Lower Inflection Point Research Articles

The Acute Effectiveness and Safety of the Constant-Flow, Pressure-Volume Curve to Improve Hypoxemia in Acute Lung Injury

To investigate the effectiveness of the constant-flow, pressure-volume curve (PVC) to prescribe positive end-expiratory pressure (PEEP) in acute lung injury (ALI) and risk of cardiopulmonary deterioration during the PVC process. A retrospective, cohort study. A surgical intensive care unit (ICU) of a tertiary, university hospital. Fifty consecutive ventilated patients diagnosed with ALI undergoing the PVC maneuver from 1999 to 2003. Titration of PEEP based on the lower inflection point of the constant-flow, pressure-volume curve. Patients were divided into 2 groups based on PVC-guided PEEP changes of <3 cm H2O (PVC-NC or "no change") or ≥3 cm H2O (PVC-CHG or "change") from the initial empiric prescription. There was a greater increase in partial pressure of arterial oxygen (PaO2)/fractional concentration of inspired oxygen (FiO2) in the PVC-CHG group, with a mean change of 80 ± 50 (95% confidence interval [CI] 61, 98) versus 42 ± 54 (95% CI 17, 67) in the PVC-NC group. Eighty-two percent of patients (41/50) showed an increase in ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) by 20% within 6 to 24 hours after the PVC test-greater in the PVC-CHG group (OR 1.44, 95% CI 1.02, 2.01). Thirteen percent (4/30) within the PVC-CHG group and none within the PVC-NC group (0/20) required a 25% increase in vasoactive infusion rates (P = .089) in relation to the procedure. Univariate logistic regression showed that PVC-CHG was significantly associated with a 20% change in PaO2/FiO2 (OR 7.54, 95% CI 1.37, 41.41). Multivariate logistic modeling showed that PVC-guided PEEP changes of ≥3 cm H2O, age ≤65 years, and pre-PVC FiO2 ≥ .85 were significantly associated with a 20% increase in PaO2/FiO2 (receiver operator area under the curve = .86). In the setting of acute lung injury, use of the constant-flow, pressure-volume curve to prescribe PEEP appears associated with improvement in oxygenation with limited risk of acute, process-related, cardiopulmonary deterioration.

Comparative study of recruitment maneuver guided by pressure-volume curve on respiratory physiology and lung morphology between acute respiratory distress syndrome of pulmonary and extrapulmonary origin in canine models

