Oleander poisoning causes cardiac toxicity primarily through which mechanism?

Explanation

## Oleander Cardiac Toxicity Mechanism **Key Point:** Oleander (Nerium oleander) contains cardiac glycosides — primarily oleandrin and neriine — that inhibit the Na⁺/K⁺-ATPase pump on cardiac myocyte membranes. This is the primary mechanism of oleander toxicity. ### Mechanism of Cardiac Glycoside Toxicity ```mermaid flowchart TD A[Oleander ingestion]:::outcome --> B[Cardiac glycosides absorbed]:::outcome B --> C[Inhibition of Na⁺/K⁺-ATPase]:::action C --> D[Increased intracellular Na⁺]:::outcome D --> E[Reduced Na⁺/Ca²⁺ exchanger activity]:::outcome E --> F[Increased intracellular Ca²⁺]:::outcome F --> G[Enhanced cardiac contractility<br/>Arrhythmias<br/>Hyperkalemia]:::urgent ``` ### Cardiac Effects of Oleander Poisoning | Effect | Mechanism | Clinical Manifestation | |--------|-----------|------------------------| | **Positive inotropism** | ↑ intracellular Ca²⁺ | Increased contractility (early) | | **Arrhythmias** | Altered automaticity, conduction block | SVT, PVCs, bradycardia, heart block | | **Hyperkalemia** | Reduced K⁺ efflux via Na⁺/K⁺-ATPase | Peaked T waves, widened QRS | | **Vagal effects** | Glycoside-mediated vagal stimulation | AV block, bradycardia | **High-Yield:** Oleander toxicity is dose-dependent and can produce a biphasic response: initial positive inotropism followed by severe arrhythmias and conduction disturbances. The Na⁺/K⁺-ATPase inhibition is the unifying mechanism. **Clinical Pearl:** Oleander poisoning mimics digoxin toxicity because both are cardiac glycosides. Hyperkalemia is a hallmark feature and a sign of severe toxicity. Serum potassium levels can rise dramatically and cause life-threatening arrhythmias. **Mnemonic:** **OLEANDER** = **O**-inhibits pump, **L**-leads to Na⁺ rise, **E**-elevated Ca²⁺, **A**-arrhythmias, **N**-no calcium channel block, **D**-digoxin-like toxicity, **E**-electrolyte shifts, **R**-rapid onset.