minute and oxygen consumption is 240 ml per minute: The Pco. rises and Po. falls. Despite the large fall in Po•• the oxygen saturation fall is only modest because at this Po, the oxyhemoglobin dissociation curve is still flat. The bottom half shows how much more oxygen is acquired and carbon dioxide excreted per 100 ml of alveolar ventilation when Po. and Peo, are elevated (right diagram) than when they are normal (left diagram).
~ [!;] [;] ~~ pC02 = 40 mm, Hg p02
=
100 mm Hg
02 Saturation = 97'.57.
pC02 = 60 mm. Hg p02 = 70 mmHg
02 Saturation = 91,,/Q
rhage and edema in the area of lungs contused by the injury increase over the first hours after injury. The disruption of the chest wall and associated pain prevent the patient from taking deep breaths or coughing effectively, so lung compliance falls and airway resistance rises. Over the first 10 to 24 hours after injury the force required to expand the lungs steadily increases. The clinical sign is an increase in the amount of paradoxical motion of the chest cage as the force or swings in pleural pressure to ventilate the stiff, high resistance lungs rises. In addition to the effects of change in compliance and resistance, paradoxical motion of the chest cage results in maldistribution of ventilation so the patient must increase his minute ventilation to provide adequate gas exchange. The respiratory work is thus steadily increased and the typical patient is eventually unable to maintain the effort necessary to breathe and so he develops progressive respiratory insufficiency. Early after the injury the changes in lung mechanics are small so ventilatory effort is not excessive. Therefore, the physician has time to provide help to these patients. Like an athletic coach he must not leave his patient in the game until he is exhausted. Unfortunately, often he is a poor coach because he fails to recognize that this patient is going to get worse rather than improve during the first 48 hours after injury. The patient will therefore be required to steadily increase his work load.
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Often the clinician only becomes cognizant of the seriousness of the patient's condition when he finds that P a02 has fallen and P aC02 has risen. A rise in arterial Pc0 2 is a clear indication of inability to perform the required level of respiratory work. By allowing his P aC02 to rise and P a02 to fall the patient increases the amount of oxygen and carbon dioxide exchange for each 100 ml of alveolar ventilation. Increase of Pc0 2 from 40 to 60 and a drop of P0 2 from 90 to 69 increases carbon dioxide excretion per 100 ml of alveolar ventilation from 5 to 8 ml and oxygen from 7 to 10 ml (Fig. 3). When P aC02 rises the last available compensatory mechanism has been called upon. Any further deterioration of pulmonary function or rise in oxygen consumption and carbon dioxide output will result in further dangerous rise in P aC02 and fall in P a02' By assessing the amount of respiratory work required of the patient, artificial ventilation can be instituted before dangerous alterations in blood-gas levels occur. In assessing preoperative or preinjury condition of patients, a lot of attention is devoted to the function of their lungs. Do they have evidence of chronic obstructive lung disease, restrictive lung disease, etc? Not as much attention is paid to the mechanical state of their chest bellows. An often neglected individual is the very muscular athlete or laborer. When he undergoes thoracotomy or suffers chest injury he is likely to be mismanaged because only his muscular strength and physical condition are'- : considered. The fact that the surgical incision or trauma results in injury to much of a large mass of muscle is neglected both in assessing the injury and providing analgesia to control pain. Obesity Obesity is another type of abnormality of the chest cage that can increase respiratory work. The excessive fat must be lifted each time the volume of the chest is changed. The Pickwickian individual is one who is so obese that he cannot do the necessary respiratory work of lifting the massive fat to maintain normal blood gases. Ascites has essentially the same effect on respiratory work as does excessive obesity. The abnormal amount of work required to move the chest cage requires increased muscular effort. The obesity or ascites exaggerates the effects on lung function of pain and splinting. These patients are difficult to move, so fluid accumulation in dependent portions of the lung is inevitable. Cough and deep breathing are inhibited. The obesity directly increases work on the chest cage and indirectly increases work on the lungs. The markedly obese patient has been performing extra respiratory work on the chest cage chronicially and so may tolerate the excessive work if care is taken to prevent pulmonary complications. However, if a ventilator is required, the mechanical effects of the obesity must be understood. The ventilator must apply a pressure at the top of the airway adequate to stretch the lungs and raise the pleural pressure to lift the mass of fat. When the pleural pressure is elevated, the heart is also compressed. To assure adequate filling of the ventricles, the central venous and wedge pressures must be proportionally elevated or cardiac output will fall. Stated in another way, these patients exaggerate the need to remember that absolute
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venous or wedge pressures have little meaning. The important parameter is the difference between pleural pressure and venous pressure. Vascular pressures measured when the patient is removed from the ventilator are useless because they signify an isolated nondescriptive measurement. If systemic pressure is low or urine output depressed in the obese patient or the patient with ascites requiring artificial ventilation, the vascular volume should be increased to provide adequate filling pressure for the ventricles. This may require a significantly elevated absolute venous pressure.
