A 57-year-old woman presents with crushing chest pressure and diaphoresis. The ECG shows ST elevation in V2 through V5 with reciprocal ST depression in III and aVF. V1 has slight elevation and aVL is involved. The QRS complexes are still narrow and there are no established Q waves.

A 66-year-old diabetic patient presents with diaphoresis and vague chest discomfort. The ECG shows ST elevation only in lead III, ST depression in multiple lateral and precordial leads, and ST elevation in aVR. Lead III looks abnormal but II and aVF do not meet classic inferior STEMI criteria.

A 59-year-old man presents with diaphoresis and epigastric pressure. The ECG shows ST elevation in II, III, and aVF with reciprocal ST depression in I and aVL. ST elevation is greater in III than II, and V1 has slight ST elevation. He becomes hypotensive after nitroglycerin given before arrival, prompting right-sided leads.

A 62-year-old man with hypertension arrives with an hour of left-sided chest heaviness radiating to the jaw. He is diaphoretic; blood pressure 148/90, heart rate 92. The monitor tech hands you the 12-lead and points to the inferior leads, where there is ST depression in III and aVF that first catches your eye. Scanning up to the high lateral leads, you see subtle ST elevation in I and aVL, and following across the precordium there is a hint of ST elevation with fattened, hyperacute T waves in V5 and V6. R wave progression is preserved and there are no Q waves yet. The prior ECG on file, from a clinic visit two years ago, is clean.

A 72-year-old man presents diaphoretic and hypotensive with chest pressure. The ECG does not meet classic STEMI criteria. Instead, it shows widespread horizontal ST depression in I, II, aVL, and V3 through V6 with 1.5 mm of ST elevation in aVR. He looks much sicker than the computer interpretation suggests.

A 52-year-old man with ischemic-sounding chest pain hands you his ECG. In the inferior leads there is ST elevation, but only a millimeter or so — not enough to satisfy your STEMI threshold. You are about to call it nonspecific when you notice lead aVL: a small but definite scoop of ST depression, the only lead truly reciprocal to the inferior wall. Nothing else jumps out. The rhythm is sinus, the QRS is narrow, and there are no established Q waves. The first troponin is pending and the man is still holding his chest. The overnight resident wants to admit him to the floor as an NSTEMI and wait for serial troponins.

A 62-year-old woman with diaphoresis and back pain has an ECG that shows ST depression of 2 mm in V1 through V3 with notably tall R waves in V1–V2 and upright T waves in those leads. Inferior leads show subtle ST elevation of about 1 mm in II, III, and aVF. The triage interpretation reads 'anterior ischemia' and no STEMI alert is called. Posterior leads V7–V9, placed at the request of the senior physician, show 1.5 mm of ST elevation. The cath lab is activated.

A 64-year-old man with inferior STEMI becomes hypotensive after a small dose of nitroglycerin. His lungs are clear and JVP is elevated. Right-sided ECG leads show ST elevation in V4R. The cath lab is already being activated, but the resuscitation plan changes immediately.

A 71-year-old man with a known left bundle branch block presents with chest pain. The old rule of 'new LBBB equals STEMI' has been retired, but ischemia in LBBB still has to be diagnosed somehow. On his ECG, lead III shows 2 mm of ST elevation in the same direction as a positive QRS — concordant ST elevation.

A 58-year-old man arrives at 0300 reporting two days of intermittent substernal pressure with exertion, each episode lasting ten minutes and resolving on its own. He has been pain-free for ninety minutes. Vitals are normal and he looks well — he is asking when he can leave. The triage ECG is read by the machine as 'nonspecific.' On a closer look, V2 and V3 show deep, symmetrically inverted T waves with preserved R wave progression and an isoelectric ST segment. There are no Q waves. The first troponin is 0.04 ng/mL.

A 47-year-old man arrives with crushing substernal chest pain that began forty minutes ago. The triage tracing shows no ST elevation. On a closer look, V2–V5 show prominent, symmetric, peaked T waves rising from upsloping ST depression of about 1.5 mm at the J point. There is small ST elevation in aVR. The pattern is identical on a repeat ECG five minutes later — it does not normalize between bursts of pain. Cardiology is paged.

A 57-year-old man presents with an hour of left-sided chest heaviness radiating to the jaw. He is diaphoretic, blood pressure 148/90. The triage ECG shows no elevation in the classic anterior or inferior clusters, so the machine reads it as nonspecific. Looking lead by lead, there is ST elevation in lead I and aVL, with a smaller bump in V2. Turn to the inferior leads and there is mirror-image ST depression and T wave inversion, most pronounced in lead III with reciprocal change also in aVF. Laid out on the 4x3 display, the elevation up top and the depression below trace out a distinctive flag-like shape. He remains in pain as the tracing prints.

A 60-year-old chronic smoker presents with mild chest pain and shortness of breath. He mentions an episode of severe chest pain about two weeks ago for which he never sought care. He is comfortable now, not diaphoretic, hemodynamically stable. His 12-lead shows ST elevation in the precordial leads with a concave contour, sitting over well-formed, deep QS-type Q waves. The T waves are conspicuously small relative to the tall QRS complexes rather than the fat hyperacute T waves you would expect early in occlusion. There is no reciprocal ST depression, and a prior ECG on the chart looks identical to today's tracing.

A 66-year-old woman with an hour of crushing chest pain and diaphoresis is brought to a resus bay. As the 12-lead prints, you make yourself read it by territory rather than lead by lead: the inferior group (II, III, aVF), the lateral group (I, aVL, V5-6), the anteroseptal precordium (V1-4), and aVR. You are looking for where a wave of ST elevation clusters and where reciprocal depression falls opposite it, so you can name the wall at risk before the troponin returns. The tracing in front of you shows changes concentrated in one of these groups, and the pattern is pointing you toward a specific culprit vessel.

