The Vascular Tree

The cardiovascular system – the vascular tree (01/10/13 lecture) The cardiovascular system exists to perfuse tissues with sufficient blood to meet their metabolic needs (which differ and change). The heart provides the energy (kinetic energy from contractile properties) and the blood vessels provide resistance to flow – this interaction generates pressure (a pump pushing against resistance = pressure), which is required in transport/distribution of fluid to counter inertia. Once the blood does start moving, the pressure is dissipated in the form of friction/heat. Blood flow through blood vessels depends on: pressure gradient, resistance, blood viscosity, tube length, and vessel radius. A pressure gradient is generated along a tube/vessel as energy is lost through friction of the fluid with walls – it is both required by and a product of flow. Flow depends on Δ pressure, not absolute pressure. Blood viscosity and tube length can be considered constant. Resistance = 1/vessel radius4. So halving the diameter increases resistance by x16, so would have to increase pressure 15x to maintain same flow – critical to controlling blood pressure and to pathology. The greatest drop in pressure throughout the circulation occurs in the arterioles, which offer the most resistance, and this bottleneck is crucial for control. Arteries have internal and external elastic lamina for elastic/pressure role, whereas veins don’t. Blood flow from the heart is intermittent but flow through the tissues is continuous – this maintenance of blood pressure and flow when the heart is relaxed is a result of passive recoil of elastic arteries. Precapillary sphincters at terminal arterioles are sensitive to local metabolic needs and control blood flow through the arterial bed that branches from the terminal arteriole. If the tissue requires perfusion, the sphincters will be open to allow blood flow. At rest, the sphincters remain closed and only the vascular shunt (the metarteriole and the thoroughfare venous channel) allow blood flow – up to 95% vessels closed at rest. The precapillary sphincters (smooth muscle) in the microcirculation respond to nerve stimulation (autonomic sympathetic), blood pressure, local metabolites (CO2, K+ etc), and circulating hormones. Capillary types: ·         Continuous: Most common; intact endothelial lining; tight inter-cell junctions so can best regulate exchange – v. tight in blood-brain barrier; e.g. in skeletal muscle and brain. ·         Fenestrated: Endothelial lining contains pores for more rapid exchange – less control; less tight inter-cell junctions between endothelial cells; e.g. in kidneys and intestines. ·         Sinusoid: Incomplete endothelial lining and basement membrane; allows movement of even cells and cellular components; e.g. in bone marrow and liver for haematopoiesis and processing of blood. Fluid exchange in capillaries is driven by forces: pressure on blood will push it forward, but also hydrostatic pressure will push it towards the periphery of the capillary, while interstitial forces will push it back, and osmotic pressure force fluid in and out of capillaries depending on composition of fluids. Oedema (build-up of fluid in the interstitial space) should occur more often due to pressures and fluid movement, but lymphatics drain it back into the right subclavian vein (~2L/day collected). Net outflow into extracellular fluid = net filtration – net absorption. The pressure gradient in the venous system is ~20 mmHg. This is too low for adequate venous return, so it is aided by the muscular pump (contraction of skeletal muscles squeezes deep veins within them which pushes blood towards heart – aided by valves) and the respiratory pump (contraction of diaphragm expands thorax, which expands great veins, which accommodates more blood filling them). Mean arterial pressure is determined by: Blood volume In turn controlled by long term mechanisms: renin release → angiotensin II production → aldosterone release → Na+ retention → ADH release → H2O retention → rise in blood volume and pressure. Cardiac output Cardiac output = heart rate x stroke volume Heart rate may be altered by autonomic nervous activity and/or epinephrine presence. Starling’s Law states that the heart will always try to pump what is returned to it – so a greater preload (set by end diastolic volume), increased contractility (e.g. caused by epinephrine) and increased afterload (pressure ventricles pump against) ↑ BP. Vessel resistance Determined by smooth muscle cell activity in arterioles, which in turn is determined by direct response to stretch, response to local metabolites and hormones (e.g. adrenaline, ADH, renin/angiotensin II, endothelium-derived factors), and sympathetic activity e.g. baroreceptor reflex. Distribution of blood between arterial and venous blood vessels In turn determined by dilation/constriction of large veins, the capacitance vessels, which hold ~65% of circulating blood. A slight constriction shifts a significant amount of blood to the arterial side – increasing pressure. This also includes plasma:interstitial fluid distribution (hydrostatic/osmotic forces). Hypertension Systolic/diastolic pressures of >140/90 mmHg. Multifactorial: genetic and environmental predispositions. Hypertension is a chronic disease (acute malignant hypertension is RARE) that is involved in major health issues such as: atherosclerosis, ischaemic heart disease, stroke, and diabetes. Cardiovascular disease is a major killer in the developed world. Greatly increased systolic pressure causes a sharper increase in mortality than increases in diastolic pressure. Salt consumption also increases blood pressure, so some populations are at a greater risk than others. Blood pressure rises ‘naturally’ with age.

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