Partitioning of respiratory mechanics in mechanically ventilated patients.

Partitioning of respiratory ventilated patients

mechanics in mechanically

G. POLESE, A. ROSSI, L. APPENDINI, G. BRAND& J. H. T. BATES, AND R. BRANDOLESE Depurtment of Anesthesia and Intensive Cure, City Hospital9 Puduu; Respiratory Division, Depurtment of Internal Medicine, University of Verona, Verona; Institute of Human Physiology, University of Paduu, Pudua, Ituly; and Meakins-Christie Luboratories, McGill University, Montreal, Quebec H2X 2P2, Cunadu POLESE,G., A. ROSSI, L. APPENDINI, G. I~RANDIJ. H. T. Am R. BRAND~LE~E. Partitioning of respimtory mechanics in mechmicdy uentihted patients. J, Appl, Physiol. 71(6): 2425-2433, 1991.--In ten mechanically ventilated patients, six with chronic obstructive pulmonary disease (COP@ and four with pulmonary edema, we have partitioned the total respiratory system mechanics into the lung (1) and chest wall (w) mechanics using the esophageal balloon technique together with the airway occlusion technique during constant-flow inflation (J. Appl. Physiol. 58: 1840-1848, 1985). Intrinsic positive end-expiratory pressure (PEEPi) was present in eight patients (range 1.1-9.8 cmHzO) and was due mainly to PEEPi,L (80%), with a minor contribution from PEEPi,w (20%), on the average. The increase in respiratory elastance and resistance was determined mainly by abnormalities in lung elastance and resistance. Chest wall elastance was slightly abnormal (7.3 * 2.2 cmH20/l), and chest wall resistance contributed only lO%, on the average, to the total. The work performed by the ventilator to inflate the lung (WL) averaged 2.04 k 0.59 and 1.25 * 0.21 J/l in COPD and pulmonary edema patients, respectively, whereas Ww was -0.4 J/l in both groups, i.e., close to normal values. We conclude that, in mechanically ventilated patients, abnormalities in total respiratory system mechanics essentially reflect alterations in lung mechanics. However, abnormalities in chest wall mechanics can be relevant in some COPD patients with a high degree of pulmonary hyperinflation.

l3mm,

pulmonary, chest wall, and total respiratory system elastance; maximum and minimum pulmonary3 chest wall, and respiratory flow resistance; work of breathing; mechanical ventilation; chronic obstructive pulmonary disease; pulmonary edema ASSESSMENT of respiratory mechanics is important in mechanically ventilated patients? because acute respiratory failure (ARF) is most often the consequence of severe abnormalities in the mechanical properties of the respiratory system that determine both the institution of mechanical ventilation and its eventual discontinuation (29, 30). In recent years, noninvasive methods for measurement of total respiratory system mechanics in mechanically ventilated patients have been used to assess the status and progress of ARF (7,11,24) and the effects of therapy (21). In anesthetized subjects9 total respiratory system mechanics has been partitioned between the lung and the chest wall (5,12,22,31). In contrast, only a few studies have measured separately the compliance or its reciprocal, elastance, and none has measured the flow resistance of the lung and the chest wall in mechanically ventilated patients (14). We reasoned that partitioning 0161~X67/91

$1.50

Copyright

of total respiratory system mechanics into its lung and chest wall components could provide a better understanding of the disease underlying ARF and eventually influence the management of the mechanically ventilated patient. We undertook this study to partition the elastic and flow-resi stive properties of the total respiratory system between the lung and the ch .est wall in mechanica .lly ventilated patients with ARF, because this has not been done before. We used the esophageal balloon technique WJ 9 together with rapid airway occlusions during constantflow inflation (2), which has already been applied in mechanically ventilated patients (24) and in anesthetized subjects for measurement of total respiratory mechanics (8). In addition, we calculated the mechanical work done by the ventilator on the respiratory system and chest wall during passive inflation. MATERIALS AND MXTHODS

Ten mechanically ventilated patients, who had been admitted to the Intensive Care Unit (ICU) of the City Hospital in Padua because of ARF, were examined in this study. The investigative protocol was approved by the Institutional Ethic& Authorities. Informed consent was obtained from the patients or from their next of kin. Six of the patients had acute exacerbation of chronic obstructive pulmonary disease (COPD) due to respiratory tract infection. These patients were all males aged 63 k 7 yr with a positive smoking history. The diagnosis of COPD was confirmed by history and physical examination as well as by previous pulmonary function tests (Table 1). In the other four patients (aged 58 k 15 yr) who did not have any history of chronic airway disease, ARF was due to pulmonary edema, as indicated by the characteristic bilateral infiltrates seen on the chest X-ray as well as by severe hypoxemia and tachypnea while they breathed room air. In one male patient, the pulmonary edema complicated an acute myocardial infarction. In two female patients, the pulmonary edema had a noncardiogenie etiology and followed a multiple trauma in one patient and major abdominal surgery in the other. In another male patient, the pulmonary edema came suddenly after an episode of sepsis, although a chronic cardiomyopathy had been present for several years and the patient was a candidate for heart transplantation. All patients were intubated with a Portex cuffed endotracheal tube (ETT, 7.5-8.5 mm ID) and were mechani-

