Congestion and Oedema Flashcards
What is the key thing to remember in congestion and oedema?
Water flows downhill, down a pressure gradient.
Things must do down a pressure gradient otherwise it won’t flow.
What is the critical relationship (ohm’s law)?
Q = deltaP/R Q = BF, P = pressure, R = resistance.
What is congestion?
Relative excess of blood in the vessels of tissue or organ.
Passive process, secondary phenomenon (not like active inflammation where it is active hyperaemia).
Is congestion acute or chronic?
Can be either.
Can become acutely congested - e.g. when grabbed by the throat, or chronic - goes on for long time.
What would a congested vein in the leg look like?
Red, almost purple coloured, full of blood, colour difference very noticeable and swollen.
(in this case due to DVT)
Give the clinical categories of congestion and give examples that fall under these categories.
Local acute congestion, e.g. CVT
Local chronic congestion, e.g. hepatic cirrhosis
Generalise acute congestion, e.g. congestive cardiac failure.
Describe how DVT leads to congestion –> ischaemia and infarction.
Vein blocked causing local acute congestion. Blood backs up in veins, venues, capillaries. Decreased outflow of blood –> local acute congestion –> decreased pressure gradient –> decreased flow across system (Ohm’s law). So no oxygen leading to ischaemia and infarction.
What is hepatic cirrhosis?
Regenerative nodules of hepatocytes with intervening fibrosis. Results from liver damage, e.g. HBV, alcohol.
What happens to the normal architecture of the liver in hepatic cirrhosis? And what is the effect of this?
Loss of normal architecture = altered hepatic BF.
Portal BF blocked - congestion in portal vein and branches, increased portal venous pressure. Collateral circulation - several sites anastomose with systemic circulation.
Local chronic congestion.
What is the major risk with hepatic cirrhosis?
Haemorrhage risk.
Describe the path of hepatic blood flow?
Blood flows from intestines to liver then to vena cava as liver wants to get proteins and detoxify things etc…
What does hepatic cirrhosis look like histologically?
Hepatocytes in lumps, bro bands of tissue b/w. Loss of normal vascular pattern that upsets hepatic BF.
What are oesophageal varices?
Result of portal hypertension, congestion causes back up of blood so enlarged thickened vessels. If puncture this absolute firing of blood out.
What are caput medusae?
Distended and engorged superficial epigastric veins Symptom of portal hypertension (result of back up of blood from blockage in liver).
What can cause congestive heart failure?
AKA biventricular failure
When the heart is unable to clear blood (right and left ventricles) - can be due to ineffective pump, e.g. ischaemia, valve disease.
What is the pathophysiology of congestive cardiac failure?
Decreased CO, decreased renal glomerular filtrate rate –> activation of renin-angiotensin-aldosterone system –> increase in sodium and therefore water retention. So increases amount of fluid in the body. Leads to fluid overload in the veins.
How do you treat this overload of fluid?
Diuretics.
How is water pulled back into the kidney tubules?
Increased ionic retention and sodium pulled back in and water pulled back in with it.
What are the effects of congestive cardiac failure?
Heart cannot clear blood from ventricles.
Back pressure, blood dammed back in veins.
Liver - central venous congestion - right heart failure dams back into the venous system. Acute and chronic changes in lung - pulmonary oedema.
What signs and symptoms are you looking for in congestive cardiac failure?
Liver - central venous congestion: increased JVP, hepatomegaly, peripheral oedema.
Pulmonary oedema: crepitations in lungs, tachycardia (working hard to clear lot of fluid in chest).
Describe the appearance of the liver in hepatic central venous congestion.
Nutmeg liver - red/brown and pale spotty appearance macroscopically.
Red = haemorrhaging, pale = poor function.
How are the pericentral hepatocytes (red) affected in hepatic central venous congestion?
Stasis of poorly oxygenated blood.
How are the periportal hepatocytes (pale) affected in hepatic central venous congestion?
