PE PBL notes

1) Anatomy of the lungs and its circulation

  • Divided into upper respiratory tract, lower respiratory tract, muscles (intercostal, abdominal, diaphragm), and skeletal elements (ribs, sternum, costal cartilage)

  • Functionally divided into conducting zone and respiratory zone

  • Blood supply: pulmonary circulation (gas exchange) + bronchial circulation (supplying lungs with blood + O2)

2) Role of peripheral and central chemoreceptors in the control of breathing

  • Chemoreceptors are sensory receptors activated by chemical stimuli (O2 level in blood + CO2 level in brain)

  • Peripheral: located on bifurcation of carotid body + aortic arch

    • Innervated by CN 9 and 10

    • Increased discharge during hypoxia

    • Signal sent to respiratory center (via cranial nerves) → Increased ventilation

  • Central: located in medulla oblongata exposed to CSF

    • Respond to H+ concentration (can't cross BBB) but not directly to CO2 (can cross BBB)

    • When blood CO2 increases, it diffuses into CSF and combines with H2O → produce HCO3 + H+

    • H+ increase detected and activated by central chemoreceptors → signals to respiratory center → hyperventilation

    • Directly respond to CSF pH (H+) and indirectly to CO2 (don't directly detect arterial CO2 tension)

    • CO2 decreases → signals to respiratory center → hyperventilation is reversed

3) Causes of PE and the mechanisms by which they cause it

  • Why do clots form:

    • Inactivity: stasis of blood

    • Causes inactivity of skeletal muscle pump → slow blood flow → increased platelets + clotting factor contact → platelet aggregation + clotting factor activation contact → clot

    • Direct injury to the vascular endothelial cells

      • Pregnancy: growing baby compresses nearby veins → slow blood flow → increased platelets + clotting factors contact with vascular endothelium → platelet aggregation + clotting factor activation

        • Hypercoagulable state (to decrease the risk of hemorrhage) mediated by increased clotting factors production, decrease in protein C (anticoagulation factor), and increase in fibrinogen level

      • Surgery: damage to endothelial cells → exposure of collagen + tissue factor → platelet aggregation + clotting factor activation

      • Antithrombin 3 (anticoagulation protein made by liver) deficiency: inherited condition of increased blood clot formation

    • Works by binding to excess thrombin and clotting factors (7, 9, 10, 11, 12)

      • Hormone replacement therapy: estrogen stimulates liver to produce more clotting factor (fibrinogen, factor 7 and 10) → procoagulant state + decreased anticoagulants (protein C + antithrombin 3)

4) Haemodynamic changes following PE and their physiological basis

  • Changes in volume and pressure (no clinical effects)

    • Embolus impact → acute increase in RV afterload → increased RV pressure → increased RA pressure → increased CVP (central venous pressure) → right heart failure

    • Embolus impact → pulmonary hypertension → increased RV volume → stretch of the tricuspid valve leaflets → stretch → tricuspid valve leaflets → regurgitation of blood in RA → increased RA blood volume + pressure → increased JVP (jugular venous pressure)

    • Embolus impact → obstruction of blood flow → decreased blood return to left side of heart → ↓EDV → ↓SV + CO → low BP

5) Clinical features of PE and their physiological basis

  • Small embolus: terminal arteries and arterioles, unlikely to cause any signs and symptoms.

    • If tissue near pleura affected (distal lung): causes pleural inflammation → pleural diffusion → pleuritic chest pain

  • Large embolus: major arterial obstruction → acute pulmonary hypertension → acute right ventricular heart failure

    • If it breaks to small clots and travels to distal lung → pleuritic chest pain

    • Clinical features:

      • Collapse (high BP)

      • Acute breathlessness

      • Pleuritic effusion

      • Heave and crackles (high RV afterload)

      • RV failure

6) Changes in arterial blood gases after major PE and their physiological basis
A. Low O2 levels

  • Obstruction of blood flow by embolus → ventilation perfusion mismatch

  • Pulmonary oedema around alveoli → impaired gas exchange → ventilation perfusion mismatch

B. Low CO2: CO2 is high initially → activation of central chemoreceptors → hyperventilation → low CO2

  • Low O2 saturation due to low PO2 due to ventilation perfusion mismatch

7) Pathogenesis of pulmonary oedema after PE to include both exudate and transudate

  • ↑ vascular permeability → leakage of inflammatory cells to lung tissue

  • Exudate oedema:

    • embolus in artery → impaired blood flow

    • Intravascular:

      • embolus inside artery → endothelial injury → inflammation → release of cytokines → phophorylation of cadherins → increased vascular permeability → leakage of inflammatory cells to lung tissue → oedema

    • Extravascular:

      • embolus in artery → obstructed blood flow → ischemia of bronchioles + lung tissue → inflammation → oedema

    • Chest Pain:

      • Tissue pleura affected → inflammation increase permeability of pleuralmembrane → entry of cells + mediators in pleural cavity → vicosity increases → pleural rub → activation of nerve ending → chest pain

  • Transudate oedema:

    • embolus in artery → obstruction of blood flow → pulmonary hypertension → increased hydrostatic pressure behind obstruction

      • Two outcomes:

        • plasma leaks into lung tissue

        • small capillaries burst → blood enters lung tissue

8) Why pale and clammy?

  • ↓ SV → low BP → activation of baroreflex → sympathetic activity → vasoconstriction → sweating

  • ↓ renal perfusion → activation of RAAS → increases angiotensin 2 → vasoconstriction → paleness

  • pleuritic chest pain → sympathetic activation → vasoconstriction → sweating

  • ↓SV→ low BP → tissue hypoperfusion → paleness (no blood perfusion)

  • Low BP and hypoxia → ↑ pulse (compensatory) → ↑ RR (compensatory)

9) Causes of Haemoptysis (coughing blood)

  • increased hydrostatic pressure→ rupture of capillaries → blood leaks into lung tissue → activation of cough receptors around alveoli → coughing blood

  • Embolus → obstruction of blood flow → hypoperfusion of distal tissue → ischemia of tissue → inflammation → inflammation damages distal tissue and bronchial arteries embedded inside affected tissue → damage to bronchial arteries → blood leaks out → activation of cough receptors in alveoli in lung tissue.