Congestion and Oedema Flashcards
Darcy’s Law
Q = difference P/R
Physiological equivalent of Ohm’s law
Q = blood flow
P = pressure
R = resistance
Congestion
Relative excess of blood in vessels of tissue or organ
Passive process, secondary phenomenon
Not like acute inflammation - active hyperaemia
Acute or chronic
Clinical pathology examples of congestion
Local acute congestion Deep vein thrombosis Local chronic congestion Hepatic cirrhosis Generalised acute congestion Congestive cardiac failure
Deep vein thrombosis of the leg
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
Hepatic cirrhosis
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
Consequence: portal-systemic shunts
Caput medusae (visible large veins in abdomen) Oesophageal varices (same in oesophagus)
Congestive cardiac failure
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)
Congestive cardiac failure - effects
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
Hepatic Central Venous Congestion
“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
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
arterial and venous pressures
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
Summary of microcirculation
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
Oedema
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
Oedema: transudate
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
Oedema: exudate
Part of inflammatory process* due to vascular permeability Tumour, inflammation, allergy Higher protein/albumin content (cells) H2O & electrolytes High specific gravity
Pathophysiology of pulmonary oedema
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
Pathophysiology of peripheral oedema
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)
Pathophysiology of lymphatic blockage
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
Pathophysiology of oedema in abnormal renal function
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
Pathophysiology of low protein oedema
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
Pathophysiology of permeability oedema
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
Summary of oedema
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
