The deadly ECG patterns — the emergency department recognition and immediate management

A small, finite set of electrocardiographic patterns carry an immediate treatment implication — the catheter-lab activation, the antidote, the defibrillation, or the avoidance of a contraindicated drug. These are the deadly patterns. The Fellowship examiner will present one in a written stem, an OSCE resuscitation station, a data-viva, or a structured clinical discussion, and the candidate is expected to recognise it on the trace, name the underlying mechanism, state the disposition, and give the drug with the dose, route, and rationale. This topic catalogues the deadly patterns by mechanism — the acutely occluded coronary artery, the channelopathy, the electrolyte derangement, the right-heart-strain state, the ventricular tachyarrhythmia, and the sodium-channel-blocker cardiotoxicity — and gives the ECG-to-drug sequence for each.[1][5]

Why a pattern is "deadly"

A deadly ECG pattern is one of three things. It is the only sign of an occluded coronary artery in a patient who still has salvageable myocardium — the de Winter and Wellens patterns, the posterior and right-ventricular infarct, and the Sgarbossa-positive left bundle branch block or paced rhythm all represent an acute or threatened occlusion that does not reach the standard ST-elevation threshold and is therefore missed if the trace is read literally. It is the precursor to a ventricular arrhythmia — the Brugada type-1 pattern, the long QT, and the hyperkalaemic sine wave all predict imminent polymorphic VT, torsades, or asystole. Or it is the arrhythmia or the toxic state itself — ventricular tachycardia, torsades de pointes, and the wide-QRS sodium-channel-blocker state, where the wrong drug (verapamil, an AV-node blocker, a class Ia or Ic antiarrhythmic) kills the patient. The recognition step is binary — present or not — and the management step is a small committed set of doses. [1]

The STEMI territories — the occlusion that meets threshold

ST-elevation myocardial infarction is the prototype deadly pattern, and the territory localises the artery. Anterior infarction (ST elevation in V1 to V4) is the left anterior descending territory; a proximal occlusion produces extensive anterior loss, cardiogenic shock, ventricular fibrillation, and a risk of left-ventricular aneurysm and rupture. Inferior infarction (ST elevation in II, III, aVF, with the elevation in III greater than in II favouring the right coronary artery) is the right coronary or the circumflex; it carries a high risk of atrioventricular block and right-ventricular involvement, and a bradycardia or a hypotensive response to nitrates is a clue. Lateral infarction (I, aVL, V5, V6) is the circumflex and is frequently under-recognised because the absolute ST elevation is modest. Posterior infarction is the mirror image — horizontal ST depression in V1 to V3 with a tall R wave and an upright T wave, confirmed by direct ST elevation in posterior leads V7 to V9; it is the territory most often missed because it is read as "anterior ischaemia" rather than what it is, a posterior occlusion.[2] Right-ventricular infarction accompanies about a third of inferior STEMIs and is identified by ST elevation in right-precordial lead V4R; it is preload-dependent, nitrates precipitate profound hypotension, and the treatment is a fluid bolus with the patient monitored for pulmonary congestion.

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The STEMI-equivalents — occlusion that does not meet threshold

The standard STEMI threshold misses a substantial minority of acutely occluded arteries, which is why the modern concept of occlusion myocardial infarction (OMI) has replaced strict millimetre counting. Five patterns must be hunted for in any trace from a patient with chest pain or an anginal equivalent, because each represents an acutely or imminently occluded coronary artery. [1]

Hyperacute T waves are the earliest electrical sign of transmural ischaemia, appearing within minutes of occlusion and before ST elevation develops. They are broad-based, bulky, and asymmetric, and they dwarf the preceding R wave in the affected leads; in anterior ischaemia they appear in V2 to V4. They are missed because they are interpreted as "normal variant tall T" or hyperkalaemia — the differentiator is the bulky asymmetric morphology and the chest pain. [1]

De Winter T waves are a proximal LAD occlusion equivalent. The pattern is upsloping ST depression at the J point of 1 to 3 millimetres in the anterior precordials (V1 to V6, most striking in V2 to V3), with tall, prominent, symmetrical T waves and no ST elevation, and it is persistent rather than evolutionary.[1] It is treated as a STEMI and the catheter lab is activated — waiting for ST elevation to develop costs myocardium.