Relatively better oxygenated due to proximity of hepatic arterioles.
Describe the normal microcirculation.
Constant movement of fluid through capillary beds, process of dynamic equilibrium.
Filtration from capillary beds to interstitial.
What forces are involved in normal circulation?
Driven by hydrostatic pressure from heart, balanced by osmotic pressures and endothelial permeability.
Involves lymphatics.
What are the three components that affect net flux and filtration?
Hydrostatic pressure
Oncotic pressure
Permeability characteristics and area of endothelium
What does disturbance in the normal components of microcirculation cause?
Oedema.
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
Define oedema.
Accumulation of abnormal amounts of fluid in the extravascular space (intracellular tissue spaces (ECP) or body cavity.
How do peripheral oedema and effusions differ?
Fluid collections in body cavity = effusions.
Peripheral oedema - increased intersistal fluid in tissues.
Give examples of effusions.
Pleural, pericardial, joint effusions.
Abdominal cavity = ascites.
Describe oedema as a transudate.
Alterations in the haemodynamic forces which act across the capillary wall. Cardiac failure, fluid overload.
Not much protein/albumin (few cells)
Lots of water and electrolytes.
Low specific gravity.
Describe oedema as an exudate.
Part of inflammatory process due to increased vascular permeability. Tumour, inflammation, allergy. Higher protein/albumin content. Water and electrolytes. High specific gravity.
What happens in pulmonary oedema?
Too much fluid going to the lungs, leaks out into alveoli and decreases gas exchange.
What is the pathophysiology of pulmonary oedema?
Hydrostatic pressure - transudate
LVF
- increased L atrial pressure –> passive retrograde flow to pulmonary veins, capillaries and arteries.
- increased pulmonary vascular pressure
- increased pulmonary blood volume
- increased pressure –> increase filtration and pulmonary oedema
What are the effects of pulmonary oedema in the lungs?
Perivascular and interstitial transudate
Progressive oedematous widening of alveolar septa
Accumulation of oedema fluid in alveolar spaces.
Describe the pathophysiology of peripheral oedema.
R heart failure - cannot empty RV in systole.
Blood retained in systemic veins –> increased P in capillaries, increased filtration –> oedema.
Also secondary portal venous congestion via liver.
What happens in congestive cardiac failure to lead to pulmonary and peripheral oedema?
R and L ventricles fail at same time.
All about hydrostatic pressure.
Describe the pathophysiology of lymphatic blockage.
Lymphatic obstruction – hydrostatic pressure upset.
Lymphatic drainage is required for normal flow. If blocked –> lymphedema.
When is lymphedema most common?
Breast cancer may req radiotherapy to axilla, which can cause fibrosis and scarring of lymph vessels, leading to blockage, decreased flow and oedema of the upper limb.
What happens during abnormal renal function?
Salt and H2O retention.
What can do you get secondary to heart failure?
Reduced renal BF.
What is the reason for primary oedema in abnormal renal function?
Acute tubular damage, e.g. hypotension.
What is the pathophysiology of oedema in abnormal renal function?
Decreased renal function, leading to increased salt and water retention, increased intravascular fluid volume, secondary increased capillary pressure –> oedema.
Describe the pathophysiology of low protein oedema.
Oncotic pressure - transudate.
Hypoabluminaemia –> decreased capillary oncotic pressure –> increased filtration.
Give examples of conditions causing low protein oedema.
Nephrotic syndrome –> leaky renal glomerular basement membrane, lose protein, generalise oedema.
Hepatic cirrhosis –> diffuse nodules and fibrosis in liver, liver unable to synthesise enough protein
Malnutrition –> insufficient protein intake.
What are examples of permeability oedema?
Acute inflammation e.g. penumonia and burns.
What occurs in permeability oedema?
Damage to endothelial lining –> increased no of pores in membrane so proteins and larger molecules as well as water leaks out.
