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To assess the time interval required to reach a new steady state of oxygenation-, ventilation-, respiratory mechanics- and hemodynamics-related variables after decreasing/increasing positive end expiratory pressure (PEEP).In 23 patients (group 1) with acute respiratory distress syndrome (ARDS), PEEP was decreased from 10 to 5 cmH2O and, after 60', it was increased from 5 to 15 cmH2O. In 21 other ARDS patients (group 2), PEEP was increased from 10 to 15 cmH2O and, after 60', decreased from 15 to 5 cmH2O. Oxygenation, ventilation, respiratory mechanics and hemodynamic variables were recorded at time 5', 15', 30' and 60' after each PEEP change.When PEEP was decreased, PaO2, PaO2/FiO2, venous admixture and arterial oxygen saturation reached their equilibrium after 5'. In contrast, when PEEP was increased, the equilibrium was not reached even after 60'. The ventilation-related variables did not change significantly with PEEP. The respiratory system compliance, when PEEP was decreased, significantly worsened only after 60'. Hemodynamics did not change significantly with PEEP. In the individual patients the change of oxygenation-related variables and of respiratory system compliance observed after 5' could predict the changes recorded after 60'. This was not possible for PaCO2.We could not find a unique equilibration time for all the considered variables. However, in general, a decremental PEEP test requires far lower equilibrium time than an incremental PEEP test, suggesting a different time course for derecruitment and recruitment patterns.

Introduction Although computed tomography (CT) is widely used to investigate different pathologies, quantitative data from normal populations are scarce. Reference values may be useful to estimate the anatomical or physiological changes induced by various diseases. Methods We analyzed 100 helical CT scans taken for clinical purposes and referred as nonpathological by the radiologist. Profiles were manually outlined on each CT scan slice and each voxel was classified according to its gas/tissue ratio. For regional analysis, the lungs were divided into 10 sterno-vertebral levels. Results We studied 53 males and 47 females (age 64 ± 13 years); males had a greater total lung volume, lung gas volume and lung tissue. Noninflated tissue averaged 7 ± 4% of the total lung weight, poorly inflated tissue averaged 18 ± 3%, normally inflated tissue averaged 65 ± 8% and overinflated tissue averaged 11 ± 7%. We found a significant correlation between lung weight and subject's height (P

To describe the physiological meaning and the clinical application of the lung stress and strain concepts.The end-inspiratory plateau pressure and ratio of tidal volume/ideal body weight are inadequate surrogates for the end-inspiratory stress (equal to the transpulmonary pressure) and the end-inspiratory strain (change in lung volume relative to the resting volume). For a given plateau pressure or tidal volume/ideal body weight, stress and strain may vary largely due to the variability of chest wall elastance and the resting lung volume. The injurious limits of stress and strain in healthy lungs are reached when stress and strain reach the total lung capacity. This occurs when the resting lung volume (the baby lung in case of acute respiratory distress syndrome) is increased by two-fold to three-fold. As these limits are rarely reached in clinical practice and damage has been reported with stress and strain well below this upper limit, this implies the presence in the lung parenchyma of regions which act as stress raisers or pressure multipliers. These are primarily linked to the inhomogeneous distribution of local stress and strain.End-inspiratory stress and strain, as well as the lung inhomogeneity and the stress raisers, must be taken in account when setting mechanical ventilation.

Crystalloids have different electrolyte composition and therefore different strong ion differences (SIDinf). The aim of the study was to investigate the response of the kidney to plasmatic acid-base changes induced by dilution with three crystalloid solutions at different SID.

Since its introduction into the management of the acute respiratory distress syndrome, mechanical ventilation has been so strongly interwoven with its side effects that it came to be considered as invariably dangerous. Over the decades, attention has shifted from gross barotrauma to volutrauma and, more recently, to atelectrauma and biotrauma. In this article, we describe the anatomical and physiologic framework in which ventilator-induced lung injury may occur. We address the concept of lung stress/strain as applied to the whole lung or specific pulmonary regions. We challenge some common beliefs, such as separately studying the dangerous effects of different tidal volumes (end inspiration) and end-expiratory positive pressures. Based on available data, we suggest that stress at rupture is only rarely reached and that high tidal volume induces ventilator-induced lung injury by augmenting the pressure heterogeneity at the interface between open and constantly closed units. We believe that ventilator-induced lung injury occurs only when a given threshold is exceeded; below this limit, mechanical ventilation is likely to be safe.

