Pathophysiology of congestion and oedema Flashcards
Critical relationship
Q = ChangeinP/R
Q = blood flow P = pressure R = resistance
What is Congestion?
Relative excess of blood in vessels of tissue or organ:
- passive process
- Not like acute inflammation: active hyperaemia
- Acute or chronic
Clinical pathology examples
Local acute congestion
- Deep vein thrombosis
Local chronic congestion
- Hepatic cirrhosis
Generalised acute congestion
- Congestive cardiac failure
What is Deep vein thrombosis of the leg, and features?
- 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
What is Hepatic cirrhosis?
- 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
What are consequences of portal-systemic shunts?
- Caput medusae
- Oesophageal varices
Features of congestive cardiac failure
Heart unable to clear blood, right & left ventricles
- ineffective pump e.g. ischaemia, valve disease
Fluid (overload) in veins (Treatment: diuretics)
Pathophysiology of congestive cardiac failure
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
What are effects of congestive cardiac failure?
- 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
Pericentral hepatocytes and Periportal hepatocytes in hepatic central venous congestion
Pericentral hepatocytes (red) - Stasis of poorly oxygenated blood
Periportal hepatocytes (pale) - Relatively better oxygenated due to proximity of hepatic arterioles
What happens in normal microcirculation?
- 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
Which three components affect net flux and filtration?
- Hydrostatic pressure
- Oncotic pressure
- Permeability characteristics and area of endothelium
What is 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
What is normal oedema?
Accumulation of abnormal amounts of fluid in the extravascular compartment
- Intercellular tissue compartment (extracellular fluid)
- Body cavities
What is peripheral oedema?
Increased interstitial fluid in tissues
What are oedema effusions?
Fluid collections in body cavities
- Pleural, pericardial, joint effusions
- Abdominal cavity: ascites
What is Oedema: exudate?
- Part of inflammatory process due to increased vascular permeability
- Tumour, inflammation, allergy
- Higher protein/albumin content (cells)
- H2O & electrolytes
- High specific gravity
Pathophysiology of pulmonary oedema in left ventricular failure
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
Pathophysiology of pulmonary oedema in lungs
- Perivascular and interstitial transudate
- Progressive oedematous widening of alveolar septa
- Accumulation of oedema fluid in alveolar spaces
Pathophysiology of peripheral oedema
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
Pathophysiology of peripheral oedema: Congestive cardiac failure
- Right and left ventricles both fail
- Pulmonary oedema and peripheral oedema at the same time
- All about hydrostatic pressure (P)
Pathophysiology of lymphatic blockage
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
Pathophysiology of low protein oedema
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
Pathophysiology of permeability oedema
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
