Ventilator-Induced Mechanical Stress and Lung Vascular Dysfunction

Abstract

By virtue of their design as a gas-exchange organ, lungs are constantly exposed to mechanical stimulation associated with inflation deflation cycles. Pulmonary vasculature experiences mechanical forces resulting from blood circulation and respiratory cycles. These forces are transduced onto pulmonary vessels in the form of shear stress, intravascular hydrostatic pressure, and tensile stress. Normally, mechanical loads on pulmonary vasculature are well tolerated even during intense exercise, several-fold elevation of inhaled air pressure during scuba diving, or ascension to high altitude. However, extreme loads experienced by elite athletes elevate the pulmonary capillary pressure beyond physiological limits and may cause transient pulmonary vascular leak. In the clinical setting, mechanical ventilation of patients at high tidal volumes leads to pulmonary edema and a severer complication, acute respiratory distress syndrome (ARDS). Chronic elevation of pulmonary artery pressure due to cardiogenic or primary pulmonary hypertension leads to vascular remodeling, vascular occlusion, and severe lung dysfunction. Relatively rare cases of pulmonary vascular leak and edema have been described when a lung collapsed for several days as a result of pneumothorax is rapidly re-expanded. In such cases, the protein concentration in sputum is very high during the onset of so-called pulmonary re-expansion edema (RPE), suggesting that RPE belongs to a type of permeability pulmonary edema caused by pulmonary microvascular dysfunction. These examples demonstrate the significance of the physiologic biomechanical milieu in the pulmonary vascular barrier regulation and proper functioning of the lung as a gas-exchange organ.