Inspiratory Pressure-volume Curve Research Articles

Cardiogenic oscillations to detect intratidal derecruitment and overdistension in a porcine model of healthy and atelectatic lungs

Low positive end-expiratory pressure (PEEP) can result in alveolar derecruitment, and high PEEP or high tidal volume (VT) in lung overdistension. We investigated cardiogenic oscillations (COS) in the airway pressure signal to investigate whether these oscillations can assess unfavourable intratidal events. COS induce short instantaneous compliance increases within the pressure-volume curve, and consequently in the compliance-volume curve. We hypothesised that increases in COS-induced compliance reflect non-linear intratidal respiratory system mechanics. In mechanically ventilated anaesthetised pigs with healthy (n=13) or atelectatic (n=12) lungs, pressure-volume relationships and the ECG were acquired at a PEEP of 0, 5, 10, and 15cm H2O. During inspiration, the peak compliance of successive COS (CCOS) was compared with intratidal respiratory system compliance (CRS) within incremental volume steps up to the full VT of 12mlkg-1. We analysed whether CCOS variation corresponded with systolic arterial pressure variation. CCOS-volume curves showed characteristic intratidal patterns depending on the PEEP level and on atelectasis. Increasing CRS- or CCOS-volume patterns were associated with intratidal derecruitment with low PEEP, and decreasing patterns above 6mlkg-1 and high PEEP showed overdistension. CCOS was not associated with systolic arterial pressure variations. Heartbeat-induced oscillations within the course of the inspiratory pressure-volume curve reflect non-linear intratidal respiratory system mechanics. The analysis of these cardiogenic oscillations can be used to detect intratidal derecruitment and overdistension and, hence, to guide PEEP and VT settings that are optimal for respiratory system mechanics.

Prone Positioning for a Morbidly Obese Patient with Acute Respiratory Distress Syndrome: An Opportunity to Explore Intrinsic Positive End-expiratory Pressure–Lower Inflexion Point Interdependence

Prone Positioning for a Morbidly Obese Patient with Acute Respiratory Distress Syndrome: An Opportunity to Explore Intrinsic Positive End-expiratory Pressure–Lower Inflexion Point Interdependence

CT-Densitometrie zur Analyse der statischen Druckvolumenkurve der Lunge bei experimentell induziertem Lungenschaden

To study quantitative changes of lung density distributions when recording in- and expiratory static pressure-volume curves by single slice computed tomography (CT). Static in- and expiratory pressure volume curves (0 to 1000 ml, increments of 100 ml) were obtained in random order in 10 pigs after induction of lung damage by saline lavage. Simultaneously, CT acquisitions (slice thickness 1 mm, temporal increment 2 s) were performed in a single slice (3 cm below the carina). In each CT image lung segmentation and planimetry of defined density ranges were achieved. The lung density ranges were defined as: hyperinflated (-1024 to -910 HU), normal aerated (-910 to -600 HU), poorly aerated (-600 to -300 HU), and non aerated (-300 to 200 HU) lung. Fractional areas of defined density ranges in percentage of total lung area were compared to recorded volume increments and airway pressures (atmospheric pressure, lower inflection point (LIP), LIP*0.5, LIP*1.5, peak airway pressure) of in- and expiratory pressure-volume curves. Quantitative analysis of defined density ranges showed no differences between in- and expiratory pressure-volume curves. The amount of poorly aerated lung decreased and normal aerated lung increased constantly when airway pressure and volume were increased during inspiratory pressure-volume curves and vice versa during expiratory pressure-volume loops. Recruitment and derecruitment of lung atelectasis during registration of static in- and expiratory pressure-volume loops occurred constantly, but not in a stepwise manner. CT was shown to be an appropriate method to analyse these recruitment process.

