Haemodynamic disorders Flashcards
Explain how fluid balance is maintained in the body?
- Interplay between hydrostatic pressure and colloid osmotic pressure
- Arteriole –> capillary –> venule
- At the arteriole end, the HP > COP, so fluid tends to escape into the tissue = filtration
- As blood continues across the microvessel, at the venule end the COP>HP due to the increasing concentration of albumin, which returns fluid from the tissues into the vessel!
6 causes of oedema?
- Increased hydrostatic pressure: Heart failure, can be localised in the limbs (DVT)
- Decreased colloid osmotic pressure: Reduction in generation of plasma proteins (albumin). Liver cirrhosis and malnutrition. Also loss of protein via skin (burns), urine (nephrotic syndrome), faeces (bowel disease)
- Lymphatic obstruction: lymph nodes blocked by parasitic worm (lymphatic filariasis) - lymph no longer circulates and drains into leg –> lymphoedema/elephantiasis
- Sodium retention: Xs salt intake or increased RAAS. This increases the hydrostatic pressure (favours fluid leaking into tissues)
- Inflammation: septic shock
Causes of the redness and oedema associated with inflammation?
Redness: blood vessels dilate to allow more blood flow to the tissue
Oedema: blood vessels are more permeable, allowing more fluid to migrate to the area, with proteins and leukocytes
Definition of hyperaemia and congestion?
Hyperaemia: increased blood flow in a particular tissue, in response to change in environment - adaptive change
Congestion: reduced blood flow out, caused by impaired venous return from the affected area - PASSIVE process
- Both based on microcirculation
Reactive vs active hyperaemia?
Reactive: Local vasodilatation in response to O2 debt or accumulation of metabolic waste. Always follows a period of ischaemia. Compensatory mechanism after a period of nutrient and O2 deprivation.
Active: Increased blood flow/vasodilatation in response to period of activation. More related to exercise, the tissue requires more blood in response to increased activity such as lifting weight
Causes & types of congestion?
- Physical obstruction of veins
- Failure of heart to pump blood away from the affected area
- Results in increased venous pressure
1. Local congestion - compression of blood vessels… tumour, venous thrombosis etc
2. Systemic congestion: associated with heart failure and can lead to widespread oedema - CONGESTION AND OEDEMA GO TOGETHER VERY COMMONLY
What is the haemostatic strategy & 3 phases?
Strategy used by the body to prevent bleeding and stop bleeding while keeping the blood within a damaged vessel
- Haemorrhage: process of bleeding
- Thrombosis: process of clotting
- Fibrinolysis: process of clot dissolution
What is a haemorrhage? Causes & consequences?
The extravasation of blood due to rupture of a blood vessel
- Caused by trauma, atherosclerosis, inflammation
- Loss of 15% blood volume = little effect
- Loss of >15% blood volume = hypovolemic shock
- Recurrent blood loss causes iron deficiency
What is the difference between a thrombus and an embolus?
A thrombus is a blood clot formed within the blood vessel that remains attached to the vessel wall. If this detaches from the vessel wall it is now called an embolus
3 main factors causing pathological thrombosis?
- Endothelial injury
- Abnormal blood flow
- Hypercoagulability
What makes up a thrombus?
- Platelets
- RBCs
- Neutrophils
- Lymphocytes
- ^ Held together by a fibrin derived from the coagulation cascade
Difference between arterial and venous thrombosis?
Arterial thrombosis:
- Platelet driven/rich
- Formed under high shear flow
- Around ruptured atherosclerotic plaques and/or damaged endothelium
Mural thrombi = do not occlude vessel. Minor clinical events e.g taking meds
Occlusive thrombi = occludes vessel. Major adverse clinical events
Venous thrombosis:
- Not mainly related to platelet function, MORE to do with stasis i.e changes in blood flow
- Formed under low shear flow (around veins)
- Fibrin and erythrocyte rich
- E.g sitting on a flight for a long period of time
- Fibrin driven response to hypercoagulation, around the valves of the veins
What is atherosclerosis? How does it progress?
Chronic inflammatory disease caused by the formation of ‘fibro-fatty’ lesions in the arterial wall
- Develops progressively through continuous evolution of arterial wall lesions centred on the accumulation of cholesterol-rich lipids and the accompanying inflammatory response
What is an atheroma? Describe the stages of atheroma development (atherogenesis)
Atheroma is an accumulation of degenerative material in the tunica intima of artery walls. Material = macrophages, debris containing lipids, calcium and fibrous connective tissue
Stages:
- Initiation - fatty streak formation
- Endothelial dysfunction
- Lipid entry and modification. Formation of lipid layer ‘fatty streak’ within the intima layer
- Leukocyte recruitment
- Foam cell formation (monocytes/macrophages that have phagocytosed lipids) - Plaque progression - fibrous cap atheroma
- Lipid-rich necrotic core, dead foam cells, macrophages, smooth muscle cells, ECM
- Necrotic core is encapsulated by a fibrous cap that separates the necrotic core and vessel
- This causes the artery to become narrower, restricting and reducing blood flow through the artery - Plaque rupture
- Mature plaques are vulnerable to rupturing, exposing thrombogenic material to the blood, this is what causes atherothrombosis/blood clot formation over the atheroma which will completely block blood flow
- The plaques can cause arteries to harden and narrow, restricting blood flow and O2 supply to vital organs (atherosclerosis), increasing risk of blood clots blocking flow to the heart (CHD) or brain
Clinical complications of atherosclerosis?
N.B acute narrowing of the vessel lumen, chronic occlusion, embolism
Can cause:
- Coronary heart disease: angina, MI, heart failure
- Carotid artery disease: brain TIA, stroke (necrosis)
- PAD: when it narrows arteries in arms or legs
- CKD
- Aneurysm