To determine effects of recruitment maneuver (RM) guided by pressure-volume (P-V) curve on respiratory physiology and lung morphology in canine models of acute respiratory distress syndrome of pulmonary or extrapulmonary origin (ARDSp and ARDSexp). Twenty-four healthy dogs were randomly divided into two groups with 12 dogs each: ARDSexp and ARDSp. Each dog in ARDSexp group was injected with oleic acid 0.1 ml/kg through femoral vein, and each dog in ARDSp group received hydrochloric acid 2 ml/kg via trachea. Subsequently, dogs with both models were randomly subdivided into lung protective ventilation strategy (LPVS) group and LPVS+RM group, respectively. Dogs in LPVS group were given LPVS only without RM. RM guided by P-V curve was performed in LPVS+RM group followed by LPVS and pressure controlled ventilation (PCV) mode was selected. Phigh was set at upper inflection point (UIP) of the P-V curve, positive end-expiratory pressure (PEEP) was set at lower inflection point (LIP)+2 cm H(2)O (1 cm H(2)O=0.098 kPa), and the duration of RM was 60 seconds. The duration of mechanical ventilation (MV) in both subgroups was 4 hours. The oxygenation index (PaO(2)/FiO(2)), relative lung mechanical indexes were measured in two ARDS models before establishment of ARDS model, and before and after RM. The UIP and LIP were calculated with P-V curve. The percentage of different volume in ventilation of lung accounting for total lung volume was compared by CT scan. The PaO(2)/FiO(2), UIP and LIP did not showed significant differences among all groups before ARDS and before RM. PaO(2)/FiO(2) and respiratory system compliance (Crs) were significantly elevated in LPVS+RM group of both models 4 hours after RM compared with corresponding LPVS group [PaO(2)/FiO(2) (mm Hg, 1 mm Hg=0.133 kPa) of ARDSexp model: 263.9±69.2 vs. 182.8±42.8, Crs (ml/cm H(2)O) of ARDSexp model: 11.3±4.2 vs. 9.7±3.7; PaO(2)/FiO(2) (mm Hg) of ARDSp model: 193.4±33.5 vs. 176.4±40.2, Crs (ml/cm H(2)O) of ARDSp model: 10.1±3.9 vs. 9.0±3.9, P<0.05 or P<0.01], and the airway pressure was significantly declined compared with corresponding LPVS group [peak inspiratory pressure (PIP), cm H(2)O ] of ARDSexp model: 24.1±7.4 vs. 30.2±8.5, plateau pressure (Pplat, cm H(2)O) of ARDSexp model: 19.1±7.3 vs. 25.6±7.7; PIP (cm H(2)O) of ARDSp model: 26.6±8.4 vs. 29.6±10.3, Pplat (cm H(2)O) of ARDSp model: 21.9±7.3 vs. 25.1±8.4, P<0.05 or P<0.01]. Moreover, PaO(2)/FiO(2), Crs, PIP and Pplat were improved better in ARDSexp model than ARDSp model (P<0.05 orP<0.01). Compared with LPVS maneuver, RM plus LPVS maneuver could significantly decrease the proportion of closure and hypoventilation region, and increase the proportion of normal ventilation region in both models [closure region of ARDSexp model: (9.9±3.1)% vs. (16.3±5.2)%, hypoventilation region of ARDSexp model: (10.2±4.2)% vs. (23.4±6.7)%, normal ventilation region of ARDSexp model: (76.2±12.3)% vs. (57.5±10.1)%; closure region of ARDSp model: (14.3±4.8)% vs. (18.2±5.1)%, hypoventilation region of ARDSp model: (17.4±6.3)% vs. (24.1±5.9)%, normal ventilation region of ARDSp model: (63.2±10.7)% vs. (54.6±11.3)%, P<0.05 or P<0.01]. All of the ventilation regions were better improved with ARDSexp model than ARDSp model (all P<0.05). RM guided by P-V curve could help obtain better oxygenation, improve pulmonary compliance and lung ventilation in ARDSexp and ARDSp, and better treatment effects are seen in ARDSexp dogs than ARDSp dogs.

Hepatic effects of lung-protective pressure-controlled ventilation and a combination of high-frequency oscillatory ventilation and extracorporeal lung assist in experimental lung injury

SummaryBackgroundVentilation with high positive end-expiratory pressure (PEEP) can lead to hepatic dysfunction. The aim of this study was to investigate the hepatic effects of strategies using high airway pressures either in pressure-controlled ventilation (PCV) or in high-frequency oscillatory ventilation (HFOV) combined with an arteriovenous extracorporeal lung assist (ECLA).Material/MethodsPietrain pigs underwent induction of lung injury by saline lavage. Ventilation was continued for 24 hours either as PCV with tidal volumes of 6 ml/kg and PEEP 3 cmH2O above the lower inflection point of the pressure-volume curve or as HFOV (≥12 Hz) with a mean tracheal airway pressure 3 cmH2O above the lower inflection point combined with arteriovenous ECLA (HFOV+ECLA). Fluids and norepinephrine stabilized the circulation. The indocyanine green plasma disappearance rate, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, alkaline phosphatase, glutamate dehydrogenase, lactate dehydrogenase and creatine kinase were determined repeatedly. Finally, liver neutrophils were counted and liver cell apoptosis was assessed by terminal deoxynucleotidyl transferase nick end labeling (TUNEL).ResultsAspartate aminotransferase increased in the PCV group about three-fold and in the HFOV+ECLA group five-fold (p<0.001). Correspondingly, creatine kinase increased about two-fold and four-fold, respectively (p<0.001). Lactate dehydrogenase was increased in the HFOV+ECLA group (p<0.028). The number of neutrophils infiltrating the liver tissue and the apoptotic index were low.ConclusionsHigh airway pressure PCV and HFOV with ECLA in the treatment of lavage-induced lung injury in pigs did not cause liver dysfunction or damage. The detected elevation of enzymes might be of extrahepatic origin.