A 64-year-old diabetic woman presents with 40 minutes of chest heaviness and nausea. She is tachycardic and diaphoretic but her pressure holds. The ECG shows flat, horizontal ST-segment depression across leads I, II and V4 through V6, each depression a half to one millimeter below baseline at the J point. In aVR the ST segment is instead elevated by more than a millimeter. The T waves in the lateral leads are shallow and inverting. A tracing from an hour earlier at triage looked different — these changes are new and evolving as you watch the monitor.

A 55-year-old man presents with anterior chest pain and a 'normal-looking' ECG. Closer inspection shows 1.5 mm of ST elevation in I and aVL, 1 mm of ST elevation in V2, and reciprocal ST depression with T-wave inversion in lead III.

A 68-year-old woman arrives with crushing substernal chest pain that began an hour after learning of her husband's sudden death. She is tearful, tachycardic, blood pressure 100/70. The ECG shows ST elevation across the precordial leads that looks, lead for lead, like an anterior STEMI. There are no reciprocal changes that reassure you and nothing on the tracing that reads as clearly non-ischemic. A troponin drawn at the bedside is mildly elevated. Her history has no prior cardiac disease, and the story is dominated by an overwhelming emotional shock rather than exertion. Looking at the tracing alone, you cannot say whether a coronary is occluded.

A 74-year-old woman with pneumonia presents tachycardic and short of breath. The ECG shows an irregularly irregular narrow-complex rhythm at 142 bpm with no consistent P waves and a fibrillatory baseline. Her blood pressure is stable, but she is febrile and hypoxic. The rhythm is real, but the infection is driving it.

A 61-year-old man presents with palpitations. The ECG shows a narrow-complex rhythm at 150 bpm that appears regular. The machine calls it sinus tachycardia. In the inferior leads, small negative sawtooth waves march through the baseline, with one buried in each QRS complex and one visible between complexes.

A 63-year-old man with crushing chest pain has repeated runs of wide-complex tachycardia with changing QRS morphology and axis. Between episodes, the QT interval is not prolonged, but there is anterior ST depression with aVR elevation. A second patient on methadone has similar twisting VT but a QTc of 610 ms. Same rhythm family, different treatment priorities.

A 28-year-old patient has sudden-onset palpitations while at rest. The ECG shows a regular narrow-complex tachycardia at 196 bpm. P waves are not clearly visible, and the QRS complexes are narrow and identical. The patient is anxious but normotensive.

A 44-year-old woman treated with methadone and ondansetron becomes lightheaded, then briefly loses consciousness. The monitor shows a rapid wide-complex rhythm whose QRS axis appears to twist above and below the baseline. Between bursts, the ECG shows a markedly prolonged QT interval with a long pause before the next run. She wakes up pale and diaphoretic as the rhythm self-terminates.

A 58-year-old patient with palpitations has a regular wide-complex tachycardia at 165 bpm. The team debates SVT with aberrancy because he is awake and talking. A closer look shows an extreme superior axis and no RS complexes in the precordial leads. There is no old ECG available.

EMS rolls in doing compressions. The monitor shows a chaotic irregular waveform without identifiable QRS complexes. There is no pulse. The team confirms pad contact and immediately defibrillates while CPR continues. After the shock, compressions resume before anyone stops to analyze the rhythm again.

A 69-year-old man with prior MI presents with palpitations and lightheadedness. The monitor shows a regular wide-complex tachycardia at 178 bpm. The QRS is very broad, concordant across the precordial leads, and occasional capture beats appear on the rhythm strip. His blood pressure is 92 systolic and he is increasingly diaphoretic.

A 62-year-old man is 40 minutes out from thrombolysis for an anterior STEMI and his chest pain has largely settled. On the monitor the rhythm becomes regular and broad, with a QRS well over 120 ms, running at about 75 per minute. There are no clearly conducted P waves in front of the wide beats; instead a dissociated P wave marches through independently, deforming an occasional complex. Every few beats a narrower, normally conducted complex breaks through, and one beat looks intermediate in width — a hybrid between the wide and narrow morphologies. He is warm, alert, and normotensive, asking whether he can sit up. The rate is too slow to call it tachycardia and too fast to call it an escape rhythm.

A 24-year-old man presents with the abrupt onset of palpitations and lightheadedness that began while lifting weights. Blood pressure is 108/70, he is alert. The monitor shows a regular narrow-complex tachycardia at 200 bpm. Studying V1, you find a small notch at the beginning of each T wave — a retrograde P wave sitting well after the QRS, giving a long RP interval. The QRS complexes are narrow, under 120 ms, and their amplitude varies slightly from beat to beat even though the baseline is steady. There are no clear delta waves during the tachycardia. He mentions he has been told before that his 'resting ECG looked unusual.'

An 80-year-old woman on digoxin for atrial fibrillation is brought in nauseated, confused, and unwell after several days of poor oral intake. On the monitor you catch a wide-complex tachycardia, and something about it is peculiar: every alternate beat looks different. Running a 12-lead, you see the frontal-plane QRS axis swing a full 180 degrees from one beat to the next — leftward, then rightward, then leftward again, a metronomic beat-to-beat alternation of the complexes. There is frequent multifocal ectopy scattered through the strip. She is hypotensive and lethargic but still perfusing. Her family mentions her kidney function has been declining and she 'takes a heart pill every day.'

A 62-year-old woman presents with a few hours of palpitations and mild breathlessness. She is comfortable, with a blood pressure of 128/76 and a regular pulse around 120. The 12-lead shows a narrow-complex tachycardia. Every QRS is preceded by a P wave, but the P waves look wrong: upright in V1 and inverted in the inferior leads II, III, and aVF. Their shape is identical from beat to beat, and the baseline between them is flat rather than sawtoothed. The QRS complexes themselves are normal. On the medication list is digoxin, and you note the ventricular response is slower than the atrial rate would suggest.