Prone positioning has been used for over 30 years in the management of patients with acute respiratory distress syndrome (ARDS). This maneuver has consistently proven capable of improving oxygenation in patients with acute respiratory failure. Several mechanisms can explain this observation, including possible intervening net recruitment and more homogeneously distributed alveolar inflation. It is also progressively becoming clear that prone positioning may reduce the nonphysiological stress and strain associated with mechanical ventilation, thus decreasing the risk of ventilator-induced lung injury, which is known to adversely impact patient survival. The available randomized clinical trials, however, have failed to demonstrate that prone positioning improves the outcomes of patients with ARDS overall. In contrast, the individual patient meta-analysis of the four major clinical trials available clearly shows that with prone positioning, the absolute mortality of severely hypoxemic ARDS patients may be reduced by approximately 10%. On the other hand, all data suggest that long-term prone positioning may expose patients with less severe ARDS to unnecessary complications.

RATIONALE: The effects of high positive end-expiratory pressure (PEEP) strictly depend on lung recruitability, which varies widely during acute respiratory distress syndrome (ARDS). Unfortunately, increasing PEEP may lead to opposing effects on two main factors potentially worsening the lung injury, that is, alveolar strain and intratidal opening and closing, being detrimental (increasing the former) or beneficial (decreasing the latter). OBJECTIVES: To investigate how lung recruitability influences alveolar strain and intratidal opening and closing after the application of high PEEP. METHODS: We analyzed data from a database of 68 patients with acute lung injury or ARDS who underwent whole-lung computed tomography at 5, 15, and 45 cm H(2)O airway pressure. MEASUREMENTS AND MAIN RESULTS: End-inspiratory nonaerated lung tissue was estimated from computed tomography pressure-volume curves. Alveolar strain and opening and closing lung tissue were computed at 5 and 15 cm H(2)O PEEP. In patients with a higher percentage of potentially recruitable lung, the increase in PEEP markedly reduced opening and closing lung tissue (P < 0.001), whereas no differences were observed in patients with a lower percentage of potentially recruitable lung. In contrast, alveolar strain similarly increased in the two groups (P = 0.89). Opening and closing lung tissue was distributed mainly in the dependent and hilar lung regions, and it appeared to be an independent risk factor for death (odds ratio, 1.10 for each 10-g increase). CONCLUSIONS: In ARDS, especially in patients with higher lung recruitability, the beneficial impact of reducing intratidal alveolar opening and closing by increasing PEEP prevails over the effects of increasing alveolar strain.

In this chapter we will illustrate the paradigmatic role that medical imaging has played in helping to define, understand, and treat a specific form of respiratory failure called acute respiratory distress syndrome (ARDS). ARDS is a life-threatening syndrome characterized by noncardiogenic (inflammatory) pulmonary edema causing mainly hypoxemic respiratory failure unresponsive to conventional therapy.

To clarify whether the gas exchange response to prone position is associated with lung recruitability in mechanically ventilated patients with acute respiratory failure.In 32 patients, gas exchange response to prone position was investigated as a function of lung recruitability, measured by computed tomography in supine position.No relationship was found between increased oxygenation in prone position and lung recruitability. In contrast, the decrease of PaCO(2) was related with lung recruitability (R(2) 0.19; P = 0.01). Patients who decreased their PaCO(2) more than the median value (-0.9 mmHg) had a greater lung recruitability (19 +/- 16 vs. 8 +/- 6%; P = 0.02), higher baseline PaCO(2) (48 +/- 8 vs. 41 +/- 11 mmHg; P = 0.07), heavier lungs (1,968 +/- 829 vs. 1,521 +/- 342 g; P = 0.06) and more non-aerated tissue (1,009 +/- 704 vs. 536 +/- 188 g; P = 0.02) than those who did not.During prone position, changes in PaCO(2), but not in oxygenation, are associated with lung recruitability which, in turn, is associated with the severity of lung injury.

