If a patient has an isolated closed fracture - for example, an isolated lower leg injury with obvious deformity making us suspect a tib/fib fracture - are they contraindicated for NSAIDS because there’s the possibility the broken bones can rupture blood vessels and cause internal bleeding (and thus the patient has “current active bleeding”)? Or can we administer NSAIDS to this type of patient?

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?

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?

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!

Could you make videos on the proper way to draw and give all of our meds ACP and PCP. Thanks