ECG Syllabus
Curriculum Pearls Must-Know 23 Tracing Library & Quiz ↗
PANCE · PANRE · ECG Curriculum · Tracing Library

ECG
Interpretation

A competency-based ECG curriculum and a visual library of high-fidelity 12-lead tracings with animated rhythm strips, worked through lead by lead. Built around the patterns boards test and codes demand.

12Curriculum Modules
23Must-Know Patterns
13Real 12-Leads
22Teaching Figures
Start the curriculum → Jump to the Must-Know 23
Rajiv Choudhary, MD, MPH · PA Clinical Bootcamp
The Curriculum · COCATS 4 aligned
Suggested order START HERE the reading spine and the highest-yield patterns THEN THESE round out the differential BACKGROUND read once — don't memorise
A 12-module path — action potential to pacemaker

Competency-based and progressive: foundational electrophysiology through advanced clinical pattern recognition, weighted toward the conditions where reading the tracing right changes what happens to the patient. Recommended training volume: ≥500 ECG interpretations (COCATS 4 Level I). Tap any part to expand.

Preview. Part 1 is open as a sample — the full 8-part syllabus, pearls, and Must-Know 23 are for enrolled bootcamp students.
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START HERE
ECG FoundationsConduction system · paper · rate · rhythm · axis · intervals · the algorithm
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Before you beginECG Foundations2 questions
Read the tracing before you read the part. Missing it is expected — attempting a question first makes the material stick better. The explanation unlocks once you submit.
ECG question 1 of 2
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
ECG from a middle-aged man shows which ONE of the following?
Click to Reveal Answer
Correct answer: A — Atrial paced rhythm
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing a regular bradycardic rhythm at about 54 per minute. A small sharp deflection precedes each P wave in most leads, and the QRS complexes that follow are narrow and normal in shape.
An atrial paced rhythm at about 54 per minute. Small but clearly evident atrial pacemaker spikes are visible in most leads. This patient has a dual-chamber (DDD) pacemaker implanted for sinus node dysfunction, and during this recording it is functioning correctly in an atrial pacing, ventricular sensing mode. The QRS complexes are native — preceded by no spike — and are normal apart from non-specific ST-T changes. The mean frontal-plane QRS axis is horizontal at roughly 0°, not frankly leftward. The A–QRS interval of about 160 ms allows physiologic AV conduction to proceed, so the ventricle activates normally through its own conduction system. That is deliberate: a goal of DDD pacing in a patient with intact AV conduction is to program the device to minimize the need for and duration of ventricular pacing.
Why the other choices are wrong
  • Sinus bradycardia with baseline artifact — artifact is random. These deflections are sharp, uniform in shape and appear at a fixed interval before every single P wave across most leads. That time-locking is what separates a pacing spike from noise.
  • Sinus rhythm with pre-excitation variant — pre-excitation means a short PR with a slurred delta upstroke and a wide QRS. Here the QRS complexes are narrow and normally shaped, and the A–QRS interval of roughly 160 ms is normal, not short.
  • AV sequential pacing with ventricular pseudo-fusion beats — AV sequential pacing would show a second spike immediately before each QRS. Every QRS here is native, preceded by no spike at all, so there is nothing for a ventricular stimulus to fuse with.
  • Ectopic atrial bradycardia — an ectopic atrial focus changes P-wave morphology but produces no spike. The discrete sharp deflection preceding each P wave is the finding that makes this paced rather than merely ectopic.
Board pearlBefore you name any bradycardia, scan for pacing spikes. They are small, easily dismissed as artifact, and they change the diagnosis completely. A sharp deflection appearing at a fixed interval before every P wave is pacing; random deflections unrelated to the P waves are noise.
Foundational skills tested here: rate, rhythm and axis · full pacemaker content in Part 3
ECG question 2 of 2
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
Which one of the following statements about this ECG from a 24-year-old man is CORRECT?
Click to Reveal Answer
Correct answer: B — The ECG is within normal limits
What the tracing shows
Twelve-lead ECG of a 24-year-old man on pink grid paper with a lead II rhythm strip beneath, showing sinus rhythm at about 60 per minute with mild beat-to-beat variation, normal intervals, normal R-wave progression across the precordial leads, and very slight concave ST elevation in V2 to V6.
Sinus rhythm with a physiologic sinus arrhythmia at an average rate of about 60, and completely normal. Every interval checks out: PR 0.15 s, QRS 0.09 s, QT 0.39 s. P-wave duration and morphology are normal. The precordial leads show normal R-wave progression with very slight ST elevation in V2–V6 consistent with normal-variant early repolarization. The QRS axis is normal at about +60°. There is no evidence of left or right ventricular hypertrophy.
Why the other choices are wrong
  • The ECG shows right ventricular hypertrophy — Right ventricular hypertrophy would need R taller than S in V1 with right axis deviation, and usually right atrial abnormality alongside it. R-wave progression across the precordium is normal here and the axis sits at +60°.
  • The ECG shows left ventricular hypertrophy — Left ventricular hypertrophy requires voltage criteria to be met — S in V1 plus R in V5 or V6 reaching 35 mm for Sokolow-Lyon. The voltages on this tracing are unremarkable.
  • The ECG is consistent with severe hypokalemia — Severe hypokalemia prolongs repolarization: a long QT–U with flattened T waves, sometimes ST sagging, and often prominent U waves. The QT here is 0.39 s and there are no prominent U waves.
  • The ECG shows left atrial abnormality — Left atrial abnormality needs a P wave of 120 ms or more in lead II, notched, or a deep wide terminal negative component in V1. P-wave duration and morphology are both normal.
Board pearlRecognizing normal is a skill in its own right, and it is tested. The slight concave ST elevation in V2–V6 in a healthy young man is benign early repolarization, not a STEMI — and being unable to leave a normal tracing alone is how normal variants get worked up as disease.
Intervals and axis are covered below · early repolarization versus STEMI in Part 7 — ECG Mimics
Cellular & conduction basisHow one impulse becomes twelve tracings.

