The Association Between Respiratory Effort Parameters During the First 48 Hours With Clinical Outcomes in Mechanically Ventilated Patients: A Prospective Observational Study.

Overview

Over-assisted mechanical ventilation (MV) is linked to respiratory muscle disuse atrophy, while under-assisted MV can lead to patient self-inflicted lung injury (P-SILI) or respiratory muscle injuries. Both scenarios result in poor outcomes. This hypothesis aims to demonstrate the association between the degree of respiratory effort which was measured by P0.1, predicted Pmus, and predicted Δtranspulmonary pressure (ΔPL) with ventilator-free days (VFD) and 28-day mortality.

Recently, the lung and diaphragm protective strategy is an important consideration when providing mechanical ventilation to critically ill patients. Although mechanical ventilation can be life-saving, improper management can cause harm. The harmful mechanical ventilator setting can result from over-assisted or under-assisted ventilation. Over-assisted ventilation can be caused by too much ventilatory support or calming down patients with high dosages of sedative drugs or muscle relaxants, which negatively affect the operation of the diaphragm leading to diaphragm muscle atrophy and weakness. This can make it more difficult to weaning and lead to prolonged use of mechanical ventilation. It appears that previous study found a correlation between percentage change in diaphragm thickness fraction, as measured by ultrasound, during the first week of mechanical ventilation and prolonged duration of mechanical ventilation, extended length of stay in the ICU, and complications. Additionally, in the study conclusions, a diaphragm thickness fraction of 15-30% during the first three days of mechanical ventilation was associated with the shortest duration of mechanical ventilation and this may potentially help guide the management of respiratory support. On the other hand, the effect of under-assist breathing or allowing excessive respiratory effort could be harmful. Some reported in chronic obstructive pulmonary disease (COPD) exacerbation patients found that the increased negative intra-thoracic pressure potentially causes injury to the diaphragm sarcomeres, which are the muscle fibers responsible for generating force during breathing and it was proportional to the degree of obstruction. And compared light microscopy of the diaphragmatic muscles necropsy in patients who died of COPD with normal subjects. They found muscular necrosis and accumulation of fibrosis and collagen deposits. The cytoplasm was scattered, disrupted, and lipofuscin accumulation with hyper-eosinophilia was observed. In addition, an excessive high respiratory effort can cause lung injury by patient-self known as patient self-inflicted lung injury (P-SILI), a theory first mentioned that the increased magnitude of negative intrathoracic pressure during inhalation may cause the fluid shift from the pulmonary capillaries to the alveoli causing pulmonary edema. This is relevant to the observational studies that the occurrence of negative intrathoracic pressure during large inhalations in obstruction airway patients, such as tracheal stenosis, also results in pulmonary edema. In latterly confirmed this hypothesis. Subsequent studies have supported this phenomenon and overall could be explained through the increase of transpulmonary pressure, pendelluft phenomenon and patient-ventilator asynchrony (PVA). However, no current studies determine the relationship between respiratory effort measurement during mechanical ventilation and clinical outcomes. Therefore, we conduct the study to determine the relationship between respiratory effort parameters and clinical outcomes.