Ventilator-Induced Lung Injury: Causes, Risks, and Prevention

Introduction

Ventilator-Induced Lung Injury (VILI) is an acute lung injury that occurs as a result of volutrauma and excessive oxygen use. While it is not a new concept, the injury occurs when the lung is damaged by the action of mechanical ventilation. Mechanical ventilation has been widely used to support acutely ill patients for many decades; however, clinicians and other medical practitioners have become increasingly aware of its complications and drawbacks, despite its life-saving potential. Since its introduction to medical practice, the use of mechanical ventilation for treating patients with acute respiratory failure has attracted significant concern. Research findings consistently indicate that mechanical ventilation may severely affect a patient's lungs, with Ventilator-Induced Lung Injury being one of the most significant possible adverse effects.

The primary cause of Ventilator-Induced Lung Injury is the over-stretching of the alveoli and airways. This over-stretching is mainly caused by mechanical ventilation, as the flow of gas into the lung tends to follow the path of least resistance during the process. During mechanical ventilation, collapsed areas of the lung or those filled with secretions become underinflated, while relatively normal areas become overinflated. As a result, these overinflated lung regions are likely to become injured or over-distended — an outcome that can be minimized through the use of smaller tidal volumes.

Etiology of VILI

While several early clinical and experimental studies suggested that mechanical ventilation could have adverse effects on the lung, other studies attempted to refute this finding (Dreyfuss & Saumon, 1998). Despite the lack of a clear medical equivalent to experimental observations, the probability that mechanical ventilation can actually worsen acute lung disease is now widely accepted. The demonstration of superimposed Ventilator-Induced Lung Injury during human acute respiratory distress syndrome may be deceptive, given that the concept is largely derived from animal studies. Nevertheless, it has contributed to a fundamental re-evaluation of mechanical ventilation for patients with acute lung diseases and forms the basis of current trends in clinical practice.

In earlier years, many patients with acute lung dysfunction could tolerate mechanical ventilation for prolonged periods without adverse consequences. Over the past two decades, it has become generally accepted that mechanical ventilation can either initiate or exacerbate lung injury, contributing to patient mortality and morbidity. This process contributes to VILI by affecting lung surfactant and compliance function and by causing air leaks (Tremblay & Slutsky, 2006).

Several studies have been conducted to determine whether mechanical ventilation can produce lung injury beyond air leaks, and to identify the specific ventilator settings at which such injuries occur. These analyses have demonstrated that ventilating normal lungs at low pressures does not cause severe injury, whereas ventilation at high pressures tends to produce perivascular edema. Furthermore, ventilation at high airway pressures without positive end-expiratory pressure results in severe lung injury and even death. This is because positive end-expiratory pressure confers protection from alveolar edema associated with high inspiratory pressure ventilation.

The overall degree of lung distention — specifically, lung volume at end-inspiration — is generally the major determinant of VILI severity. This is because injury and edema typically occur when a particular threshold of lung over-inflation is reached (Ricard, Dreyfuss & Saumon, 2003). Lung over-inflation occurs when ventilation is increased at a specific end-inspiratory pressure. Conversely, when positive end-expiratory pressure is added to achieve a similar end-inspiratory pressure, it tends to slow the development of edema and reduce the severity of tissue injury. However, positive end-expiratory pressure does not prevent changes in microvascular permeability, and greater edema occurs when it contributes to additional over-inflation.

Significance of Lung Distention

It is now well established that ventilation-induced pulmonary edema is the outcome of significant changes in the permeability of the alveolar-capillary barrier. Edema severity is likely to be compounded when small increases in microvascular transmural pressure add to the effects of altered permeability. In response to relatively high airway pressures, edema develops more slowly in larger animals, a finding that adds complexity to the clinical picture.

High mechanical ventilation without positive end-expiratory pressure may reduce the aerated lung volume and gradually contribute to mechanical non-uniformity. The resulting lung inhomogeneity facilitates over-inflation of the more distensible, relatively healthier zones, creating a positive feedback loop that further aggravates injury.

Conclusion

Ventilator-Induced Lung Injury is one of the common illnesses that occur among patients with acute lung injury. This disease is mainly attributed to the use of a mechanical ventilator to save these patients, though there are other risk factors that contribute to the injury.