Pulmonary Embolism

Pathophysiology

Leading source of PE is DVT in the legs from the proximal veins. 20% of VTE in the calves end up extending into the proximal veins as opposed to resolving spontaneously
Upper extremity DVT in the axillary or subclavian veins result in PE in only 10-15% of patients.
Classically, VTE is thought to be result of Virchow triad of endothelial cell activation, stasis, and hypercoagulability though inflammation is now also thought of as a key precipitant

PE represents 1/3 of symptomatic VTE
Acquired risks include advanced age, history of prior VTE, obesity, and active cancer
Hereditary risk factors include genetic conditions associated with hypercoagulability of the blood (e.g. Factor V Leiden, protein C and prothrombin gene mutations)
Triggering factors are surgery, immobilization, and pregnancy (and other high estrogen-related states)
Unprovoked VTE (or VTE without any risk or trigger factors) make up almost half of first episodes of VTE

Patients living in zip codes with lower socioeconomic status have higher mortality rates in the hospital and are less likely to receive thrombolysis as compared with patients located in zip codes with higher socioeconomic status

Acute

Typical symptoms include dyspnea at rest (50%) and pleuritic chest pain (39%)
Massive PE can have dyspnea at rest, hypotension, and syncope due to hypoxemia and low cardiac output

Look for evidence of DVT (edema, erythema, and warmth in the extremity) which is found in 50% of patients with PE. Wells Scoring can be used to determine probability of DVT.
Tachycardia and tachypnea are frequent signs
Increased pulmonary artery pressure from increased pulmonary vascular resistance (due to vascular obstruction and associated inflammatory mediators, vasoconstriction from hypoxemia, and other neurohumoral agents) can result in right heart failure from the increased afterload on the right ventricle.
- Signs of right heart failure include gallop rhythm, widely split second heart sound with loud pulmonic component, distended jugular veins, and right ventricular heave

Use validated risk assessment models for PE to evaluate the pretest probability of VTE
- If low or moderate, can consider use of d-dimer to rule out PE
- If high, diagnosis should be assessed by computed tomography pulmonary angiography (CTPA)

For low-risk PE, anti-coagulation is all that is necessary
For massive PE (sustained hypotension), thrombolytics and / or embolectomy maybe used. some submassive PEs (evidence of heart damage) may also qualify.
if unprovoked PE, evaluate for underlying causes

Essien, Eno-Obong, et al. “Pulmonary Embolism.” Medical Clinics of North America, vol. 103, no. 3, 1 May 2019, pp. 549–564
Goldhaber, Samuel. “Pulmonary Embolism.” Braunwald’s Heart Disease: a Textbook of Cardiovascular Medicine, by Douglas P. Zipes, Elsevier, 2019, pp. 1681–1698
McGee, Steven R. “Edema and Deep Vein Thrombosis.” Evidence-Based Physical Diagnosis, by Steven R. McGee, Elsevier, 2018, pp. 473-480.
Weitz, Jeffrey I., and Jeffrey S. Ginsberg. “Venous Thrombosis and Embolism.” Goldman-Cecil Medicine, by Lee Goldman et al., Elsevier, 2019, pp. 476-486

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