ARTERIAL BLOOD PRESSURE
Systemic blood flow is pulsatile in large arteries because of the heart’s cyclic activity; by the time blood reaches the systemic capillaries, flow is con-tinuous (laminar). The mean pressure falls to less than 20 mm Hg in the large systemic veins that return blood to the heart. The largest pressure drop, nearly 50%, is across the arterioles, and the arterioles account for the majority of SVR.MAP is proportionate to the product of SVR × CO. This relationship is based on an analogy to Ohm’s law, as applied to the circulation:
MAP − CVP ≈ SVR × CO
Because CVP is normally very small compared with MAP, the former can usually be ignored. From this relationship, it is readily apparent that hypo-tension is the result of a decrease in SVR, CO, or both: To maintain arterial blood pressure, a decrease in either SVR or CO must be compensated by an increase in the other. MAP can be measured as the integrated mean of the arterial pressure waveform.Alternatively, MAP may be estimated by the follow-ing formula:
where pulse pressure is the difference between sys-tolic and diastolic blood pressure. Arterial pulse pressure is directly related to stroke volume, but is inversely proportional to the compliance of the arte-rial tree. Thus, decreases in pulse pressure may be due to a decrease in stroke volume, an increase in SVR, or both. Increased pulse pressure increases shear stress on vessel walls, potentially leading to atherosclerotic plaque rupture and thrombosis or rupture of aneurysms. Increased pulse pressure in patients undergoing cardiac surgery has been associ-ated with adverse renal and neurological outcomes.
Transmission of the arterial pressure wave from large arteries to smaller vessels in the periphery is faster than the actual movement of blood; the pres-sure wave velocity is 15 times the velocity of blood in the aorta. Moreover, reflections of the propagating waves off arterial walls widen pulse pressure before the pulse wave is completely dampened in very small arteries.
Arterial blood pressure is regulated by a series of immediate, intermediate, and long-term adjust-ments that involve complex neural, humoral, and renal mechanisms.
Minute-to-minute control of blood pressure is pri-marily the function of autonomic nervous system reflexes. Changes in blood pressure are sensed both centrally (in hypothalamic and brainstem areas) and peripherally by specialized sensors (barorecep-tors). Decreases in arterial blood pressure result in increased sympathetic tone, increased adrenal secre-tion of epinephrine, and reduced vagal activity. Theresulting systemic vasoconstriction, increased heart rate, and enhanced cardiac contractility serve to increase blood pressure.
Peripheral baroreceptors are located at the bifurcation of the common carotid arteries and the aortic arch. Elevations in blood pressure increasebaroreceptor discharge, inhibiting systemic vaso-constriction and enhancing vagal tone (barorecep-tor reflex). Reductions in blood pressure decreasebaroreceptor discharge, allowing vasoconstriction and reduction of vagal tone. Carotid baroreceptors send afferent signals to circulatory brainstem centers via Hering’s nerve (a branch of the glossopharyngeal nerve), whereas aortic baroreceptor afferent signals travel along the vagus nerve. Of the two peripheral sensors, the carotid baroreceptor is physiologi-cally more important and is primarily responsible for minimizing changes in blood pressure that are caused by acute events, such as a change in posture. Carotid baroreceptors sense MAP most effectively between pressures of 80 and 160 mm Hg. Adapta-tion to acute changes in blood pressure occurs over the course of 1–2 days, rendering this reflex inef-fective for longer term blood pressure control. All volatile anesthetics depress the normal barorecep-tor response, but isoflurane and desflurane seem to have less effect. Cardiopulmonary stretch receptors located in the atria, left ventricle, and pulmonary circulation can cause a similar effect.
In the course of a few minutes, sustained decreases in arterial pressure, together with enhanced sym-pathetic outflow, activate the renin–angiotensin– aldosterone system, increase secretion of arginine vasopressin (AVP), and alter normal capillary fluid exchange. Both angiotensin II and AVP are potent arteriolar vasoconstrictors. Their immedi-ate action is to increase SVR. In contrast to forma-tion of angiotensin II, which responds to relatively smaller changes, sufficient AVP secretion to pro-duce vasoconstriction will only occur in response to more marked degrees of hypotension. Angiotensin constricts arterioles via AT 1 receptors. AVP medi-ates vasoconstriction via V 1 receptors and exerts its antidiuretic effect via V 2 receptors.
Sustained changes in arterial blood pressure can also alter fluid exchange in tissues by their sec-ondary effects on capillary pressures. Hypertension increases interstitial movement of intravascular fluid, whereas hypotension increases reabsorption of interstitial fluid. Such compensatory changes in intravascular volume can reduce fluctuations in blood pressure, particularly in the absence of ade-quate renal function .
The effects of slower renal mechanisms become apparent within hours of sustained changes in arte-rial pressure. As a result, the kidneys alter total body sodium and water balance to restore blood pres-sure to normal. Hypotension results in sodium (and water) retention, whereas hypertension generally increases sodium excretion in normal individuals.
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