Say bon voyage to MONA for treating ACS
Treat acute cardiac syndrome patients with the appropriate order of operations, and consider when traditional treatments may be contraindicated
MONA has retired ... and now she lives at Del Boca Vista with the Costanzas.
For those of you who remember introducing your chest pain patients to MONA (or for those of you who still do), this four-part acronym was a staple answer for nearly any acute coronary syndrome patient:
Much to our acronym-infatuated dismay, however, MONA was actually out of order and didn’t accurately align with the proper sequence of medication administration for our cardiac patients. This big piece of the puzzle was often overlooked as some providers simply followed the order of the acronym rather than really evaluating which medications were truly warranted (and their proper sequence).
Nevertheless, advanced life support guidelines for managing acute coronary syndrome patients have evolved. MONA lived her life in EMS and the emergency department, but now it’s time to let her sit on a beach with a cocktail in one hand and a longboard in the other.
Let’s break down the relevance of MONA in today’s management of ACS patients, starting with the appropriate order of operations.
That’s right; the first consideration that should cross our mind for cardiac-origin chest pain patients is aspirin. Aside from any contraindications, aspirin still holds a place in the management of ACS patients.
The key to this equation is ACS patients. Any random, undifferentiated or unspecified sign of chest pain or torso pain should not automatically equate to aspirin administration. In its true sense, aspirin (being an antiplatelet medication) is not benign; it can have side effects. Improperly – or blindly – administering it should not be a part of your clinical practice.
Properly identifying patients that meet ACS criteria, have ischemic changes on a 12-, 15- or 18-lead ECG, and otherwise do not show signs of active gastrointestinal bleeding, does meet its criteria. Beyond that, simply administering aspirin “just because” doesn’t constitute as a valid answer, and certainly doesn’t constitute as clinical justification.
Replace MONA’s morphine with fentanyl. Yes, morphine sulfate is still listed as part of the formulary of options for ACS pain management, but considering its longer onset and slurry of side effects (nausea, vomiting and acute hypotension, to name a few), transitioning toward fentanyl is showing to be a safer alternative.
In the event that you still do administer (or even carry) morphine, please consider an antiemetic chaser to coincide with it. After all, strapping your patient to a cot and facing them backwards in a moving ambulance is only asking for trouble.
Third on the list, oxygen deserves an asterisk, because it really is a consideration, not a necessity. Recent (and even prior) AHA guidelines have very quietly emphasized that ACS patients may not need supplemental oxygen administration if their pulse oximetry values are greater than 94%.
Unnecessarily applying oxygen (especially at 25 Lpm with a non-rebreather mask levitating off of the patient’s face) is truly overkill, and can lead to negative outcomes. Yes, it makes sense that if coronary blood flow and oxygen supply are decreased, therefore, supplemental oxygen is warranted. However, the other side of this equation is related to exactly how much ... and of what concentration ... the oxygen being delivered actually is.
Think of it this way; you take a breath in, you’re breathing in approximately 21% atmospheric oxygen. If you apply a nasal cannula flowing at 4 Lpm, then you’re already hyper-saturating your patient with 40-50% oxygen concentration (or FiO2). Your body isn’t used to this over-saturation, so it reacts. It releases free-radicals and results in vasoconstriction (which is something that we don’t want in the presence of an acute myocardial infarction).
If your patient isn’t showing physical signs of respiratory distress, and his/her oxygen saturation is greater than (or even equal to) 94%, then they likely don’t need supplemental oxygen. Simply applying it because it makes you feel better is not justification for its use.
As a strong word of caution related to nitroglycerin administration, I strongly suggest acquiring (and interpreting) – at a minimum – a 12-lead ECG prior to its administration (with an IV established, of course).
Why? Nitroglycerin is a preload affecting medication, essentially affecting the right side of the heart. If you suspect that your patient may be having a right-sided infarct, then taking away their compensatory blood pressure may cause a collapse of the system ... it may kill them.
You should not administer nitroglycerin without being prepared to counteract its potential side effects. No, I’m not talking about an acute headache or fizzing sensation underneath the tongue. I’m talking about hypotension.
As a vasodilator, it seems right that increasing the size of the pipe would increase blood flow and, therefore, decrease chest pain. This, however, has not really been proven to be effective. The vasodilation part, don’t get me wrong, is effective – but the pain management part – not so much.
Plus, we’re administering 400 micrograms to our patients via tablet or spray; yet when we administer nitroglycerine via IV drip, it’s at a fraction of this amount, and extended over minutes or hours, not seconds. That’s enough to make me want to reconsider my own practice of why we do it this way. If we have IV access and we can control (titrate) nitroglycerine administration, then why not administer it this route, instead?
Overall, things have changed; ACS management has evolved. We no longer need to focus on introducing our chest pain patients to MONA, or even her cousin, FONA. Instead, we should focus on appropriate-order treatment that is case-dependent and tailored to meet the needs of our patients. Instead, we should focus more on the initials AF, and allow MONA to enjoy her retirement and reading the “Boca Breeze.”