Alexander B. Adams

Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury

Elevated lung volumes and increased pleural pressures associated with recruitment maneuvers (RM) may adversely affect pulmonary vascular resistance and cardiac filling or performance. We investigated the hemodynamic consequences of three RM techniques after inducing acute lung injury. Design:Prospective, randomized, controlled experimental study. Setting:Hospital research laboratory. Subjects:Thirteen anesthetized, mechanically ventilated pigs. Interventions:We induced three types of acute lung injury: oleic acid injury (n = 4); ventilator-induced lung injury (n = 4); and pneumonia (n = 5). All three models were designed to initiate a similar severity of oxygenation impairment. RM methods tested were sustained inflation, incremental positive end-expiratory pressure (PEEP) with a limited peak pressure, and pressure-controlled ventilation with increased PEEP and a fixed driving pressure. From a baseline PEEP of 8 cm H2O, all interventions were tested using post-RM PEEP levels of 8, 12, and 16 cm H2O. Cardiac output by thermodilution and systemic and pulmonary artery pressures were measured frequently during the RM and for 15 mins after its completion. Measurements and Main Results:During the RM, cardiac output decreased to a greater extent in the pneumonia model (0.49 of baseline cardiac output) than in the oleic acid injury (0.67 of baseline) or ventilator-induced lung injury (0.79 of baseline) models. Cardiac output recovered to the baseline value by 5 mins post-RM in oleic acid injury and ventilator-induced lung injury models. However, cardiac output remained decreased 15 mins post-RM in the pneumonia model. There were no differences in hemodynamic parameters among RM methods in oleic acid injury and ventilator-induced lung injury models. In the pneumonia model, however, cardiac output decreased to a greater extent during the RM with sustained inflation (to 0.33 of baseline cardiac output) compared with pressure-controlled ventilation (to 0.68 of baseline). Conclusions:We conclude that RM transiently but profoundly depressed cardiac output in three models of acute lung injury. The results imply that a lung recruiting maneuver should be used with caution, especially when using sustained inflation in the setting of pneumonia.

Intercomparison of recruitment maneuver efficacy in three models of acute lung injury

To compare the relative efficacy of three forms of recruitment maneuvers in diverse models of acute lung injury characterized by differing pathoanatomy. Design:We compared three recruiting maneuver (RM) techniques at three levels of post-RM positive end-expiratory pressure in three distinct porcine models of acute lung injury: oleic acid injury; injury induced purely by the mechanical stress of high-tidal airway pressures; and pneumococcal pneumonia. Setting:Laboratory in a clinical research facility. Subjects:Twenty-eight anesthetized mixed-breed pigs (23.8 ± 2.6 kg). Interventions:The RM techniques tested were sustained inflation, extended sigh or incremental positive end-expiratory pressure, and pressure-controlled ventilation. Primary Measurements:Oxygenation and end-expiratory lung volume. Main Results:The post-RM positive end-expiratory pressure level was the major determinant of post-maneuver Pao2, independent of the RM technique. The pressure-controlled ventilation RM caused a lasting increase of Pao2 in the ventilator-induced lung injury model, but in oleic acid injury and pneumococcal pneumonia, there were no sustained oxygenation differences for any RM technique (sustained inflation, incremental positive end-expiratory pressure, or pressure-controlled ventilation) that differed from raising positive end-expiratory pressure without RM. Conclusions:Recruitment by pressure-controlled ventilation is equivalent or superior to sustained inflation, with the same peak pressure in all tested models of acute lung injury, despite its lower mean airway pressure and reduced risk for hemodynamic compromise. Although RM may improve Pao2 in certain injury settings when traditional tidal volumes are used, sustained improvement depends on the post-RM positive end-expiratory pressure value.