@ 1991 the American Physiological

Society

2425

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2426 TABLE

liters

1.80 LO*50

RESPIRATORY

MECHANIC3

DURING

1. k&?tg volumes in COPD patients

%pred

36 11

liters

0.64 kO.10

%pred

18 4

liters

6.10 kO.70

%pred

89 12

liters

4.70 Iko.73

FRWTLC

0.77 kO.04

Values are means k SD. COPD, chronic obstructive pulmonary disease; VC, vital capacity; FE&, forced expiratory vulume in 1 s; TLC, total lung capacity; FRC, functional residual capacity.

tally ventilated with the Siemens *Servo 9OOC ventilator with constant inspiratory flow (VI). The patients had been mechanically ventilated on the synchronized intermittent mandatory mode (SIMV) for a period of l-3 days before the present investigation. Three patients with pulmonary edema had 5-8 cmHZO positive end-expiratory pressure (PEEP) set by the ventilator. Settings of mechanical ventilation had been established by the caring physicians according to standard criteria (e.g., tidal volume lo-15 ml/kg, frequency 12-15 breaths/min). Flow was measured with a heated pneumotachograph (Fleisch no. 1) inserted between the proximal tip of the ETT and the “Y” of the ventilator tubings by means of a flexible T connector and connected to a Hewlett-Packard 47304A flow transducer. Volume was determined by numerical integration of the flow signal. Pressure at the airway opening (Pao) was sampled proximal to the pneumotachograph by means of a differential pressure transducer (Honeywell l43PCO3D). Tracheal pressure (Ptr) was recorded by means of a polyethylene catheter (90 cm long and 1.7 mm ID) whose distal tip with a few spiral side holes was positioned in the trachea 2-3 cm below the distal side of the ETT, while the proximal tip was connected to a differential pressure transducer (Honeywell l43PCO3D). Esophageal pressure (Pes) was recorded using a double-lumen nasogastric tube with a thin-walled vinyl balloon (10 cm long, 3J! cm circumference) incorporated in the lower midportion of the tube and connected to a differential pressure transducer (Honeywell 143PCO3D) through a polyethylene catheter (90 cm long, 1.7 mm ID). This tube-ballooncatheter system allows measurement of Pes in patients requiring nasogastric tube placement. Because most patients require a nasogastric tube for nutrition during mechanical ventilation, this system is ideally suited for the measurement of Pes without additional invasive procedures in ICU patients (10, 28) The balloon was filled with 05-l ml of air and was properly positioned using the “occlusion test” (OT), as previously described (4, 13). Briefly, the OT consisted of occluding the external airway at the end of a tidal expiration and allowing the patient to perform a series of inspiratory efforts while Ptr and Pes were simultaneously recorded. When the esophageal balloon was properly positioned, swings in Ptr and Pes were essentially equal (Fig. 1). The transpulmonary pressure (PL) was obtained either by connecting the catheter coming from the esophageal balloon and the tracheal catheter to the two sides of a differential pressure transducer (Honeywell l43PCO3D) or by subtracting Pes from Ptr. Flow, Pao, Ptr, and Pes were continuously displayed on a four-channel pen recorder (Gould),

MECHANICAL

VENTILATION

and all physiological variables were fed into a personal computer (CPU 80286 with 80287 math coprocessor IBM-AT compatible) via a l&bit analog-to-digital converter (Data Translation DT28OUA) at a sampling rate of 50 Hz and stored on 3.&n. floppy diskettes. A standard set of ventilator tubings supplied with the machine for adult patients was used, and the humidifier was omitted from the inspiratory line during the experimental procedure to reduce the effects of the compliance of the system connecting the patients to the ventilator. Special care was taken to avoid gas leaks in the equipment, particularly around the tracheal cuff, which was checked frequently (8). The esophageal balloon was also checked frequently throughout the procedure. Particular attention was paid to keeping the tracheal catheter free from secretions. Procedure and data analysis. After a patient entered the study, a light sedation (benzodiazepine) was administered to ensure that the respiratory muscles were relaxed throughout the procedure. In a few minutes, the SIMV gave 100% intermittent mandatory ventilation, i.e., the patients were ventilated on control mode. PEEP was removed in the three patients in whom it had been set, so that all patients were studied while ventilated with zero end-expiratory pressure (ZEEP). The medical treatment was left unaltered; it consisted of aminophylline infusion at a constant rate (0.6 mg/min) for COPD patients who were also receiving a single dose of 40 mg of methylprednisone intravenously in the morning. All patients were treated with antibiotics. Ventilatory patterns and blood gases before the start of the measurements are reported in Table 2. Blood gases were measured with a blood gas analyzer (model 1302, Instrumentation Laboratories). Patients were examined in the recumbent or semirecumbent position, and a physician not involved in the procedure was always present. An electrocardiogram was monitored throughout the study. The airway was suctioned before the start of the measurements and when needed throughout the procedure. Regular mechanical ventilation was recorded for several breaths to ensure steady state; then respiratory mechanics were measured, as previously described (7,8,21). 1

la.eI

1 48.0 0.6 38. a. APeSi @JIBEm)

FIG. 1. Relationship between changes in tracheal pressure (Ptr) and esophageal pressure (Pes) in a representative patient during respiratory efforts against occluded airway to perform occlusion test (OT) (4). Dots are points sampled through analog-to-digital converter and are all close to identity line. With this configuration, which was obtained in all patients, OT was accepted as satisfactory, so changes in Pes were assumed to reflect changes in mean pleural pressure.