The ECG is the sum of millions of action potentials projected onto the skin. One rule explains every deflection: depolarization toward a lead reads up, away reads down.

Action potential — 5 phases

  • 0 — rapid depolarization: Na⁺ influx in working myocytes; Ca²⁺ influx in nodal cells.
  • 1 — early repolarization (K⁺ efflux).
  • 2 — plateau (Ca²⁺ in balances K⁺ out); the long refractory period unique to cardiac cells — stops tetany.
  • 3 — repolarization (K⁺ efflux dominates).
  • 4 — resting −90 mV; pacemaker cells slope upward here (automaticity).
The cardiac action potential — five phases and the currents behind them
Fast-response ventricular myocyte, with the slow-response nodal cell below
The ventricular myocyte action potential plotted as membrane potential against time, with each of the five phases color-coded and annotated with its ion current and channel, refractory periods marked below the trace, a five-column summary of each phase, and a lower panel contrasting the slow-response nodal pacemaker cell. FAST-RESPONSE CELL · VENTRICULAR MYOCYTE +300−50−90 0100200300 time (ms) membrane potential (mV) threshold ≈ −70 mV 4 0 1 2 3 4 Na⁺ influx K⁺ efflux, transient Ca²⁺ influx, L-type K⁺ efflux · IKr, IKs K⁺ efflux · IK1 fast Na⁺ channels open Ito channels open balances K⁺ efflux andsustains the plateau Ca²⁺ channels close;voltage falls to rest maintains resting potential ABSOLUTE REFRACTORY — no stimulus can excite RELATIVE 0 1 2 3 4 Rapid depolarization Early repolarization Plateau phase Repolarization Resting potential Na⁺ IN · fast channels K⁺ OUT · Ito Ca²⁺ IN · L-type K⁺ OUT · IKr, IKs K⁺ IK1 · Na⁺/K⁺ pump Voltage-gated fast Na⁺channels open. Nodalcells use Ca²⁺ here. Na⁺ channels shut; atransient K⁺ effluxcuts the notch. Inward Ca²⁺ balancesoutward K⁺ — the longrefractory period. Ca²⁺ channels close,K⁺ efflux dominates,voltage falls to rest. Stable near −90 mV.Pacemaker cells driftupward here. SLOW-RESPONSE CELL · SA AND AV NODE dashed line = threshold No true resting potential: phase 4 drifts upward on its own — the funny current, If. Reaching threshold fires phase 0, carried here by slow L-type Ca²⁺ rather than Na⁺. A steeper drift means a faster intrinsic rate; that slope is automaticity, and vagal tone flattens it.
Why it matters84-word note
the plateau is the phase with clinical consequences. It gives cardiac muscle a refractory period far longer than skeletal muscle, which is why the heart cannot tetanize and why re-entry requires a critically timed extra beat to start. It is also the drug target: class IV agents and the non-dihydropyridine calcium blockers act on the L-type current, class III agents on IKr, and class I agents on the fast sodium current of phase 0. Every antiarrhythmic class maps onto a phase of this curve.
From action potential to ECG — what writes each wave
Which phase of the action potential writes which part of the tracing
The sequence that writes the tracing: atrial depolarization produces the P wave, ventricular depolarization the QRS, ventricular repolarization the T wave, and the flat TP and ST segments correspond to phase 4 and phase 2 respectively, when every cell sits at the same potential and no current flows. THE SEQUENCE THAT WRITES THE TRACING P QRS T PRSTTP Atrial depolarization Ventricular depolarization Ventricular repolarization The flat segments SA node spreads acrossboth atria, towardlead II → a smallupright P wave. His → bundles →Purkinje; septum, thenfree walls. Big, sharpQRS. Epicardium repolarizesfirst, so this wave runsopposite to the QRS —so the T stays upright. TP: all cells at rest(phase 4). ST: all cellsdepolarized (phase 2).No gradient either way. PHASE 0 · ATRIAL CELLS PHASE 0 · VENTRICLES PHASE 3 PHASE 4 AND PHASE 2
Why TP and ST are both flat109-word note
Two segments on every tracing are flat for opposite reasons, and the figure pairs each with its phase. During TP every cell is at rest in phase 4; during ST every cell is depolarized in phase 2. A lead records a difference in potential, so when all the tissue agrees — whether it agrees on resting or on depolarized — there is nothing to record and the pen sits at baseline. That is also why the ST segment is the diagnostic battleground: it is the one stretch that should be flat, so any deviation from it means part of the ventricle is not doing what the rest is doing.