Lung injury caused by a ventilator results from nonphysiologic lung stress (transpulmonary pressure) and strain (inflated volume to functional residual capacity ratio).To determine whether plateau pressure and tidal volume are adequate surrogates for stress and strain, and to quantify the stress to strain relationship in patients and control subjects.Nineteen postsurgical healthy patients (group 1), 11 patients with medical diseases (group 2), 26 patients with acute lung injury (group 3), and 24 patients with acute respiratory distress syndrome (group 4) underwent a positive end-expiratory pressure (PEEP) trial (5 and 15 cm H2O) with 6, 8, 10, and 12 ml/kg tidal volume.Plateau airway pressure, lung and chest wall elastances, and lung stress and strain significantly increased from groups 1 to 4 and with increasing PEEP and tidal volume. Within each group, a given applied airway pressure produced largely variable stress due to the variability of the lung elastance to respiratory system elastance ratio (range, 0.33-0.95). Analogously, for the same applied tidal volume, the strain variability within subgroups was remarkable, due to the functional residual capacity variability. Therefore, low or high tidal volume, such as 6 and 12 ml/kg, respectively, could produce similar stress and strain in a remarkable fraction of patients in each subgroup. In contrast, the stress to strain ratio-that is, specific lung elastance-was similar throughout the subgroups (13.4 +/- 3.4, 12.6 +/- 3.0, 14.4 +/- 3.6, and 13.5 +/- 4.1 cm H2O for groups 1 through 4, respectively; P = 0.58) and did not change with PEEP and tidal volume.Plateau pressure and tidal volume are inadequate surrogates for lung stress and strain. Clinical trial registered with www.clinicaltrials.gov (NCT 00143468).

Objectives: The lung-protective strategy employs positive endexpiratory pressure to keep open otherwise collapsed lung regions (anatomical recruitment). Improvement in venous admixture with positive end-expiratory pressure indicates functional recruitment to better gas exchange, which is not necessarily related to anatomical recruitment, because of possible global/ regional perfusion modifications. Therefore, we aimed to assess the value of venous admixture (functional shunt) in estimating the fraction of nonaerated lung tissue (anatomical shunt compartment) and to describe their relationship. Design: Retrospective analysis of a previously published study. Setting: Intensive care units of four university hospitals. Patients: Fifty-nine patients with acute lung injury/acute respiratory distress syndrome. Interventions: Positive end-expiratory pressure trial at 5 and 15 cm H2O positive end-expiratory pressures. Measurements and Main Results: Anatomical shunt compartment (whole-lung computed tomography scan) and functional shunt (blood gas analysis) were assessed at 5 and 15 cm H2O positive end-expiratory pressures. Apparent perfusion ratio (perfusion per gram of nonaerated tissue/perfusion per gram of total lung tissue) was defined as the ratio of functional shunt to anatomical shunt compartment. Functional shunt was poorly correlated to the anatomical shunt compartment (r 2 .174). The apparent perfusion ratio at 5 cm H2O positive end-expiratory pressure was widely distributed and averaged 1.25 0.80. The apparent perfusion ratios at 5 and 15 cm H2O positive endexpiratory pressures were highly correlated, with a slope close to identity (y 1.10·x 0.03, r 2 .759), suggesting unchanged blood flow distribution toward the nonaerated lung tissue, when increasing positive end-expiratory pressure. Conclusions: Functional shunt poorly estimates the anatomical shunt compartment, due to the large variability in apparent perfusion ratio. Changes in anatomical shunt compartment with increasing positive end-expiratory pressure, in each individual patient, may be estimated from changes in functional shunt, only if the anatomicalfunctional shunt relationship at 5 cm H2O positive end-expiratory pressure is known. (Crit Care Med 2008; 36:669‐675)

Traditionally, ARDS obese patients are ventilated with higher tidal volumes and higher PEEP due to expected increased in pleural pressure. However, data from the literature regarding the influence of body mass on lung mechanics and, particularly, on chest wall elastance are not univocal [1,2]. Failure to account for how the increase in body weight could affect the respiratory function can result in injurious mechanical ventilation and in the onset of VILI. The aim of this study was to evaluate the role of the body weight on respiratory mechanics in ARDS patients.

CT has provided new insights on the pathophysiology of acute respiratory distress syndrome (ARDS), demonstrating that ARDS does not affect the lung parenchyma homogeneously. These findings suggest that lung edema, as assessed by CT scan, should be included in the definition. Lung CT findings may provide a firm rationale for tailoring tidal volume during mechanical ventilation. Ideally, tidal volume should be proportional to the portion of the lung open to ventilation, as assessed by CT scan, rather than to the body weight. CT assessment of lung recruitability seems to be a prerequisite for a rational setting of positive end-expiratory pressure.

