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2. Cardiovascular System > 32. Pathophysiology of Congestion and Oedema > Flashcards

32. Pathophysiology of Congestion and Oedema Flashcards

1
Q

What is Darcy’s law?

A

Blood flow= (difference in pressure)/ resistance

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2
Q

Define congestion.

A
  • Abnormal or excessive accumulation of blood or bodily fluid in vessels of tissue or organ
  • Passive process
  • acute or chronic
  • can be active hyperaemia (excess blood in vessels supplying organs or other parts of the body-too much blood)
  • blood (or any fluid) is going in and not going out
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3
Q

Why is congestion NOT like an acute inflammatory process?

A
  • In acute inflammation, vessels deliberately open up and allow more blood into tissues with inflammatory process
  • Whereas in congestion, it’s a PASSIVE process and there are no instructions for it since it happens automatically (the body doesn’t mean to do it for any benefit)
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4
Q

What is an example of local acute congestion?

A

deep vein thrombosis

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5
Q

What is an example of local chronic congestion?

A

hepatic cirrhosis

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6
Q

What is an example of generalised acute congestion?

A

congestive cardiac failure

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7
Q

Describe what happens in deep vein thrombosis of the leg in terms of congestion.

A
  • blood backs up in veins, venules and capillaries and gets stuck in vessels
  • local acute congestion
  • decreased outflow of blood
  • decreased pressure gradient
  • decreased flow across system (decrease in pressure difference therefore decrease in flow)
  • flow is proportional to resistance (if you increase resistance, you decrease flow)
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8
Q

What does acute local congestion in deep vein thrombosis eventually lead to?

A
  • since no O2

- ischaemia and infarction can occur

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9
Q

What happens in hepatic cirrhosis that leads to local chronic congestion?

A
  • regenerative nodules of hepatocytes with intervening fibrosis
  • due to liver damage
  • loss of normal architecture leading to altered hepatic flow
  • liver structure is damaged so therefore so is function
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10
Q

What is the aetiology of hepatic cirrhosis?(6)

A
  • alcohol
  • hepatitis B and C
  • liver injury
  • reaction to prescription medication
  • toxic substances
  • repeated episodes of heart failure with liver congestion
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11
Q

Which blood flow channel is blocked in hepatic cirrhosis?

A

Portal blood flow is blocked (congestion in portal vein and branches)

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12
Q

What happens in hepatic cirrhosis to the portal blood flow?

A
  • increased portal venous pressure
  • collateral circulation; several sites anastomose with systemic circulation (circulation around a blocked pathway)
  • chronic inflammation in hepatocytes also occurs
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13
Q

What is the portal blood flow in the liver?

A
  • carries blood from gastrointestinal tract gallbladder, and spleen to the liver (from gut to liver)
  • venous drainage
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14
Q

What is the main risk associated with local chronic congestion like hepatic cirrhosis?

A

haemorrhage risk

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15
Q

What is the common consequence of cirrhosis? (2)

A
  • Oesophageal varices

- Caput Medusae

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16
Q

What are oesophageal varices?

A
  • very dilated sub-mucosal veins in the lower third of the oesophagus
  • if these veins are damaged then blood can spill into oesophagus and blood exits forcefully through the mouth
  • mainly as a consequence of hepatic portal system hypertension
  • have tendency to start bleeding
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17
Q

What is Caput Medusae?

A
  • anastamosis of veins in the abdominal wall
  • engorged superficial epigastric veins which are seen radiating from umbilicus across the abdomen
  • caused by dilation of paraumbilical veins which become recanalised (usually close within 1 week after birth) due to portal hypertension
  • paraumbilical veins usually carry oxygenated blood from mother to foetus
  • anastomosis between the veins of the anterior abdominal wall and the hepatic portal, hypogastric, and iliac veins.
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18
Q

What happens in congestive heart failure?

A
  • heart unable to clear blood from right and left ventricles
  • ineffective pump due to ischamia or valve disease for example
  • heart works very hard to make up for its loss of function
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19
Q

What is the aetiology of congestive cardiac failure? (9)

A
  1. coronary artery disease
  2. MI
  3. high BP
  4. faulty valves (valve disease)
  5. cardiomyopathy (damage to heart muscle)
  6. myocarditis
  7. heart defects( congenital)
  8. heart arrhythmias
  9. chronic disease e.g. diabetes, HIV, hyperthyrodism, hypothyrodism, hemochromatosis, amyloidosis (build up of protein)
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20
Q

What is the pathophysiology of congestive cardiac failure in terms of:

  • CO
  • GFR
  • Na and H2O retention
  • fluid in the body and veins
A
  • decreased cardiac output
  • decreased renal glomerular filtration rate (GFR)
  • increase in Na and H2O retention
  • increase in amount of fluid in the body
  • increase in fluid overload in veins
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21
Q

What is the treatment for fluid overload in the body?