A 28-year-old man with no medical history presents with palpitations and lightheadedness that started at rest. He is alert and talking, blood pressure 108/70. The monitor shows a regular broad-complex tachycardia, but the QRS looks oddly narrow for a wide-complex rhythm — around 120 ms. There is an RBBB morphology with an RSR' in V1 and marked left axis deviation. Running the lead II rhythm strip, you catch occasional P waves that march through independently, and one beat mid-strip is suddenly narrow and early. The rate is fast and sustained, and he has had brief episodes like this before that resolved on their own.

An 80-year-old woman on digoxin for atrial fibrillation is brought in lethargic. The rate is regular at 60. The QRS complexes are narrow, under 120 milliseconds, and they march out at perfectly even intervals. The baseline, though, is not flat — it is a chaotic, irregular fibrillatory line with atrial activity far faster than the ventricles. Nowhere is there a consistent P wave tied to a QRS; the atrial chaos and the crisp regular ventricular rhythm are utterly dissociated. A once-irregular atrial fibrillation has become strikingly regular on the monitor.

A 74-year-old man with severe COPD is in respiratory distress from an exacerbation, on continuous nebulized beta-agonists and looking exhausted. The monitor shows a fast, irregular rhythm, and you order a 12-lead to sort out whether this is atrial fibrillation. On the tracing the rhythm is irregularly irregular at about 130 bpm — but there clearly are P waves, and they keep changing shape. Studying a single lead you count at least three distinct P-wave morphologies, each with its own PR interval, and the baseline between them is flat with no flutter waves. There is right axis deviation with a dominant R wave in V1. His potassium is low and he is tiring.

A 15-year-old girl is brought in by her parents for fatigue and feeling faint. She is thin and quiet; heart rate reads 35 on the monitor. The 12-lead shows a regular sinus rhythm — a normal upright P wave before every QRS in lead II — but the rate is strikingly slow. Scanning the precordial leads, you notice prominent U waves after the T waves. Blood pressure is low-normal and she is mentating well. Her parents mention she has been eating very little and has lost a lot of weight over the past several months.

A 78-year-old woman presents after a syncopal episode at home, now recovered but shaken, describing weeks of fatigue, dizziness and palpitations. Her telemetry tells a strange story: runs of a fast, narrow-complex junctional tachycardia around 140 bpm abruptly give way to profound slowing, with the sinus rate dropping from 40 bpm to nearly nothing and a pause stretching to six seconds before the next beat surfaces. At other moments there are stretches with no P waves at all for more than three seconds. She takes a beta-blocker and digoxin. Between episodes her rhythm looks almost ordinary, which is why three prior clinic visits found nothing.

A 34-year-old presents feeling their heart racing. On the monitor the rate is 150 and regular, with narrow QRS complexes. You look for P waves and at first can't find them — then you notice each T wave has an odd extra hump on its upstroke, a 'camel hump' where the P wave is buried in the preceding T. The rhythm is regular but not rigidly so, and it doesn't start or stop abruptly. The patient is warm and mildly diaphoretic. There is no bundle branch pattern, no delta wave — just a fast, narrow, regular tracing with hidden P waves.

A 76-year-old woman is brought in obtunded and profoundly bradycardic after feeling dizzy at home. Her blood pressure is barely palpable. The monitor shows a regular but extremely slow rhythm, around 25 bpm. Each beat is a wide QRS, well over 120 ms, with a left bundle branch appearance. On the 12-lead you can find occasional P waves marching at their own independent rate, bearing no consistent relationship to the broad complexes below them. There are no pacing spikes. The complexes are uniform and regular but agonizingly slow. You reach for her medication list and the potassium result while the nurse places pads.

A 74-year-old woman on digoxin for atrial fibrillation is brought in feeling nauseated and 'off,' with some blurred vision. She is stable, and the monitor shows a regular narrow-complex rhythm at about 80. On the 12-lead the QRS complexes are narrow, but the P waves are strange: inverted in the inferior leads II, III, and aVF and upright in aVR and V1, and they sit oddly close to the QRS — appearing just before some complexes, buried in others. In places the atria and ventricles seem to march independently. The rate is too fast for a normal junctional escape yet not a tachycardia, and vagal pressure barely nudges it.

A 74-year-old woman in known atrial fibrillation is on the monitor for palpitations. The rhythm is irregularly irregular, as expected. During one stretch a relatively long R-R interval is followed by a noticeably short one, and the beat that closes that short cycle comes out wide, with a right-bundle morphology — a tall secondary R in V1. The very next beats are narrow again. There is no fully compensatory pause around the wide complex, and the initial vector of that broad QRS looks the same as the surrounding conducted beats. She is asymptomatic and hemodynamically well throughout.

A 66-year-old man is being monitored during a run of regular wide-complex tachycardia. Scanning the strip, most of the beats are broad and uniform, but one complex stands out: it is neither as narrow as his baseline conducted beats nor as wide as the surrounding ectopics, sitting midway in both width and shape. A couple of beats nearby look fully narrow and normally conducted, as if the supraventricular impulse briefly won out. That single in-between complex is the clue — a supraventricular and a ventricular impulse have collided to stamp out one blended morphology on the tracing.

A 52-year-old presents with palpitations and a sensation of the heart 'skipping.' The underlying rhythm is sinus and regular. Interrupting it, early and unexpected, is a wide QRS complex of at least 120 milliseconds with a bizarre morphology unlike the sinus beats. Its ST segment and T wave point in the opposite direction to the main QRS deflection. There is no preceding P wave, and after the odd beat comes a pause — the next sinus beat arrives at an interval equal to double the normal R-R. Scanning the strip, a second early beat appears with a different shape from the first.