The plasmatic strong ion difference (SID) is the difference between positively and negatively charged strong ions. At pH 7.4, temperature 37 degrees C and partial carbon dioxide tension 40 mmHg, the ideal value of SID is 42 mEq/l. The buffer base is the sum of negatively charged weak acids ([HCO3(-)], [A-], [H2PO4(-)]) and its normal value is 42 mEq/l. According to the law of electroneutrality, the amount of positive and negative charges must be equal, and therefore the SID value is equal to the buffer base value. The easiest assessment of metabolic acidosis/alkalosis relies on the base excess calculation: buffer base(actual) - buffer base(ideal) = SID(actual) - SID(ideal). The SID approach allows one to appreciate the relationship between acid-base and electrolyte equilibrium from a unique perspective, and here we describe a comprehensive model of this equilibrium. The extracellular volume is characterized by a given SID, which is a function of baseline conditions, endogenous and exogenous input (endogenous production and infusion), and urinary output. Of note, volume modifications vary the concentration of charges in the solution. An expansion of extracellular volume leads to acidosis (SID decreases), whereas a contraction of extracellular volume leads to alkalosis (SID increases). A thorough understanding of acid-base equilibrium mandates recognition of the importance of urinary SID.

Computed tomography (CT) has been utilized to study acute respiratory distress syndrome (ARDS) since the middle 1980s, when it revealed the inhomogeneous pattern of the lung lesion. Its advantages rely on the strict correlation between CT density and the lung physical density, allowing a quantification of lung compartments with different degrees of aeration. By CT scans, ARDS lung appeared to be "small" rather than "stiff," leading to the "baby lung" concept. The regional analysis revealed that this appearance derives from an evenly distributed lung edema, which tends, because of gravitational forces, to lie predominantly in the most dependent regions, leading to alveolar collapse. New data suggest that such a "sponge lung" is made by a "core," consolidated, lung portion, from which, through an inflammatory reaction, lung edema will spread, determining the collapsed and recruitable lung portion. The amount of recruitable lung varies among ARDS patients. This knowledge is necessary for a rational positive end-expiratory pressure (PEEP) setting because the amount of tissue maintained aerated by PEEP is closely associated with the amount of recruitable lung. CT scans may also help to diagnose ARDS because CT provides a good estimate of the high-permeability lung edema, the characteristic lesion of this syndrome.

Objective To investigate if prone position delays the progression of experimental ventilator-induced lung injury, possibly due to a more homogeneous distribution of strain within lung parenchyma. Design Prospective, randomized, controlled trial. Setting Animal laboratory of a university hospital. Subjects Thirty-five Sprague Dawley male rats (weight 257 +/- 45 g). Interventions Mechanical ventilation in either supine or prone position and computed tomography scan analysis. Measurements : Animals were ventilated in supine (n = 15) or prone (n = 15) position until a similar ventilator-induced lung injury was reached. To do so, experiments were interrupted when respiratory system elastance was 150% of baseline. Ventilator-induced lung injury was assessed as lung wet-to-dry ratio and histology. Time to reach lung injury was considered as a main outcome measure. In five additional animals, computed tomography scans (GE Light Speed QX/I, thickness 1.25 mm, interval 0.6 mm, 100 MA, 100 Kv) were randomly taken at end-expiration and end-inspiration in both positions, and quantitative analysis was performed. Data are shown as mean +/- sd. Measurements and main results Similar ventilator-induced lung injury was reached (respiratory system elastance, wet-to-dry ratio, and histology). The time taken to achieve the target ventilator-induced lung injury was longer with prone position (73 +/- 37 mins vs. 112 +/- 42, supine vs. prone, p = .011). Computed tomography scan analysis performed before lung injury revealed that at end-expiration, the lung was wider in prone position (p = .004) and somewhat shorter (p = .09), despite similar lung volumes (p = .455). Lung density along the vertical axis increased significantly only in supine position (p = .002). Lung strain was greater in supine as opposed to prone position (width strain, 7.8 +/- 1.8% vs. 5.6 +/- 0.9, supine vs. prone, p = .029). Conclusions Prone position delays the progression of ventilator-induced lung injury. Computed tomography scan analysis suggests that a more homogeneous distribution of strain may be implicated in the protective role of prone position against ventilator-induced lung injury.

