Systolic blood pressure is the peak blood pressure in the arterial portion of the systemic circulation that results from contraction of the left ventricle and continues into the aorta and through its branches into the arteries when the aortic valve is open. Peak blood pressure depends on several fixed and variable factors, including cardiac output, vascular wall elasticity, and vascular tone.
What is systolic blood pressure?
Systolic blood pressure embodies the peak blood pressure that occurs in the arterial portion of the great circulation for a brief moment during the contraction phase (systole) of the left ventricle. Systolic blood pressure embodies the peak blood pressure that occurs in the arterial part of the great circulation for a brief moment during the contraction phase (systole) of the left ventricle. The peak pressure in the arteries depends on the cardiac output, the elasticity and tone of the arterial vessel walls, and the functionality of the aortic valve. The aortic valve must open during systole to allow blood to flow into the aorta under the pressure generated by the left ventricle. During the subsequent diastole, the relaxation and resting of the heart chambers, the aortic valve closes to maintain a residual pressure, diastolic blood pressure, in the arterial system and to prevent blood from flowing from the aorta back into the left ventricle. Systolic blood pressure can be adjusted almost without delay within certain limits to changing demands by the autonomic nervous system via the release of stress hormones. Systolic blood pressure is regulated by the tension or relaxation of smooth muscle cells, which enclose the arterial vessels in a helical fashion and can dilate their lumen by contraction to reduce vascular resistance.
Function and Purpose
The control and short-term adaptation of the circulatory system to rapidly changing demands is accomplished by the heart‘s beating rate and by influencing systolic blood pressure in the arterial portion of the great circulatory system. The processes are controlled by stress hormones, which are mainly produced by the adrenal gland. Stress hormones cause the smooth muscle cells in the so-called muscular arteries to tense, thus widening the lumen of the arterial vascular system so that lower vascular resistance leads to higher throughput. The necessary supply to muscles and organs can thus be adapted to short-term peaks in demand. In addition to the short-term adaptation of the blood circulation to changing requirements, systolic blood pressure also fulfills another essential task. In the pulmonary circulation, the exchange of carbon dioxide for oxygen takes place in the alveoli, the air sacs in the lungs, and the exchange of substances between blood and tissue cells within the systemic circulation takes place in the capillaries, which form the transition from the arterial to the venous side of the circulation. To perform their mass transfer function, both systems depend on a blood flow that is as continuous as possible and on a certain residual pressure in the microscopically fine veins. If the pressure falls below a certain value, alveoli and capillaries tend to collapse, which is not reversible. In collapsed alveoli and capillaries, adhesion forces cause their membranes to stick together so tightly that even elevated blood pressure cannot restore their functionality. Systolic blood pressure serves to build up pressure in the arterial part of the systemic and pulmonary circulation in such a way that the necessary residual pressure is maintained during the recovery phase of the chambers to sustain the alveolar and capillary systems. In this process, the arterial vascular system exerts a kind of Windkessel function due to its elasticity. This means that when the pressure decreases, the elastic arterial vessels contract again a little and are actively involved in maintaining the diastolic pressure. This results in a smoothed, nearly continuous blood flow in the alveoli and capillaries. Because of the peculiarity of the cardiac musculature, which is not controllable by analogy as is skeletal muscle, but knows only the responses contracticon or noncontraction, the ventricles cannot assume the function of pressure control or maintenance in the arterial vascular system. The contraction phase of the chambers always lasts 300 milliseconds with only slight deviations.This means that until the next systole occurs at a low heart rate of less than 60 Hz. there is a “resting phase” of 700 to 900 milliseconds, which the arterial vascular system must overcome without suffering a complete loss of pressure.
Diseases and ailments
Although systolic blood pressure is allowed to fluctuate within certain limits on an individual basis and depending on the demand situation, compliance with generally accepted limits requires that all system components function properly. In principle, a basic requirement for maintaining a normal systolic blood pressure, which should be between 120 and 140 mm Hg. at rest, is a fully functional and efficient heart and heart valves. Another prerequisite is a functional arterial vein system that has both its elasticity and the hormonal controllability of its lumen. The systolic – and also the diastolic – blood pressure can already move into a chronically pathological range, mostly unnoticed, in the case of a functional impairment of one system component and, as secondary damage, cause serious health problems such as cardiovascular diseases, heart attack, stroke or hypertensive retinal disease. In addition to the functioning of the “mechanical” components of the cardiovascular system, maintaining the limits of systolic blood pressure also requires functioning hormonal control via the renin-angiotensin-aldosterone system (RAAS). This is, in effect, the control software of the system. One of the most common pathological changes that can directly affect systolic blood pressure is atherosclerosis. This is a kind of progressive sclerotization of certain arteries, which consequently lose their elasticity and their cross-section narrows. The function of the arteries in terms of controlling systolic blood pressure is thus severely restricted. In up to 80 percent of cases of arterial hypertension, no organic defects are detectable. Such hypertension is termed primary or essential.