COPD The incidence of chronic obstructive airway disease (COPD) in surgical patients is increasing. One need only look at such patients to know they they are doing increased respiratory work They have a resting minute ventilation that is greater than normal to compensate for the incoordination of ventilation and perfusion. In addition, the high resistance to airflow and poor elastic recoil of the lungs make their lungs mechanically inefficient. Without any injury or operation their cough mechanism is inefficient. To ventilate such lungs these patients develop considerable increase in strength in their respiratory muscles. Since they are using their chest cage at near maximum capacity, any operative or traumatic description of the chest cage is very poorly tolerated. However, use of a ventilator is also hazardous in these patients. The respirator does the work of inspiration but the elastic recoil of lung and chest cage must do the work of expiration. The high airway resistance and poor elastic recoil of their lungs make it difficult for air to be expelled by the passive recoil of the lungs and chest cage during the expiratory phase. The work of expiration is only that to overcome the high airway resistance. Given adequate time, the alveolar pressure will fall to atmospheric at the end of expiration, no matter how high the resistance or low the compliance. However, if time is inadequate, the next inspiration will occur before the previous expiration is completed. In a stepwise fashion the lungs and chest cage will be progressively hyperinfiated until recoil force is adequate to expel the inspired tidal volume. If end expiratory volume is increased, pleural pressure will be increased, thus decreasing venous return as in the obese patient. There is also risk of hyperexpanding the lungs and creating a spontaneous pneumothorax. It is theoretically possible to determine the time of expiration required to prevent hyperinfiation of the lungs: it equals three times the product of the resistance times the compliance. A practical method is to ascertain whether the venous pressure remains elevated at end expiration. In addition to the difficulties of using a respirator because of the mechanical properties of the lungs in patients with COPD, respirator support also puts their respiratory muscles at rest and so deconditions them. If they stay on a ventilator for any extended period over 48 hours, it is difficult to wean them from the ventilator because of the fall in muscle strength. We feel that these patients should have optimal control of pain to minimize any splinting of the chest cage. Epidural block for the first 48 to 72 postoperative hours in patients with moderately advanced to ad-
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vanced disease may avoid the need for a respirator and its many complications in these patients by making them able to continue to maintain the high required levels of work and minimizing the effects of operation on lung mechanics.
Post-Traumatic Respiratory Distress A group of patients whom much attention is being paid now are those with acute posttraumatic respiratory distress. These are individuals who prior to injury or operation have essentially normal lungs and develop acute mechanical changes which result in greatly increased ventilatory work. The mechanical abnormalities are the result of interstitial edema which makes the lungs stiffer, lowers lung compliance and increases work to stretch the lungs. Edema of the small airways results in significant increase in airway resistance and so resistive work. The fall in lung compliance affects the mechanical interaction between lungs and chest cage which results in a decrease in the amount of air in the lungs at the end of expiration - functional residual capacity (FRC). At the end of quiet expiration all respiratory muscles are relaxed. In the normal individual, if the lungs were not in the chest cage resting volume would be larger than when the lungs are in the chest cage. Likewise, the resting volume of lungs when removed from the chest cage is smaller than when they are in the closed chest. Thus, the FRC is a volume determined by the interaction between the lungs trying to pull the chest cage to a smaller volume and the chest wall trying to increase the volume. If the lungs become stiffer due to interstitial edema, their recoil force will be greater and will pull the chest to a smaller volume at rest. Functional residual capacity will fall. When FRC falls more, alveoli are near critical closing volumes and so tend to collapse further, lowering lung compliance and decreasing efficiency of gas exchange due to development of intrapulmonary shunt. Patients with post-traumatic respiratory distress must hyperventilate inefficient lungs. A number of factors combine to increase respiratory woi-k (1) Compliance falls making the lungs stiffer, hard to ventilate; (2) resistance to airflow increases, probably due to swelling of small airways; (3) collapsed alveoli lead to intrapulmonary shunt; (4) intrapulmonary shunt requires hyperventilation to prevent hypercapnia and combat hypoxemia. Measurement of compliance, resistance, and shunt fraction are all useful methods of assessing the severity of acute RDS. Measuring respiratory work seems to correlate as well as any measure and better than most in assessing the severity of this syndrome. It includes information about all four factors listed above and so is an information-rich determination. In patients with pulmonary congestion due to cardiac failure, the sequence of events in the lungs is very similar to that in acute RDS.l In these patients, respiratory work rises markedly due to fall in lung compliance, rise in airway resistance, and imbalance in ventilation-perfusion. The added work increases oxygen consumption, which requires either a rise in cardiac output or a widening of arteriovenous oxygen difference. If the work becomes excessive in cardiac patients, artificial ventilation can improve ventilatory function, reduce the work required of the heart, and often reverse acute pulmonary edema.
