When the heart contracts and forces blood into the arteries the pressure created is known?

8.2.1 Systolic and diastolic pressure

Arterial blood pressure consists of several distinct components—systolic and diastolic pressures, pulse pressure, and mean arterial pressure (Fig. 8.1). The systemic arterial blood pressure in the normal healthy young adult is 110–120 mmHg systolic and 70–80 mmHg diastolic. The systolic pressure indicates the arterial pressure resulting from the ejection of blood during ventricular contraction, whereas the diastolic pressure represents the arterial pressure of blood during ventricular relaxation. These values change with age, being lower in infants and children than in adults. Moreover, the blood pressure values of women are 5–10 mmHg lower than those of males until the age of 50, after which there is no appreciable difference. In the elderly, an increase in the systolic and diastolic pressures is partially due to loss of elasticity of the arteries.

Control Mechanisms

Arterial blood pressure is controlled by the kidney. Too much fluid causes the pressure to rise, too little fluid causes the pressure to drop. The two determinants of arterial blood pressure are the volume of renal output and the amount of salt and water in the system. The kidneys control renal output by changing the extracellular fluid volume. An increase in extracellular fluid increases blood volume and ultimately cardiac output, which increases arterial pressure. This increase in arterial pressure is accomplished by controlling the amount of salt in the system, which is the main determinant of the amount of extracellular fluid.

As part of the endocrine system, the kidneys have an additional means of controlling arterial pressure. The renin-angiotensin system is a more powerful and complex mechanism than the one previously described. After a drop in blood pressure, the kidneys release renin, which enzymatically causes the release of angiotensin I. Within seconds, angiotensin I is converted by an enzyme in the lungs to angiotensin II. The latter produces systemic vasoconstriction and decreased excretion of salt and water by the kidney. Angiotensin can secondarily cause fluid retention by stimulating the adrenal gland to secrete aldosterone. The renin-angiotensin system maintains normal arterial blood pressure despite wide fluctuations in salt intake. The system takes about 20 minutes to become fully active.

Determinants of Levels of Arterial Pressure

Arterial pressure derives from the pumping action of the left ventricle of the heart; therefore, the level of arterial pressure at any point in the arterial vascular compartment reflects functioning of the left ventricle. During each contraction of the left ventricle (termed systole), the highest systemic pressure generated within the arteries is termed the “systolic pressure.” When the left ventricle stops contracting, the heart valve controlling outflow from the left ventricle into the aorta closes and the left ventricle relaxes and refills (between beats). This phase of the heart is termed diastole. During diastole the arterial pressure drops as the arterial blood rapidly flows out of the arterial compartment into the capillaries. The lowest arterial pressure during this rest phase of the left ventricle is termed the “diastolic pressure.” The rate of drop of arterial pressure is primarily controlled by the terminal resistance arterioles, located at the junction of artery to the capillaries, which meter the rate of outflow of blood from the arteries. A second factor is the interbeat interval, the time between contractions of the left ventricle, the heart rate (HR). At constant arteriole resistance, increasing HR may increase apparent diastolic pressure since there is less time for blood to leave the arterial compartment. A third factor is the rebound of the conduit arteries, the windkessel energy effect that sustains the arterial pressure during diastole. Diastolic pressure also is indirectly determined by the systolic pressure in that an increase in systolic pressure leads to a higher starting point from which the arterial pressure may descend between contractions. This leads to a higher diastolic pressure starting point. In a normally functioning and contracting heart, the lowest systemic arterial pressure level is reached just prior to the next contraction. Thus, systolic pressure reflects multiple contributions—the action of the heart, resistance to outflow from the arterial compartment, and the windkessel effect.

The pressure difference between systolic and diastolic pressure is termed the “pulse pressure.” Pulse pressure, which is sensed by the blood vessel elements, has recently been deemed a potential contributor to the development of both systemic arterial hypertension and arterial wall damage contributory to atherosclerosis.

Arterial pressure is influenced by many factors. These include age, gender, body weight, level of physical conditioning, current physical activity, and behaviors of all kinds, for example, stress, eating, drinking, and exercise. Arterial pressure can also be influenced by many agents, both prescription and over-the-counter drugs, herbal products, caffeine-loaded energy drinks, psychoactive drugs, and drugs of abuse. Further, arterial pressure varies continuously with variations caused by changes in heart beat-to-beat intervals, periods of rest and sleep, as well as levels of psychological stress.