Conduction hierarchy (intrinsic rates)

SA 60–100AV junction 40–60His 40–60Purkinje/vent 20–40Rest −90 mV

Fastest pacemaker wins (overdrive suppression); lower sites are backups. The AV node's built-in delay = the PR segment, and it's your drug target in narrow-complex SVT. Sympathetic → ↑rate/conduction/contractility; vagal → ↓SA rate, ↓AV conduction.

The conduction system — anatomy, rates and speeds
One impulse, six stations, from the SA node to the last Purkinje fiber
Schematic anterior view of the heart showing the conduction pathway from SA node through the atria, AV node, bundle of His, bundle branches and Purkinje network, numbered one to six, alongside a cascade listing each station with its intrinsic pacemaker rate and conduction velocity. RALA RVLV 1 2 3 4 5 6 ANTERIOR VIEW · SCHEMATIC SA node Atrial myocardium AV node Bundle of His Left & right bundle branches Purkinje network Right atrium, near the SVC Internodal tracts · Bachmann's The only gate, atria → ventricles Penetrates the AV septum Down either side of the septum Subendocardium, apex toward base 1 2 3 4 5 6 60–100 / minno pacemaker 40–60 / min40–60 / min 20–40 / min20–40 / min 0.05 m/s1.0 m/s 0.05 m/s · slowest1.0–1.5 m/s 2.0 m/s2.0–4.0 m/s · fastest INTRINSIC RATE / CONDUCTION SPEED Sympathetic → ↑ SA rate, ↑ AV conduction Vagal → ↓ SA rate, ↓ AV conduction The fastest pacemaker wins — overdrive suppression. Every site below it stays silent until the one above fails.
Why it matters85-word note
the AV node is the slowest tissue in the chain, and that deliberate bottleneck is the PR segment: it buys time for the atria to finish emptying, and it is the reason AV-nodal blockers work in narrow-complex SVT. The His bundle sits on the boundary of the two escape tiers, so a rhythm arising at or above it is junctional at 40–60, while anything below the bifurcation falls to 20–40 — which is exactly why a wide, slow escape rhythm is the more frightening tracing.
The paper, the leads, the normal tracingWhat a box is worth and what each lead sees.

Standardize before you interpret. Wrong paper speed, bad calibration, or a swapped lead manufactures pathology that isn't there.