A

diuretic (so more urine is excreted)

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22
Q

What general and systemic effects does congestive heart failure have on other systems?

A
  1. heart can’t clear blood from ventricles
  2. blood dammed back in veins (back pressure)
  3. central venous congestion in the liver
  4. acute and chronic changes in lungs (pulmonary oedema)
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23
Q

Which side of heart is affected for central venous congestion to occur for example in liver?

A

right heart failure

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24
Q

What does central venous congestion from liver cause which is due to r.heart failure? (3)

A
  • raised JVP
  • hepatomegaly (liver swollen)
  • peripheral oedema
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25
Q

Which side of the heart is affected for acute and chronic lung changes to occur leading to pulmonary oedema?

A

left heart failure

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26
Q

What does pulmonary oedema cause in terms of clinical features? (2)

A
  1. crepitations in lungs

2. tachycardia

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27
Q

What does a liver look like which has hepatic central venous congestion?

A
  • “nutmeg liver”

- red/brown and pale spotty appearance

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28
Q

What type of hepatocytes are red in colour in hepatic central venous congestion? What is their oxygenation like?

A

Pericentral hepatocytes:

stasis of poorly oxygenated blood (worse inside) which menas central hepatocytes will not receive as much blood

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29
Q

What type of hepatocytes are pale in colour in hepatic central venous congestion? What is their oxygenation like?

A

Periportal hepatocytes: relatively better oxygenated due to proximity of hepatic arterioles (better outside)

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30
Q

Describe how normal microcirculation works.

A
  • constant movement of fluid through capillary beds
  • process of dynamic equilibrium
  • filtration from capillary beds to interstitium
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31
Q

What forces drive microcirculation?

A
  • driven by hydrostatic forces from heart (pushes fluid OUT)

- balanced by osmotic pressure and endothelila permeability (favours ABSORPTION, fluid IN)

32
Q

Which end of the systemic circulation favours hydrostatic forces/ pressure?

A

arterial end of the capillary (want to push fluid OUT since)

33
Q

Which end of the systemic circulation favours osmotic (oncotic) forces/pressure?

A

venous end of the capillary (want to absorb fluid back from lymphatics)

34
Q

Describe the movement of fluid in microcirculation.

A

Capillaries- Interstitum (tissue space) - Capillaries and Lymphatics (fluid enters lymphatic which is then circulating in lymphatic vessels and returns through venous side back into circulation)

35
Q

Describe what is meant by hydrostatic and osmotic/oncotic pressures.

A

In the capillaries hydrostatic pressure increases filtration by pushing fluid and solute OUT of the capillaries, while capillary oncotic pressure (also known as colloid osmotic pressure) pulls fluid into the capillaries and/or prevents fluid from leaving.

36
Q

What 3 components affect net flux and filtration?

A
  1. hydrostatic pressures
  2. oncotic/osmotic pressures
  3. permability characteristics and areas of endothelium
37
Q

What does Starling’s Hypothesis state?

A
  • Fluid movement due to filtration across the wall of a capillary is dependent on the balance between hydrostatic pressure gradient and oncotic pressure gradient across capillaries. It’s the relationship between net filtration being affected by force favouring filtration and flow out of fluid out of vessel.
  • Endothelial permeability to proteins and H2O and area of capillary bed is also a factor which affects net filtration
38
Q

What does disturbances of normal components of microcirulation cause according to Starling’s hypothesis?

A

Oedema

39
Q

Define oedema.

A
  • Accumulation of abnormal amounts of fluid in the extravascular space.
  • Includes intercellular tissues spaces between cells (extracellular fluid) and body cavities)
40
Q

Define peripheral oedema.

A

Increased interstitial fluid in tissues

41
Q

Define effusions.

A

-fluid collection in body cavities

42
Q

What is fluid collection in between cells called?

A

oedema

43
Q

What are the most common effusions? (4)

A
  1. pleural
  2. pericardial
  3. joint
  4. ascites (abdominal cavity)
44
Q

Is oedema a transudate or exudate?

A

it can be a TRANSUDATE and EXUDATE

45
Q

What is the difference between transudate and exudate fluids?

A 
Transudate= fluid pushed through the capillary due to high pressure within the capillary; alteration in the haemodynamic forces which act across capillary wall 
Exudate= fluid that leaks around the cells of the capillaries caused by inflammation; part of the inflammatory process due to increase in vascular permeabiltiy
46
Q

What makes up a transduate fluid? (3)

A
  • water
  • electrolytes
  • little protein/ albumin with few cells
47
Q

What are the main causes for oedema that is made up of transudates? (2)

A
  1. cardiac failure

2. fluid overload

48
Q

What are the main causes for oedema that is made up of exudates? (3)

A
  1. tumour
  2. inflammation
  3. allergy
49
Q

What makes up exudate fluid? (3)

A
  1. water
  2. electrolytes
  3. high protein content/albumin content (cells)
50
Q

What is the specific gravity in transudates and exudates?

