• Mechanism of action: epinephrine’s mechanism of action can be divided into low-dose (2-3 μg/min) and high-dose (≥ 3 μg/min) actions. At low doses, epinephrine favors β1 and β2 agonism. As β1 receptors are on the heart, epinephrine at low doses increases both chronotropy and inotropy. β2 receptors are on the vasculature, and they cause vasodilation. Thus, epinephrine at low doses decreases preload, afterload, and systemic vascular resistance. Agonism of β2 receptors with epinephrine also causes bronchodilation, and low doses of epinephrine can be useful for patients with obstructive pulmonary pathology. However, at high doses, the β2 effect falls off, and the α1 effect becomes more significant. Thus, at high doses, epinephrine increases preload, afterload, and systemic vascular resistance.  

• Uses: go-to agent for anaphylaxis and cardiac arrest. Also great for cardiogenic shock because of its effects on chronotropy and inotropy  

• Avoid: can worsen primary tachyarrhythmias because of its propensity to increase chronotropy and inotropy, and can worsen supply/demand mismatch in critical aortic stenosis due to the fact that the heart is now beating harder against a fixed afterload  

For comparison, here's our 'obligatory' pressor table:

References: