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Comprehensive CRNA Interview Review Study
Guide
1.Norepinephrine Mechanism of Action (MOA): A1, A2, B1 agonist.
Primary agent used in distributive shock because it's ability to recruit
venous volume and augment preload, while increasing arterial tone, and
increasing cardiac output.
Alpha one causing peripheral smooth muscle contraction. (low dose
venous, high dose venous and arterial).
Alpha 2 adrenoreceptor agonism actually antagonizes the release of
norepinephrine in the CNS, but these receptors are less present in
peripheral vasculature and thus, their anti-hypertensive effects are
overtaken by A1 agonism.
These alpha effects can increase SVR and thereby increase cardiac
workload, decrease cardiac output, and increase coronary perfusion
pressure.
The slight B1 agonism increases inotropy and chonotropy sufficiently to
overcome these A1 effects and result in a fairly "pure" vasopressor.
Increasing contraction of the heart and increasing AV nodal conduction.
**First line agent in septic shock
2.Epinephrine MOA:
A1 A2
B1 - Stimulate Heart Rate through SA node, increase conduction
through AV node. Increase contractility to ATRIAL and VENTRICULAR
cardiac muscle.
B2 - Smooth muscle relaxation. Resulting in dilation of the bronchial
tree, coronary arterial dilation. Also plays a role in insulin and glucagon
secretion in the pancreas. Also increases cardiac inotropy/chonotropy
