In conversation with colleagues, I have been getting mixed opinions with applying CPAP to a pt with a DNR. Some see it as artificial ventilation other see it as treatment. Inwould love to hear base hospitals perspective on this.

Is it true that providing salbutamol for a wheezing CHF patient may cause “flooding” in the lungs? Often distinguishing between CHF vs asthma exacerbations can be difficult when the patient has both wheezing and crackles in bases. Is providing salbutamol potentially dangerous in this situation?

I was curious if Hepatitis A/B/C counts as a contraindication for Acetaminophen (Under the "Liver Disease" point)?

I have noticed that a clinical consideration has been removed from the ACP Analgesia medical directive in regards to Morphine and Fentanyl administration. I recall that in previous versions of the ALS PCS it stipulated that you can only administer Morphine or Fentanyl when providing opioid analgesia to a patient, without a patch. I notice this has been taken out, am I now authorized to be able to administer Fentanyl then morphine or vice versa to a patient. An example would be: giving morphine to a patient who then presents with a histamine reaction and I want to switch to Fentanyl, or I have maxed my patient out on Fentanyl and want to continue pain management treatment with Morphine? Thank you

Can midazolam be administered to treat a dysphoric reaction to an analgesic dose of ketamine?

Can a Primary Care Paramedic (PCP) remain with their original patient and continue transport after an Advanced Care Paramedic (ACP) administers opioid analgesia, assuming the patient has had good effect, does not require further dosing, and the transport is short? Historically, we have treated this as out-of-scope for PCPs, requiring the ACP to take over the call. Has this changed with version 5.4 of the ALS PCS, or was this addressed in CME?

The ALS PCS 5.4 Companion Document (page 10) notes that “ketamine would be the preferred analgesic option for hypotensive patients or when there is a risk of hemorrhagic shock or respiratory depression.” How does this align with CEPCP’s expectations around ketamine use in the field?

Is ASA considered an NSAID for analgesia purposes?

If we want to admin morphine/fentanyl to a breast feeding parent, how long afterwards do we have to worry about the breast milk containing opioids?

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.

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

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

After a patient goes VSA from a suspected asthma attack, why is IM epi no longer indicated?

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.

A patient with a history of AAA repair two years ago presents with severe lower abdominal pain and concurrent chest pain with cardiac features. Vital signs show hypertension with equal bilateral pressures. In this situation, is ASA still appropriate for suspected ACS, or should it be withheld due to concern for a possible AAA related complication?

Under the nitroglycerin contraindications it notes phosphdiesterase inhibitors. In the companion document it references PDE5s, but I do not recall reading that other forms are disclosed from the definition. What about PDE-4 inhibitors?

I have a question about the contraindication in the Analgesia Medical Directive that lists “suspected ischemic chest pain.” My understanding has always been that this meant we should not administer analgesia for ischemic chest pain itself, except for morphine under the Cardiac Ischemia directive. However, if another pain source, such as a headache, occurred alongside suspected ischemia, I thought we could treat that secondary pain with something like acetaminophen.After reviewing some recent discussions and material from other Base Hospital Physicians, I am beginning to wonder if that interpretation is correct. Does the presence of suspected ischemic chest pain act as an absolute contraindication to all analgesia outside of the Cardiac Ischemia directive, or can we still manage unrelated pain once appropriate treatment for ischemia has been initiated?Lastly, if we have administered 160 mg of ASA, does that contraindicate the use of an NSAID due to overlap or interaction?

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?

Aggrenox is a combo drug of ASA and dipyridamole that may be prescribed to cardiac patients. However I just read that dipyridamole is a phosphodiesterase inhibitor. Just to confirm, does this mean patients with pre-existing cardiac conditions who are on Aggrenox are contraindicated for nitroglycerin administration? What if their doctor has prescribed them both Aggrenox and nitro?

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)?

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?

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 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.

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?

In medical cardiac arrest cases where a potentially reversible cause cannot be corrected in the field, such as hypothermia, mixed overdose, pregnancy, or a remaining foreign body airway obstruction, should Paramedics continue rhythm analysis every two minutes once transport is prioritized and initiated, or should only one analysis be performed prior to departure similar to a traumatic cardiac arrest?

During an FBAO, if the patient has a pulse but is unconscious with a valid DNR. Are we allowed to perform CPR & ventilations to dislodged the obstruction? Or should CPR & ventilations be withheld and the patient should be put on an NRB / suction as needed then transport to the hospital? Thank you.

What is the correct approach if a patient rearrests after achieving ROSC following double sequential external defibrillation (DSED) or vector change defibrillation? Should the directive be restarted with standard pad placement, or should the advanced defibrillation strategy be continued?

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.

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?

