Effects of catecholamines on BP

Keynotes

Both NE and E increase contractility via beta-1

E

Vasodilation in skeletal muscle and liver (beta-2 receptor)
--> Overall vasodilation

Reflex bradycardia insufficient

• Decrease PVR, DBP
• Increase HR, SBP, pulse pressure, CO
• MABP increase slightly

NE

Overall vasocontriction (alpha-1)

Reflex bradycardia sufficent to dominate

• Decrease HR, CO
• Increase SBP, DBP, PVR
• MABP increase

Norepinephrine = NE

Epinephrine = E

Effects on heart

NE and E both increase HR and contractility in isolated heart, via beta-1 receptors.

Also see ANS innervation of the heart

Epinephrine on vasomotor tone

Epinephrine causes vasodilation in skeletal muscles and liver via beta-2 receptors

--> This vasodilation overwhelms vasoconstriction caused by E elsewhere

--> PVR decrease (not increase)

Thus,

• DBP decreased
  * Due to decreased SVR
• SBP increased
  * Due to increased stroke volume
• HR increased
  * Direct effect of catecholamine on heart
  * Reflex bradycardia secondary to BP increase is insufficient to override the direct tachycardic effect
• Cardiac output increased
  * Due to increased HR and stroke volume

NB:

[BL8:p245] Low doses of epinephrine cause muscle vasodilation, but high doses cause muscle constriction

Norepinephrine on vasomotor tone

Norepipherine causes vasoconstriction in almost all organs via alpha-1 receptors.

Thus,

• Both SBP and DBP increased
  * Due to increased SVR
• HR decreased
  * Stimulation of baroreceptors
  * Compensatory reflex bradycardia overrides NE's direct (bradycardic) effect on HR
• Stroke volume
  * ?? Unchanged or slightly increased
• Cardiac output decreased
  * Due to decreased HR