3. Secure the ABCs！
Airway-Intubate if necessary
Breathing-Oxygenate/ventilate/monitor SpO2
Circulation-place IV/fluids for ↓BP/telemetry/EKG
Yes No
Is the patient confused,
somnolent, or comatose?
1. Check blood glucose or
Give 1amp D50W IV
2. Thiamine 100 mg IV
3. Naloxone 0.4-2.0 mg IV
1. Brief history and physical examination
2. Collect critical labs:
• Serum electrolytes and glucose
• Liver & renal profiles
• CBC
• Serum levels: EtOH, acetaminophen,
salicylates
•Urine drug screen with TCA
Specific toxin(s) identified
or highly suspected?
Give antidote/therapy
And
Contact Poison Control
Yes
Patient improving?
Yes
1. Continue supportive care
2. Psychiatry consult for
Intentional ingestions
No No
1. Review available data
2. Detailed history and PE
3. Consider coingestion(s)
4. Toxicology consult
Consider nonpoisoning
etiology of symptoms
Ref: The Washington Manual of Critical Care
A direct relationship exists between the action potential in a single myocardial fiber and the recorded ECG (Figure 2). This key point demonstrates that drug-induced prolongation of the QT interval is directly linked to modification of the action potential. The shape of the action potential is based on the balance between the inflow of positive ions (sodium and calcium) and outflow of positive ions (potassium).[5] When an electrical impulse reaches a myocardial fiber (Figure 2), it initially results in the brisk movement of sodium ions inward, resulting in a sharp, rapid upstroke of the action potential (phase 0). After this initial rapid sodium influx, calcium and additional sodium ions enter slowly, potassium exits the cell, and at the end of the action potential there is electrolyte equilibration. Factors that impair rapid inward or outward ion movement (e.g., fast sodium influx or potassium efflux) widen the action potential, prolong repolarization, and hence lengthen the QT interval. A decrease in the net outward current and/or increase in inward current may facilitate early afterdepolarizations. When early after-depolarizations occur with abnormal ventricular repolarization, it may prompt torsade de pointes.[3]
Physostigmine is an acetylcholinesterase inhibitor that has historically been used in the treatment of anticholinergic poisoning. Patients with a tricyclic antidepressant (TCA) overdose often present with an anticholinergic-like toxidrome. Caution must be used when administering physostigmine to an anticholinergic poisoning because the combination of TCAs and physostigmine can lead to life-threatening bradyarrhythmias.
