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Cardiovascular System > Pathophysiology of Congestion & Oedema > Flashcards

Pathophysiology of Congestion & Oedema Flashcards

1
Q

Flow (Q) = ______

A

pressure gradient (deltaP) / resistance (R)

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2
Q

What happens to the floe with an increased pressure gradient?

A

it increases also

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3
Q

What is congestion?

A

excess of blood in vessels of tissue/organ

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4
Q

How would you describe the process of congestion?

Is it a physiological mechanism?

A

passive

It is not a physiological mechanism, it is a pathological process.

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5
Q

Give examples of active hyperaemia.

4

A
  • exercise/digestion
  • release of blockage
  • inflammation (exudation)
  • heat loss (vasodilation)
  • menopause/blushing
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6
Q

Give examples of passive hyperaemia (congestion).

3

A
  • local acute congestion (e.g. DVT)
  • local chronic congestion (e.g. liver cirrhosis)
  • generalised acute congestion (e.g. CHF)
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7
Q

What is deep vein thrombosis, in basic terms?

A

vein in lower limb is blocked by clot causing congestion

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8
Q

Outline the pathophysiology of DVT, in terms of pressure, flow and resistance.

A
  • 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
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9
Q

What is a serious complication of DVT?

A

pulmonary thromboembolism

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10
Q

What type of drug is digoxin?

What are its effects? (2)

A

cardiac glycoside

  • treats HF
  • stimulates heart to beat stronger and with more regular rhythm
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11
Q

Outline briefly what hepatic cirrhosis is.

2

A
  • late stage scarring (fibrosis) of the liver

- caused by hepatitis and chronic alcoholism.

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12
Q

What is a complication of hepatic cirrhosis?

A

portal hypertension (congestion)

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13
Q

Which hepatic vessels/circulation is affected by congestion?

A

portal veins (circulation)

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14
Q

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)

A

portal-systemic shunts

  • haemorrhage risk
  • oesophageal varices (can lead to severe bleeding/death)
  • caput medusae (medusa snakes head)
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15
Q

Briefly outline what congestive heart failure is?

A
  • ineffective pump (affects LV and RV)

- many causes inc. IHD, vascular disease

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16
Q

Explain the pathophysiology behind congestive heart failure i.e. why is there less cardiac output and what is the consequence of this?

A
  • reduced CO
  • reduced renal GFR
  • increased renin production
  • increased Na+/H2O retention
  • increased PV/fluid overload
  • increased congestion
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17
Q

Outline problems caused secondary to congestive heart failure.

A
  • pulmonary oedema (LVF)

- cardiac (liver) cirrhosis (RVF)

18
Q

What are the clinical signs of pulmonary oedema?

2

A
  • peripheral oedema

- crepitations

19
Q

What are the clinical signs of liver cirrhosis?

3

A
  • raised JVP
  • hepatomegaly
  • peripheral oedema
20
Q

What are the two blood supplies to the liver? Name the vessels.

A

systemic: hepatic artery
portal: portal vein - hepatic vein

21
Q

Pericentral hepatocytes (_____) - stasis of poorly oxygenated blood.

A

red

22
Q

Periportal hepatocytes (____) Relatively better oxygenated due to proximity of hepatic arterioles

A

pale

23
Q

Explain Starling’s forces relating to capillary fluid exchange starting from the arterial end of the capillary?

A
  • 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.
24
Q

What are the three components which affect net flux and filtration?

A

hydrostatic pressure
oncotic pressure
permeability characteristics

25
Q

What does disturbance of normal components of fluid exchange result in?

Give an example.

A

oedema

Increased hydrostatic pressure (hypertensive, congestion)

26
Q

What is oedema?

A

Accumulation of abnormal amounts of fluid in the extravascular compartment .

27
Q

What constitutes as ‘extravascular’ compartments?

Give examples.

A
  • ECF (e.g peripheral oedema)

- body cavities (e.g. pleural effusion)

28
Q

What do you call effusions in the abdominal cavity?

A

ascites

29
Q

Briefly outline the difference between transudate and exudate.

A

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
30
Q

What would the fluid found in pulmonary oedema be: exudate or transudate?

Why?

A

transudate - caused by congestive heart failure, no inflammatory process.

31
Q

Explain the pathophysiology of pulmonary oedema.

A
  • LVF/CHF
  • increased LA pressure
  • increased pulmonary vascular pressure/blood volume
  • increased filtration
  • increased transudate/oedema
32
Q

Explain the pathophysiology of peripheral oedema.

A
  • RVF/CHF
  • blood back flow into venous circulation
  • increased hydrostatic pressure in capillaries
  • increased filtration
  • increased transudate (oedema)
33
Q

Which vessel is affected by congestion in the liver?

A

hepatic vein (portal circulation)

34
Q

What else can lead to oedema other than increased hydrostatic pressure within capillaries?

A

lymphatic blockage

35
Q

What is the result of lymphatic blockage?

A

lymphoedema

36
Q

What might result in reduced renal blood flow i.e. what is this secondary to?

A

congestive heart failure

37
Q

Explain how abnormal renal function can result in oedema?

What can this be a primary and secondary cause of?

A
  • increased Na+/H2O retention
  • secondary to HF
  • or primary to acute tubular damage e.g. hypotension
  • increased PV
  • Increased P(h)
  • oedema
38
Q

Explain the pathophysiology of low protein oedema.

A
  • e.g. hypoalbuminaemia
  • low solute concentration
  • low oncotic pressure gradient
  • high hydrostatic pressure gradient
  • increased filtration/oedema
39
Q

Name situations where low protein can cause oedema.

A
  • liver cirrhosis
  • malnutrition
  • nephrotic syndrome
40
Q

How does the oncotic pressure work to keep fluid in the capillary vessels?

A

increased solute concentration (e.g. plasma proteins) build up an oncotic pressure which drives fluid back into vessel from interstitial

Cardiovascular System (37 decks)

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