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In patients with stiff lungs due to the acute respiratory distress syndrome, the mechanical derangements tend to lower pleural pressure throughout the respiratory cycle. Without change in cardiac filling pressure, the venous and wedge pressure may be decreased, particularly during spontaneous ventilation. The stiff lung requires a greater negative pleural pressure to stretch it. If the enthusiastic physician uses only venous or wedge pressure as an index of adequate resuscitation, he can easily give such a patient excessive amounts of fluids. Low venous or wedge pressures are not indications for further infusion unless there is evidence of decreased systemic perfusion, i.e., low systemic pressure, peripheral vasoconstriction, or low urine output. In patients with severe RDS, the pleural pressure may be depressed even while the patient is being ventilated using positive end-expiratory pressure. In all of these patients respiratory work is markedly elevated. Respiratory Work Measurements The concept of respiratory work measurements as a means of control for patient care has sound theoretical basis. We have for the past 3 years been testing the clinical significance of quantitative measurements of respiratory work. 9 The determination of respiratory work is most useful in predicting the need for initiating artificial ventilation and the safety of discontinuing support. In our studies, work levels have proven more predictive than measurements of resistance or compliance. We are in the process of assessing work measurements in comparison to measurements of FRC, shunt fraction, etc., in the control of postoperative therapy. Table 1 lists our present indications for use of a respirator. These particular values are being constantly reassessed, but the levels for work seem to be quite reliable. They are particularly useful in deciding about the safety of discontinuing respirator support in patients with acute RDS. Until work falls below 0.18 kg-m per L, discontinuance of respirator therapy is rarely successful and often dangerous even for a short trial period. Ifpatients with these high work levels have respirator support discontin-
Table 1. Values for Work and Lung Mechanics Which Indicate Need for Respirator Support of Ventilation
Total work per minute (kg-m) Total work per liter (kg-m) Resistive work per minute (kg-m) Compliance (ml per cm H 2 0) Resistance (cm per L per sec) Q,(per cent) VDiVT P aCO, (mm Hg) PaO, (mm Hg on room air) pH
EARLY
RESPIRATOR
WARNINGS
INDICATED
>0.85 >0.08 >0.5 <60 >10 >15 >0.4 45-53 <80 <7.35
>1.800 >0.180 >1.0 <40 >13 >20 >0.6 >55 <60 <7.35
WORK OF BREATHING AND ABNORMAL MECHANICS
965
ued even for a short trial period, they can develop severe fatigue, a fall in P a02, a rise in P aC02, and respiratory or cardiac arrest. A more subtle and less recognized consequence of premature unsuccessful attempts to wean patients from the respirator is significant deterioration in mechanics during the trial period off the ventilator. As a result of this deterioration in function, the total period of respirator support is longer than would be required if an attempt at weaning had been delayed until function had improved adequately and work per liter decreased. Use of measurement of work to determine the need for artificial ventilation is not useful in patients with neuromuscular diseases. In these patients, assessments of muscle strength and blood gases are proper criteria. Assessment of work as criteria for need to continue respirator support can also lead to erroneous conclusions in patients with crushing chest injuries. These patients often develop acute post-traumatic respiratory insufficiency, so monitoring of respiratory work levels is a useful method of determining the need to initiate artificial ventilation and in assessing the effectiveness of therapy for the acute RDS. However, it may be a poor indicator of the time for discontinuing respirator support. The lungs recover faster than the rib fractures can stabilize. The mechanics of the chest cage control the need for respirator support in these patients as much as do the mechanics of the lungs. One must ascertain whether the fractures are stable and paradoxical respiration has stopped. Premature removal of the ventilator may only result in recurrence of acute respiratory distress. Perhaps the real problem in these patients is our inability to truly measure the work being done by the muscles of respiration to compensate for the paradoxing chest cage. The concept of work of breathing as an important clinical parameter is sound and its quantification useful. However, like all laboratory determinations, it must be placed in the context of the patient's disease. If one could measure the work done by the muscles of the chest cage in a patient with flail chest during spontaneous respiration, it would probably be found to be very great (Fig. 4).
RESPIRATORY
WORK
Figure 4. Interaction of factors in postoperative patients which leads to increased work of breathing.
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SUMMARY The clinician responsible for the care of postoperative and posttraumatic patients must be aware that in most forms of respiratory failure the individual increases his respiratory effort-work-to try to compensate for the abnormal blood-gas levels. The amount of work required to compensate for the low P a02 and/or high P aC02 controls whether the patient will be able to prevent a dangerous fall in P a02 and how long he can maintain adequate spontaneous ventilation. The timely use of a ventilator to do the work of respiration for a patient can shorten the duration of need for artificial ventilation. Assessing respiratory work can provide objective evidence of the time to start weaning from respirator support.
REFERENCES 1. Garzon, A. A., Seltzer, B., Lichtenstein, S., and Karlson, K. E.: Influence of open-heart surgery on respiratory work. Dis. Chest, 52:392-396, 1967. 2. Gump, F. E., Price, J. B., Jr., and Kinney, J. M.: Whole body flow and oxygen consumption measurements in patients with intraperitoneal infection. Ann. Surg., 171 :321, 1970. 3. Gump, F. E., Price, J. B., Jr., and Kinney, J. M.: Blood flow and oxygen consumption in patients with severe burns. Surg. Gynec. Obstet., 130:23, 1970. 4. Hilberman, M., Stacy, R. W., and Peters, R. M.: A phase method of calculating respiratory mechanics using a digital computer. J. Appl. Physiol., 32:535-541, 1972. 5. Hilberman, M., Patitucci, P. J., and Peters, R. M.: One-line assessment of cardiac and pulmonary pathophysiology in the acutely ill. J. Assoc. Adv. Med. Instru., 6:65-69, 1972. 6. Osborn, J. J., Beaumont, J. 0., Raison, J. C. A., Russell, J., and Gerbode, F.: Measurements and monitoring of acutely ill patients by digital computer. Surgery, 64:1057,1969. 7. Peters, R. M.: In The Mechanical Basis of Respiration: An Approach to Respiratory Pathophysiology. Boston, Little, Brown & Co., Inc., 1969, pp. 195-211. 8. Peters, R. M.: In The Mechanical Basis of Respiration: An Approach to Respiratory Pathophysiology. Boston, Little, Brown & Co., Inc., 1969, pp. 247-279. 9. Peters, R. M., Hilberman, M., Hogan, J. S., and Crawford, D. A.: Objective indications for respiratory therapy in post-trauma and postoperative patients. Amer. J. Surg., 124:262269,1972. University Hospital 225 West Dickinson Street San Diego, California 92103
Work of Breathing and Abnormal Mechanics
Richard M. Peters, M.D.*
Astute clinicians have always evaluated the degree of pulmonary dysfunction by assessing the respiratory effort of their patients. One need only look at an Olympic athlete immediately after a swimming or running race to recognize that he would be unable to continue indefinitely the high minute ventilation present at the end of the race. Even such a superbly conditioned individual has a limit on his ability to perform excessive respiratory work. The postoperative or injured patient has fewer reserves and also has abnormalities of his lungs and chest wall which make them inefficient. As a result, the work of breathing is increased without the hyperventilation of exercise. The elderly or debilitated patient with low physical reserves may exceed his work capacity with only moderate degrees of dysfunction of the respiratory system. On the other hand an otherwise strong young patient may tolerate quite severe derangements of pulmonary function.
