Abstract
Recent data have suggested that the elastic properties of the chest wall (CW) may be compromised in patients with ARDS because of abdominal distension (4). We partitioned CW and lung (L) mechanics, assessed the role of abdominal distension, and verified whether the underlying disease responsible for ARDS affects the impairment of respiratory mechanics. Volume-pressure (V-P) curves (interrupter technique) were assessed in nine patients with surgical ARDS and nine patients with medical ARDS. Relative to nine patients undergoing heart surgery, V-P curves of the respiratory system (rs) and L of patients with surgical or medical ARDS showed a rightward displacement. V-P curves of the CW and the L showed an upward concavity in patients with medical ARDS and a downward concavity in patients with surgical ARDS. Although the CW and the abdomen (abd) V-P curves in patients with medical ARDS were similar to those obtained in patients undergoing heart surgery, they showed a rightward shift and a downward flattening in patients with surgical ARDS. In five of these patients, a reduction in static end-inspiratory pressure of the abd (69 ± 4%), rs (30 ± 3%), CW (41 ± 2%), and L (27 ± 3%) was observed after abdominal decompression for acute bleeding. Abdominal decompression therefore caused an upward and leftward shift of the V-P curves of the respiratory system, chest wall, lung, and abdomen. In conclusion we showed that impairment of the elastic properties of the respiratory system may vary with the underlying disease responsible for ARDS. The flattening of the V-P curve at high pressures observed in some patients with ARDS may be due to an increase in chest wall elastance related to abdominal distension. These observations have implications for the assessment and ventilatory management of patients with ARDS.
The acute respiratory distress syndrome (ARDS) is known to be characterized by a reduction in FRC and an increase in static elastance of the respiratory system (1). Given the underlying pulmonary injury that is present in patients with ARDS, the increase in static elastance is thought to reflect mainly alterations of the mechanical properties of the lung rather than those of the chest wall (2). However, a number of studies have also reported an increase in chest wall elastance in mechanically ventilated patients with acute lung injury (3, 4).
Mutoh and coworkers (5) showed in an animal model that abdominal distension markedly altered respiratory mechanics by its effect on the mechanical properties of the chest wall. On the basis of these results, the increase in chest wall elastance found in patients with ARDS was ascribed to abdominal distension (4). However, the role played by abdominal distension in the impairment of the mechanical properties of the respiratory system has never been assessed in patients with ARDS.
The main purposes of this study were (1) to determine the relative contribution of the chest wall and the lung to the overall impairment of the volume-pressure relationship of the respiratory system in patients with ARDS, (2) to assess the role of abdominal pressure in the impairment of respiratory mechanics in such patients, (3) to verify whether the underlying disease responsible for ARDS may qualitatively and quantitatively affect the degree of impairment or respiratory mechanics, and (4) to assess the effect of altered chest wall mechanics on estimation of the upper and lower inflection points of the volume-pressure (V-P) curve.
After obtaining approval of the protocol from the Ethical Committee of the Policlinico Hospital and informed consent from the patients or the next of kin, we studied 18 patients with severe ARDS of varying etiology admitted to the intensive care unit of the Policlinico Hospital (University of Bari, Bari, Italy). As a control group, nine patients scheduled for elective open heart surgery were studied after induction of general anesthesia and before the onset of the surgical procedure (Table 1). The diagnosis of ARDS was based on the criteria recently proposed by the American-European Consensus Conference on ARDS: acute onset, presence of hypoxemia (PaO2 /Fi O2 < 200 mm Hg regardless of positive end-expiratory pressure [PEEP] level), bilateral and diffuse opacities seen on frontal chest radiographs, absence of left ventricular failure with a pulmonary arterial occlusion pressure ⩽ 18 mm Hg (6). On the basis of the presence or absence of major abdominal surgery, patients were divided into surgical (n = 9) or medical (n = 9) ARDS.
