Module 4A: Venous Thromboembolism Flashcards
DVT risk factors
blood stasis, vessel wall injury, altered blood coagulation
virchow’s triad
endothelial damage, venous stasis, altered coagulation
DVT prevention
↑ mobility, compression stockings, intermittent pneumatic compression devices, prophylactic anticoagulation therapy, lifestyle changes (normal BMI, no smoking, regular exercise)
DVT s/s
swelling, pain, cool or warm to touch, often asymptomatic
PE s/s
dyspnea, tachypnea, ↓ SpO2, chest pain of “pleuritic” nature (worsened by breathing), cough, hemoptysis, anxiety
VTE diagnostic tests
D-Dimer, PTT, PT-INR, platelets (GFR + creatinine if CT w/ contrast is ordered d/t contrast secreted via kidneys), ultrasound - deep veins in legs, CT chest w/ contrast, chest x-ray (CXR)
d-dimer
body’s natural reaction to clot development is fibrinolysis & is produced by action of plasmin on fibrin polymer clot
VTE non-pharmacological interventions
monitor CWMS, measure limb, monitor SpO2, monitor resp status, OPQRSTUV assessment
VTE pharmacological interventions
monitor and treat pain, administer anticoagulants, thrombolytics, PE = administer O2
reasons someone is on an anticoagulant
immobility, history of VTE/pulmonary embolism, dysrhythmias (a-fib), mechanical heart valve, post iM or stroke
anticoagulants
increase clotting time to prevent thrombi from forming or growing larger, inhibit specific clotting factors in coagulation cascade, do not breakdown clot
heparin
IV or SQ, brief-half life (90 mins), increase risk of thrombocytopenia
IV heparin
rapid onset, weight-based, frequent monitoring of PTT and signs of bleeding
SQ heparin
non or infrequent monitoring of PTT, monitor signs of bleeding, usually given BID/TID
heparin antidote
protamine sulfate