Aims:

A quick recap of MI, then walk through how to approach chest pain and recognise a STEMI. After that we will dive into the clinical practice of managing a STEMI - basic initial management, reperfusion pathways, monitor for key complications, and what to do when a patient starts to deteriorate. 

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Preclinical:

So when people think about STEMI, the usual understanding is that there is a complete occlusion of the coronary artery from a ruptured plaque, and actually, that is true..but really only for what we call Type 1 MI. 

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In reality, MI is a bit more nuanced, because, well, it’s medicine - nothing is ever that simple. We actually classified MI into 5 different types, based on what is causing them. Type 1 is the one we all know - plaque rupture, platelet aggregation, acute thrombosis. Type 2, on the other hand, is a supply and demand issue. Think anaemia, sepsis, coronary spasm - situations where the heart is not getting enough oxygen as it should. Then you’ve got type4/5 which are linked to procedures like PCI or CABG. 

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So when we say STEMI, what we’re really talking about is transmural ischaemia - an injury affecting the full thickness of the myocardium - not just ‘there is a blocked artery’. That distinction actually matters…because the CODE STEMI pathway and guidelines we will be discussing are really designed for type 1 MI. 

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Presentations:

The classic presentation of STEMI is dull central chest pain, squeezing/tightening in nature, radiating to the left jaw/arm, associated with nausea/diaphoresis/presyncope. The pain is often poorly localised given the visceral innervation of myocardium, and comes on suddenly and importantly, IT LASTS. We are talking longer than 15 minutes.

 

Certain demographics can also have atypical presentation of STEMI, such as elderly, women, Aboriginal and Torres Strait Islander and those that are renally impaired. You should really have that at the back of your mind because the last thing you want to do is to miss a STEMI. These patients may not have any chest pain at all but they may have severe nausea, syncope or isolated dyspnoea. 

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There are a few things in the patient's history that should really ring alarm bells for possible STEMI. Things like previous episodes of chest pain that resolve on their own, pain that’s brought on by exertion, or relief with GTN, obesity/poor diet, sedentary lifestyle, smoking, family history of MI. 

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Risk factors:

The classic triad of hypertension, diabetes, and hypercholesterolaemia. A known history of IHD is also really important - that should definitely raise your suspicion. 

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Differentials:

Now, of course, not all chest pain is STEMI—and this is where keeping a few key differentials in the back of your mind really matters.

So really quickly—how do we actually exclude these in the ED?

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You’re not trying to prove every diagnosis. You’re just looking for red flags that pull you away from your suspicion of STEMI.

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Here are some classic exam trigger phrases to know:

 

For cardiac causes—

Tamponade: think hypotension, raised JVP, and muffled heart sounds—Beck’s triad.

Dissection: sudden, tearing chest pain radiating to the back, maybe unequal pulses or a widened mediastinum on CXR.

Pericarditis: pleuritic chest pain, worse lying flat, better sitting forward, with a possible pericardial rub.

 

For the lungs—

PE: tachycardia, hypoxia, risk factors from Virchow’s triad, maybe calf tenderness.

Pneumothorax: sudden onset with unilateral reduced breath sounds, and in severe cases, tracheal deviation.

Pneumonia: fever, productive cough, and focal crackles on exam.

 

For GI causes—

Reflux or peptic ulcer disease is usually more burning, often post-prandial, and may improve with antacids or PPIs.

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But the key point is this— Nothing should delay an ECG.

 

If you could only take in one thing from today’s podcast, let it be that. 

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Queensland Guidelines:

All patients with suspected MI should have a 12-lead ECG and vital signs and be reviewed by senior clinicians within the first 10 minutes of medical contact. Anything beyond that, and you’re delaying care. So once you’ve got your ECG within that first 10 minutes—this is where things start to get real.

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Because at the end of the day, STEMI is an ECG diagnosis. So what are we actually looking for?