Wellens syndrome is the signature of critical proximal LAD stenosis in a patient whose chest pain has resolved by the time of the ECG — the resting trace is recorded in a pain-free window, which is precisely why it is missed. The two patterns are type A, deeply biphasic T waves in V2 and V3 (and often V1 to V4), and type B, deeply inverted symmetrical T waves in the same leads; both show preserved R waves and no pathological Q, and no or minimal ST elevation. The cardinal error is to send the patient for a stress test, which precipitates an acute occlusion and ventricular fibrillation. The correct management is urgent coronary angiography. [1]

Sgarbossa criteria apply to left bundle branch block and to a paced rhythm, where the standard ST-elevation thresholds are useless because the broad QRS itself displaces the ST segment. The original three Sgarbossa criteria, adapted and now refined by the Smith-modified third criterion, identify occlusion in this population with high specificity.[2] Concordant ST elevation — the ST vector points the same way as the dominant QRS — is the most specific (≈98 per cent). Concordant ST depression in V1 to V3 is the second. The third is excessively discordant ST elevation, defined by the original criterion as at least 5 millimetres, and by the Smith-modified criterion as a ratio of ST elevation to the depth of the S wave of at least 25 per cent (one quarter), which corrects for the depth of the underlying QRS.

Hyperacute equivalents in paced rhythm use the same Sgarbossa logic, and the paced Sgarbossa criteria carry comparable specificity to the LBBB version.[2]

The Brugada pattern — the coved type-1 trace

Brugada syndrome is an autosomal-dominent sodium-channel channelopathy (most commonly a loss-of-function SCN5A mutation) that produces a characteristic right-precordial pattern and a risk of polymorphic ventricular tachycardia and sudden cardiac death, typically in young and middle-aged men. Three patterns are described in V1 to V3, but only the type-1 pattern is diagnostic of the syndrome. [1]

The type-1 pattern is a coved ST elevation of at least 2 millimetres in at least one right-precordial lead (V1 to V3, recorded in standard or higher intercostal spaces), descending into a negative T wave. The type-2 pattern is a saddle-back ST elevation of at least 2 millimetres with a high takeoff, a trough of at least 1 millimetre, and a positive or biphasic T wave. The type-3 pattern is either morphology with ST elevation under 2 millimetres. Type-2 and type-3 are not diagnostic; they are converted to a type-1 by sodium-channel-blocker provocation (ajmaline, flecainide, procainamide) when the diagnosis is suspected. A spontaneous type-1 with symptoms (syncope, nocturnal agonal breathing, documented VT/VF) or a family history of sudden death under 45 confers a high arrhythmic risk and is an indication for an implantable cardioverter-defibrillator. [1]

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Hyperkalaemia — the progression from peaked T to sine wave

Hyperkalaemia is the electrolyte emergency with the most predictable ECG evolution, and the trace is the first — and often the only — investigation available before the laboratory returns. The progression reflects rising extracellular potassium and the inactivation of cardiac sodium channels.[3]

The treatment ladder matches the trace. Membrane stabilisation with calcium comes first in any patient with a widened QRS, a sine wave, or haemodynamic instability — calcium chloride 10 mL of 10 per cent (6.8 mmol) intravenously over 5 to 10 minutes, repeated as needed; calcium gluconate 30 mL of 10 per cent is an alternative if a central line is not available. Potassium shift into cells follows: insulin 10 units with 50 mL of 50 per cent dextrose intravenously (the dextrose prevents hypoglycaemia, monitor glucose for several hours), salbutamol 10 to 20 mg nebulised (a beta-2 agonist that drives potassium into cells), and sodium bicarbonate if there is coexistent acidosis. Potassium removal is then achieved with a gastrointestinal cation-exchange resin or, definitively, haemodialysis in the refractory or the renal-failure patient. ECG changes that resolve with calcium confirm the diagnosis at the bedside. [1]