RESPIRATURY

MECHANICS

DURING

Briefly, the airway opening was occluded at the end of a tidal expiration with the end-expiratory hold button of the ventilator for direct measurement of PEEPi, i.e., the end-expiratory elastic recoil pressure (20, 25). Because all patients were ventilated on ZEEP, the plateau in Pao during the occlusion (-1 s) equaled the PEEPi of the total respiratory system (PEEPi,rs). During the end-expiratory occlusion, PL and sometimes Pes increased (Fig. ZA). We have assumed that the difference in PL and Pes between the preinterruption level and the plateau during the occlusion equaled the amount of PEEPi due to the recoil of the lung (PEEPi,L) and of the chest wall (PEEPi,w), respectively. Then the occlusion was released for the mechanical lung inflation. After a few regular mechanical breaths, the airway opening was occluded again at the end of the constantflow inflation by means of the end-inspiratory hold button of the ventilator. After the occlusion, there was an immediate drop in Pao9 Ptr, and PL from the maximum value (Pmax) to a lower value (PI), followed by a gradual decrease until an apparent plateau (PJ was achieved (Fig. 2@(24). After the plateau was observed (-1.5-Z s from the occlusion), the occlusion was released, and the relaxed expiration was allowed until the expiratory flow became zero, i.e., the elastic equilibrium volume of the respiratory system was reached (Vr) (7). In those patients in whom complete expiration went below the tidal end-expiratory lung volume (EELV), the difference between EELV during tidal ventilation and Vr was termed 6EELV. During the occlusion, Pmax and Pz were easily identified on each tracing of Pao, Ptr, PL, and Pes, although particularly in Pes cardiac oscillations were present. P1 was measured by back extrapolation of a computer-fitted curve (8,X5,16) to the point at which the rapid decrease from Pmax changed sharply to the slow decrease to Pz (Fig. 2Z3). Pz, i-e*, the plateau pressure on each tracing, represented the static end-inspiratory elastic recoil of the total respiratory system (Pst,rs), lung (Pst,L), and chest wall (Pst,w). Measurements of Pz were taken between 1.5 and 2 s in all instances, with care taken to ensure that the system was leak free. During this 1.5-2 s, the contribution of reduction in pressures due to volume loss by continuing gas exchange should be negligible (8). 2. Preliminary blood gases

TABLE

ventilatory patterns and arterial . COPD

VT, b2

f, breaths/mm TI, s Ts t3 VI, l/s

bz Paoz, Torr Pacoz, Torr PH

0.78HLO8 11&l l.OHILl

4.4M.8 0.77kO.U7 0.3-0.5 98k38 46*2&4*9 7.44kO.03

PE

0.76M.08 12kl 1.3~0.1 3.9k0.6 0.58kO.07 0.5 llZk42 32.7k4.8 7.47kO.06

Values are means k SD for 6 COPD patients and 4 patients with pulmonary edema (PE). VT, tidal volume; f, frequency of breathing; TI, inspiratory time, including 0.2-s end-inspiratory pause; TIZ, expiratory time; VIM constant inspiratory flow; FIEF, fraction of inspired Oz; Paoz mci &oz 9 arterial POT and Pco~, respectively.

MECHANICAL

VENTILATION

2427

Ptr (mm) 20

I

PL (cmH20) 101 Pes (cmH20)

6I

6

I

FIG. 2. Tracings (top to bottom) of flow, volume (obtained by mathematical integration of flow signal), pressure at the airway opening proximal to the pneumotachograph (Pao), Ptr? transpulmonary pressure (PL), and Pes in a representative patient with chronic obstructive pulmonary disease (COPD) in whom the end-expiratory occlusion (A) and the end-inspiratory occlusion (B) have been performed. During end-expiratory occlusion, increase in Pao and Ptr was due to end-expiratory elastic recoil of respiratory system (PEEPi,rs), and increase in PL reflected end-expiratory elastic recoil of lung (PEEPi,L). End-expiratory elastic recoil of chest wall (PEEPi,w) was computed by subtracting PEEPi,L from PEEPi,rs. After end-inspiratory occlusion, there was an immediate drop from maximum cycling pressure value (Pmax) to a lower value (PI), which was computed through a computerfitted curve, followed by a gentle decay to a plateau (PJ that represented end-inspiratory elastic recoil of respiratory system, lung, and chest wall on Pao, Ptr, PL, and Pes, respectively.

The dynamic and static elastances of the total respiratory system (Edyn,rs and Est,rs) and of the lung (Edyn,L and Est,L) were computed by dividing PI-PEEPi and Pz-PEEPi from Pao (and Ptr) and PL records, respectively9 by the tidal volume (VT) (8,25). The dynamic and static elastances of the chest wall (Edyn,w and Est,w, respectively) were computed by subtracting Edyn,L and Est,L from Edyn,rs and Est,rs, respectively. The flow resistance of the ETT and measuring equipment was obtained by dividing the difference between peak Pao and peak Ptr by the preceding constant VI. Then, according to a previously described method (8,X, 16,24), maximum and minimum resistances of the total respiratory system (Rmax,rs and Rmin,rs) and of the lung (Rmax,L and Rmin,L) were computed by dividing Pmax-P1 and Pmax-P9 from the Ptr and PL records, respectiv;ly, by the VI preceding the occlusion. Mini: mum and maximum resistances of the chest wall (Rmin,w and Rmax,w) were obtained by subtracting


2428

RESPIRATORY

MECHANICS

DURING

12 y=o.22+ -038

14% pNWI 1 1

l

1

0

4

8

12

PEEPi,L(cmH20)

3. Relationship between PEEPi,rs and PEEPi,L. Symbols are individual data for COPD (e) and pulmonary edema patients (A). Continuous line, identity line; dashed line, regression line computed with least-squares method. FIG.