Lung morphology predicts response to recruitment maneuver in patients with acute respiratory distress syndrome

The impact of recruitment maneuvers on gas exchange, hemodynamics, alveolar recruitment, and hyperinflation is highly variable among patients with acute respiratory distress syndrome. The objective was to determine whether differences in lung morphology, defined as differences in the pulmonary distribution of aeration loss, predict the response to recruitment maneuvers. Prospective study. A 16-bed medical-surgical intensive care unit in a university hospital. Nineteen consecutive patients with early acute lung injury/acute respiratory distress syndrome were studied. Computed tomography scans, respiratory mechanics, hemodynamics, and gas exchange were obtained at zero end-expiratory pressure during an open-lung ventilation (controlled mode, tidal volume 6 mL/kg of ideal body weight, positive end-expiratory pressure set 2 cm H2O above the lower inflection point of the inspiratory pressure volume curve at zero end-expiratory pressure) during a recruitment maneuver (continuous positive airway pressure of 40 cm H2O for 40 secs), and, finally, 5 mins after the recruitment maneuver during open-lung ventilation. Nine patients presented focal and 10 presented nonfocal lung morphology at zero end-expiratory pressure. Recruitment maneuver-induced recruited volume after 5 mins of open-lung ventilation was 48 +/- 66 mL and 417 +/- 293 mL in patients with focal and nonfocal lung morphology, respectively (p = .0009). Recruitment maneuver-induced alveolar hyperinflation represented 23% +/- 14% and 8% +/- 9% of total lung volume in patients with focal and nonfocal morphology, respectively (p = .007). In patients with focal lung morphology, hyperinflated lung volume was significantly greater during and 5 mins after (316 +/- 155 mL) than immediately before recruitment maneuvers (150 +/- 175 mL; p = .0407. Lung morphology at zero end-expiratory pressure predicts the response to recruitment maneuvers. Patients with focal lung morphology are at risk for significant hyperinflation during the recruitment maneuvers, and lung recruitment is rather limited.

Hepatic effects of an open lung strategy and cardiac output restoration in an experimental lung injury

Ventilation with high positive end-expiratory pressure (PEEP) can lead to liver dysfunction. We hypothesized that an open lung concept (OLC) using high PEEP impairs liver function and integrity dependent on the stabilization of cardiac output. Juvenile female Pietrain pigs instrumented with flow probes around the common hepatic artery and portal vein, pulmonary and hepatic vein catheters underwent a lavage-induced lung injury. Ventilation was continued with a conventional approach (CON) using pre-defined combinations of PEEP and inspiratory oxygen fraction or with an OLC using PEEP set above the lower inflection point of the lung. Volume replacement with colloids was guided to maintain cardiac output in the CON(V+) and OLC(V+) groups or acceptable blood pressure and heart rate in the OLC(V-) group. Indocyanine green plasma disappearance rate (ICG-PDR), blood gases, liver-specific serum enzymes, bilirubin, hyaluronic acid and lactate were tested. Finally, liver tissue was examined for neutrophil accumulation, TUNEL staining, caspase-3 activity and heat shock protein 70 mRNA expression. Hepatic venous oxygen saturation was reduced to 18 + or - 16% in the OLC(V-) group, while portal venous blood flow decreased by 45%. ICG-PDR was not reduced and serum enzymes, bilirubin and lactate were not elevated. Liver cell apoptosis was negligible. Liver sinusoids in the OLC(V+) and OLC(V-) groups showed about two- and fourfold more granulocytes than the CON(V+) group. Heat shock protein 70 tended to be higher in the OLC(V-) group. Open lung ventilation elicited neutrophil infiltration, but no liver dysfunction even without the stabilization of cardiac output.

Positive end-expiratory pressure-induced functional recruitment in patients with acute respiratory distress syndrome*

In acute respiratory distress syndrome, alveolar recruitment improves gas exchange only if perfusion of the recruited alveolar units is adequate. To evaluate functional recruitment induced by positive end-expiratory pressure, we assessed pulmonary conductance for gas exchange based on lung diffusion for carbon monoxide and its components, including pulmonary capillary blood volume. Prospective, randomized, crossover study. Medical intensive care unit of a university hospital. Sixteen patients with lung injury/acute respiratory distress syndrome as well as eight control patients under invasive ventilation and eight healthy volunteers. Mechanical ventilation with two levels of positive end-expiratory pressure (5 and 15 cm H2O). Lung diffusion for carbon monoxide and lung volumes, arterial blood gas analysis, and pressure-volume curves. In patients with acute respiratory distress syndrome, high positive end-expiratory pressure induced a 23% mean lung diffusion for carbon monoxide increase (4.4 +/- 1.7 mm Hg . min vs. 3.6 +/- 1.4 mL . mm Hg . min). In control patients and in healthy volunteers, lung diffusion for carbon monoxide values were (median [interquartile range]) 5.5 [3.8-8.0] mm Hg . min and 19.6 [15.1-20.6] mL . mm Hg . min, respectively. Among patients with acute respiratory distress syndrome, eight showed a >20% lung diffusion for carbon monoxide increase (responders) when increasing positive end-expiratory pressure. In the other eight, lung diffusion for carbon monoxide decreased or showed a <5% increase (nonresponders) with high positive end-expiratory pressure. Compared with nonresponders, responders at low positive end-expiratory pressure had smaller lungs with higher capillary blood volume-to-lung-volume ratio, higher values of the lower inflection point, and significantly greater increases in pulmonary capillary blood volume with high positive end-expiratory pressure. High positive end-expiratory pressure increased PaO2/Fio2 only in the responders. The functional response to positive end-expiratory pressure in patients with acute lung injury/acute respiratory distress syndrome seems better when the lungs are smaller and with a higher capillary blood-volume-to-lung-volume ratio. Lung diffusion for carbon monoxide measurement supplies additional information about functional lung recruitment, which is not synonymous with mechanical recruitment.

