Week 2: Pulmonary embolism Flashcards
1
Q
venous thromboembolic (VTE) diseases summary
A
type-hemodynamics-treament
- DVT- stable -anticoagulation
- Non-massive PE-stable-anticoag
- Massive PE-unstable-thrombolysis
- massive PE can cause right heart failure, long term consequence is chronic pulmonary HTN
2
Q
Risk factors for PE
A
Virchow's triad 1. Venous stasis -CHF, immobility, obesity, surgery, trauma 2. Endothelial injury -hx of VTE, trauma, catheters 3. hypercoaguable states -inherited, acquired MAJOR RISK FACTORS -major surgery, lower extremities fractures, pregnancy, h/o VTE, malignancy, varicose veins, prolonged immobility
3
Q
Pathophysiology of PE: respiratory consequences
A
- decreased perfusion from occlusion of pulmonary artery. Leads to increased dead space with decreased CO2 excretion
- compensation: hyperventilation, causes hypocapnia - Decreased perfusion leads to decreased surfactant synthesis
- more difficult for alveoli to stay open, more prone to collapse
- hypocapnia may cause bronchioconstriction of small airways
- hypoxemia and atelectasis - widened A-a gradient
4
Q
Cardiac/hemodynamic consequences of PE
A
- increased pulmonary vascular resistance due to occlusion of pulmonary artery
- usually not significant unless large - pulmonary HTN and RV failure
- if PE is large enough and cardiopulmonary reserve is poor
- RV dilation compresses LV, leads to decrease CO and hypotension, syncope or death - release of mediators may result in vasoconstriction and increase in pulmonary vascular resistance
5
Q
Possible outcomes of PE
A
- usually not ischemia infart because dual perfusion from bronchial and pulmonary
- Most PEs come from DVTs
1. fragmentation of emboli+clot lysis - no changes
2. reorganization and partial recanalization (~3 months)
3. infarction leading to scar formation
6
Q
Symptoms and signs of PE
A
SYMPTOMS -acute dyspnea -pleuritic chest pain -hemoptysis -anxiety, cough, palpitation -sycope, rare SIGNS -tachypnea -tachycardia, S4, accentuated P2 -fever, friction rub -signs of DVT -evidence of R heart failure
7
Q
Radiographic findings
A
- X-ray: usually normal. May see prominent PA, pleural effusion, decreased perfusino (westermark’s sign), wedge shaped infarct (Hamptom’s hump)
- CT w/ contrast: FIRST LINE. appear as filing defect and may find vessel cut off
8
Q
D-dimer test for PE
A
- degradation product of cross-linked fibrin
- good sensitivity but low specificity
- a negative D dimer rules out PE but a positive can’t diagnose
9
Q
Diagnosis of DVT
A
-Doppler Ultrasound
10
Q
Treatment for PE
A
- anticoagulation to prevent reoccurrence of PE
- goal is PTT 2x normal achieved within 24 hours
- if stable; LMWH or fondaparonox
- if unstable: IV heparin
- followed by oral coumadin for 3-6 months - Thrombolytics to clot bust
- tPA, urokinase
11
Q
Pulmonary HTN
A
- when mPAP is greater than 25 mmHg
- characteristic feature: remodeling of pulmonary vasculature
- plexogenic lesion: intralumenal growth of fibrous network, from endothelial or fibroblasts in the intimalbasement
- thrombogenic arteriopathy: clot organization