Rmin,L and Rmax,L from Rmin,rs and Rmax,rs, respectively. We have corrected all resistance values for the finite occlusion time of the ventilator occlusion valve according to the technical considerations of Kochi and colleagues (7,15,16). We also computed the differences between Rmax and Rmin for the respiratory system, lung and chest wall; these differences have been termed aRrs, ~RL, and ~Rw, respectively. According to the analysis by Bates and associates (3), Rmin represents the “ohmic” resistance and reflects mostly airway resistance (Z), whereas 6R reflects both viscoelastic properties of the tissues and “pendelluft” due to time constant inhomogeneities (2, 3, 8). In the normal lung, the great majority of 6R is due to viscoelasticity (2,3), whereas in disease it is possible for considerable time constant inequality to exist and so to contribute to 6R significantly (2). Therefore, Rmax represents the total flow resistance, which includes airway resistance, i.e., Rmin, plus the additional component due to viscoelastic phenomena of the respiratory tissues and time constant inequality, i.e., 6R. The mechanical work done by the ventilator to inflate the respiratory system through the ETT and measuring equipment (WT) was computed by integrating the area of Pao during inspiration over the inflation volume. Then the WT was partitioned using the Ptr, PL, and Pes changes during inspiration over inflation volume integrals to obtain the wurk done on the respiratory system excluding the measuring equipment and the ETT (Wrs) and that done on the lung (WL) and chest wall (WW)~ The mean value from three measurements was used for each physiological variable. Statistical analysis was performed using the Student’s t test for paired observation and the regression analysis with the least-squares method. P < 0.05 was accepted as significant. RESULTS

A satisfactory OT (Fig. 1) was obtained in all patients examined in this study, and the aPtr-to-apes ratio during occluded respiratory efforts ranged between 0.9 and 1.1. As illustrated by the example in Fig* 2, after the endexpiratory occlusion, Pao and Ptr clearly increased from

MECHANICAL

VENTILATION

the preinterruption level (Fig. 2A) in all the COPD patients of this study and in two of the patients with pulmonary edema. The plateaus in Pao and Ptr, which were equal during the occlusion, reflected the end-expiratory elastic recoil of the total respiratory system (PEEPi,rs). PL and Pes also increased during the end-expiratory occlusion, reflecting PEEPi,L and PEEPi,w, respectively (Fig. !ZA)* As illustrated in Fig. 3, most of PEEPi,rs is due to PEEPi,L, and the two are significantly correlated (r = 0.98, P < 0.001). However, in one COPD patient PEEPi,w amounted to 2.3 cmHzO and contributed 30% to PEEPi,rs. In all the COPD patients and in one patient with pulmonary edema, the expired volume during the complete expiration went well below the tidal end-expiratory position, and in one COPD patient the fiEELV was as large as 1.48 liters. Table 3 shows individual as well as average values of PEEPi and 6EELV. After the end-inspiratory occlusion, Pmax decreased to a lower value in all patients and in all the pressure tracings, and an apparent plateau was observed in any instance -1.5-Z s from the occlusion. On Pao, Ptr, and PL signals, there was a rapid drop from Pmax to P1 (Fig. 2@, which was clearly separated from the subsequent slower decay from P1 to Pz, i.e., the plateau pressure. In contrast, the fall from Pmax to Ps was much smaller and progressive on Pes signal. We were unable to identify any P1 on the Pes record. This means that the immediate drop from Pmax to P1 for the total respiratory system was due to the lungs alone and is therefore essentially due to airways resistance (3). In this connection it should be mentioned that P1 and Pz measurements on Pao and Ptr records were virtually identical. The dynamic and static elastances of the total respiratory system, lung, and chest wall are given in Table 4. Edyn,rs and Edyn,L were significantly higher than Est,rs and Est,L, respectively (P < O.Ol), in all patients. In contrast, Edyn,w was not significantly different from Est,w. Edyn,L and Est,L were on the average 61.3 and 51.6% of TABLE 3. htrinsic PEEP of totd respiruto?y system, lwtg, und chest wall und 6EELV Subj NO.

PEEPi,rs, cmH20

PEEPi,L, cmH20

PEEPi,w, cmH20

I

9.8

2 3 4 5 6

6.6 7.7 9.2 3.8 6.5

7.5 5.5 6.9 8.5 2.7 5.4

1.1

0.56 I.48 0.66 0.44 0.31 0.18

Means k SD

7.3~2.2

6.lkZ.O

l.ZzkO.6

0.6OzkO.46

I 2

0 0

3 4

2.1

0.9 2.0

0.8kl.O

0.7kl.O

6EELV, liter

COPLI

Means 2 SD

1.1

PE 0 0

2.3 1.1 0.8 0.7 1.1

0 0

0 0

0.2 0.4

0 0.27

0.2~0.2

0.07kO.13

PEEPi, rs, L, w, intrinsic positive end-expiratory pressure, i.e., endexpiratory elastic recoil of total respiratory system, lung, and chest wall; 6EELV, delta end-expiratory lung volume, i.e., difference between EELV and relaxation volume.


