Key Characteristics of the Arterial Pulse
When evaluating arterial pulsation, several key parameters are considered that reflect heart function and the state of the vascular bed:
- Rate. Directly determined by the heart rate (HR).
- Rhythm. Can be regular or irregular. This parameter demonstrates the regularity of heart function.
- Amplitude. Characterizes the stroke volume of blood and the degree of elasticity of the arterial walls.
- Rate of rise (speed). Reflects the speed at which pressure in the arteries changes (rises and falls) during left ventricular contraction. The pulse can be rapid or slow.
- Tension. Evaluated by the resistance of the arterial wall — determined by the pressing force required to completely compress the vessel and stop the pulsation. Based on tension, the pulse is classified as hard or soft.
Sphygmography: Graphical Recording of the Pulse
Sphygmography is a method for graphically recording the arterial pulse. The resulting curve (sphygmogram) consists of first-order waves, each corresponding to a specific phase of the cardiac cycle.
The mechanism of these waves is based on the stretching of the aortic wall during blood ejection and its subsequent return to original dimensions due to elasticity.
Main elements of the sphygmogram:
- Anacrotism (anacrotic wave) — the ascending part of the curve (rise). It reflects the moment of opening of the semilunar valves and active blood ejection into the aorta. The duration of this stage is about 0.08 s.
- Systolic plateau — the peak of the pulse curve, lasting approximately 0.14 s. The total period of systolic rise and plateau takes about 0.25 s.
- Catacrotism (catacrotic wave) — the descending part of the curve (fall), which shows the pressure drop in the arterial system during diastole. The period of diastolic decline lasts about 0.4 s.
- Incisura (dicrotic notch) — a sharp, short-term drop on the catacrotism. This element precisely corresponds to the moment the aortic semilunar valves snap shut.
- Dicrotic wave — a secondary, lower-amplitude wave rise immediately following the incisura. It is caused by elastic recoil: blood rebounds from the closed aortic valves back into the vascular bed.
Propagation of the Pulse Wave
The mechanical oscillation, originating in the aorta, is transmitted to arteries and arterioles. The propagation velocity of the pulse wave is always higher than the actual blood flow velocity.
To calculate the pulse wave velocity, a specialized formula is used that takes into account the physical characteristics of the vessel:
- Internal radius of the vessel.
- Thickness of the vessel wall.
- Density of the blood and vessel wall.
- Modulus of elasticity (compliance) of the vessel.
For instance, when recording the pulse at the radial artery (a. radialis), located about 1 meter from the heart, the wave transit time is approximately 100 ms. This is precisely the delay by which pulsation at the wrist lags behind myocardial contraction.
As the wave travels from the heart to the periphery, the pressure oscillations gradually attenuate. However, the amplitude of each pulse phase in peripheral arteries increases (the phenomenon of peripheral pulse amplification). Final attenuation of the pulse wave occurs in the arterioles.
Venous Pulse (Jugular Vein Example)
In addition to the arterial pulse, there is a venous pulse, which is recorded in large veins (such as the jugular vein) and correlated with the electrocardiogram (ECG). The venous pulse curve has a complex structure consisting of positive and negative waves.
Positive waves:
- Wave a: caused by right atrial systole, which impedes outflow and causes partial blood reflux.
- Wave c: transmitted pulsation (mechanical impulse) from the adjacent carotid artery.
- Wave v: reflects right atrial filling and blood stagnation while the tricuspid valve is closed.
Negative waves (collapses):
- x descent (x-collapse): relaxation in the atria at the beginning of ventricular systole (the valve plane shifts toward the apex) and active venous blood inflow.
- y descent (y-collapse): corresponds to the rapid ventricular filling phase when the tricuspid valve opens and veins rapidly empty.