Arterial Pressure Waveforms

Abstract

What is the Windkessel effect? During systole, the LV ejects around 70 mL of blood into the aorta (the SV). The elastic aortic walls expand to accommodate the SV, moderating the consequent increase in intra-aortic pressure from a DBP of 80 mmHg to an SBP of 120 mmHg. The ejected blood possesses kinetic energy, whilst there is storage of potential energy in the stretched aortic wall. In diastole, recoil of the aortic wall converts the stored potential energy back into kinetic energy. This maintains the onward flow of blood during diastole, thereby maintaining DBP; this is known as the ‘Windkessel effect’. This effect converts the sinusoidal pressure wave generated in the heart into a positive and constant pressure at the tissues, much like converting AC to DC electricity. With advancing age, there is degeneration of elastin in the wall of the aorta. The aortic wall becomes less compliant, and its ability to accommodate SV without a large increase in pressure reduces. This accounts for the development of systolic hypertension in the elderly. What is the arterial pressure wave? Ejection of blood into the aorta generates both an arterial pressure wave and a blood flow wave. The arterial pressure wave is caused by the distension of the elastic walls of the aorta during systole. The wave propagates down the arterial tree at a much faster rate (around 4 m/s) than the mean aortic blood velocity (20 cm/s). It is the arterial pressure wave that is felt as the ‘radial pulse’, not the blood flow wave.