Effect of core body temperature on ventilator-induced lung injury

ObjectiveVentilator-induced lung injury is a risk in patients requiring elevated ventilatory support pressures. We hypothesized that thermal stress modulates the development of ventilator-induced lung injury. DesignExperimental study. SettingUniversity laboratory. SubjectsAnesthetized rabbits. InterventionsTwo experimental studies were designed to determine the role of temperature as a cofactor in ventilator-induced lung injury. In the first study, three groups of anesthetized rabbits were randomized to be ventilated for 2 hrs at core body temperatures of 33, 37, or 41°C while ventilated with pressure control ventilation of 15/3 cm H2O (noninjurious settings—control) or 35/3 cm H2O (potentially injurious settings—experimental). To exclude effects arising from cardiac output fluctuations or from extrapulmonary organs, an isolated lung model was used for the second study, perfused at a fixed rate and studied at either 33°C or 41°C. Measurements and Main ResultsIn the first study, the hyperthermic group compared with the hypothermic animals had significantly reduced mean Pao2 (−114 vs. + 14 mm Hg, p < .05), increased lung edema formation (mean wet weight/dry weight ratio of 8.1 vs. 5.7), and altered pressure-volume curves. The hyperthermic isolated, perfused lungs had an increased ultrafiltration coefficient, formed more edema, and experienced greater alveolar hemorrhage than hypothermic lungs. ConclusionsIn two studies of ventilator-induced lung injury in rabbits, maintaining hyperthermia compared with hypothermia augmented the development of lung injury. Similar results from both the in vivo and isolated, perfused lung studies suggest that the observed effects were not due to cardiovascular factors or consequences of heating nonpulmonary organs.

Relative roles of vascular and airspace pressures in ventilator-induced lung injury.

ObjectiveTo determine whether elevations in pulmonary vascular pressure induced by mechanical ventilation are more injurious than elevations of pulmonary vascular pressure of similar magnitude occurring in the absence of mechanical ventilation. DesignProspective comparative laboratory investigation. SettingUniversity research laboratory. SubjectsMale New Zealand white rabbits. InterventionsThree groups of isolated, perfused rabbit lungs were exposed to cyclic elevation of pulmonary artery pressures arising from either intermittent positive pressure mechanical ventilation or from pulsatile perfusion of lungs held motionless by continuous positive airway pressure. Peak, mean, and nadir pulmonary artery pressures and mean airway pressure were matched between groups (35, 27.4 ± 0.74, and 20.8 ± 1.5 mm Hg, and 17.7 ± 0.22 cm H2O, respectively). Measurements and Main Results Lungs exposed to elevated pulmonary artery pressures attributable to intermittent positive pressure mechanical ventilation formed more edema (6.8 ± 1.3 vs. 1.1 ± 0.9 g/g of lung), displayed more perivascular (61 ± 26 vs. 15 ± 13 vessels) and alveolar hemorrhage (76 ± 11% vs. 26 ± 18% of alveoli), and underwent larger fractional declines in static compliance (88 ± 4.4% vs. 48 ± 25.1% decline) than lungs exposed to similar peak and mean pulmonary artery pressures in the absence of tidal positive pressure ventilation. ConclusionsIsolated phasic elevations of pulmonary artery pressure may cause less damage than those occurring during intermittent positive pressure mechanical ventilation, suggesting that cyclic changes in perivascular pressure surrounding extra-alveolar vessels may be important in the genesis of ventilator-induced lung injury.

Effects of ventilatory pattern on experimental lung injury caused by high airway pressure

ObjectiveTo determine the influence of clinician-adjustable ventilator settings on the development of ventilator-induced lung injury, as assessed by changes in gas exchange (Pao2), compliance, functional residual capacity, and wet weight to dry weight ratio. DesignRandomized in vivo rabbit study. SettingHospital research laboratory. SubjectsForty-four anesthetized, mechanically ventilated adult rabbits. InterventionsVentilation for 2 hrs with pressure control ventilation at 45 cm H2O, Fio2 = 0.6, and randomization to one of five ventilatory strategies using combinations of positive end-expiratory pressure (3 or 12 cm H2O), inspiratory time (0.45, 1.0, or 2.0 secs), and frequency (9 or 23/min). Measurements and Main ResultsAmong the ventilator strategies applied, PEEP at 12 cm H2O (elevated positive end-expiratory pressure) and inspiratory time at 0.45 secs (reduced inspiratory time) best preserved Pao2 (p < .003) and compliance (p < .035). During injury development, two consistent changes were observed: Tidal volume increased, and airway pressure waveform was transformed by extending the time to attain target pressure. ConclusionsIn this preclinical model, lung injury was attenuated by decreasing inspiratory time. As lung injury occurred, tidal volume increased and airway pressure waveform changed.

