Systolic pressure refers to the pressure in the arterial system at its highest and diastolic pressure refers to the lowest pressure. Blood pressure is normally measured at the brachial artery with a sphygmomanometer (pressure cuff) in mm of Hg and given as systolic over diastolic pressure. Normal pressure is said to be 120/70 on average but normal for an individual varies with the height, weight, fitness level, health, emotional state and age of a person.
This is because blood pressure is a product of cardiac output and total peripheral resistance. Blood pressure is normally maintained within narrow limits but can be as low as 60/40 during sleep or increase dramatically in exercise. Chronically high blood pressure is called hypertension and is a life threatening condition that must be managed and or treated.
Blood pressure is maintained by regulation of cardiac output and peripheral resistance at the arterioles, postcapillary venules, and heart. The kidney contributes to maintenance of blood pressure by regulating blood volume.
An example of the dependence of blood pressure on cardiac output and peripheral resistance occurs when the blood pressure is taken on an excited person with an increased cardiac output due to an increased heart rate. Increases in cardiac output generally cause increases in systolic pressure while increases in peripheral resistance (caused by vasoconstriction, for example) cause increases in diastolic pressure. With age, the arterial wall become less elastic causing systolic pressure to rise as the heart has to pump against a less compliant system.
Capillary pressure is higher on the arterial side than the venous end and can range from 30-15 mm Hg from one end to the other. Pressure in the venules is 12-18 mm Hg and falls as the diameter of the vein increases to under 5 mm Hg in the great veins. The pressure in the vena cava fluctuates with respiration and stage of the cardiac cycle.
Central control of blood pressure is integrated and regulated by diffuse neurons within a region of the medulla oblongata loosely called the vasomotor center. Hypoxia or carbon dioxide directly stimulate the vasomotor center. It also receives input from sensors within the walls of the large arteries. Output from the vasomotor center alters heart rate and vascular tone to return blood pressure to acceptable levels. As a general rule, anything that increases heart rate also increases blood pressure and anything that decreases heart rate causes a decrease in blood pressure. This is because of the relationship of heart rate to cardiac output.
Hormonal and nervous regulation of blood flow
Tissues can regulate their own blood flow through autoregulation. Local factors such as decreased oxygen, increased carbon dioxide, or increased osmolarity relax arterioles and precapillary sphincters. Increased temperature also causes vasodilation as in heat induced erythema. Lactate and potassium ion concentrations also cause local vasodilation. Injury causes arteries and arterioles to constrict to limit blood loss. Temperature decreases cause vasoconstriction in localized areas as well.
Circulating or local hormonal factors can change the caliber of the arterioles. Histamine, atrial natriuretic peptide, epinephrine, kinins, nitric acid, and adenosine are all vasodilators. Vasoconstrictors include vasopressin, norepinephrine, angiotensin II, and serotonin. The action of any of many of these substances depend on the tissue and receptor compliment of the cells there. For instance, Epinephrine causes vasodilation in skeletal muscle and the liver but causes vasoconstriction in other tissues because of the types of receptors present in the tissues.
With the exception of capillaries and venules, all blood vessels have direct neural input from the sympathetic nervous system. The fibers form a network or plexus in the adventitia and some extend into the outer surfaces of the media. Vascular innervation to the arterial and venous sides of the vascular system regulate tissue blood flow, arterial pressure and the venous blood volume. Veins are not well innervated except those in serving the gastrointestinal system.
Vasoconstrictor fibers that release norepinephrine innnervate vessels in all parts of the body. Vessels in skeletal muscle are also innervated by vasodilator fibers that release acetylcholine. The vasoconstrictor fibers normally maintain some tonal discharge but the vasodilator fibers must be stimulated to have an effect and in most tissues regulation is accomplished by modulating the vasoconstrictor influence alone.
Baroreceptors & Chemoreceptors
Within the heart and large arteries are stretch receptors that send pressure information to the vasomotor center. The receptors are located in the walls of the right and left atria, in the wall of the left ventricle and in the pulmonary circulation. These cardiopulmonary receptors sense distension in their respective structures and discharge at a higher rate when the pressure rises. Carotid sinuses and the aortic arch contain stretch receptors (baroreceptors) that are sensitive to arterial pressure.
Impulses generated in the baroreceptors inhibit the tonic discharge of the vasoconstrictor nerves and excite the vagal center causing vasodilation, venodilation and a drop in blood pressure, decreased heart rate, and a decrease in cardiac output.
Conversely, a drop in blood pressure causes a decrease in discharge at the baroreceptors which removes inhibition from the vasomotor center and a compensatory increase in blood pressure and cardiac output. Therefore, the baroreceptors act to fine tune the activity of the vasomotor center based on fluctuations in pressure. They are responsible for rapid adjustments in blood pressure such as that needed when one moves from a reclining to a standing position.
The atrial baroreceptors are also important in the endocrine regulation of extracellular volume. Decreased discharge of the atrial baroreceptors caused vasopressin release and increased renin secretion from the kidney. Aldosterone secretion is stimulated as well. The combined effect is to limit water and sodium loss.
Chemoreceptors in the carotid bodies sense decreased oxygen in the blood and those in the aortic bodies sense increased carbon dioxide and hydrogen ion concentrations. Stimulation of these chemoreceptors causes an increase in respiratory rate and also stimulates the vasomotor center such that heart rate, cardiac output, and blood pressure are modified. Low oxygen or high carbon dioxide also directly stimulate the vasomotor center. The net effect of these peripheral and central inputs varies with the source and cause with the goal of achieving proper blood flow to tissues, especially the brain and kidneys.
A decrease in cardiac output sufficient to deprive the tissues of necessary blood flow may be caused by a loss of blood volume as in hemorrhage (hypovolemic shock). Or the decrease in tissue perfusion can be due to peripheral pooling in the venous system (distributive shock) or failure of the heart to pump efficiently (cardiogenic shock).
Hypovolemic shock can be caused by blood loss, trauma, surgery or burns. Distributive shock may be caused by sepsis, anaphylaxis, or from neurogenic causes.
Neurogenic shock is where nervous impulses cause vasodilation and pooling of the blood in the extremities, an example of which is fainting after an emotional event. Cardiogenic shock occurs with severe damage to the left ventricle as my occur in myocardial infarction.
Hemorrhage is compensated for by several methods that are both acute and chronic fixes for the problem. Rapid compensation for low blood volume include vaso and venoconstriction, increased heart rate (tachycardia), adrenergic output from the adrenal medulla, secretion of vasopressin, glucocorticoids, renin, aldosterone and erythropoetin, and hepatic plasma protein synthesis. By decreasing urine formation, retaining sodium and water, increasing blood pressure, stimulation of blood cell formation and increasing plasma oncotic pressure the net effect is to feed the brain and heart while restoring normal blood volume.
In moderate hemorrhage blood volume is restored in about 12-72 hours. Plasma proteins are restored in 3-4 days and red blood cells in 4-8 weeks. The goal of treatment is to augment physiologic compensatory mechanisms and if due to blood loss, treatment may include the use of plasma expanders which are solutions of large molecular weight sugars. In anaphylactic shock, epinephrine is used to constrict vessels. Often raising the foot of the patient’s bed is beneficial to return blood to the heart, but only periodically due to the possibility of complications.