Long QT and torsades de pointes

A long QT is the substrate for torsades de pointes, the characteristic polymorphic broad-complex tachycardia on a prolonged QT with a twisting of the QRS axis around the baseline, often in short self-terminating runs ("salvos") that can degenerate to ventricular fibrillation. The corrected QT is calculated by Bazett's formula (QTc equals QT divided by the square root of the R-to-R interval in seconds). The thresholds are over 440 milliseconds in men and over 460 milliseconds in women for abnormal, and over 500 milliseconds for high torsades risk. The risk is multiplicative — long QT plus a trigger (a premature ventricular beat, an electrolyte disturbance, a bradycardia) produces the arrhythmia. [1]

Torsades is treated with magnesium sulphate 2 g intravenously over 10 to 15 minutes regardless of the serum magnesium, withdrawal of the offending drug, and potassium correction to a high-normal level (4.5 to 5.0 mmol/L). A sustained or recurrent torsades is managed by overdrive pacing (transvenous or transcutaneous at a rate of 100 to 120 to shorten the QT) and isoprenaline for the bradycardia-dependent form. A defibrillator is applied from the outset because degeneration to ventricular fibrillation is treated with an unsynchronised shock.[4]

Pulmonary embolism — the right-heart-strain trace

The ECG is neither sensitive nor specific for pulmonary embolism, but in the right patient it carries the diagnosis. The commonest finding is sinus tachycardia. The classic but uncommon finding is the S1Q3T3 pattern (an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III), described by McGinn and White in 1935; it reflects acute right-heart strain with right-axis deviation and is most often seen with a massive or submassive embolus. The most diagnostically useful findings are new T-wave inversion in V1 to V4 (right-heart strain), right-axis deviation, a right-bundle-branch-block pattern (new or rate-related), an S wave in V1 with an R-prime, and new atrial fibrillation. The changes resolve as the embolus lyses or is lysed. The ECG in suspected pulmonary embolism is most valuable for excluding the alternative diagnosis (an anterior or inferior STEMI) and for risk-stratification — a trace showing right-heart strain plus haemodynamic compromise points to a massive embolus that may need thrombolysis or embolectomy. [1]

Ventricular tachycardia — the broad-complex tachycardia to assume

A regular broad-complex tachycardia (QRS at least 120 milliseconds, rate over 100) is ventricular tachycardia until proven otherwise, and the burden of proof is on the dissenting clinician. The features that confirm VT are the AV dissociation sign — independent P waves marching through the broad QRS complexes, visible on a long rhythm strip — the capture beat (a narrow normally-conducted QRS appearing among the broad ones, capturing the moment the AV node conducts through), and the fusion beat (a hybrid QRS that is a summation of a conducted and a ventricular beat). Concordance of the precordial QRS — all positive or all negative from V1 to V6 — and an extreme axis (northwest) also favour VT. The morphological criteria of Brugada and Griffith apply to V1 and V6 to distinguish VT from SVT with aberrancy. [1]

The stable regular broad-complex tachycardia receives amiodarone 300 mg intravenously over 20 to 60 minutes followed by an infusion (900 mg over 24 hours); the alternative for a clearly monomorphic stable VT is procainamide. The unstable regular broad-complex tachycardia — hypotension, shock, ischaemic chest pain, acute heart failure, or altered consciousness — is treated with synchronised cardioversion. The cardiac arrest dose of amiodarone for shockable VT or VF is 300 mg as an intravenous bolus, with a further 150 mg if required. Verapamil is absolutely contraindicated in any broad-complex tachycardia: it is a negative inotrope that has caused cardiovascular collapse and death when given for what was in fact VT. [1]

Sodium-channel-blocker toxicity — the wide QRS with R-prime in aVR

A wide QRS in the poisoned patient is sodium-channel blockade until proven otherwise, and the trace carries both the diagnosis and the antidote. The causative agents are the tricyclic antidepressants, the class Ia antiarrhythmics (quinidine, procainamide, disopyramide), the class Ic antiarrhythmics (flecainide, propafenone), the antihistamines (diphenhydramine), the antimalarials (chloroquine, hydroxychloroquine), carbamazepine, lamotrigine, lacosamide, and cocaine — all sodium-channel blockers, and all treatable with the same antidote.[5]

