Pulmonary embolism represents a spectrum from incidental subsegmental PE to massive PE causing obstructive shock. The pathophysiology centers on acute right ventricular pressure overload: the thin-walled RV cannot acutely generate pressures >40 mmHg, and sudden increases in pulmonary vascular resistance cause RV dilation, decreased RV output, interventricular septal deviation (D-shaped LV), decreased LV preload, and systemic hypotension. Neurohormonal activation of the sympathetic nervous system and release of vasoactive mediators (serotonin, thromboxane A2) from activated platelets worsen pulmonary vasoconstriction. Risk stratification guides management: massive PE (hypotension/shock) requires thrombolysis, submassive PE (RV dysfunction without hypotension) requires close monitoring with possible escalation, and low-risk PE can be managed as outpatient. The clinician must apply clinical prediction rules, order and interpret advanced diagnostics, prescribe anticoagulation, determine disposition, and manage long-term VTE prevention.