Selection of ideal tidal volume according to pressure-volume curve for instruction of mechanical ventilation nursing

Objective To study the influence of the different tidal volume on hemodynamics,pulmonary ventilation and pulmonary mechanics during mechanical ventilation in patients with acute lung injury.Methods To adopt contrast method,making use of the VIIP +0.196 kPa of P-V curve to decide PEEP,then according to the VUIP of P-V curve,obtaining the three different data of humidity 100%Vt,85% Vt and 70 Vt.At the same time,monitoring the change of static compliance,the changing of hemodynamics and P-V curve.Results 85%Vt group was better than 100%Vt group and 70%Vt group in the heart rates,CVP,PaO_2,the peak airway pressure(PIP) and mean pressure(Pm),Cst,PaO_2/FiO_2.Conclusions When insuring the PEEP data in low inflection point pressure (Pinf) of breathing system P-V curve,and 85% humidity in upper inflection point pressure,which is in accordance with individual protecting breathing strategy.The curative effect is the best for improving static compliance and decreasing the harm of lung injury.The change of pressure-volume curve should be paid attention to in nursing. Key words: Lung-protective ventilation; Pressure-volume curve; Tidal volume; Nursing

Pulmonary Capillary Blood Flow and Cardiac Output Measurement by Partial Carbon Dioxide Rebreathing in Patients with Acute Respiratory Distress Syndrome Receiving Lung Protective Ventilation

Partial carbon dioxide rebreathing noninvasively measures the pulmonary capillary blood flow and estimates the cardiac output with the use of a predicted shunt value. It has been reported that the accuracy of the method is decreased in patients with high pulmonary shunt. The aim of this study was to investigate the agreement between partial rebreathing and thermodilution for the determination of pulmonary capillary blood flow and cardiac output in the setting of acute respiratory distress syndrome. Twenty consecutive patients with the acute respiratory distress syndrome were enrolled. Ventilator settings include low tidal volume (6 ml x kg(-1)) and positive end-expiratory pressure + 2 cm H2O higher than the lower inflection point if present or 10 cm H2O if not. Seven pairs of cardiac output and pulmonary capillary blood flows were recorded every 20 min over a 2-h period. The authors determined bias, SD, limit of agreement (95% confidence interval) and percentage error. Bias and agreement for cardiac output measurement were 0.8 +/- 1.2 l x min(-1) (-2.1 to 3.7 l x min(-1)), and percentage error was 36%. Bias and agreement for pulmonary capillary blood flow measurement were -0.1 +/- 0.8 l x min(-1) (-2.1 to 1.9 l x min(-1)), and percentage error was 35%. Dead space, arteriovenous oxygen content difference, mean pulmonary arterial pressure, and baseline cardiac output were independently associated with differences between methods. In patients with the acute respiratory distress syndrome, partial rebreathing cannot yet replace thermodilution for measuring pulmonary capillary blood flow or cardiac output. However, accuracy of the method is close to the boundary of clinical relevance.

