FLOW THROUGH TUBES

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 r4)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? • Decrease • Decreased viscosity, therefore SVR decrease, and CO rises • 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] • Chronic endothelial injury (e.g. HTN, smoking) • Endothelial dysfunction (becomes more permeable, cholesterol-rich LDLs enter and becomes oxidised • Monocytes enter, becomes macrophages and attempt to digest the cholesterol – become foam cells (visible as a fatty streak) • Foam cells release growth factors, stimulating SMC infiltration from the media, which then proliferate • Collagen and ECM becomes deposited, forming fibrofatty plaque • 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