RESPIRATORY

MECHANICS

DURING

TABLE 4. Dynumic wad stutic elustunces of tutu1 respirutory system, luag, und chest wull in COPD und PE putients Subj NO.

Edyn,rs

Edyn,L

Edyn,w

Est,rs

Est,L

Est,w

16.4 22.4 16.1 13.3 12.7

9.4 6.8 11.4 7.7 5.8 6.5

4.2 11.3 a.4 7.5 6.2

15.3k4.0

7.9k2.1

7.4k2.4

COPD 1 2 3 4 5 6

24.7 18.7 30.9 23.0 17.4 17.5

16.0 14.8 16.2 11.9 9.9 11.9

Means I!I SD

22.0k5.3

13.5k2.6

8.7

3.9 14.7 11.1

7.5 5.7

8.6k3.9

11.0

7.0

PE 1 2 3

28.3 28.4 36.1

20.7 22.7 32.4

7.6 5.7 3.7

4

21.9

12.7

9.2

Means k SD

28.7k5.8

22.lk8.1

6.6k2.4

25.6 25.6

18.8 15.6

33.4 17.5

28.8 10.0

10.0 4.3 7.5

18.3k7.9

‘7.2k2.3

25.5k6.5

6.8

Values are cmH@/l. Edyn, rs, L, w, dynamic elastance of total respiratory system, lung, and chest wall; Est, rs, L, w, static elastance of total respiratory system, lung, and chest wall.

Edyn,rs and Est,rs, respectively, in COPD patients. In patients with pulmonary edema the contribution of lung elastances to the respiratory system elastances amounted, on the average, to 77 and 71.7%, respectively. Figure 4 shows that individual values of lung and respiratory system elastances were significantly correlated, indicating that changes in total Edyn,rs and Est,rs, in our patients, were determined by aEdyn,L and aEst,L rather than 6Edyn,w and SEst,w* However, in some individual patients, e.g., putient 3 with COPD and putient 2 with pulmonary edema in Table 4, Edyn,w and Est,w were increased enough to contribute significantly to the increase in total Edyn,rs and Est,rs. Individual and average values of maximum and minimum resistance of the total respiratory system (Rmax,rs and Rmin,rs), lung (Rmax,L and Rmin,L), and chest wall (Rmax,w and Rmin,w) are shown in Table 5. The added resistance of ETT and measuring equipment was flow dependent and amounted on the average to 18.1 & 5.9 and 14.0 & 3.4 crnHgO. l-‘. s in COPD and pulmonary edema patients, respe&ively$ for the range of VI and inflation volume used in this study (Table 2). In all patients, Rmax,L and Rmin,L were a substantial part of Rmax,rs and Rmin,rs (Fig. 5), whereas Rmax,w amounted to 10% of Rmax,rs, on the average, in both groups of patients. Rmin,w was small and sometimes within the error of measurement (Table 5). This latter result may not be surprising in view of the faot that Rmin reflects essentially the resistance of the airways. However, in one COPD patient Rmax,w was large, amounting to 4.5 cmHzO. 1-l. s, i.e., 27.3% of RmaxYrs. As illustrated in Fig. 5, 6Rrs was mainly due to ~RL, and a significant correlation was also found between 6Rrs and ~RL (P < 0.05). 6Rrs averaged 5.9 & 1.6 and 6.0 k 1.4 cmHzO 1-l s, respectively9 in COPD and pulmonary edema patients, while ~RLwas, on the average, 4.9 k 1.4 cmHzO 1-l. s in l

l

l

MECHANICAL

2429

VENTILATION

the former and 5.2 & 2.1 cmHzO. 1-l. s in the latter. On the average, ~Rw contributed to 6Rrs 17% in COPD patients and 13.3% in pulmonary edema patients. Individual and mean values of the mechanical work done by the ventilator per liter of ventilation are given in Table 6. A significant amount (-32% on the average) of the total work was performed by the ventilator to drive the VI through the ETT and measuring equipment. Because the flow resistance of the ETT is markedly flow dependent, this part of WT was higher in COPD patients (1.18 J/l), who were ventilated with a higher VI, than in pulmonary edema patients (1.01 J/l). Most of the work on the respiratory system was done to expand the lung. In fact, WL amounted on the average to 81.9 and 75.8% of Wrs in COPD and pulmonary edema patients, respectively. The work done on the chest wall was not different between the two groups of patients and averaged -0.4 J/l. DISCXJSSION

Descriptions of chest wall mechanics in mechanically ventilated patients are scanty. This work provides the first partitioning of both elastic and flow-resistive properties of the total respiratory system between lung and chest wall mechanics in mechanically ventilated patients with acute respiratory failure. y- 1.12+0.0x r-O.87 ptO.001

Edyn,L (cmH2O/L) y-O*~+OAMx f-o.@8 pto*OO1

0

10

20

30

4

40

Eat,L(cmH2O/L) 4. Relationship between dynamic elastance of total respiratory system (Edyn,rs) and that of lung (Edyn,L) (kq3) and between static elastance of total respiratory system (Est,rs) and that of lung (Est,IJ (bottom). Symbols and lines as in Fig. 3. FIG.