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The antidote is sodium bicarbonate: a 1 to 2 milliequivalent per kilogram intravenous bolus of 8.4 per cent sodium bicarbonate (typically 50 to 100 mL), repeated every few minutes until the QRS narrows (under 100 milliseconds), the R-prime in aVR resolves, the blood pressure improves, and the serum pH is between 7.45 and 7.55. It works by providing a sodium load (overcoming the channel blockade), alkalinising the blood (which traps the drug off the sodium channel), and correcting the acidosis that itself worsens channel blockade. Hyperventilation to a target pH of 7.45 to 7.55 augments the alkalinisation in the intubated patient. The unstable or arresting sodium-channel-blocker patient is treated with high-dose sodium bicarbonate, and intralipid is considered for the refractory case (the local cardiac-arrest protocol for the lipophilic sodium-channel blockers — bupivacaine, verapamil, and the local-anaesthetic-class drugs). [1]

Differential diagnosis — the patterns that masquerade as each other

The deadly patterns overlap on the trace, and the differential is the difference between the right antidote and a fatal misclassification. [1]

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The two trace-level distinctions that cost the most lives when missed are hyperacute T (ischaemia) versus peaked T (hyperkalaemia) — giving an LAD occlusion to a hyperkalaemic patient as "STEMI" delays calcium, and giving thrombolysis to a hyperkalaemic peaked T precipitates arrest — and sodium-channel-blocker VT versus structural VT — treating a sodium-channel-blocker wide-QRS with amiodarone alone (without bicarbonate) delays the antidote, while treating a true VT with verapamil collapses the ventricle. [1]

Immediate management and resuscitation — the ECG-to-drug sequence

The deadly patterns are treated at the bedside from the trace, and the doses are committed to memory because the unstable patient cannot wait for a lookup. [1]

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A stable regular narrow-complex SVT is treated with vagal manoeuvres, then adenosine 6 mg as a rapid intravenous bolus followed by a flush, escalating to 12 mg then a further 12 mg if the rhythm persists. Adenosine transiently blocks the AV node and terminates the re-entrant circuit; warn the patient of the brief flush, dyspnoea and chest tightness, and avoid it in asthma and high-grade block. A stable monomorphic VT receives amiodarone 300 mg intravenously over 20 to 60 minutes, with the unstable rhythm cardioverted synchronised. Torsades on a long QT receives magnesium sulphate 2 g intravenously, withdrawal of the offending drug, and potassium correction. Hyperkalaemia with a wide QRS or a sine wave receives calcium chloride 10 mL of 10 per cent intravenously for membrane stabilisation, then insulin with dextrose and a beta-agonist to shift potassium. Sodium-channel-blocker cardiotoxicity receives sodium bicarbonate to narrow the QRS and alkalinise the serum. [1]

Subtypes and scenarios — the patient who already has a confounder

The patient with a left bundle branch block, a paced rhythm, or a known channelopathy is the highest-risk group for a missed deadly pattern, because the baseline trace is already abnormal. In left bundle branch block and paced rhythm, occlusion is judged only by the Sgarbossa or Smith-modified Sgarbossa criteria — concordant ST change or excessively discordant ST elevation.[2] In known Brugada syndrome with fever, treat the fever aggressively (it unblocks the type-1 pattern and the arrhythmic risk) and monitor. In the dialysis patient with chest pain, hyperkalaemia and ischaemia coexist — the peaked T of hyperkalaemia can precede and obscure the ST elevation of an infarct, so calcium is given for the wide QRS and serial ECGs are taken. In the pregnant patient, adenosine, a synchronised cardioversion, magnesium, calcium, and sodium bicarbonate are all safe; thrombolysis is relatively contraindicated but used for life-threatening PE or STEMI when percutaneous intervention is not available.