Safety of Pressure-Volume Curve Measurement in Acute Lung Injury and ARDS Using a Syringe Technique

To assess the safety of frequent pressure-volume (PV) curve measurement in patients with acute lung injury (ALI)/ARDS. Prospective observational study. Academic medical-surgical critical care unit. Consecutive patients with ALI or ARDS. Static inspiratory PV curves of the respiratory system were determined twice on day 1, then once daily for up to 6 days using a syringe. At each time point, three separate measurements of the PV curve were made. A 100-mL graduated syringe was used to inflate patients' lungs with 50- to 100-mL increments up to an airway pressure of 45 cm H(2)O or a total volume of 2 L; each volume step was maintained for 2 to 3 s until a plateau airway pressure was recorded. Outcome measures were mean arterial BP, heart rate (HR), and oxyhemoglobin saturation (SpO(2)) prior to and immediately after PV curve measurement. There were a priori criteria for procedure discontinuation if poorly tolerated. Eleven patients were enrolled with a total of 134 PV curves generated. SpO(2) was 93 +/- 4% (mean +/- SD) before and fell to a nadir of 89 +/- 5% during PV curve measurement (p < 0.001), but increased to 97 +/- 4% immediately afterwards (p < 0.001, before vs after). HR rose from 106 +/- 22 to 108 +/- 22 beats/min immediately after the maneuver (p < 0.001). Mean arterial BP was 93 +/- 15 mm Hg before and 100 +/- 17 mm Hg immediately afterwards (p < 0.001). During PV curve measurement, systolic BP in one patient fell to 64 mm Hg from 113 mm Hg; in another patient, SpO(2) dropped to 79% from 89%. Both changes were transient. The study was discontinued in one patient because of inability to tolerate zero positive end-expiratory pressure; in another patient, the study was discontinued because of the development of subcutaneous emphysema. PV curve measurement by syringe technique is well tolerated in most patients. Nonetheless, the maneuver may cause significant changes in oxygenation and/or hemodynamics, necessitating close monitoring.

Pressure-volume curves in acute respiratory distress syndrome: clinical demonstration of the influence of expiratory flow limitation on the initial slope.

The presence of an initial segment with a low compliance on the static pressure-volume (PV) curve in patients with acute respiratory distress syndrome (ARDS) indicates that some lung compartments do not initially receive insufflated gas. We tested the hypothesis that an uneven distribution of time constants, producing a "slow compartment," was in part responsible for the change in compliance between the initial and the intermediate segment of the PV curve. In 16 patients with ARDS submitted to mechanical ventilation in volume-controlled mode with a supportive respiratory rate of 15 breaths/minute, we constructed the static PV curve on the first day of respiratory support and determined the intrinsic positive end-expiratory pressure (PEEPi4) during a prolonged end-expiratory pause (4 seconds). We also measured the volume of a "slow compartment" during a prolonged expiration (> 6 seconds), and determined an external PEEP (PEEPe) suppressing PEEPi4. Among the 16 patients studied, 11 exhibited a low inflection point, associated with a "slow compartment" of 172 +/- 83 ml, responsible for a PEEPi4 of 3 +/- 2 cm H2O. Conversely, the five remaining patients had a linear PV curve, associated with a minimal "slow compartment" of 28 +/- 10 ml, responsible for a negligible PEEPi4. We observed that individual slopes of the initial segment of the PV curve were inversely and significantly correlated with the proportion of the "slow compartment" (r = -0.85). We concluded that the shape of the inspiratory PV curve in ARDS might be dependent on the presence of a "slow compartment," and demonstrated that a low external PEEP appeared sufficient to achieve a substantial mechanical improvement in clinical practice.

Inspiratory pressure-volume curves at different positive end-expiratory pressure levels in patients with ALI/ARDS.

In lung protective strategy, positive end-expiratory pressure (PEEP) slightly higher than the Pflex (the airway pressure corresponding to the lower inflection point (LIP) on the inspiratory pressure-volume (P-V) curve measured with ZEEP) is generally recommended. However, this method to determine optimal PEEP lacks a theoretical background and there is no clinical report that investigated how the P-V relationship would be with such PEEP. Therefore, we measured inspiratory P-V curves at different PEEP levels to increase our knowledge about the inspiratory P-V curve with PEEP. In eight consecutive patients with ALI/ARDS, inspiratory P-V curves were repeatedly measured at different PEEP levels by low flow inflation technique and LIP was assessed in all inspiratory P-V curves. Afterwards, the minimum PEEP level at which LIP was not identifiable (PEEP(LIP)(-)) was determined and the relationship between Pflex and PEEP(LIP)(-) was investigated. Pflex and PEEP(LIP)(-) could be determined in all patients. Pflex was 9.4+/-2.0 cmH2O (range: 7 to 12 cmH2O) and PEEP(LIP)(-) was 7.9+/-1.6 cmH2O (range: 5 to 10 cmH2O) (mean+/-SD, P=0.0877). PEEP(LIP)(-) was lower than the Pflex in five patients, and significantly lower than the Pflex + 2 cmH2O (P=0.0024). From the analysis of inspiratory P-V curves at different PEEP levels, PEEP 2 cmH2O higher than the Pflex may not be necessary to prevent cyclic collapse and reopening of alveoli, at least in some ALI/ARDS patients. Further studies are needed to confirm this preliminary result.

