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Effect of APRV vs. LTV on Right Heart Function in ARDS Patients: a Single-center Randomized Controlled Study
Acute Respiratory Distress Syndrome (ARDS) is often complicated by Right Ventricular Dysfunction (RVD), and the incidence can be as high as 64%. The mechanism includes pulmonary vascular dysfunction and right heart systolic dysfunction. Pulmonary vascular dysfunction includes acute vascular inflammation, pulmonary vascular edema, thrombosis and pulmonary vascular remodeling. Alveolar collapse and over distension can also lead to increased pulmonary vascular resistance, Preventing the development of acute cor pulmonale in patients with acute respiratory distress. ARDS patients with RVD have a worse prognosis and a significantly increased risk of death, which is an independent risk factor for death in ARDS patients. Therefore, implementing a right heart-protective mechanical ventilation strategy may reduce the incidence of RVD. APRV is an inverse mechanical ventilation mode with transient pressure release under continuous positive airway pressure, which can effectively improve oxygenation and reduce ventilator-associated lung injury. However, its effect on right ventricular function is still controversial. Low tidal volume (LTV) is a mechanical ventilation strategy widely used in ARDS patients. Meta-analysis results showed that compared with LTV, APRV improved oxygenation more significantly, reduced the time of mechanical ventilation, and even had a tendency to improve the mortality of ARDS patients However, randomized controlled studies have shown that compared with LTV, APRV improves oxygenation more significantly and also increases the mean airway pressure. Therefore, some scholars speculate that APRV may increase the intrathoracic pressure, pulmonary circulatory resistance, and the risk of right heart dysfunction but this speculation is not supported by clinical research evidence. In addition, APRV may improve right ventricular function by correcting hypoxia and hypercapnia, promoting lung recruitment and reducing pulmonary circulation resistance. Therefore, it i
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