Prescribe the damn aspirin. Then think about it.

ACS is not just about sorting out the meds and organise the PCI ASAP, then moving on. If the patient is still alive and sitting front of you following an MI, we need to remember they are at high risk right now of reinfarcting as well other complications.

With this in mind, we should get the treatment on board as soon as possible. If the diagnosis is clear from the history/ECG/troponin, then of course this is no problem. Similarly, if another diagnosis e.g. gastritis seems to be far more likely and there is a negative ECG/troponin (although a negative troponin does not in itself rule out an MI until 12 hours from the symptoms) then it seems reasonable to hold off treatment.

The problem arises when you have those in between patients. I recently saw a 59 year old man with a background of gastritis presenting with chest pain lasting 10 minutes and starting three hours ago. There were no other cardiac features of the pain, but it was different from his usual gastric pain, and more severe. His ECG and initial troponin were normal. Should we start the ACS meds now?

It’s tricky. Perhaps we could classify the ACS drugs into high risk and low risk drugs. The main risk with the ACS drugs is bleeding, and we are most worried about intracranial and gastrointestinal bleeds, as these can have high morbidity/mortality. The high risk drugs, like clopidogrel and heparin and thrombolysis, could be given once we are confident we are dealing with ACS and they meet the relevant criteria within the ACS guidelines. The low risk ones (aspirin, morphine, GTN) can be given immediately provided that there are no contraindications. In fact, in the UK, the prehospital treatment of suspected ACS includes aspirin 300mg provided that there is no allergy. A history of gastritis is not a contraindication in these circumstances.

I had a look at the evidence to support aspirin in MI and also its risks. In the ISIS-2 trial, the main risk of aspirin at 160mg OD for a month was a 0.6% increase in minor bleeding, with no increase in major bleeds (defined as intracranial or gastrointestinal bleeds). There were 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets vs 1016/8600 (11.8%) among those allocated placebo tablets, which is an absolute risk reduction of 11.8% – 9.4% = 2.4%. The number needed to treat to prevent one vascular death I make as 100/2.4 =  41. That’s pretty good compared to most interventions we do.

I don’t think we should be giving oxygen in ACS by default. Oxygen is a vasoactive substance. It causes vasoconstriction everywhere but in the lungs, where it causes vasodilation. Overenthusiastic administration of oxygen in ACS is bad. It decreases coronary blood flow through vasoconstriction, as well as worsening reperfusion injury through the formation of reactive oxygen species. A recent Cochane review also found no benefit and possibly some harm from giving oxygen to MI patients compared to room air. The BTS states:

Most patients with acute coronary artery syndromes are not hypoxaemic and the benefits/harms of oxygen therapy are unknown in such cases.

NICE  says oxygen only to keep sats > 94% (or at 88-92% in those at risk of retaining CO2).

Let’s get back to that 56 year old man waiting for us. We should check that the initial dose of aspirin has been given, and if it has not been given for whatever reason, we need to get it in there ASAP. The benefit in terms of lives saved for aspirin is as good as the benefit thrombolysis offers. We can also give the other low risk meds like morphine and PRN GTN if there are no contraindications, and hold the high risk meds pending the 12 hour troponin. This way, the patient is getting most of the benefits and little of the harm until we know more about his condition, which will allow us to make a better informed risk/benefit decision on the rest of the meds. I disagree with a school of thought I have seen which does nothing until ACS is confirmed.

I now like to think about groups of ACS patients based on something I read from Dr Tabas at the San Francisco General Hospital:

1.        Definite ACS

Diagnostic ECG changes and/or diagnostic troponin rise

 2.        Possible ACS

Good history, possible ischemic changes on ECG, trace troponin rise (or complicated by other causes of chronically elevated troponin rise e.g. renal failure, heart failure)

3.        Not ACS

Not a convincing story, no evidence from ECG or troponin.

