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