Blood Pressure (third part): Physiology

The physics of the circulatory system is very complex. That said, there are many physical factors that influence arterial pressure. Each of these may in turn be influenced by physiological factors, such as diet, exercise, disease, drugs or alcohol, obesity, excess weight and so-forth.

Some physical factors are:

* Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at which blood (the fluid) is pumped by the heart. The volume of blood flow from the heart is called the cardiac output which is the heart rate (the rate of contraction) multiplied by the stroke volume (the amount of blood pumped out from the heart with each contraction). The higher the heart rate, the higher the arterial pressure, assuming no reduction in stroke volume.
* Volume of fluid or blood volume, the amount of blood that is present in the body. The more blood present in the body, the higher the rate of blood return to the heart and the resulting cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response.
* Resistance. In the circulatory system, this is the resistance of the blood vessels. The higher the resistance, the higher the arterial pressure upstream from the resistance to blood flow. Resistance is related to vessel radius (the larger the radius, the lower the resistance), vessel length (the longer the vessel, the higher the resistance), as well as the smoothness of the blood vessel walls. Smoothness is reduced by the buildup of fatty deposits on the arterial walls. Substances called vasoconstrictors can reduce the size of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the size of blood vessels, thereby decreasing arterial pressure. Resistance, and its relation to volumetric flow rate (Q) and pressure difference between the two ends of a vessel are described by Poiseuille's Law.
* Viscosity, or thickness of the fluid. If the blood gets thicker, the result is an increase in arterial pressure. Certain medical conditions can change the viscosity of the blood. For instance, low red blood cell concentration, anemia, reduces viscosity, whereas increased red blood cell concentration increases viscosity. Viscosity also increases with blood sugar concentration—visualize pumping syrup. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of blood, but studies found[22] that they act by reducing the tendency of the blood to clot instead.

In practice, each individual's autonomic nervous system responds to and regulates all these interacting factors so that, although the above issues are important, the actual arterial pressure response of a given individual varies widely because of both split-second and slow-moving responses of the nervous system and end organs. These responses are very effective in changing the variables and resulting blood pressure from moment to moment.

[edit] Mean arterial pressure

The mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP),[23]

\! MAP = (CO \cdot SVR) + CVP

MAP can be approximately determined from measurements of the systolic pressure \! P_{sys} and the diastolic pressure \! P_{dias} while there is a normal resting heart rate,[23]

\! MAP \approxeq P_{dias} + \frac{1}{3} (P_{sys} - P_{dias})

[edit] Pulse pressure

The up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. The pulse pressure is determined by the interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta, and the resistance to flow in the arterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way the pulse pressure is reduced from what it would be if the aorta wasn't compliant.[24]

The pulse pressure can be simply calculated from the difference of the measured systolic and diastolic pressures,[24]

\! P_{pulse} = P_{sys} - P_{dias}

[edit] Vascular resistance

The larger arteries, including all large enough to see without magnification, are low resistance conduits (assuming no advanced atherosclerotic changes) with high flow rates that generate only small drops in pressure. For instance, with a subject in the supine position, blood travelling from the heart to the toes typically only experiences a 5 mmHg drop in mean pressure.

[edit] Vascular pressure wave

Modern physiology developed the concept of the vascular pressure wave (VPW). This wave is created by the heart during the systole and originates in the ascending aorta. Much faster than the stream of blood itself, it is then transported through the vessel walls to the peripheral arteries. There the pressure wave can be palpated as the peripheral pulse. As the wave is reflected at the peripheral veins it runs back in a centripetal fashion. Where the crests of the reflected and the original wave meet, the pressure inside the vessel is higher than the true pressure in the aorta. This concept explains why the arterial pressure inside the peripheral arteries of the legs and arms is higher than the arterial pressure in the aorta,[25][26][27] and in turn for the higher pressures seen at the ankle compared to the arm with normal ankle brachial pressure index values.

[edit] Regulation

The endogenous regulation of arterial pressure is not completely understood. Currently, three mechanisms of regulating arterial pressure have been well-characterized:

* Baroreceptor reflex: Baroreceptors detect changes in arterial pressure and send signals ultimately to the medulla of the brain stem. 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 total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.[28]

* 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.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. Currently, the RAS system is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. 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.