A practical emergency medicine case about treating risk before the diagnosis is complete

A 45-year-old man presents to a community emergency clinic with acute central chest pain.

He is haemodynamically stable:

• Blood pressure: 120/70 mmHg
• Heart rate: 57 beats/min
• SpO₂: 97% on room air
• No clinical evidence of shock
• No acute pulmonary oedema

The clinic has cardiac monitoring, laboratory testing and resuscitation capability, but there is no echocardiography service and no cardiologist on site.

A PCI-capable hospital is approximately 40 minutes away.

A 12-lead ECG is obtained.

The ECG

Figure 1. Initial 12-lead ECG obtained during chest pain. Sinus rhythm at approximately 57 beats/min, high QRS voltage, mild intraventricular conduction delay, and marked anterior–lateral repolarization abnormalities with deep T-wave inversion.

The ECG is striking.

But before attaching a diagnosis to it, I ask a more useful question:

What does this ECG actually tell me right now?

There is substantial voltage and extensive ST-T abnormality. Possible explanations include acute myocardial ischaemia, significant left ventricular hypertrophy with secondary repolarization change, an underlying cardiomyopathy, or more than one process occurring simultaneously.

Related reading: Differential Diagnosis of ST Elevation Patterns

What I should not do is diagnose a specific structural cardiomyopathy from this ECG alone.

And I should not allow the dramatic appearance of the tracing to distract me from the patient in front of me.

The 2025 ACS guideline emphasizes rapid ECG acquisition, focused clinical assessment, cardiac troponin testing and serial ECG assessment when ACS remains clinically suspected.

The diagnosis is not complete.

The management, however, has already started.

Minute 0–5: Is the patient unstable?

Before thinking about medications, I reassess the physiology.

Is he hypotensive?

No.

Is there pulmonary oedema?

No.

Is there a malignant arrhythmia?

No.

Is he showing signs of poor perfusion, altered consciousness or cardiogenic shock?

No.

So this is not currently a resuscitation problem.

It is a potentially high-risk cardiac presentation in a stable patient.

I place him on continuous cardiac monitoring, establish reliable IV access, keep defibrillation immediately available and obtain blood samples for:

• high-sensitivity troponin;
• full blood count;
• electrolytes;
• renal function;
• glucose; and
• coagulation studies.

I also request any previous ECG immediately. An old ECG showing the same repolarization pattern would be extremely valuable.

Most importantly, I contact the receiving cardiac centre early.

I do not wait for every test result before beginning the transfer process.

Minute 5: Aspirin — yes

Unless there is active major bleeding, a significant aspirin hypersensitivity or a clinical concern for an acute aortic syndrome, I give an aspirin loading dose—for example:

Aspirin 300 mg chewed, according to local ACS protocol.

Aspirin loading followed by low-dose aspirin is recommended in ACS because it reduces death and major adverse cardiovascular events.

This is a relatively straightforward decision.

ACS remains a major working diagnosis, and I do not need an echocardiogram or coronary angiogram before giving aspirin.

Oxygen — no

His oxygen saturation is 97% and he has no respiratory distress.

I monitor his oxygen saturation, but I do not give supplemental oxygen routinely.

Supplemental oxygen is indicated when clinically significant hypoxaemia or respiratory distress is present rather than simply because the patient has chest pain.

This sounds like a small detail, but it illustrates an important principle:

Do not treat “chest pain” with an automatic package of medications. Treat the patient’s physiology and the likely pathology.

What about nitroglycerin?

This decision deserves more nuance.

The patient has chest pain and a blood pressure of 120/70 mmHg.

For ongoing ischaemic discomfort, sublingual nitroglycerin is a reasonable symptomatic treatment when there is no significant hypotension, suspected right ventricular infarction or other important contraindication. The current ACS guidance lists sublingual nitroglycerin as an option for symptom control; analgesic therapy itself has not been shown to improve clinical outcomes.

So I would not say that this ECG alone contraindicates nitrates.

We do not yet know the structural diagnosis.

However, I also do not regard nitroglycerin as mandatory.

If the patient’s pain is mild or improving, his haemodynamics are stable and definitive cardiac assessment is only 40 minutes away, there is no need to aggressively chase the symptom with vasodilators.

If he has significant ongoing ischaemic-type pain, his blood pressure remains adequate and there are no contraindications, I would consider:

Nitroglycerin 0.4 mg sublingually, with close reassessment of symptoms and blood pressure.

If hypotension develops, I stop.

Later, if obstructive hypertrophic physiology were demonstrated, vasodilator therapy would require additional caution because reductions in preload or afterload can aggravate dynamic outflow obstruction in susceptible patients. The 2024 HCM guideline specifically advises reconsideration of vasodilating drugs in symptomatic obstructive HCM.

