The Windkessel Effect
Arterial Pressure Determinants
– CO
– TPR
Changes in the Pulse Waveform
Hydraulic filtering converts the intermittent output of the heart to a steady flow through the capillaries.
Part of the energy of cardiac contraction is dissipated as forward capillary flow.
The remaining energy is stored as potential energy in the distensible arteries.
During diastole, the elastic recoil of the arterial walls converts this potential energy into blood flow.
The mean arterial pressure is the pressure in the large arteries, averaged over time.
MAP can be measured from the arterial pressure tracing by measuring the area under the pressure curve.
It can also be estimated by the formula: MAP = Pd + (Ps-Pd)/3
The physiological (alterable) factors are the cardiac output and the peripheral resistance.
The two physical (dependent) factors are the blood volume within the arterial system and the compliance of the system .
The change in pressure in response to a change in cardiac output can be appreciated by considering:
Let the cardiac output = 5 L/min and
MAP = 100 mmHg.
The total peripheral resistance is; R
= P/Q = 100/5 = 20 mmHg/L/min
( Omh’s Law: R=V/I)
If cardiac output (Qh) suddenly increased to
10 L/min, P will initially remain unchanged.
Outflow (Qr) remains unchanged at 5 L/min because it depends on depends on P and R.
When Qh > Qr, mean arterial blood volume increases.
Because P depends on the arterial blood volume (V) and on the arterial compliance
(C), an increase in V will increase P.
Similar reasoning can explain the changes in
P that accompany alterations in peripheral resistance.
Increase R suddenly to 40 mmHg/L/min.
Qr = P/R = 2.5 L/min.
Thus, the peripheral runoff would only be 2.5
L/min, even though cardiac output was 5
L/min.
If Qh remained constant at 5 L/min, Qh would exceed Qr and V would increase; therefore, P would rise.
The radial stretch of descending aorta from ejection initiates a pressure wave that is propagated down the aorta and its branches.
The pressure wave travels much faster than does the blood itself.
The velocity of the pressure wave varies inversely with the vascular compliance.
The pulse velocity increases progressively as the wave travels from aorta towards the periphery.
The arterial pressure contour becomes distorted as the wave is transmitted down the arterial system.
– Three major changes occur in the arterial pulse contour.
First, the incisura (a notch that appears at the end of ventricular ejection), is damped and disappears.
Second, the systolic portions of the pressure wave become narrow and elevated.
Third, a hump may appear on the diastolic portion of the pressure wave.
– The dampening of the high-frequency components of the arterial pulse is caused largely by the viscoelastic properties of the arterial walls.
– The precise mechanism for the peaking of the pressure wave is controversial.
– Several factors contribute to these changes, including reflection, tapering of the arteries, resonance, and velocity of transmission.
The Windkessel Effect
Arterial Pressure Determinants
– CO
– TPR
Changes in the Pulse Waveform