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The classic finding is ST elevation in contiguous leads, in a pattern that fits a coronary artery territory. To keep it simple, inferior leads II, III, aVF, anterior leads V1 to V4, lateral leads I, aVL, V5 and V6. ST elevations across multiple territories should make you think of pericarditis/Takotsubo cardiomyopathy, since it’s less typical for STEMI. But the key point is, if you are not sure, you treat it as a STEMI first. Because missing a STEMI is far worse than over-calling one. 

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If your initial ECG is in-conclusive but suspicion remains, perform serial ECGS every 15-30 minutes as per guidelines but also consider alternatives. 

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So once you’ve diagnosed a STEMI on the ECG, you’re activating the Queensland Health suspected Acute Coronary Syndrome pathway.

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Management:

But before we jump into all the definitive management—always go back to your basics. These patients are in pain, they’re anxious, and they’re often nauseous—so treat that first.

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And for nausea, something like metoclopramide or ondansetron works well.

 

For analgesia, small IV boluses like fentanyl 25 to 50 micrograms, or morphine 2.5 to 5 milligrams, are all very reasonable.

 

For MI specifically, GTN is great pain relief as it reduces preload via venodilation to drop myocardial oxygen demand and also afterload via arterial dilation, lowering systemic vascular resistance. But here is the trap, there are certain situations where GTN should not be given. You would have noticed that our candidate in the shift did not administer Julie GTN. As per guidelines, GTN should not be given in hypotension SBP<110mmHg and should be given with extreme caution if you are dealing with an inferior STEMI, which may have potential right ventricle involvement. The RV is preload-dependent, so if you drop the preload with GTN, it may precipitate significant hypotension. 

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Coming back to the basics, make sure you’ve got at least two IV lines—you’re going to need access for medications and potentially fluids. Oxygen is not given routinely—only if the SpO₂ is less than 93%.

A portable chest X-ray is often done—not to diagnose STEMI—but to help rule out other serious differentials we talked about earlier, like pneumothorax or a widened mediastinum.

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Next up—bloods. You’ll want to send off your standard set: FBC, U&Es, and a VBG if needed.
And importantly—if you’re suspecting an MI, you need a troponin.

If available, always use a high-sensitivity cardiac troponin assay—that’s the current standard. But if your centre doesn’t have it, send whatever troponin assay is available—something is better than nothing. Now, a really important point—

If the initial troponin is negative, that does not rule out an MI. Like in Julie’s case on our night shift, if the first troponin is negative, you need to repeat it— usually at around the 2 to 3 hour mark, depending on your local protocol.

Because with troponin, it’s not just the absolute value— It's the trend over time that matters.

And when you’re doing serial testing, make sure you’re using the same assay so you can actually compare results. And just to be very clear— you never wait for the troponin to come back before treating a suspected STEMI. The ECG makes the diagnosis. Troponin supports it—but it should never delay management.

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And this is the big one - both for exams and real life: Give aspirin early. A 300mg oral loading dose should be given as soon as possible, unless contraindicated. After that, patients should be on a maintenance dose of 100mg daily for life. If you do nothing else - get the ECG and give the aspirin. 

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So we’ve given aspirin—what’s next?

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The next thing to think about is a P2Y12 inhibitor. Now, you might be wondering—why don’t we just give it straight away with aspirin?

And the reason is, the choice of P2Y12 inhibitor depends on your reperfusion strategy.

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If your patient is going for primary PCI—so they’re in a PCI-capable centre, or can be transferred there quickly—then agents like ticagrelor or prasugrel are preferred.

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On the other hand, if your patient is in a rural setting—like our patient Julie in Miles Hospital—and is more likely to receive fibrinolysis, then clopidogrel is usually the agent of choice, as per ETG.

And the reason for that is ticagrelor and prasugrel are more potent, which means a higher bleeding risk, especially when combined with thrombolytic therapy.

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When you combine aspirin with a P2Y12 inhibitor, that’s what we call dual antiplatelet therapy—DAPT.

