Systemic Vascular Resistance

Systemic Vascular Resistance
(Total Peripheral Resistance)

Systemic vascular resistance (peripheral vascular resistance, SVR) is the resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function.

• Majority of resistance in systemic system results from arterioles – state of contraction and relaxation of smooth muscle cells of arterioles which determines distribution of blood to organs
• The % of each organ blood flow is dependent on the organ vascular resistance
• Systemic vascular resistance is the resistance of several circuits in parallel, which have both common and independent factors in their regulation.
  • As they are in parallel the sum of reciprocals is used to determine the overall value.

Control

• As per Hagen Poiseuille Equation:

where: η = blood viscosity
L = length of vessel
r = radius of vessel

• radius is the most important factor

Extrinsic Control

• Extrinsic SNS control
  • Arterioles have profuse SNS supply → NAd from nerve endings act on α1-adrenoceptors to cause vasoconstriction (and β2-adrenoceptors to cause vasodilation – but effect is weaker!)
  • Due to the tonic SNS outflow from medullary vasomotor centres, arterioles have a basal level of vasoconstriction → the degree of basal vasoconstriction (and arteriolar resistance) can be varied by altering SNS outflow
• Extrinsic PNS control
  • PNS control of arterioles is less important → vessels of external genitalia have dual ANS supply with PNS dilator nerves and SNS constrictor supply; PNS activation in heart, brain and lungs have an uncertain role
• Extrinsic hormonal control
  • Adrenaline (from adrenal medulla) → effect on organ blood flow depends on the relative % of α1- and β2-adrenoceptors present in the arteriole
  • AII (from RAAS) → vasoconstriction (via AT2R)
  • ADH (from posterior pituitary) → vasoconstriction (via V1R)
  • ANP (from RA) → vasodilation (via ANPR)

Intrinsic Control

• Autoregulation
  • Ability of an organ to maintain relatively constant blood flow across variations in perfusion pressure
  • flow = pressure/ resistance → as the P changes, the R also changes to maintain flow
  • Outside limits of autoregulation: flow = dependent on driving pressure
  • Kidneys, brain, heart
• Autoregulation is dependent on 2 mechanisms:
  • Pressure autoregulation: myogenic stretch response to ↑ and ↓ in pressure → vasoconstriction, and vasodilation
  • Metabolic or vasoactive autoregulation: direct action of locally derived metabolites and vasoactive substances e.g. platelets release thromboxane A2 → constriction in damage

Bianca / Kerr 2016

Answer by Bianca, Kerr