10 Cardiac Emergencies Every Physician Must Know: Recognise, Act, Avoid the Trap

It is 2 am in a busy emergency department. In the next hour you will see a breathless woman with clear lungs and a low blood pressure, a man with chest pain whose ECG “doesn’t quite meet criteria”, and a dialysis patient who feels weak and whose pulse is 38. None of them looks like the textbook picture. Each can die before morning if the first decision is wrong. This guide is for the physician who makes that decision, often alone.

Key points

• Most deaths in cardiac emergencies follow a wrong first step, not a missing rare diagnosis.
• Several STEMI equivalents never show classical ST elevation; recognise the patterns and activate the reperfusion pathway.
• Before any irreversible step (thrombolysis, anticoagulation, intubation, large fluid volumes, AV nodal blockers), pause and ask what would happen if the working diagnosis were wrong.
• Haemodynamic instability changes the order of everything: stabilise, then image.
• Each emergency below has one classic trap; knowing it in advance is the cheapest safety measure available.

The ten emergencies

1. STEMI equivalents: de Winter, Wellens, posterior MI, LBBB and paced rhythms

Recognise: Ischaemic pain with an ECG that signals acute coronary occlusion without classical ST elevation. De Winter: upsloping ST depression at the J point across V1–V6 with tall, symmetrical T waves. Wellens: biphasic or deeply inverted T waves in V2–V3, often recorded when the pain has settled. Posterior MI: ST depression in V1–V3 with dominant R waves; record V7–V9. LBBB or paced rhythm: apply Sgarbossa or modified Sgarbossa criteria.

Act now: Treat de Winter, confirmed posterior MI and Sgarbossa-positive LBBB or paced rhythm as STEMI and activate primary PCI. Treat Wellens as a critical proximal LAD lesion: admit, manage as very high-risk NSTE-ACS and arrange early angiography.

The trap: Sending the pain-free Wellens patient for a treadmill test. In LBBB with suspected ongoing ischaemia, ESC guidance advises managing as STEMI whether or not the block is known to be old.

2. Acute aortic dissection

Recognise: Abrupt, severe chest, back or interscapular pain, often tearing; pulse deficit or a systolic difference of more than 20 mmHg between arms; a new aortic regurgitation murmur; focal neurological deficit or syncope with pain.

Act now: Analgesia, IV beta-blocker first to bring heart rate towards 60/min, then a vasodilator if needed, aiming for a systolic pressure of roughly 100–120 mmHg as tolerated. Urgent CT aortography and immediate cardiothoracic referral for Type A.

The trap: An inferior STEMI caused by a dissection flap involving the right coronary ostium, treated with a thrombolytic or full anticoagulation.

3. Massive (high-risk) pulmonary embolism

Recognise: Sudden dyspnoea, syncope or hypotension with hypoxia, a raised JVP and clear lung fields; a dilated, hypokinetic right ventricle on bedside echo.

Act now: Unfractionated heparin bolus immediately unless contraindicated; systemic thrombolysis; noradrenaline for hypotension; catheter-directed or surgical reperfusion when thrombolysis is contraindicated or has failed.

The trap: Large fluid boluses that further distend a failing right ventricle, and an unplanned intubation, where induction and positive-pressure ventilation can precipitate arrest.

4. Cardiac tamponade

Recognise: Hypotension, tachycardia, raised JVP, pulsus paradoxus above 10 mmHg; on echo, an effusion with right atrial and right ventricular diastolic collapse and a plethoric IVC. A small effusion that accumulates quickly, as after a procedure, can be enough.

Act now: Echo-guided pericardiocentesis; modest fluid as a bridge.

The trap: Diuretics or vasodilators, which drop preload further. In haemopericardium from Type A dissection or free-wall rupture, surgery, not needle drainage, is the definitive treatment.

5. Cardiogenic shock

Recognise: Systolic pressure below 90 mmHg for more than 30 minutes or the need for vasopressors, with hypoperfusion: cold peripheries, oliguria, confusion, rising lactate. Early shock may be normotensive.

