## Distinguishing Cyanide from Carbon Monoxide Poisoning ### Key Pathophysiological Difference **Key Point:** Cyanide causes **histotoxic hypoxia** (cells cannot use oxygen), whereas carbon monoxide causes **hypoxic hypoxia** (reduced oxygen delivery). ### Comparison Table | Feature | Cyanide Poisoning | Carbon Monoxide Poisoning | |---------|-------------------|-------------------------| | **Mechanism** | Blocks cytochrome c oxidase (Complex IV) | Binds Hb with affinity 200× higher than O₂ | | **PaO₂ / SaO₂** | Normal or high | Low (reflects true hypoxemia) | | **Venous O₂ saturation** | High (tissues cannot extract O₂) | Low (tissues extract available O₂) | | **Arteriovenous O₂ difference** | Narrow (poor tissue extraction) | Wide (compensatory extraction) | | **Skin colour** | Normal or cyanosed | Cherry-red (carboxyhemoglobin) | | **Carboxyhemoglobin** | Absent | Present (diagnostic) | | **Lactate** | Markedly elevated (anaerobic metabolism) | Elevated but usually less severe | ### Clinical Pearl **Clinical Pearl:** The **paradox of normal SaO₂ with severe acidosis** is the hallmark of cyanide poisoning. The pulse oximeter reads normal because it detects oxygenated hemoglobin, but the tissues are dying from inability to use that oxygen. This creates a "metabolic emergency with normal vital signs" picture. ### High-Yield Discriminator **High-Yield:** The **normal or elevated SaO₂ in the presence of severe metabolic acidosis and elevated lactate** is the single best bedside clue that cyanide, not carbon monoxide, is the culprit. CO poisoning would show low SaO₂ or low SpO₂ readings. ### Why Each Wrong Option Fails - **Cherry-red skin:** This is classic for CO poisoning (carboxyhemoglobin), not cyanide. - **Delayed neurological onset:** Cyanide causes **rapid** onset (minutes), not delayed (24–48 hrs). - **Elevated carboxyhemoglobin:** This is diagnostic of CO, not cyanide. [cite:Reddy's Forensic Medicine 34e Ch 18]
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