| Patient No. | Sex | Fi O2 | PaO2 *(mm Hg) | Underlying Disease | ||||
|---|---|---|---|---|---|---|---|---|
| Preoperative cardiac surgery | ||||||||
| 1 | M | 0.3 | 303 | Mitral stenosis | ||||
| 2 | F | 0.3 | 315 | Aortic stenosis | ||||
| 3 | M | 0.3 | 288 | Coronary artery disease | ||||
| 4 | M | 0.3 | 301 | Coronary artery disease | ||||
| 5 | M | 0.3 | 285 | Coronary artery disease | ||||
| 6 | F | 0.3 | 296 | Aortic insufficiency | ||||
| 7 | M | 0.3 | 285 | Aortic insufficiency | ||||
| 8 | M | 0.3 | 328 | Coronary artery disease | ||||
| 9 | M | 0.3 | 288 | Coronary artery disease | ||||
| Surgical ARDS | ||||||||
| 1 | M | 0.8 | 85 | Abdominal aortic aneurysm | ||||
| 2 | M | 1.0 | 95 | Intenstinal obstruction, sepsis | ||||
| 3 | M | 0.8 | 88 | Mesenteric infarction | ||||
| 4 | M | 0.8 | 86 | Abdominal abscess drainage | ||||
| 5 | M | 0.8 | 82 | Mesenteric infarction | ||||
| 6 | F | 1.0 | 84 | Portacaval shunt | ||||
| 7 | M | 1.0 | 88 | Intenstinal obstruction, laparotomy | ||||
| 8 | M | 0.8 | 78 | Resection pelvic tumor | ||||
| 9 | M | 0.8 | 81 | Abdominal aortic aneurysm | ||||
| Medical ARDS | ||||||||
| 1 | M | 0.7 | 70 | Lymphoma, bone marrow transplant | ||||
| 2 | M | 0.8 | 55 | Drug overdose | ||||
| 3 | M | 0.8 | 78 | Pneumonia | ||||
| 4 | M | 0.6 | 61 | Lymphoma, bone marrow transplant | ||||
| 5 | M | 0.8 | 84 | Pneumonia | ||||
| 6 | F | 1.0 | 57 | Urinary tract infection, sepsis | ||||
| 7 | F | 1.0 | 65 | Pneumonia | ||||
| 8 | M | 1.0 | 84 | Drug overdose | ||||
| 9 | F | 0.8 | 80 | Urinary tract infection, sepsis |
All patients included in the study were mechanically ventilated with a Siemens Servo Ventilator 900C (Siemens Elema AB, Berlin, Germany). Patients with ARDS were nasotracheally intubated, whereas patients undergoing cardiac surgery were orotracheally intubated (inner diameters of the tubes varied from 7 to 8 mm and from 8 to 9 mm, respectively). Duration of mechanical ventilation prior to the study was 3 ± 1 d (range, 1 to 4 d) and 2 ± 1 d (range, 1 to 3 d) in the surgical and the medical ARDS, respectively. Patients with ARDS were sedated (diazepam, 0.1 to 0.2 mg/kg, and fentanyl, 2 to 3 μg/kg) and paralyzed (pancuronium bromide, 0.1 to 0.2 mg/kg). In patients undergoing cardiac surgery, anesthesia was induced with intravenous doses of fentanyl (5 to 10 μg/kg), thiopenthon (1 to 2 mg/kg), and vecuronium (0.7 mg/kg). All patients were in the semirecumbent position during the study period. Breathing pattern and inspiratory fraction of oxygen (Fi O2 ) in the three groups of patients during the study period are indicated in Table 2.
| Preoperative Cardiac Surgery | Surgical ARDS | Medical ARDS | ||||
|---|---|---|---|---|---|---|
| Vt, ml/kg | 11 ± 2 | 9 ± 2 | 10 ± 1 | |||
| Ti, s | 0.58 ± 0.05 | 0.66 ± 0.05 | 0.63 ± 0.03 | |||
| Ti/Ttot | 0.14 ± 0.01 | 0.15 ± 0.02 | 0.15 ± 0.08 | |||
| RR, min−1 | 15 ± 2 | 15 ± 1 | 15 ± 2 | |||
| Flow, L/s | 1.05 ± 0.07 | 1.02 ± 0.07 | 1.03 ± 0.08 | |||
| PEEPi,rs, cm H2O | 0.31 ± 0.05 | 7.67 ± 0.81† | 3.84 ± 0.44† | |||
| PEEPi,cw, cm H2O | 0.12 ± 0.03 | 3.29 ± 0.24† | 1.21 ± 0.17† | |||
| PEEPi, l , cm H2O | 0.16 ± 0.04 | 4.37 ± 0.44† | 2.65 ± 0.69† | |||
| ΔEELV, ml | 27 ± 2 | 298 ± 29† | 144 ± 31† |
To better evaluate the role of abdominal distension, measurements of the static V-P curves were also obtained in five patients with surgical ARDS (Patients 1, 3, 4, 7 and 9) after abdominal reexploration and decompression for acute intra-abdominal bleeding (7, 8).
Flow was measured with a heated No. 2 pneumotachograph (Fleisch, Lausanne, Switzerland) connected to a differential pressure transducer (MP 45, ± 2 cm H2O; Validyne, Northridge, CA), which was inserted between the Y-piece of the ventilator circuit and the endotracheal tube (ET). The pneumotachograph was linear over the experimental range of flows and was calibrated using the same gas mixtures used to ventilate the patient at the moment of the study. Equipment dead space (not including the ET tube) was 60 ml.