Grid & calibration

Speed 25 mm/sSmall box 0.04 s · 0.1 mVBig box 0.20 sCalibration 10 mm = 1 mV
The ECG grid — reading time and voltage
Standard calibration: 25 mm/s paper speed, 10 mm = 1 mV
An ECG grid drawn to scale with a calibration pulse, one small box and one big box highlighted, and tables converting box counts into time on the horizontal axis and voltage on the vertical axis. DRAWN TO SCALE · 1 SMALL BOX = 1 mm CALIBRATION PULSE · 10 mm tall = 1 mV one small box one big box 5 big boxes = 1 second HORIZONTAL AXIS = TIME 1 small box 0.04 s · 40 ms 1 big box = 5 small 0.20 s · 200 ms 5 big boxes 1 full second VERTICAL AXIS = VOLTAGE 1 small box 1 mm · 0.1 mV 1 big box = 5 small 5 mm · 0.5 mV 10 small boxes 10 mm · 1.0 mV The calibration pulse is printed at the edge of every tracing. Check it before you measure. 1 small box = 1 mm = 0.04 s = 0.1 mV · 1 big box = 5 mm = 0.20 s = 0.5 mV · 10 mm = 1 mV A wrong paper speed or a mis-set gain manufactures pathology that is not there — half standard gain halves every voltage criterion.
Board move68-word note
every duration on the tracing is a box count, so the two conversions above are the only arithmetic ECG interpretation requires. At 25 mm/s a PR of 4 small boxes is 160 ms and normal; at 5 small boxes it is 200 ms and at the ceiling. If a tracing looks impossibly fast or the complexes look impossibly small, read the calibration pulse before you read the rhythm.

Intervals to own

PR 120–200 msQRS <120 msP wave <120 msQTc <440 M / <460 FQTc >500 torsades risk
QRS width and height — the box rules
Count boxes for duration; use voltage criteria, never eyeballing, for amplitude
Four QRS complexes drawn to scale on an ECG grid at two, two and a half, three and more than three small boxes wide, with the corresponding durations, the differential for a wide QRS, and guidance on QRS height in limb and precordial leads. NORMAL QRS WIDTH · 1 SMALL BOX = 40 ms 80 ms 2 small boxes normal 100 ms 2.5 small boxes normal 120 ms 3 small boxes upper limit >120 ms more than 3 wide — find the cause More than 3 small boxes — the wide-QRS differential Bundle branch block · ventricular rhythm · hyperkalemia · WPW pre-excitation · ventricular pacing NORMAL QRS HEIGHT Limb leads There is no single normal height. It varies with: · age· cardiac axis· heart size · body habitus· lead placement So we use voltage criteria instead of impression. a "tall" R is often ≥ 11 mm (1.1 mV) in I or aVL Precordial leads R waves in V5 and V6 commonly become quite tall in normal hearts. On their own they are not diagnostic of anything. What matters is whether the tracing meets a formal LVH criterion — Sokolow-Lyon or Cornell.
Board move71-word note
width and height are read in completely different ways, and conflating them is a common error. Duration is absolute: 3 small boxes is 120 ms in every patient, in every lead. Amplitude is relative: it depends on body habitus, lead placement and chest wall thickness, so a tall R wave is only meaningful once it satisfies a named criterion. A thin young patient can out-voltage an obese patient with genuine hypertrophy.

Limb leads (I, II, III, aVR, aVL, aVF) view the frontal plane; precordials (V1–V6) the horizontal. Einthoven: lead II = lead I + lead III. P = atrial depolarization; QRS = ventricular depolarization; T = repolarization; U = late repolarization (tall in hypokalemia).