Automated measurement of the lower inflection point in a pediatric lung model*

To determine which flow setting most accurately detects the lower inflection point (Pflex) using an automated constant flow method and varying endotracheal tube (ETT) sizes with and without an airleak in a pediatric lung model. Interventional laboratory study. Children's hospital research center. A pediatric lung model was created with Pflexs of the inspiratory pressure-volume (P-V) curve set at 5 and 10 cm H2O using the ASL 5000 Test Lung (IngMar Medical, Pittsburgh, PA). Three ETT sizes (3.0, 4.0, 5.0 mm) were tested with and without a 25% airleak. P-V curves were obtained using an automated constant flow method at ten different flow rates. Without an ETT airleak, the lowest flow of 0.5 L/min led to the most accurate determination of Pflex regardless of ETT size or set Pflex (p < 0.001). When a 25% leak was introduced, accuracy of measured Pflex depended on both ETT size (p < 0.001) and flow rate (p < 0.001). Optimum flow rates for Pflex determination were 0.5, 1.0, and 1.5 L/min at Pflex of 5 cm H2O, and 2.0, 3.5, and 4.5 L/min at 10 cm H2O for 3.0, 4.0, and 5.0 mm ETTs, respectively (p < 0.001). Estimation of Pflex can be achieved using automated P-V curves with ETTs appropriate for pediatric use, with and without an airleak. ETT size and flow rate affect the accuracy of these measurements when an airleak is present, and use of increased flow rates to create the automated P-V curves can reduce error. These data support the idea that a low-flow technique provides the most accurate determination of Pflex in pediatric patients without a leak around their ETT, whereas increased flows are needed to compensate when an ETT airleak is present.

Differences in regional pulmonary pressure–impedance curves before and after lung injury assessed with a novel algorithm

Global pressure–volume (PV) curves are an adjunct measure to describe lung characteristics in patients with acute respiratory distress syndrome (ARDS). There is convincing evidence that high peak inspiratory pressures (PIP) cause barotrauma, while optimized positive end-expiratory pressure (PEEP) helps avoid mechanical injury to the lungs by preventing repeated alveolar opening and closing. The optimal values of PIP and PEEP are deduced from the shape of the PV curve by the identification of so-called lower and upper inflection points. However, it has been demonstrated using electrical impedance tomography (EIT) that the inflection points vary across the lung. This study employs a simple curve-fitting technique to automatically define inflection points on both pressure–volume (PV) and pressure–impedance (PI) curves to asses the differences between global PV and regional PI estimates in animals before and after induced lung injury. The results demonstrate a clear increase in lower inflection point (LIP) along the gravitational axis both before and after lung injury. Moreover, it is clear from comparison of the local EIT-derived LIPs with those derived from global PV curves that a ventilation strategy based on the PV curve alone may leave dependent areas of the lung collapsed. EIT-based PI curve analysis may help choosing an optimal ventilation strategy.

Changes of splanchnic perfusion after applying positive end expiratory pressure in patients with acute respiratory distress syndrome

Background:Positive end-expiratory pressure (PEEP) improves oxygenation and can prevent ventilator- induced lung injury in patients with acute respiratory distress syndrome (ARDS). Nevertheless, PEEP can also induce detrimental effects by its influence on the cardiovascular system. The purpose of this study was to assess the effects of PEEP on gastric mucosal perfusion while applying a protective ventilatory strategy in patients with ARDS.Materials and Methods:Thirty-two patients were included in the study. A pressure–volume curve was traced and ideal PEEP, defined as lower inflection point + 2cmH2O, was determined. Gastric tonometry was measured continuously (Tonocap). After baseline measurements, 10, 15 and 20cmH2O PEEP and ideal PEEP were applied for 30 min each. By the end of each period, hemodynamics, CO2 gap (gastric minus arterial partial pressures), and ventilatory measurements were taken.Results:PEEP had no effect on CO2 gap (median [range], baseline: 18 [2–30] mmHg; PEEP 10: 18 [0–40] mmHg; PEEP 15: 17 [0–39] mmHg; PEEP 20: 16 [4–39] mmHg; ideal PEEP: 19 [9–39] mmHg; P = 0.19). Cardiac index also remained unchanged (baseline: 4.7 [2.6–6.2] l min−1 m−2; PEEP 10: 4.4 [2.5–7] l min−1 m−2; PEEP 15: 4.4 [2.2–6.8] l min−1 m−2; PEEP 20: 4.8 [2.4–6.3] l min−1 m−2; ideal PEEP: 4.9 [2.4–6.3] l min−1 m−2; P = 0.09).Conclusion:PEEP of 10–20 cmH2O does not affect splanchnic perfusion and is hemodynamically well tolerated in most patients with ARDS, including those receiving inotropic supports.

