Congestion and Oedema

Question 1

Darcy’s Law

Q = difference P/R

Answer 1

Physiological equivalent of Ohm’s law
Q = blood flow
P = pressure
R = resistance

Question 2

Congestion

Answer 2

Relative excess of blood in vessels of tissue or organ
Passive process, secondary phenomenon
Not like acute inflammation - active hyperaemia
Acute or chronic

Question 3

Clinical pathology examples of congestion

Answer 3

Local acute congestion
Deep vein thrombosis
Local chronic congestion
Hepatic cirrhosis
Generalised acute congestion
Congestive cardiac failure

Question 4

Deep vein thrombosis of the leg

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
decreased flow across system (Flow = difference in P/R) hence decreased pressure difference P causes decreased flow
No O2 supply causes ischaemia and infarction

Question 5

Hepatic cirrhosis

Answer 5

Results from serious liver damage eg HBV, alcohol
Regenerating liver forms nodules of hepatocytes with intervening fibrosis
Loss of normal architecture
altered hepatic blood flow
Portal blood flow blocked
congestion in portal vein and branches
increased portal venous pressure
collateral circulation - several sites anastomose with systemic circulation
Local chronic congestion - haemorrhage risk

Question 6

Consequence: portal-systemic shunts

Answer 6

Caput medusae (visible large veins in abdomen)
Oesophageal varices (same in oesophagus)

Question 7

Congestive cardiac failure

Answer 7

Heart unable to clear blood, right & left ventricles
ineffective pump eg ischaemia, valve disease
Pathophysiology
decreased Cardiac Output (CO)
 Renal Glomerular Filtration Rate (GFR)*
activation of renin-angiotensin-aldosterone system
Na and H2O retention*
increased amount of fluid in body
Fluid (overload) in veins (Treatment: diuretics)

Question 8

Congestive cardiac failure - effects

Answer 8

Heart cannot clear blood from ventricles
Back pressure, blood dammed back in veins
Lungs - pulmonary oedema – see later
Left heart failure – blood dams back into lungs
Clinically, crepitations in lungs, tachycardia
Liver - central venous congestion
Right heart failure- blood dams back to systemic circulation
 JVP, hepatomegaly, peripheral oedema

Question 9

Hepatic Central Venous Congestion

Answer 9

“Nutmeg” liver red/brown & pale spotty appearance macroscopically
Pericentral hepatocytes (red) Stasis of poorly oxygenated blood
Periportal hepatocytes (pale) Relatively better oxygenated due to proximity of hepatic arterioles

Question 10

Normal microcirculation

Answer 10

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 11

arterial and venous pressures

Answer 11

Arterial side: PC > piC sofiltration
Venous side: piC > PC so reabsorption

Pc=capillary hydrostatic pressure
Pi=intersitial hydrostatic pressure
pii=interstitial oncotic pressure
pic=capillary oncotic pressure

Question 12

Summary of microcirculation

Answer 12

Three components affect net flux and filtration
Hydrostatic Pressure
Oncotic Pressure
Permeability characteristics and area of Endothelium

Starling's Hypothesis
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

Disturbances of normal components =oedema

Question 13

Oedema

Answer 13

Accumulation of abnormal amounts of fluid in the extravascular compartment
intercellular tissue compartment (extracellular fluid)
body cavities
Peripheral oedema : increased interstitial fluid in tissues
Effusions: fluid collections in body cavities
Pleural, pericardial, joint effusions
Abdominal cavity - ascites

Question 14

Oedema: transudate

Answer 14

Alterations in the haemodynamic forces which act across the capillary wall
Cardiac failure, fluid overload
Not much protein/albumin (few cells)
Lots of H2O & electrolytes
Low specific gravity

Question 15

Oedema: exudate

Answer 15

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

Question 16

Pathophysiology of pulmonary oedema

Answer 16

Hydrostatic pressure - transudate
Left ventricular failure
 left atrial pressure  passive retrograde flow to pulmonary veins, capillaries and arteries
 pulmonary vascular pressure
 pulmonary blood volume
PC  filtration and pulmonary oedema
In lungs
perivascular and interstitial transudate
progressive oedematous widening of alveolar septa
accumulation of oedema fluid in alveolar spaces

Question 17

Pathophysiology of peripheral oedema

Answer 17

Right heart failure – cannot empty RV in systole
Blood retained in systemic veins so increase P in capillaries so increase filtration so peripheral oedema
also, secondary portal venous congestion via liver

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

Question 18

Pathophysiology of lymphatic blockage

Answer 18

Lymphatic Obstruction – hydrostatic pressure upset
Lymphatic drainage is required for normal flow
If lymphatic system blocked  lymphoedema
e.g. breast cancer may require radiotherapy to axilla  fibrosis  outflow  oedema of upper limb

Question 19

Pathophysiology of oedema in abnormal renal function

Answer 19

Abnormal renal function results in Salt (NaCl) and H2O retention
Secondary in heart failure - reduced renal blood flow
Primary: acute tubular damage eg hypotension
decreased renal function is the result of both
increase salt and H2O
increase intravascular fluid volume
 secondary  PC
 oedema

Question 20

Pathophysiology of low protein oedema

Answer 20

Oncotic Pressure (pi ) - transudate
piC requires normal protein levels
Hypoalbuminaemia decreaes piC so increases filtration
e.g. nephrotic syndrome  leaky renal glomerular basement membrane; lose protein; generalised oedema
e.g. hepatic cirrhosis  diffuse nodules and fibrosis in liver; liver unable to synthesise enough protein
e.g. malnutrition  insufficient intake of protein

Question 21

Pathophysiology of permeability oedema

Answer 21

Endothelial Permeability - exudate
Damage to endothelial lining increase”pores” in membrane (osmotic reflection coefficient of endothelium) towards zero
Proteins and larger molecules can leak out (not just H2O)
e.g. acute inflammation such as pneumonia
e.g. burns

Question 22

Summary of oedema

Answer 22

Normal fluid flux is a complex dynamic balance across the endothelial membrane
Achieves a steady state
Upsetting any of the Starling forces can lead to oedema
Oedema is clinically relevant – morbidity and mortality – understanding the pathology allows rational treatment