A 68-year-old woman on a beta blocker presents feeling intermittently 'skippy.' She is stable, with a pulse in the 60s. Her rhythm strip shows a run of normal sinus beats, then an abrupt gap where an entire P-QRS-T is missing, then the rhythm resuming on schedule. When you caliper it, the P waves before and after are otherwise regular, and the pause bracketing the absent P wave measures almost exactly twice the surrounding P-P interval. On a second strip you see a different pattern: the P-P intervals gradually shorten into a cluster before a P wave drops, giving the beats a grouped appearance.

A healthy 18-year-old man presents for a pre-participation sports evaluation with no complaints. Vitals are normal. His 12-lead shows a regular rhythm at 84 bpm. Each QRS is narrow, under 100 ms, and is preceded by a P wave that is upright in leads I and II and inverted in aVR. The PR interval is constant from beat to beat, and every P wave is followed by a QRS. The complexes are of normal amplitude with no ST or T wave abnormality. Nothing on the tracing departs from what you would expect in a well young adult.

A healthy 19-year-old has an ECG done before minor elective surgery. The rhythm looks irregular at a glance, and the automated read flags an 'irregular ventricular rate.' On inspection every P wave is a normal sinus P wave, upright in I and II, with identical morphology beat to beat. Each P wave is followed by a QRS at a constant PR interval. What varies is the spacing between beats: the P-P interval lengthens and shortens smoothly and cyclically, speeding up and slowing down in a rhythmic way that seems to track the patient's breathing. There are no premature P waves and no dropped beats.

A 76-year-old patient with dizziness has an ECG showing regular sinus P waves at 75 bpm. Most P waves conduct with a constant PR interval, but every third P wave is suddenly not followed by a QRS complex. The conducted QRS complexes are wide with a right bundle branch block morphology. There is no progressive PR lengthening before the dropped beat.

An 82-year-old man presents with weakness and near-syncope. The ECG shows P waves marching through at 80 bpm while the QRS complexes appear independently at 32 bpm. The PR intervals vary randomly because the atria and ventricles are not communicating. His blood pressure is 84/48 and he looks gray.

A 66-year-old man presents with an hour of central chest pressure and diaphoresis. He is pale but hemodynamically stable. The ECG shows a broad QRS with an RSR' pattern in V1 through V3 and slurred S waves in the lateral leads — a right bundle branch block. Layered on top, the frontal axis is markedly leftward, with a dominant negative deflection inferiorly. Looking closer at the precordium there are concordant ST-segment changes best seen in V2 and the inferior T waves look fuller and more peaked than they should. No lead meets a millimeter threshold for classic ST elevation. The pain persists as the tracing prints.

A 60-year-old man with well-controlled hypertension comes in after a minor fall and gets a routine ECG. He is asymptomatic, hemodynamically normal, and the tracing is otherwise unremarkable. Every P wave is followed by a QRS, and the rate and rhythm are regular — but the PR interval is strikingly long, well beyond five small squares, and constant from beat to beat. On careful inspection some of the P waves are almost lost in the upstroke of the preceding T wave. There is no dropped beat and no progressive lengthening; the conduction delay is fixed across the entire strip.

A 70-year-old woman with hypertension and aortic stenosis presents with chest pressure. Her vitals are stable. The 12-lead shows a wide QRS, clearly beyond 120 ms. In V1 there is a deep, dominant S wave with only a tiny initial R wave; in leads I, aVL, and V5-V6 there is a broad, notched, M-shaped R wave with no preceding Q waves. R-wave progression across the precordium is poor and the axis is leftward. In the lateral leads with the tall R waves you see some ST depression and T-wave inversion, while the right precordial leads with deep S waves carry a modest amount of ST elevation. You study the proportions of those ST shifts against the QRS.

A 62-year-old man with risk factors presents with an hour of central chest pain. He is diaphoretic, and the pain is ongoing. The QRS is broad, beyond 120 ms. Lead V1 shows an M-shaped RSR' with a tall, broad secondary R wave, and leads I and V6 carry wide, slurred terminal S waves. The right precordial leads show some ST and T-wave change, but in V2 the ST shift looks concordant rather than discordant, and the inferior T waves are tall and bulky. A prior ECG on file, the nurse notes, had a normal QRS width. The pain has not eased.

A 55-year-old man is brought in obtunded after a suspected overdose. He is hypotensive and poorly responsive. The ECG shows a broad QRS — clearly beyond 100 ms — but the morphology fits no clean template: there is no RSR' in V1 to call it a right bundle block, and no dominant broad S in V1 with a notched R in V6 to call it a left bundle block. The complex is just widened and bizarre across the precordium. The rate is a touch fast and the terminal forces look prolonged. Nothing about the QRS conforms to a typical bundle-branch pattern.

A 68-year-old man presents for evaluation of exertional chest discomfort. He is hemodynamically stable and the rhythm is regular sinus. On the 12-lead the frontal axis is markedly leftward, between -45 and -90 degrees. Leads I and aVL show qR complexes with small Q waves and tall R waves, while the inferior leads II, III and aVF show rS complexes with small R waves and deep S waves. The QRS duration is only slightly prolonged, around 100 ms. The R wave in aVL peaks late, its onset-to-peak time exceeding 45 ms, and the limb-lead voltages look generous. There is no ST-segment strain pattern in the lateral leads.

A 70-year-old man presents with dyspnea. His ECG shows a markedly rightward frontal axis: leads I and aVL are dominantly negative while II, III, and aVF are dominantly positive. Looking at the morphology, leads I and aVL show rS complexes with small R waves and deep S waves, and the inferior leads show qR complexes with small Q waves and tall R waves. The QRS is only slightly widened, and the R-wave peak time in aVF looks prolonged. There is no chest wall deformity, and you have no prior tracing to compare against as you work through why his axis has swung so far right.

A 78-year-old man presents after a syncopal episode. He is now alert, bradycardic in the low 30s, and mildly lightheaded. The ECG shows a broad QRS with an RSR' in V1 typical of right bundle disease and a markedly leftward axis. The P waves march out at their own rate, and the QRS complexes come slower and entirely independently — there is no consistent relationship between atria and ventricles. The escape complexes carry that same right-bundle-plus-left-axis appearance. Across the strip the atria and ventricles beat on separate clocks.

