Vascular resistance refers to the resistance that must be overcome to push blood through the circulatory system and create flow. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR) or may sometimes be referred to the antiquated term total peripheral resistance (TPR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). Systemic vascular resistance is used in calculations of blood pressure, blood flow, and cardiac function. 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.
|Systemic vascular resistance||700–1600||70–160||9–20|
|Pulmonary vascular resistance||20–130||2–13||0.25–1.6|
- 1 Calculation of vascular resistance
- 2 Regulation of vascular resistance
- 3 Systemic vascular resistance
- 4 Pulmonary vascular resistance
- 5 Coronary vascular resistance
- 6 References
- 7 Literature
- 8 See also
Calculation of vascular resistance
The basic tenet of calculating resistance is that flow is equal to driving pressure divided by resistance.
- R is Resistance
- ΔP is the change in pressure across the circulation loop (systemic / pulmonary) from its beginning (immediately after exiting the left ventricle / right ventricle) to its end (entering the right atrium / left atrium)
- Q is the flow through the vasculature (when discussing SVR this is equal to cardiac output)
Systemic vascular resistance calculations
The systemic vascular resistance can therefore be calculated in units of dyn·s·cm−5 as
where mean arterial pressure is 2/3 of diastolic blood pressure plus 1/3 of systolic blood pressure [or Diastolic + 1/3(Systolic-Diastolic)].
In other words:
- Systemic Vascular Resistance = 80x(Mean Arterial Pressure - Mean Venous Pressure or CVP) / Cardiac Output
Mean arterial pressure is most commonly measured using a sphygmomanometer, and calculating a specialized average between systolic and diastolic blood pressures. Venous pressure, also known as central venous pressure, is measured at the right atrium and is usually very low (normally around 4 mm Hg). As a result, it is sometimes disregarded.
Pulmonary vascular resistance calculations
The pulmonary vascular resistance can be calculated in units of dyn·s·cm−5 as
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. 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:
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.
Regulation of vascular resistance
There are many factors that alter the vascular resistance. Factors that influence vascular resistance are represented in an adapted form of the Hagen–Poiseuille equation:
- R = resistance to blood flow
- L = length of the vessel
- η = viscosity of blood
- r = radius of the blood vessel
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. But according to Thurston, there is a plasma release-cell layering at the walls surrounding a plugged flow. It is a fluid layer in which at a distance δ, viscosity η is a function of δ written as η(δ), and these surrounding layers do not meet at the vessel centre in real blood flow. Instead, there is the plugged flow which is hyperviscous because holding high concentration of RBCs. Thurston assembled this layer to the flow resistance to describe blood flow by means of a viscosity η(δ) and thickness δ from the wall layer.
The blood resistance law appears as R adapted to blood flow profile :
- R = resistance to blood flow
- c = constant coefficient of flow
- L = length of the vessel
- η(δ) = viscosity of blood in the wall plasma release-cell layering
- r = radius of the blood vessel
- δ = distance in the plasma release-cell layer
Blood resistance varies depending on blood viscosity and its plugged flow size as well, and on the size of the vessels.
Blood viscosity increases as blood is more hemoconcentrated, and decreases as blood is more dilute. The greater the viscosity of blood, the larger the resistance will be. In the body, blood viscosity increases as red blood cell concentration increases, thus more hemodilute blood will flow more readily, while more hemoconcentrated blood will flow more slowly.
The major regulator of vascular resistance in the body is regulation of vessel radius. In humans, there is very little pressure change as blood flows from the aorta to the large arteries, but the small arteries and arterioles are the site of about 70% of the pressure drop, and are the main regulators of SVR. 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. Because resistance is inversely proportional to the fourth power of vessel radius, changes to arteriole diameter can result in large increases or decreases in vascular resistance.
The blood flow resistance in a vessel is mainly regulated by the vessel radius and viscosity when blood viscosity too varies with the vessel radius. According to very recent results showing the sheath flow surrounding the plug flow in a vessel, the sheath flow size is not neglictible in the real blood flow velocity profile in a vessel. The velocity profile is directly linked to flow resistance in a vessel. The viscosity variations, according to Thurston, are also balanced by the sheath flow size around the plug flow. The secondary regulators of vascular resistance, after vessel radius, is the sheath flow size and its viscosity.
Thurston, as well, shows that the resistance R is constant, where, for a defined vessel radius, the value η(δ)/δ is constant in the sheath flow.
Vascular resistance depends on blood flow which is divided into 2 adjacent parts : a plug flow, highly concentrated in RBCs, and a sheath flow, more fluid plasma release-cell layering. Both coexist and have different viscosities, sizes and velocity profiles in the vascular system.
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 most likely does not 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, 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.
Systemic vascular resistance
Effects of systemic vascular resistance on the body
A decrease in SVR (e.g., during exercising) will result in an increased flow to tissues and an increased venous flow back to the heart. An increased SVR will decrease flow to tissues and decrease venous flow back to the heart.
Pulmonary 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 5 to 10 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.
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. POnis, 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.
- 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.
- 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.
- Derived from values in dyn·s/cm5
- University of Virginia Health System."The Physiology: Pulmonary Artery Catheters"
- GB Thurston, Viscosity and viscoelasticity of blood in small diameter tubes, Microvasular Research 11, 133 146, 1976
- "Cardiac Output and Blood Pressure". biosbcc. Retrieved 7 April 2011.
- Measurement of real pulsatile blood flow using X-ray PIV technique with CO2 microbubbles, Hanwook Park, Eunseop Yeom, Seung-Jun Seo, Jae-Hong Lim & Sang-Joon Lee, NATURE, Scientific Reports 5, Article number: 8840 (2015), doi:10.1038/srep08840.
- 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.