Fio2 and acute respiratory distress syndrome definition during lung protective ventilation*

PaO2/FIO2 ratio (P/F) is the marker of hypoxemia used in the American-European Consensus Conference on lung injury. A high FIO2 level has been reported to variably alter PaO2/FIO2. We investigated the effect of high FIO2 levels on the course of P/F in lung protective mechanically ventilated patients with acute respiratory distress syndrome. Prospective, controlled, interventional study. University teaching French medical intensive care unit. Twenty-four patients with acute respiratory distress syndrome having P/F between 100 and 200 mm Hg at FIO2 0.5 received low-volume controlled ventilation (V(T) = 6 mL/kg predicted body weight) with a positive end-expiratory pressure at 2 cm H2O above the lower inflection point if present, or 10 cm H2O. The following FIO2 levels were applied randomly for 20 mins: 0.5, 0.6, 0.7, 0.8, 0.9, and 1. Increasing FIO2 above 0.7 was associated with a significant increase in P/F (p < 0.001). The mean P/F change between FIO2 0.5 and 1 (Delta P/F) was 47% +/- 35%. Sixteen patients (67%) had a P/F >200 at FIO2 1 whereas P/F was <200 at FIO2 0.5. Venous admixture (Q(VA)/Q(T)) decreased linearly for each FIO2 step (p < 0.001). The Q(VA)/Q(T) change between FIO2 0.5 and 1 was strongly correlated with Delta P/F (r = 0.84). Delta P/F was higher in patients with true shunt <30% (64% [54-93]) than in those with shunt >30% (20% [10-36]; p = 0.003). The P/F ratio increased significantly with a FIO2 >0.7. P/F variation, induced by a switch from FIO2 0.5 to 1, was responsible for two thirds of patients changing from the acute respiratory distress syndrome to the acute lung injury stage of the American-European Consensus Conference definition. FIO2 should be carefully defined for the screening of lung-injured patients.

Arteriovenous extracorporeal lung assist allows for maximization of oscillatory frequencies: a large-animal model of respiratory distress

BackgroundAlthough the minimization of the applied tidal volume (VT) during high-frequency oscillatory ventilation (HFOV) reduces the risk of alveolar shear stress, it can also result in insufficient CO2-elimination with severe respiratory acidosis. We hypothesized that in a model of acute respiratory distress (ARDS) the application of high oscillatory frequencies requires the combination of HFOV with arteriovenous extracorporeal lung assist (av-ECLA) in order to maintain or reestablish normocapnia.MethodsAfter induction of ARDS in eight female pigs (56.5 ± 4.4 kg), a recruitment manoeuvre was performed and intratracheal mean airway pressure (mPaw) was adjusted 3 cmH2O above the lower inflection point (Plow) of the pressure-volume curve. All animals were ventilated with oscillatory frequencies ranging from 3–15 Hz. The pressure amplitude was fixed at 60 cmH2O. At each frequency gas exchange and hemodynamic measurements were obtained with a clamped and de-clamped av-ECLA. Whenever the av-ECLA was de-clamped, the oxygen sweep gas flow through the membrane lung was adjusted aiming at normocapnia.ResultsLung recruitment and adjustment of the mPaw above Plow resulted in a significant improvement of oxygenation (p < 0.05). Compared to lung injury, oxygenation remained significantly improved with rising frequencies (p < 0.05). Normocapnia during HFOV was only maintained with the addition of av-ECLA during frequencies of 9 Hz and above.ConclusionIn this animal model of ARDS, maximization of oscillatory frequencies with subsequent minimization of VT leads to hypercapnia that can only be reversed by adding av-ECLA. When combined with a recruitment strategy, these high frequencies do not impair oxygenation

Does a solitary lobar collapse give pressure–lung volume relationship similar to that found in acute respiratory distress syndrome? A porcine experimental study

The underlying pathophysiology causing different shapes of static pressure-lung volume (PV) curves is not fully elucidated. In this study the aim was to examine the influence of a solitary lobar collapse on inflation-deflation PV curves. The hypothesis was that a lobar collapse would induce the same changes in the PV-curve as those found in experimental acute lung injury (ALI) and in acute respiratory distress syndrome (ARDS). In four mechanically ventilated, anaesthetized pigs, the right lower lobe was collapsed by selective lavage and exsufflation. End-expiratory lung volume and static inflation-deflation PV curves of the respiratory system, the chest wall and the lung were obtained before formation of the collapse. After creation of the collapse, the same measurements were performed in the non-collapsed lung and in the whole lung including the lobar collapse. In two animals computed tomography was performed to verify the lobar collapse. The solitary lobar collapse changed the PV curve by inducing a significant hysteresis and a right shift of lower inflexion point (LIP) on the inflation limb, but had minimal influence on the deflation limb. After creation of the lobar collapse, LIP was found at the pressure at which the collapse started to expand. PV curves of lungs with solitary lobar collapse are similar to those found in ALI/ARDS. Inspiratory LIP indicated start of recruitment, and expiratory curves did not indicate the pressure at which collapse occurred.

