Congestion and oedema Flashcards
define congestion
Relative excess of blood in vessels of tissue or organ
- secondary phenomenon- usually occurs as a result of primary pathology
how is congestion dissimilar to acute inflammation?
Congestion is passive whereas acute inflammation is active hyperaemia.
Congestion may be associated with active hyperaemia - it can be acute or chronic
example of clinical pathology example of local acute congestion
deep vein thrombosis
example of clinical pathology example of local chronic congestion
Hepatic cirrhosis - scarring/fibrosis of liver - scar tissue prevents normal function. Liver is unable to clear toxins from the blood
example of clinical pathology example of generalised acute congestion
congestive heart failure
effects of deep vein thrombosis of the leg on blood flow
blood backs up in veins, venules and capillaries
there is a decreased outflow of blood
decrease in pressure gradient because the pressure rises
no O2 leads to ischaemia and venous infarction (uncommon form of stroke)
effects of hepatic cirrhosis on blood flow
cells in the liver become damaged as well as the surrounding supportive structures. This loss of normal architecture means altered hepatic blood flow as cells promote flow of blood around them - different route
portal blood flow becomes blocked - congestion in portal vein and branches causes an increase in portal venous pressure
what risk is there of local chronic congestion in hepatic cirrhosis?
haemorrhage risk
What do you see as a consequence of portal vein hypertension?
portal-systemic shunts
what is a portosystemic shunt
because the pressure in the portal system is so high, blood goes backwards through veins to get into the systemic circulation. It means blood bypasses the liver.
2 clinical signs of portal-systemic shunts
caput medusae
oesophageal varices
caput medusae
swollen superficial epigastric veins seen on the abdomen
oesophageal varices
dilated submucosal veins in lower part of oesophagus
What happens with congestive heart failure
the heart is unable to clear blood from the right and left ventricles. It becomes an ineffective pump and leads to ischaemia or valve disease etc
Pathophysiology of congestive heart failure
decreased cardiac output
decreased glomerular filtration rate - activate renin-angiotensin aldosterone system to increase MAP
increased fluid due to H20 retention so more fluid in veins.
effects of congestive heart failure in regards to the lungs
left heart failure causes blood to dam back into the lungs causing pulmonary oedema
what would you find on examination of person with congestive cardiac failure?
rattling/crackling sound in lungs
tachycardia
effects of congestive heart failure in regards to the liver
right heart failure causes blood to dam back into systemic circulation which causes central venous congestion. An increased JVP, hepatomegaly (abnormal enlargement of the liver) and peripheral oedema can occur
macroscopic sign of hepatic central venous congestion
nutmeg liver - red/brown and pale spotty appearance
Define oedema
Accumulation of abnormal amounts of fluid in the extravascular compartment ie intercellular tissue compartment (ECF) or body cavities
what is peripheral oedema
increased interstitial fluid in tissues
define an effusion and where you can get these
fluid collections in body cavities
Pleural, pericardial, joint effusions, or Abdominal cavity
what is the normal fluid movement through capillaries driven and balanced by
driven by hydrostatic pressure from the heart and balanced by oncotic pressures and endothelial permeability
what does disturbances in the normal components of fluid movement lead to?
oedema
What is starling’s hypothesis
fluid movement due to filtration across the wall of a capillary is dependent on the balance between the hydrostatic pressure gradient and the oncotic pressure gradient across the capillary
what is a transudate
an ultrafiltrate of plasma that contains few, if any, cells and doesn’t contain large plasma proteins - has H20 and electrolytes
What is an exudate
mass of fluid and cells that have seeped out of blood vessels or an organ
when is it most common for an exudate to arise
occurs especially in inflammation due to increased vascular permeability
out of transudate and exudate which has a low and which has a high specific gravity
transudate - low
exudate - high (means that it is denser than water)
how/ why does a transudate come about?
due to alterations in the haemodynamic forces which act across the capillary wall
what can cause an overload of fluid due to high vascular hydrostatic pressure or low oncotic pressure
cardiac failure
what is pitting oedema
often due to water retention as a result of peripheral oedema
after pressure is applied to a small area, the indentation persists after the release of the pressure
how can left ventricular failure cause pulmonary oedema?
it increases L atrial pressure as result of blood not being pumped out of the heart by LV
passive backwards flow of blood to the pulmonary veins, capillaries and arteries
increase in pulmonary vascular pressure and blood volume
therefore increased capillary hydrostatic pressure meaning an increase in fluid and solute being pushed out of the vessel into the interstitial space and so more filtration and pulmonary oedema
How does oedema arise in the lungs between alveoli
perivascular and interstitial transudate
caused by progressive oedematous widening of alveolar septa so oedema accumulates in the alveolar spaces
peripheral oedema caused by right heart failure
cannot empty RV in systole
Blood retained in systemic veins so pressure in capillaries increases causing more filtration –> peripheral oedema
when might you get peripheral and pulmonary oedema occuring at the same time?
in person with congestive cardiac failure - both the L and R ventricles fail
why is lymphatic drainage so important
it is required for normal flow
what is the oedema called cause when the lymphatic system becomes blocked
lymphoedema
abnormal renal function and oedema
Abnormal renal function results in Salt (NaCl) and H2O retention which increases intravascular fluid volume and capillary hydrostatic pressure
low protein oedema
transdute due to oncotic pressure decreasing meaning water isn’t being pulled into the circulatory system
this is all due to low protein levels in blood
what 3 conditions could bring about low protein oedema
nephrotic syndrome
malnutrition
hepatic cirrhosis - liver can’t synthesise enough protein
how does endothelial permeability come about? - exudate
damage to endothelial lining increases number of pores in membrane
proteins and larger molecules can leak out, not just H20
e.g acute inflammation or burns
what is Darcy’s law?
Q = change in P/R
Q = blood flow P = pressure R= resistance
what does it mean that congestion is a secondary phenomenon?
secondary to something else going on, it is not a primary pathology
3 examples of pathology in local acute congestion, local chronic congestion and generalised acute congestion
local acute congestion - deep vein thrombosis
local chronic congestion - hepatic cirrhosis
generalised acute congestion - congestive cardiac failure
what happens to form transudate and exudate?
increased hydrostatic pressure (pressure exerted by blood onvessel wall) pushes H20 out of the vessel
or
decrease in oncotic pressure where H20 moves from high to low pressure out of the vessel.
The reason there is more protein in an exudate is because there is often a decrease in oncotic pressure in this and it is also often due to inflammation. Inflammation causes the capillaries to be more leaky (larger pores) which allow movement of large proteins like albumin
values for protein content in an exudate
> 35 g/L
values for protein content in an transudate
<25 g/L