Regional pressure volume curves by electrical impedance tomography in a model of acute lung injury.

A new noninvasive method, electrical impedance tomography (EIT), was used to make pressure-impedance (PI) curves in a lung lavage model of acute lung injury in pigs. The lower inflection point (LIP) and the upper deflection point (UDP) were determined from these curves and from the traditional pressure-volume (PV) curves to determine whether the PI curves resemble the traditional PV curves. Furthermore, regional differences in the mentioned determinants were investigated. Prospective, experimental study. Animal research laboratory. In nine anesthetized pigs, repeated lung lavage was performed until a Pao2 <80 torr was reached. Thereafter, an inspiratory PV curve was made using a constant flow of oxygen. During the intervention, EIT measurements were performed. In this study, the LIP(EIT) was within 2 cm H2O of the LIP(PV). Furthermore, it was possible to visualize regional PI curves by EIT. No significant difference was found between the LIP(PV) (21.3+/-3.0 cm H2O) and the LIP(EIT) of the total lung (21.5+/-3.0 cm H2O) or the anterior parts of the lung (21.5+/-2.9 cm H2O). A significantly higher LIP (29.5+/-4.9 cm H2O) was found in the posterior parts of the lung. A UDP(PV) could be found in three animals only, whereas in all animals a UDP(EIT) could be determined from the anterior part of the lung. Using EIT, determination of LIP and UDP from the regional PI curves is possible. The obtained information from the regional PI curves may help in understanding alveolar recruitment. The use of this new bedside technique for clinical decision making remains to be examined.

The lower inflection point of the inspiratory pressure-volume curve overestimates optimal PEEP in surfactant-treated immature lambs

The lower inflection point of the inspiratory pressure-volume curve overestimates optimal PEEP in surfactant-treated immature lambs

Tidal ventilation at low airway pressures can augment lung injury.

Intermittent positive pressure ventilation with large tidal volumes and high peak airway pressures can result in pulmonary barotrauma. In the present study, we examined the hypothesis that ventilation at very low lung volumes can also worsen lung injury by repeated opening and closing of airway and alveolar duct units as ventilation occurs from below to above the infection point (Pinf) as determined from the inspiratory pressure-volume curve. We ventilated isolated, nonperfused, lavaged rat lungs with physiologic tidal volumes (5 to 6 ml/kg) at different end-expiratory pressures (above and below Pinf) and studied the effect on compliance and lung injury. In the groups ventilated with positive end-expiratory pressure (PEEP) below Pinf compliance fell dramatically after ventilation. It did not change in either the control group or the group ventilated with PEEP above Pinf. Lung injury assessed morphologically was significantly greater in the groups ventilated with a PEEP below Pinf, and in these groups the site of injury was dependent on the level of PEEP. The group ventilated without PEEP had significantly greater respiratory and membranous injury to bronchioles, while the group ventilated with PEEP of 4 cm H2O had significantly greater alveolar duct injury. In conclusion, ventilation at lung volumes below those found at Pinf caused a significant decrease in lung compliance and progression of lung injury. Therefore, in addition to high airway pressures, end-expiratory lung volume is an important determinant of the degree and site of lung injury during positive-pressure ventilation.

Investigation of Inspiratory Pressure-Volume Curves on Mechanically Ventilated Patients Using Least Square Polynomial Fit

An on-line method for the registration of pressure volume 1 oops TrT mechanically ventilated patients was developed using a personal computer with analog/digital interface. A third order polynomial function was fitted to the measured inspiratory pressure volume pairs. The significance of the fitting procedure was calculated using regression ANOVA. The inflection point of the pressure-volume curve was determinated by calculating the root of the second derivative of the polynomial. The method was teseted on 20 patients without major pulmonary dysfunction and on 6 patients with severe ARDS.

Use of total inspiratory pressure-volume curves for determination of appropriate positive end-expiratory pressure in newborns with hyaline membrane disease.

