1. FLOW THROUGH TUBES By Joshua Bower Peer Support 2013/2014 J.Bower@warwick.ac.uk

2. WARNING I am not a physicist.

3. Where is the largest pressure drop in the systemic circulation? Between the arteries- arterioles

4. For a given pressure gradient, what is flow determined by? Resistance of the vessel (dependent on its radius) The arterioles are high resistance – narrow with stretch-resistant muscular walls

5. What is the clinical relevance? Arteriolar constriction/dilatation (e.g. at the renal bed) controls the blood supply to an organ or capillary bed

6. Blood pressure = ? Blood pressure = cardiac output x systemic vascular resistance Pressure gradient = flow x resistance BP = CO x SVR

7. What term denotes normal blood flow in a tube? Laminar Laminar flow means velocity is at its lowest at the edges – Why is this good?

8. Laminar flow means the width of the tube greatly affects its resistance (flow proportional to r 4 ) What is the clinical significance? If there is an occlusion of the vessel (i.e. atherosclerosis) by 50% of the radius, flow will fall by 16x if pressure is constant OR pressure gradient will rise by 16x if flow is constant

10. The basics so far… Pressure gradient = flow x resistance Blood pressure = CO x SVR Laminar flow means velocity is lowest at the edges, and the width of the tube will affect resistance. Halving the vessel radius means either flow will fall by 16x (>>ischaemia) or pressure has to rise by 16x (>>hypertension)

11. What THREE factors increase the likelihood of turbulent flow? [3] High velocity Low blood viscosity Large vessel diameter

12. (i) How would the blood viscosity change in anaemia? (ii) What term denotes increased RBCs? (i)Decrease  Decreased viscosity, therefore SVR decrease, and CO rises (ii)Polycythaemia  Increased SVR and BP

13. What is the clinical significance of turbulent flow? [2] We can hear it! Bruits in arteries, wheeze in airways Turbulent flow causes damage to endothelium

14. List the steps leading to atheroma development [6] 1.Chronic endothelial injury (e.g. HTN, smoking) 2.Endothelial dysfunction (becomes more permeable, cholesterol-rich LDLs enter and becomes oxidised 3.Monocytes enter, becomes macrophages and attempt to digest the cholesterol – become foam cells (visible as a fatty streak) 4.Foam cells release growth factors, stimulating SMC infiltration from the media, which then proliferate 5.Collagen and ECM becomes deposited, forming fibrofatty plaque 6.SMCs calcify as they degenerate in aged plaques, making them more vulnerable to rupture

15. How can atheroma be treated? [3] Reduce risk factors Stenting by PCTA Bypass grafting via CABG

16. What is the relationship between flow and pressure within vessels, bearing in mind they are distensible? With a distensible tube, an increase in pressure stretches the walls lowering resistance

17. What is the clinical relevance? Distensibility gives them capacitance – Vessels widen with increasing pressure, so more blood will flow in than out – Thus the venous system can store blood (~67%) However, at low intravascular pressures the vessels may close

18. So what do you really need to know? Occlusion = bad – Rise pressure or reduce flow BP = CO x SVR – So think about factors affecting SVR (vasoconstrictors) and CO Turbulent flow can damage endothelium At low intravascular/high extravascular pressures, vessels can collapse

19. QUESTIONS? By Joshua Bower Peer Support 2013/2014 J.Bower@warwick.ac.uk