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.  

• Sodium Bicarbonate IV / IO if the patient is tachypneic - reduce acidosis 

• Dextrose IV / IO regardless of indicated BGL if the patient is altered - patient has a central hypoglycemia 

• Sodium Bicarbonate if airway maintenance is necessary - this is bad all around, but help minimize the acidosis that will be created by taking the airway and inevitability underventilating the patient. 

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.

• Most commonly methamphetamines / cocaine

• Treated by combating the stimulant with a major depressant - usually a benzodiazepine

• Hyperthermia from the hypermetabolic state treated with cooling measures - cool fluids, A/C, fans, misting, cold packs

• IV fluid bolus for dehydration / tachycardia

• 12 lead required - increased heart rate = increased myocardia oxygen demand

• If complaints of chest pain - and STEMI with stimulant use - likely vasospastic occasion of the coronary arteries rather than a clot. Hold Ticagrelor (Brilinta) and Heparin until discussion with medical control. Additional and potentially higher doses of benzodiazepines may be needed. 

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.

• One treatment modality may be insufficient, multiple may be needed in profound poisoning cases

• Bata heavy agents to overcome the beta blockade are the staple of treatments - Push Dose Epi / Epi drips common for EMS

• Transcutaneous Pacing (TCP) may be necessary, and may be used in conjunction with medications - capture may be difficult or impossible in these cases - move on if not working

• Calcium helps speed of conduction and helps increase heart rate

• Fluid boluses will help maintain BP and cerebral perfusion

• Atropine may be added, but is unlikely to have dramatic effect. Use aforementioned treatments

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.

• Commonly tricyclic antidepressants, antiarrhythmics, some anti-seizure, and large doses of diphenhydramine (Benadryl) can impart a sodium channel blockade

• Overdose widens the QRS, and causes dysrhythmia

• Overcome sodium blockade with large dose of sodium

• Largest quantity of sodium available is as sodium bicarbonate - not using to modify acidosis here, just delivering the most sodium available. There will be an temporary increase in PH with this treatment. Accepted side effect to get the sodium blockade addressed. 

• Look at AVR - terminal R wave here suggestive of TCA / sodium channel blocker OD

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.

• Profound bradycardia and hypotension are hallmark signs

• Overcome calcium channel blockade with calcium 

• 2 calcium salts commonly available to EMS - Calcium chloride / Calcium gluconate

• The chloride salt has 3x the elemental calcium as compared to the gluconate salt

• Calcium gluconate can cause less phlebitis than the chloride, but more will need to be given to match the delivered calcium by the chloride preparation

• All heart rate increasing therapies fair game here

• Transcutaneous Pacing (TCP) may be necessary, and may be used in conjunction with medications - capture may be difficult or impossible in these cases - move on if not working

• Fluid boluses will help maintain BP and cerebral perfusion

• Atropine may be added, but is unlikely to have dramatic effect. Use aforementioned treatments

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

• Patients who lack capacity to make decisions and are combative are legally allowed to be restrained

• Patients shall never be restrained with any technique that impedes breathing

• Patients shall never be restrained prone

• Neurovascular checks on restrained limbs shall be conducted a minimum of every 15  min

• Commonly one arm is restrained over head, on arm down to side

• Use purpose made restraints whenever possible - posey type restraints or non-locking leather restraints

• If Police have patient handcuffed or shackled, officer must go with patient to unlock if there is an emergency

• Once restrained, sedatives and / or antipsychotics should be used to keep the patient from injuring themselves

RSI - 2023 Update

• Change in paralytic agent in 2023 EMS protocol

• Primary agent switched from succinylcholine to rocuronium

• Rocuronium is a non-depolarizing neuromuscular blocker as compared to succinylcholine which is a depolarizing neuromuscular blocker

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. 

Benefits 

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

• They can be re-dosed for longer effect if necessary

• Does not worsen hyperkalemia

• Last longer for easier management of the patient 

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

• Etomidate is a good short acting induction agent - causes amnesia and sedation

• Ketamine is a longer acting induction agent that cause amnesia, sedation, analgesia, and disassociation at the same time. It also is not cardio depressant, helping  maintain and often augmenting hemodynamics.