Ana Villagrá

Massive brain injury enhances lung damage in an isolated lung model of ventilator-induced lung injury

Objective:To assess the influence of massive brain injury on pulmonary susceptibility to injury attending subsequent mechanical or ischemia/reperfusion stress. Design:Prospective experimental study. Setting:Animal research laboratory. Subjects:Twenty-four anesthetized New Zealand White rabbits randomized to control (n = 12) or induced brain injury (n = 12) group. Interventions:After randomization, brain injury was induced by inflation of an intracranial balloon-tipped catheter, and animals were ventilated with a tidal volume of 10 mL/kg and zero end-expiratory pressure for 120 mins. Following heart-lung block extraction, isolated and perfused lungs were subjected to injurious ventilation with peak airway pressure 30 cm H2O and positive end-expiratory pressure 5 cm H2O for 30 mins. Measurements and Main Results:No difference was observed between groups in gas exchange, lung mechanics, or hemodynamics during the 2-hr in vivo period following induction of brain injury. However, after 30 mins of ex vivo injurious mechanical ventilation, lungs from the brain injury group showed greater change in ultrafiltration coefficient, weight gain, and alveolar hemorrhage (all p < .05). Conclusions:Massive brain injury might increase lung vulnerability to subsequent injurious mechanical or ischemia-reperfusion insults, thereby increasing the risk of clinical posttransplant graft failure.

Improvement in oxygenation by prone position and nitric oxide in patients with acute respiratory distress syndrome.

Objective: Inhaled nitric oxide (NO) and prone position improve arterial oxygenation in patients with the acute respiratory distress syndrome. This study was undertaken to assess the combined effects of NO and prone position in these patients. Design: Prospective clinical study. Setting: General intensive care service in a community teaching hospital. Patients: 14 mechanically ventilated adult patients with the acute respiratory distress syndrome (mean lung injury score 3.23 ± 0.27). Measurements and results: We measured hemodynamic and oxygenation parameters in the supine position and 2 h later in the prone position, before and during inhalation of 10 ppm NO. A positive response in oxygenation was defined as a ≥ 20 % increment in the arterial oxygen tension/fractional inspired oxygen ratio (PaO2/FIO2). In the prone position PaO2/FIO2 increased significantly (from 110 ± 55 to 161 ± 89 mmHg, p < 0.01) and venous admixture decreased (from 38 ± 12 to 30 ± 7 %, p < 0.01) compared to the supine position. Ten of the 14 patients were responders in the prone position. In the supine position, inhalation of NO improved oxygenation to a lesser extent, increasing PaO2/FIO2 to 134 ± 64 mmHg (p < 0.01) and decreasing venous admixture to 35 ± 12 %, (p < 0.01). Five of the 14 patients responded to NO inhalation supine and 8 of 14 responded prone (p = 0.22). The combination of NO therapy and prone positioning was additive in increasing PaO2/FIO2 (197 ± 92 mmHg) and decreasing venous admixture (27 ± 8 %) (p < 0.01). This combination also showed a positive oxygenation response on compared to the supine value without NO in 13 of the 14 patients (93 %). NO-induced changes in PaO2/FIO2 were correlated to changes in pulmonary vascular resistance only in the prone position. Conclusions: In patients with the acute respiratory distress syndrome, the combination of NO and prone position is a valuable adjunct to mechanical ventilation.

Contributions of vascular flow and pulmonary capillary pressure to ventilator-induced lung injury.

Objective:To evaluate the influence of vascular flow on ventilator-induced lung injury independent of vascular pressures. Design:Laboratory study. Setting:Hospital laboratory. Subjects:Thirty-two New Zealand White rabbits. Interventions:Thirty-two isolated perfused rabbit lungs were allocated into four groups: low flow/low pulmonary capillary pressure; high flow/high pulmonary capillary pressure; low flow/high pulmonary capillary pressure, and high flow/low pulmonary capillary pressure. All lungs were ventilated with peak airway pressure 30 cm H2O and positive end-expiratory pressure 5 cm H2O for 30 mins. Measurements and Main Results:Outcome measures included frequency of gross structural failure (pulmonary rupture), pulmonary hemorrhage, edema formation, changes in lung compliance, pulmonary vascular resistance, and pulmonary ultrafiltration coefficient. Lungs exposed to high pulmonary vascular flow ruptured more frequently, displayed more hemorrhage, developed more edema, suffered larger decreases in compliance, and had larger increases in vascular resistance than lungs exposed to low vascular flows (p < .05 for each pairwise comparison between groups). Conclusions:These findings suggest that high pulmonary vascular flows might exacerbate ventilator-induced lung injury independent of their effects on pulmonary vascular pressures.