A 71-year-old man with a known ventricular aneurysm and heart failure presents with fatigue and near-syncope. He is stable but bradycardic. The QRS is broad. In the precordial leads V1–3 there is a clear RSR' pattern typical of right bundle disease. But look at the limb leads and the picture changes: lead I has almost no S wave at all, the axis is markedly leftward with QS complexes in II, III, and aVF, and aVL shows an M-shaped complex resembling a left bundle pattern. The two territories seem to be telling different stories on the same tracing.

A 24-year-old man is brought in with palpitations, chest tightness, and lightheadedness that began abruptly an hour ago. He is anxious, diaphoretic, and pale, with a blood pressure of 96/58. The monitor shows a wide, chaotic tachycardia. The 12-lead is a rapid, irregular, broad-complex rhythm with an overall rate around 200 and stretches touching 300 in places — far too fast to be conducted through the AV node. The QRS width shifts subtly from beat to beat, and the axis stays fixed rather than rotating. Scattered among the wide beats are a couple of narrower complexes in the right precordial leads. It looks almost like a polymorphic ventricular rhythm, but there is no twisting envelope.

A 23-year-old man presents with palpitations. His baseline ECG shows a PR interval under 120 ms, a slurred upstroke at the beginning of the QRS, and a mildly widened QRS complex. Later, he develops an irregular very rapid wide-complex rhythm with beat-to-beat QRS variation, and the monitor alarms.

A 24-year-old man presents after a self-terminating episode of palpitations, now asymptomatic with normal vitals. His resting 12-lead is unusual: the PR interval is strikingly short, under 120 ms, and the initial upstroke of each QRS is not sharp but slurred, rising slowly before the complex takes off. The QRS is broadened, though not as wide as a bundle branch block, and the ST segments and T waves point opposite to the main QRS deflection. There is a dominant R wave in V1 with T-wave inversions in the right precordial leads, and a negative deflection at the start of the complex in aVL that could be mistaken for an old lateral Q wave.

A 40-year-old woman presents after a self-terminating run of rapid palpitations, her third this year. Between episodes she feels well, with normal vitals. Her resting 12-lead shows a strikingly short PR interval, under 120 milliseconds, but the P-wave axis is normal and the QRS is narrow and entirely normal in shape — there is no slurred upstroke, no delta wave to be found on careful inspection of every lead. The tracing looks almost ordinary apart from that tight PR. The story of recurrent paroxysmal tachycardia is what makes the short PR interesting rather than incidental.

A 32-year-old man presents after a syncopal episode. His father died of a cardiac arrest in his early 40s. He is afebrile and looks well. The ECG shows V1 and V2 with a coved-shape ST elevation of 2.5 mm, an inverted T wave, and a pseudo-RBBB pattern. The pattern is unchanged on a repeat tracing.

A 36-year-old woman presents after syncope while taking escitalopram, hydroxyzine, and azithromycin for a respiratory illness. Her ECG shows a QTc over 560 ms with broad-based T waves and a pause-dependent premature ventricular beat. Potassium returns at 3.1 mmol/L and magnesium is low. She is currently awake.

A 22-year-old soccer player collapses on the field, is briefly unconscious, and walks into your ED insisting he is fine. He mentions his cousin died suddenly in his twenties. Vitals are normal. His resting 12-lead shows deeply inverted T waves across V1, V2, and V3, yet the QRS is not broad in the way a bundle branch block would make it, and there is no RSR' pattern. Looking closely at the terminal QRS in V1 you can make out a small, low-amplitude deflection riding just after the S wave, before the ST segment. The precordial S waves rise sluggishly. On the monitor you catch a run of broad-complex beats with a left bundle pattern and an inferior axis.

A 28-year-old man presents after a syncopal episode and a scare of rapid palpitations. He is healthy, athletic, and has no structural heart disease on prior evaluation; a maternal uncle died suddenly in his thirties. Vitals are normal. His 12-lead catches your eye because the interval from the QRS to the end of the T wave looks unusually compressed, with a very short or almost absent ST segment. The T waves are tall, narrow, and peaked, most striking across the precordial leads. On a rhythm strip taken while his heart rate slowed into the 60s, the short interval does not lengthen the way you would expect. You pull his old tracings to compare.

A 46-year-old woman presents with chest pain, and her ECG raises immediate alarm: concave-upward ST depression spread across at least seven leads — I, II, aVL, aVF and V2 through V6 — with reciprocal ST elevation in lead aVR. It looks exactly like the left-main-insufficiency pattern that would send you racing to the cath lab. But the story doesn't fit: serial troponins are flat, and when the angiogram comes back it is pristine, with no coronary disease and no ischemia. Digging up an old ECG from years earlier, you find the identical pattern, unchanged. On close inspection there is a subtle notch in the ascending limb of the ST segment in V3-4. Her father died suddenly and young.

A 68-year-old dialysis patient arrives weak and nauseated after missing dialysis. The monitor shows a slow wide-complex rhythm. The 12-lead has tall narrow-based T waves that look too sharp for ischemia, PR prolongation, flattening P waves, and a QRS that is beginning to widen in the precordial leads. The nurse is waiting for the chemistry panel.

A 62-year-old woman on chronic furosemide presents with palpitations and generalized weakness after a week of vomiting. Heart rate is 96, blood pressure normal. The monitor shows frequent ventricular ectopics. On the 12-lead, the T waves are strikingly flat and the precordial leads V2 and V3 carry tall, rounded humps riding just after each T. There is widespread ST depression. The computer flags a markedly prolonged QT, but on close inspection the T and U waves have fused into a single long deflection with no clear separation. The P waves look taller than expected and the PR interval is stretched. While you are reading the tracing, a run of polymorphic ventricular beats crosses the strip.