But that information is not available to me yet.

That distinction is important.

What about a beta-blocker?

The current ACS guideline supports early oral beta-blocker treatment in appropriate patients who do not have contraindications.

But this patient already has a heart rate of approximately:

57 beats/min.

He is not hypertensive.

He has no tachyarrhythmia.

I therefore do not give an IV beta-blocker simply because the ECG is abnormal.

There is no need to produce bradycardia in someone who is already relatively bradycardic.

A beta-blocker may become appropriate later, depending on the final diagnosis, ventricular function, rhythm and cardiology assessment.

The principle is simple:

Treat the physiology you have—not the diagnosis you are imagining.

Morphine or fentanyl?

Not routinely.

If the patient is experiencing severe pain that remains uncontrolled, carefully titrated opioid analgesia can be used.

But morphine is not an obligatory component of modern ACS treatment.

The 2025 guideline places IV morphine or fentanyl as options for pain resistant to maximally tolerated anti-ischaemic therapy and notes that opioids can delay the action of oral P2Y12 inhibitors. Analgesics improve symptoms but have not themselves demonstrated improved ACS outcomes.

If the patient continues to have severe chest pain despite treatment, my concern should increasingly become:

Why is the ischaemic-type pain continuing, and does this patient need even more urgent invasive assessment?

Not simply:

What stronger analgesic can I give?

The troponin returns positive

The initial high-sensitivity troponin is elevated.

Now the case feels different.

We have:

• acute chest pain;
• a markedly abnormal ECG; and
• objective myocardial injury.

But this is where terminology matters.

A positive troponin means myocardial injury.

It does not independently establish the mechanism of injury.

It does not tell me whether the patient has plaque rupture, another coronary mechanism, myocarditis, structural myocardial disease, supply–demand imbalance, or another cause.

Nevertheless, in a patient with acute chest pain and this ECG, acute coronary syndrome remains a serious working diagnosis.

This patient needs definitive cardiac assessment.

And that assessment is only approximately 40 minutes away.

Anticoagulation — this is where I pause for a safety check

Before administering anticoagulation, I briefly reopen the differential.

Could this be an acute aortic syndrome?

I reconsider:

• Was the pain maximal at onset?
• Was it described as tearing or ripping?
• Does it radiate prominently to the back?
• Is there syncope?
• Is there a neurological deficit?
• Are the pulses or blood pressures asymmetric?
• Is there known aortic disease?

I also assess for active bleeding and other significant anticoagulation contraindications.

If there is no meaningful concern for these alternatives and NSTE-ACS remains the leading working diagnosis, I start parenteral anticoagulation according to the local ACS and receiving-centre protocol.

With early invasive assessment planned, unfractionated heparin is a practical strategy in many systems.

The 2025 ACS guideline states that IV unfractionated heparin is useful in NSTE-ACS to reduce ischaemic events and recommends parenteral anticoagulation in patients undergoing coronary revascularization during the admission.

I document the exact agent, dose and administration time so that the interventional team knows precisely what the patient has received.

Should I load ticagrelor or clopidogrel before transfer?

This is one of the most useful modern teaching points in the case.

The cath lab is only approximately 40 minutes away.

Aspirin has already been given.

Should I automatically add a P2Y12 loading dose before the coronary anatomy is known?

Not necessarily.

The 2025 ACS guideline specifically states that in NSTE-ACS patients planned for an invasive strategy, upstream clopidogrel or ticagrelor may be considered when angiography is expected to be delayed beyond 24 hours. That is quite different from saying that every NSTE-ACS patient must be preloaded immediately before early angiography.

In this case, angiography is potentially available very soon.

My practical approach would therefore be to contact the receiving cardiologist, transmit the ECG and coordinate the P2Y12 strategy.

Unless the receiving pathway specifically requests pretreatment, I would not make P2Y12 loading at the clinic automatic.

The interventional team can select the agent once the invasive strategy and coronary anatomy are clearer.

High-intensity statin — yes

If there is no contraindication, I give high-intensity statin therapy—for example:

Atorvastatin 80 mg orally.

The 2025 ACS guideline recommends high-intensity statin therapy for patients with ACS.

This treatment does not require me to know the coronary anatomy first.

Meanwhile, do not stop thinking

One of the easiest mistakes at this stage is to believe the work is finished.

Aspirin given.

Heparin started.

Cardiology called.

Ambulance requested.

Now we wait.

No.

Those 20–30 minutes are clinically important.