A

in transdutes= low specific gravity

in exudates= high specific gravity

51
Q

What is the main pathophysiology of pulmonary oedema?

A
  • linked to hydrostatic pressures therefore it’s a TRANSUDATE
  • caused by left ventricular failure
52
Q 
Describe what happens to: 
- l.atrial pressure 
- pulmonary vascular pressure
- pulmonary blood volume 
- cardiac pressure and filtration
in pulmonary oedema.
A
  1. increase in l. atrial pressure (causes passive retrograde flow to pulmonary veins, capillaries and arteries)
  2. increase in pulmonary vascular pressure
  3. increase in pulmonary blood volume
  4. increase in cardiac pressure which increases filtration and pulmonary oedema
53
Q

What type of fluid accumulates in lungs in pulmonary oedema?

A
  • perivascular and interstitial transduate
54
Q

What happens pathophysiologically in lungs during pulmonary oedema?

A
  • progressive oedematous widening of the alveolar septa

- accumulation of oedema fluid in alveolar spaces

55
Q

What is pulmonary oedema caused by?

A

LEFT ventricular failure (left cardiac failure)

56
Q

What is peripheral oedema caused by?

A

RIGHT heart/cardiac failure (cannot empty r. ventricle in systole)

57
Q

Describe the pathophysiology of peripheral oedema.

A
  • blood retained in systemic veins
  • increase in capillaries pressure
  • increase in secondary portal venous congestion in liver
  • increase in filtration leading to peripheral oedema
58
Q

What is congestive cardiac failure caused by?

A
  • right AND left ventricles fail at the same time

- pulmonary oedema (failure on the left) and peripheral oedema (failure on the right) at the same time

59
Q

Problems in which pressures lead to congestive cardiac failure?

A

hydrostatic pressures

60
Q

What is caused if there is lymphatic obstruction?

A

lymphoedema (normal lymphatic drainage is affected)

61
Q

What patients are highly at risk of lymphoedema? Why?

A

Breast cancer patients:

  • radiotherapy in axilla causes fibrosis to surrounding tissues
  • decreases outflow of blood
  • leads to oedema of upper limb
62
Q

Why does oedema happen in abnormal renal function?

A
  • results in salt and H2O retention in the kidneys

- can be primary (wide range of conditions) or secondary in heart failure which causes reduced renal blood flow

63
Q

What is an example of primary cause for abnormal renal function which can lead to oedema?

A

acute tubular damage (e.g. hypotension)

64
Q

What is an example of a secondary cause for abnormal renal function which can lead to oedema?

A

reduced renal blood flow

65
Q

What can cause a decrease in renal function which can ultimately lead to oedema? (4)

A
  1. increase in salt and H2O (retention)
  2. increase in intravascular fluid volume
  3. secondary to cardiac failure
  4. oedema
66
Q

What can protein reduction be caused by? (3)

A
  1. reduction in dietary protein, malnutrition, insufficient intake of protein
  2. nephrotic syndrome: leaky renal glomerular basement membrane means protein is lost and causes generalised oedema
  3. hepatic cirrhosis: diffuse nodules and fibrosis in liver, liver unable to synthesise enough protein (metabolic dysfunction)
67
Q

Is low protein oedema a transudate or exudate?

A

Transudate (linked to oncotic pressure)

68
Q

What does hypoalbuminaemia cause?

A

-increase in filtration and eventually oedema

69
Q

What happens to fluid at the:

  • arterial side
  • venous side
A 
arterial= fluid pushed out 35mmHg (more than taken in: 25mmHg )
venous= fluid reabsorbed 25mmHg(more than pushed out 15mmHg)
70
Q

Is permeability oedema a transudate or exudate?

A

EXUDATE= endothelial permeability oedema

71
Q

Describe the pathophysiology of permeability oedema.

A
  • damage to endothelial lining occurs
  • this increases pores in membrane (osmotic reflection coefficient of endothelium decreases towards zero)
  • proteins and larger molecules can leak out (not just H2O)
72
Q

What can increase endothelial permability? (2)

A
  • acute inflammation such as pneumonia
  • burns
    Therefore exudate since damage to endothelium (inflammatory link)
73
Q

What is normal fluid flux dependent upon?

A

complex dynamic balance across the endothelial membrane to achieve a steady state (normal)

74
Q

Can upsetting any of the Starling’s forces lead to oedema?

A

Yes

75
Q

Overall, what leads to transudate oedema? (3)

A
  1. cardiac failure
  2. fluid overload
  3. low protein (hypoalbuminaemia)
76
Q

Overall, what leads to exudate oedema? (4)

A
  1. tumour
  2. inflammation
  3. allergy
  4. endothelial damage (due to inflammation or burns)

2. Cardiovascular System (42 decks)

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