A 41-year-old man with known parathyroid disease is brought in critically unwell — confused, dehydrated, and profoundly weak. While the nurse hangs fluids you glance at the monitor and the 12-lead. The QRS complexes look strange and misshapen, and the interval from the QRS to the end of the T wave is strikingly compressed — the T wave seems to sit almost on top of the QRS with barely any ST segment between them. In lead V1 there is a notch on the terminal portion of the QRS complex. The stat chemistry panel is still pending, but you know a J-wave notch and a QT this short in a sick patient is a warning. Moments later the rhythm degenerates on the monitor.

A 45-year-old woman who had a thyroidectomy weeks ago presents with tingling around the mouth, cramping hands, and intermittent muscle spasms. Her fingers draw into a claw when the blood-pressure cuff inflates. Vitals are stable. The ECG is in sinus rhythm, but the QTc measures around 500 ms. Looking closely, the prolongation comes from a markedly lengthened, flat ST segment that pushes the T wave later and later; the T wave itself is normal in shape and width. There are no U waves and no ectopy, just that stretched isoelectric segment between the QRS and an unremarkable T.

A 76-year-old man presents with palpitations. He is intermittently symptomatic and looks anxious but perfused. The 12-lead shows sinus rhythm with a markedly prolonged QTc measured at 510 ms and a slightly long PR interval. Over a few minutes on the monitor you catch frequent ventricular ectopics and then a short run of nonsustained polymorphic ventricular tachycardia that self-terminates. His serum potassium and calcium are pending. The QRS duration and ST segments look unremarkable. As you are drawing up your plan, the monitor alarms again — this time the run is longer and the patient briefly loses consciousness before it breaks.

A 54-year-old unhoused patient is found outside overnight and arrives confused with a core temperature of 29°C. The ECG shows sinus bradycardia, a prolonged PR and QT interval, and prominent positive deflections at the J point in the inferior and lateral leads. The monitor intermittently shows atrial fibrillation with a slow ventricular response.

A 45-year-old patient is brought in after ingesting an unknown number of propranolol tablets. The ECG shows sinus bradycardia with a prolonged PR interval. The patient is hypotensive and then has a generalized seizure. A repeat ECG shows QRS widening.

A 52-year-old patient arrives altered and hypotensive after a suspected overdose. The ECG shows sinus bradycardia with first-degree AV block that progresses to junctional bradycardia. Glucose is 340 despite no diabetes history.

An 82-year-old woman on digoxin and a diuretic for atrial fibrillation is brought in with two days of nausea, vomiting, and vague visual disturbance — she keeps mentioning that lights look yellow. She is bradycardic at 44 and mildly confused. The monitor shows an atrial rate around 150 with regular P waves, but only one QRS conducts for every four atrial beats, and frequent wide premature complexes interrupt the rhythm. On another strip her underlying fibrillation has become strikingly regular at a slow rate, with a narrow escape rhythm marching out independently. The rhythm keeps shifting between these patterns as you watch.

A 29-year-old patient is brought in somnolent after an unknown ingestion. The ECG shows sinus tachycardia with a QRS of 142 ms, a tall terminal R wave in aVR, and a slurred S wave in lead I. Blood pressure is soft and the patient has intermittent ventricular ectopy. The pill bottle history is unclear.

A 70-year-old woman on long-standing digoxin for atrial fibrillation comes in for a pre-operative evaluation, entirely asymptomatic. Her ECG catches your eye: across the lateral leads V4-6, I and aVL, the ST segments sag downward in a smooth downsloping curve that looks like a reverse tick — a shape someone once dubbed Salvador Dali's moustache. The T waves are biphasic, dipping negative first and then rising to a small terminal peak continuous with the depressed ST segment. The QT interval looks short, the PR is mildly long, and there are prominent U waves. You find yourself wondering whether this tracing is telling you she is poisoned.

A 51-year-old woman with sudden dyspnea, pleuritic chest pain, and syncope has an ECG showing sinus tachycardia, a new right bundle branch block, right-axis deviation, and deep T-wave inversions in V1 through V4 and lead III. The classic S1Q3T3 pattern is present but subtle. Bedside echo shows RV dilation.

A 67-year-old woman presents with acute dyspnea and pleuritic chest pain after a long flight. She is tachycardic and hypoxic on room air. The 12-lead shows T wave inversions across the right precordial leads V1 to V4, and simultaneously in the inferior leads, most pronounced in lead III. The axis is deviated rightward and V1 carries a dominant R wave with a deep S wave persisting into V6. There is downsloping ST depression in the same right-sided leads. The left-sided leads I, aVL, V5 and V6 are relatively spared. She looks unwell and her heart rate is climbing.

A 70-year-old man with a long smoking history presents with worsening breathlessness. He is barrel-chested, tachycardic, and using accessory muscles. The 12-lead shows a vertical QRS axis around +90 degrees. The P waves are peaked and tall in the inferior leads but flattened and inverted in leads I and aVL, sitting on a rightward axis. The precordial leads show delayed R/S transition with clockwise rotation and near-absent R waves in V1 to V3. The QRS voltages are strikingly low over the left precordium in V4 to V6, and the PR and ST segments sag below the baseline. On the rhythm strip you notice the rate is irregular, with the P waves changing shape from beat to beat.

A 54-year-old woman with longstanding dyspnea on exertion has an ECG done for palpitations. The frontal axis is swung far to the right, around +150 degrees. In V1 the QRS is dominated by a tall R wave over 7 mm with an R/S ratio greater than 1, while V6 shows a correspondingly deep dominant S wave. The right precordial leads V1-4 carry down-sloping ST depression with T wave inversion, and the same strain pattern reaches into the inferior leads. The P wave in lead II is tall and peaked at over 2.5 mm. The QRS is not wide enough to be a bundle branch block. The overall picture is of a right-sided chamber under strain.

