## Systemic Complications of Diphtheria: Myocarditis and Conduction Abnormalities ### Pathophysiology of Diphtheritic Myocarditis **Key Point:** Diphtheria toxin is absorbed systemically and causes direct myocardial damage through ADP-ribosylation of elongation factor 2 (EF-2), leading to inhibition of cardiac protein synthesis and myocyte necrosis. ### Cardiac Manifestations | Feature | Details | |---------|----------| | **Timing** | Appears 1–3 weeks after onset of pseudomembrane | | **Pathology** | Myocardial inflammation, edema, and necrosis | | **ECG findings** | Prolonged PR interval, heart block (1st, 2nd, or 3rd degree), ST-T wave changes | | **Clinical signs** | Tachycardia, hypotension, arrhythmias, cardiogenic shock | | **Mortality** | Accounts for 50–60% of diphtheria deaths | ### Mechanism of Conduction Abnormalities 1. **Direct toxin effect:** Myocardial necrosis and inflammation damage the conduction system 2. **Edema:** Inflammatory edema compresses conduction pathways (especially AV node) 3. **Electrolyte disturbance:** Toxin-induced cellular dysfunction alters ion homeostasis 4. **Progressive block:** May progress from 1st-degree to complete heart block **Clinical Pearl:** Heart block in diphtheria is often **reversible** if the patient survives the acute phase; conduction abnormalities may resolve over weeks to months as inflammation subsides. ### High-Yield Fact **High-Yield:** Diphtheritic myocarditis is the **leading cause of death** in untreated or inadequately treated diphtheria. Early antitoxin administration reduces cardiac complications. **Mnemonic:** **CARD** — **C**onduction abnormalities, **A**rrhythmias, **R**educed contractility, **D**eath risk in diphtheritic myocarditis. [cite:Park 26e Ch 10; Harrison 21e Ch 132] 
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