DEFINITION OF RESPIRATORY WORK Work is done when a force moves an object through a distance. Work has the dimension of kilogram-meters. In a volume system such as the lungs, distance is measured by determining the change in volume of the system and has ,the dimensions of liters or cubic centimeters. Force is measured by determining the pressure acting on the system and has the dimensions of grams per square centimeter or kilograms per square meter. Change in volume multiplied by forcing pressure equals work. For example, if the forcing pressure equals 10 cm of H 2 0 or 0.01 kg, and the volume change is 500 ml or 0.5 liter, the work done would be 10 gm of H 2 0 cm
-=-:'~=--:'::2:"=c:...::.. X
500 cm 3
=
5000 gm-cm of work or 0.005 kg-m.
'Professor of Surgery and Bioengineering, University of California, San Diego, School of Medicine; Head, Division of Thomcic Surgery, University Hospital of San Diego County
Surgical Clinics of North America- Vol. 54, No.5, October 1974
955
956
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900
~
~
~
600
Figure 1. Graphic representation of elastic work. Change in force required to stretch the lung. pleural pressure, is plotted on the horizontal axis, change in lung volume on the vertical axis. The elastic work to expand the lungs for first 300 ml, equivalent to the area covered by oblique lines, is '/3 that required for the second 300 ml, the stippled area. It takes 4.5 times as much work for the third 300ml.
--P.-i~~~-¥
....I
o >
t!)
~ 300 ....I
o
2
4
6
8
PLEURAL PRESSURE Volume change in the lungs can be measured with a spirometer, or with a pneumotachograph and integration of the airflow signal. It is possible to measure the force acting on the lungs by measuring the difference between the intrapleural pressure and the pressure at the mouth or top of an artificial airway. Intrapleural pressure can be approximated by measuring intraesophageal pressure. It is not possible to measure the forces acting on the chest cage during spontaneous ventilation, since this would require measuring the forces applied by each muscle group. When a patient is being ventilated with a mechanical respirator, the pressure in the airway is the force moving the chest cage and lungs. In this manner the work done on both the chest cage and lungs can be measured. In the example cited above, it was assumed that the force of 10 cm of H 2 0 pressure was the same throughout during the 500 ml volume change. This would be the case if the lungs and chest cage were simple pistons and the only opposing force was the friction between piston and cylinder. However, the lung and chest cage are not simple pistons; they change volume by stretching elastic elements in their structure. Like all elastic structures, they require a stretching force that is directly proportional to the change in volume. As the volume increases the force must increase. The compliance of the lungs defines the force or pressure required per unit of volume change. At resting volume, forces acting on the lungs and chest cage are zero. For a respirator to pump air into a patient whose lungs and chest cage have a compliance of 0.1 liter per centimeter of water, the pressure in the airway would increase from 0 to 1 cm H 2 0 during the first 100 ml, from 1 to 2 cm of H 2 0 for the second 100 ml, and so forth (Fig. 1). The work for the second 100 ml is 21/2 times that required for the first 100 ml, the work required for the third 100 ml is 31/2 times that of the first, etc. The pressure to overcome elastic work is continually changing during inspiration. The elastic work, done to stretch the lung during inspiration, is stored as potential energy in the stretched components of the lungs. When the inflating force is removed from the airway, the stored potential energy is available to do work during expiration.
WORK OF BREATHING AND ABNORMAL MECHANICS
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Work must also be done to overcome the resistance to airflow in the airways and the small frictional resistance of the tissues. The resistance to airflow also varies throughout the respiratory cycle. During inspiration the pressure in the lumen of the airways is higher than pressure in the surrounding lung. This force tends to stretch the airways during inspiration, increasing their cross-sectional area and lowering resistance. During expiration, pressure in the lumen is less than pressure surrounding the airways, so they tend to collapse and resistance is greater. In normal quiet breathing, the potential energy stored in the stretched tissues by the work done during inspiration provides adequate force to overcome airway resistance during expiration. If the airway resistance is high or there is marked hyperventilation, the stored potential energy in the stretched lungs and chest cage will not be adequate to push the air out of the lungs, and positive muscular effort will be required. This muscular effort raises the pleural pressure above atmospheric and so increases the difference between the pressures around and within the airways. This results in greater compression of the airways, which decreases their cross-sectional area and increases resistance. Even in normal individuals, hyperventilation increases the work per unit of ventilation or work per liter as well as the work per minute. 7 The ventilatory apparatus is similar to the reciprocating engine; it becomes less efficient as it increases its speed. The physiologic highway patrolman is dyspnea, which signals the individual that the speed of ventilation is excessive and the work must be decreased or the system will fail. The clinician's radar is to measure the amount of respiratory work being done.