Purpose of review The purpose of this paper is to review the mechanisms of ventilator-induced lung injury as a basis for providing the less damaging mechanical ventilation in patients with acute respiratory failure. Recent findings In normal lungs, high tidal volume causes an immediate gene upregulation and downregulation. Although the importance of alveolar inflammatory reaction is well known, recent findings suggest the potential role of airway distension in causing ventilator-induced lung injury. The initial activation has been shown to occur in the airways, accounting for the damages induced by high peak flow. The healthier lung regions are more exposed to the injury, since they may be subjected to strain. Challenge with endotoxin enhances in a synergistic manner the pulmonary inflammation induced by mechanical ventilation. However, mechanical strain and endotoxin seem to trigger lung inflammation through two different pathways. Despite convincing experimental and clinical evidences of lung injury, the clinical implementation of low tidal volume ventilation is still limited and has not yet become part of standard clinical practice. Setting positive end-expiratory pressure remains an open problem because the ALVEOLI study did not provide any exhaustive answers, likely because of methodologic problems and, unphysiologic design. Summary Gentle lung ventilation must be standard practice. Because stress and strain are the triggers of ventilator-induced lung injury, their clinical equivalents should be measured (transpulmonary pressure and the ratio between tidal volume and end-expiratory lung volume). For a rational application of positive end-expiratory pressure, the potential for recruitment in any single patient should be estimated.

The concept of ‘inadequate’ hemodynamics is traditionally based on low flow and/or low arterial pressure. However it has been hypothesized that hemodynamics may be ‘inadequate’ for physiological organ function even if perfusion pressures and cardiac output are within the normal values. This concept was mainly introduced by Shoemaker, who originally observed that critically ill patients who survived major surgery had significantly greater cardiac index and oxygen transport parameters than those who ultimately died [1]. This led many investigators to consider ‘supra-normal’ hemodynamic values as the essence of ‘adequate’ hemodynamics in critically ill patients, and hundred of papers have dealt with this issue over the last 25 years. In this brief chapter, we would like to discuss the physiological basis of ‘adequate hemodynamics’, in the context of cell bioenergetics. Our interpretation, however, does not pretend to preclude or invalidate other views of the problem.

Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H(2)O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H(2)O significantly lowered the gas content, leaving the tissue content unchanged. In OA-injured lung at aIAP 0 cm H(2)O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 +/- 24% of the original tissue weight (455 +/- 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H(2)O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 +/- 37% (tissue weight 905 +/- 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OA-injured lung, the increase of IAP increases the amount of edema.

Objective: To determine whether gas exchange improvement in response to the prone position is associated with an improved outcome in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Design: Retrospective analysis of patients in the pronation arm of a controlled randomized trial on prone positioning and patients enrolled in a previous pilot study of the prone position. Setting: Twenty-eight Italian and two Swiss intensive care units. Patients: We studied 225 patients meeting the criteria for ALI or ARDS. Interventions: Patients were in prone position for 10 days for 6 hrs/day if they met ALI/ARDS criteria when assessed each morning. Respiratory variables were recorded before and after 6 hrs of pronation with unchanged ventilatory settings. Measurements and Main Results: We measured arterial blood gas alterations to the first pronation and the 28-day mortality rate. The independent risk factors for death in the general population were the Pao 2/F102 ratio (odds ratio, 0.992; confidence interval, 0.986-0.998), the minute ventilation/Paco2 ratio (odds ratio, 1.003; confidence interval, 1.000-1.006), and the concentration of plasma creatinine (odds ratio, 1.385; confidence interval, 1.116-1.720). Pao2 responders (defined as the patients who increased their Pao2/F10 2 by ≥20 mm Hg, 150 patients, mean increase of 100.6 ± 61. 6 mm Hg [13.4 ± 8.2 KPa]) had an outcome similar to the nonresponders (59 patients, mean decrease -6.3 ± 23.7 mm Hg [-0.8 ± 3.2 KPa]; mortality rate 44% and 46%, respectively; relative risk, 1.04; confidence interval, 0.74-1.45, p = .65). The Paco2 responders (defined as patients whose Paco2 decreased by ≥1 mm Hg, 94 patients, mean decrease -6.0 ± 6 mm Hg [-0.8 ± 0.8 KPa]) had an improved survival when compared with nonresponders (115 patients, mean increase 6 ± 6 mm Hg [0.8 ± 0.8 KPa]; mortality rate 35.1% and 52.2%, respectively; relative risk, 1.48; confidence interval, 1.07-2.05, p = .01). Conclusion: ALI/ARDS patients who respond to prone positioning with reduction of their Paco2 show an increased survival at 28 days. Improved efficiency of alveolar ventilation (decreased physiologic deadspace ratio) is an important marker of patients who will survive acute respiratory failure.