Act now: Noradrenaline as first-line vasopressor, an inotrope such as dobutamine for persistent low output, urgent echo to exclude a mechanical complication, and immediate angiography with culprit-lesion PCI in MI-related shock. Involve a shock team early.

The trap: Routine immediate multivessel PCI (CULPRIT-SHOCK favoured a culprit-only strategy) and routine intra-aortic balloon pumping, which did not reduce mortality in IABP-SHOCK II.

6. Unstable tachyarrhythmias

Recognise: Any tachyarrhythmia with adverse features: shock, syncope, myocardial ischaemia or heart failure.

Act now: Synchronised DC cardioversion under sedation or anaesthesia. If it fails, amiodarone 300 mg IV over 10–20 minutes before repeating the shock, per resuscitation council algorithms.

The trap: Giving verapamil for a broad-complex tachycardia presumed to be SVT with aberrancy; treat it as VT until proven otherwise. In irregular, broad, varying-QRS tachycardia (pre-excited AF), avoid all AV nodal blockers, including adenosine.

7. Complete heart block

Recognise: P waves and QRS complexes that bear no relationship to each other, with a regular slow escape rhythm. A narrow escape suggests a nodal level; a broad, slow escape suggests infranodal block and a less reliable rhythm.

Act now: Atropine as a first step, transcutaneous pacing, an isoprenaline or adrenaline infusion as a bridge, and temporary transvenous pacing. Look for reversible causes.

The trap: Repeating atropine in broad-complex escape, where infranodal block will not respond, and missing hyperkalaemia or AV nodal blocking drugs as the cause.

8. Acute pulmonary oedema

Recognise: Acute breathlessness, orthopnoea, crackles and hypoxia, frequently with high blood pressure; B-lines on lung ultrasound.

Act now: Sit the patient up, give oxygen if saturation is below 90%, start CPAP or non-invasive ventilation early, give IV furosemide and IV nitrates if systolic pressure exceeds about 110 mmHg. Identify the trigger: ACS, arrhythmia, acute mitral regurgitation, uncontrolled hypertension.

The trap: Routine morphine, which ESC guidance does not recommend routinely, and nitrates given without caution in hypotension, right ventricular infarction or severe aortic stenosis.

9. Hypertensive emergency

Recognise: Severe hypertension with acute organ damage: encephalopathy, retinal haemorrhages or papilloedema, pulmonary oedema, ACS, dissection, acute kidney injury, pre-eclampsia. The number alone does not define it.

Act now: Titratable IV therapy (labetalol, nicardipine, glyceryl trinitrate, depending on the organ involved) in a monitored setting. In most cases, lower mean arterial pressure by no more than about 25% over the first hours; dissection, pulmonary oedema and pre-eclampsia need faster, specific targets.

The trap: Sublingual nifedipine or precipitous lowering in asymptomatic severe hypertension, which risks stroke and myocardial ischaemia. Acute ischaemic stroke has its own thresholds.

10. Severe hyperkalaemia

Recognise: Potassium of 6.5 mmol/L or above, or any hyperkalaemia with ECG change: peaked T waves, PR prolongation, P-wave flattening, QRS widening, bradyarrhythmia, sine wave.

Act now: IV calcium gluconate 10% 30 mL over 5–10 minutes to stabilise the myocardium; insulin 10 units with glucose to shift potassium; nebulised salbutamol as an adjunct; then remove potassium by dialysis, binders or diuresis.

The trap: Believing calcium lowers potassium (it does not) and acting on a haemolysed sample without checking for pseudohyperkalaemia.

One habit that protects against all ten

Every trap above is an irreversible action taken on an unchallenged first impression. Before a thrombolytic, a heparin bolus, an induction agent, a litre of fluid or an AV nodal blocker, ask: what else could this be, and what happens if I am wrong? That thirty-second pause costs almost nothing.

For physicians who want to build these decisions into everyday practice, the structured 12-week Practical Cardiology Certificate for Physicians opens with its founding cohort on 23 November 2026.

This article is educational content intended for registered medical practitioners. It does not replace clinical judgement. Always follow your local protocols and current national and international guidelines when managing patients.