Q - Can I synchronize cardiovert an uncontrolled AFib?
A - There are some main concerns with treating atrial fibrillation/irregular rhythms prehospitally, mainly thromboembolism, as these patients may not have been anti-coagulated prior to treatment. Often rapid atrial fibrillation is secondary to a different cause that requires treatment beyond simply managing the rhythm alone. A.Fib is a complex entity and needs a complete assessment to determine the cause (primary or secondary). There is some literature that states an amiodarone bolus followed by an infusion had positive outcomes in reducing ventricular rates in some atrial fibrillation patients. However, it must be the right patient, who has a history of A.Fib/A.Flutter, in a primary arrythmia without secondary cause, is fully anticoagulated and compliant with anticoagulation, is very symptomatic (SOB/Chest Pain/Respiratory Distress), is not unstable enough for synchronized cardioversion, and often a considerable distance to hospital. Amiodarone works as a rate controller from the beta-blockade, which controls the rate-related symptoms, and can also cardiovert the patient out of the A.Fib/A.Flutter.
Rapid A.Fib is often the "sinus tach" for sick patients. They are septic, bleeding, or have PE's, and they are hypotensive and in rapid A.Fib. Paramedics will ask to do a synchronized cardioversion, but we can often tell from their medical history that it's not the primary treatment of choice. They may also be chronically A.Fib (in which case the shock often doesn't work and was never going to work), they may not be anticoagulated and the thromboembolic stroke risk in cardioverting is unacceptable, and it may be missing the primary problem altogether (ie: they are dehydrated, septic, or bleeding and the heart is doing what it is supposed to - it is their sinus tach). Therefore, the calls for rapid A.Fib with hypotension rarely result in a recommendation to cardiovert.
Q - Should I be providing sedation/pain management prior to carrying out Synchronized Cardioversion?
A - Intravenous analgesics or sedatives should be cautiously administered to ensure that the blood pressure tolerates their use. The use of such agents must be balanced against the risks of further hemodynamic deterioration and therapy should not be unnecessarily delayed if the ability to administer conscious sedation is not readily available. If your patient requires sedation/analgesia consider low and slow. Dosing for FentaNYL would remain within the 25-75mcg/dose, with an interval of 5 mins to a max of 150mcg. Midazolam would remain with the 0.1mg/kg/dose, with a max dose of 5mg, with an interval of 5min, to a max total of 10mg. Once the arrythmia is corrected, there will be no need for these medications, so use them sparingly and only if your patient really requires them.
Q - For the Medical Directors, do you have any insight on how often these patches (cardioversion) are being accepted/declined? We're wondering if one of the reasons is not due to the rarity of the patient but rather declined orders? Also, why is there still a mandatory patch point in this directive?
A - Yes, it’s infrequent. Traditional ACLS teaching is that if they're tachycardic and unstable the treatment is synchronized cardioversion. This is simple to teach but not so simple in practice. We frequently find that when medics are calling to do synchronized cardioversion, we are recommending a different course of action that we think is beneficial, but on the basis of principles that would take a lot of time to teach. Hence the patch point. Some examples: Rapid A-fib is often the "sinus tach" for sick patients. SVT with hypotension is often patched for cardioversion and we say try adenosine as it is chemical cardioversion, just as effective and you don't have the risk of sedation or a painful shock. "Unstable" doesn't mean they require emergent cardioversion - if they are awake and not in too much distress it is often okay to transport to hospital where sedation and synchronized cardioversion is much safer (even if that means they remain hypotensive for a bit longer)- more people and more tools.
Q - Let’s discuss wording, more specifically, sedation. Is our goal to sedate the patients we are going to cardiovert? Synchronized cardioversion is not part of the Procedural Sedation Medical Directive, what should we do/use?
A - Currently the direction is to follow the Procedural Sedation Medical Directive as a guiding directive for medications to use and dosing regimens to consider/use. Please note, Ketamine is not part of the sedation medical directive and is not recommended for synchronized cardioversion. Midazolam has dissociative and amnestic properties and works well for procedures such as synchronized cardioversion. Additionally, if pain is expected, Fentanyl is available through that Medical Directive.
Q - We had a conversation during today's TtT about overdrive pacing for Torsade's de Pointe (TdP). A medic had the discussion with cardiologists from the UOHI about TdP and prehospital management. They were saying that overdrive pacing was our "bailout" treatment until definitive care or Magnesium (Mg) administration. Since we don't carry Mg, would this be something that could be done with a BH patch? Are there situations where you would consider providing these orders such as long transport times?
A - The recommendation is synchronized cardioversion for polymorphic VT with instability along with rapid transport. Pacing or using meds to increase heart rate for conditions other than bradycardia would be an incredibly rare requirement and recurrence of unstable VT can be managed with cardioversion. I never say never and patching is always an option, but this would be incredibly rare.
Q - To consider- Pacing to maximum mA WITHOUT achieving capture and the use of dopamine to increase excitability to then achieve capture. While doing the treatments, do you decrease the mA to zero, start dopamine at your initial dose and then increase the mA again or do you simply add your dopamine to the mA setting currently at (no capture)?
A - irstly, we want to emphasize troubleshooting of failure to capture by optimizing pad placement and contact. This could include Vector Change. This is by far the most common cause of capture failure, the pacer runs up to 200mA, however capture is usually obtained around 100mA. Utilizing 1mA/kg is also another guide you can consider, but do note that capture is often affected by influenced by body size, impedance, past medical history, medications, etc. However, if you max out and have done troubleshooting and it’s still not working, dopamine is a good thought. If the patient is in pain from the pacing and it’s not working, it probably should be stopped as it’s causing harm with no clear benefit. If the patient is tolerating it, like they’re unconscious, it’s fine to keep going as you dial up the dopamine. Also consider treatments for hyperkalemia or MI if indicated, along with rapid transport. It is not wrong to stop and switch therapies, but this is not mandatory “you must stop” before switching therapies.
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