Cardiac Poisons

Cardiac Glycosides - Foxglove's Fury

• Source: Digitalis purpurea (Foxglove), D. lanata. Active principles: Digoxin, Digitoxin.
  • Clinical Context: While cardiac glycosides like digoxin are still used, their role as first-line treatment has largely been superseded by ACE inhibitors and beta-blockers due to narrow therapeutic window and potential for severe toxicity.
• Mechanism (MoA): Inhibits Na+/K+ ATPase → ↑ intracellular Na+ → ↑ intracellular Ca2+ (via Na+/Ca2+ exchanger) → ↑ inotropy, ↓ AV conduction (chronotropy & dromotropy).
• Clinical Features:
  • GI: Nausea, vomiting, abdominal pain.
  • CNS: Confusion, drowsiness, visual disturbances (xanthopsia - yellow/green halos around objects).
  • CVS: Bradycardia (commonest), AV blocks, various arrhythmias (e.g., ventricular bigeminy, VT), hyperkalemia (indicates severe toxicity).
• ECG Changes: 📌 DALI mnemonic
  • Depression of ST segment (characteristic scooping - "Salvador Dali moustache" sign).
  • AV block (all degrees).
  • Lengthened PR interval.
  • Inversion or flattening of T wave, shortened QT interval.
• Fatal Dose: Digoxin ~2-3 mg; Digitoxin ~10-20 mg.
• Treatment: First-line for severe arrhythmias: Digoxin immune Fab (DigiFab, Digibind) for significant dysrhythmias. Magnesium sulfate may be life-saving in VT/VF. Stop drug. Gastric lavage/activated charcoal (if early). Correct hyperkalemia (glucose-insulin, K+-binding resins; AVOID Ca2+). Atropine for bradycardia. Lidocaine/Phenytoin for arrhythmias.
• Postmortem (PM): Often non-specific. Drug detectable in blood, urine, bile, liver, kidney, vitreous humor (good for recent intake). BNS Section 103 (culpable homicide) considerations in suspicious cases.

  ⭐ Hyperkalemia is a significant indicator of severe digitalis toxicity and correlates with mortality. Digitalis toxicity remains forensically relevant due to digoxin's narrow therapeutic window - thorough history of source, amount, timing, and comorbidities essential.

More Plant Poisons - Aconite's Agony

• Aconite (Monkshood, Wolfsbane, Meetha Zehr): Known as "sweet poison".
  • Active Principle: Aconitine (highly toxic diterpenoid alkaloid).
  • Mechanism: Locks open voltage-gated Na+ channels → sustained depolarization, affecting heart & nerves.
  • Key Symptoms:
    • Initial: Tingling/numbness of mouth, tongue, throat (pathognomonic).
    • GIT: Nausea, vomiting, severe abdominal pain.
    • CVS: Hypotension, bradycardia → ventricular tachyarrhythmias (VT/VF).
    • CNS: Paresthesias, muscle weakness, convulsions, respiratory paralysis.
  • Fatal Dose: Aconitine 1-2 mg; Root 1-2 g.
  • Fatal Period: Rapid, typically 1-6 hours.
  • PM: Non-specific; froth at mouth/nostrils, organ congestion.
  • Treatment: Gastric lavage, charcoal. Supportive: atropine, amiodarone. No specific antidote.

  ⭐ Pathognomonic: initial tingling/burning sensation in mouth, lips, tongue, spreading to face/limbs.

Drug Cardiotoxicity - Pill Perils

Many pharmaceuticals induce cardiac damage. Key offenders:

• Tricyclic Antidepressants (TCAs):
  • $Na^+$ channel blockade → QRS widening, arrhythmias.
  • Anticholinergic effects.
  • 📌 Mnemonic: "Tri-C's" - Convulsions, Coma, Cardiac (arrhythmias, hypotension).
• Antipsychotics (e.g., Haloperidol, Risperidone):
  • $K^+$ channel blockade → QT prolongation (TdP risk).
• Antiarrhythmics (e.g., Amiodarone, Sotalol):
  • Class-specific effects; can be pro-arrhythmic.
• Anthracyclines (e.g., Doxorubicin):
  • Dose-dependent cardiomyopathy (oxidative stress, mitochondrial damage).
• Cocaine:
  • Vasospasm, MI, arrhythmias ($Na^+$/$K^+$ channel blockade).

ECG Clues:

• QTc > 500 ms: High TdP risk.
• QRS > 120 ms (sodium channel blocker toxicity): General indicator for toxicity; specific thresholds vary per current guidelines.

⭐ Digoxin toxicity classically presents with "reverse tick" sign (scooped ST segments) on ECG and visual disturbances (xanthopsia - yellow halos).

💡 Clinical Note: ECG parameters and risk thresholds are subject to ongoing refinement. Always refer to latest clinical toxicology guidelines and cardiology recommendations for current diagnostic criteria and management protocols.

Inorganic & Gaseous - Ion & Gas Attack

• Phosphorus (Yellow): Protoplasmic poison. Myocardial damage, fatty degeneration. Garlic odor. Red phosphorus is non-toxic, but yellow phosphorus is highly toxic causing severe symptoms. Treat with 2-3 glasses of water, seek immediate medical attention without inducing vomiting.
• Arsenic ($As_2O_3$): Sulfhydryl enzyme inhibitor. Capillary damage, QT prolongation. FD: 100-300 mg.
• Thallium: Interferes with K+ processes. Tachycardia, hypertension. Alopecia (delayed). FD: 1 g.
• Carbon Monoxide (CO): Forms carboxyhemoglobin (COHb). Myocardial ischemia, arrhythmias. Cherry-red skin. COHb >20% symptomatic.
  • Binds myoglobin & cytochrome oxidase.

⭐ CO has 200-250 times greater affinity for hemoglobin than oxygen.

• Cyanide (HCN/KCN): Inhibits cytochrome c oxidase. Rapid cardiovascular collapse. Bitter almond odor. FD (HCN): 50-60 mg.
  • Histotoxic hypoxia.
• Barium Salts (Soluble): Blocks K+ channels $\rightarrow$ hypokalemia. Arrhythmias (VPCs, VT), hypertension.

High‑Yield Points - ⚡ Biggest Takeaways

• Aconite: Tingling/numbness (mouth, fingers), bradycardia, arrhythmias; no specific antidote.
• Oleander (Nerium): Contains cardiac glycosides; causes hyperkalemia, bradycardia. Treat with Digoxin Fab.
• Digitalis (Foxglove): Xanthopsia, scooped ST segment; hypokalemia potentiates toxicity. Antidote: Digibind.
• Quinine: Cinchonism (tinnitus), QT prolongation, Torsades de Pointes.
• Potassium Chloride (KCl): Hyperkalemia causes peaked T waves, wide QRS, then asystole.
• Cerbera thevetia (Yellow Oleander): Potent cardiac glycosides; causes vomiting, hyperkalemia, heart block.