CVS Module
AIM Concept Integration
Venous Thromboembolism: Deep Vein Thrombosis & Pulmonary Embolism
Connect risk factors → thrombus formation → DVT → embolization → pulmonary vascular obstruction → diagnosis → treatment.
1. THE TOPIC IN ONE CONNECTED FLOW
Venous thromboembolism is best understood as one continuous process. A patient develops a venous thrombus because of stasis, endothelial injury or increased coagulation tendency. The thrombus may remain in the deep veins and cause local leg symptoms, or part of it may detach and obstruct the pulmonary circulation, producing pulmonary embolism and, in severe cases, right ventricular failure and shock.
Immobility • surgery • malignancy • hypercoagulable state
Stasis • endothelial injury • hypercoagulability
Venous obstruction → unilateral pain, swelling, warmth
Thrombus detaches → right heart → pulmonary arteries
V/Q mismatch + increased pulmonary vascular resistance
Dyspnea • pleuritic pain • RV strain • shock if severe
Anticoagulation ± reperfusion when hemodynamically unstable
2. KEY CLINICAL CONNECTIONS
Unilateral pain + swelling + VTE risk context → increased clinical probability of DVT → D-dimer may help rule out disease when probability is low → non-compressible deep vein on ultrasound supports DVT.
Deep venous thrombus → embolization to pulmonary arteries → reduced perfusion of ventilated lung → V/Q mismatch → hypoxemia, tachypnea and pleuritic chest pain → CTPA demonstrates pulmonary arterial filling defect.
Large embolic burden → sudden rise in pulmonary vascular resistance → acute right ventricular pressure overload → reduced left ventricular filling → reduced cardiac output → hypotension, syncope or shock.
Confirmed DVT or stable PE → anticoagulation prevents further thrombus propagation and recurrent embolization. PE with persistent hypotension or shock → urgent stabilization + assessment for reperfusion therapy.