Episode 4 - Toxicology



May 2023


Scott Wildenheim

Caleb Ferroni

Ray Pace


Dr. Jordan Singer

Episode Videos

Cardiotoxins & the Drug Box, Part 1 

Drug Toxicity - Excited Delirium Syndrome and Restraints, Part 2

Drug Toxicity - The Revamp of the RSI Protocol, Part 3

Toxicology Live, Part 4

Episode Audio

Show Notes

In this episode Scott, Ray and Caleb speak with Dr. Jordan Singer from UH Elyria about the changes to the overdose and toxicology. In the third part, we discuss the changes to the RSI protocol that Dr. Singer was instrumental in bringing to UH. 

Aspirin (ASA) Overdose

Newly added to the toxic ingestion ingestions / exposure / overdose protocol for 2023. 

Not to be confused with Tylenol (acetaminophen) overdose or Ibuprofen overdose - require medications not in EMS boxes, early recognition and supportive care in these non-aspirin cases.

Salicylate poisoning causes a variety of metabolic disorders. Direct stimulation of the cerebral medulla causes hyperventilation and respiratory alkalosis. As it is metabolized, it causes an uncoupling of oxidative phosphorylation in the mitochondria. Lactate levels then increase due to the increase in anaerobic metabolism. The lactic acid along with a slight contribution from the salicylate metabolites result in metabolic acidosis. Hyperventilation worsens in an attempt to compensate for the metabolic acidosis. Eventually, the patient fatigues and is no longer able to compensate via hyperventilation, and metabolic acidosis prevails. This results in hemodynamic instability and end-organ damage. 

Patients with salicylate toxicity are volume depleted due to hyperventilation, fever, and increased metabolic activity. Patients should be volume resuscitated to correct the volume depletion. Sodium bicarbonate will help correct the metabolic acidosis. Dextrose will treat the central nervous system (CNS) hypoglycemia. 

The hyperventilation is a response to the metabolic acidosis. The body is creating a respiratory alkalosis to offset the metabolic acidosis. Let these people breathe on their own as long as possible, as we cannot meet the needed ventilatory demand with our devices  (BVM  / ventilators). Likewise, patients who require airway and breathing management has grossly decompensated and will likely not survive.  

Sympathomimetic Overdose (Stimulants)

The etiology of acute sympathomimetic toxicity is related to its effect on the inhibition of norepinephrine and dopamine reuptake at the preganglionic synapse. This leads to an excess of norepinephrine and dopamine at the postsynaptic terminal and synaptic space. This prolonged exposure is what causes most of the untoward effects of sympathomimetics due to the end organ being affected. Cardiac effects include tachycardia, hypertension, and vasoconstriction leading to cardiac ischemia and dysrhythmias. Neurologically it can cause vasoconstriction and stroke-like syndromes and intracranial hemorrhage.

Beta Blocker Overdose

Traditionally, beta-blockers are classified as selective and non-selective depending on the receptor specificity. Specificity is, however, lost in cases involving overdose. To better understand the toxicity, beta-blockers are classified as lipophilic or lipophobic. Highly lipophilic beta-blockers can easily cross the blood-brain barrier and may cause various central nervous system (CNS) manifestations. While CNS manifestations secondary to beta-blocker overdose are primarily attributed to lipophilicity, water-soluble beta-blockers, for example, atenolol, may also cause tiredness and fatigue.  

Various metabolic and circulatory pathways are dependent on circulating catecholamine that, in turn, is switched off by beta-blockade. While hypotension, bradycardia, decreased myocardial contractility and oxygen consumption account for the hemodynamic instability, hypoglycemia secondary to inhibition of glycogenolysis and gluconeogenesis may also occur.

Sodium Channel Blocker Overdose

Sodium channel blockade produces a variety of cardiac effects as demonstrated by their impact on the action potential. With varying degrees of potency, sodium channel blocking agents decrease the slope and amplitude of phase 0, and thereby reduce the rate of depolarization and the conduction velocity. This leads to a slower depolarization of the cell and is important for the desired therapeutic suppression of tachydysrhythmias through reentrant mechanisms.

Calcium Channel Blocker Overdose

Calcium channel blockers (CCBs) are among the most commonly used cardiovascular drugs in the adult population. They are used to treat a broad array of clinical conditions, including hypertension, supraventricular tachycardia, vasospasm, and migraine headaches.  

Accidental over-ingestion, suicidal ingestion, and exploratory ingestion in children can all lead to severe toxicity. Therapeutic use can lead to toxicity through drug interactions with other cardiac medications or increased drug exposure because of interference with metabolism or elimination. Poisoning with these agents can have severe hemodynamic effects and be fatal.

Potassium Channel Blocker Overdose

Potassium channel blockers result in QT prolongation that can set up for ventricular arrhythmias such as Torsades de Pointes or heart block. Continuous cardiac monitoring for arrhythmia disturbances is the mainstay of management for suspected potassium channel blocker overdose. 

Magnesium should be added to prevent Torsades de Pointes

Normally necessary if QT > 500 ms (2.5 large boxes)

2 grams slow  IV / IO

Restraint Use

RSI - 2023 Update

The key difference between depolarizing and nondepolarizing neuromuscular blockers is that depolarizing neuromuscular blockers act as acetylcholine receptor agonists while nondepolarizing neuromuscular blockers act as competitive antagonists. 


The intermediate duration non-depolarizing neuromuscular blocking agents (NMBA) are believed to be better choices because;

In addition the primary induction agent is being switched from etomidate to ketamine

The Protocols

Episode Shorts

From The Episode

Dr. Singer discusses aspirin killing the brain

Caleb hammers down on fluid resuscitation

Ray discusses capnography - making it easier

Scott discusses things he often misses in peoples medicine cabniet