As a caveat, we need to bear in mind patients who may be having silent MIs – for example women, the elderly, diabetics, or post-operative and critically ill patients. Depending on the presentation, following a normal ECG and initial troponin they may justify a 12 hour troponin to rule MI out in the absence of any specific ACS-sounding symptoms, especially if they have CV risk factors.

It’s that middle group (possible ACS) which is the trickiest. I think that as long as the prescriber know the contraindications and risks of the low risk drugs and how they apply to the patient in front of them, then they should be given more routinely and more quickly in possible ACS cases.

How do we classify ACS?

ACS is cardiac sounding pain at rest, lasting at least 15 minutes. The first split is into ST Elevation ACS and non ST Elevation ACS based on the ECG. The universal definition of myocardial infarction with ST elevation on the ECG is:

New ST elevation at the J point [which is where the QRS complex joins the ST segment] in two contiguous leads with the cut-points: ≥0.1 mV in all leads other than leads V2–V3 where the following cut points apply: ≥0.2 mV in men ≥40 years; ≥0.25 mV in men <40 years, or ≥0.15 mV in women.

This reflects the fact that V2/V3 are the most likely leads to have a little bit of ST elevation in normal health. They are also the leads most likely to demonstrate high take off. High take off is a normal variant that usually occurs in the young athletes and represents early repolarisation. There is an upwards curving shape to the ST elevation and the ST segment does not evolve over hours or days.

Non ST elevation ACS is then classified into NSTEMI and unstable angina on the troponin levels, using the cut offs at your local lab.

I’ll write up some more stories from the nights. As a teaser for the next post, this is the ECG of a farmer in his early 50s who had two collapses in 3 days. He had never had a fall or collapse before, and his only medical problem was osteoarthritis of the hip (a classic occupational risk, with all the jumping from tractors). A previous ECG 6 months ago was normal. What does the ECG show and how could that explain the collapses?

Right bundle branch block

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4 thoughts on “Prescribe the damn aspirin. Then think about it.

  1. Is the ECG showing right bundle branch block (tall R’ in lead V1-V2)? The episodes of collapse could be syncope (loss of consciousness due to inadequate cerebral perfusion) due intermittent complete heart block or ventricular tachyarrhythmias.

    1. Hey Bibek,

      Thanks for commenting. Yup, it is RBBB (the ST depression and T wave inversions in V1-V3 are part of the deal in RBBB).

      Am I right in that you are suggesting a Stokes-Adams attack? It would fit. However, from my knowledge and googling (well, mostly googling) isolated RBBB very rarely progresses to complete heart block (http://www.annualreviews.org/doi/abs/10.1146/annurev.me.32.020181.002435?journalCode=med). It is more likely to progress if it is part of a trifasicular block, though even this is pretty rare.

      As for tachyarrythmias, I guess any cause of widened QRS is going to put you at risk of re-entry and other funny rhythms. However, I’m not sure if there are any cause and effect links between RBBB and tachyarrythmias and google didn’t help me find any. You may of course be right, so I would be grateful if you would clarify whether you are saying that the tachy causes the RBBB, or the RBBB causes the tachy?

      Thanks again for commenting, and hope to hear from you soon.

      1. Actually on looking into this, you’re probably right to say that that RBBB rarely progresses to CHB. Braunwald’s mentions that RBBB is very common and often benign, and only in Brugada syndrome is there a “RBBB-like pattern with persistent ST-segment elevation in the right precordial leads which is associated with susceptibility to ventricular tachyarrhythmias and sudden cardiac death”. Also “new onset of RBBB predicts a higher rate of coronary artery disease, congestive heart failure, and cardiovascular mortality” but this still doesn’t directly link RBBB to episodes of collapse. Will be interested to hear the case.

  2. Nice case dude. Re the o2 – i think the standpoint of only using oxygen if sats drop below 94% (in a non-COPD pt) is used for stroke as well as ACS.

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