Week 5 Respiratory Flashcards
What is the bronchial arterial system?
Low flow, high pressure system that supplies the visceral pleura, the bronchi, and the bulk of the intestinal connective tissues supporting these structures
Where do the bronchial arteries arise?
Directly from the aorta or from the intercostal or subclavian arteries
What does the pulmonary arterial system supply?
Alveolar capillary beds and the distal bronhchioles (in carnivores, it may also supply the visceral pleura)
What are the dual venous drainage routes from the lungs?
Pulmonary veins (left heat) and azygous veins (right heart)
What are the two lymphatic vessels that drain the lungs?
Superficial lymphatic channels (connective tissue of the visceral pleura and drain in the interlobular septa towards the hilus) and the deep bronchovascular lymphatic channels (connective tissue surrounding the distal bronciholes and drain proximally towards the hilus. Anastomoses between the deep and superficial lymphatics.
What makes up the blood air barrier?
alveolar capillary endothelial cells with their basement membrane, alveolar interstitium (collagen, elastin fibres, fibrocytes, mast cells, and interstitial macrophages), layer of epithelial cells (mostly type I pneumocytes) with their basement membrane, thin layer of surfactant containing alveolar fluid
What are the mechanisms that prevent fluid from filling the alveoli?
- the volume of fluid that enters the alveolar interstitium is Limited by interstitial oncotic pressure augmented by the transport of albumin into it by alveolar capillary endothelial cells
- type I pneumocytes lining the alveoli have tight junctions that seal off the alveolar lumina- these cells play a major role in preventing fluid movement across the blood-air barrier so that fluid emerging from teh capillaries remains largely in the alveolar interstitium
- type II pneumocytes draw slowly and osmotically fluid that does enter the alveoli…. type II pneumocytes have passive sodium channels on their luminal surfaces and Na+ K+ ATPase pumps on their basolateral surfaces (also surfactant, side note)
- Clara cells of the distal bronchioles can also extract osmotically any alveolar fluid that has been drawn proximally by surface tension into the lumina of the distal airways and return it to the peribronchiolar interstitial tissues
- the pressure within the interstitial tissues of the lungs is lower than the intra alveolar pressure and becomes increasingly subatmospheric towards the hilus of the lung
What enhances and what impairs the active transport of alveolar fluid back into the interstitium by type II pneumocytes and Clara cells?
Enhances: catecholamines and glucocorticoids
Impairs: hypoxia, reactive oxygen and nitrogen species (during inflammation e.g.), use of halogenated anaesthetics, malnutrition, and if the alveolar fluid is highly proteinaceous
* the bronchovascular interstitium (loose connective tissues surrounding the airways and major blood vessels of the lungs) and the pulmonary lymphatics constitute a highly compliant sump taht has excess capacity in health)
What does the pressure differential between the interstitial tissues and the intra-alveolar do?
Promotes rapid drainage of fluid via the deep bronchovascular interstitial lymphatics and the superficial pleura and interlobular lymphatics to the hilus of the lungs and mediastinum
What is pulmonary oedema?
Oedema fluid flooding the alveoli and filling the luminal terminal bronchioles prevents ventilation and gas exchange
What occurs with pulmonary oedema?
Prevents ventilation and gas exchange, reduced lung compliance so that increased effort is required to expand the lungs, in the presence of surfactant, the oedema fluid forms a stable foam by mixing with air; the foam further compromises ventilation, phagocytic function of the alveolar macrophages is also compromised by pulmonary oedema and intra-alveolar hypoxia, predisposes to secondary bacterial infections of the lungs
What are the causes of pulmonary oedema?
Two major mechanisms: increased hydrostatic pressure in alveolar capillaries and increased permeability of the blood alveolar barrier
What causes increased hydrostatic pressure in alveolar capillaries?
Left sided congestive heart failure (cardiogenic pulmonary oedema), hypervolaemia due to excessive intravaneous fluid administration (over hydration), gravitational pooling of blood in dependent areas of the lungs of large animals that are rebument for prolonged periods, horses with acute severe exercise induced pulmonary haemorrhage.
What is the mechanism of action of pulmonary oedema due to increased hydrostatic pressure in alveolar capillaries?
Increased hydrostatic pressure in the alveolar capillaries–> excess fluid formation–> overloading the drainage sump–> intitial accumulation of oedema fluid in the bronchovascular interstitium (esp. near the hilus)–> ultimate spillage into the alveoli via an unidentified pathway close to the bronchiolar alveolar junction (oedema fluid that is low in protein)
What causes increased permeability of the blood-alveolar barrier?
