1) migration of thrombus or other materials to pulmonary arterial vasculature 2) most common cause is venous thrombus – from “deep veins” of iliac, femoral, and pelvic systems 3) factors that contribute to arterial and venous thrombus formation classically described as Virchow’s triad – stasis of blood, vessel wall injury, hypercoagulable state 4) generally – big embolism, big complications.
Signs and Symptoms
1) tachypnea 2) dyspnea 3) chest pain 4) tachycardia 5) systemic hypotension 6) hemoptysis 7) cyanosis 8) chest splinting 9) friction rub 10) new heart gallop
Characteristic Test Findings
EKG – 1) sinus tachycardia 2) right-sided heart volume overload – Q waves in lead 3, S waves in lead 1, inverted T wabes in lead 3 3) ST segment depression 4) atrial fibrillation Echocardiogram – 5) right ventricle overload 6) tricuspid regurgitation Nuclear medicine – 7) mismatch on xenon ventilation/technetium perfusion scan Laboratory – 8) presence of lupus anticoagulant 9) deficiency of activated protein C/protein S/antithrombin 3 Radiology – 10) deep venous thrombus on Doppler ultrasound 11) mass defect on pulmonary arteriogram/spiral CT 12) Westermark’s sgin (loss of lung vasculature markings at site of emboli) and Hampton’s hump on chest radiograph.
venous thrombus – 1) forms when platelets adhere to venous sinus 2) enlarges by successive deposition of aggregated platelets, leukocytes, and fibrin 3) elongates both antegrade and retrograde
increased incidence with – 1) pregnancy/bedrest 2) postoperatively 3) hip and femur fractures 4) atrial fibrillation 5) post-MI 6) cancer (especially prostate and pancreas) 7) oral contraceptives (especially in smokers) 8) spinal cord injury 9) emphysema 10) sytemic infection 11) renal cell carcinoma (50% risk) 12) tumors in right heart
1) 600,000 cases/200,000 deaths yearly in USA 2) 64% of patient over age of 40 have subclinical PE in lungs at autopsy 3) more common in right lung and lower lobes 4) most common in middle to old age
1) best treatment is prevention 2) low molecular weight or unfractionated heparin 3) pneumatic compression devices on legs (must be placed pre-op and data are mixed on whether they work on the arms 4) early mobilization After PE diagnosis – 5) infusion of unfractionated heparin or administration of low-molecular weight heparin followed by 3-6 months of warfarin or continued low-molecular weight heparin shots 6) surgical removal if life-threatening via modified Trendelenburg procedure 7) tPA, if life-threatening is also an option 8) caval interruption (e.g., Greenfield’s filter), if anticoagulation post-PE is not possible or PE is recurrent while patient is on anticoagulation.
Tips for USMLE
1) paradoxical embolus is embolus that moves from venous system to arterial system via intracardiac defect (most commonly patent foramen ovale, atrial septal defect, and ventricular septal defect) 2) most common EKG finding is sinus tachycardia 3) if question mentions “S1-Q3-T3” pattern on EKG, think PE 4) chronic PE, as opposed to the acute PE described above, are recurrent PE that manifest as pulmonary hypertension leading to pulmonary and heart failure
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