The Vascular Tree

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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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