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As per guidelines, patients with STEMI should be on DAPT for at least 12 months, regardless of whether they’ve had PCI or fibrinolysis. After that, the P2Y12 inhibitor is usually stopped, and the patient continues on the maintenance dose of aspirin for life. 

 

Reperfusion Therapy:

Next, let’s talk about reperfusion therapy—because this is what actually saves myocardium.

The key principle in STEMI management is simple — Time is muscle.

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For patients presenting within 12 hours of symptom onset, the goal is to reperfuse the myocardium by reopening the occluded artery—either with primary PCI or fibrinolysis.

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Now, even if a patient presents outside that 12-hour window, they may still benefit from PCI—especially if they’re haemodynamically unstable, have ongoing chest pain, or show signs of ongoing ischaemia.

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So how do we choose between PCI and fibrinolysis?

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Primary PCI is the preferred option, if it can be performed within 120 minutes of first medical contact.

But in reality—especially in Queensland—not every hospital is PCI-capable.

So for many rural or regional patients, an early transfer decision is critical.

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If the patient can get to a PCI centre and have the artery opened within that 120-minute window— great, PCI is the way to go.

But if that’s not possible— if you can’t achieve reperfusion in time— then you should proceed with fibrinolysis instead.

So let’s briefly talk about PCI.

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PCI, or percutaneous coronary intervention, is a catheter-based procedure where a balloon is used to open the blocked artery, and a stent is placed to keep it open long-term.

During the procedure, patients are given anticoagulation, like IV heparin, to prevent clot formation. And one of the key complications we’re trying to avoid is stent thrombosis, which is why antiplatelet therapy is so important.

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Our other option is fibrinolysis.

This involves giving a tissue plasminogen activator—most commonly tenecteplase—to dissolve the clot and restore blood flow.

But before you give it, you must screen for contraindications—because the biggest risk here is bleeding, especially intracranial haemorrhage.

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A simple way to remember this is—think, where could bleeding be catastrophic?

So ask:

• any previous intracranial haemorrhage

• any ischaemic stroke within the last 3 months

• any active bleeding

Once you’ve given tenecteplase, you don’t just walk away—you reassess.

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Successful reperfusion is suggested by:

• improvement in chest pain

• and more than 50% resolution of ST elevation within 60 to 90 minutes

If it’s successful—great. You’ve bought your patient time.

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They’ll still need to be transferred to a PCI-capable centre for coronary angiography within 24 hours. If it’s not successful— that’s a failed lysis, and the patient needs urgent rescue PCI.

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Now, just like with PCI, these patients also need anticoagulation—most commonly low molecular weight heparin.

And this is where it can feel a bit counterintuitive—If we’re worried about bleeding, why are we giving anticoagulation?

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The key is this: Yes, thrombolysis breaks down the clot—but it also creates a pro-thrombotic state.

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You’ve still got a ruptured plaque sitting there, and by breaking down the fibrin clot, you expose that surface again—triggering platelet aggregation.

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So the artery you’ve just opened is actually at high risk of re-occluding. Lysis opens the artery—anticoagulation keeps it open.

So we’ve restored blood flow - but the job doesn’t end there. 

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As soon as you diagnose a STEMI, the patient needs to be on continuous telemetry monitoring. And the reason is simple - the most dangerous time is right at the start. In the first few minutes to hours, this is where most deaths happen. And the big one you’re watching for? Ventricular arrhythmia - VT or VF. After thrombolysis, reperfusion arrhythmia can occur, so patients should be closely monitored with a defibrillator and senior staff on standby. 

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Post-MI Complications:

Over the next few days, the problem shifts. Now you start to see the consequences of myocardial damage. The heart just can’t pump effectively - leading to cardiogenic shock or RV failure. These are your hypotensive, cold and clammy patients - they need urgent escalation.