Ventilator-induced lung injury (VILI) is a well-known side effect of mechanical ventilation. The pressures and volumes needed to induce VILI in healthy animals are far greater than pressure and volumes applied in clinical practice [1]. A possible explanation may be the presence of local pressure multipliers (stress raisers).

Chloride shift is the movement of chloride between red blood cells (RBC) and plasma (and vice versa) caused by variations in pCO2. The aim of our study was to investigate changes in plasmatic strong ion difference (SID) during acute variations in pCO2 and their possible role in the compensation for hypocapnic alkalosis.

The plasmatic strong ion difference (SID) is the difference between positively and negatively charged strong ions. At pH 7.4, temperature 37°C and partial carbon dioxide tension 40 mmHg, the ideal value of SID is 42 mEq/l. The buffer base is the sum of negatively charged weak acids ([HCO3-], [A-], [H2PO4-]) and its normal value is 42 mEq/l. According to the law of electroneutrality, the amount of positive and negative charges must be equal, and therefore the SID value is equal to the buffer base value. The easiest assessment of metabolic acidosis/alkalosis relies on the base excess calculation: buffer baseactual - buffer baseideal = SIDactual - SIDideal. The SID approach allows one to appreciate the relationship between acid–base and electrolyte equilibrium from a unique perspective, and here we describe a comprehensive model of this equilibrium. The extracellular volume is characterized by a given SID, which is a function of baseline conditions, endogenous and exogenous input (endogenous production and infusion), and urinary output. Of note, volume modifications vary the concentration of charges in the solution. An expansion of extracellular volume leads to acidosis (SID decreases), whereas a contraction of extracellular volume leads to alkalosis (SID increases). A thorough understanding of acid–base equilibrium mandates recognition of the importance of urinary SID.

During pressure support ventilation (PSV) a part of the breathing pattern is controlled by the patient, and synchronization of respiratory muscle action and the resulting chest wall kinematics is a valid indicator of the patient's adaptation to the ventilator. The aim of the present study was to analyze the effects of different PSV settings on ventilatory pattern, total and compartmental chest wall kinematics and dynamics, muscle pressures and work of breathing in patients with acute lung injury. In nine patients four different levels of PSV (5, 10, 15 and 25 cmH2O) were randomly applied with the same level of positive end-expiratory pressure (10 cmH2O). Flow, airway opening, and oesophageal and gastric pressures were measured, and volume variations for the entire chest wall, the ribcage and abdominal compartments were recorded by opto-electronic plethysmography. The pressure and the work generated by the diaphragm, rib cage and abdominal muscles were determined using dynamic pressure-volume loops in the various phases of each respiratory cycle: pre-triggering, post-triggering with the patient's effort combining with the action of the ventilator, pressurization and expiration. The complete breathing pattern was measured and correlated with chest wall kinematics and dynamics. At the various levels of pressure support applied, minute ventilation was constant, with large variations in breathing frequency/ tidal volume ratio. At pressure support levels below 15 cmH2O the following increased: the pressure developed by the inspiratory muscles, the contribution of the rib cage compartment to the total tidal volume, the phase shift between rib cage and abdominal compartments, the post-inspiratory action of the inspiratory rib cage muscles, and the expiratory muscle activity. During PSV, the ventilatory pattern is very different at different levels of pressure support; in patients with acute lung injury pressure support greater than 10 cmH2O permits homogeneous recruitment of respiratory muscles, with resulting synchronous thoraco-abdominal expansion.

