Vascular resistance and flow

Question 1

What determines arterial blood pressure (ABP)?

Answer 1

• Level of arterial blood pressure is determined in elastic arteries, is the driving force for flow
• ABP is determined by blood volume in the arterial system (cardiac output) and determined by resistance offered by all vessels in peripheral arterial system (TRP = total peripheral resistance)
• ABP = CO X TPR
• Determinants of systole pressure in the aorta:
  1. stroke volume (the larger the SV ejected by the left ventricle the higher the systolic pressure)
  2. aortic/arterial distensibility
  3. ejection velocity
  4. diastolic pressure of previous beat
• Increases in EDV, contractility, venous return, exercise, ageing, and decreased aortic compliance all lead to an increased systolic pressure
• Determinants of diastolic pressure:
  1. arteriolar resistance
  2. increases vasoconstriction, arteriosclerosis, and atherosclerosis lead to increase of diastolic pressure
• At very high heart rates, time for diastole is shortened, time available for pressure to fall during diastole is less therefore does not fall to such a low level → high heart rate leads to increased diastolic pressure

Question 2

Properties of elastic arteries

Answer 2

• Primary function of blood vessels: act as a conduit for blood flow away from the heart, towards cells, or back to heart from tissues
• Larger arteries (elastic arteries) have walls rich in smooth muscle and elastin fibres
• Function of larger arteries: damped pulsatile pressure to ensure continuous flow into circulation and ensure blood pressure is maintained during diastole
• Projection of blood into aorta = pressure wave, maximum pressure in aorta is developed during systole when heart is contracting and ejecting blood (systolic pressure) and is progressively damped in smaller arteries
• Pressure drops in aorta during diastole and reaches a minimum at beginning of the next systole (diastolic pressure)
  * SP - DP = pulse pressure
  * MAP = (SP - DP)/3 + DP
• Arterial pressure rises and falls during cardiac cycle
• From blood ejected into aorta, 20-50% of SV passes into peripheral circulation
• Aorta has greater levels of elastin in walls than levels of either smooth muscle or collagen as elastin offers least resistant to stretch allowing walls of aorta to expand to accommodate increase in blood volume during ejection
• During systole, elastic wall distends out this stores some energy of pressure wave, but during diastole, elastic walls recoil, propels blood forward and releases stored energy (Windkessel effect) driving pressure is maintained during diastole for continuous blood flow
• Blood re-enters heart at minimal pressure (central venous pressure)
• Arteriosclerosis: loss of compliance and stiffening of arteries with age leading to increased pulse pressure, elastic component of aorta degenerates, reduced SV increases systolic pressure but reduced elastin decreases diastolic pressure

Question 3

Arterioles and resistance

Answer 3

• Vasoconstriction and vasodilation of arterioles alter resistance to flow in vascular bed they supply, all arterioles are slightly constricted at rest (known as tone)
• 4 different control mechanisms for changing vessel diameter: endothelial factors, local mechanisms, central neural mechanisms, and hormonal mechanisms
• Constriction to multiple organs can increase TPR and ABP
• Endothelium in arteries are joined together by very tight junctions, it produces vasoactive substances the effect vascular smooth muscle cells
• NO is the most important endothelial factor released in arterioles (synthesised continuously in endothelium by NO synthase) release of NO leads to falls in Ca2+ levels and vasodilation by relaxing smooth muscle
• Prostaglandins and endothelial derived hyperpolarisation factors cause vasodilation
• Endothelin causes contraction and acts via intracellular Ca2+ release
• Tissues can regulate their flow through local mechanisms, cells are constantly releasing by-products of metabolism that increase during metabolic activity, resistance vessels close by are sensitive to these by-products
• Active hyperaemia: increased flow due to increased metabolic activity
• Reactive hyperaemia: transient increased flow after period of no flow due to arterial occlusion
• Resistance of arterioles is innovated by sympathetic nervous system, most vascular smooth muscle has tonic vasomotor tone due to sympathetic nerve activity (SNA)
• Decrease in SNA causes vasodilation, increases causes vasoconstriction
• Noradrenaline (released from sympathetic nerve fibres) bind to α1 adrenal receptors causing vasoconstriction
• Presence of α and β receptors shows circulating adrenaline can change radius (tends to cause vasodilation, higher affinity for β receptors)