Under the opioid toxicity directive, how should 'persistent need to assist ventilations' be interpreted? If a patient is experiencing decreased respiratory rate and oxygen saturation but has not yet received assisted ventilations, does this meet the criteria for naloxone administration? Or is there a requirement to attempt ventilation before naloxone can be given?

Is it permissible to administer palliative care medications, as outlined in the directive, to patients who are clinically appropriate for such treatment but are not enrolled in a palliative care program, following consultation with a Base Hospital Physician (BHP)? For example, administering hydromorphone for cancer-related pain in a patient currently prescribed this medication, or using haloperidol for delirium, agitation, behavioral issues, or as an antiemetic.

Using the newborn resuscitation flowchart for PCP, once you've gone through 30s of warm/dry, reassess, ventilate for 30s, reassess, and then CPR for 30s. I read it as continuing reassessments every 30s. However, under NRP it states reassessments after 60s. Just wondering what the standard for time between reassessments is once we have moved to CPR. Does it differ for ACPs and PCPs. Thank you!

Chronic headaches notwithstanding, is there indication for opiate analgesia in the severe acute headache, ie; thunderclap, first-time cluster etc., and if not why?

Is it appropriate to patch for glucagon for esophageal obstructions or is there not enough supporting evidence for this?

For neonatal resuscitation, we have the option of IV or IO route for med administration. But even the 25 mm (Blue) IO needle is likely to be too large for a child under 24 hrs of age. Are there any limitations on our options for IV placement? I know there are a number of unusual spots utilized in infants by NICU staff, etc. but are we able to attempt cranial, saphenous, jugular, sites etc. for IVs given we usually haven't practiced or trained on them?

The medical cardiac arrest medical directive states “There is no clear role for routine administration of Naloxone in confirmed cardiac arrest”. With the new emerging evidence on the administration of naloxone in the setting of opioid-overdose related PEA cardiac arrest, what is CEPCP’s stance on this treatment? And can Naloxone be administered in a opioid-overdose VSA presenting in PEA as long as high quality CPR and all other priorities are being managed accordingly?

So let's talk about combative patients. I feel like there's a bit of a knowledge/training gap in the implementation of the ketamine component of sedation. I get why we're administering a whack of dissociative to a highly violent and agitated pt - it's effective, and rapidly eliminates the immediate physical risk to pt and crew. But when we look at hyperactive delerium, and realize that the proximal cause in many (most?) cases is the use of stimulants/sympathomimetics, I wonder why our proscribed front-line med is one that has a not-insignificant risk of potentiating these effects. Would our benzo, midazolam, not be more appropriate in this situation particularly if the cause is rooted in stimulant use? Sure, we should be trying to establish a hx, but how exhaustive can one be when faced with an immediate threat? I just worry that we might be putting our pts at risk by effectively not addressing the underlying cause. Tldr; wouldn't Midaz be better for hyperactive delerium?

Should oxytocin be administered if baby is delivered but the placenta has not been delivered. The conditions of administration I find aren't clear and are open for interpretation when they state "postpartum delivery and/or placental delivery" to me both of these options indicate after the placenta is delivered.

Are antiplatelets, such clopidogrel/plavix, count as a contraindication to advil and ketorolac?

Prior to our arrival on scene of a short of breath call, a clinic doctor gave a dose of prednisone for the acute reaction. The pt required full utilization of the bronchoconstriction medical directive, however because the prednisone was not prescribed and just given as an emergency dose, we were unclear if that was a valid contraindication for dexamethasone. As we were 4 minute transport time we decided to withhold due to uncertainty.

When giving a bolus for hypotension what is considered "normotensive" or a systolic blood pressure that is considered acceptable to terminate the bolus. Of course assuming the pt is not symptomatic and no fluid overload.

Is it possible to transport a patient directly to a PCI center under the STEMI bypass protocol based on a 15 lead showing an isolated posterior STEMI? It is my understanding that if a patient's 12-lead meets the provincial STEMI bypass criteria we can transport directly to the PCI center after calling the PCI team to advise them that we are coming. Does the directive allow us to follow the same process based on a 15-lead showing STEMI only in V8 and V9?

In neonatal patients, obtaining IV access can be challenging, often requiring the use of an IO for D10W administration, which typically requires a base hospital patch. If IV or IO access is unavailable, would it be appropriate to administer D10W via the endotracheal tube (ETT)? If not, what are the physiological and pharmacological reasons for this (e.g., fluid viscosity, drug absorption)?

When performing DSED, should the first shock be delivered using the anterior-lateral or anterior-posterior pad placement? Or does the placement not significantly impact effectiveness? In the 2025 Double Sequential Review: Advanced Emergency Defibrillation Techniques (self-study 2025 package) at 16:34, the first shock is shown using the anterior-posterior placement. However, I recall you mentioning in an earlier video that the anterior-lateral placement is the recommended approach for the first shock. Could you please clarify which placement is most appropriate? Thank you.

For trauma arrest, should we be continuing to analyze/shock after the first analyze if we are transporting as long as it does not delay transport to the hospital? Or is it only one defibrillation for the entire arrest? Also, are PCPAIVs allowed to give a fluid bolus or only ACPs?

If we had a patient presenting with nausea/vomiting and abdominal pain who could not receive oral medications due to the vomiting and the medic treated with IM ketorolac and IM dimenhydrinate but throughout transport improved to no longer have any bouts of nausea/vomiting but was still in pain, would we be permitted to give acetaminophen since it is not contraindicated and would achieve the synergistic effect desired of giving an NSAID and acetaminophen.

I was just reviewing the Gastric port suctioning directive and it's mentioned that we can only suction for 15 seconds if "there are no gastric secretions". My two questions about this are: 1- If we are trying to remove air from the stomach, would it not appear as "no secretions" and if we have. suspicion of more air are we allowed to suction for greater than 15 seconds? 2- If we suspect heavy amounts of blood in the stomach, say from swallowing during a ruptured varricies event, should we be trying to remove that blood to avoid the body trying to vomit it up or do we stop suctioning once we see blood in case it's actually us causing damage?

Are PICC lines considered central access lines and as an ACP can we only access them with the medications approved for CVAD administration and if they are in a pre-arrest or in cardiac arrest state (CVAD directive)?

If I have been called to support a PCP crew (not AIV) for ACP back up and find that the patient only needed PCP AIV level treatment/monitoring can my partner run the call with the primary crew or is the expectation that I attend as the higher medical authority?