I repeatedly reassess:

• Is the chest pain improving?
• Is it becoming more severe?
• Is the blood pressure falling?
• Is the heart rate changing?
• Is pulmonary oedema developing?
• Has a new murmur appeared?
• Is there an arrhythmia?
• Is the patient becoming presyncopal or syncopal?

And particularly:

Is the ECG changing?

If the pain continues or changes, I repeat the 12-lead ECG and compare it directly with the first tracing.

Serial ECG assessment is recommended when clinical suspicion for ACS remains high.

The first ECG is not a permanent answer.

The cardiology call

I send the ECG electronically to the receiving cardiologist.

My handover might sound like this:

“I have a 45-year-old man with acute central chest pain. He is haemodynamically stable: BP 120/70, heart rate 57 and SpO₂ 97%. His ECG has high voltage with marked anterior and lateral ST-T abnormalities and deep T-wave inversion. Initial high-sensitivity troponin is positive. There is no echo available here. He has received aspirin, high-intensity statin and ACS anticoagulation. I have not routinely preloaded a P2Y12 inhibitor because invasive assessment is readily accessible. He is being transferred now.”

The objective of that call is not to persuade the cardiologist that I have already made the final diagnosis.

Quite the opposite.

It communicates:

This patient has significant myocardial injury and an abnormal ECG, the diagnosis remains incomplete, and he needs definitive cardiac evaluation.

Current ACS guidance recommends an invasive strategy during hospitalization for intermediate- or high-risk NSTE-ACS, with urgent invasive assessment for patients who develop refractory angina, haemodynamic instability, electrical instability or acute heart failure.

What I do not do

I do not keep the patient in the clinic for several hours simply to obtain more troponins.

Serial troponin measurements remain diagnostically useful, but they should not create an unnecessary delay in transferring a patient who already has significant symptoms, a markedly abnormal ECG and an elevated troponin when definitive cardiac care is nearby. The 2025 guideline incorporates serial troponin into the initial ACS assessment while also emphasizing risk-based invasive management.

I do not wait for an outpatient echocardiogram.

I do not diagnose a cardiomyopathy solely from the ECG.

And I do not allow the automated ECG interpretation to make the clinical decision for me.

Approximately 40 minutes later: the diagnostic picture changes

The patient reaches the cardiac centre.

Now information becomes available that I did not have when making those initial decisions.

Echocardiography is performed.

Figure 2. Transthoracic echocardiographic view obtained following transfer. Prominent thickening of the apical left ventricular myocardium with relative narrowing of the apical cavity is visible, raising suspicion for an apical hypertrophic phenotype. Complete characterization requires formal measurements and assessment across multiple echocardiographic views.

Now go back and look at Figure 1 again.

The ECG suddenly has a different context.

The high voltage and profound anterior–lateral T-wave inversion may be explained, at least in part, by the structural abnormality now visible on echocardiography.

But we should not make the opposite diagnostic error.

The echo does not allow us to say:

“The chest pain and troponin no longer matter.”

Structural heart disease and acute coronary disease can coexist.

The coronary arteries still need to be assessed.

The 2024 HCM guideline recommends transthoracic echocardiography as part of the initial evaluation of suspected HCM and recognizes additional advanced imaging, including cardiac MRI, as important when further diagnostic characterization is required.

The coronary result

Coronary angiography was subsequently performed.

According to the treating cardiologist, the coronary arteries were normal, with no significant obstructive coronary artery disease.

The angiographic images were not available for independent review.

That limitation should be stated explicitly rather than presenting an angiographic interpretation that we did not personally review.

Now the case becomes considerably more interesting.

We began with:

Chest pain + dramatic ECG + elevated troponin

and therefore appropriately treated the patient as a potentially significant ACS presentation.

After definitive evaluation, however, no obstructive coronary lesion was identified.

The echocardiographic appearance instead raised strong suspicion for an apical hypertrophic phenotype.

Importantly, I would not automatically label this case MINOCA from the information currently available.

MINOCA is a working diagnosis that requires the patient first to fulfil criteria for acute myocardial infarction and then to have no obstructive coronary disease, with further investigation directed toward alternative coronary and non-coronary mechanisms. A positive troponin alone is not sufficient.

Likewise, I would not state that the hypertrophic phenotype definitely “caused” the troponin elevation unless the complete clinical investigation supports that conclusion.

A more accurate description is:

Chest pain with myocardial injury, marked ECG abnormalities, an apical hypertrophic phenotype on echocardiography, and coronary angiography reported as showing no significant obstructive coronary artery disease.

Further formal echocardiographic characterization and, where clinically appropriate, cardiac MRI can help define the phenotype and assess myocardial scar and other diagnostic possibilities.

