Search Results (6)

Airway pressure release ventilation (APRV) is a protective mechanical ventilation mode for patients with acute respiratory distress syndrome (ARDS) that theoretically may reduce ventilator-induced lung injury (VILI) and ARDS-related mortality. However, there is no standard method to set and adjust the APRV mode shown to be optimal. Therefore, we performed a meta-regression analysis to evaluate how the four individual APRV settings impacted the outcome in these patients. Methods: Studies investigating the use of the APRV mode for ARDS patients were searched from electronic databases. We tested individual settings, including (1) high airway pressure (P_High); (2) low airway pressure (P_Low); (3) time at high airway pressure (T_High); and (4) time at low pressure (T_Low) for association with PaO₂/FiO₂ ratio and ICU length of stay. Results: There was no significant difference in PaO₂/FiO₂ ratio between the groups in any of the four settings (P_High difference −12.0 [95% CI −100.4, 86.4]; P_Low difference 54.3 [95% CI −52.6, 161.1]; T_Low difference −27.19 [95% CI −127.0, 72.6]; T_High difference −51.4 [95% CI −170.3, 67.5]). There was high heterogeneity across all parameters (P_hHgh I² = 99.46%, P_Low I² = 99.16%, T_Low I² = 99.31%, T_High I² = 99.29%). Conclusions: None of the four individual APRV settings independently were associated with differences in outcome. A holistic approach, analyzing all settings in combination, may improve APRV efficacy since it is known that small differences in ventilator settings can significantly alter mortality. Future clinical trials should set and adjust APRV based on the best current scientific evidence available. Full article

Background/Objectives: This study aimed to investigate the hypothesis that an alveolar recruitment maneuver can restore lung compliance to initial values after laparoscopic gynecological surgery. Methods: A total of 31 patients who underwent laparoscopic gynecological surgery were enrolled. Protective mechanical ventilation was applied, and the radial artery was catheterized in all patients. An alveolar recruitment maneuver (incremental and decremental positive end-expiratory pressure) was applied ten minutes after the release of pneumoperitoneum. The respiratory mechanics and blood gas results were recorded at eight different time points: after induction of anesthesia (T1), in the lithotomy position (T2), in the Trendelenburg position (T3), 10 and 90 min after insufflation of carbon dioxide (T4 and T5), in the supine position (T6), after desufflation (T7), and 10 min after an alveolar recruitment maneuver at the end of surgery (T8). Results: Pneumoperitoneum and the Trendelenburg position caused a decline of 15 units in compliance (T7 vs. T1; p < 0.05) compared to baseline. After the alveolar recruitment maneuver, compliance increased by 17.5% compared with the mean value of compliance at time T1 (T8 vs. T1; p < 0.05). The recruitment maneuver had favorable results in patients with low initial compliance (41.5 mL/cmH₂O, IQR: 9.75 mL/cmH₂O), high Body Mass Index 30.32 kg/m² (IQR: 1.05 kg/m²), and high initial plateau airway pressure (16.5 cmH₂O, IQR: 0.75 cmH₂O). Conclusions: Lung compliance does not return to initial values after performing laparoscopic gynecological procedures. However, after the release of pneumoperitoneum, an alveolar recruitment maneuver is beneficial as it improves compliance and gas exchange. Full article

Acute respiratory distress syndrome (ARDS) is associated with a heterogeneous pattern of injury throughout the lung parenchyma that alters regional alveolar opening and collapse time constants. Such heterogeneity leads to atelectasis and repetitive alveolar collapse and expansion (RACE). The net effect is a progressive loss of lung volume with secondary ventilator-induced lung injury (VILI). Previous concepts of ARDS pathophysiology envisioned a two-compartment system: a small amount of normally aerated lung tissue in the non-dependent regions (termed “baby lung”); and a collapsed and edematous tissue in dependent regions. Based on such compartmentalization, two protective ventilation strategies have been developed: (1) a “protective lung approach” (PLA), designed to reduce overdistension in the remaining aerated compartment using a low tidal volume; and (2) an “open lung approach” (OLA), which first attempts to open the collapsed lung tissue over a short time frame (seconds or minutes) with an initial recruitment maneuver, and then stabilize newly recruited tissue using titrated positive end-expiratory pressure (PEEP). A more recent understanding of ARDS pathophysiology identifies regional alveolar instability and collapse (i.e., hidden micro-atelectasis) in both lung compartments as a primary VILI mechanism. Based on this understanding, we propose an alternative strategy to ventilating the injured lung, which we term a “stabilize lung approach” (SLA). The SLA is designed to immediately stabilize the lung and reduce RACE while gradually reopening collapsed tissue over hours or days. At the core of SLA is time-controlled adaptive ventilation (TCAV), a method to adjust the parameters of the airway pressure release ventilation (APRV) modality. Since the acutely injured lung at any given airway pressure requires more time for alveolar recruitment and less time for alveolar collapse, SLA adjusts inspiratory and expiratory durations and inflation pressure levels. The TCAV method SLA reverses the open first and stabilize second OLA method by: (i) immediately stabilizing lung tissue using a very brief exhalation time (≤0.5 s), so that alveoli simply do not have sufficient time to collapse. The exhalation duration is personalized and adaptive to individual respiratory mechanical properties (i.e., elastic recoil); and (ii) gradually recruiting collapsed lung tissue using an inflate and brake ratchet combined with an extended inspiratory duration (4–6 s) method. Translational animal studies, clinical statistical analysis, and case reports support the use of TCAV as an efficacious lung protective strategy. Full article

One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation. Full article

Burn patients are a unique population when considering strategies for ventilatory support. Frequent surgical operations, inhalation injury, pneumonia, and long durations of mechanical ventilation add to the challenging physiology of severe burn injury. We aim to provide a practical and evidence-based review of mechanical ventilation strategies for the critically ill burn patient that is tailored to the bedside clinician. Full article

This study aimed to investigate whether a selective phosphodiesterase-3 (PDE3) inhibitor olprinone can positively influence the inflammation, apoptosis, and respiratory parameters in animals with acute respiratory distress syndrome (ARDS) model induced by repetitive saline lung lavage. Adult rabbits were divided into 3 groups: ARDS without therapy (ARDS), ARDS treated with olprinone i.v. (1 mg/kg; ARDS/PDE3), and healthy ventilated controls (Control), and were oxygen-ventilated for the following 4 h. Dynamic lung–thorax compliance (Cdyn), mean airway pressure (MAP), arterial oxygen saturation (SaO₂), alveolar-arterial gradient (AAG), ratio between partial pressure of oxygen in arterial blood to a fraction of inspired oxygen (PaO₂/FiO₂), oxygenation index (OI), and ventilation efficiency index (VEI) were evaluated every hour. Post mortem, inflammatory and oxidative markers (interleukin (IL)-6, IL-1β, a receptor for advanced glycation end products (RAGE), IL-10, total antioxidant capacity (TAC), 3-nitrotyrosine (3NT), and malondialdehyde (MDA) and apoptosis (apoptotic index and caspase-3) were assessed in the lung tissue. Treatment with olprinone reduced the release of inflammatory mediators and markers of oxidative damage decreased apoptosis of epithelial cells and improved respiratory parameters. The results indicate a future potential of PDE3 inhibitors also in the therapy of ARDS. Full article