Situation: A 34-year-old woman with generalized myasthenia gravis (MG) is admitted to the medical ward with fever and a productive cough. She weighs 60 kg. She takes pyridostigmine 60 mg by mouth every 6 hours and prednisone 10 mg once daily. She has no drug allergies. By day 4 her fever has resolved, and her pyridostigmine dose was increased this morning. One hour after the new dose she is weak and anxious, with gurgling respirations and saliva pooling in her mouth. Respiratory rate is 30/min, oxygen saturation (SpO2) 89%, heart rate 52/min, pupils 2 mm, and she has abdominal cramps. Which action should the nurse take FIRST?

Cramps, small pupils, bradycardia, and heavy secretions soon after a dose increase point to cholinergic crisis from excess acetylcholinesterase inhibitor. All four actions have a place, but in either crisis the first action is to clear the airway and support breathing, because secretions are already lowering her oxygen saturation. The drug is then held, atropine is given as ordered, and blood gases follow.

Pathophysiology of the presentation
The patient’s symptoms began 1 hour after an increased pyridostigmine dose. Pyridostigmine inhibits acetylcholinesterase, so more acetylcholine remains at nicotinic and muscarinic receptors. When the dose is too high, excessive cholinergic stimulation produces a cholinergic crisis: muscarinic effects include bronchorrhea, salivation, abdominal cramps, miosis, and bradycardia, while nicotinic effects produce muscle weakness. The gurgling respirations, pooled saliva, small pupils, heart rate of 52/min, and abdominal cramps fit this pattern. The respiratory rate of 30/min and SpO2 of 89% show that secretions are already compromising ventilation and oxygenation. In cholinergic crisis, airway obstruction from excessive secretions is the immediate threat to life, not the bradycardia or cramps alone.

Why airway and breathing come first
The question asks for the FIRST action. The airway-breathing-circulation (ABC) framework applies even when the underlying cause is pharmacologic. Secretions pooling in the mouth and gurgling respirations indicate that the upper airway is not protected. Suctioning clears the obstruction, and supplemental oxygen supports the falling SpO2. No medication or diagnostic test can correct hypoxemia if the airway remains full of secretions. After airway and breathing are stabilized, the next steps are to hold the offending drug, notify the prescriber, give atropine as ordered, and obtain blood gases.

Distinguishing cholinergic crisis from myasthenic crisis
Both conditions cause weakness and respiratory failure, but the bedside clues differ. Myasthenic crisis results from too little acetylcholine effect, while cholinergic crisis results from too much. The table below compares the key features.

Feature	Cholinergic crisis	Myasthenic crisis
Cause	Excess acetylcholinesterase inhibitor effect	Insufficient acetylcholine effect at the neuromuscular junction
Secretions	Increased, profuse, gurgling respirations	Usually not increased
Pupils	Small (miosis)	Normal or dilated
Heart rate	Bradycardia	Tachycardia
Gastrointestinal	Abdominal cramps, diarrhea	Not prominent
Muscle weakness	Present, with fasciculations	Present, without fasciculations

Watch out! A patient with MG who becomes weaker after a dose increase should be assessed for cholinergic crisis. A common exam trap is to assume all weakness in MG is myasthenic crisis. The small pupils, bradycardia, and heavy secretions point the opposite direction.

Role of atropine and other interventions
Atropine is a muscarinic antagonist. It dries secretions and raises the heart rate, but it does not reverse nicotinic muscle weakness. In cholinergic crisis, atropine is given after the airway is cleared and oxygenation is supported. Atropine is an important treatment, but it is not the first action when secretions are actively obstructing the airway. Holding pyridostigmine prevents further cholinergic stimulation, and notifying the physician is essential, but both are secondary to immediate airway management. Arterial blood gas analysis confirms hypoxemia and hypercapnia, but pulse oximetry and clinical signs already indicate hypoxemia, so a blood gas draw should not delay suctioning and oxygen.

Clinical relevance from the evidence
Cholinergic crisis is rare but life-threatening because of excessive cholinergic stimulation ^[1]. Pyridostigmine is primarily excreted by the kidneys, so standard doses can become excessive in renal impairment, but this patient has no reported renal dysfunction; the trigger here is the dose increase itself ^[1]. Myasthenia gravis crisis is defined as an MG exacerbation requiring mechanical ventilation, and acute management begins with supportive care of the airway and breathing ^[2]. Respiratory failure in MG can have unclear causes, so a rapid bedside assessment of secretions, pupils, heart rate, and bowel sounds helps differentiate the type of crisis before definitive treatment ^[2][3].