Clinical review: The implications of experimental and clinical studies of recruitment maneuvers in acute lung injury

Mechanical ventilation can cause and perpetuate lung injury if alveolar overdistension, cyclic collapse, and reopening of alveolar units occur. The use of low tidal volume and limited airway pressure has improved survival in patients with acute lung injury or acute respiratory distress syndrome. The use of recruitment maneuvers has been proposed as an adjunct to mechanical ventilation to re-expand collapsed lung tissue. Many investigators have studied the benefits of recruitment maneuvers in healthy anesthetized patients and in patients ventilated with low positive end-expiratory pressure. However, it is unclear whether recruitment maneuvers are useful when patients with acute lung injury or acute respiratory distress syndrome are ventilated with high positive end-expiratory pressure, and in the presence of lung fibrosis or a stiff chest wall. Moreover, it is unclear whether the use of high airway pressures during recruitment maneuvers can cause bacterial translocation. This article reviews the intrinsic mechanisms of mechanical stress, the controversy regarding clinical use of recruitment maneuvers, and the interactions between lung infection and application of high intrathoracic pressures.

Application of continuous positive airway pressure to trace static pressure-volume curves of the respiratory system

ObjectiveTo evaluate a new technique for pressure-volume curve tracing. DesignProspective experimental study. SettingAnimal research laboratory. SubjectsSix anesthetized rats. InterventionsTwo pressure-volume curves were obtained by means of the super-syringe method (gold standard) and the continuous positive airway pressure (CPAP) method. For the CPAP method, the ventilator was switched to CPAP and the pressure level was raised from 0 to 50 cm H2O in 5 cm H2O steps and then decreased, while we measured lung volume using respiratory inductive plethysmography. Thereafter, lung injury was induced using very high-volume ventilation. Following injury, two further pressure-volume curves were traced. Pressure-volume pairs were fitted to a mathematical model. Measurements and Main ResultsPressure-volume curves were equivalent for each method, with intraclass correlation coefficients being higher than .75 for each pressure level measured. Bias and precision for volume values were 0.46 ± 0.875 mL in basal measurements and 0.31 ± 0.67 mL in postinjury conditions. Lower and upper inflection points on the inspiratory limb and maximum curvature point on the deflation limb obtained using both methods and measured by regression analysis also were correlated, with intraclass correlation coefficients (95% confidence interval) being .97 (.58, .99), .85 (.55, .95), and .94 (.81, .98) (p < .001 for each one). When inflection points were estimated by observers, the correlation coefficient between methods was .90 (.67, .98) for lower inflection points (p < .001). However, estimations for upper inflection points and maximum curvature point were significantly different. ConclusionsThe CPAP method for tracing pressure-volume curves is equivalent to the super-syringe method. It is easily applicable at the bedside, avoids disconnection from the ventilator, and can be used to obtain both the inspiratory and the deflation limbs of the pressure-volume curve. Use of regression techniques improves determination of inflection points.

Mecanismos biofísicos, celulares y modulación de la lesión pulmonar inducida por la ventilación mecánica

Ventilator-induced lung injury (VILI) is associated to a high rate of mortality with an important social impact. Mechanical ventilation induces structural and ultrastructural alterations in all cell types of the lung and can derive in the transduction of intracellular signals, as well as in changes in the expression of genes, a process known as mechanotransduction. Some of the conditions involved, such as inflammation and/or coagulation, apoptosis/necrosis can lead to the propagation of the injury outside the lung, resulting in multiorganic failure. VILI can be modulated by means of diverse interventions as the use of protective ventilatory modes, therapeutic approaches based on vasoactive and antioxidative drugs, and more recently treatments based on the use of repairing substances of the surfactant like poloxamers among others. Knowledge of the mechanisms involved in VILI is definitive for a better approach to this condition.

