Lungs Circulatory - Pathology

()Map CARDIORESPIRATORY SYSTEM (Map) LUNGS DEGENERATIVE

Hyperaemia

• Localised of diffuse as part of acute inflammation

Congestion

• Decreased outflow of venous blood
• Most commonly caused by left-sided or bilateral cardiac failure
  • Stagnant blood in pulmonary vessels -> red blood cells move into alveoli and are phagocytosed -> haemosiderin in macrophages (heart failure cells)
• One-sided in post-mortem hypostatic congestion
• Acute pulmonary congestion is seen after barbiturate euthanasia
• Leads to pulmonary oedema (below)

Pulmonary oedema

• Excessive fluid in the lung
• Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See functional anatomy)
• Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
• Generally a sequel to or part of congestion or inflammatory process
• Generally begins as interstitial oedema characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
• Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing alveolar oedema
• Gross pathology:
  • Heavy wet lungs which do not properly collapse
  • Subpleural and interstitial tissue distended with fluid
  • Foamy fluid oozing from the cut surface and airways
• Micro pathology:
  • Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
  • Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
  • In slowly developing cases, macrophages contain haemosiderin
• The major causes of pulmonary oedema are:
  • Increased capillary or type I epithelial permeability caused by
    • Systemic toxins
    • Shock
    • Inhaled caustic gases
  • Increased capillary hydrostatic pressure (cardiogenic oedema - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
  • Decreased plasma oncotic pressure (hypoalbuminaemia)
  • Overloading in excessive fluid therapy
  • As part of inflammatory process

Pulmonary haemorrhage

Pulmonary haemorrhage (Image sourced from Bristol Biomed Image Archive with permission)

• Potential sequel of septicaemias, bleeding disorders, disseminated intravascular coagulation, and severe congestion, severe acute inflammation, "back splashing" at slaughter (aspiration of blood)
• Exercise-induced pulmonary hemorrhage (EIPH) occurs commonly in horses during racing or training
  • Shows as epistaxis
  • Undetected in many horses
  • Haemorrhage is dorsocaudal, large brown areas
  • Micro - alveolar haemorrhage, macrophages containing haemosiderin, mild interstitial fibrosis

Embolism, thrombosis and infarction

Pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)

Segmental pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)

• Lungs are strategically situated to catch emboli carried in venous blood
• Because the lung is supplied by both pulmonary and bronchial arteries and has extensive collateral channels, infarction usually does not follow embolism or thrombosis unless pulmonary circulation is already compromised
• In animals, greatest risk comes from:
  • Tumor emboli
    • From e.g.: osteosarcoma and haemangiosarcoma in dogs, uterine carcinoma in cattle
  • Septic emboli
    • From bacterial endocarditis, jugular thrombophlebitis, hepatic abscesses etc.
    • May cause unexpected death if in large numbers
    • May develop suppurative pneumonia -> pulmonary abscesses, arteritis, thrombosis
• Pulmonary infarcts usually occur when there is embolisation or thrombosis during general circulatory collapse or passive congestion of heart failure
• Pulmonary thromboembolism is a sequel to in cattle to large emboli from liver abscesses close to the vena cava
  • Death may ocur due to massive haemorrhaging into lung tissue
• Parasites (e.g. Dirofilaria immitis, Angiostrongylus vasorum) may be responsible
• Long-term intravenous catheterisation may cuse thrombi pieces breaking off and lodging in pulmonary vessels

Pulmonary hypertension

• Caused by left-to-right vascular shunts or increased resistance of the pulmonary vascular system

• In animals, it is most commonly a sequel of widespread fibrosis in the lung or chronic bronchitis or bronchiolitis which stimulates hypertrophy in the walls of small arteries
• Severe prolonged pulmonary hypertension leads to cor pulmonale, right-sided heart failure secondary to primary lung disease