MEASUREMENT OF MECHANICAL WORK OF RESPIRATION To measure the driving force ventilating the lungs, it is necessary to know the distance or volume change that occurs at each different forcing pressure, in other words, the rate of change of volume with respect to forcing pressure. Flow rate into or out of the mouth or artificial airway is the rate of change of volume and can be measured with a pneumotachograph. Multiplying flow at any instant by forcing pressure at the same instant gives the instantaneous work or power. Power is the rate of doing work (kg-m per sec). The work per minute is equal to the sum of all of the power units applied to the system during a minute. In mathematical terms, work per minute is the integral of power during one minute. Because this forcing pressure and flow rate are constantly changing, flow and pressure must be recorded, multiplied by one another, and the products assumed at least 25 times per second. The work should be measured for a period of 2 minu tes to get a sample of data large enough to be indicative of the patient's clinical state. Such calculations are impossible without some form of automation but are relatively simple with it. Systems for this type of measurement are becoming available. Simple analog devices are commercially available, although these require skilled operators at this stage of development. ,; There are also systems using *Medical Electronics Division of Hewlett-Packard, Waltham, Mass.
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digital computers.4-fi Clinical instruments for these determinations will be more effective and easier to use in the near future. Integrated circuit technology that has made pocket caculators generally available will be applied to these types of measurements with the same success. The only deterrent at present is the medical question of what type of instruments will be most useful so industry can be assured of recovering engineering investment in instrument development. Useful information can also be gained by calculating resistance and compliance. Airflow and trans pulmonary pressure provide the signals necessary for such calculations, and either a digital or analog processor can be used for these calculations. Like all objective determinations in medical practice, quantitation will increase the precision of treatment of 'patients with respiratory disease. AutOInation also permits collection of an adequate sample of data to diminish errors due to the unsteady state of sick patients. The value of quantitation or work can best be illustrated by discussing the effect of the mechanical derangements of the lungs and chest wall on the work of breathing.
FACTORS INCREASING RESPIRATORY WORK The amount of work required of the respiratory muscles is determined by (1) oxygen consumption and carbon dioxide output, i.e., the amount of gas exchange needed; (2) the mechanical efficiency of the chest cage; (3) the mechanical properties of the lungs; and (4) the coordination of ventilation and perfusion-the efficiency of the lungs in gas exchange. Gas Exchange Oxygen consumption and carbon dioxide output are moderately increased in the uncomplicated postoperative and postinjury patient. In the severely injured or septic patient, or in patients with bums, the oxygen uptake and carbon dioxide output can be markedly elevated. 2 • 3 This elevation in demand for gas exchange increases work of respiration because the patient must hyperventilate. The postoperative hyperventilation would therefore increase work per minute and per liter. Postoperative and postinjury patients have alterations in the chest cage. s This may range in degree from splinting due to pain, to severe disruption resulting from multiple rub fractures. Splinting of the chest cage which results in fast shallow respirations significantly increases respiratory work. To decrease pain, the patient increases rate and decreases tidal volume. One hundred and fifty ml of each breath are wasted to ventilate the dead space regardless of the size of the tidal volume. To maintain the same amount of alveolar ventilation fast shallow respiration requires higher minute ventilation than a normal pattern of ventilation. The rise in minute ventilation required to maintain alveolar ventilation increases respiratory work per minute. Shallow fast respirations also lead to a decrease in lung compliance. To remain open, alveoli must be periodically hyperinflated by deep
959
WORK OF BREATHING AND ABNORMAL MECHANICS
3900 3700
Work/min.
3500 3300 3100 2900 2700 2500 f - - - - - 2300 2100 1900
o
2
4
6
8
10 12 14 16
Figure 2. The increased work required when breathing is fast and shallow. On the left side the work per breath is smaller for shallow respiration but the proportion of work wasted in dead space ventilation results in increased work per minute and per ml of alveolar ventilation. The difference is shown in the bar graph on the right.
breaths. Pain also inhibits the patient's ability to change position. As a result, areas of lung remain dependent and tend to develop interstitial edema which makes .them stiffer and results in a fall in compliance. Cough is also inhibited, causing retention of secretions and an increase in airway resistance. All of these factors interact to impair the matching of ventilation and perfusion. Dependent areas of lung that are edematous are stiffer and get less ventilation than more compliant areas, while maintaining their blood flow. The same is true of regions of lung distal to bronchi with retained secretions. To maintain normal blood gases, well ventilated areas of lung must be hyperventilated enough to compensate for the poorly ventilated areas. As a result, the total amount of ventilation required for a given amount of gas exchange is increased. The failure to control pain adequately can set a chain reaction of alterations in lung and chest wall mechanics which increases the amount of respiratory work per minute and per liter (Fig. 2). Chest Cage If there is serious injury to the chest cage such as with crushing chest injury, the disruption of lung and chest wall function further compromises the system in addition to inefficiency of ventilation due to pain. When ribs are crushed, the chest cage loses its stability and paradoxical motion of the chest cage occurs. Portions of the chest cage which should be expanding during muscular effort are pulled inward. A large amount of muscular effort is wasted and work is thereby increased. The amount of paradoxical motion of the chest cage depends on two factors, the degree of disruption of the chest cage and the amount of force needed to ventilate the lungs. The degree of chest cage disruption is a finite result of the injury. The amount of force needed to ventilate the lungs will depend on the mechanical properties of the lungs. Hemor-
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RESPIRATORY RATE 12!MIN. CO 2 OUTPUT 192cc /MIN. 02 CONSUMPTION 240 cc /MIN. DEAD SPACE 150cC 6000 5000 DEAD SPACE VENTILATION 1800
4000
DEAD SPACE 3000
VENTILATION 1800 ALVEOLAR
2000
VENTILATION 3600
1000
ALVEOLAR VENTILATION 2400
=40 mm. Hg =100 mm Hg 02 Sat. =97.5'1·,
=60 mm Hg =69 mm Hg O2 Sat. =9lY.,
pC0 2
pC0 2
p02
p02
02 ACQUISITION CO2 EXCRETION PER 100ee OF ALVEOLAR VENTILATION
Figure 3. The effect of rise in Pco, on the alveolar ventilation needed to exchange cMbon dioxide and oxygen. Top shows the effect of decreasing alveolar ventilation from 3600 to 2400 ml when carbon dioxide output is 192 ml per minute and oxygen consumption is 240 ml per minute: The Pco. rises and Po. falls. Despite the large fall in Po•• the oxygen saturation fall is only modest because at this Po, the oxyhemoglobin dissociation curve is still flat. The bottom half shows how much more oxygen is acquired and carbon dioxide excreted per 100 ml of alveolar ventilation when Po. and Peo, are elevated (right diagram) than when they are normal (left diagram).