Interpretación de las curvas del respirador en pacientes con insuficiencia respiratoria aguda

Mechanical ventilation is a therapeutic intervention involving the temporary replacement of ventilatory function with the purpose of improving symptoms in patients with acute respiratory failure. Technological advances have facilitated the development of sophisticated ventilators for viewing and recording the respiratory waveforms, which are a valuable source of information for the clinician. The correct interpretation of these curves is crucial for the correct diagnosis and early detection of anomalies, and for understanding physiological aspects related to mechanical ventilation and patient-ventilator interaction. The present study offers a guide for the interpretation of the airway pressure and flow and volume curves of the ventilator, through the analysis of different clinical scenarios.

Effects of vascular flow and PEEP in a multiple hit model of lung injury in isolated perfused rabbit lungs.

BACKGROUND High vascular flow aggravates lung damage in animal models of ventilator-induced lung injury. Positive end-expiratory pressure (PEEP) can attenuate ventilator-induced lung injury, but its continued effectiveness in the setting of antecedent lung injury is unclear. The objective of the present study was to evaluate whether the application of PEEP diminishes lung injury induced by concurrent high vascular flow and high alveolar pressures in normal lungs and in a preinjury lung model. METHODS Two series of experiments were performed. Fifteen sets of isolated rabbit lungs were randomized into three groups (n = 5): low vascular flow/low PEEP; high vascular flow/low PEEP, and high vascular flow/high PEEP. Subsequently, the same protocol was applied in an additional 15 sets of isolated rabbit lungs in which oleic acid was added to the vascular perfusate to produce mild to moderate lung injury. All lungs were ventilated with peak airway pressure of 30 cm H2O for 30 minutes. Outcome measures included frequency of gross structural failure, pulmonary hemorrhage, edema formation, changes in static compliance, pulmonary vascular resistance, and pulmonary ultrafiltration coefficient. RESULTS In the context of high vascular flow, application of a moderate level of PEEP reduced pulmonary rupture, edema formation, and lung hemorrhage. The protective effects of PEEP were not observed in lungs concurrently injured with oleic acid. CONCLUSIONS Under these experimental conditions, PEEP attenuates lung injury in the setting of high vascular flow. The protective effect of PEEP is lost in a two-hit model of lung injury.

Bedside evaluation of pressure-volume curves in patients with acute respiratory distress syndrome.

Purpose of reviewTo describe the physiologic and diagnostic utility of static pressure–volume curves of the respiratory system at the bedside in patients with acute lung injury or acute respiratory distress syndrome. Recent findingsThe pressure–volume curve of the respiratory system is a useful tool for the measurement of respiratory system mechanics in patients with acute lung injury or acute respiratory distress syndrome. The pressure–volume curve has a sigmoid shape, with lower and upper points on the inspiratory limb and a point of maximum curvature on the expiratory limb. Visual and mathematical pressure–volume curve analysis may be useful for understanding individual lung mechanics and for selecting ventilator settings. Among the different techniques for acquiring pressure–volume curves at the bedside, the constant slow flow method is the simplest to perform, the most clinically reliable and has the fewest limitations. SummaryMeasurement of pressure–volume curves at the bedside in critically ill patients with acute lung injury or acute respiratory distress syndrome should be considered a useful respiratory monitoring tool to assess physiologic lung status and to adjust ventilator settings, when appropriate, to minimize superimposed lung injury associated with mechanical ventilators.

Thenar oxygen saturation during weaning from mechanical ventilation: an observational study

Our aim was to determine whether thenar tissue oxygen saturation (StO2), measured by noninvasive near-infrared spectroscopy, and its changes derived from an ischaemic challenge are associated with weaning outcome. Our study comprised a prospective observational study in a 26-bed medical–surgical intensive care unit. Patients receiving mechanical ventilation for >48 h, and considered ready to wean by their physicians underwent a 30-min weaning trial. StO2 was measured continuously on the thenar eminence. A transient vascular occlusion test was performed prior to and at the end of the 30-min weaning trial, in order to obtain StO2 deoxygenation and reoxygenation rates, and estimated local oxygen consumption. 37 patients were studied. Patients were classified as weaning success (n=24) or weaning failure (n=13). No significant demographic, respiratory or haemodynamic differences were observed between the groups at inclusion. Patients who failed the overall weaning process showed a significant increase in deoxygenation and in local oxygen consumption from baseline to 30 min of weaning trial, whereas no significant changes were observed in the weaning success group. Failure to wean from mechanical ventilation was associated with higher relative increases in deoxygenation after 30 min of spontaneous ventilation. Failure to wean from mechanical ventilation is associated with increases in deoxygenation after spontaneous ventilation http://ow.ly/pUn5B