Looking back: did we manage the first 40 minutes correctly?

Yes.

And this is the central educational point.

The emergency physician did not know the angiography result.

The emergency physician did not have the echocardiogram.

The emergency physician did not need to establish the final structural diagnosis before acting.

The information available at the clinic was:

acute chest pain + markedly abnormal ECG + positive troponin.

That patient deserved serious ACS evaluation, antithrombotic treatment when appropriate, continuous reassessment and rapid transfer for definitive cardiac investigation.

The later diagnosis does not make the initial ACS approach incorrect.

It demonstrates why emergency medicine is often about managing probability and risk before certainty exists.

The first-40-minute medication summary

For this patient, my practical initial approach would be:

Aspirin

Yes.

Give an appropriate loading dose—for example 300 mg chewed according to local protocol—unless contraindicated.

Anticoagulation

Yes, if NSTE-ACS remains the working diagnosis after excluding important contraindications and dangerous mimics.

UFH is a reasonable strategy when early invasive management is anticipated, according to the receiving-centre protocol.

High-intensity statin

Yes.

For example, atorvastatin 80 mg unless contraindicated.

Oxygen

No routine oxygen at SpO₂ 97%.

Continue monitoring and treat clinically significant hypoxaemia if it develops.

Nitroglycerin

Individualize.

For significant ongoing ischaemic-type pain with adequate blood pressure and no contraindications, sublingual nitroglycerin can be used with close haemodynamic monitoring. It is symptomatic therapy rather than definitive treatment. Do not give it simply because every patient with chest pain is expected to receive it.

Beta-blocker

Not immediately in this patient.

His resting heart rate is already approximately 57 beats/min and there is no tachycardia or hypertension requiring urgent treatment. Early oral beta-blockade can be considered later if clinically appropriate.

Morphine or fentanyl

Not routinely.

Reserve carefully titrated opioid analgesia for severe refractory pain. Opioids can delay oral P2Y12 activity and do not improve ACS outcomes themselves.

P2Y12 loading

Do not make pretreatment automatic when angiography is imminent.

With the cath lab approximately 40 minutes away, discuss the strategy with the receiving interventional team. Current guidance particularly identifies upstream clopidogrel or ticagrelor as an option when invasive evaluation is expected to be delayed beyond 24 hours.

And perhaps most importantly

Monitor. Repeat the ECG. Reassess the patient. Call cardiology early. Transfer early.

What this case teaches us

There are three potential cognitive errors in a case like this.

Error 1: Anchoring on acute coronary syndrome

Chest pain plus a positive troponin does not guarantee an obstructive coronary culprit lesion.

Troponin tells us that myocardial injury is present. The clinical context and further investigation determine why.

Error 2: Anchoring on the ECG morphology

A dramatic ECG does not necessarily provide the final diagnosis.

High voltage and profound T-wave inversion should broaden the differential rather than immediately close it.

Error 3: Anchoring on the later echocardiogram

Once structural heart disease is found, it is tempting to retrospectively dismiss the original ACS concern.

That is also a mistake.

The emergency physician must make decisions using the information available at that moment, not using the diagnosis that becomes apparent 40 minutes later.

The take-home message

The most important question in this case is not:

“Can I diagnose the final cardiac condition from this ECG?”

The better question is:

“What does this patient need during the next 40 minutes while the diagnosis is still uncertain?”

The answer is:

• Recognize the risk.
• Treat credible acute coronary syndrome while the diagnosis remains uncertain.
• Avoid unnecessary medication.
• Do not overinterpret the ECG.
• Repeat the ECG when symptoms persist or evolve.
• Monitor and reassess the patient closely.
• Communicate early with the receiving cardiologist.
• Move the patient rapidly toward the tests that can answer the questions you cannot answer in the clinic.

The echocardiogram and coronary angiogram may eventually provide diagnostic clarity.

But the emergency management comes before the diagnostic reveal.

Continue learning

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References

1. Rao SV, O’Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025. doi:10.1161/CIR.0000000000001309.
2. Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2024. doi:10.1161/CIR.0000000000001250.
3. Tamis-Holland JE, Jneid H, Reynolds HR, et al. Contemporary Diagnosis and Management of Patients With Myocardial Infarction in the Absence of Obstructive Coronary Artery Disease: A Scientific Statement From the American Heart Association. Circulation. 2019;139:e891–e908. doi:10.1161/CIR.0000000000000670.

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Educational case for healthcare professionals. Treatment decisions, medication dosing, anticoagulation strategy and transfer pathways should be individualized and follow local emergency medicine and cardiology protocols. Identifying patient information should be removed from all ECG and imaging figures before publication.