~ [!;] [;] ~~ pC02 = 40 mm, Hg p02
=
100 mm Hg
02 Saturation = 97'.57.
pC02 = 60 mm. Hg p02 = 70 mmHg
02 Saturation = 91,,/Q
rhage and edema in the area of lungs contused by the injury increase over the first hours after injury. The disruption of the chest wall and associated pain prevent the patient from taking deep breaths or coughing effectively, so lung compliance falls and airway resistance rises. Over the first 10 to 24 hours after injury the force required to expand the lungs steadily increases. The clinical sign is an increase in the amount of paradoxical motion of the chest cage as the force or swings in pleural pressure to ventilate the stiff, high resistance lungs rises. In addition to the effects of change in compliance and resistance, paradoxical motion of the chest cage results in maldistribution of ventilation so the patient must increase his minute ventilation to provide adequate gas exchange. The respiratory work is thus steadily increased and the typical patient is eventually unable to maintain the effort necessary to breathe and so he develops progressive respiratory insufficiency. Early after the injury the changes in lung mechanics are small so ventilatory effort is not excessive. Therefore, the physician has time to provide help to these patients. Like an athletic coach he must not leave his patient in the game until he is exhausted. Unfortunately, often he is a poor coach because he fails to recognize that this patient is going to get worse rather than improve during the first 48 hours after injury. The patient will therefore be required to steadily increase his work load.
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Often the clinician only becomes cognizant of the seriousness of the patient's condition when he finds that P a02 has fallen and P aC02 has risen. A rise in arterial Pc0 2 is a clear indication of inability to perform the required level of respiratory work. By allowing his P aC02 to rise and P a02 to fall the patient increases the amount of oxygen and carbon dioxide exchange for each 100 ml of alveolar ventilation. Increase of Pc0 2 from 40 to 60 and a drop of P0 2 from 90 to 69 increases carbon dioxide excretion per 100 ml of alveolar ventilation from 5 to 8 ml and oxygen from 7 to 10 ml (Fig. 3). When P aC02 rises the last available compensatory mechanism has been called upon. Any further deterioration of pulmonary function or rise in oxygen consumption and carbon dioxide output will result in further dangerous rise in P aC02 and fall in P a02' By assessing the amount of respiratory work required of the patient, artificial ventilation can be instituted before dangerous alterations in blood-gas levels occur. In assessing preoperative or preinjury condition of patients, a lot of attention is devoted to the function of their lungs. Do they have evidence of chronic obstructive lung disease, restrictive lung disease, etc? Not as much attention is paid to the mechanical state of their chest bellows. An often neglected individual is the very muscular athlete or laborer. When he undergoes thoracotomy or suffers chest injury he is likely to be mismanaged because only his muscular strength and physical condition are'- : considered. The fact that the surgical incision or trauma results in injury to much of a large mass of muscle is neglected both in assessing the injury and providing analgesia to control pain. Obesity Obesity is another type of abnormality of the chest cage that can increase respiratory work. The excessive fat must be lifted each time the volume of the chest is changed. The Pickwickian individual is one who is so obese that he cannot do the necessary respiratory work of lifting the massive fat to maintain normal blood gases. Ascites has essentially the same effect on respiratory work as does excessive obesity. The abnormal amount of work required to move the chest cage requires increased muscular effort. The obesity or ascites exaggerates the effects on lung function of pain and splinting. These patients are difficult to move, so fluid accumulation in dependent portions of the lung is inevitable. Cough and deep breathing are inhibited. The obesity directly increases work on the chest cage and indirectly increases work on the lungs. The markedly obese patient has been performing extra respiratory work on the chest cage chronicially and so may tolerate the excessive work if care is taken to prevent pulmonary complications. However, if a ventilator is required, the mechanical effects of the obesity must be understood. The ventilator must apply a pressure at the top of the airway adequate to stretch the lungs and raise the pleural pressure to lift the mass of fat. When the pleural pressure is elevated, the heart is also compressed. To assure adequate filling of the ventricles, the central venous and wedge pressures must be proportionally elevated or cardiac output will fall. Stated in another way, these patients exaggerate the need to remember that absolute
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venous or wedge pressures have little meaning. The important parameter is the difference between pleural pressure and venous pressure. Vascular pressures measured when the patient is removed from the ventilator are useless because they signify an isolated nondescriptive measurement. If systemic pressure is low or urine output depressed in the obese patient or the patient with ascites requiring artificial ventilation, the vascular volume should be increased to provide adequate filling pressure for the ventricles. This may require a significantly elevated absolute venous pressure.