Airway opening pressure (Pao) was measured proximal to the ET tube with a pressure transducer (Validyne MP 45 ± 100 cm H2O). To reduce the effects of compliance and resistance of the system connecting the endotracheal tube to the ventilator circuit, a single length of standard low compliance tubing supplied with the ventilator was used (2 cm ID, 60 cm long). During the measurements the humidifier was disconnected from the inspiratory tubing. The compliance of the system connecting the subjects to the ventilator was 0.4 ml/cm H2O. Special care was taken to avoid gas leaks in the equipment, particularly around the tracheal cuff, which was frequently checked. Changes in intrathoracic and abdominal pressures were evaluated by assessment of esophageal (ΔPes) and gastric (ΔPga) pressures. ΔPes and ΔPga were measured using thin latex balloon-tipped catheter systems. Both balloons were 10 cm in length and 2.4 cm in circumference and were connected by polyethylene catheters (length, 70 cm; internal diameter, 1.7 mm) to separate differential pressure transducers (Validyne MP 45 ± 100 cm H2O). The esophageal balloon was positioned in the middle third of the esophagus and filled with 0.75 ml of air. The gastric balloon contained 1.0 ml of air and was positioned in the stomach. Two tests were performed to ensure correct positioning of the catheters: first, an occlusion test to assess the validity of the esophageal pressure measurement (9); second, a search for positive deflections on gastric pressure tracings, made while one of the operators applied gentle pressure to the patient's stomach (10). Both tests were performed prior to administration of sedative and paralyzing agents in patients with ARDS and before entering the operating theater in patients undergoing cardiac surgery. Estimates of absolute pleural pressure with an esophageal balloon are prone to artifacts in supine subjects. However, the likelihood that such artifacts were significant in our study is small because our calculations are based on the variability of changes in Pes instead of on its absolute values.
All of the above variables were displayed on an eight-channel strip-chart recorder (7718A; Hewlett-Packard Co., Cupertino, CA) and collected on a personal computer through a 12-bit analog-to-digital converter at a sample rate of 100 Hz. Subsequent data analysis was performed using the software package ANADAT (RHT-InfoDat, Montreal, PQ). Tidal volume (Vt) was computed by digital integration of the flow signal. Measurements were obtained on PEEP = 0.
Test breath. During baseline ventilation an end-expiratory airway occlusion (EEO) was performed by pressing the end-expiratory hold knob on the ventilator. When an end-expiratory plateau in pressure was reached, EEO was released. At the end of the following breath, an end-inspiratory occlusion (EIO) was performed by pressing the end-inspiratory hold knob on the ventilator until an apparent plateau was observed in Pao, Pes, and Pga. During the EIO, the patient was disconnected from the ventilator and let to expire through the pneumotachograph to the atmosphere (Figure 1). In this way, when the EIO was released, a complete expiration to the elastic equilibrium volume of the respiratory system (Vr) was obtained. To confirm that Vr had been reached, the airway was repeatedly occluded. If during the occlusion there was no increase in Pao, Vr was achieved. After each test breath, the baseline ventilation was resumed until ΔV, flow, and pressures returned to their baseline values (11-13).
Fig. 1. Records of flow, changes in lung volume (ΔV), airway opening (Pao), esophageal pressure (ΔPes) and gastric pressure (ΔPga) from Patient 5 with surgical ARDS illustrating a test breath. To confirm that the elastic equilibrium volume of the respiratory system had been reached, the airway was repeatedly occluded. See text for further details.
[More] [Minimize]Intrinsic PEEP. Whenever the time required to complete passive expiration is greater than the expiratory duration set by the ventilator, the end-expiratory lung volume (EELV) will exceed the relaxation Vr during mechanical ventilation, and the respiratory system will exert positive static pressure at end-expiration. This pressure is termed intrinsic PEEP (PEEPi). PEEPi in the respiratory system (PEEPi,rs) and in the chest wall (PEEPi,w) was measured as the plateau pressure during EEO in Pao and Pes, respectively, referred to their values at Vr. PEEPi in the lung (PEEPi,L) was determined as the difference between PEEPi,rs and PEEPi,w. The increase in lung volume because of the presence of PEEPi was quantified as the difference between EELV during mechanical ventilation and Vr (11-13).
Static inflation volume-pressure curve. This was measured as previously described (14) by intermittently performing a series of the above-described test breaths at different inflation volumes that ranged between 0.1 and 1.0 L. Different volumes were achieved by changing the respiratory frequency of the ventilator while keeping the inspiratory flow constant at baseline level. The static V-P curves of the respiratory system, chest wall, and lung were obtained by plotting the different inflating volumes (expressed relative to Vr) against the corresponding pressure values at 3 to 5 s after EIO (13, 14). The static end-inspiratory recoil pressure of the respiratory system (Pst,rs) and chest wall (Pst,w) were measured as the plateau pressure on Pao and Pes during EIO referenced to their values at Vr. Static end-inspiratory recoil pressure of the lung (Pst,L) was calculated as the difference between Pst,rs and Pst,w. Static end-inspiratory pressure of the abdomen (Pst,ab) was measured as the EIO gastric plateau pressure referred to its value at EELV, and the static V-P curve of the abdomen was obtained by plotting the different volumes, referred in this case to EELV, against the corresponding values of Pst,ab.
The experimental points were fit to a power equation (11, 13):
| Equation 1 |
where coefficients a and b are constant. Coefficient a represents static elastance of the relevant component at ΔV of 1 L, and coefficient b is a dimensionless number that indicates the variation of elastance with inflating volume. For values of coefficient b < 1 elastance decreases with inflating volume, whereas it increases for values of coefficient b > 1 (11, 13).
Measurement of inflection points. Values of the volumes at the upper (UIP) and lower inflection points (LIP) of the V-P curves were quantified using a step-by-step regression analysis on samples of four consecutive experimental points (15). The zone of lowest elastance was determined by the computer (Mathcad; Mathsoft Inc., Cambridge, MA). The same analysis was than performed on samples of three consecutive points, allowing the calculation of the slopes at the different segments of the V-P curves. In the presence of a consistent change in slope of at least 20%, the point before (Figure 2, bottom panels) and after (Figure 2, middle panels) the linear tract identifying the zone of lowest elastance were identified as LIP and UIP, respectively (15).
