What will the nurse administer to a client with sustained supraventricular tachycardia?

Choice A rationale

Sodium thiosulfate is primarily utilized in the management of cyanide poisoning, not nerve agent exposure. It works by acting as a sulfur donor for the enzyme rhodanese, which converts toxic cyanide into less toxic thiocyanate for renal excretion. Tabun is an organophosphate nerve agent that inhibits acetylcholinesterase, leading to a cholinergic crisis. Therefore, sodium thiosulfate would not address the underlying mechanism of neuromuscular blockade or the overstimulation of muscarinic receptors caused by Tabun.

Choice B rationale

Sodium nitrate is used to treat cyanide toxicity by inducing methemoglobinemia, which has a high affinity for cyanide, pulling it away from cytochrome oxidase. This treatment is irrelevant for nerve agents like Tabun. Nerve agents require medications that counteract excess acetylcholine at the receptor level or reactivate the inhibited enzyme. Using nitrates in this context would not alleviate the respiratory distress, miosis, or bradycardia associated with the specific toxidrome produced by organophosphate nerve agent exposure.

Choice C rationale

While maintaining an airway is a priority in any emergency, the use of a plastic airway or intubation alone does not treat the physiological effects of Tabun. Tabun causes a massive accumulation of acetylcholine, leading to bronchorrhea and bronchospasm, often referred to as "killer B's.”. Without pharmacological intervention to dry secretions and relax the airway, mechanical ventilation may be ineffective due to extremely high airway resistance and excessive fluid within the pulmonary tree.

Choice D rationale

Atropine is the definitive treatment for the muscarinic effects of nerve agent poisoning. It is a competitive antagonist at postganglionic muscarinic receptor sites, effectively blocking the excess acetylcholine resulting from the inhibition of acetylcholinesterase by Tabun. It helps reverse life-threatening symptoms such as severe bradycardia, excessive bronchial secretions, and bronchospasm. Standard dosing in nerve agent exposure involves rapid administration until secretions dry up and heart rate increases, typically alongside an oxime to reactivate the enzyme.

Choice A rationale

Atropine is an anticholinergic medication that blocks the effects of the vagus nerve on the sinoatrial node. This action increases the heart rate, which is the primary goal when treating symptomatic sinus bradycardia. By increasing the heart rate, cardiac output is improved, helping to resolve hypotension and dizziness. A normal heart rate is 60 to 100 beats/min; therefore, a rate below 60 accompanied by clinical symptoms requires this rapid pharmacological intervention.

Choice B rationale

Digoxin is a cardiac glycoside used to treat heart failure and certain atrial arrhythmias like atrial fibrillation. It has positive inotropic effects but also possesses negative chronotropic properties, meaning it slows the heart rate by increasing vagal tone and slowing conduction through the atrioventricular node. Administering digoxin to a patient who is already bradycardic and symptomatic would be contraindicated, as it would likely worsen the low heart rate and associated dizziness.

Choice C rationale

Lidocaine is a Class 1b antiarrhythmic primarily used to treat ventricular arrhythmias, such as premature ventricular contractions or ventricular tachycardia. It works by blocking sodium channels in the myocardial cell membranes. It does not have a role in increasing the heart rate for sinus bradycardia. Using it in this context provides no benefit for the bradycardia and could potentially introduce unwanted side effects without addressing the underlying cause of the hypotension.

Choice D rationale

Metoprolol is a beta-adrenergic blocker that decreases the heart rate, blood pressure, and myocardial oxygen demand by blocking beta-1 receptors. Like digoxin, it is a negative chronotrope and is specifically contraindicated in patients with sinus bradycardia or high-degree heart blocks. Giving metoprolol to a patient with a slow heart rate and hypotension would dangerously exacerbate the condition, potentially leading to a complete circulatory collapse or cardiogenic shock.