COPD The incidence of chronic obstructive airway disease (COPD) in surgical patients is increasing. One need only look at such patients to know they they are doing increased respiratory work They have a resting minute ventilation that is greater than normal to compensate for the incoordination of ventilation and perfusion. In addition, the high resistance to airflow and poor elastic recoil of the lungs make their lungs mechanically inefficient. Without any injury or operation their cough mechanism is inefficient. To ventilate such lungs these patients develop considerable increase in strength in their respiratory muscles. Since they are using their chest cage at near maximum capacity, any operative or traumatic description of the chest cage is very poorly tolerated. However, use of a ventilator is also hazardous in these patients. The respirator does the work of inspiration but the elastic recoil of lung and chest cage must do the work of expiration. The high airway resistance and poor elastic recoil of their lungs make it difficult for air to be expelled by the passive recoil of the lungs and chest cage during the expiratory phase. The work of expiration is only that to overcome the high airway resistance. Given adequate time, the alveolar pressure will fall to atmospheric at the end of expiration, no matter how high the resistance or low the compliance. However, if time is inadequate, the next inspiration will occur before the previous expiration is completed. In a stepwise fashion the lungs and chest cage will be progressively hyperinfiated until recoil force is adequate to expel the inspired tidal volume. If end expiratory volume is increased, pleural pressure will be increased, thus decreasing venous return as in the obese patient. There is also risk of hyperexpanding the lungs and creating a spontaneous pneumothorax. It is theoretically possible to determine the time of expiration required to prevent hyperinfiation of the lungs: it equals three times the product of the resistance times the compliance. A practical method is to ascertain whether the venous pressure remains elevated at end expiration. In addition to the difficulties of using a respirator because of the mechanical properties of the lungs in patients with COPD, respirator support also puts their respiratory muscles at rest and so deconditions them. If they stay on a ventilator for any extended period over 48 hours, it is difficult to wean them from the ventilator because of the fall in muscle strength. We feel that these patients should have optimal control of pain to minimize any splinting of the chest cage. Epidural block for the first 48 to 72 postoperative hours in patients with moderately advanced to ad-
WORK OF BREATHING AND ABNORMAL MECHANICS
963
vanced disease may avoid the need for a respirator and its many complications in these patients by making them able to continue to maintain the high required levels of work and minimizing the effects of operation on lung mechanics.
Post-Traumatic Respiratory Distress A group of patients whom much attention is being paid now are those with acute posttraumatic respiratory distress. These are individuals who prior to injury or operation have essentially normal lungs and develop acute mechanical changes which result in greatly increased ventilatory work. The mechanical abnormalities are the result of interstitial edema which makes the lungs stiffer, lowers lung compliance and increases work to stretch the lungs. Edema of the small airways results in significant increase in airway resistance and so resistive work. The fall in lung compliance affects the mechanical interaction between lungs and chest cage which results in a decrease in the amount of air in the lungs at the end of expiration - functional residual capacity (FRC). At the end of quiet expiration all respiratory muscles are relaxed. In the normal individual, if the lungs were not in the chest cage resting volume would be larger than when the lungs are in the chest cage. Likewise, the resting volume of lungs when removed from the chest cage is smaller than when they are in the closed chest. Thus, the FRC is a volume determined by the interaction between the lungs trying to pull the chest cage to a smaller volume and the chest wall trying to increase the volume. If the lungs become stiffer due to interstitial edema, their recoil force will be greater and will pull the chest to a smaller volume at rest. Functional residual capacity will fall. When FRC falls more, alveoli are near critical closing volumes and so tend to collapse further, lowering lung compliance and decreasing efficiency of gas exchange due to development of intrapulmonary shunt. Patients with post-traumatic respiratory distress must hyperventilate inefficient lungs. A number of factors combine to increase respiratory woi-k (1) Compliance falls making the lungs stiffer, hard to ventilate; (2) resistance to airflow increases, probably due to swelling of small airways; (3) collapsed alveoli lead to intrapulmonary shunt; (4) intrapulmonary shunt requires hyperventilation to prevent hypercapnia and combat hypoxemia. Measurement of compliance, resistance, and shunt fraction are all useful methods of assessing the severity of acute RDS. Measuring respiratory work seems to correlate as well as any measure and better than most in assessing the severity of this syndrome. It includes information about all four factors listed above and so is an information-rich determination. In patients with pulmonary congestion due to cardiac failure, the sequence of events in the lungs is very similar to that in acute RDS.l In these patients, respiratory work rises markedly due to fall in lung compliance, rise in airway resistance, and imbalance in ventilation-perfusion. The added work increases oxygen consumption, which requires either a rise in cardiac output or a widening of arteriovenous oxygen difference. If the work becomes excessive in cardiac patients, artificial ventilation can improve ventilatory function, reduce the work required of the heart, and often reverse acute pulmonary edema.