Thirty newborns with hyaline membrane disease were treated by mechanical ventilation with individualized appropriate positive end-expiratory pressure (APEEP) from inspiratory pressure-volume curves of the total respiratory system. APEEP was started before H24 in group 1 (19 patients), and after H24 in group 2 (11 patients). Until APEEP, the 2 groups had classical PEEP levels (lower than 0.8 kPa) either without or with incomplete improvement in arterial hypoxia. The mean APEEP of each group was greater than classical PEEP (p less than 0.001). In group 1 the time of exposure to FiO2 greater than 0.4 was shorter (23.8 +/- 13.7 h) than in group 2 (88.6 +/- 56.9 h) (p less than 0.001) and rapid improvement in blood gas exchanges was seen in group 1 compared to group 2 that was independent of the severity of the disease. Tolerance was excellent. APEEP ventilation started before H24 is of special interest in the management of newborns with severe alveolar injury.

Effects of neuromuscular blockade on respiratory mechanics in conscious man.

The effect of submaximal neuromuscular blockade (SMNB) on lung and chest wall mechanics was studied in six normal, awake subjects infused with pancuronium. Measurements of static lung volumes, specific airway conductance (sGaw), maximum expiratory and inspiratory flow-volume (MEFV, MIFV) curves, and static pressure-volume (PV) curves of the lung and of the relaxed chest wall were obtained after lung recoil pressure (Pst(L)) at full inflation had been reduced to 60 +/- 10% of control. Inspiratory capacity was decreased, but residual volume was not increased. Inspiratory PV curve of the lung was not modified, and the observed decrease in expiratory compliance and the slight increase in Pst(L) during deflation were compatible with the altered lung volume history. SMNB did not modify sGaw nor the relationship between Pst(L) and MEF; by contrast it markedly reduced MIF rates. Finally, SMNB transposed the chest wall PV curve to higher levels on the pressure axis (it decreased the outward pull of the chest wall) without greatly affecting its slope, and thereby it reduced the resting level of the respiratory system. We conclude that 1) muscle weakness per se does not affect the eleastic properties of the lungs and airways, and 2) involuntary respiratory muscle activity influences the elastic recoil of the chest wall. We believe this muscle activity originates from muscle spindles, and lies essentially in the inspiratory portion of the intercostal musculature.

Lung recoil and gas trapping during oxygen breathing at low lung volumes.

If airways are closed at lung volumes less than the closing volume (CV), there should be correlations among 1) the volume of trapped N2 (VTN) during N2-washout performed below CV, 2) the increase in static lung recoil pressure (delta P) while breathing below CV after denitrogenation compared with breathing air (due to absorption atelectasis distal to closed airways), and 3) the CV. Static inspiratory pressure-volume (PV) curves and CV were measured in 18 seated normal volunteers (ages 24-48 yr). Subjects then breathed air for 30 s and O2 for 2.5 min at RV + 0.6 liter (LVB-air), and an inspiratory PV curve and VTN were determined. While still breathing O2, the subjects repeated the 3 min of low-volume breathing (LVB-O2). There was a significant (P less than 0.001) delta P with LVB but no difference between delta P (LVB-air) and delta P (LVB-O2). CV was not related to VTN or to either delta P. VTN was not related to delta P (LVB-O2)--delta P (LVB-air) nor to delta P (LVB-air), but was related to delta P (LVB-O2). Evidence of airway closure could not be demonstrated in all subjects by LVB and when present showed no correlation with CV.

The mechanism of increase in total lung capacity during acute asthma

In order to investigate the mechanism underlying the increased total lung capacity (TLC) observed during an acute asthmatic attack, we measured respiratory mechanics in a specially trained, exercise-induced, asthmatic. During the acute attack his TLC (determined plethysmographically) increased from 7.8 to 9.2 liters. The static pressure-volume curve of the lung shifted to the left and expiratory compliance increased from 0.24 to 0.55 liter/cm H 2O. There was a parallel shift of the static pressure-volume curve of the chest wall resulting in an increase in the outward recoil of this structure. The maximum inspiratory pressure-volume curve of the total respiratory system was shifted so that the inspiratory muscles were able to generate greater pressures at any given lung volume during the attack. The findings indicate that the increase in TLC during acute bronchospasm results from the combination of loss of lung recoil, increased outward recoil of the chest wall and increased strength of contraction of the inspiratory muscles.