In the hydraulic version of Ohm's law, sometimes called Ohm’s law of fluid flow, vascular resistance is analogous to electrical resistance, the pressure difference is analogous to the electrical voltage difference, and volumetric flow is analogous to electric current flow:[4] where The SVR can therefore be calculated in units of dyn·s·cm−5 as where the pressures are measured in mmHg and the cardiac output is measured in units of litres per minute (L/min).
For this reason the BP is frequently used as a practical but somewhat inadequate definition of shock or the state of blood flow.
[6] Therefore, the numerator of the above equation is the pressure difference between the input to the pulmonary blood circuit (where the heart's right ventricle connects to the pulmonary trunk) and the output of the circuit (which is the input to the left atrium of the heart).
Vascular compliance is determined by the muscle tone in the smooth muscle tissue of the tunica media and the elasticity of the elastic fibers there, but the muscle tone is subject to continual homeostatic changes by hormones and cell signaling molecules that induce vasodilation and vasoconstriction to keep blood pressure and blood flow within reference ranges.
[citation needed] In a first approach, based on fluids dynamics (where the flowing material is continuous and made of continuous atomic or molecular bonds, the internal friction happen between continuous parallel layers of different velocities) factors that influence vascular resistance are represented in an adapted form of the Hagen–Poiseuille equation:[citation needed] where Vessel length is generally not subject to change in the body.
In Hagen–Poiseuille equation, the flow layers start from the wall and, by viscosity, reach each other in the central line of the vessel following a parabolic velocity profile.
[citation needed] Counteracting this effect, decreased viscosity in a liquid results in the potential for increased turbulence.
Turbulence can be viewed from outside of the closed vascular system as increased resistance, thereby countering the ease of flow of more hemodilute blood.
When environmental changes occur (e.g. exercise, immersion in water), neuronal and hormonal signals, including binding of norepinephrine and epinephrine to the α1 receptor on vascular smooth muscles, cause either vasoconstriction or vasodilation.
[8] If the resistance is inversely proportional to the fourth power of vessel radius, the resulting force exerted on the wall vessels, the parietal drag force, is inversely proportional to the second power of the radius.
So the total force on the wall is proportional to the pressure drop and the second power of the radius.
Thus the force exerted on the wall vessels is inversely proportional to the second power of the radius.
The secondary regulators of vascular resistance, after vessel radius, is the sheath flow size and its viscosity.
[citation needed] Combining Thurston's work with the Hagen-Poiseuille equation shows that blood flow exerts a force on vessel walls which is inversely proportional to the radius and the sheath flow thickness.
Most of the adenosine that is produced leaves the cell and acts as a direct vasodilator on the vascular wall.
[citation needed] Adenosine causes vasodilation in the small and medium-sized resistance arterioles (less than 100 μm in diameter).
[12] The coronary steal and the stress test can be quickly terminated by stopping the adenosine infusion.
Vasoconstriction and an increased SVR is particularly true of drugs the stimulate alpha(1) adrenergic receptors.
They are sometimes known as autoregulatory vessels since they can dynamically change in diameter to increase or reduce blood flow.
The highly compliant nature of the pulmonary circulation means that the degree of lung distention has a large effect on PVR.
PVR is calculated as a sum of the alveolar and extra-alveolar resistances as these vessels lie in series with each other.
Because the alveolar and extra-alveolar resistances are increased at high and low lung volumes respectively, the total PVR takes the shape of a U curve.
There are a number of mechanisms for regulating coronary vascular tone, including metabolic demands (i.e. hypoxia), neurologic control, and endothelial factors (i.e. EDRF, endothelin).