Fig. 2. Static inflation volume-pressure curves of the respiratory system (rs), chest wall (cw), and lung (L) in three representative preoperative cardiac surgery (top), surgical ARDS (middle), and medical ARDS (bottom) patients. Intrinsic positive end-expiratory pressure (PEEPi) and the corresponding increase in end-expiratory lung volume (EELV) relative to the elastic equilibrium volume of the respiratory system (Vr) are indicated on the volume-pressure curves (closed symbols). Experimental points above EELV were fitted with Equation 1. Dotted line indicates zone of lowest elastance determined by a step-by-step regression analysis on samples of four consecutive experimental points. ΔPst = changes in end-inspiratory static pressure; ΔV = changes in lung volume relative to Vr; UIP = upper inflexion point; LIP = lower inflection point. See text for further details.
[More] [Minimize]All results are expressed as mean ± SEM. Regression analysis was made using the least-squares method. Values obtained in the different groups of patients were compared using the two-way analysis of variance (ANOVA) of repeated measures. If significant (p < 0.05), the values were compared using the Bonferroni test (software package StatView; Abacus Inc., Berkeley, CA).
The static inflation V-P relationship of the respiratory system, chest wall, and lung in three representative patients of the three groups is illustrated in Figure 2. Individual and average values of coefficients a and b in Equation 1 for the total respiratory system, chest wall, and lung in the three groups of patients are given in Table 3. The correlation coefficients ranged between 0.99 and 1.00.
| Patient No. | RS | CW | L | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| a | b | a | b | a | b | |||||||
| Preoperative cardiac surgery | ||||||||||||
| 1 | 13.96 | 0.98 | 5.91 | 0.91 | 8.05 | 0.98 | ||||||
| 2 | 13.85 | 0.98 | 5.19 | 0.90 | 8.66 | 0.97 | ||||||
| 3 | 12.55 | 0.98 | 6.06 | 0.94 | 6.49 | 0.93 | ||||||
| 4 | 12.15 | 0.95 | 5.14 | 0.91 | 7.01 | 0.95 | ||||||
| 5 | 13.33 | 0.93 | 6.08 | 0.95 | 7.25 | 0.97 | ||||||
| 6 | 14.56 | 0.95 | 5.02 | 0.96 | 9.54 | 0.90 | ||||||
| 7 | 14.07 | 0.96 | 5.01 | 0.92 | 9.06 | 0.94 | ||||||
| 8 | 12.72 | 0.96 | 5.98 | 0.95 | 6.74 | 0.98 | ||||||
| 9 | 13.58 | 0.97 | 6.51 | 0.91 | 7.07 | 0.91 | ||||||
| Mean ± SEM | 13.42 ± 0.27 | 0.96 ± 0.01 | 5.66 ± 0.19 | 0.93 ± 0.01 | 7.76 ± 0.37 | 0.95 ± 0.01 | ||||||
| Surgical ARDS | ||||||||||||
| 1 | 32.55 | 1.17 | 9.44 | 1.25 | 23.11 | 1.33 | ||||||
| 2 | 32.69 | 1.06 | 8.49 | 1.22 | 24.20 | 1.49 | ||||||
| 3 | 32.54 | 1.25 | 9.81 | 1.12 | 22.73 | 1.57 | ||||||
| 4 | 38.46 | 1.06 | 7.96 | 1.23 | 30.50 | 1.66 | ||||||
| 5 | 39.05 | 1.26 | 9.21 | 1.28 | 29.84 | 1.32 | ||||||
| 6 | 32.06 | 1.45 | 9.91 | 1.13 | 22.15 | 1.37 | ||||||
| 7 | 31.32 | 1.04 | 8.76 | 1.35 | 22.56 | 1.19 | ||||||
| 8 | 32.02 | 1.18 | 7.97 | 1.22 | 24.05 | 1.24 | ||||||
| 9 | 32.17 | 1.55 | 8.95 | 1.19 | 23.22 | 1.19 | ||||||
| Mean ± SEM | 33.65 ± 0.98* | 1.22 ± 0.06* | 8.94 ± 0.24* | 1.22 ± 0.02* | 24.71± 1.06* | 1.37 ± 0.06* | ||||||
| Medical ARDS | ||||||||||||
| 1 | 30.12 | 0.81 | 5.22 | 0.94 | 24.90 | 0.88 | ||||||
| 2 | 28.04 | 0.88 | 5.83 | 0.91 | 24.21 | 0.81 | ||||||
| 3 | 33.24 | 0.98 | 5.25 | 0.91 | 28.09 | 0.94 | ||||||
| 4 | 28.17 | 0.81 | 5.59 | 0.94 | 26.71 | 0.85 | ||||||
| 5 | 34.30 | 0.98 | 5.13 | 0.95 | 29.17 | 0.91 | ||||||
| 6 | 27.29 | 0.88 | 5.29 | 0.98 | 25.85 | 0.83 | ||||||
| 7 | 35.25 | 0.97 | 4.98 | 0.94 | 30.27 | 0.91 | ||||||
| 8 | 29.15 | 0.84 | 5.87 | 0.97 | 23.28 | 0.87 | ||||||
| 9 | 28.28 | 0.75 | 5.52 | 0.93 | 22.76 | 0.80 | ||||||
| Mean ± SEM | 30.20 ± 1.12* | 0.88 ± 0.03* | 5.40 ± 0.11 | 0.94 ± 0.01 | 26.14 ± 0.71* | 0.87 ± 0.02* | ||||||
