Week 2: Pulmonary embolism Flashcards

1
Q

venous thromboembolic (VTE) diseases summary

A

type-hemodynamics-treament

  1. DVT- stable -anticoagulation
  2. Non-massive PE-stable-anticoag
  3. Massive PE-unstable-thrombolysis
    - massive PE can cause right heart failure, long term consequence is chronic pulmonary HTN
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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
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3
Q

Pathophysiology of PE: respiratory consequences

A
  1. decreased perfusion from occlusion of pulmonary artery. Leads to increased dead space with decreased CO2 excretion
    - compensation: hyperventilation, causes hypocapnia
  2. 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
  3. widened A-a gradient
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4
Q

Cardiac/hemodynamic consequences of PE

A
  1. increased pulmonary vascular resistance due to occlusion of pulmonary artery
    - usually not significant unless large
  2. 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
  3. release of mediators may result in vasoconstriction and increase in pulmonary vascular resistance
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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
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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
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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
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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
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9
Q

Diagnosis of DVT

A

-Doppler Ultrasound

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10
Q

Treatment for PE

A
  1. 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
  2. Thrombolytics to clot bust
    - tPA, urokinase
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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
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