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Related Subjects: |Drug Toxicity - clinical assessment |Metabolic acidosis |Aspirin or Salicylates toxicity |Ethylene glycol toxicity |Ethanol toxicity |Methanol toxicity |Ricin toxicity |Carbon Tetrachloride Toxicity |Renal Tubular Acidosis |Lactic acidosis |Iron Toxicity |Tricyclic Antidepressant Toxicity |Opiate Toxicity |Carbon monoxide Toxicity |Benzodiazepine Toxicity |Paracetamol (Acetaminophen) toxicity |Amphetamine toxicity |Beta Blocker toxicity |Calcium channel blockers toxicity |Cannabis toxicity |Cyanide toxicity |Digoxin Toxicity |Lithium Toxicity |NSAIDS Toxicity |Ecstasy toxicity |Paraquat toxicity |Quinine toxicity |SSRI Toxicity |Theophylline Toxicity |Organophosphate (OP) Toxicity |Toxin elimination by dialysis |Drug Toxicity with Specific Antidotes
Tight affinity
All bound same vicinity
Space heater on fritz
Household red, barely alive
Force free heme, O2, deep dive Link to author
CO poisoning is not apparent on a pulse oximeter and needs an ABG if suspected. Key to prognosis is removal from the source of carbon monoxide as quickly as possible and instigation of high flow oxygen treatment. Normally CO is <10%. In city dwellers or smokers, levels can be raised up to 10%. A carboxyhaemoglobin level of 30% indicates severe exposure.
Administration of 15 L/min of oxygen via a non-rebreather mask (NRB) is an integral part of the initial management of acute carbon monoxide poisoning.