# Vascular resistance

Vascular resistance is 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. Vasoconstriction (i.e., decrease in blood vessel diameter) increases SVR, whereas vasodilation (increase in diameter) decreases SVR.

Units for measuring vascular resistance are dyn·s·cm−5, pascal seconds per cubic metre (Pa·s/m³) or, for ease of deriving it by pressure (measured in mmHg) and cardiac output (measured in l/min), it can be given in mmHg·min/l. This is numerically equivalent to hybrid reference units (HRU), also known as Wood units, frequently used by pediatric cardiologists. 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.[1]

Measurement Reference Range
dyn·s/cm5 MPa·s/m3 mmHg·min/l or
HRU/Wood units
Systemic vascular resistance 700–1600[2] 70–160[3] 9–20[3]
Pulmonary vascular resistance 20–130[2] 2–13[3] 0.25–1.6[3]

## Calculation of resistance

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

The systemic vascular resistance can therefore be calculated in units of dyn·s·cm−5 as

$\frac {80 \cdot (mean\ arterial\ pressure - mean \ right \ atrial \ pressure)} {cardiac\ output}$

where mean arterial pressure is 2/3 of diastolic blood pressure plus 1/3 of systolic blood pressure.

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

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

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). The pulmonary artery wedged pressure (also called pulmonary artery occlusion pressure or PAOP) is a measurement in which one of the pulmonary arteries is occluded, and the pressure downstream from the occlusion is measured in order to approximately sample the left atrial pressure.[4] 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). The above equation contains a numerical constant to compensate for the units used, but is conceptually equivalent to the following:

$R = \frac{\Delta P}{Q}$

where R is the pulmonary vascular resistance (fluid resistance), ΔP is the pressure difference across the pulmonary circuit, and Q is the rate of blood flow through it.

As an example: If Systolic pressure: 120 mmHg, Diastolic pressure: 80 mmHg, Right atrial mean pressure: 3 mmHg, Cardiac output: 5 l/min, Then Mean Arterial Pressure would be : (2 Diastolic pressure + Systolic pressure)/3 = 93.3 mmHg, and Systemic vascular resistance: (93 - 3) / 5 =18 Wood Units. or Systemic vascular resistance: 18 x 80 = 1440 dyn·s/cm5 These values are in the normal limits.

## 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 since they can dynamically change in diameter to increase or reduce blood flow.

Any change in the viscosity of blood (such as due to a change in hematocrit) would also affect the measured vascular resistance.

## 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 vasodilation. If the endothelium is damaged, cholinergic stimulation causes vasoconstriction.

Adenosine probably doesn't play a role in maintaining the vascular resistance in the resting state. However, it causes vasodilation 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 vasodilation.

Adenosine causes vasodilation 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,[5] where the vessels in healthy tissue dilate as much as the ischemic tissue and more 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.

## 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 (i.e.: hypoxia), neurologic control, and endothelial factors (i.e.: 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.

## References

1. ^ Fuster, V.; Alexander, R.W.; O'Rourke, R.A. (2004) Hurst's the heart, book 1. 11th Edition, McGraw-Hill Professional, Medical Pub. Division. Page 513. ISBN 978-0-07-143224-5.
2. ^ a b Table 30-1 in: Trudie A Goers; Washington University School of Medicine Department of Surgery; Klingensmith, Mary E; Li Ern Chen; Sean C Glasgow (2008). The Washington manual of surgery. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 0-7817-7447-0.
3. ^ a b c d Derived from values in dyn·s/cm5
4. ^ University of Virginia Health System."The Physiology: Pulmonary Artery Catheters"
5. ^ Masugata H, Peters B, Lafitte S, et al. (2003). "Assessment of adenosine-induced coronary steal in the setting of coronary occlusion based on the extent of opacification defects by myocardial contrast echocardiography". Angiology 54 (4): 443–8. doi:10.1177/000331970305400408. PMID 12934764.

## Literature

1. Grossman W, Baim D. Grossman's Cardiac Catheterization, Angiography, and Intervention, Sixth Edition. Page 172, Tabe 8.1 ISBN 0-683-30741-X