August 3, 2026

Good morning,

This month we will be focusing on the prehospital management of the poisoned patient. A key component that needs to occur for any potentially poisoned patient, no matter what was ingested, is a 12-lead EKG. Today we will review one of the key things to look for on the EKG, sodium (Na) channel poisoning, and how to treat it. 

The effect of Na channel poisoning on the heart

Drugs that have this effect will bind to Na channels in the heart and prevent them from working, too. The effect of this on the heart is slower conduction between heart cells. The effect on the EKG is that the QRS widens, eventually having a sine wave appearance. If too many channels get blocked, the heart cannot conduct any electricity and goes into asystole. A wide QRS in the setting of acute overdose should be considered sodium channel poisoning until proven otherwise. This EKG depicts the sine wave appearance of a severe Na channel poisoning.

A key clue that you are dealing with an Na channel poison and not ventricular tachycardia is that there will be a tall terminal R wave in aVR. This is a wide and tall R wave with the R component being the final part of the QRS. This sign clinches that you are dealing with an Na channel poison and not ventricular tachycardia. An example of this finding is in the picture below. 

Common examples of Na channel poisons

What types of drugs classically cause Na channel poisoning? Some examples include carbamazepine, cyclic antidepressants (TCAs), diphenhydramine (Benadryl), propranolol, and hydroxychloroquine, among many others. It does not matter what drug caused the Na channel poisoning; all are managed the exact same way! 

Treatment for sodium channel poisoning

Sodium bicarb: We can treat the sodium channel poison by giving the patient more sodium. The bicarb component just happens to be along for the ride. The effect is that more sodium will make it through the channels despite some not working. The effect on the EKG will be that the QRS will shorten. The best part is that this effect is immediate. If the QRS narrows right after pushing sodium bicarb, you both diagnosed and treated Na channel poisoning at the same time. Here is how to manage in the field: 

• QRS > 120ms + acute OD → give sodium bicarb 

• This assumes normal QRS at baseline 

• Note: most patients will be young and likely have normal baseline QRS 

• When in doubt, give the sodium bicarb 

• Dose: 1-2 mEq/kg sodium bicarb 

• 70kg person → 1-2 amps slow IV push 

• Goal: QRS < 120ms 

• If first dose is not effective, consult online medical command for order of additional sodium bicarb

Na channel poisoning is one of the most life-threatening effects of overdoses. OD + prolonged QRS = sodium bicarb!

Be safe and keep up the awesome work! 

Jordan Singer, MD

Images sourced from https://litfl.com/.

August 10, 2026

Good morning,

This month we will be focusing on the prehospital management of the poisoned patient. A key component that needs to occur for any potentially poisoned patient, no matter what was ingested, is a 12-lead EKG. Last week, we reviewed Na channel poisoning. This week, we will review another key thing to look for on the EKG: potassium (K) channel poisoning.

The effect of K channel poisoning on the heart 

For the heart to reset after an electrical signal is sent and a contraction occurs, potassium must leave the cardiac cells, which allows the cells to repolarize. K channel poisons block the channels that allow this repolarization to occur, leading to slowed repolarization. The effect on the EKG is a delayed and widened T wave, which in turn leads to a long QTc interval. If the QTc gets too long, the patient can go into Torsade de Pointes.

How do we calculate QTc and when should we worry?

The “c” in QTc stands for "corrected." The reason this is used over QT is that QT varies with heart rate, making it hard to provide recommendations for cutoffs, since they would differ with heart rate. QTc attempts to correct for this variation. QTc = QT/ √ (R-R), which is not easy to calculate on the fly. The good news is that the EKG computer will calculate this for you, and it is pretty accurate the majority of the time. Alternatively, you can estimate the QTc by ensuring that the end of the T-wave is less than ½ of the R-R interval. If this is true, the QTc is likely not long enough to be clinically significant and does not need prehospital management. The normal QTc for men is〈 440 ms and for women is〈 460 ms. The risk of torsade de pointes increases significantly if the QTc is 〉500.

Common examples of K channel poisons

What types of drugs classically cause K channel poisoning? TONS of medications prolong the QTc. The common offenders can be remembered by the Anti-ABCDEs mnemonic. Antiarrhythmics, antibiotics, antipsychotics (anti-C-chotics), antidepressants, and antiemetics. It is important to remember that the degree of QTc prolongation varies from patient to patient, and taking multiple medications that are QTc prolonging has an additive effect.