2430

RESPIRATURY

MECHANICS

DURING

MECHANICAL

VENTILATI0N

5. Maximum and minimum resistances of total respiratury system, lung, and chest wall in COPD and PE patients

TABLE

Subj No.

Rmax*rs

Rmax,L

Rmax,w

Rminps

Rmin,L

Rmin,w

6.4 9.9 14.7 9.5 14.0 9-8

6.6 9.8 13.2 8.5

-0.2

corn 1

2 3 4 5

6

14.7 15.3 21.5 16.5

13.6

1.1

14.7 19.1 12.0

17.6 15.0

15.6 14.2

0.6 1.4 4*5 2.0 0.8

121

9.5

0.1 1.5 1.0

1.9 0.3 1

Means I!I SD

0 16.6k2.2

14e9k2.4

1.7kl.4

1.1 3.4 2.8 6.4 3.422.2

1 2 3 4

6.6 8.6 10.8 11.5

4.8 7.8 10.4 9.7

FE 1.8 0.8 0.4 1.5

Means k SD

9.4k2.2

8s322.6

1.120.6

10.7k3.1

10.0k2.4 1.0 2.5 2.7 6.2 3.lk2.2

5

10

0.8kO.8

20

15

25

RmhpL(cmH20*L%)

0.1 0.9 OS 0.2

10 0-

y-2.em+cmh f-o.71 pto.05

0.3kO.4

Values are cmH@ 1-l s. Rmax, rs, Lo w, maximum resistance of total respiratory system, lung, and chest wall; Rmin, rs, L, w, minimum resistance of total respiratory system? lung, and chest wall. l

l

Intrinsic PEEP. In line with our previous work, we found PEEPi in all the COPD patients and in some pulmonary edema patients, although the values of PEEPi found in this study are lower than those reported in the previous studies (7). However, the expiratory time in the patients of this study was longer (~4 s) than in the previous studies (~2-3 s), and the COPD patients were receiving aminophylline infusion at a constant rate at the time of the study. In the eight patients in whom PEEPi was present, it was almost entirely due to the end-expiratory elastic recoil of the lung, i.e., PEEPi,L (Fig. 3). However in four COPD patients, FEEPi,w ranged from 1.1 to 2.3 cmHZO, reflecting a small degree of end-expiratory inward elastic recoil of the chest wall due to hyperinflation, as indicated by the systematic presence of a 6EELV (Table 3). The presence of PEEPi,w, i.e., the end-expiratory chest wall inward recoil, indicates that the chest wall was recoiling inward throughout expiration, thus providing a possible explanation for the flow limitation observed in mechanically ventilated COPD patients during the tidal expiration (11). Respiratov elastarzces. In normal subjects, a shift from the upright or sitting to the supine position decreases the functional residual capacity because of the effect of gravity on the abdomen-diaphragm compartment (I), but it has no effect on respiratory elastance (6). Dynamic and static elastances of the total respiratory system have been measured with a method similar to the present one, i.e., rapid airway occlusion during constant-flow inflation, only in anesthetized subjects (8, 9). Because it is well known that anesthesia increases respiratory elastance (3l), we will compare our data only with values obtained in normal supine awake subjects, although different techniques were used (Table 7). Overall, both dynamic and static elastances of our mechanically ventilated patients are higher, on the average, than values found in normal awake subjects, as illustrated in

FIG. 5. Relationship tory system (Rmin,rs) difference in maximum &R) of total respiratory lines as in Fig. 3.

between minimum resistance of total respiraand that of lung (Rmin,L) (top) and between and minimum resistance (Rmax - Rmin, i.e., system and that of lung @CIUOTTI). Symbols and

6. Passive inspiratq system, lung, and chest wall

work of total respiratory

TABLE

Subj No.

WT

wrs

WL

ww

1.91 2.13

COPD 4.82 3.60 4.30 3.39 3.47 2.42

2.41 3.29 2.8 2.41 1.46

2.95 2.11 2.05 1.10

0.62 0.28 0.34 0.70 0.36 0.35

3.67k0.83

2.49kO.60

2.041kO.59

0.44kO.17

1 2 3 4

2.41 2.31 2.49 2.63

PE 1.61 1.26 1.85 1.89

1.01 1.14 1.44 1.42

0.60

Means k SD

2.46kO.14

1.6520.29

1.25kO.21

0.4OkO.21

Means k SD

2.53

0.11

0.40 0.48

Values are J/l. WT, Wrs, WL, and Ww, passive work for respiratory system + endotracheal tube and measuring equipment, respiratory system, lung, and chest wall, respectively.

