Pathophysiology of Congestion & Oedema Flashcards
Flow (Q) = ______
pressure gradient (deltaP) / resistance (R)
What happens to the floe with an increased pressure gradient?
it increases also
What is congestion?
excess of blood in vessels of tissue/organ
How would you describe the process of congestion?
Is it a physiological mechanism?
passive
It is not a physiological mechanism, it is a pathological process.
Give examples of active hyperaemia.
4
- exercise/digestion
- release of blockage
- inflammation (exudation)
- heat loss (vasodilation)
- menopause/blushing
Give examples of passive hyperaemia (congestion).
3
- local acute congestion (e.g. DVT)
- local chronic congestion (e.g. liver cirrhosis)
- generalised acute congestion (e.g. CHF)
What is deep vein thrombosis, in basic terms?
vein in lower limb is blocked by clot causing congestion
Outline the pathophysiology of DVT, in terms of pressure, flow and resistance.
- blood clot/thrombus causes block
- outflow of blood is reduced (Q reduced)
- venous pressure increases (to match arterial pressure)
- pressure gradient decreases, Q decreases further
- haemostasis, further thrombosis
- O2 delivery decreases, ischaemia and infarction
What is a serious complication of DVT?
pulmonary thromboembolism
What type of drug is digoxin?
What are its effects? (2)
cardiac glycoside
- treats HF
- stimulates heart to beat stronger and with more regular rhythm
Outline briefly what hepatic cirrhosis is.
2
- late stage scarring (fibrosis) of the liver
- caused by hepatitis and chronic alcoholism.
What is a complication of hepatic cirrhosis?
portal hypertension (congestion)
Which hepatic vessels/circulation is affected by congestion?
portal veins (circulation)
Where there is congestion in the portal venous system, several sites anastomose with the systemic circulation.
What are they called?
What complications can this lead to?
(3)
portal-systemic shunts
- haemorrhage risk
- oesophageal varices (can lead to severe bleeding/death)
- caput medusae (medusa snakes head)
Briefly outline what congestive heart failure is?
- ineffective pump (affects LV and RV)
- many causes inc. IHD, vascular disease
Explain the pathophysiology behind congestive heart failure i.e. why is there less cardiac output and what is the consequence of this?
- reduced CO
- reduced renal GFR
- increased renin production
- increased Na+/H2O retention
- increased PV/fluid overload
- increased congestion
Outline problems caused secondary to congestive heart failure.
- pulmonary oedema (LVF)
- cardiac (liver) cirrhosis (RVF)
What are the clinical signs of pulmonary oedema?
2
- peripheral oedema
- crepitations
What are the clinical signs of liver cirrhosis?
3
- raised JVP
- hepatomegaly
- peripheral oedema
What are the two blood supplies to the liver? Name the vessels.
systemic: hepatic artery
portal: portal vein - hepatic vein
Pericentral hepatocytes (_____) - stasis of poorly oxygenated blood.
red
Periportal hepatocytes (____) Relatively better oxygenated due to proximity of hepatic arterioles
pale
Explain Starling’s forces relating to capillary fluid exchange starting from the arterial end of the capillary?
- at arterial end, hydrostatic (blood) pressure is high
- oncotic pressure P(o) is low as solute is diluted.
- P(h) > P(o) therefore net flow is water out of the capillary.
- somewhere in the middle of the capillary bed, the hydrostatic and oncotic pressures equilibriate.
- solute diffusion happens according to concentration gradients only (not Starling Forces).
- this includes small molecules such as O2, glc, H2O and CO2.
- at venous end, hydrostatic (blood) pressure is low
- oncotic pressure P(o) is high as there is high solute concentration in vessel.
- P(o) > P(h) therefore net flow is water into the capillary.
What are the three components which affect net flux and filtration?
hydrostatic pressure
oncotic pressure
permeability characteristics
What does disturbance of normal components of fluid exchange result in?
Give an example.
oedema
Increased hydrostatic pressure (hypertensive, congestion)
What is oedema?
Accumulation of abnormal amounts of fluid in the extravascular compartment .
What constitutes as ‘extravascular’ compartments?
Give examples.
- ECF (e.g peripheral oedema)
- body cavities (e.g. pleural effusion)
What do you call effusions in the abdominal cavity?
ascites
Briefly outline the difference between transudate and exudate.
transudate:
- only fluid, no protein
- caused by congestion/CHF
- low specific weight
- lots of H2O
exudate:
- inflammatory process
- fluid and proteins
- increased permeability
- high specific gravity
What would the fluid found in pulmonary oedema be: exudate or transudate?
Why?
transudate - caused by congestive heart failure, no inflammatory process.
Explain the pathophysiology of pulmonary oedema.
- LVF/CHF
- increased LA pressure
- increased pulmonary vascular pressure/blood volume
- increased filtration
- increased transudate/oedema
Explain the pathophysiology of peripheral oedema.
- RVF/CHF
- blood back flow into venous circulation
- increased hydrostatic pressure in capillaries
- increased filtration
- increased transudate (oedema)
Which vessel is affected by congestion in the liver?
hepatic vein (portal circulation)
What else can lead to oedema other than increased hydrostatic pressure within capillaries?
lymphatic blockage
What is the result of lymphatic blockage?
lymphoedema
What might result in reduced renal blood flow i.e. what is this secondary to?
congestive heart failure
Explain how abnormal renal function can result in oedema?
What can this be a primary and secondary cause of?
- increased Na+/H2O retention
- secondary to HF
- or primary to acute tubular damage e.g. hypotension
- increased PV
- Increased P(h)
- oedema
Explain the pathophysiology of low protein oedema.
- e.g. hypoalbuminaemia
- low solute concentration
- low oncotic pressure gradient
- high hydrostatic pressure gradient
- increased filtration/oedema
Name situations where low protein can cause oedema.
- liver cirrhosis
- malnutrition
- nephrotic syndrome
How does the oncotic pressure work to keep fluid in the capillary vessels?
increased solute concentration (e.g. plasma proteins) build up an oncotic pressure which drives fluid back into vessel from interstitial
