1. Nerve Agents. Before the past century, it was unthinkable that rogue states or terrorists would use chemical agents. But today there is no doubt in anyone's mind that chemical agents will be used again in the future. The nerve agents are so named because of their mechanisms of action.
   1. Similar to organophosphate insecticides and the anticholinesterase drugs anesthesiologists use daily, nerve agents inhibit acetylcholinesterase at preganglionic muscarinic and postganglionic muscarinic and nicotinic receptors, leading to copious secretions, meiosis, arrhythmias, bronchospasm, tonic muscle contractions, respiratory paralysis, seizures, and death.
      1. Similar to managing the side effects of neostigmine, a cholinergic agent and competitive muscarinic blockers (atropine or glycopyrrolate) is administered to attenuate and block the muscarinic side effects of the agents.
      2. When anticipating a nerve agent attack, US military personnel pretreat themselves with low-dose pyridostigmine and don personal protective equipment (preventing the agent from contacting and wetting skin from, which it is readily absorbed.)
      3. US military personnel carry syringes of atropine and pralidoxime chloride (2-PAM chloride), an oxime that reactivates acetylcholinesterase by removing the nerve agent from its binding site on the enzyme.
   2. Diagnosis (Table 53-3: Diagnosis of Nerve Agent Toxicity)
   3. Treatment. The treatment for nerve agent poisoning is one with which every anesthesiologist is familiar.
      1. Atropine (2–6 mg every 5–10 minutes until secretions begin to decrease) is a competitive muscarinic blocker.
      2. Pralidoxime chloride is the better long-term treatment because it reactivates acetylcholinesterase by removing the organophosphate compound.
      3. Depending on the extent of exposure, treatment is different. Patients with moderate (and severe) poisoning require treatment with atropine and 2-PAM chloride intramuscularly.
      4. With nerve injury casualties, decontamination is critical. It needs to be done as quickly as possible, first by leaving the area of exposure. Patients are decontaminated by removing their clothing and washing with copious amounts of water in 5% hypochlorite (household bleach).
2. Pulmonary Agents
   1. Chlorine and phosgene are the considered the classical pulmonary agents and the two most likely to be used by terrorists. If quantities are released that are sufficient to displace O₂, then death results from asphyxia. In addition, these two gases are extremely toxic to the lungs; individuals who survive the acute exposure who have inhaled even small amounts often develop acute lung injury or acute respiratory distress syndrome.
   2. The treatment of the resulting noncardiogenic pulmonary edema from NO₂ or the pulmonary agents is supportive: mechanical ventilation using small tidal volumes (6–8 mL/kg), peak airway pressures <30 cm H₂O, and positive end-expiratory pressure and inspired oxygen concentrations of 50% to 60% or less.
3. Blood Agents
   1. Cyanide inhibits cellular respiration by interrupting the oxidative electron transfer process in mitochondria.
   2. The treatment for cyanide toxicity is similar to treatment of someone who had an accidental overdose of sodium nitroprusside (intravenous thiosulfate and supportive care, including tracheal intubation, ventilation with 100% oxygen, and inotropes and vasopressors to stabilize the cardiovascular system).

Emergency Preparedness for and Disaster Management of Casualties from Natural Disasters and Chemical, Biologic, Radiologic, Nuclear, and High-Yield Explosive (Cbrne) Events

1. Preparation: Personal Preparedness
2. Role of Anesthesiologist in Management of Mass Casualties
3. Chemical
4. Biologic
5. Nuclear Radiation