This study sought to assess whether the use of thoraco-pelvic supports during prone positioning in patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS) improves, deteriorates or leaves unmodified gas exchange, hemodynamics and respiratory mechanics. We studied 11 patients with ALI/ARDS, sedated and paralyzed, mechanically ventilated in volume control ventilation. Prone positioning with or without thoraco-pelvic supports was applied in a random sequence and maintained for a 1-hour period without changing the ventilation setting. In four healthy subjects the pressures between the body and the contact surface were measured with and without thoraco-pelvic supports. Oxygenation variables (arterial and central venous), physiologic dead space, end-expiratory lung volume (helium dilution technique) and respiratory mechanics (partitioned between lung and chest wall) were measured after 60 minutes in each condition. With thoraco-pelvic supports, the contact pressures almost doubled in comparison with those measured without supports (19.1 ± 15.2 versus 10.8 ± 7.0 cmH2O, p ≤ 0.05; means ± SD). The oxygenation-related variables were not different in the prone position, with or without thoraco-pelvic supports; neither were the CO2-related variables. The lung volumes were similar in the prone position with and without thoraco-pelvic supports. The use of thoraco-pelvic supports, however, did lead to a significant decrease in chest wall compliance from 158.1 ± 77.8 to 102.5 ± 38.0 ml/cmH2O and a significantly increased pleural pressure from 4.3 ± 1.9 to 6.1 ± 1.8 cmH2O, in comparison with the prone position without supports. Moreover, when thoraco-pelvic supports were added, heart rate increased significantly from 82.1 ± 17.9 to 86.7 ± 16.7 beats/minute and stroke volume index decreased significantly from 37.8 ± 6.8 to 34.9 ± 5.4 ml/m2. The increase in pleural pressure change was associated with a significant increase in heart rate (p = 0.0003) and decrease in stroke volume index (p = 0.0241). The application of thoraco-pelvic supports decreases chest wall compliance, increases pleural pressure and slightly deteriorates hemodynamics without any advantage in gas exchange. Consequently, we stopped their use in clinical practice.

We previously found that optoelectronic plethysmography can be used to measure the chest wall volume and its compartments: rib cage and abdomen [1]. We evaluated the breathing pattern and the chest wall displacement during pressure support (PSV) in patients with acute respiratory failure. Nine intubated patients (age 57 ± 12 years, BMI 26 ± 5 kg/m2, PaO2/FiO2 293 ± 67) were studied first at four levels of PSV (5, 10, 15, 25 cmH2O) at 10 cmH2O of PEEP and then at three levels of PEEP (5, 10, 15 cmH2O) at 10 of PSV. We measured the breathing pattern, the ribcage contribution to tidal volume (RC/VT) and the inspiratory asynchrony (IA) [2]. IA was calculated as the area enclosed by the inspiratory portion of rib cage abdomen loop and the line connecting the commencement and the terminal of inspiration. Our results suggest that only the level of PSV affects the breathing pattern. Table 1

The pressure volume (P-V) curve of the total respiratory system is drawn assuming the changes of chest wall (?Vcw) equal to the volume displaced from the syringe (?Vgas). We compared ?Vgas and ?Vcw during P-V curves obtained by supersyringe and opto-electronic plethysmography [1]. Eight sedated paralysed intubated ALI/ARDS patients (5 M/3 F, age 70 ± 13 years, BMI 25.6 ± 3 kg/m2, PaO2/FiO2 220 ± 76) were studied. During the manoeuvre ?Vcw was recorded by optoelectronic plethysmography. The volume injected and withdrawn by the supersyringe step by step (100 ml) was corrected by temperature, humidity, pressure and gas exchange [2]. The discrepancy was computed as the difference between the volume of air inflated and the chest volume measured. The compliance of the total respiratory system was measured between zero and maximum airway pressure values on the inflation (Crsinf) and deflation (Crsdef) limbs of the P-V curves. Hysteresis loops of the corrected P-Vgas and P-Vcw curves were calculated as the percentage ratio between the area of the P-V curves and the product of maximal volume by maximal pressure. Even considering thermodynamics and gas exchange correction, ?Vgas values were systematically higher than ?Vcw probably due to blood shifts from the thorax to the extremities. As a consequence, the standard supersyringe method provides an overestimation of the inspiratory and expiratory compliance of the total respiratory system on the inflation limb and an overestimation of the hysteresis area. Table 1

