When a thrombus lodges in the pulmonary vasculature, it creates mechanical obstruction and triggers reflex vasoconstriction via thromboxane A2 and serotonin release from activated platelets. The obstructed segment becomes ventilated dead space — alveoli receive air but no blood flow, preventing gas exchange. Simultaneously, blood is shunted to non-obstructed lung zones, creating areas of low V/Q ratio and intrapulmonary shunting. In massive PE (>50% vascular occlusion), acute right ventricular afterload increases dramatically. The thin-walled RV cannot generate pressures >40 mmHg acutely, leading to RV dilation, interventricular septal bowing leftward (D-sign on echo), reduced LV filling, decreased cardiac output, and obstructive shock. Neurohormonal activation (catecholamine surge) initially compensates with tachycardia, but progressive RV ischemia from elevated wall tension and decreased coronary perfusion pressure leads to cardiovascular collapse.