Pulse Pressure Wave Velocity (07/10/13 prac)

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Pulse Pressure Wave Velocity

(07/10/13 prac)

The pulse pressure wave is the wave of pressure/volume changes that

occurs down an elastic arterial blood vessel to maintain blood pressure and

flow during diastole. Completely rigid arteries would result in an equal volume

of blood being returned to the heart as is ejected from it – but this would

move blood at too rapid a speed for exchange and would not allow for control.

The rate at which the pulse pressure wave travels

along the blood vessels depends on the rigidity/elasticity of the blood vessel

walls – the more ‘relaxed’ they are, the more blood pushes and stretches the

wall rather than pushing on the blood further down, so the slower the

pressure wave travels; the ‘stiffer’ the blood vessels are, the less able blood

is to stretch the blood vessel wall and the greater the ‘push’ on blood further

downstream, so that the pulse pressure wave travels faster.

In order to measure

the speed (distance/time), we used the R wave from an ECG (subject had

positive, negative and earth attached to wrists and ankle) as the start of the

pulse pressure wave (ventricular systole) and the peak blood volume at the

index finger to indicate the blood arriving at distal arteries (using a

plethysmograph). To calculate the speed in metres per second, we measured the

distance from the subject’s sternum to their fingertip in millimetres (1),

established the time delay in milliseconds (2) and then divided 1 by 2.

We recorded repeated measurements of pulse pressure wave under the

following conditions: quiet/relaxed; supine; recording arm above head (increase

in gravity); non-recording hand in ice (vasoconstriction); after two minutes of

moderate exercise (step-ups)(increased heart rate and cardiac output); and

immediately after two minutes of occlusion of forearm blood flow using a sphygmomanometer

cuff (build-up of pressure behind cuff).

A study found that the

average pulse pressure wave velocity in the quiet/relaxed conditions was 4.67±0.41

m/s. My value was 3.12 m/s which is either very slow or inaccurate.

Class

data:

·

Using an unpaired T-test to establish p

values, there was evidence (@ 5%) that male and female pulse pressure wave

velocities differed in quiet/relaxed, arm raised, and ice experimental

conditions. This is likely tied in to the physiological difference of males

having a higher blood pressure overall (as established in the blood pressure

practical).

·

Using a paired T-test to establish p values,

there was no evidence for a significant difference in pulse pressure wave

velocity when the subject was in quiet/relaxed, arm raised and ice experimental

conditions. We deduced that this was because the non-recording arm underwent

the change in conditions and it may not have had time to cause a systemic

effect.

Aortic pulse pressure wave velocity is considered the gold standard

for assessing arterial stiffness; this is most commonly calculated from

carotid-to-femoral pulse pressure wave velocity, and is one of the most robust

parameters for the prediction of cardiovascular events. The four major

determinants of pulse pressure wave velocity are:

·

Age: With increasing age the pulsatile strain breaks the elastic fibres (in elastic

arteries such as the aorta, carotid, or iliac), which are replaced by

collagen. These changes in the arterial structure lead to increased arterial

stiffness, and consequently to increased central PWV.

·

Blood pressure: The pulse pressure wave is matched by a reflective

wave travelling back to the heart. Increased arterial stiffness increases the

velocity of the reflective wave so that it interferes with systole rather than

arriving at the ascending aorta during diastole. This increases the afterload

and thus blood pressure.

·

Gender: pre-menopausal women have lower pulse pressure wave

velocities than age-matched men, but post-menopausal women have similar values

to age-matched men.

·

Heart rate: If heart rate increases, the time for vessels to

distend is reduced, resulting in increased rigidity of the arterial wall. Also,

sympathetic activation is associated

with increased stiffness of the arteries due to an increase in heart

rate, blood pressure and smooth muscle cells tonus.

Increased arterial stiffness can lead to endothelial damage, which

is the first stage in the development of atherosclerosis.

Increased arterial stiffness leads to an

increase in central systolic pressure associated with an increased afterload,

which in turn can lead to left ventricular hypertrophy. The associated lowered

diastolic pressure can then prevent the increased muscle mass from receiving the

correct oxygen level, resulting in ischaemic events.

Increased

arterial stiffness and blood pressure affects vascular beds in the brain and

kidneys, which receive a high-volume flow throughout systole and diastole with

minimal vasoconstrictive protection. This can lead to vascular injuries.

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