Vascular resistance

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Vascular resistance is a term used to define the resistance to flow that must be overcome to push blood through the circulatory system. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). The systemic vascular resistance may also be referred to as the total peripheral resistance.

Units for measuring vascular resistance are dyn·s·cm^-5 or pascal seconds per cubic metre (Pa·s/m³). Pediatric cardiologists use hybrid reference units (HRU), also known as Wood units, as they were introduced by Dr. Paul Wood. To convert from Wood units to MPa·s/m³ you must multiply by 8, or to dyn·s·cm^-5 you must multiply by 80.

Measurement	Reference Range
Systemic vascular resistance	900–1200 dyn·s/cm⁵ (90–120 MPa·s/m³)
Pulmonary vascular resistance	100–200 dyn·s/cm⁵ (10–20 MPa·s/m³)

1 Calculation of resistance
2 Determinants of vascular resistance
3 Regulation of vascular resistance
- 3.1 Role of adenosine
4 Coronary vascular resistance
5 References
6 See also

[edit] Calculation of resistance

The basic tenet of calculating resistance is that flow is equal to driving pressure divided by resistance.

The pulmonary vascular resistance can therefore be calculated in units of dyn·s·cm^-5 as

$\frac {80 \cdot (mean\ pulmonary\ arterial\ pressure - pulmonary\ capillary\ wedge\ pressure)} {cardiac\ output}$

where the pressures are measured in units of millimetres of mercury (mmHg) and the cardiac output is measured in units of litres per minute (L/min).

[edit] Determinants of vascular resistance

The major determinant of vascular resistance is small arteriolar (known as resistance arterioles) tone. These vessels are from 450 µm down to 100 µm in diameter. (As a comparison, the diameter of a capillary is about 3 to 4 µm.)

Another determinant of vascular resistance is the pre-capillary arterioles. These arterioles are less than 100 µm in diameter. They are sometimes known as autoregulatory vessels.

[edit] Regulation of vascular resistance

There are many factors that alter the vascular resistance. Many of the platelet-derived substances, including serotonin, are vasodilatory when the endothelium is intact and are vasoconstrictive when the endothelium is damaged.

Cholinergic stimulation causes release of endothelium-derived relaxing factor (EDRF) (later it was discovered that EDRF was nitric oxide) from intact endothelium, causing vasodilatation. If the endothelium is damaged, cholinergic stimulation causes vasoconstriction.

[edit] Role of adenosine

Adenosine probably doesn't play a role in maintaining the vascular resistance in the resting state. However, it causes vasodilatation and decreased vascular resistance during hypoxia. Adenosine is formed in the myocardial cells during hypoxia, ischemia, or vigorous work, due to the breakdown of high-energy phosphate compounds (e.g., adenosine monophosphate, AMP). Most of the adenosine that is produced leaves the cell and acts as a direct vasodilator on the vascular wall. Because adenosine acts as a direct vasodilator, it is not dependent on an intact endothelium to cause vasodilatation.

Adenosine causes vasodilatation in the small and medium sized resistance arterioles (less than 100 µm in diameter). When adenosine is administered it can cause a coronary steal phenomenon, where the vessels in health tissue dilate as much as the ischemic tissue and more and blood is shunted away from the ischemic tissue that needs it most. This is the principle behind adenosine stress testing.

Adenosine is quickly broken down by adenosine deaminase, which is present in red cells and the vessel wall.

[edit] Coronary vascular resistance

The regulation of tone in the coronary arteries is a complex subject. There are a number of mechanisms for regulating coronary vascular tone, including metabolic demands (ie: hypoxia), neurologic control, and endothelial factors (ie: EDRF, endothelin).

Local metabolic control (based on metabolic demand) is the most important mechanism of control of coronary flow. Decreased tissue oxygen content and increased tissue CO₂ content act as vasodilators Acidosis acts as a direct coronary vasodilator and also potentiates the actions of adenosine on the coronary vasculature.