Fluid And Harmodynamic Derangements Flashcards
Basement membrane
Comprised of collagen type 4
Connects capillary to surround tissue
Acts as a sieve or filter
Where endothelial cells sit
Hydrostatic pressure
Forces fluid out of capillary
Proportional to blood pressure
Therefore, hydrostatic pressure at the arterioles end of the capillary is larger than the hydrostatic pressure and the venule end of the capillary.
Oncotic pressure
Forces fluid into capillary, due to plasma proteins.
Equal fluid exchange at arteriole and venule end of capillaries due to no change in plasma concentration.
Hence, considering hydrostatic pressure, we have a small positive pressure forcing fluid out of capillary at arteriole end, whilst at venule end we have a slight pressure forcing fluid back into the vessel; therefore balancing fluid exchange.
Effusion
Fluid accumulation in these body cavities
Ascites
Oedema within the peritoneal (abdominal) cavity
Anasarca
Generalised oedema in all interstitial tissues and body cavities .
Transudate
Fluid that accumulates in interstitial tissues and body cavities in non-inflammatory situations. Basically an ultrafiltration of plasma, that is, contains little protein and no white blood cells.
Oedema
Accumulation of excess fluid in interstitial spaces and/ or body cavities.
Oedema due to an increase in hydrostatic pressure: localised
Example: person with deep leg vein thrombosis in right leg.
Causes oedema in right leg because thrombosis increases hydrostatic pressure within that vein, which impacts on capillaries to also increase hydrostatic pressure and thus force fluid out of the capillary beds within the right leg. May also retard wound healing or allow infected wound to persist.
Other localised oedemas may be fatal, such as cerebral oedema compressing the brain stem, thus damaging medullary centres.
Oedema due to an increase in hydrostatic pressure: systemic
Example: right sided congestive heart failure
If the right side of the heart is not pumping blood efficiently to the lungs there will be a build up of pressure in the inferior vena cava (which enters right atrium). This results in an increase in venous pressure and therefore an increase in capillary pressure to force fluid out of capillaries into interstitial spaces of most tissues (apart from the lungs).
Oedema due to decrease in oncotic pressure
If an individual with cirrhosis of the liver progresses to hepatic failure, the liver will gradually reduce the formation of plasma proteins which are essential for maintaining oncotic pressure within blood vessels. This drop in oncotic pressure will result in the person eventually developing anasarca (generalised oedema).
Similarly, a person who is protein malnourished will see the same result.
Oedema due to lymphatic obstruction
Most common form through cancer invasion of lymphatic vessels or resection of a cancer that has invaded lymphatics. (Lymphoedema)
Parasites such as worms that infiltrate lymphatics can also cause lymphoedema.
Thrombosis
Process of forming a thrombus, a coagulated mass of blood in an uninterrupted cardiovascular system.
Blood is continually trying to coagulate via the coagulation cascade, which is instigated by collagen exposure and forms fibrin. This is opposed by anti-coagulating factors such as protein C and antithrombin 3 in plasma. Laminar blood flow also impedes by restricting cellular elements of blood and platelets to a central region in vessels, whilst plasma is confined to other regions alongside endothelial cells.
Disruption to laminar flow such as in some arteries and chambers of the heart increase likelihood of thrombus developing.
Fibrinolytic system also dissolves fibrin, thus preventing thrombosis.
Factors increasing likelihood of developing thrombosis
- Injury to endothelial cells. releases thromboplastin (instigates coagulation cascade along with collagen) and connective tissue collagen.
- static and turbulent blood flow. Disruption of laminar flow in vessels allows for platelets to come into contact with endothelium; therefore instigation of the coagulation cascade.
Stasis is prominent within veins and initiation of thrombus formation occurs behind vein valve leaflets where stasis is most evident.
Turbulence in arteries also damages endothelial cells by reducing oxygenation of these cells and therefore increasing the likelihood of cholesterol infusion and subsequent atheroma formation.
Turbulence in heart chambers, aneurysms, diseased heart valves creates eddy currents (pockets of stasis) which impede anti coagulating factors from entering, thereby increasing predisposition of thrombosis. - hypercoaguability of blood: Increased risk of coagulation in many situations:
After long trauma or burns (release of thromboplastin)
Certain cancers (released thrombogenic agents)
Nephrotic syndrome (urinary excretion of anti coagulating proteins)
People who smoke and the obese
Fate of thrombosis
- lysis: Most thrombi that form are small and easily dissolved by fibrinolytic system through the generation of plasmin.
- propagation: Can occur in lesions with the heart (on scar of healed myocardial infarcts) and arteries as well as within veins with no apparent lesions. Propagation of thrombus in coronary artery for example may block the lumen and lead to infarction.
- embolus and embolism: An embolus is an entity that normally doesn’t travel in the blood stream. Embolism on the other hand is/ are where an embolus/ emboli lodge. vast majority of emboli are thrombo- emboli.
- organisation to result in scar: Thrombus that is formed in an aneurysm can be converted to scar through the repair process. The scar is this incorporated into the wall of the artery/ ventricle. The resultant scar will increase the likelihood of thrombosis on top of this scar.
- recanalisation: the formation of granulation tissue from an organising thrombus in either an artery or vein to reconstitute blood flow in that vessel.
