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

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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