5. Increased Hydrostatic pressure
→↑pressure in pulmonary veins
→which is transmitted to pulmonary
capillaries
→imbalance between pulmonary hydrostatic
pressure and plasma oncotic pressure
→excess fluid move into interstitial tissue of
lung
17. Later on fibrosis and thickening of alveolar
walls with haemosiderin laden
macrophages
ie Brown induration
- These changes impair respiratory
functions and predispose to infection.
18. Oedema caused by microvascular
injury
- Injury to capillary of the alveolar septa
- Damage to endothelial cells or alveolar
epithelial cells.
19. - Increased leakage of fluid into interstitial
space and later into alveoli
- Oedema may be
localized → pneumonia
Diffuse → ARDS
29. Route Cause
Inflammatory cells → production of
chemical mediators of inflammation
- Cytokines
- Oxygen free radicals
- Complement fragments
- Eicosanoids
30. Endotoxin induces the release of pro-
inflammatory cytokines from macrophages
and induces endothelial expression of
adhesion molecules
31. Endotoxin also amplifies compliment
mediated responses of neutrophils
Neutrophils – Release toxic Oxygen free
radicals
- Enzymes
32. - Extra pulmonary activation of
compliment pathway e.g. in:-
Haemodialysis
Cardiopulmonary bypass
33. Sepsis also causes activation of the
compliment system
Macrophages elaborate
- Oxygen toxic free radicals
- Proteases
- Arachidonic acid metabolites
- PAF
- Cytokines
- Interleukin – 8
34. Other physiologic effects
- Vasoconstriction
- Platelet aggregation
These two mechanisms may decrease
blood supply to tissues in the lungs
36. Lungs are focally stiff
- Infiltrated
- Consolidated
- Collapsed
In some areas the lungs are normal
Mortality approximately 60%.
37. Pulmonary Embolism, Infarction,
Haemorrhage
Occlusion of pulmonary arteries by blood
clot are almost always embolic in origin.
Source – thrombi in deep veins of legs in
more than 95% of cases.
Cause:-
- Burns
- Trauma
- Fracture
38. Morphology:-
Depends on size of the embolic mass and
state of circulation
Large emboli may impact in major vessels
e.g. saddle embolus
Death
- Blockage of Blood supply
- Acute cor pulmonale
39. Small emboli may travel to peripheral
areas of the lungs:-
- May cause infarction
- Haemorrhage
Infarction in 10% of cases
40. Clinical Course
- Pulmonary embolism may follow
Cardiac disease
Cancer
Immobilization for a long time
- Hypercoagulable states
49. Pathogenesis
Secondary forms of pulmonary
hypertension.
Endothelial cells play an important role
Increased shear and mechanical injury
associated with
- Left to right shunts → ASD,VSD
- Biochemical injury produced by fibrin
in thromboembolism.
50. In Primary Pulmonary Hypertension;
Endothelial cell injury is idiopathic
May be associated with
- autoimmune disorders (collagen
diseases)
51. - Toxic substances
- Genetic determinants (family history)
- Decreased prostacylin
- Decreased NO
- Increased endothelin
All these promote pulmonary
vasoconstriction
53. Endothelial activation
→ endothelial cells thrombogenic
→ promotes the persistence of fibrin
Cytokines
GF → these induce the migration and
replication of vascular smooth muscle cells
→ elaboration of extracellular matrix
54. Some patients have vasospastic
component
- Widespread and sustained hypoxic -
vasoconstriction and alveolar
hyperventilation → Pulmonary
hypertension eg high altitude
56. Pathologic changes
• May lead to cor-pulmonale
• Pathological changes are seen in Right
heart and pulmonary arterial tree in the
lungs
• Right- ventricular hypertrophy
• Right- atrial dilatation
57. Vascular changes
• 1) Arterioles and small pulmonary arteries
Medial hypertrophy
Thickening and redublication of elastic
laminae
Plexiform pulmonary arteriopathy
58. 2) Medium sized pulmonary arteries
concentric intimal thickening
Medial hypertrophy
Adventitial fibrosis
Thickening and redublication of elastic
laminae
3) Large pulmonary arteries
Atheromatous deposits