Hi there, I'm a second year Fleming College paramedic student, Could you confirm that in dual sequential defibrillation, if no other paramedic monitor (Lifepak or Zoll) is available, an AED that the local fire department has on scene can be used? Have fire departments in Kawartha, Peterborough and Haliburton agreed and been informed?

In the case of a moderate to severe allergic reaction, where epi and 25mg of diphenhydramine have already been administered, are we permitted to administer another full 50mg of diphenhydramine, or should we just top up the dose and administer a additional 25mg to make a total of 50mg for the patient.

Does base hospital use "two or more body systems" when defining anaphylaxis?

Can you please define “unavailable” in terms of the nausea/vomiting directive where it phrases **if ondansetron is unavailable..

In neonatal resuscitation, it seems possible to get stuck in a decision loop, and I am wondering whether NRP offers any explicit guidance for this scenario.Consider a freshly delivered neonate who is breathing but has a persistent heart rate of approximately 80 bpm. The infant is receiving oxygenated positive-pressure ventilation, which appears effective, yet there is no improvement in heart rate after repeated 30-second reassessments. The infant continues to appear clinically unwell.Following the algorithm strictly, progression to chest compressions does not occur because the heart rate remains above 60 bpm. However, 80 bpm is clearly abnormal for a term newborn, and after several ventilation cycles it can feel uncomfortable to continue without escalation. My instinct in this situation would be to consider starting compressions, particularly if the overall clinical picture is deteriorating.Does NRP provide any guidance for exiting this loop, or is management primarily based on the global clinical picture and provider judgment?

While reviewing Newborn Resus vs Pediatric VSA I noticed the concentration for epinephrine are different for ETT. I am just curious as to why we use 1:1000 for the pediatric VSA but 1:10000 for the newborn resus.

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!

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 there any consideration of adding a directive for CPR-induced consciousness (CPRIC) with the increased use of mechanical CPR devices?

What is your opinion on treatment of suspected pseudo seizures? Is there any negative outcome from treating with Midazolam? Additionally, how would you recommend we identify these types of seizures and document our reasoning to not treat them if we choose that route?

What is CEPCP stance on chest needle site location for pediatrics? The latest companion document states 2nd intercostal space as the prefer location for pediatrics; however, I was always taught this anterior location is dangerous with an 80% failure rate and especially dangerous for pediatrics due to their large thymus and other important structures. I have noticed other base hospitals advising against this and that the 4th intercostal, anterior axillary location to be preferred to pediatrics.

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?

Does LVH mimic STEMI only because a larger-than-usual repolarization voltage typically follows a larger-than-usual negative QRS deflection? Or can it cause ST elevation by some other mechanism in other leads where we don't have that huge negative QRS we get in, say, V1? So if I have a pt with new onset of chest pain who meets LVH criteria based on their precordial voltages, but they have ST elevation in II, III, and aVF (especially if their inferior QRS complexes are also all upright), can I still STEMI bypass them? Related: what if a pt were to meet LVH criteria based only on R wave height in aVL, but their precordial lead voltages are normal. Does LVH in this case also cause ST elevation that can mimic an MI, or could I STEMI bypass this patient if they had chest pain and met STEMI criteria?

Do LVH and LBBB also affect the ST segment in V4R, potentially causing right-sided ST elevation that can mimic right ventricular infarct? I recently wanted to give nitro to a patient with the most classic cardiac ischemia symptoms you could ask for. He had LBBB that sounded potentially new onset, as well as 1mm of elevation in V4R - sign of RVI or mimic? I called the BHP to ask about whether I could/should give nitro in this case and, being put on the spot in the moment with a question about those right-sided leads almost nobody ever talks about, the doctor didn't know and couldn't look up an answer quickly (he ultimately said just make sure I have an IV first and then follow the nitro directive as usual - I did that, the patient's pressure stayed totally fine the whole time, and his chest pain improved somewhat). I'm wondering if there even is an established answer to this question, given a little more time to come up with it than the BHP had when I patched. Thank you!

Is there any evidence to suggest applying a tourniquet to an individual whose sustained a prolonged crush injury to an extremity will improve outcomes before releasing them? This came up in the current CME with hyperkalemia in terms of an unconscious person laying on their limbs for prolonged time. Thanks!

In the event of a postpartum hemorrhage is external bimanual compression something that can be delegated to allied resources on scene (ex. FD) if the paramedic has other tasks to attend to? Or since it is listed a delegated medical act is it something only a certified paramedic can do?

When handling a patient that is experiencing a miscarriage under 20 weeks, what can we do to control excessive bleeding? I understand we can consider patching for oxytocin, but can we consider bimanual compression, voiding bladder, etc.?

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.