Lecture 68 - Dx and Tx of PE Flashcards
what is a DVT? where is it most likely to originate?
DVT = Deep venous thrombosis
○ Femoral, popliteal, greater saphenous – most commonly
Pelvic veins
Upper extremity veins – but usually catheter associated
What is a PE and how does it kill you? q
Pulmonary Embolism
• Results in an anatomical obstruction --- resulting In physiological disruption
○ Effects on the RV: Increased RV Afterload
○ Death is usually from RV failure
what is the recurrence rate following a thrombo-embolytic event ?
rank the following contexts in which a DVT/PE can occur in terms of likelihood of recurrence: surgically provoked, non surgically provoked, idiopathic
Recurrence: Following thromboembolic event – recurrence rate at 8 years is 30%
§ Surgery: highly unlikely to manifest another clot
§ Non-surgical provoked event (eg truama) – higher risk
§ Idiopathic clot – most likely to have recurrence
PE Physiology: what happens to V/Q?
how do patients typically present ?
what does this mean in terms of blood gas levels?\
Creates Dead Space: (High V/Q) (low perfusion, normal ventilation) —
Patients present dyspnea but hyperventilating and able to get expel sufficient CO2 such that they are Hypocapnic
In what context might patients with PE present with hypercapnea?
COPD
Is it possible for patients with PE to present with hypoxemia?
Describe this physiology?
○ Hypoxemia is Observed – Some areas of the Lung Develop Low V/Q Physiology
- Bronchoconstriction, areas of atelectasis
§ Loss of surfactant; also leads to atelectasis
§ Pulmonary HTN can lead to shunting –
High RV Pressure can shunt through a Patent Foramen Ovale
Risk Factor for PE: what is virchow’s triad?
Increased Clotting Risk: Virchows Triad -
Venous stasis
Vascular/Endothelial Injury
Hypercoagulability
what causes venous stasis?
What causes vascular/endothelial injury?
what types of surgery most commonly lead to DVT/PE?
Venous Stasis -Immobility
Vascular/Endothelial Injury – surgery, trauma, post partum, vascular catheters
hip, knee, vascular)
what are some inherited Hypercoagulopathies ?
Factor V Leiden (protein C resistnace; most common inherited disorder)
□ Antithrombin Deficiency; Protein C deficiency, Protein S deficiency
Prothrombin Gene mutations
what are some acquired hypercoagulopathies?
□ Malignancy
□ Hormone replacement
□ Oral Contraceptives
□ Antiphospholipid antibody syndrome
□ Elevated homocysteine
describe a common presentation for DVT vs PE?
§ PE – Sudden onset dyspnea and CP (can be insidious, can be pleuritic in nature);+/- hemoptysis
§ DVT – Asymmetric leg swelling and pain
□ Risk factors: Surgery, OCP, immobilization, catheters
Physical exam findings for DVT?
what is homan’s sign?
Is it useful for diagnosis of DVT?
leg edema, warmth, or asymmetry; Palpable cord (indurated, tender subQ vein)
Homan’s = pain in calf with dorsiflexion
Not useful for DVT Dx
Physical exam findings for PE?
tachycardic, tachypnic, febrile, hypotensive (severe clot)
Heart Exam – possible loud P2 or tricuspid murmur (LLSB)
Best tool for diagnosis of DVT?
what lab is commonly drawn
○ Compression Ultrasound – best test; non invasive, quick, accurate
○ D Dimer – a fibrin degradation product
§ Sensitive but not specific
Tools for Dx of PE?
which is the current standard evaluative test for PE?
EKG, CXR, ECHo, VQ Scan, Pulmonary Arteriogram , CT Scan with IV Contrast
standard: CT Scan with IV Contrast
Classical EKG findings of a PE?
S1Q3T3
S1 – S waves in lead 1 = RBBB
Lead III Q waves or T wave inversion = right sided pressure and volume overload causing repolarization abnormalities
Classical CXR findings for PE:
CXR — A “normal” CXR with someone presenting with sudden onset hypoxemia and SOB is a PE!!!
how is an echocardiogram use?
how is V/Q scan used ?
Echo – § Can evalutae for Tamponade, aortic disection, MI
§ Can help assess right heart function
Right Ventricular Dilation implies – “submassive” PE
V/Q Scan – § Look for areas that have mismatch
In PE – Getting air but not blood
What is the difference between a massive and submassive PE?
Some Classifications:
• Massive PE – big enough to effect blood pressure (hypotension)
• "Submassive PE" -- big enough to lead to Right heart strain, dilation
Clot SIZE visualized on imaging – does not determine massive vs submassive
DVT/PE Prophylaxis?
• Minimize Risk Factors:
• Low dose prophylactic anticoagulation therapy
○ unfractionated heparin, low molecular weight heparin
• Mechanical
○ venous compression devices
Three methods to treat DVT/PE?
Anticoagulation – LMW Heparin, Unfractioned Heparin (paraenteral), Wafarin (oral)
Mechanical – IVC filter, Surgical Embolectomy
Thrombolytic Therapy – TPA – only for massive PE
when should you initiate treatment for PE?
for how long do you treat?
Initiate Treatment (with LMW Heparin) before getting confirmatory results — once it is suspected – or high pre test probability
- Temporary risk factor — 3 months – surgery, fracture
- Idiopathic , recurrent or malignancy – life
Long term Complications of PE
Chronic Thromboembolic Pulmonary Hypertension –
====High clot burden in the pulmonary vasculature; RV can’t handle this resistance… results in Pulm HTN
