HSNCPC

What is the differentiating QRS for paediatric tachycardia? As per PALS guidelines they utilize a QRS less than 0.09 for narrow complex and greater than 0.09 for wide complex. As per BH hospital can we use these guidelines?

Thank you for your question. In the clinical scenario of tachycardia with a pediatric patient, an EKG showing a QRS complex that is <= 0.09 seconds would be an appropriate interval cutoff for decision making in determining a Narrow vs. Wide complex tachycardia. The Base Hospital supports the use of this interval cutoff for pediatric patients. Quite often a quick visual of the QRS complex suffices to determine if its narrow or wide. However, in the pediatric patient, the tachycardias are usually of such high rates that this quick visual can sometimes be challenging. Therefore using the rule of thumb of a QRS cut off of 0.09 in the pediatric patient is helpful in this decision making.

Opinion on co-administration of Tylenol and Ibuprofen with opioids. With some studies showing lower doses of opioids needed with co-administration of a NSAID or Tylenol and ibuprofen. Would this be beneficial practice in the field?

Great question. The co-administration of acetaminophen and/or ibuprofen (NSAID) with an opioid has been shown in several studies to reduce the opioid utilization and maintain effective pain control. Quite often some of the most severe acute pain conditions we treat (ie. Renal Colic) can be reduced significantly with a single dose of NSAID. Many of these patients who present via EMS having received an NSAID en-route will often require no further immediate pain (opioid) medication administered in the emergency department.

Smoking calculation for dexamethasone administration Do we include vaping as part of the 20-pack/year smoking calculation for potential dexamethasone administration?

Thank you for the question regarding vaping and pack/year of smoking. I would consider any type of smoking (vape, cigarettes, cannabis, etc) as part of the calculation towards the 20 pack/year history. Although vaping does not carry the same ingredients as cigarettes, we do know that it still causes lung damage.

Can we co-administer Toradol and Acetaminophen? I did a call today where the pt was contraindicated for acetaminophen as she had taken it 3.5 hours prior, however we ended up giving her Toradol IV anyways, as the pt stated when she ingested anything she felt nauseous. Our transport time was over 30mins so my student asked about administering acetaminophen enroute, once the 4 hour time frame was over. He was taught in school that it was ok to administer Toradol and acetaminophen in conjunction with one another. My partner and I both were under the impression that it was ibuprofen and acetaminophen OR Toradol, even though they are 2 different classifications of meds.

Thank you for your question. Ibuprofen and ketorolac (Toradol) are both NSAIDS. The two drugs share all the same indications and contraindications with the one main difference being that Toradol is injectable. NSAIDS have analgesic, antipyretic and anti-inflammatory properties due to their suppression of prostaglandin release and other unknown factors. It is this anti-inflammatory effect which makes all NSAIDS potent analgesics.
Acetaminophen (Tylenol) has only analgesic and antipyretic properties, it is not an anti-inflammatory. Although both agents are metabolized in the liver, they are done so by different pathways, and so any NSAID and acetaminophen can be taken together for a short, defined period.
There is emerging evidence that NSAIDS and acetaminophen work synergistically when taken together which is why you now see Tylenol with Ibuprofen advertised.
In short acetaminophen can be administered with any NSAID, if there are no contraindications.

Tibial IO Can a Tibial IO be inserted if there is suspected pelvis fracture?

Thank you for your question. In trauma patients, the most important prehospital treatment is to ensure rapid transport to hospital, preferably a trauma center if possible. In a patient with hypotension, IV access for fluid bolus would be the best choice if this will not delay transport or interfere with other more crucial treatments such as hemorrhage control. If IV access is not achievable, IO access may be used for fluid or any other IV treatments.
In a patient with presumed pelvic fracture, humeral IO would be the preferred site as fluids would reach the central circulation faster and there would be less concern for fluid extravasation via injured pelvic vessels.

Which sedative would be most appropriate in treating a combative head injury patient? Would ketamine or midazolam be the best treatment when having to sedate a patient who is combative due to a head injury?

Thank you for your question. Both ketamine and midazolam are ideal agents for agitation secondary to a head injury due to their short time of onset and relatively short half time. They have made the job of agitation management easier. In most cases, the decision is based upon the patients clinical condition i.e. GCS, airway, degree of agitation, and physician preference. Ketamine is preferred over midazolam because we do not have to worry about the possibility of respiratory depression with escalating doses and we achieve quicker sedation at lower doses than we do with midazolam. The issue with ketamine in the past was the unfounded allegation that it increased ICP and therefore was contraindicated in head injury patients. This has since been disproven thereby giving us another useful agent in the treatment of head injured patients.
In summary, both agents are acceptable for the treatment of agitation secondary to a head injury.

Would you give NTG in a cardiac Ischemia call but their is no presence of pain? I am seeking clarification regarding the administration of Nitro during a cardiac ischemia call. Specifically, if the patient does not exhibit pain, should Nitro still be administered? My understanding from training is that Nitro should not be given in the absence of pain, with pain defined as discomfort, heaviness, or tightness.

Thank you for your question. You are correct. Nitro is a symptom relief and chest pain, or its cardiac equivalent, needs to be present as a symptom to relieve. No symptoms means no nitro regardless of the EKG.

What is the criteria for aVR STEMI? In the context of calling a STEMI Alert to a receiving hospital for suspected aVR elevation; does there need to be >1mm of elevation in aVR, with ST depression in the lateral leads? Or is the criterion completely different?

Thank you for your question. aVR was once considered the "nothing" lead - a ground if you will. However, new evidence throughout the years has shown that STE in aVR with diffuse depression in a patient with chest pain is indicative of a critical left main occlusion. This is more so if there is STE in aVR, aVL and V1 with diffuse ST depression.
However, the key is in the history. STE in aVR with diffuse ST depression can be seen in the context of diffuse multivessel disease or poor endocardial perfusion secondary to a shock state (GI Bleed, PE, sepsis, etc.) When there is a clinical picture that is consistent with ischemia, and you have STE in aVR, in order for a critical left main occlusion to be considered there must be concurrent diffuse ST depression.

Does any med administration raise the CTAS?

Thank you for your question. Medication administration could possibly raise the CTAS level, however it would have to correlate with patient condition. An example of this would be arriving to a patient whose chief complaint is shortness of breath and is displaying moderate respiratory distress with evidence of bronchoconstriction. You administer Ventolin to this patient and begin extrication. This patient would be considered a CTAS 2 upon arrival. However, during transport the patient worsens and is displaying fatigue from excessive work of breathing, confusion and cyanosis. You now administer intramuscular epinephrine followed by Ventolin. The worsened patient condition along with medication administration would now make this patient a CTAS 1.