Pathophysiology of congestion and oedema

Question 1

Critical relationship

Answer 1

Q = ChangeinP/R

Q = blood flow 
P = pressure 
R = resistance

Question 2

What is Congestion?

Answer 2

Relative excess of blood in vessels of tissue or organ:

• passive process
• Not like acute inflammation: active hyperaemia
• Acute or chronic

Question 3

Clinical pathology examples

Answer 3

Local acute congestion
- Deep vein thrombosis

Local chronic congestion
- Hepatic cirrhosis

Generalised acute congestion
- Congestive cardiac failure

Question 4

What is Deep vein thrombosis of the leg, and features?

Answer 4

• Vein blocked causing localised acute congestion
• Blood backs up in veins, venules, capillaries
• Decreased outflow of blood
• Local, acute congestion
• Decreased pressure gradient
• No O2 therefore ischaemia and infarction

Question 5

What is Hepatic cirrhosis?

Answer 5

• Results from serious liver damage e.g. HBV, alcohol
• Regenerating liver forms nodules of hepatocytes with intervening fibrosis
• Loss of normal architecture: altered hepatic blood flow
• Portal blood flow blocked
• Local chronic congestion: haemorrhage risk

Question 6

What are consequences of portal-systemic shunts?

Answer 6

• Caput medusae

- Oesophageal varices

Question 7

Features of congestive cardiac failure

Answer 7

Heart unable to clear blood, right & left ventricles
- ineffective pump e.g. ischaemia, valve disease

Fluid (overload) in veins (Treatment: diuretics)

Question 8

Pathophysiology of congestive cardiac failure

Answer 8

Decreased cardiac output (CO)

Decreased renal glomerular filtration rate (GFR)

• Activation of renin-angiotensin-aldosterone system
• Increased Na and H2O retention

Increased amount of fluid in body

Question 9

What are effects of congestive cardiac failure?

Answer 9

• Heart cannot clear blood from ventricles
• Back pressure, blood dammed in veins
• Lungs -pulmonary oedema
• Liver: central venous congestion:
  Right heart failure
  Increased JVP, hepatomegaly, peripheral oedema

Question 10

Pericentral hepatocytes and Periportal hepatocytes in hepatic central venous congestion

Answer 10

Pericentral hepatocytes (red) - Stasis of poorly oxygenated blood

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

Question 11

What happens in normal microcirculation?

Answer 11

• Constant movement of fluid through capillary beds; process of dynamic equilibrium
• Driven by hydrostatic pressure from heart
• Balanced by osmotic pressures and endothelial permeability
• Filtration from capillary beds to interstitium
• Capillaries-interstitium-capillaries and lymphatics

Question 12

Which three components affect net flux and filtration?

Answer 12

• Hydrostatic pressure
• Oncotic pressure
• Permeability characteristics and area of endothelium

Question 13

What is Starling’s hypothesis?

Answer 13

Net filtration (Jv)= [(force favouring filtration/flow of fluid out of vessel) - endothelial permeability to proteins x (forces opposing filtration/keeping fluid in vessel)] x endothelial permeability to H2O x area of capillary bed

Question 14

What is normal oedema?

Answer 14

Accumulation of abnormal amounts of fluid in the extravascular compartment

• Intercellular tissue compartment (extracellular fluid)
• Body cavities

Question 15

What is peripheral oedema?

Answer 15

Increased interstitial fluid in tissues

Question 16

What are oedema effusions?

Answer 16

Fluid collections in body cavities

• Pleural, pericardial, joint effusions
• Abdominal cavity: ascites

Question 17

What is Oedema: exudate?

Answer 17

• Part of inflammatory process due to increased vascular permeability
• Tumour, inflammation, allergy
• Higher protein/albumin content (cells)
• H2O & electrolytes
• High specific gravity

Question 18

Pathophysiology of pulmonary oedema in left ventricular failure

Answer 18

Hydrostatic pressure - transudate

• Increased left atrial pressure > passive retrograde flow to pulmonary veins, capillaries and arteries
• Increased pulmonary vascular pressure
• Increased pulmonary blood volume
• Increased Pc > Increased filtration and pulmonary oedema

Question 19

Pathophysiology of pulmonary oedema in lungs

Answer 19

• Perivascular and interstitial transudate
• Progressive oedematous widening of alveolar septa
• Accumulation of oedema fluid in alveolar spaces

Question 20

Pathophysiology of peripheral oedema

Answer 20

Right heart failure – cannot empty RV in systole
Blood retained in systemic veins > Increased pressure in capillaries > increased filtration > peripheral oedema
also, secondary portal venous congestion via liver

Question 21

Pathophysiology of peripheral oedema: Congestive cardiac failure

Answer 21

• Right and left ventricles both fail
• Pulmonary oedema and peripheral oedema at the same time
• All about hydrostatic pressure (P)

Question 22

Pathophysiology of lymphatic blockage

Answer 22

Lymphatic obstruction - hydrostatic pressure upset

• Lymphatic drainage is required for normal flow
• If lymphatic system is blocked > lymphoedema
  e. g. breast cancer may require radiotherapy to axilla > fibrosis > decreased outflow > oedema of upper limb

Question 23

Pathophysiology of low protein oedema

Answer 23

Oncotic pressure - transudate

• Oncotic pressurec requires normal protein levels
• Hypoalbuminaemia > decreased oncotic pressurec > increases filtration
  e. g nephrotic syndrome
  e. g. hepatic cirrhosis
  e. g. malnutrition

Question 24

Pathophysiology of permeability oedema

Answer 24

Endothelial permeability - exudate

• Damage to endothelial lining > Increases “pores” in membrane > osmotic reflection coefficient of endothelium decreases towards zero
• Proteins and larger molecules can leak out (not just H2O)
  e. g. acute inflammation such as pneumonia
  e. g. burns