The term blood pressure, the force of blood against the wall of the blood vessels, usually refers to arterial blood pressure in the systemic circuit-in the aorta and its branches. Arterial blood pressure is greatest during ventricular contraction (systole) as blood is pumped into the aorta and its branches. This pressure is called the systolic blood pressure, and it optimally averages 110 millimeters of mercury (mm Hg) when measured in the brachial artery. The lowest arterial pressure occurs during ventricular relaxation (diastole). This pressure is called the diastolic blood pressure, and it optimally averages 70 mm Hg.
The difference between the systolic and diastolic blood pressures is known as the pulse pressure. The alternating increase and decrease in arterial blood pressure during ventricular systole and diastole causes a comparable expansion and contraction of the elastic arterial walls. This pulsating expansion of the arterial walls follows each ventricular contraction, and it may be detected as the pulse by placing the fingers on a superficial artery.
Three major factors affect blood pressure: cardiac output, blood volume, and peripheral resistance. An increase in any of these factors causes an increase in blood pressure, while a decrease in any of these causes a decrease in blood pressure.
Blood volume may be decreased by severe hemorrhage, vomiting, diarrhea, or reduced water intake. The decrease in blood volume causes a decrease in blood pressure. Many drugs used to treat hypertension (abnormally high blood pressure) act as diuretics, meaning they increase urine volume and as a result decrease blood volume. As soon as the lost fluid is replaced, blood pressure returns to normal. Conversely, if the body retains too much fluid, blood volume and blood pressure increase. A high-salt diet is a risk factor for hypertension because it causes the blood to retain more water as a result of osmosis, leading to an increase in blood volume.
Peripheral resistance is the opposition to blood flow created by friction of blood against the walls of blood vessels. Increasing peripheral resistance will increase blood pressure, while decreasing peripheral resistance decreases blood pressure. Peripheral resistance is determined by vessel diameters, total vessel length, and blood viscosity. Arterioles play a critical role in controlling blood pressure by changing their diameters. As arterioles constrict, peripheral resistance increases and blood pressure increases accordingly. As arterioles dilate, peripheral resistance and blood pressure decrease. Peripheral resistance is directly proportional to the total length of the blood vessels in the body: the longer the total length of the vessels, the greater their resistance to flow. Obese people tend to have hypertension partly because their bodies contain more blood vessels to serve the extra adipose tissue. Viscosity is the resistance of a liquid to flow. For example, water has a low viscosity, while honey has a high viscosity. Blood viscosity is determined by the ratio of plasma to formed elements and plasma proteins. Increasing viscosity, or shifting the ratio in favor of the formed elements and plasma proteins, increases peripheral resistance and blood pressure. Both dehydration (loss of water from plasma) and polycythemia (elevated RBC count) can increase viscosity. Abnormally high levels of blood lipids and sugar are also risk factors for hypertension because they increase blood viscosity, in addition to promoting the formation of plaque on the vessel walls. Decreasing viscosity through over-hydration or certain types of anemia will decrease peripheral resistance and blood pressure.
Control of Peripheral Resistance
The sympathetic division of the ANS controls peripheral resistance primarily by regulating the diameter of blood vessels, especially arterioles. The integration center is the vasomotor center in the medulla oblongata. An increase in the frequency of sympathetic nerve impulses to the smooth muscle of blood vessels produces vasoconstriction, which increases resistance. The increase in resistance increases blood pressure and blood velocity. This response accelerates the rate of oxygen transport to cells and the removal of carbon dioxide from blood by the lungs. A decrease in sympathetic nerve impulse frequency results in vasodilation, which decreases resistance. The decrease in resistance decreases blood pressure and blood velocity.
Like the cardiac control center, the activity of the vasomotor center is modified by nerve impulses from higher brain areas, and sensory nerve impulses from baro- receptors and chemoreceptors in the aortic arch and the internal and external carotid arteries. For example, a decrease in pressure, pH, or oxygen concentration of the blood stimulates vasoconstriction. Conversely, an increase in these values promotes vasodilation.
In addition, arterioles and precapillary sphincters are affected by localized changes in blood concentrations of oxygen, carbon dioxide, and pH. These local effects override the control by the vasomotor center, through a process called autoregulation, and increase the rate of exchange of materials between tissue cells and the capillaries. For example, if a particular muscle group is active for an extended period, a localized decrease in oxygen concentration and an increase in carbon dioxide concentration result. These chemical changes stimulate the vasodilation of local arterioles and precapillary sphincters, which increases the flow of blood into capillary networks of the affected muscles to provide more oxygen and to remove more carbon dioxide.