Cardiac systole and diastole Blood flow velocity waveforms in the central retinal artery (red) and vein (blue), measured by alt During each heartbeat,<unk>  varies between a maximum (systolic) and a minimum (diastolic) pressure. The<unk>  in the circulation is principally due to the pumping action of the heart. However,<unk>  is also regulated by neural regulation from the brain (see Hypertension and the brain), as well as osmotic regulation from the kidney. Differences in mean<unk>  drive the flow of blood around the circulation. The rate of mean blood flow depends on both<unk>  and the resistance to flow presented by the blood vessels. In the absence of hydrostatic effects (e.g. standing), mean<unk>  decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean<unk>  drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles. Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries. Schematic of pressures in the circulation Gravity affects<unk>  via hydrostatic forces (e.g., during standing), and valves in veins, breathing, and pumping from contraction of skeletal muscles also influence<unk> , particularly in veins. Hemodynamics A simple view of the hemodynamics of systemic arterial pressure is based around mean arterial pressure (MAP) and pulse pressure. Most influences on<unk>  can be understood in terms of their effect on cardiac output, systemic vascular resistance, or arterial stiffness (the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) the end diastolic volume or filling pressure of the ventricle acting via the Frank Starling mechanism - this is influenced by blood volume; 2) cardiac contractility; and 3) afterload, the impedance to blood flow presented by the circulation. In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased<unk> ; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the renin–angiotensin system, changes in plasma osmolarity may also be important. In the longer-term the relationship between volume and<unk>  is more complex. In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the Hagen-Poiseuille's equation (resistance∝1/radius4). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance) and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial stenosis increases resistance to flow, however this increase in resistance rarely increases systemic<unk>  because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow. Substances called vasoconstrictors reduce the caliber of blood vessels, thereby increasing<unk> . Vasodilators (such as nitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents. Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances. In practice, each individual's autonomic nervous system and other systems regulating<unk> , notably the kidney, respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term. Mean arterial pressure MAP is the average of<unk>  over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP)): ::::::::::: In practice, the contribution of CVP (which is small) is generally ignored and so ::::::::::: MAP is often estimated from measurements of the systolic pressure, and the diastolic pressure, using the equation: where k = 0.333 although other values for k have been advocated. Pulse pressure A schematic representation of the arterial pressure waveform over one cardiac cycle. The notch in the curve is associated with closing of the aortic valve. The pulse pressure is the difference between the measured systolic and diastolic pressures, ::::::::::: The pulse pressure is a consequence of the pulsatile nature of the cardiac output, i.e. the heartbeat. The magnitude of the pulse pressure is usually attributed to the interaction of the stroke volume of the heart, the compliance (ability to expand) of the arterial system—largely attributable to the aorta and large elastic arteries—and the resistance to flow in the arterial tree. Regulation of<unk>  The endogenous, homeostatic regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized: * Baroreceptor reflex: Baroreceptors in the high pressure receptor zones detect changes in arterial pressure. These baroreceptors send signals ultimately to the medulla of the brain stem, specifically to the rostral ventrolateral medulla (RVLM). The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the systemic vascular resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch. * Renin–angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II. * Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure. * Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone (ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results in an increased cardiac output by the Frank–Starling law of the heart, in turn increasing arterial<unk> . These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When<unk>  falls many physiological cascades commence in order to return the<unk>  to a more appropriate level. # The<unk>  fall is detected by a decrease in blood flow and thus a decrease in glomerular filtration rate (GFR). # Decrease in GFR is sensed as a decrease in Na+ levels by the macula densa. # The macula densa causes an increase in Na+ reabsorption, which causes water to follow in via osmosis and leads to an ultimate increase in plasma volume. Further, the macula densa releases adenosine which causes constriction of the afferent arterioles. # At the same time, the juxtaglomerular cells sense the decrease in<unk>  and release renin. # Renin converts angiotensinogen (inactive form) to angiotensin I (active form). # Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs where angiotensin-converting enzyme (ACE) acts on it to convert it into angiotensin II. # Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output. # Angiotensin II also causes an increase in the release of aldosterone from the adrenal glands. # Aldosterone further increases the Na+ and H2O reabsorption in the distal convoluted tubule of the nephron. Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists, also known as angiotensin receptor blockers (ARBs). The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may suffer from orthostatic hypotension and fainting. Taking<unk>  with a sphygmomanometer
Blood pressure
Heart rate
Mean arterial pressure
Pulse pressure
Oxygen saturation 
Oxygen saturation
Blood protein
Respiratory rate