Respiratory System Model for Quasistatic Pulmonary Pressure-Volume (P-V) Curve: Inflation-Deflation Loop Analyses

A respiratory system model (RSM) is developed for the deflation process of a quasistatic pressure-volume (P-V) curve, following the model for the inflation process reported earlier. In the RSM of both the inflation and the deflation limb, a respiratory system consists of a large population of basic alveolar elements, each consisting of a piston-spring-cylinder subsystem. A normal distribution of the basic elements is derived from Boltzmann statistical model with the alveolar closing (opening) pressure as the distribution parameter for the deflation (inflation) process. An error minimization by the method of least squares applied to existing P-V loop data from two different data sources confirms that a simultaneous inflation-deflation analysis is required for an accurate determination of RSM parameters. Commonly used terms such as lower inflection point, upper inflection point, and compliance are examined based on the P-V equations, on the distribution function, as well as on the geometric and physical properties of the basic alveolar element.

Maximal hysteresis: a new method to set positive end‐expiratory pressure in acute lung injury?

No methods are superior when setting positive end-expiratory pressure (PEEP) in acute lung injury (ALI). In ALI, the vertical distance (hysteresis) between the inspiratory and expiratory limbs of a static pressure-volume (PV) loop mainly indicates lung recruitment. We hypothesized that PEEP set at the pressure where hysteresis is 90% of its maximum (90%MH) would give similar oxygenation, but less cardiovascular depression than PEEP set at the pressure at lower inflection point (LIP) on the inspiratory limb or at the point of maximal curvature (PMC) on the expiratory limb in ALI. In 12 mechanically ventilated pigs, ALI was induced in a randomized fashion by lung lavage, lung lavage plus injurious ventilation, or by oleic acid. From a static PV loop obtained by an interrupted low-flow method, the pressures at LIP [25 (25, 25) cmH(2)O, mean and 25, 75 percentiles], at PMC [24 (20, 24) cmH(2)O], and at 90% MH [19 (18, 19) cmH(2)O] were determined and used for the PEEP-settings. We measured lung inflation (by computed tomography), end-expiratory lung volume (EELV), airway pressures, compliance of the respiratory system (Crs), blood gases, cardiac output and arterial blood pressure. There were no differences between the PEEP settings in EELV or oxygenation, but the 90%MH setting gave lower end-inspiratory pause pressure (P<0.025), higher Crs (P<0.025), less hyper-aeration (P<0.025) and better maintained hemodynamics. In this porcine lung injury model, PEEP set at 90% MH gave better lung mechanics and hemodynamics, than PEEP set at PMC or LIP.

Utilization of the Lower Inflection Point of the Pressure-Volume Curve Results In Protective Conventional Ventilation Comparable to High Frequency Oscillatory Ventilation in an Animal Model of Acute Respiratory Distress Syndrome

Studies comparing high frequency oscillatory and conventional ventilation in acute respiratory distress syndrome have used low values of positive end-expiratory pressure and identified a need for better recruitment and pulmonary stability with high frequency. To compare conventional and high frequency ventilation using the lower inflection point of the pressure-volume curve as the determinant of positive end-expiratory pressure to obtain similar levels of recruitment and alveolar stability. After lung lavage of adult rabbits and lower inflection point determination, two groups were randomized: conventional (positive end-expiratory pressure = lower inflection point; tidal volume=6 ml/kg) and high frequency ventilation (mean airway pressures= lower inflection point +4 cmH2O). Blood gas and hemodynamic data were recorded over 4 h. After sacrifice, protein analysis from lung lavage and histologic evaluation were performed. The oxygenation parameters, protein and histological data were similar, except for the fact that significantly more normal alveoli were observed upon protective ventilation. High frequency ventilation led to lower PaCO2 levels. Determination of the lower inflection point of the pressure-volume curve is important for setting the minimum end expiratory pressure needed to keep the airways opened. This is useful when comparing different strategies to treat severe respiratory insufficiency, optimizing conventional ventilation, improving oxygenation and reducing lung injury. Utilization of the lower inflection point of the pressure-volume curve in the ventilation strategies considered in this study resulted in comparable efficacy with regards to oxygenation and hemodynamics, a high PaCO2 level and a lower pH. In addition, a greater number of normal alveoli were found after protective conventional ventilation in an animal model of acute respiratory distress syndrome.

