Pathophysiology

• Why do you get right ventricular strain in thrombosis?

  Due to increase in pulmonary vascular resistance (due to thrombus & vasoconstriction by hypoxia mediators) -> increased right ventricular afterload -> increased right ventricular muscle stretch, increased wall tension & right ventricular dilatation -> right ventricular strain
• What are the physiological consequences of PE?

  Blocks oxygenated blood to body

  Hypoxic vasoconstriction (changes amount of ROS)

  Increases resistances in pulmonary system

  Gas exchange reduced -> increases alveolar dead space

  Pleural effusion - fluid build up between pleural layer
• What problems can chronic thromboembolic pulmonary HTN cause?

  Right ventricle dilation

  Tricuspid valve reguritation

  Right ventricle failure

  Change in ventricular pressure -> interventricular septum to shift to left

  Compresses left ventricle -> less CO by left ventricle -> affects coronary arteries -> heart ischaemia
• What does a decreased left ventricular compliance cause?

  Diminished diastolic performance -> less filling
• How does the pulmonary circulation react to hypoxia?

  Pulmonary circulation reacts differently to hypoxia -> vasoconstriction -> sends blood to highly oxygenated areas in lungs

  Pulmonary resistance vessels is insensitive to sympathetic & chemical control
• How is an air embolism resolved naturally?

  Air bubble is eventually reabsorbed by surrounding blood or tissue and recovery without intervention may occur
• What is Virchow's triad?

  Venous stasis

  Hypercoagulability

  Endothelial injury
• Pathophys PE

  Damage to endothelium of veins → vasoconstriction → limit blood flow → platelets adhere to endothelium & become activated by collagen & tissue factor → recruit more platelets → activates coagulation cascade → cleave fibrinogen to fibrin → fibrin clot formation → clot grows, reduces blood flow → increase venous pressure

  Clot can breakdown → increased D-dimer

  OR

  High venous pressire -> part of clot breaks off to become thromboembolism -> travel towards heart & can become lodged in lungs → PE
• What are the 2 types of thrombus?

  Arterial

  Venous
• What are the possible fates of a thrombus?

  Lysis - thrombolytic activity of blood

  Propagation - increase in size

  Organisation - thrombus becomes firm & greyish white

  Canalisation - new lumen

  Embolisation - part/all of thrombus becomes dislodged & travels through circulation
• Fill in the blanks

  A) Factor XII

  B) Factor XIIa

  C) Factor XI

  D) Factor XIa

  E) Factor IX

  F) Factor IXa

  G) Factor VIIIa

  H) Tissue factor

  I) Factor VII

  J) Factor VIIa

  K) Factor X

  L) Factor Xa

  M) Factor II

  N) Factor IIa

  O) Factor I

  P) Factor Ia