Inspiratory tidal volume sparing effects of tracheal gas insufflation in dogs with oleic acid-induced lung injury

PURPOSEnTracheal gas insufflation (TGI) improves the efficiency of conventional mechanical ventilation (CMV) by reducing the series dead space of the airways. Consequently, application of TGI as an adjunct to CMV may permit reducing tidal volume (VT) while limiting CO2 retention. We tested the extent to which panexpiratory TGI allows reduction of VT while maintaining PaCO2 constant in an oleic acid-induced lung injury model.nnnMETHODSnWe studied six anesthetized, paralyzed, and mechanically ventilated dogs. Oleic acid injury was induced by injecting 0.09 mL/kg of oleic acid into the right atrium. After stabilization of lung injury the VT-sparing effect of TGI was tested by progressively increasing catheter flow rate (Vc) from 2 to 5, 10, and 15 L/min while decreasing VT by an amount that maintained PaCO2 constant (approximately 47 mm Hg) with respect to baseline (Vc = 0 L/min).nnnRESULTSnTidal volume was decreased from a baseline value of 0.360 +/- 0.030 L to 0.238 +/- 0.054 L at Vc of 15 L/min. The reduction in VT was associated with a decrement in peak and end-inspiratory plateau airway opening pressure from 32 +/- 3 to 28 +/- 6 cm H2O and from 25 +/- 2 to 21 +/- 3 cm H2O, respectively. Total physiological dead space fraction decreased from a baseline value of 0.60 +/- 0.08 to 0.31 +/- 0.20 during TGI at 15 L/min. TGI did not affect cardiac output, PaO2, or pulmonary venous admixture.nnnCONCLUSIONnWe conclude that TGI can be a useful adjunct to CMV during acute lung injury to limit VT while avoiding CO2 retention.

Experimental intra-abdominal hypertension influences airway pressure limits for lung protective mechanical ventilation.

BACKGROUND Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) may complicate monitoring of pulmonary mechanics owing to their impact on the respiratory system. However, recommendations for mechanical ventilation of patients with IAH/ACS and the interpretation of thoracoabdominal interactions remain unclear. Our study aimed to characterize the influence of elevated intra-abdominal pressure (IAP) and positive end-expiratory pressure (PEEP) on airway plateau pressure (PPLAT) and bladder pressure (PBLAD). METHODS Nine deeply anesthetized swine were mechanically ventilated via tracheostomy: volume-controlled mode at tidal volume (VT) of 10 mL/kg, frequency of 15, inspiratory-expiratory ratio of 1:2, and PEEP of 1 and 10 cm H2O (PEEP1 and PEEP10, respectively). A tracheostomy tube was placed in the peritoneal cavity, and IAP levels of 5, 10, 15, 20, and 25 mm Hg were applied, using a continuous positive airway pressure system. At each IAP level, PBLAD and airway pressure measurements were performed during both PEEP1 and PEEP10. RESULTS PBLAD increased as experimental IAP rose (y = 0.83x + 0.5; R2 = 0.98; p < 0.001 at PEEP1). Minimal underestimation of IAP by PBLAD was observed (−2.5 ± 0.8 mm Hg at an IAP of 10–25 mm Hg). Applying PEEP10 did not significantly affect the correlation between experimental IAP and PBLAD. Approximately 50% of the PBLAD (in cm H2O) was reflected by changes in PPLAT, regardless of the PEEP level applied. Increasing IAP did not influence hemodynamics at any level of IAP generated. CONCLUSION With minimal underestimation, PBLAD measurements closely correlated with experimentally regulated IAP, independent of the PEEP level applied. For each PEEP level applied, a constant proportion (approximately 50%) of measured PBLAD (in cm H2O) was reflected in PPLAT. A higher safety threshold for PPLAT should be considered in the setting of IAH/ACS as the clinician considers changes in VT. A strategy of reducing VT to cap PPLAT at widely recommended values may not be warranted in the setting of increased IAP.