Table 7. This abnormality is more severe in pulmonary edema patients, in whom lung elastances are markedly increased, reflecting the reduction in the amount of aer-


RESPIRATCRY

7. Respirutov study und in others

TABLE

Study

Ref. 6 Ref. 22 Ref. 31 Ref. 17 Ref. 27 Present study COPD PE

Est,rs

MECHANICS

DURING

elastance values obtained in this E&L

Est,w

Edyn,w

10.7k2.4

5.8-11.7 8.lkO.9

4.6-8.3 4.Ok2.1

4.lkO.5

8.9zkl.6

4.8k2.0

4.2kl.9

7.9k2.1 18.3Ik7.9

7.4k2.4 7.2k2.3

6.ZkO.7 15.3k4.0 25.51k6.5

8.6k3.9 6.6k2.3

Values are means k SD or range expressed in cmH$J/l. Values in Refs. 6,17,22, and 31 are for normal subjects, and those in Ref. 27 are for stable COPD patients for whom means have been recomputed from original compliance vaIues.

ated tissue due to alveolar flooding (14). On the average, both lung and chest wall elastances are increased in our COPD patients with ARF compared with values found in COPD patients in stable condition (27), probably reflecting a greater degree of hyperinflation (Table 7). Table 4 shows that chest wall elastances were not substantially different between patients with pulmonary edema and those with COPD, whereas lung elastances were markedly increased in the former, reflecting the characteristic of the underlying pathology. Respiratory resistance. We have found, in this study, that the resistance of the ETT (plus measuring equipment) obtained in vivo was very high, amounting on the average to -50% of the total flow resistance. Wright and colleagues (33) have found that flow resistance of the ETT was higher when measured in vivo than in vitro because of kinking and compression of the tube as well as the presence of secretions. These factors cannot easily be predicted in the individual measurements and could explain some differences between results obtained in different groups of patients when values with the in vitro subtraction are compared with in vivo measurements (7, 32). In this connection it should be noted that the flow resistance of the ETT is markedly flow dependent, so that its contribution to total flow resistance can change remarkably with different inspiratory flows. In fact, in our study, the resistance of the ETT plus measuring equipment was higher, on the average, in COPD patients who were ventilated with higher VI (Table 2). According to the analyses by Bates and colleagues (2, 3) and by D’Angelo et al. (8), the ETT is a pure “ohmic” resistance. Indeed, whereas Pmax on Ptr tracing was always clearly lower than Pmax on Pao tracing, P1 was virtually the same in the two records, and the slow decay from P1 to PZ was identical, indicating that it was determined only by the intrinsic mechanical properties of the respiratory system. In Table 8 the mean values of Rmax?rs found in this study are compared with values from the literature. Rmax,rs is higher not only in our COPD patients but also in patients with pulmonary edema, in agreement with results of our previous studies (7). As shown by Table 5, the increase in Rmax,rs was due mainly to the increase in lung resistance in both groups of patients. The contribution of chest wall resistance to the total was rather small, iSee,Rmax,w was only -10% of Rmax,rs in both groups, on the average. As illustrated in Table 8, our values of

MECHANICAL

2431

VENTILATION

chest wall resistance are on the average similar to those found by Behrakis and colleagues (5) in normal anesthetized young subjects. Values of pulmonary resistance in our patients with pulmonary edema (Table 5) are on the average higher than normal values and similar to those obtained by Wright and colleagues (32) in patients with the adult respiratory distress syndrome. This increase in resistance in patients with pulmonary edema, both cardiogenic and noncardiogenic, is in line with experimental results, although the underlying mechanism is not yet fully elucidated (18, 32). D’Angelo and colleagues (8) have measured Rmin,rs, and 6Rrs with a method similar to the present one in anesthetized subjects. Values of Rmin,rs in all our COPD patients were higher than values reported by D’Angelo and colleagues for any range of VI and volume, whereas in only one patient with cardiogenic pulmonary edema Rmin,rs was clearly increased (Table 5). In anesthetized cats (15, 16) and dogs (3), Rmin,L essentially reflected airways resistance, but Rmin,w contributed ~40% to Rmin,rs at low flow rates. In contrast, Robatto and colleagues (23) found recently that, in normal anesthetized humans, Rminrs was due entirely to Rmin,L. Their result (23) is in line with our finding in mechanically ventilated patients. According to the analysis by Bates and colleagues (2), our data and the data of Robatto et al. (23) suggest that there is no ohmic resistive behavior of the chest wall in humans, in contrast to animals. In this study, 6Rrs was larger than values of normal subjects (8) in five of our COPD and in all pulmonary edema patients (Fig. 5). 6Rrs was essentially due to ~RL, and ~Rw contributed only 17 and 13% to 6Rrs, on the average, in COPD and pulmonary edema patients, respectively. According to the analyses by Bates et al. (2) and D’Angelo et al. (8), 6Rrs reflects the respiratory tissues-stress adaptation phenomena and “pendelluft” due to time constant inhomogeneities. In the normal lung, “pendelluft” contributes very little to SRrs (3); therefore the larger 6Rrs, and ~RL, in mechanically ventilated patients could reflect a larger amount of time constant inequalities within the lungs. This is likely to be the case in COPD patients, who are well known to have diffuse time constant inequalities within the lungs (l2), but it is still unclear for pulmonary edema patients. However, the end-inspiratory occlusion method does not allow one to differentiate between stress adaptation phenomena and time constant inhomogeneities. 8. Maximum respirutory resistunce vulues obtuined in this study and in others