Normative Levels of Arterial Pressure in Humans

ABP is a ‘quantitative trait’ because values vary with age, sex, body weight, and physical activity of the individual. A pressure considered ‘normal’ in one individual may be judged abnormal in another. ABP increases with age for both genders (Figure 11) and generally is lower in premenopausal women than in men of the same age. ABP increases with increased body mass such that some hypertensive subjects can normalize their ABP by losing only 5–10% of body mass. Once hypertension is evident, gender differences tend to be obscured (see Figure 11).

Since ABP is a quantitative trait, what are ‘normal values’ (Kaplan, 1986)? Through measurements of very large numbers of adult subjects, in apparent good health, values of 120 mmHg for SBP and 80 mmHg for DBP have entered our vocabulary to imply ‘normal’ ABP; however, Figure 12 illustrates that the spread of arterial pressures, even for ‘normals,’ is very broad. Values of 120/80 may be good approximations for the population as a whole; however, biological variability results in a range of ‘normal’ arterial pressures with some being outliers, either low or high.

Since ABP varies widely across the population being measured, classification of an individual as hypertensive and the type of therapy to use have been controversial. Further, what pressure is most informative, SBP, DBP, or MAP? DBP informs about the cardiovascular system during cardiac rest, thereby potentially reflecting the state of the arterial blood vessels. SBP equals DBP plus pulse pressure, and pulse pressure reflects both cardiac contractility and conduit artery compliance. Therefore, SBP is informative about cardiac function contributions to the ABP. But it is really more complicated. Vessel compliance, or distensibility, leads to reflected waves of arterial pressure moving through the arterial system that can change local pressure profiles. Further, as shown in Figure 11, DBP appears to track better with hypertension before the age of 50 years but poorly after 50 years, while SBP continues to increase after 50 years. Which pressure should a physician rely upon for diagnosis and treatment? The fact is that there are sufficient data to consider that for both genders, high ‘normal’ ABP increases the risk of subsequent cardiovascular disorders (Figure 13).

Many studies of adult populations have yielded general guidelines for classifying a state of hypertension. Figure 14 illustrates the recommendations of both the 6th and 7th Joint National Commissions on Hypertension (JNC6 and JNC7) (JNC7, National Heart Lung and Blood Institute, 2003). For adults, above 18 years of age, the JNC7 classification now defines normal pressure as an SBP less than 120 mmHg and a DBP less than 80 mmHg. This is the ideal target for arterial pressure; however in practice, age, body weight, and gender must still be considered for each subject in setting goals and objectives. The area of controversy still lies in the ABP classified by the JNC7 as ‘prehypertension,’ previously termed ‘borderline hypertension.’

The issue of the best classification of hypertension is very serious. Many antihypertensive drugs have undesirable side effects with long-term usage, and such side effects must be monitored and prevented. Some drugs target SBP while others DBP, or both SBP and DBP. Hypertension may be evident even in young children. Does transient hypertension in children identify increased risks in adults? Nondrug therapy for children and behavior modification may have major cardiovascular benefits beyond hypertension. Hypertension is closely associated with obesity and Type I and II diabetes, and the current epidemic of obesity and Type II diabetes warrants implementation of at least behavioral modification in overweight children, especially those exhibiting episodes of high ABP.

Systolic hypertension, with normal or low DBP, is associated with the elderly and attributed to a loss of arterial vessel compliance. Systolic hypertension in young individuals may be associated with stress or anxiety, but could also arise from other organ system dysfunctions. ‘White coat hypertension’ is high ABP in the presence of a physician or a health professional. While it may represent anxiety-associated sympathetic activation, it could reflect inheritance of genes predisposing to stress-induced hypertension. Transient and reversible episodes of elevated ABP would not necessarily constitute a diagnosis of hypertension; however, sustained or repeated episodes of high SBP or DBP could indicate altered homeostatic regulation or an identifiable origin of hypertension.

Invasive or noninvasive arterial pressure monitoring?

Arterial pressure is a key determinant of organ perfusion and is routinely measured in critically ill patients, either noninvasively or invasively. Noninvasive measurements can reliably be used in less severely ill patients but are unfortunately less reliable in patients with shock, when accuracy of measurements is most important.9 For example, an overestimate of 5–10 mm Hg will have minimal impact on patient management if real mean arterial pressure (MAP) is 80 mm Hg, but could have important consequences if MAP is 55 mm Hg. Hence invasive arterial pressure monitoring is recommended in patients with circulatory failure.5

Arterial pressure

Arterial pressure results from the pressure exerted by the blood in the large arteries. Blood pressure depends on cardiac output and total peripheral resistance. Arterial pressure fluctuates with each heart beat, according to the pumping of the heart. It:

increases during the emptying phase (ventricular systole)

decreases during the filling phase (ventricular diastole).

