**Core Concept**
Beta blockers induce excessive bradycardia and/or decreased cardiac output by blocking beta-1 adrenergic receptors in the heart, leading to decreased heart rate and contractility. In such scenarios, treatment involves administering drugs that counteract these effects by increasing heart rate and cardiac output.

**Why the Correct Answer is Right**
Glucagon is a potent agonist of the glucagon receptor, which stimulates adenylate cyclase activity, thereby increasing cAMP levels within cardiac cells. This leads to an increase in heart rate and contractility, effectively countering the effects of beta blockers. Glucagon also has a positive inotropic effect, which helps to increase cardiac output.

**Why Each Wrong Option is Incorrect**
**Option A:** Atropine, a muscarinic receptor antagonist, can increase heart rate by blocking parasympathetic tone. However, it is not the most effective agent for treating beta blocker-induced bradycardia and decreased cardiac output.

**Option B:** Dobutamine, a beta-1 agonist, can increase heart rate and contractility but may not be as effective as glucagon in countering the effects of beta blockers. Dobutamine also has a shorter duration of action compared to glucagon.

**Option C:** Epinephrine, a non-selective adrenergic agonist, can increase heart rate and contractility but may cause significant vasodilation and hypotension, which can worsen cardiac output.

**Clinical Pearl / High-Yield Fact**
When treating beta blocker-induced excessive bradycardia and/or decreased cardiac output, it's essential to remember that glucagon is a more effective agent than atropine or dobutamine due to its potent positive inotropic and chronotropic effects.

**Correct Answer:** C. Epinephrine