A 58-year-old woman with longstanding COPD presents with worsening dyspnea and leg swelling. Her ECG shows sinus rhythm, and the P waves catch your eye: in the inferior leads (II, III, aVF) they are tall and sharply peaked, taller than 2.5 mm, rather than the usual gentle dome. In V1 and V2 the P wave is also prominent, exceeding 1.5 mm. The QRS and ST segments look unremarkable, but the atrial signal alone is telling you the right heart is under strain as you consider what is driving her presentation.

A toddler is brought in by worried parents after a brief unexplained spell. The child is now playful and well-perfused, with vitals that look reasonable for age. A 12-lead is obtained with pediatric lead placement, and the tracing looks nothing like an adult's: the proportions, the axis, and the wave amplitudes are all shifted from what you are used to reading at 3 a.m. on grown patients. Reflexively applying adult thresholds, one of the residents flags several 'abnormalities.' You pause before deciding whether the tracing is normal for this child's age or whether it is pointing at something real underneath.

A 78-year-old with a dual-chamber pacemaker arrives feeling faint and short of breath. Heart rate is 38 and blood pressure is soft. The monitor shows a P wave before each QRS, and tiny pacing spikes march out ahead of the ventricular complexes, most visible in V3 through V6 and again in I, aVR and V1. But the spikes are not followed by a QRS — the ventricle does not respond. The native P waves themselves fail to reach the ventricles, and between the dropped paced beats there is a long, silent pause before an escape complex crawls through. The spike is there; the depolarization is not.

An 82-year-old man with a dual-chamber device comes in for a fall. Vitals are stable. On his 12-lead you see, before each beat, a pair of sharp vertical spikes of very short duration — one preceding a small P wave, a second preceding the QRS. Each atrial spike is followed by a P wave and each ventricular spike by a broad QRS, beat after beat. The QRS complexes are wide with a left bundle branch look, and the ST segments and T waves point in the opposite direction to the main QRS deflection. A couple of complexes in the middle of the strip are narrower and shaped differently, without the same relationship to the spikes. The rhythm is regular and the rate is adequate.

A 48-year-old cancer patient presents with dyspnea, tachycardia, and hypotension. The ECG shows low-voltage QRS complexes and beat-to-beat alternation in QRS amplitude and axis. The chest x-ray shows an enlarged cardiac silhouette, and a bedside echo is performed.

A 31-year-old man presents with sharp pleuritic chest pain that improves when leaning forward. The ECG shows diffuse concave ST elevation in I, II, aVL, aVF, and V2 through V6 with PR depression in multiple leads and reciprocal PR elevation in aVR. There is no focal reciprocal ST depression except in aVR and V1.

A 24-year-old man is sent in from a walk-in clinic after an ECG done for palpitations showed 'ST elevation.' He feels well, has no chest pain, and his vitals are normal. On the tracing there is widespread concave ST elevation, most prominent across the mid-to-left precordial leads V2-5, with smaller elevation in the inferior limb leads. Look closely at V4 and there is a notch at the J point — a small hook where the QRS meets the ST segment. The T waves are tall, peaked and slightly asymmetrical, concordant with the QRS. In V6 the ST elevation is dwarfed by the T wave. There is no reciprocal ST depression anywhere.

A 30-year-old man presents after several episodes of exertional lightheadedness and palpitations. He is well-appearing now, with normal vitals. His 12-lead meets voltage criteria for left ventricular hypertrophy across the precordial and limb leads, with nonspecific ST-segment and T-wave changes riding along. In the lateral leads I, aVL, and V5-6 there are deep but strikingly narrow Q waves, each under 40 milliseconds wide, with a couple echoed inferiorly. The computer, and even the reviewing team, are drawn to the words 'lateral infarct, age undetermined.' The R waves are tall, the young man looks fit, and he is asking to go home.

A 68-year-old man with long-standing hypertension and a harsh systolic murmur presents with exertional breathlessness. He is stable. The ECG shows enormous QRS voltages: the S wave in V2 and the R wave in V5 together far exceed 35 mm, and adjacent precordial complexes overlap each other. R-wave peak time in V5–6 is prolonged with some QRS broadening. In the lateral leads — I, aVL, V5–6 — there is downsloping ST depression with T-wave inversion, while V1–3 show ST elevation proportional to the deep S waves. The axis is leftward and prominent U waves appear in the right precordial leads.

A 71-year-old woman is placed on the monitor for palpitations and the printed 12-lead looks alarming. Lead I is completely inverted — P wave, QRS, and T wave all pointing down — aVR has become upright, and there is marked right axis deviation. At a glance it suggests dextrocardia or a strange ectopic rhythm. But the precordial leads march out with entirely normal R wave progression across V1 to V6. On a second tracing from a different day, instead lead II records as a perfectly flat line at zero, while aVR and aVF look identical to each other. The patient is comfortable and asymptomatic, and the nurse is reaching to re-check the cables.

A 58-year-old woman presents with progressive dyspnea and chest heaviness. She is tachycardic at 118, blood pressure 96/68, and looks uncomfortable sitting forward. The 12-lead is unremarkable at first glance, but every QRS complex is tiny — under 5 mm in all the limb leads and under 10 mm across the precordium. Then you notice the R wave height marches up and down from beat to beat, a regular alternation in complex amplitude against a steady rhythm. The rate is fast, the voltages are small, and the complexes are swinging. Her neck veins are full and the heart sounds are muffled.

A 24-year-old presents with pleuritic chest pain and dyspnea a week after a flu-like illness. Heart rate is 118, and he looks more unwell than a simple viral syndrome should make him. The ECG shows a sinus tachycardia with nonspecific ST segment and T wave changes that don't fit a single coronary territory. In another young patient with the same story, the tracing instead shows widespread concave ST elevation across multiple leads — the pattern of pericardial inflammation. Elsewhere the QRS looks slightly prolonged and the QT stretched, and there are scattered T wave inversions. The rhythm strip catches a run of ventricular ectopy. Nothing on the tracing is diagnostic on its own.

