Antiarrhythmic Agents Part 2 Flashcards
(30 cards)
Natural Catecholamines
Epinephrine
Norepinephrine
Dopamine
Synthetic Catecholamines
Isoproterenol
Dobutamine
Synthetic NonCatecholamines
Ephedrine
Phenylephrine
Alpha Receptor Affinity
norepi>epi>iso
Beta Receptor Affinity
Iso>epi>norepi
Alpha 1 Receptor Locations
post-synaptic
vasculature, heart, glands, and gut
activation causes vasoconstriction and relaxation at the GI tract
Alpha 2 Receptor Locations
Presynaptic: peripheral vascular smooth muscle, coronaries, brain. Activation causes inhibition of norepi release and inhibition of SNS outflow leading to decreased BP, HR and inhibition of CNS activity.
Postsynaptic: coronaries and CNS. Activation causes constriction, sedation and analgesia.
Beta 1 Receptor Locations
myocardium, SA node, ventricular conduction system, coronaries, and kidney.
increases inotropy, chronotrophy, myocardial conduction velocity, coronary relaxation and renin release.
Beta 2 Receptor Locations
vascular, bronchial, smooth muscle in the skin, myocardium, coronaries, kidneys and GI tract and uterine smooth muscle.
Vasodilation, bronchodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake (hypokalemia)
Use of CV agents in Anesthesia
- improve arterial BP
- improve myocardial contractility
- improve oxygenation through bronchodilation
- anaphylaxis treatment
- ACLS protocols
- Additive to L.A.
- sedation and analgesia (alpha2)
Alpha Adrenergic Receptors
GPCR
Ligands: NE, EPI, DOPA
Alpha 1: increases DAG + IP3, increased calcium leading to contraction
Alpha2: decreased camp leads to inhibition of Norepi
Beta Adrenergic Receptors
activation of adenyl cyclase, increased camp, increased kinase production and phosphorylation.
Classes of Drugs to treat HTN: Sympathetic Nervous System
beta antagonists
alpha 1 antagonists
mixed alpha & beta antagonists
centrally acting alpha 2 agonists
Classes of Drugs to treat HTN: RAAS
ACE-I
ARB
Diuretics
Classes of Drugs to treat HTN: Endothelium derived mediator and/or ion channel modulators
direct vasodilators (nitro, hydralazine) calcium channel antagonists potassium channel opener
When to Treat HTN
> 120/80 “lifestyle modifications”
<140/90 18-59 no comorbidities OR >60 with diabetes and/or CKD
<150/90 60 or older with no DM or kidney disease
First Line Therapy HTN
Thiazide diuretic UNLESS compelling indication such as already showing organ decompensation
I.E. elevated BUN/Cr or cardiac hypertrophy
Hypertensive Emergency
diastolic >120 with evidence of progressive end organ damage
Goal: decrease DBP to 100-105 within 24 hours (clonidine)
Hypertensive Crisis
diastolic >120 with evidence of end organ FAILURE
Goal: decrease DBP to 100-105 ASAP
nitroprusside, nitroglycerin, labetalol, fenoldapam
Alpha Antagonists
bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response
Phenoxybenzamine
binds covalently, nonselective (less alpha 2)
less tachycardia with decreased SVR
PO med for preop BP control in pheochromocytoma
PRODRUG (1 hr onset, long acting 24 half time)
Phentolamine
non selective, competitive alpha antagonist
reflex mediated and alpha2 associated increases in HR and CO
produce vasodilation and decrease in SVR
Prazosin
selective alpha 1 competitive alpha antagonist
less likely to cause tachycardia
dilates arteries and veins
used preop for pheo patients, essential HTN with thiazides, decreasing afterload in HF, raynaud phenomenon
Yohimibine
Competitive alpha antagonist
alpha 2 selective
increases release of NE from post-synaptic neuron (vasoconstriction)
used for orthostatic hypotension and impotence