Arterial Baroreceptor Reflex

Arterial blood pressure is maintained within narrow limits by a negative feedback system called the arterial baroreceptor reflex.35,36 Its major components of this system are (Figure 21-15, A): (1) an afferent limb composed of baroreceptors in the carotid artery and aortic arch and their respective afferent nerves, the glossopharyngeal and vagus nerves; (2) cardiovascular centers in the medulla that receive and integrate sensory information; and (3) an efferent limb composed of sympathetic nerves to the heart and blood vessels and the parasympathetic (vagus) nerve to the heart. Figure 21-15, B, presents the neural relationships of the arterial baroreceptor reflex.37 Baroreceptors are stimulated by stretch of the vessel wall by increased transluminal pressure. Impulses originating in the baroreceptors tonically inhibit discharge of sympathetic nerves to the heart and blood vessels, and tonically facilitate discharge of the vagus nerve to the heart. A rise in arterial pressure reduces baroreceptor afferent activity, resulting in further inhibition of the sympathetic and facilitation of parasympathetic output. This produces vasodilation, venodilation, and reductions in stroke volume, heart rate, and cardiac output, which combine to normalize arterial pressure. A decrease in arterial pressure has opposite effects. The cardiovascular centers in the medulla are also under the influence of neural influences arising from the arterial chemoreceptors, hypothalamus, and cerebral cortex, and of local changes in PCO2 and PO2.

INTEGRATION AND REDUNDANCY OF CARDIOVASCULAR CONTROL

Arterial blood pressure is regulated by neural and endocrine mechanisms and augmented by exchange between the vascular and other body fluid spaces. Neural control is mostly by the SNS, with a minor role played by the PNS in controlling heart rate and some local vascular beds. Endocrine agents that control vascular smooth muscle tone include the vasoconstrictors catecholamines, angiotensin II, and ADH and the vasodilator nitric oxide. Physical mechanisms include exchange of fluid between the plasma and the interstitial fluid at the capillaries of the microcirculation, and the loss of plasma from filtration at the renal glomerulus. The renal regulation of blood pressure is augmented by the same agents that constrict vascular smooth muscle—the catecholamines, angiotensin II, and ADH—as well as the steroid hormone aldosterone. It is useful to understand the vascular control systems on the basis of both the pressure range over which they operate and the time frame in which they operate.

Cardiovascular control systems can be grouped by the pressure range over which they act. Baroreceptor control operates in the normal arterial pressure range and is important in compensating for both increases and decreases in blood pressure. Some vascular control systems become important only during a drop in arterial pressure. During hypotension, angiotensin II and fluid translocation are important compensatory mechanisms. Severe hypotension activates the CNS ischemic response, a massive activation of the SNS. Renal regulation of fluid volume is effective over the entire range of arterial pressures (Fig. 9-6).

Cardiovascular control systems can also be grouped by the time delay before they become effective (Fig. 9-7). Nervous system reflexes are the most rapid, causing a physiologic response within seconds. Peptide and catecholamine hormones become effective within minutes. Fluid translocation effects are noticeable after 10 minutes. Steroid hormones take hours to exert effects. Renal fluid retention requires days to alter arterial pressure. Consequently, acute cardiovascular responses center on the autonomic nervous system, and chronic cardiovascular disorders are tied more closely to body fluid regulation.

Cerebral Blood Flow

Systemic arterial pressure is the primary determinant of cerebral blood flow. Normal cerebral blood flow remains remarkably constant from birth to adult life and is generally 50–60 mL/min/100-g brain weight. The autonomic innervation of blood vessels on the surface and at the base of the brain is richer than vessels of any other organ. These nerve fibers allow the autoregulation of cerebral blood flow. Autoregulation refers to a buffering effect by which cerebral blood flow remains constant despite changes in systemic arterial perfusion pressure. Alterations in the arterial blood concentration of carbon dioxide have an important effect on total cerebral blood flow. Hypercarbia dilates cerebral blood vessels and increases blood flow, whereas hypocarbia constricts cerebral blood vessels and decreases flow. Alterations in blood oxygen content have the reverse effect, but are less potent stimuli for vasoconstriction or vasodilation than are alterations in the blood carbon dioxide concentration.

Cerebral perfusion pressure is the difference between mean systemic arterial pressure and ICP. Reducing systemic arterial pressure or increasing ICP may reduce perfusion pressure to dangerous levels. The autoregulation of the cerebral vessels is lost when cerebral perfusion pressure decreases to less than 50 cm H2O, or in the presence of severe acidosis. Arterial vasodilation or obstruction of cerebral veins and venous sinuses increases intracranial blood volume. Increased intracranial blood volume, similar to increased CSF volume, results in increased ICP.