Complications and pitfalls

The recurring errors with the deadly patterns are: reading a trace literally and missing the occlusion-equivalent (de Winter, Wellens, posterior, RV, Sgarbossa-positive) because the ST-elevation threshold is not met; giving a nitrate to an inferior STEMI before recording V4R and precipitating hypotension in an RV infarct; sending a Wellens patient for a stress test; treating a regular broad-complex tachycardia with verapamil; giving an AV-node blocker (adenosine, verapamil, beta-blocker, digoxin) to pre-excited atrial fibrillation and accelerating conduction down the accessory pathway to ventricular fibrillation; giving amiodarone alone — without bicarbonate — to sodium-channel-blocker cardiotoxicity; reaching for thrombolysis before excluding hyperkalaemia in a patient with peaked T waves and renal failure; and stopping the read at the first abnormality, missing a second. The discipline is to finish the systematic read on every trace and to compare with the previous one. [1]

Special populations

In the elderly, atypical presentations (breathlessness, syncope, confusion) and baseline ECG abnormalities (bundle branch block, paced rhythm, old infarcts) obscure the deadly pattern; a high index and serial traces are mandatory. In women, the STEMI threshold in V2 to V3 is lower (1.5 millimetres vs 2.0 in men over 40), and ischaemic T-wave inversion may be misread as normal variant. In children and young athletes, early repolarisation and the juvenile T-wave pattern overlap with hyperacute and ischaemic T waves — the clinical context and a comparison with a baseline trace settle the matter. In renal failure and on dialysis, hyperkalaemia is the first assumption for any arrhythmia or conduction abnormality; calcium first, then ask why. [1]

Evidence and regional guidelines

The modern concept of occlusion myocardial infarction, of which the de Winter and Wellens patterns are the prototypes, has displaced strict millimetre ST-elevation counting as the operational standard for catheter-lab activation.[1] The Sgarbossa criteria and the Smith-modified third criterion are the accepted method for diagnosing occlusion in left bundle branch block and paced rhythm.[2] The hyperkalaemia ECG progression is reproducible but imperfect — a normal ECG does not exclude a high potassium, and a borderline trace should not delay calcium in the unwell hyperkalaemic patient.[3] The QT-prolonging effect of antipsychotics is dose- and route-dependent and has been quantified in meta-analysis.[4] The wide-QRS sodium-channel-blocker state is treated with sodium bicarbonate by the ACMT (American College of Medical Toxicology) and the ANZ tox guidelines; intralipid is the rescue therapy for the refractory case.[5]

Digoxin toxicity — the scooped ST and the "reverse tick"

Digoxin is the cardiac glycoside that produces a characteristic repolarisation abnormality even at therapeutic levels, and a constellation of arrhythmias and conduction blocks at toxic levels. The pathognomonic trace finding is the downsloping, "scooped" ST-segment depression (the "sagging" or "reverse tick" sign, likened to Salvador Dalí's moustache) — most evident in the lateral leads with a small or negative T wave; it is a digoxin effect, not by itself toxicity, but it is the pattern the examiner expects the candidate to recognise and to contextualise against the clinical picture. [1]

The lethal toxicity is far subtler than the scoop. Digoxin inhibits the sodium–potassium ATPase, raises intracellular calcium (the inotropic effect), and directly suppresses atrioventricular nodal conduction; toxicity therefore expresses as a heightened automaticity coupled with AV block — the classic rhythm is atrial tachycardia with block (an atrial rate of 150 to 250 with a 2:1 or variable AV response), but also bidirectional ventricular tachycardia (alternating QRS axis, beat to beat — virtually pathognomonic), bradycardia with premature ventricular complexes, and high-grade AV block. The single most useful bedside clue to life-threatening toxicity is hyperkalaemia — digoxin poisoning drives serum potassium up by inhibiting the Na⁺/K⁺ pump, and a potassium above 5.0 mmol/L in the setting of digoxin predicts a high mortality and is itself a trigger for the antidote. [1]

