Pulse Pressure = Systolic Blood Pressure – Diastolic Blood Pressure
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, usually approximately 120 mm Hg. The diastolic blood pressure is defined as the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle, often approximately 80 mm Hg. Normal pulse pressure is, therefore, approximately 40 mm Hg.
A change in pulse pressure (Delta Pp) is proportional to volume change (Delta V) but inversely proportional to arterial compliance (C):
Delta Pp = Delta V/C
Because the change in volume is due to the stroke volume of blood being ejected from the left ventricle (SV), we can approximate pulse pressure as:
Pp = SV/C
A normal young adult at rest has a stroke volume of approximately 80 mL. Arterial compliance is approximately 2 mL/mm Hg, which confirms that normal pulse pressure is approximately 40 mm Hg.
Arterial compliance is equal to the change in volume (Delta V) over a given change in pressure (Delta P):
C = Delta V/Delta P
Because the aorta is the most compliant portion of the human arterial system, pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again.
A pulse pressure that is less than 25% of the systolic pressure is inappropriately low or “narrowed,” whereas, a pulse pressure of greater than 100 is high or “widened.”
Arteries are efferent vessels that lead away from the heart. They are lined by endothelial cells and consist of 3 different layers, which can be seen in the figure below. The innermost layer, the tunica intima, consists primarily of an endothelial layer, subendothelial layer, and an internal elastic lamina. The middle layer, also called the tunica media, has concentric layers of helically arranged smooth muscle cells, as well as varying amounts of elastic and reticular fibers and proteoglycans. Some of the larger arteries also contain an external elastic lamina. Finally, the tunica adventitia also called the tunica externa, is the outermost layer made up of longitudinally oriented type-I collagen fibers.
There are 2 main types of arteries in the human body. The first, which is the more prominent of the 2, 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 main 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 in that in the tunica media; they have elastic fibers interspersed in between the smooth muscle cells. This 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 also be seen 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 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 be seen 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 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 called “hardening of the arteries.” As the left ventricle contracts against stiffer, less compliant arteries, systolic and diastolic pressures increase and can result in a widening of the pulse pressure. In response, the left ventricular tends to hypertrophy. When excessive pulse pressure is transmitted through the microcirculation of vital organs such as the brain and kidneys, extensive tissue damage tends to occur.
Valvular disease states such as aortic regurgitation and aortic stenosis result in changes in pulse pressure. In aortic regurgitation, the aortic valve insufficiency results in a backward, or regurgitant, flow of blood from the aorta back into the left ventricle, so that blood that was ejected during systole returns during diastole. This leads to an increase in the systolic pressure and a decrease in the diastolic pressure, which results in an increase in pulse pressure. In aortic stenosis, there is a narrowing of the aortic valve which interferes with the ejection of blood from the left ventricle into the aorta, which results in a decrease in stroke volume and subsequent decrease in pulse pressure.
Significant blood loss, such as seen in trauma or acute hemorrhage, leads to a decrease in both the preload and stroke volume and subsequently a decrease in pulse pressure.
The research done by Blacher et al. has shown that pulse pressure is a significant risk factor in the development of heart disease. It has even been shown to be more of a determinant than the mean arterial pressure, which is the average blood pressure that a patient experiences in a single cardiac cycle. In fact, as little as a 10-mm Hg increase in the pulse pressure increases the cardiovascular risk by as much as 20%. This finding was found to be consistent in both Caucasian and Asian populations.
Pulse pressure is also independently associated with an increased risk of developing atrial fibrillation. A study done by Mitchell et al. showed that patients with a pulse pressure of 40 mm Hg or less developed atrial fibrillation at a rate of 5.6%, whereas patients with a pulse pressure greater than 61 mm Hg developed atrial fibrillation at a rate of 23.3%. In fact, for every 20-mm Hg increase in pulse pressure, the adjusted hazard ratio for developing atrial fibrillation is 1.28. This risk is independent of mean arterial pressure.
Other research has focused on helping to maintain a normal pulse pressure. One of the most effective ways to do this is to increase arterial compliance. According to Thorin-Trescases et al., endurance aerobic exercise is the only intervention that has been shown to help mitigate age-related arterial stiffening by reducing age-related increases in collagen I and III and calcification. These same benefits were not seen with resistance training, such as bench press, as this actually decreases the arterial compliance and increases the pulse pressure.
In addition to aerobic exercise training, Dart et al. demonstrated that one could also increase arterial compliance by increasing estrogen compounds (as in hormone replacement in post-menopausal women), increasing the consumption of n-3 fatty acids, and decreasing salt intake. There has also been some evidence that supports the notion that ACE inhibitors have beneficial arterial wall effects and may be of use. Finally, research by Williams et al. showed that folic acid supplementation (a 3-week treatment with 5 mg of folic acid per day) could decrease the plasma homocysteine concentrations, which improves endothelial dysfunction and causes a reduction in the stiffness of large arteries.
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