A decremental PEEP trial for determining open‐lung PEEP in a rabbit model of acute lung injury

A positive end-expiratory pressure (PEEP) above the lower inflection point (LIP) of the pressure-volume curve has been thought necessary to maintain recruited lung volume in acute lung injury (ALI). We used a strategy to identify the level of open-lung PEEP (OLP) by detecting the maximum tidal compliance during a decremental PEEP trial (DPT). We performed a randomized controlled study to compare the effect of the OLP to PEEP above LIP and zero PEEP on pulmonary mechanics, gas exchange, hemodynamic change, and lung injury in 26 rabbits with ALI. After recruitment maneuver, the lavage-injured rabbits received DPTs to identify the OLP. Animals were randomized to receive volume controlled ventilation with either: (a) PEEP = 0 cm H2O (ZEEP); (b) PEEP = 2 cm H2O above OLP (OLP + 2); or (c) PEEP = 2 cm H2O above LIP (LIP + 2). Peak inspiratory pressure and mean airway pressure were recorded and arterial blood gases were analyzed every 30 min. Mean blood pressure and heart rate were monitored continuously. Lung injury severity was assessed by lung wet/dry weight ratio. Animals in OLP + 2 group had less lung injury as well as relatively better compliance, more stable pH, and less hypercapnia compared to the LIP + 2 and ZEEP groups. We concluded that setting PEEP according to the OLP identified by DPTs is an effective method to attenuate lung injury. This strategy could be used as an indicator for optimal PEEP. The approach is simple and noninvasive and may be of clinical interest.

Static pressure–volume curves of the respiratory system: were they just a passing fad?

The aim of this article is to describe the physiologic utility, correlation with lung morphology, difficulties in interpretation and current clinical applications of static respiratory system pressure-volume curves at the bedside in patients with acute lung injury or acute respiratory distress syndrome. Complex interpretation of pressure-volume curves indicates that alveolar reopening continues past the lower inflection point on the linear part of the curve and suggests the presence of homogeneous lung disease in which recruitment is still possible by positive end-expiratory pressure application. Setting positive end-expiratory pressure above the lower inflection point and tidal ventilation (approximately 6 ml/kg) in the linear portion of the respiratory system pressure-volume curve improved mortality and ameliorated lung and plasma inflammatory mediators compared with ventilation with the lowest positive end-expiratory pressure at traditional tidal volumes. Recent studies have found that regular use of pressure-volume curves provides useful physiological data that help to optimize mechanical ventilation at the bedside. The physiologic data obtained by measuring the static pressure-volume curves have helped clinicians to better understand the behavior of the respiratory system when positive-pressure ventilation is applied. The advanced technology incorporated into modern ventilators allows routine measurement of pressure-volume curves under sedation without paralysis, with acceptable variability and no serious adverse effects.

Peripheral airways injury in acute lung injury/acute respiratory distress syndrome

Peripheral airways are less than 2 mm in diameter and comprise a relatively large cross-sectional area, which allows for slower, laminar airflow. They include both membranous bronchioles and gas exchange ducts, and have been referred to in the past as the 'quiet zone', partly because these structures were felt to contribute little to lung mechanics, and partly because they are difficult to study directly. Recent studies suggest that peripheral airway dysfunction plays a significant role in acute respiratory distress syndrome, which may be exacerbated by injurious mechanical ventilation strategies. The presence of elevated airways resistance, intrinsic positive end-expiratory pressure or a lower inflection point on a pressure-volume curve of the respiratory system may indicate presence of impaired peripheral airway function. In-vitro animal and human studies have begun to elucidate the signaling mechanisms responsible for stretch and shear mediated cellular injury. Understanding the pathophysiology of peripheral airway dysfunction in acute respiratory distress syndrome and mechanical ventilation continues to evolve. Greater insight into the signaling mechanisms involved in cellular injury and repair will lead to further alterations in mechanical ventilation strategies, and may lead to specific treatment options.