In the cardiac surgery patients, the static V-P relationship of the respiratory system, chest wall, and lung (Figure 2, top panels) were almost linear. However, coefficients b in Equation 1 were always slightly < 1, indicating that elastance of the respiratory system, chest wall, and lung progressively decreased with inflating volume. V-P curves of the respiratory system and lung of patients with surgical (Figure 2, middle panels) and medical (Figure 2, bottom panels) ARDS exhibited a rightward displacement with an increase in coefficient a in Equation 1 (i.e., elastance at ΔV = 1 L) (p < 0.0001) (Table 3). However, although elastance of the respiratory system and of the lung perceptibly decreased with inflation volume in patients with medical ARDS and the relative V-P curves showed an upward concavity (Figure 2, bottom panels), in patients with surgical ARDS the V-P curve of the respiratory system of the lung showed an upward convexity, indicating that elastance increased with inflating volume (Figure 2, middle panels). Consequently, in patients with surgical ARDS coefficients b in Equation 1 for the respiratory system and lung ranged between 1.06 and 1.55 and 1.19 and 1.66, respectively. On the other hand, in patients with medical ARDS coefficient b in Equation 1 for the respiratory system and lung ranged between 0.75 and 0.98 and 0.80 and 0.94, respectively (Table 3).
The static inflation V-P curve of the chest wall also differed between patients with surgical and medical ARDS. Although the V-P curves of the chest wall in patients with medical ARDS (Figure 2, bottom panels) were virtually superimposable to the curves obtained in preoperative cardiac surgery patients (Figure 1, top), the V-P curve of patients with surgical ARDS showed a rightward shift and an upward convexity (Figure 2, bottom panels). As a consequence, values of coefficients a and b in Equation 1 for the chest wall in patients with medical ARDS did not differ statistically from those observed in preoperative cardiac patients, whereas in patients with surgical ARDS, values of coefficients a and b ranged between 7.96 and 9.91 and 1.12 and 1.35 cm H2O/L, respectively, and were statistically (p < 0.0001) higher than those found in patients undergoing cardiac surgery.
Values of PEEPi in preoperative cardiac patients were close to zero, ranging between 0.18 and 0.50 cm H2O. On the other hand, PEEPi ranged between 5.01 and 9.77 and 2.77 and 5.02 cm H2O in patients with ARDS secondary to surgical and medical causes, respectively. PEEPi,w was, on average, 43 ± 3 and 30 ± 2% of PEEPi,rs (p < 0.001) in surgical and medical ARDS, respectively.
The mean V-P curves of the abdomen in the three groups of patients obtained during inflation of the respiratory system and end-inspiratory occlusions are shown in Figure 3. In patients undergoing cardiac surgery, coefficients a and b in Equation 1 were 3.78 ± 0.08 and 0.81 ± 0.06 cm H2O/L, respectively. Patients with medical ARDS had V-P curves of the abdomen virtually superimposable to those of the cardiac surgery patients, with coefficients a and b equal to 3.69 ± 0.04 and 0.80 ± 0.07. A rightward shift of the V-P curve of the abdomen was observed in patients with surgical ARDS as indicated by the significant (p < 0.0001) increase in coefficient a (9.90 ± 0.01). In these patients, the coefficient b was 0.84 ± 0.08 and did not differ from those observed in preoperative cardiac surgery patients and those with medical ARDS.
Fig. 3. Mean static inflation volume-pressure curves of the abdomen (abd). Changes in lung volume and abdominal pressure are expressed relative to end-expiratory lung volume (EELV). Circles indicate preoperative cardiac surgery; diamonds indicate medical ARDS; squares indicate surgical ARDS. Details and abbreviation as in Figure 2.
[More] [Minimize]Effects of abdominal decompression on the inspiratory V-P curves of the respiratory system, chest wall, lung, and abdomen in three representative patients are shown in Figure 4. Average values of coefficients a and b in Equation 1 for the respiratory system, chest wall, lung, and abdomen in the five patients are shown in Table 4. Abdominal decompression for acute bleeding decreased Pst,ab from 6.58 ± 2.22 to 2.39 ± 0.98 cm H2O (69 ± 4%). Consequently, Pst,rs, Pst, w , and Pst,L decreased from 30.37 ± 3.33 to 21.24 ± 2.98 cm H2O (30 ± 3%), from 6.51 ± 2.29 to 3.87 ± 1.65 cm H2O (41 ± 2%), and from 23.88 ± 4.01 to 17.35 ± 3.88 cm H2O (27 ± 3%), respectively. Similar behavior was shown by PEEPi,rs, PEEPi, w , and PEEPi,L, which decreased from 6.05 ± 2.08 to 2.55 ± 1.27 (58 ± 37%), from 1.59 ± 1.08 to 0.59 ± 0.18 (63 ± 4%), and from 4.44 ± 1.83 to 1.95 ± 0.58 (56 ± 3%) cm H2O, respectively. Abdominal decompression therefore caused an upward and leftward shift of the V-P curves of the respiratory system, chest wall, lung, and abdomen.