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The antidote is the digoxin-specific antibody (Fab) fragment — the original ovine Fab (Digibind / DigiFab), which binds circulating digoxin and is renally excreted as the inactive complex.[10] The indications for Fab are life-threatening arrhythmia (ventricular tachyarrhythmia, symptomatic bradycardia or high-grade AV block unresponsive to atropine), hyperkalaemia above 5.0 mmol/L in acute overdose (the Fab corrects the potassium by restoring pump function), haemodynamic instability, and a serum digoxin above 10 ng/mL in the acute ingestion or above 6 ng/mL in the chronic setting. The dose is calculated from the ingested dose or from the steady-state serum concentration using the published nomograms; where these are unknown, an empirical loading dose (typically 5 to 10 vials in the acute, life-threatening presentation) is given. Atrial tachyarrhythmias may transiently worsen as the AV block is reversed, and the Fab is given in a monitored setting. Magnesium sulphate, and the avoidance of calcium (calcium may potentiate the intracellular calcium overload — though this is debated, it is a sensible caution in the examiner's mind), round out the supportive management. Cardioversion of a digoxin-toxic rhythm risks asystole and is a last resort — correct with Fab first.

[1] [1]

Wolff–Parkinson–White and pre-excitation — the delta wave and the short PR

The Wolff–Parkinson–White (WPW) pattern is the electrocardiographic signature of an accessory atrioventricular pathway (the bundle of Kent) that bypasses the AV node and pre-excites the ventricles. The three features are the short PR interval (under 120 milliseconds), the delta wave (a slurred upstroke of the QRS from the premature depolarisation of a small portion of ventricle through the pathway ahead of the AV node), and the broadened QRS (the fusion of the accessory-pathway and the normal nodal depolarisation). The pattern is common (about 1 to 3 per 1000) and most carriers are asymptomatic; the concern is the pre-excited tachyarrhythmia — atrioventricular re-entrant tachycardia (AVRT) and, the lethal one, atrial fibrillation conducting rapidly down the accessory pathway. [1]

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The lethal rhythm is pre-excited atrial fibrillation. Atrial fibrillation conducts down the accessory pathway, which (unlike the AV node) has no rate-limiting property — the ventricular rate can exceed 250 per minute, the broad irregularly irregular QRS with the delta wave degenerates to ventricular fibrillation, and sudden death is the well-described outcome in the young WPW patient. The cardinal error is to give an AV-nodal-blocking drug (adenosine, verapamil, diltiazem, a beta-blocker, or digoxin) — these block the AV node, preferentially funnel the atrial fibrillation down the accessory pathway, and accelerate the ventricular rate to ventricular fibrillation. Pre-excited atrial fibrillation is treated by synchronised cardioversion if unstable, or by an intravenous antiarrhythmic that blocks the accessory pathway (procainamide, flecainide, or amiodarone) if stable; the AV-node blockers are absolutely contraindicated. [1]

[1] [1]

Ventricular tachycardia versus SVT with aberrancy — the Brugada algorithm

A regular broad-complex tachycardia is ventricular tachycardia until proven otherwise, and the burden of proof is on the clinician who claims an SVT with aberrancy. The morphological and the structural criteria that distinguish the two are codified in the Brugada algorithm (not to be confused with the Brugada syndrome), a four-step flow with a high sensitivity for the diagnosis of VT.[6]

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The hyperkalaemia treatment ladder — the three-tiered response

The hyperkalaemia ECG progression is matched by a three-tiered treatment ladder that the candidate must recite by mechanism and by the dose: membrane stabilisation (to buy time), potassium shift (to lower the level), and potassium removal (for the definitive and the renal-failure patient).[3]

[1] [1]

The differential of the ST elevation — the territory that says the artery

The ST-elevation territory localises the occluded artery, and the candidate is expected to read the territory and to name the vessel. The five territories, with the vessel and the high-yield correlate, are: [1]

[1] [1] [1] [1] [1]

The landmark evidence — the trials and the consensus papers

[7] [1] [11]