Then in the weeks that follow, that’s when the mechanical complications can appear. Things like papillary muscle rupture - acute severe mitral regurgitation, ventricular septal rupture with new pansystolic murmur and free wall rupture leading to cardiac tamponade. Also in this late phase - don’t forget Dressler’s syndrome. This is a form of post-MI pericarditis, caused by an autoimmune response myocardial injury. Patient weeks after MI presenting with pleuritic chest pain, fever and pericardial friction rub? That’s something you need to think about. 

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Secondary Prevention:

So we’ve managed the acute event—but what we do next is equally important. Because STEMI isn’t a one-time event, and secondary prevention is what changes long-term outcomes. And this is a very high-yield area for exams.

 

First—dual antiplatelet therapy, or DAPT. That’s aspirin plus a P2Y12 inhibitor for at least 12 months, followed by lifelong aspirin in most patients. 

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Next—statins. And this is important— they’re given regardless of baseline cholesterol. Because it’s not just about lowering lipids—it’s about stabilising plaques.

 

Then—beta-blockers. Typically used for around 12 months, they reduce myocardial oxygen demand and help prevent arrhythmias.

 

And finally—ACE inhibitors. These are key for cardiac remodelling after myocardial injury, and help reduce the risk of developing heart failure.

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So that’s STEMI management from start to finish.

 

I know that’s a lot to take in - so let’s quickly summarise the key points.

 

Key Points:

Get an ECG within the first 10 minutes. Remember — STEMI is an ECG diagnosis. A normal or inconclusive ECG, and even a negative troponin should never delay management if your clinical suspicion is high. Next —give aspirin 300mg early, and be cautious with nitrates, especially in hypotensive patients or those with possible RV involvement. When it comes to reperfusion — PCI is preferred if it can be done within 120 minutes of first medical contact. If not — don’t wait. Thrombolyse. 

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And finally—stay alert for complications. Because as we saw in Julie’s case, STEMI doesn’t just affect the myocardium— it can also affect the cardiac conduction system.

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The right coronary artery supplies the AV node, so when you get an infarct in that territory, you can end up with bradycardia or even complete heart block. So let’s walk through the bradyarrhythmia pathway - in particular, complete heart block, and how we manage these patients in the ED.

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Bradyarrhythmia:

Quick reminder what complete heart block, or third degree AV block is. This is when there is no conduction between atria and ventricles, so they are essentially beating independently of each other.

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So the first question you always want to ask is—  is this patient stable or unstable? Start with your primary survey. Look for hypotension, chest pain, signs of shock, altered mental state. If the patient is unstable, or has a high-degree block—like Mobitz type II or in this case, complete heart block—they will need urgent pacing. There are two types of pacing: Transcutaneous pacing— which is non-invasive, can be done immediately in ED, and is your first-line temporising measure. And transvenous pacing— which is more definitive, but requires a procedure to insert a pacing wire, usually via central venous access.

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And a really important point—don’t forget analgesia and sedation. Transcutaneous pacing is uncomfortable— and repeatedly capturing the heart without pain control can be quite distressing for patients. Now, as an interim measure, you can try atropine. Give 500–600 micrograms IV, and repeat every 3 to 5 minutes, up to a maximum of 3 mg.

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But here’s the key— In complete heart block, atropine often doesn’t work, because the block is below the AV node. You can also consider infusions like: adrenaline, isoprenaline or dopamine. But in the context of STEMI—like Julie’s case— these are often just bridges, not definitive management.

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And that brings us to the end of this week’s deep dive on STEMI.

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We’ve covered a lot—from recognising it on ECG, to managing it in those first critical minutes, to thinking about reperfusion, complications, and what happens after the dust settles.

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And hopefully, through Julie’s case, you can see that these aren’t just textbook concepts— this is exactly how things unfold on a real night shift.

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Thanks so much for tuning in!

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If you found this helpful, feel free to share it with a friend, a study buddy, or someone about to start their ED term.

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And stay tuned—because next time, we’ll be diving into another case, and seeing whether our next student will… sink or think.