Fig. 4. Static inflation volume-pressure curves of the respiratory system (rs), chest wall (cw) and lung (L) in three representative patients with surgical ARDS before (open squares) and after (closed squares) surgical reexploration and abdominal decompression for acute intra- abdominal bleeding. The difference in volume between the curve obtained before and after abdominal decompression at Pst,L of 20 cm H2O (vertical line) indicates recruited volume. Details and abbreviation as in Figure 2.
[More] [Minimize]| Abdominal Reexploration | ||||||
|---|---|---|---|---|---|---|
| Before | After | |||||
| Respiratory system | ||||||
| a | cm H2O/L | 33.65 ± 1.72 | 22.62 ± 3.94† | |||
| b | 1.09 ± 0.03 | 0.83 ± 0.01† | ||||
| Chest wall | ||||||
| a | cm H2O/L | 8.72 ± 0.33 | 5.00 ± 0.56† | |||
| b | 1.27 ± 0.03 | 0.92 ± 0.01† | ||||
| Lung | ||||||
| a | cm H2O/L | 25.39 ± 1.98 | 18.21 ± 1.74† | |||
| b | 1.39 ± 0.10 | 0.82 ± 0.01† | ||||
| Abdomen | ||||||
| a | cm H2O/L | 9.64 ± 0.17 | 3.63 ± 0.05† | |||
| b | 0.83 ± 0.01 | 0.84 ± 0.01 | ||||
Cardiac patients did not have a measurable LIP or UIP on the V-P curves of the respiratory system, chest wall, and lung (Figure 2). The LIP and UIP were identified only on the V-P curves of the respiratory system and lung of patients with medical and surgical ARDS, respectively (Figure 2). In the patients with medical ARDS, the values of pressures corresponding to LIP were about 28% lower when calculated from the V-P curve of the lung (Table 5), whereas in the patients with surgical ARDS, the values of Vt (above the end-expiratory volume) that corresponded to the UIP were about 28% greater when estimated from the lung V-P curve of the respiratory system (Table 6).
| Patient No. | LIP | |||
|---|---|---|---|---|
| Pst,rs(cm H2O) | Pst,L(cm H2O) | |||
| 1 | 18.34 | 14.30 | ||
| 2 | 16.88 | 10.88 | ||
| 3 | 15.76 | 12.09 | ||
| 4 | 12.31 | 8.34 | ||
| 5 | 11.89 | 9.09 | ||
| 6 | 17.79 | 12.32 | ||
| 7 | 18.34 | 14.09 | ||
| 8 | 14.89 | 10.54 | ||
| 9 | 13.78 | 8.69 | ||
| Mean ± SEM | 15.55 ± 0.83 | 11.15 ± 0.74* | ||
| Vt Above EELV (L) | ||||
|---|---|---|---|---|
| Patient No. | RS | L | ||
| 1 | 0.51 | 0.72 | ||
| 2 | 0.64 | 0.80 | ||
| 3 | 0.58 | 0.77 | ||
| 4 | 0.65 | 0.82 | ||
| 5 | 0.77 | 0.95 | ||
| 6 | 0.81 | 1.08 | ||
| 7 | 0.53 | 0.77 | ||
| 8 | 0.78 | 0.98 | ||
| 9 | 0.75 | 0.88 | ||
| Mean ± SEM | 0.67 ± 0.04 | 0.86 ± 0.04 | ||
Our data show that in mechanically ventilated patients with ARDS, impairment of the mechanical properties of the respiratory system varies greatly with the underlying disease responsible for ARDS. In patients in whom ARDS was consequent to major abdominal surgery (surgical ARDS), the static inspiratory V-P relationship of the respiratory system and lung showed an upward convexity, indicating that elastance increased with tidal volume causing alveolar overinflation with inflating volume (14). Patients with ARDS not consequent to major surgery (medical ARDS) had an upward concavity on the static inspiratory V-P curves of the respiratory system and lung, indicating a progressive decrease in elastance and alveolar recruitment with lung inflation (14). Whereas in patients with medical ARDS the V-P curves of the chest wall and the abdomen were essentially superimposable with the curves observed in patients during general anesthesia for cardiac surgery, a rightward shift of the thoracic and abdominal V-P curves was observed in patients with surgical ARDS. These data seem to suggest that the flattening of the V-P curves of the respiratory system and lung observed in some patients with ARDS (14) may in part be due to the increase in chest wall elastance related to abdominal distension.