To test the capability of optoelectronic plethysmography (OEP) to monitor positive end-expiratory pressure (PEEP)-induced changes of end-expiratory lung volume (EELV) changes in mechanically ventilated paralyzed patients.Laboratory and clinical investigation.Intensive care unit of the Ospedale Maggiore Policlinico di Milano.A total of eight patients with respiratory failure of various degrees, sedated and paralyzed.PEEP variations (+/-5 cm H2O) relative to the baseline PEEP of 10 cm H2O.In the model protocol, we tested the reproducibility of the OEP by repeating volume measurements of a plastic torso model over a 21-hr period, every 30 mins. The variations of OEP measurements of the torso model (9337 mL value) were encountered in a range of 16 mL (sd = 4 mL). In the patient protocol, we measured the end-expiratory volume of the chest wall (EEVCW) breath-by-breath by OEP before, during, and after the PEEP increase/decrease and we compared its variations with the corresponding variations of EELV measured by helium dilution technique. The regression line between EELV changes measured by helium and EEVCW changes measured by OEP resulted very close to the identity line (slope 1.06, intercept -0.02 L, r(2) = 0.89) and their difference was not related to their absolute magnitude. After PEEP increase, the new steady state of EEVCW was reached approximately in 15 breaths; and, after PEEP decrease, in 3-4 breaths. The slow increase in EEVCW was mainly because of the abdominal compartment.OEP measurements of EEVCW accurately reflect the changes of EELV. Furthermore, OEP allows a continuous compartmental analysis, even during unsteady conditions.

Bicarbonate infusion is traditionally used to increase pH during metabolic acidosis, but it has been also suggested to increase the pH during permissive hypercapnia. In this paper we will discuss the physicochemical effect of adding (Na+ HCO3-), first in a closed system (venous blood) and then in an open system (the blood after the lung). According to Stewart model, in the closed system two independent variables are changed (CO2 and strong ion difference). As a first result changes in pH are negligible. If the CO2 is cleared by the lung and the PCO2 is maintained as before the infusion, the rise in pH is due to the SID increase caused by the (Na+) rise. The effect is independent on (HCO3-) infusion and equivalent to adding (Na+ OH-) instead of (Na+ HCO3-).

Background High tidal volume can cause ventilator-induced lung injury (VILI), but positive end-expiratory pressure (PEEP) is thought to be protective. We aimed to find the volumetric VILI threshold and see whether PEEP is protective per se or indirectly. Methods In 76 pigs (22 ± 2 kg), we examined the lower and upper limits (30.9–59.7 mL/kg) of inspiratory capacity by computed tomography (CT) scan at 45 cmH2O pressure. The pigs underwent a 54-h mechanical ventilation with a global strain ((tidal volume (dynamic) + PEEP volume (static))/functional residual capacity) from 0.45 to 5.56. The dynamic strain ranged from 18 to 100 % of global strain. Twenty-nine pigs were ventilated with end-inspiratory volumes below the lower limit of inspiratory capacity (group “Below”), 38 within (group “Within”), and 9 above (group “Above”). VILI was defined as death and/or increased lung weight. Results “Below” pigs did not develop VILI; “Within” pigs developed lung edema, and 52 % died before the end of the experiment. The amount of edema was significantly related to dynamic strain (edema 188–153 × dynamic strain, R2 = 0.48, p

Positive end-expiratory pressure (PEEP) is commonly used in patients with ARDS to prevent end-expiratory collapse. The increase in gas volume and/or change in mechanical properties of the lung are used at the bedside to estimate lung recruitment and individualize PEEP selection.

Ventilator-induced lung injury is a side-effect of mechanical ventilation. Its prevention or attenuation implies knowledge of the sequence of events that lead from mechanical stress to lung inflammation and stress at rupture. A literature review was undertaken which focused on the link between the mechanical forces in the diseased lung and the resulting inflammation/rupture. The distending force of the lung is the transpulmonary pressure. This applied force, in a homogeneous lung, is shared equally by each fibre of the lung9s fibrous skeleton. In a nonhomogeneous lung, the collapsed or consolidated regions do not strain, whereas the neighbouring fibres experience excessive strain. Indeed, if the global applied force is excessive, or the fibres near the diseased regions experience excessive stress/strain, biological activation and/or mechanical rupture are observed. Excessive strain activates macrophages and epithelial cells to produce interleukin-8. This cytokine recruits neutrophils, with consequent full-blown inflammation. In order to prevent initiation of ventilator-induced lung injury, transpulmonary pressure must be kept within the physiological range. The prone position may attenuate ventilator-induced lung injury by increasing the homogeneity of transpulmonary pressure distribution. Positive end-expiratory pressure may prevent ventilator-induced lung injury by keeping open the lung, thus reducing the regional stress/strain maldistribution. If the transpulmonary pressure rather than the tidal volume per kilogram of body weight is taken into account, the contradictory results of the randomised trials dealing with different strategies of mechanical ventilation may be better understood. Eur Respir J 2003; 22: Suppl. 47, 15s-25s.