Perfusion 3 Flashcards
Why are calcium channel blockers not first line for HTN?
They decrease CO by dilating arterioles but their specificity is not absolute
Body Parts that have only SNS innervation
Adrenal medulla, arrector pili muscles, sweat glands, some blood vessels.
Alpha 1 receptors
cause vasoconstriction
pupil dilation
increased closure of internal urinary sphincter
secretions
Alpha 2 receptors
vasoconstriction of arteries vasoconstriction of veins decreased GI motility Decreased smooth muscle motility Contraction of male genitalia during ejaculation
Beta 1 Receptors
increased myocardial activity and increased HR
Beta 2 receptors
Smooth muscles in blood vessels, bronchi. Stimulation leads to vasodilation/BRONCHODILATION
increased muscle and liver breakdown of glycogen and increased release of glucagon from alpha cells in pancreas.
Antagonism would cause constriction in bronchi***and hypoglycemic traits
Adrenergic Antagonist action
block catecholamine activity:
DECREASE IN: HR, conduction rate, contractility.
-also vasodilation
MEds:
Atenolol (beta 1-vasodilaton), Propanolol (beta 1/2 decreased AV node conduction) antiarrythmic
Metoprolol (beta 1, high dose beta 2)
Prazosin (alpha 1-peripheral vasodilation),
Phentolamine (alpha “)
What to watch for in pts on Beta blockers
their vital signs will not compensate in state of emergency bc we have blocked the receptors.
Beta 1 Specific Meds: what to watch for
may decrease HR so much that we need to make sure we have peripheral pulses and adequate skin color
Centrally acting Alpha 2 adrenergic agonists
Stimulate CNS alpha 2 in the vasomotor directly.
Drugs: Clonidine, methyldopa
SE: hypotension, headache. bc they cross the BBB. Second line tx for pts who didn’t respond to meds