Measurements of the inspiratory V-P curves of the respiratory system have been used in mechanically ventilated patients with ARDS as a means of assessing the patients' status and progress (1) and to optimize the use of PEEP and of mechanical ventilation (15-17). Abnormalities in the mechanical properties of the respiratory system in patients with ARDS have been generally attributed to alteration in lung rather than to chest wall mechanics (18), eventhough a few investigators have reported an increase in chest wall elastance in patients with ARDS (3, 4, 19, 20). We recently observed that with a baseline tidal volume of 10.4 ± 0.5 ml/kg, five patients with ARDS consequent to major abdominal surgery exhibited a static inflation V-P curve of the respiratory system with a convex shape and a progressive increase in elastance with increasing tidal volume (14). In contrast, in patients who were not submitted to major abdominal surgery, the static inflation V-P curves exhibited a concave shape with a progressive decrease in elastance (14). Data obtained in the present investigation confirm those preliminary observations. The V-P relationship of the respiratory system and lung in nine patients with ARDS caused by major abdominal surgery showed an upward convexity and a V-P relationship of the chest wall that was shifted to the right and flattened (Figure 2). In the patients with medical ARDS, the V-P relationship of the respiratory system and lung showed an upward concavity and the V-P relationship of the chest wall was superimposable with the one observed in the control group (Figure 2). In addition, in the patients with medical ARDS, values of Pst,ab were not statistically different from those of the control group, whereas in patients with surgical ARDS, values of Pst,ab were about four times greater than the values observed in the control patients (p < 0.0001). Consistent with these findings, the static inflation V-P curve of the abdomen in patients with medical ARDS was superimposable to the one measured in the control group, whereas a rightward shift was observed in patients with surgical ARDS (Figure 3). These data therefore indicate that when the underlying disease responsible for ARDS is an abdominal pathologic process requiring major abdominal surgery, abdominal distension may occur, and alteration of the mechanical properties of the chest wall may contribute to the derangement of respiratory mechanics. However, measurements of absolute lung volume were not performed in this study, and therefore differences between cardiac patients with those with ARDS may reflect the downward displacement along the same V-P relationship or an overall change of the characteristic V-P relationship of the respiratory system because of ARDS.
Although in this study the increase in abdominal distension occurred in the surgical patients, it may also occur in some patients with medical ARDS as well. The key factor is increased abdominal pressure, which can occur in a variety of clinical situations such as tense ascites, abdominal hemorrhage, abdominal obstruction, laparoscopy, large abdominal tumors, and peritoneal dialysis, all of which can adversely affect respiratory, cardiac, renal, and metabolic functions (7, 8, 21, 22). Elevations in intra-abdominal pressure will occur when the distensible components of the peritoneal cavity (peritoneum, abdominal muscles, and diaphragm) become less compliant because of increased intra-abdominal volume (i.e., ascites, abdominal hemorrhage). Under these circumstances, direct compression of the abdominal contents occurs, venous return from the lower extremities is impaired, and intra-abdominal pressure is transmitted via the diaphragm to the thoracic cavity (23, 24). Whether increase in abdominal pressure in absence of overt distension, perhaps as a result of bowel wall edema or ileus, may affect lung mechanics remain to be established.
The respiratory system may be partitioned into two compartments; the chest wall and the lung. Although the diaphragm forms the caudal boundary of the chest cavity, the diaphragm is mechanically coupled to the abdominal wall and contents. Any increase in abdominal pressure may therefore affect lung mechanics by increasing the propensity for the development of atelectasis and by decreasing FRC (5, 21), which may also indirectly alter chest wall mechanics by shifting the V-P curve of the chest wall to a lower lung volume (25). Abdominal distension may also directly impact on chest wall mechanics by affecting chest wall configuration, and/or changing in the interaction at the zone at which the lungs are opposed to the lateral surface of the diaphragm, and/or causing inhomogeneity in the displacement among different parts of the chest wall (22). Mutoh and coworkers (5) studied the effects of abdominal distension on lung and chest wall mechanics in anesthetized, paralyzed, and mechanically ventilated pigs. Abdominal distension was induced by inflating a liquid-filled balloon placed in the abdominal cavity. During baseline conditions, Pst,ab was 2.8 ± 1.0 cm H2O and increased to 15.2 ± 1.5 cm H2O after inflation of the abdominal balloon. Abdominal distension caused a rightward and downward shift of the static V-P curves of the respiratory system, chest wall, lung, and abdomen. Consequently, compliance (i.e., 1/elastance) of the respiratory system, chest wall, and lung was reduced by 47, 48, and 39%, respectively, after abdominal distension. FRC decreased by 54% from control values. In patients with ARDS after major abdominal surgery, we found values of Pst,ab that were markedly higher than those found in patients undergoing general anesthesia for cardiac surgery and patients with medical ARDS. Further evidence that abdominal distension may play a specific role in the abnormalities observed in patients with surgical ARDS was obtained from the five patients who underwent surgical decompression (Figure 4).
