Finally, the tunica adventitia also called the tunica externa, is the outermost layer made up of longitudinally oriented type-I collagen fibers. There are two main types of arteries in the human body. The first, which is the more prominent of the two, is the muscular artery. Muscular arteries have a thin intimal layer with a well-developed internal elastic lamina.
They also have a muscular wall that can be up to forty layers thick. The primary function of these arteries is to regulate blood flow through adjustment of blood vessel caliber.
The other main type of artery is the elastic artery. Elastic arteries are unique as they have elastic fibers interspersed in between the smooth muscle cells of the tunica intima, which allows elastic arteries to store kinetic energy to smooth out the surge in blood pressure that occurs during systole, known as the Windkessel effect. An increase in pulse pressure can occur in a well-conditioned endurance runner.
As he or she continues to exercise, the systolic pressure will progressively increase due to an increase in stroke volume and cardiac output. Diastolic pressure, on the contrary, will continually decrease due to a decrease in the total peripheral resistance.
This effect is due to the accumulation of red slow-twitch muscle tissue in the arterioles instead of white fast-twitch tissue. As a result, the pulse pressure is going to increase; this can also occur in individuals with larger amounts of muscle mass. Aging impacts pulse pressure and arterial compliance. With aging, there is a decrease in the compliance of the large elastic arteries. This change is due to structural molecular changes in the arterial wall, including decreased elastin content, increased collagen I deposition, and calcification, which increases the stiffness of the wall.
This process is often described as "hardening of the arteries. In response, the left ventricular tend to hypertrophy. The rise in aortic pressure from its diastolic to systolic value is determined by the compliance of the aorta as well as the ventricular stroke volume. In the arterial system, the aorta has the highest compliance, due in part to a relatively greater proportion of elastin fibers versus smooth muscle and collagen.
This serves the important function of dampening the pulsatile output of the left ventricle, thereby reducing the pulse pressure systolic minus diastolic arterial pressure.
If the aorta were a rigid tube, the pulse pressure would be very high. So, that's a way to reason through this answer. However, one might point out that, from the point of view of the left ventricle, there is no distinction between the effects of the distal and the proximal arteries on variables affecting afterload.
The ventricle is working against the entire systemic circuit. What, then, is the relationship of arterial resistance and compliance in the total arterial circulation? Fortunately, this question has a handy answer. Here's a graph of arterial compliance and systemic vascular resistance from Wohlfahrt et al As you can see, the relationship is hyperbolic. As SVR increases, compliance decreases, and vice versa. As mentioned above, changes in arterial compliance result in a more rapid drop of blood pressure in diastole, because of a steep arterial pressure-volume relationship.
This brings diastolic time, and therefore heart rate, into the equation. Because the pulse pressure is dependent on arterial compliance, the site of measurement becomes very important.
Consider putting your pressure probe inside some hypothetical infinitely compliant aneurysmal sack. Of course, the pulse pressure here will be zero, as each time the sack receives more volume it distends without increasing its pressure.
The human aorta is not infinitely compliant, but it is certainly the most compliant vessel in the proximal arterial circulation, and so the pulse pressure measured there is usually much lower than peripheral pulse pressure. Another aspect of this is distal pulse pressure amplification , the phenomenon of constructive interference between reflected waves from the distal circulation and the "forward" pressure waves propagating from the left ventricle.
Thus, the most distal vessels, such as the dorsalis pedis artery, should have the greatest pulse pressure because the reflected waves are strongest there. The consequence of both of these factors is an increase in the systolic pressure and a decrease in diastolic pressure as one moves distally through the circulatory tree.
There is no better way to illustrate this than by using an excellent diagram from Gedde's Handbook of Blood Pressure Measurement Apart from the already mentioned physiological processes, there are all sorts of structural and functional problems which could give rise to changes in pulse pressure.
Without going into too much detail, they can be listed in broad groups:. Sure, pulsatile flow is the natural free-range gluten-free way of running your circulatory system, but is it essential for life?
For example, here is an arterial line waveform of a patient on VA ECMO, in whom the circulation is sustained by a nonpulsatile rotary pump, and whose left ventricle is producing a barely registered pulse pressure of 6 mmHg. It would be disingenuous to pretend that this patient is completely fine, but ECMO patients can remain like this for weeks, and their overall trajectory is often one of improvement. So the question remains: is there anything special about the pulse, apart from its association with life-sustaining forward flow of blood?
Is pulsatile flow somehow superior to constant flow, or is flow the objective, irrespective of how it is delivered? Turns out, our preoccupation with the arterial pulse is probably just a quaint anachronism, arising from a traditionalist reliance on a biological mammalian heart.
That thing has significant limitations from an engineering standpoint. The myocardial cells need rest periods, the muscle requires diastole for perfusion, and the device a duplex diaphragm positive displacement pump requires alternating periods of filling and emptying to function, making the pulse a mandatory component of "normal" biological circulation.
However, it is purely a phenomenon of the proximal circulation. As one moves distally into the arterioles, the pulse pressure is essentially obliterated by the windkessel effect where elastic energy of the pulse is stored during the high-pressure period and then released during the low-pressure period , producing a "smoothing" of peaks and troughs until they almost disappear.
Gore , while measuring the pressure in cat capillaries, noted that the pulse pressure width there was somewhere around mmHg. In short, the tissues the main consumer base for blood flow couldn't possibly care less whether the flow is pulsatile or not. Russel et al and Saito et al were able to confirm this by means of cruel experiments which were essentially endurance marathons for VAD devices fitted into healthy experimental animals or humans and adjusted to a flow rate at which pulsatile flow was absent.
The systolic blood pressure is defined as the maximum pressure experienced in the aorta when the heart contracts and ejects blood into the aorta from the left ventricle approximately mmHg. The diastolic blood pressure is the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle approximately 80 mmHg.
Normal pulse pressure is, therefore, approximately 40 mmHg.
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