Treatment for K channel poisoning

Magnesium sulfate – Magnesium (Mg) sulfate does not decrease the QTc. The only thing that decreases the QTc is the body metabolizing the poison, which takes time. The benefit of magnesium is that it decreases the risk of Torsade de Pointes. The treatment depends on exactly what is going on: 

• Pulseless polymorphic VT: defibrillation + chest compressions + ACLS + Mg 2 grams (IV push) 

• Unstable polymorphic VT: defibrillation + ACLS + Mg 2 grams (slow push) 

• Stable or intermittent Torsades: 

• Pads on the patient (they will likely become unstable shortly) 

• Mg load (2 grams over 20 minutes 

• Avoid exacerbating drugs: ondansetron, amiodarone 

K channel poisoning, in addition to Na channel poisoning, is an important life-threatening effect that can be seen in many overdoses. OD + QTc over 500 = magnesium load!

Be safe and keep up the awesome work! 

Jordan Singer, MD

August 17, 2026

Good morning,

This month we are focusing on the prehospital management of the poisoned patient. A commonly used medication that is life-threatening in overdose is aspirin. This week we will focus on the key aspects of managing aspirin overdoses.

Where is aspirin found?

The chemical that forms aspirin is known as salicylic acid. Similar compounds can be found in other common drugs such as Pepto-Bismol, Excedrin, Maalox, and Alka-Seltzer, and are naturally occurring in wintergreen. While it is fantastic at decreasing thrombus formation in MI, it is incredibly dangerous in overdose. Thirty full-strength aspirin tablets can be fatal in the average adult, and nine full-strength tablets can be fatal for children. It only takes 6 mL of oil from wintergreen to be fatal in an adult, and only 4 mL to be fatal in children.

Why is aspirin so dangerous in overdose?

In an overdose, aspirin disrupts the process that lets cells turn glucose into usable energy. The effect is that glucose is used, but instead of usable energy, the body just makes heat. This is especially bad if aspirin gets into the brain since the brain needs tons of glucose to function. Once the excess aspirin enters the brain, the brain's glucose supply runs out, leading to seizures, altered mental status, and death.

Blood pH is critical in aspirin overdose 

The goal of treating aspirin overdose is to keep it out of the brain. Too much aspirin in the blood is tolerable; too much aspirin in the brain is deadly. If the blood pH is acidotic, aspirin will be uncharged and can freely enter the brain. If the blood is basic, aspirin will be charged. This charge will prevent it from entering the brain and prevent the damage it causes there. As we know, ventilation affects pH through blowing off CO2. Patients should be breathing quickly and deeply if poisoned with aspirin. If they are breathing shallowly or even normally, this is a sign their pH is starting to drop, and cardiac arrest for profound aspirin overdose is imminent.

Treatment for aspirin poisoning 

Sodium Bicarb – For Na channel toxicity, we gave sodium bicarb for the sodium component; in aspirin overdose, we give it for the bicarb component. By giving bicarb, we can increase the pH of the blood, make aspirin charged, and prevent it from wreaking havoc in the brain. The dose of sodium bicarb for aspirin overdose is 1-2 amps, slow push IV.

Monitor Ventilation closely – Patients should be hyperventilating if they are poisoned with aspirin. We should monitor their ventilation with continuous waveform ETCO2. We want their ETCO2 to be slightly low. If it is normal or elevated, aspirin will start to move into the brain. To prevent this, we should perform BVM ventilation to support their ventilation.

Monitor neuro status – Confusion in the setting of aspirin overdose implies that so much has entered the brain that brain glucose levels have reached a critically low level. These patients decompensate and die rapidly. If there are signs of confusion, give an additional dose of 1-2 amps of sodium bicarb. You can also consider giving D10 IV since some of that sugar will enter the brain and temporize the situation.

While aspirin is a widely utilized drug with many benefits, it is incredibly deadly in overdose. The key to treating these overdoses is aggressive use of sodium bicarb and closely monitoring mental status and ventilation.

Be safe and keep up the awesome work! 

Jordan Singer, MD