Inflammation of the lung parenchyma with an increase in vascular permeability via opening of gaps between endothelial cells (esp. in the interstitial and bronchointersitital pneumonias), direct damage to alveolar capillary endothelium e.g. uraemia, septicaemia, endotoxaemia, clostridial toxins, anaphylaxis, toxins such as paraquat and fumonisin, adverse drug reactions, DIC, direct damage to type I pneumocytes- e.g. influenza viruses, bovine respiratory syncytial virus, reactive oxygen species, toxins such as 3-methylindole, noxious gases such as NH3, NO2, SO2, H2S, smoke, increased permeability–> rapid development of pulmonary oedema with direct movement of fluid from the alveolar capillaries into the alveolar lumina–> high risk of fatality (acute respiratory distress syndrome), (OEDEMA WITH HIGH PROTEIN CONCENTRATION)
How does hypoalbuminaemia cause pulmonary oedema?
Reduced plasma oncotic pressure due to chronic hepatic dysfunction, protein-losing nephropathy, protein losing enteropathy, chronic malnutrition, often overshadowed by oedema in other sites
What are some other causes of pulmonary oedema?
Lymphatic obstruction (e.g. intra-thoracic neoplasia), neurogenic pulmonary oedema (traumatic injury to the CNS–> catecholamine release–> increased pressure within the pulmonary arterial system and hence increased hydrostatic pressure within the alveolar capillaries; followed by increased capillary permeability, acute upper airway obstruction (strangulation or hanging), Impaired active transport of alveolar fluid from distal airspaces (direct damage to type II pneumocytes or distal bronchiolar clara cells- hypoxia, reactive oxygen species or nitrogen species, malnutrition, halogenated anaesthetics, presence of highly proteinaceous fluid within alveoli, lack or inhibition of surfactant (high surface tension at the blood air interface tends to draw fluid into the alveolus), near drowning
Gross appearance of pulmonary oedema
Wet and heavy lungs, wet and rubbery, do not collapse, watery fluid oozes from cut surface. distended. stable frothy foam possible (oedema fluid, surfactant, and air bubbles) in the lumina of the trachea, primary bronchi, and lower airways and may even flow from the nostrils, leads to interstitial fibrosis chronic… firmer than normal
When is passive congestive seen most often?
Left sided congestive heart failure
What causes passive congestion?
Left sided congestive heart failure, prolonged recumbency, lung lobe torsion
What does passive congestion look like?
Lung parenchyma is congested, dark-red purple (cyanotic), heavier than normal, pulmonary oedema
What happens with chronic passive congestion?
Fibrosis of alveolar septa and accumulation of haemosiderin pigment by alveolar macrophages (heart failure cells)– lungs can become grossly discoloured tan brown- “bronzing”
What does pulmonary hyperaemia look like?
Acute hyperaemia during acute or subacute phase of lung injury and inflammation. Affected areas are bright red due to arteriolar vasodilation and increased blood volume within the alveolar capillaries. Some accompanying of pulmonary oedema due to increased vascular permeability. (RED PHASE OF PNEUMONIA- SUBSIDES IN 7 days)
How can pulmonary haemorrhage be distinguished from pulmonary congestion?
Multifocal or patchy distribution and its more pronounced red to red-black color
What are some causes of pulmonary haemorrhage in domestic animals?
Blunt chest trauma with lung contusion, penetrating injuries (rib), haemostatic disorders (thrombocytopenia, DIC), septicaemia, bacteraemia, endotoxaemia, viraemia, pulmonary thrombosis, erosion of pulmonary vessel by adjacent inflammation, bleeding lung tumours, pulmonary vasculitis, exercise induced pulmonary haemorrhage in horses
What is haemoptysis?
Coughing of blood
What is Exercise Induced Pulmonary Haemorrhage (EIPH) in horses?
TB and SB horses >80% have episodes of bleeding into the lungs by vigorous exercise. Mostly subclinical.
What are some signs of EIPH?
epistaxis (uncommon), poor race performance
What causes EIPH?
Stress induced Rupture of alveolar capillaries (bleeding into alveolar spaces and pulmonary interstitium), due to exercise induced increase in transmural pressure (pressure difference between the lumen of the capillary and the alveolar space), increase in pulmonary arterial and hence alveolar capillary pressure from exercise, marked decrease in negative pleural pressure and therefore the intra-alveolar pressure
Where does EIPH haemorrhage typically occur?
Dorsocaudal areas of the diaphragmatic lung lobes