Prior to surgical reexploration, the V-P curve of the lung showed an upward convexity, thus indicating a progressive increase in elastance with inflating volume caused by alveolar overdistension; after abdominal decompression, the V-P curve of the lung showed an upward concavity, indicating that elastance progressively decreased with tidal volume because of alveolar recruitment (14). We have previously shown that the upward displacement along the volume axis of the V-P curves, termed recruited volume and quantified as the increase in volume at a static end-inspiratory pressure of 20 cm H2O, could be used as an index of recruitment of previously collapsed units with PEEP (14). We therefore quantified recruited volume as the upward shift along the volume axis of the inspiratory V-P curve of the lung after abdominal decompression relative to the curve prior to surgical exploration at the same Pst,L (20 cm H2O). We found that recruited volume consequent to abdominal decompression was 236 ± 36 ml. In line with a previous study (7), we found that PaO2 /Fi O2 increased with abdominal decompression from 103 ± 4 to 178 ± 21 mm Hg; this improvement was correlated (p < 0.0001) with the recruited volume. However, measurements of abdominal V-P curves made using a method that is independent of the change in lung volume would be required to distinguish between recruited volume and a shift of the equilibrium volume. Therefore, these data suggest that abdominal distension may be present in patients with ARDS; this distension may cause flattening of the inspiratory V-P curve of the respiratory system by either stiffening the chest wall and/or causing further alveolar atelectasis (5), both of which may be reversed by abdominal decompression.
Mutoh and coworkers (28) compared V-P curves of the respiratory system, chest wall, and lung in pigs before and after fluid loading (volume intravenously infused equal to 15 to 20% of the pig's body weight). Volume infusion caused abdominal distension and decreased FRC by 62% (p < 0.05). This caused a rightward shift of the V-P curves of the respiratory system, chest wall, and lung (28). The effects of abdominal distension induced by inflating a balloon placed in the abdominal cavity (at the same pressure obtained during fluid loading) were similar to those of volume infusion. Mutoh and coworkers concluded that infusing large volumes of fluid markedly alters chest wall mechanics mainly by causing abdominal distension. A positive fluid balance (1.63 ± 0.46 L) was found only in patients with surgical ARDS. In these patients, values of coefficients a and b for the chest wall, values of coefficient a for the abdomen, and values of Pst,ab were positively (p < 0.01) correlated with the amount of positive fluid balance. Volume overloading may contribute to abdominal distension in any number of ways: (1) engorging abdominal vessels, (2) generating ascites, and (3) causing increased urine production and bladder distension (28, 29). Because abdominal surgery and sepsis are associated with third spacing and permeability changes, edema of abdominal organs may also contribute to abdominal distension (29, 30).
Our results may have potential clinical implications with respect to the appropriate ventilatory stategies for these patients. In an attempt to limit the lung injury caused by ventilation at high lung volumes, it has been suggested that one should limit the Vt to maintain the end-inspiratory volume less than the upper inflection point (15-17, 31). The concept is that the UIP represents the point where elastance starts to increase and hence represents the volume at which stretching and overdistension of at least some alveolar structures occurs (15). Our results indicate that, in the presence of alteration in chest wall mechanics caused by abdominal distension, the Vt at which elastance starts to increase is on average 28% greater when the lung V-P curve is analyzed compared with the respiratory system V-P curve. Because one is interested in limiting overdistension of the lung, it is the analysis of the V-P curve of the lung that should be used to determine the appropriate Vt. However, in clinical practice, it is the respiratory system V-P curve that is routinely assessed, thus potentially leading to an underestimation of the “permissible” Vt. Similarly, it has been suggested that ventilation should occur above LIP (2, 15-17, 31-33) to ensure recruitment of the lung since LIP is thought to represent the average critical pressure required to reopen previously closed peripheral airways and/or alveoli. Our results indicate that analysis of the V-P curve of the respiratory system indicates that the LIP should be 25 to 30% higher than calculated on the basis of lung mechanics. Thus, in using a lung protective strategy, analysis of mechanics based on respiratory system V-P curves may lead to much higher PEEP and lower Vt levels (because of lower UIP and higher PEEP), potentially leading to substantially higher levels of PaCO2 than if the lung V-P curves had been analyzed. These considerations seem to have particular relevance in the presence of alteration of chest wall mechanics caused by abdominal distension (30).
In conclusion, in the present study we showed that interpretation of the mechanical properties of the respiratory system requires assessment of both lung and chest wall mechanics and may vary with the underlying disease responsible for ARDS. In patients with medical ARDS, the inspiratory V-P curve of the respiratory system and lung showed a progressive reduction in elastance with inflating volume because of alveolar recruitment. In patients in whom ARDS followed major abdominal surgery, abdominal distension with increased values of chest wall elastance were observed. When abdominal pressure was normalized by surgical reexploration, improvement of the mechanical properties of the respiratory system, lung, and chest wall was observed. These data suggest that the flattening of the V-P curve at high pressures observed in some patients with ARDS may be due to increase in chest wall elastance related to abdominal distension. These results may also have importance for the optimal ventilatory management of critically ill patients with ARDS with respect to the selection of optimal PEEP and Vt levels to minimize ventilator- induced lung injury.
The writers thank L. Gattinoni and P. Pelosi for the stimulating discussions that motivated this study. They also thank the physicians and nursing staff of the ICUs and operating theaters of the Policlinico Hospital for their valuable cooperation and Mary V. C. Pragnell, B.A., for help in revising the manuscript.
Supported by Grant 95.00934.CT04 from the Consiglio Nazionale delle Ricerche.
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