Additional red flags

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Exam pearls

• A regular broad-complex tachycardia is VT until proven otherwise — give amiodarone 300 mg if stable, cardiovert if unstable, never give verapamil.
• De Winter and Wellens are anterior STEMI-equivalents — both represent a critical proximal LAD lesion and are treated as a STEMI activation; Wellens is recorded pain-free.
• Sgarbossa in LBBB and paced rhythm — concordant ST elevation, concordant ST depression in V1–V3, or excessively discordant ST elevation (at least 5 mm original, or at least 25 per cent of S-wave depth Smith-modified).
• Hyperkalaemia peaked T is narrow and symmetric; hyperacute T of ischaemia is broad and bulky. Calcium chloride 10 mL of 10 per cent for the wide QRS.
• Long QT over 500 ms is high torsades risk — give magnesium 2 g, stop the offending drug, correct potassium.
• Brugada type-1 is coved ST elevation of at least 2 mm in V1–V3 with a negative T wave — only type-1 is diagnostic; consider a phenocopy from fever or hyperkalaemia.
• Sodium-channel-blocker wide QRS with R-prime in aVR — give sodium bicarbonate 1 to 2 mEq/kg to narrow the QRS.
• Inferior STEMI — record V4R before nitrates; treat the RV infarct with fluid.
• Always compare with the old ECG — a borderline change that is new is the one that matters.
• Pre-excited atrial fibrillation (WPW) — irregularly irregular broad-complex tachycardia; never give AV-node blockers (adenosine, verapamil, digoxin), they funnel conduction down the accessory pathway to VF — cardiovert if unstable, procainamide / flecainide / amiodarone if stable.
• Digoxin toxicity — the scoop / reverse-tick ST is an effect, not toxicity; toxicity is the arrhythmia (atrial tachycardia with block, bidirectional VT, AV block) with a potassium above 5.0 — give the Fab fragments, never IV calcium.
• WPW pseudo-infarction — the delta wave can mimic an inferior or lateral STEMI; recognise the short PR and the slurred upstroke before activating the lab.
• Posterior STEMI — horizontal ST depression, tall R wave, upright T wave in V1–V3 (the mirror image); confirm with V7–V9; treat as a STEMI.
• The hyperkalaemia treatment ladder — membrane stabilisation (calcium chloride 10 mL of 10 per cent), then shift (insulin–dextrose, salbutamol, bicarbonate), then removal (dialysis); the calcium does not lower the potassium.
• The Brugada algorithm for the broad-complex tachycardia — no RS complex in the precordials, R-to-S over 100 ms, AV dissociation, morphology in V1/V6; sensitive but treat as VT when in doubt. [1]

[1]

Red flags

[1]

References

1. [1]de Winter RW, Verouden NJW, Wellens HJJ, et al. Precordial junctional ST-segment depression with tall symmetric T-waves signifying proximal LAD occlusion, case reports of STEMI equivalence J Electrocardiol, 2016.PMID 26560436
2. [2]Maloy KR, Bhardwaj A, Zimetbaum PJ, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers West J Emerg Med, 2010.PMID 21079708
3. [3]Quintero JA, Galvis LM, Saavedra AC, et al. Electrocardiographic Abnormalities in Patients with Hyperkalemia: A Retrospective Study in an Emergency Department in Colombia Open Access Emerg Med, 2024.PMID 38952854
4. [4]Berling I, Isoardi KZ, Lopresti D, et al. QT interval prolongation in acute antipsychotic poisoning: systematic review and recommendations Clin Toxicol (Phila), 2025.PMID 41255343
5. [5]Chua-Tuan JL, Hayes BD, Jani-Majewski P, et al. Cardiac sodium channel blockade after an intentional ingestion of lacosamide, cyclobenzaprine, and levetiracetam: Case report Clin Toxicol (Phila), 2015.PMID 25951877
6. [6]Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex Circulation, 1991.PMID 2022022
7. [7]Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report J Am Coll Cardiol, 1992.PMID 1309182
8. [8]de Zwaan C, Bär FWHM, Wellens HJJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction Am Heart J, 1982.PMID 6121481
9. [9]Tzivoni D, Banai S, Schuger C, et al. Magnesium therapy for torsades de pointes Am J Cardiol, 1984.PMID 6695782
10. [10]Smith TW, Haber E, Yeatman L, Butler VP. Reversal of advanced digoxin intoxication with Fab fragments of digoxin-specific antibodies N Engl J Med, 1976.PMID 943040
11. [11]Anselm DD, Baranchuk A, et al. Link between Brugada phenocopy and myocardial ischemia: Results from the International Registry on Brugada Phenocopy Pacing Clin Electrophysiol, 2019.PMID 30924150