A comatose 55-year-old woman is wheeled in after a sudden collapse preceded by the worst headache of her life. She is unresponsive with a sluggish pupil, and the monitor shows a slow heart rate. The 12-lead is dramatic: deep, giant, symmetric T-wave inversions sprawling across nearly every lead, with a grossly prolonged QT interval measuring around 600 ms. The T-wave morphology looks unsettlingly like an anterior ischemic pattern, but the patient has no chest pain — she has no history you can obtain at all. There is a whisper of ST depression in a couple of leads. The bradycardia is new and deepening.

A 40-year-old man presents for an unrelated complaint and a routine ECG is done. The machine flags it as abnormal. Lead I is upside-down: the P wave, QRS, and T wave are all inverted — global negativity. aVR, which is normally negative, shows an upright P wave, positive QRS, and upright T wave. Across the precordium the expected growth of the R wave never happens; instead there are dominant S waves from V1 through V6. The frontal axis is markedly rightward. The patient is asymptomatic and unaware of any cardiac history.

A 58-year-old man presents with weeks of worsening dyspnea, orthopnea and ankle swelling. He is tachypneic with crackles at both bases. The ECG shows tall precordial voltages meeting criteria for left ventricular hypertrophy, with a downsloping ST depression and asymmetric T-wave changes in the lateral leads. The limb leads, by contrast, look relatively small in amplitude. In V1 the P wave has a broad, deep terminal negative component, and across V1 through V4 the R waves fail to build, leaving QS complexes that look like an anterior scar. The QRS is broad, approaching a bundle branch pattern but not quite typical.

A thin, tremulous 34-year-old woman presents with palpitations, heat intolerance, and weight loss over two months. She is anxious and diaphoretic. Her heart rate is 132. The 12-lead shows an irregularly irregular rhythm with no discernible P waves and a rapid ventricular response. The QRS voltages are tall enough to meet criteria for left ventricular hypertrophy, yet there is no accompanying ST depression or T-wave inversion of a strain pattern. Scattered through the tracing are nonspecific ST and T-wave changes and an occasional early wide beat. You note her staring gaze and the fine tremor of her outstretched hands as you order labs.

A 79-year-old man is referred to the ICU with coma, hypothermia, and hypotension that is not responding to inotropes. He is profoundly bradycardic. The admission 12-lead confirms a heart rate around 30. The QRS complexes are strikingly small in amplitude, especially in the limb leads, and there are widespread T-wave inversions across the tracing without accompanying ST-segment shift. The QT looks long. Nothing on the ECG points to an acute coronary event, and the low voltages and diffuse T-wave changes together give the tracing a flat, blunted appearance out of keeping with a primary cardiac catastrophe.

A 55-year-old man with known cardiomyopathy presents with worsening exertional dyspnea. He is stable in sinus rhythm. On the 12-lead the P waves in lead II are both tall and broad — a bifid complex at least 2.5 mm in amplitude and over 120 ms wide. In V1 the P wave is distinctly biphasic, with a tall initial positive deflection nearly 3 mm high followed by a deep, wide terminal negative component exceeding 1 mm in depth and 40 ms in duration. The notched, prolonged P waves carry through to V5 and V6. The rest of the tracing reflects his underlying disease.

A 6-year-old with a known ventricular septal defect comes in for a febrile illness and gets a screening ECG. The tracing shows enormous QRS voltages, and across the mid-precordial leads V2-5 the complexes are large and biphasic — tall R waves stacked over deep S waves in the same leads. There are voltage criteria that would satisfy LVH, yet there are also persistent deep S waves carried out to V5-6 and peaked P waves in lead II. The forces seem to be pulling in both directions at once, and no single hypertrophy pattern fully explains what you are seeing.

A young, healthy man has an ECG for a pre-participation physical. The tracing is otherwise unremarkable, but at the junction where each QRS ends and the ST segment begins, the baseline sits slightly above the isoelectric line. In several precordial leads there is a subtle notch or slur at that terminal-QRS-to-ST transition, lifting the takeoff of the ST segment upward. There is no chest pain, no reciprocal change, no evolution on a repeat tracing. The elevation is at the very junction point, not a discrete separate wave, and the young man feels completely well.

A 63-year-old woman with exertional dyspnea and a soft diastolic murmur has a 12-lead recorded. The rhythm is sinus, but the P waves draw the eye. In lead II each P wave is broad, running beyond 110 ms, and clearly bifid — two humps separated by more than 40 ms, an M-shaped 'P mitrale'. Over in V1 the P wave is biphasic, and its terminal negative portion is both wide, more than 40 ms, and deep, dipping over 1 mm below baseline. The QRS and ST segments look unremarkable. Everything abnormal here lives in the P wave.

A 68-year-old man presents for a routine pre-operative evaluation, asymptomatic. Vitals are unremarkable. On his 12-lead you run the quick axis check: lead I shows a clearly dominant, upright R wave, while leads II, III, and aVF each show a dominant downward S wave. Lead aVL, like lead I, is upright. Putting those together, the frontal-plane QRS axis sits more negative than -30 degrees. The QRS duration itself is normal and there are no acute ST-segment changes. You look back through the rest of the tracing for the features that would tell you which of several causes is responsible.

A 60-year-old man with long-standing COPD presents short of breath. Working through his 12-lead systematically, you check the axis: the QRS is upright with a dominant R wave in leads II, III and aVF, but in lead I the complex is predominantly negative, a deep S wave dragging it below the baseline. Lead aVL is negative as well. Estimating the frontal-plane vector on the hexaxial system puts the axis past +90 degrees, swung rightward. The rest of the tracing shows a tall R wave in V1. He is tachypneic and hypoxic, and you are trying to decide whether this axis is his chronic lung disease talking or something acute.