Good morning,

This month we will be focusing on the prehospital management of the poisoned patient. A key component or 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. The effect on the heart is slower conduction between heart cells. The effect on the EKG is 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. It 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, 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 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 simultaneously.  

• 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 à 1-2 amps slow IV push

• Goal: QRS < 120ms

*If the first dose is not effective, consult online medical command to order 

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!

Dr. Singer

Poisoning - March 14, 2022

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 re-set after an electrical signal is sent and a contraction occurs, potassium must leave the cardiac cells which allow the cells to repolarize. K channel poisons block the channels that allow 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 the QT is that QT varies with heart rate. It makes it hard to give recreations for cut-offs since they would be different depending on the heart rate. QTc attempts to correct this variation. QTc = QT/ √ (R-R), is not an easy thing to calculate quickly. The good news is the EKG computer will calculate this for you, and it is pretty accurate the majority of the time. Alternatively, you can estimate the QTc ensuring the end of the T-wave is less than ½ the R-R interval. If this is true, the QTc is likely not long enough to be clinically significant and need prehospital management. The normal QTc for men is <440ms and for women <460ms. 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 Na channel poisoning? TONS of medications prolong the QTc. The following 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: defibration + chest compressions + ACLS + Mg (IV push)

• Unstable polymorphic VT: cardioversion + ACLS + Mg (slow push over 5m)

• Stable or intermittent torsades:

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

*Mg Load (slow push over 5m)

*Avoid exacerbating drugs: ondansetron, amiodarone

What is the dose of a magnesium load?

• 25-50 mg/kg IV over 5 minutes

• For average adult: 2-4g

• Note: pushing too fast can lead to respiratory depression and hypotension

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!

Dr. Singer

University Hospitals

Poisoning - March 21, 2022

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 naturally occur in wintergreen. While it is fantastic at decreasing thrombus formation in MI, it is incredibly dangerous in overdose. Thirty (30) full-strength aspirin tablets can be fatal in the average adult, and nine (9) full-strength tablets can be fatal for children. It only takes 6ml of oil of wintergreen to be fatal in an adult and only 4ml to be fatal in children.

Why is Aspirin so dangerous in overdose?

In overdose, aspirin disconnects the process that lets cells turn glucose into usable energy. As a result, glucose is used. Instead of usable energy, the body only makes heat. It 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, but 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 by blowing off CO2. Patients should be breathing quickly and deeply if poisoned with aspirin. If they are breathing shallow or even naturally, 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 its glucose levels reach 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 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 keys to treating these overdoses are an aggressive use of sodium bicarb and to monitor mental status and ventilation.

Be safe and keep up the awesome work!

Dr. Singer

University Hospitals

 Poisoning - March 28, 2022

Good morning,

This month we are focusing on the prehospital management of the poisoned patient, with a focus this week on stimulants. When a patient overdoses on stimulants, it causes a syndrome known as sympathomimetic toxidrome.

What is the sympathomimetic toxidrome?

Sympathomimetic means mimicking the sympathetic nervous system. It is the part of our nervous system that regulates the fight or flight response and releases epinephrine and norepinephrine to do this. When a drug causes this type of response, it is called a sympathomimetic. Symptoms include elevated heart rate, elevated blood pressure, dilated pupils, sweatiness, and warm flushed skin. In large excess, they can cause ventricular tachycardia, cardiac ischemia, seizures, agitation, and heatstroke.

What are some examples of sympathomimetics?

While the most obvious examples are cocaine and amphetamines, many drugs can cause this toxidrome. Others include bupropion, albuterol, theophylline, and caffeine.

Treatment for sympathomimetic toxicity

Supportive care – Patients with this type of toxicity should have the specific symptoms and complications managed as they arise. The key is to use benzodiazepines whenever possible to treat these symptoms.

• Agitation: benzos

• Seizures: benzos

• Hyperthermia: cold IVF and misting; the goal temperature is 38-39C

• IV fluids: sweating and agitation leads to volume loss

Chest pain – Patients with chest pain caused by stimulant use are more likely to have ischemia from vasospasm than from a ruptured plaque-forming thrombus (but they can still have both!). The treatment for this type of chest pain is slightly different than usual.

• Benzodiazepines: Midazolam 2.5mg IV q5m for pain with a maximum dose of 10mg

• Nitroglycerin and aspirin: same dosing as for non-stimulant chest pain

• If STEMI on EKG: heparin, ticagrelor, notify receiving hospital

Likely is vasospasm if <1 hour after ingestion, but we treat the same as a STEMI for non-stimulant CP

Stimulant toxicity can occur both in patients who overdid it with recreational drug use and in patients who accidentally or purposefully overdid it on certain prescribed drugs. The key to treating this toxicity is that first, second, and third-line treatments for seizure, agitation, and chest pain are benzothiazines.

Be safe and keep up the awesome work!

Dr. Singer

University Hospitals