Arterial pulses

Arterial pulse

The blood forced into the aorta during systole not only moves the blood in the vessels forward but also sets up a pressure wave that travels along the arteries. The pressure wave expands the arterial walls as it travels, and the expansion is palpable as the "pulse".
The rate at which the wave travels, is about 4 m/s in the aorta,
8 m/s in the large arteries, and 16 m/s in the small arteries of young adults. Consequently, the pulse is felt in the radial artery at the wrist about 0.1 second after the peak of systolic ejection into the aorta. With advancing age, the arteries become more rigid, and the pulse wave moves faster.
The pulse is weak "thready" in shock. It is strong when stroke volume is large; for example during exercise. When the pulse pressure is high, the pulse waves may be large enough to be felt or even heard by the individual "palpitation or pounding heart". When the aortic valve is incompetent (aortic insufficiency), the pulse is particularly strong, and the force of systolic ejection maybe sufficient to make the head nod with each heartbeat. The pulse in aortic insufficiency is called "collapsing or water-hammer pulse".
The "dicrotic notch", a secondary upstroke in the descending part of the pulse wave caused by vibrations set up when the aortic valve snaps shut, is visible if the pressure wave is recorded but is not palpable at the wrist. The pulmonary artery pressure curve also has a dicrotic notch produced by the closure of the pulmonary valves.
Atrial pressure changes and the jugular pulse

Atrial pressure rises during atrial systole and continues to rise during isovolumetric ventricular contraction when the A-V valves bulge into the atria. When the A-V valves are pulled down by the contracting ventricular muscle, pressure falls rapidly and then rises as blood flows into the atria until the A-V valves open early in diastole. The return of the A-V valves to their relaxed position also contributes to this pressure rise by reducing atrial capacity. The atrial pressure changes are transmitted to the great veins, producing three characteristic waves in the record of jugular pressure:

The a wave: It is due to atrial systole. As mentioned previously, some blood regurgitates into the great veins when the atria contract. In addition, venous inflow stops, and the resultant rise in venous pressure contributes to the a wave.

The c wave: It is due to the rise in atrial pressure produced by the bulging of the tricuspid valve into the atria during isovolumetric ventricular contraction.

The v wave: It is due to the rise in atrial pressure with passive atrial filling before the tricuspid valve opens during diastole.