**Core Concept**
β-blocker toxicity occurs when excessive levels of β-blockers, a class of medications used to treat hypertension, angina, and arrhythmias, lead to over-activation of β-adrenergic receptors. This results in a complex clinical picture characterized by bradycardia, hypotension, and decreased cardiac output.

**Why the Correct Answer is Right**
Glucagon is the correct treatment for β-blocker toxicity because it acts as a β-adrenergic agonist, bypassing the β-blocker blockade and stimulating the heart to increase its rate and contractility. Glucagon also has a direct inotropic effect, increasing cardiac contractility, which helps to counteract the negative effects of β-blocker toxicity. This is particularly useful in the setting of cardiac arrest or severe bradycardia.

**Why Each Wrong Option is Incorrect**
**Option A:** Atropine is a muscarinic antagonist that can be used to treat bradycardia caused by other mechanisms, such as excessive vagal tone. However, it does not directly address β-blocker toxicity and may even worsen the situation by increasing heart rate without addressing the underlying blockade.

**Option B:** Insulin is not a treatment for β-blocker toxicity. While insulin can be used to manage glucose levels in diabetic patients, it does not have a direct effect on β-adrenergic receptors or cardiac function in the context of β-blocker toxicity.

**Option C:** Fomepizole is a specific antidote for methanol and ethylene glycol poisoning, not β-blocker toxicity. It works by inhibiting alcohol dehydrogenase, preventing the formation of toxic metabolites.

**Clinical Pearl / High-Yield Fact**
In the setting of β-blocker toxicity, the use of glucagon is a high-yield fact that can be remembered using the mnemonic "GIG" - Glucagon, Insulin, Glucose (which is often given concurrently with glucagon to help manage hypoglycemia). This approach can help to rapidly reverse the effects of β-blocker toxicity and improve cardiac function.

**Correct Answer Line**
✓ Correct Answer: D. Glucagon