TABLE

Study

Ref. 9 Ref. 5 Ref. 17 Ref. 32 Present study CUPD PE

Rmax,rs 6.2k2.5 2.3kO.2

Rmax,L

Rmax,w

oAko.4 2.7kO.4

1.5kO.5

(at 1 l/s) 6.15kO.89

16.6k2.2 9.4k2.2

14.9k2.4

1.7kl.4

8.3k2.6

lSkO.6

Values are means k SD expressed in cmH& 4-l s. Those from Refs. 9 and 5 are from normal subjects, those from Ref. 17 are from normal subjects by use of the elastic subtraction method (19), and those from Ref. 32 are from patients with adult respiratory distress syndrome. l


2432

RESPIRATORY

MECHANICS

DURING

Wurk of breuthing. Measurement of the work of ventilation during passive inflation is probably a poor reflection of the actual work done by the respiratory muscles during spontaneous breathing because of the large differences in tidal volume and frequency between the two conditions. However, the work done by the ventilator can provide useful clinical information. Recently, the total work during passive inflation has been measured in normal nonintubated supine awake subjects by Marini and colleagues (l7), who found average values amounting to 0.98-1.08 J/l for the kind of ventilator (i.e., the Servo 9OOC) and the range of VI used in this study. As shown in Table 6, the values found in all our patients were higher. In our patients, the work done on the respiratory system was due mainly to WL/~, while Ww/l amounted, on the average, to O-4 J/l in both groups of patients. For comparison, Sharp and colleagues (26), using a tank ventilator, have obtained a mean value of Ww amounting to 0.37 J/l in normal supine subjects. This normal Ww/l in our patients is not surprising in view of the normal chest wall resistance and the small increase in chest wall elastance in both groups of patients. However, the work done on the chest during spontaneous breathing might be slightly higher in view of the stiffer thorax when the inspiratory muscles contract (5) In conclusion, we have provided in this paper the first data on partitioning of total respiratory system mechanics between lung and chest wall in mechanically ventilated patients with ARF due to COPD and pulmonary edema. In this study, the abnormalities in total respiratory system mechanics mainly reflected alterations of lung mechanics, rather than changes in chest wall mechanics. The magnitude of PEEPi and the increase in lung elastance and resistance were clearly different in the two groups of patients because of the difference in underlying disease between COPD and pulmonary edema. In contrast, chest wall mechanics in the patients were only slightly different from normal subjects and did not exhibit’ any significant difference between the two groups of patients with different diagnosis. In a few patients PEEPi,w, Rmax,w, and Est,w were higher than values found in normal subjects, indicating that measurement of chest wall mechanics may sometimes help explain changes in total respiratory system mechanics, particularly in patients with pulmonary hyperinflation. Overall, our work supports the idea that noninvasive measurements of total respiratory system mechanics can reliably reflect changes in lung mechanics, at least for clinical purposes in these kinds of patients. The authors are grateful to the medical and nursing staff of the Intensive Care Unit in Padua for their kind cooperation and skill and to the chief of the unit Prof. E. Manzin. This study was supported by National Research Council Grant 88~01888~04 and the Ministry of Education, Special Project on Respiratory Pathophysiology, Rome, Italy. J. H. T. Bates is a Scholar of the Medical Research Council of Canada. Address for reprint requests: A. Rossi, Fisiopatologia Respiratoria, Divisione di Pneumologia, Ospedale Civile Maggiore, USL 25, Piazzale Stefani 1, I-37126 Verona, Italy. Received 4 February 1991; accepted in final form 5 June 1991.

MECHANICAL

2.

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Changes in respiratory mechanics during respiratory physiotherapy in mechanically ventilated patients.

To: Changes in respiratory mechanics during respiratory physiotherapy in mechanically ventilated patients.

Determination of volume-dependent respiratory system mechanics in mechanically ventilated patients using the new SLICE method.

Influence of different degrees of head elevation on respiratory mechanics in mechanically ventilated patients.

Myopathic characteristics in septic mechanically ventilated patients.

Conservative oxygen therapy in mechanically ventilated patients.

Ofloxacin pharmacokinetics in mechanically ventilated patients.

Optimizing Communication in Mechanically Ventilated Patients.

Angiopoietin-2 Levels as Predictors of Outcome in Mechanically Ventilated Patients with Acute Respiratory Distress Syndrome.

Music interventions for mechanically ventilated patients.

Cardiopulmonary resuscitation among mechanically ventilated patients.

A method for increasing confidence in respiratory gas exchange measurements in mechanically ventilated patients.

A respiratory-gated micro-CT comparison of respiratory patterns in free-breathing and mechanically ventilated rats.

Prediction of mortality from respiratory distress among long-term mechanically ventilated patients.

Severe hypercapnia and outcome of mechanically ventilated patients with moderate or severe acute respiratory distress syndrome.

Respiratory CO2 response depends on plasma bicarbonate concentration in mechanically ventilated patients.

Lower respiratory tract virus findings in mechanically ventilated patients with severe community-acquired pneumonia.

Dose-response effects and time course of effects of inhaled fenoterol on respiratory mechanics and arterial oxygen tension in mechanically ventilated patients with chronic airflow obstruction.

Chest physiotherapy on the respiratory mechanics and elimination of sputum in paralyzed and mechanically ventilated patients with acute lung injury: a pilot study.

Communication of mechanically ventilated patients in intensive care units.

Severe and early quadriceps weakness in mechanically ventilated patients.

Microbial profiling of dental plaque from mechanically ventilated patients.

Management and outcome of mechanically ventilated patients after cardiac arrest.

Cost comparison of mechanically ventilated patients across the age span.