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In patients with stiff lungs due to the acute respiratory distress syndrome, the mechanical derangements tend to lower pleural pressure throughout the respiratory cycle. Without change in cardiac filling pressure, the venous and wedge pressure may be decreased, particularly during spontaneous ventilation. The stiff lung requires a greater negative pleural pressure to stretch it. If the enthusiastic physician uses only venous or wedge pressure as an index of adequate resuscitation, he can easily give such a patient excessive amounts of fluids. Low venous or wedge pressures are not indications for further infusion unless there is evidence of decreased systemic perfusion, i.e., low systemic pressure, peripheral vasoconstriction, or low urine output. In patients with severe RDS, the pleural pressure may be depressed even while the patient is being ventilated using positive end-expiratory pressure. In all of these patients respiratory work is markedly elevated. Respiratory Work Measurements The concept of respiratory work measurements as a means of control for patient care has sound theoretical basis. We have for the past 3 years been testing the clinical significance of quantitative measurements of respiratory work. 9 The determination of respiratory work is most useful in predicting the need for initiating artificial ventilation and the safety of discontinuing support. In our studies, work levels have proven more predictive than measurements of resistance or compliance. We are in the process of assessing work measurements in comparison to measurements of FRC, shunt fraction, etc., in the control of postoperative therapy. Table 1 lists our present indications for use of a respirator. These particular values are being constantly reassessed, but the levels for work seem to be quite reliable. They are particularly useful in deciding about the safety of discontinuing respirator support in patients with acute RDS. Until work falls below 0.18 kg-m per L, discontinuance of respirator therapy is rarely successful and often dangerous even for a short trial period. Ifpatients with these high work levels have respirator support discontin-
Table 1. Values for Work and Lung Mechanics Which Indicate Need for Respirator Support of Ventilation
Total work per minute (kg-m) Total work per liter (kg-m) Resistive work per minute (kg-m) Compliance (ml per cm H 2 0) Resistance (cm per L per sec) Q,(per cent) VDiVT P aCO, (mm Hg) PaO, (mm Hg on room air) pH
EARLY
RESPIRATOR
WARNINGS
INDICATED
>0.85 >0.08 >0.5 <60 >10 >15 >0.4 45-53 <80 <7.35
>1.800 >0.180 >1.0 <40 >13 >20 >0.6 >55 <60 <7.35
WORK OF BREATHING AND ABNORMAL MECHANICS
965
ued even for a short trial period, they can develop severe fatigue, a fall in P a02, a rise in P aC02, and respiratory or cardiac arrest. A more subtle and less recognized consequence of premature unsuccessful attempts to wean patients from the respirator is significant deterioration in mechanics during the trial period off the ventilator. As a result of this deterioration in function, the total period of respirator support is longer than would be required if an attempt at weaning had been delayed until function had improved adequately and work per liter decreased. Use of measurement of work to determine the need for artificial ventilation is not useful in patients with neuromuscular diseases. In these patients, assessments of muscle strength and blood gases are proper criteria. Assessment of work as criteria for need to continue respirator support can also lead to erroneous conclusions in patients with crushing chest injuries. These patients often develop acute post-traumatic respiratory insufficiency, so monitoring of respiratory work levels is a useful method of determining the need to initiate artificial ventilation and in assessing the effectiveness of therapy for the acute RDS. However, it may be a poor indicator of the time for discontinuing respirator support. The lungs recover faster than the rib fractures can stabilize. The mechanics of the chest cage control the need for respirator support in these patients as much as do the mechanics of the lungs. One must ascertain whether the fractures are stable and paradoxical respiration has stopped. Premature removal of the ventilator may only result in recurrence of acute respiratory distress. Perhaps the real problem in these patients is our inability to truly measure the work being done by the muscles of respiration to compensate for the paradoxing chest cage. The concept of work of breathing as an important clinical parameter is sound and its quantification useful. However, like all laboratory determinations, it must be placed in the context of the patient's disease. If one could measure the work done by the muscles of the chest cage in a patient with flail chest during spontaneous respiration, it would probably be found to be very great (Fig. 4).
RESPIRATORY
WORK
Figure 4. Interaction of factors in postoperative patients which leads to increased work of breathing.
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SUMMARY The clinician responsible for the care of postoperative and posttraumatic patients must be aware that in most forms of respiratory failure the individual increases his respiratory effort-work-to try to compensate for the abnormal blood-gas levels. The amount of work required to compensate for the low P a02 and/or high P aC02 controls whether the patient will be able to prevent a dangerous fall in P a02 and how long he can maintain adequate spontaneous ventilation. The timely use of a ventilator to do the work of respiration for a patient can shorten the duration of need for artificial ventilation. Assessing respiratory work can provide objective evidence of the time to start weaning from respirator support.
REFERENCES 1. Garzon, A. A., Seltzer, B., Lichtenstein, S., and Karlson, K. E.: Influence of open-heart surgery on respiratory work. Dis. Chest, 52:392-396, 1967. 2. Gump, F. E., Price, J. B., Jr., and Kinney, J. M.: Whole body flow and oxygen consumption measurements in patients with intraperitoneal infection. Ann. Surg., 171 :321, 1970. 3. Gump, F. E., Price, J. B., Jr., and Kinney, J. M.: Blood flow and oxygen consumption in patients with severe burns. Surg. Gynec. Obstet., 130:23, 1970. 4. Hilberman, M., Stacy, R. W., and Peters, R. M.: A phase method of calculating respiratory mechanics using a digital computer. J. Appl. Physiol., 32:535-541, 1972. 5. Hilberman, M., Patitucci, P. J., and Peters, R. M.: One-line assessment of cardiac and pulmonary pathophysiology in the acutely ill. J. Assoc. Adv. Med. Instru., 6:65-69, 1972. 6. Osborn, J. J., Beaumont, J. 0., Raison, J. C. A., Russell, J., and Gerbode, F.: Measurements and monitoring of acutely ill patients by digital computer. Surgery, 64:1057,1969. 7. Peters, R. M.: In The Mechanical Basis of Respiration: An Approach to Respiratory Pathophysiology. Boston, Little, Brown & Co., Inc., 1969, pp. 195-211. 8. Peters, R. M.: In The Mechanical Basis of Respiration: An Approach to Respiratory Pathophysiology. Boston, Little, Brown & Co., Inc., 1969, pp. 247-279. 9. Peters, R. M., Hilberman, M., Hogan, J. S., and Crawford, D. A.: Objective indications for respiratory therapy in post-trauma and postoperative patients. Amer. J. Surg., 124:262269,1972. University Hospital 225 West Dickinson Street San Diego, California 92103