The standard limb leads — why a deflection goes up or down
Six viewing angles onto the same heartbeat
Einthoven's triangle formed by the right arm, left arm and left leg electrodes, with the three bipolar limb leads drawn along its sides pointing toward their positive electrode and the three augmented leads drawn as dashed lines from the center. The single rule governing deflection: a wave traveling toward the positive electrode writes an upright deflection, a wave traveling away writes an inverted one, and a wave traveling perpendicular writes a biphasic or flat one. Applied to a normal heart depolarizing down and left at about plus 60 degrees, leads I, II, III, aVL and aVF are all upright with lead II tallest, while aVR is negative because it views the heart from the right shoulder. Why a lead reads up or down Each lead is a camera angle — the deflection says whether the wave is coming or going WHERE THE ELECTRODES SIT LEAD I LEAD II LEAD III aVR aVL aVF RA LA LL − + + Solid red = bipolar (I, II, III) · dashed green = augmented (aVR, aVL, aVF) THE ONE RULE + Wave travels TOWARD the + electrode UPRIGHT deflection + Wave travels AWAY from the + electrode INVERTED deflection + Wave travels PERPENDICULAR to the lead BIPHASIC or flat SO IN A NORMAL HEART, WITH DEPOLARIZATION HEADING DOWN AND LEFT (≈ +60°) I 0° moderate R II +60° TALLEST R III +120° smaller R aVR −150° NEGATIVE aVL −30° small R aVF +90° moderate R WHY aVR IS THE ODD ONE OUT It looks in from the right shoulder, so a wave heading down and left is heading straight away from it. P, QRS and T should all be negative.
Alignment, not just voltage148-word note
The rule is the whole of electrocardiography — everything else is bookkeeping about which lead points where. Two consequences worth holding onto. First, the size of a deflection depends on alignment, not just on voltage: lead II is tallest in a normal heart not because it is closer, but because it points at +60° and so sits almost parallel to the depolarizing wavefront, while aVL at −30° catches it obliquely and records less. A lead reading small is often a lead reading sideways. Second, this figure is the foundation for axis determination — once you accept that lead I looks left and aVF looks down, checking whether each is upright is simply asking which quadrant the wavefront is heading into, which is exactly the two-lead method in the systematic approach.
How each stage appears across the six limb leads
The same electrical event, viewed from six different angles
A grid showing how each of the five activation stages appears in the six limb leads. The P wave and T wave are upright in leads one, two, three, aVL and aVF but negative in aVR. The PR segment is isoelectric in every lead. A small q may appear or be absent in any lead. The R wave is tallest in lead two, moderate in leads one, three, aVL and aVF, and replaced by a deep S in aVR. STAGE I II III aVR aVL aVF 1 SA node activation P wave Atrial depolarization. The wavefront runs leftward and downward. UPRIGHT UPRIGHT UPRIGHT NEGATIVE UPRIGHT UPRIGHT 2 AV node delay PR segment An electrical pause. No large muscle mass is depolarizing. ISOELECTRIC ISOELECTRIC ISOELECTRIC ISOELECTRIC ISOELECTRIC ISOELECTRIC 3 Early ventricular activation Q wave Septal depolarization, left to right. Small or absent in any lead. SMALL q SMALL q SMALL q SMALL q SMALL q SMALL q 4 Ventricular depolarization R wave Mass depolarization toward the left and downward. MODERATE R TALLEST R MODERATE R DEEP S MODERATE R MODERATE R 5 Ventricular repolarization T wave Runs opposite to the depolarizing wavefront, so the T stays upright. UPRIGHT UPRIGHT UPRIGHT NEGATIVE UPRIGHT UPRIGHT
Why aVR is the odd one out120-word note
the normal cardiac vector points down and to the patient's left, roughly toward lead II at +60°, which is why lead II carries the tallest R and the clearest upright P. aVR looks from the opposite shoulder at −150°, so it sees that same vector receding and inverts everything: P negative, QRS predominantly negative, T negative. That makes aVR a built-in error check — an upright P in aVR means limb-lead reversal far more often than it means disease. Two normal variants worth knowing: an isolated inverted T wave in lead III or aVL can be entirely normal, particularly when the QRS in that lead is small, and a small q in any of these leads may simply be absent.
The five-step readThe algorithm you run on every ECG, in order, every time.

Run the same five steps on every tracing, every time. The disciplined read is how you catch the quiet killer hiding behind the obvious finding.

1 · Rate

Count big boxes between R waves: 300 – 150 – 100 – 75 – 60 – 50. Slow/irregular → QRS in a 6-second strip ×10.

2 · Rhythm

Regular? A P before every QRS and a QRS after every P? An upright P in lead II = sinus origin.

3 · Axis — read leads I and aVF

PatternLead IaVF
Normalupup
LAD (confirm w/ II)updown
RADdownup
Extremedowndown

4 · Intervals  ·  5 · Morphology

Intervals: PR, QRS, QT. Morphology: chamber size, ST/T changes, pathologic Q waves.

ECG fundamentals — principal waves, intervals and complexes
What you are measuring in step 4, and what each part of the tracing means
An annotated ECG complex identifying the P wave, PR segment, PR interval, QRS complex, J point, ST segment and T wave with their normal values, followed by four detail cards covering P wave morphology and atrial enlargement, the purpose of the PR segment delay, the wide QRS differential, and the J point. P QRS T PR segmentST segment J point PR INTERVAL · 120–200 ms QRS · <120 ms P WAVE PR INTERVAL QRS DURATION < 2.5 mm and < 120 ms 120 – 200 ms < 120 ms P wave — atrial depolarization Normally under 2.5 mm tall and under 120 ms wide. MORPHOLOGY Tall and peaked → right atrial enlargement (P pulmonale) Notched and wide → left atrial enlargement (P mitrale) PR segment The flat stretch from the end of the P wave to the start of the QRS — the delay inside the AV node. WHY THE DELAY? 1. Lets the atria finish emptying 2. Gives the ventricles time to fill the flat part QRS complex Ventricular depolarization. Normally under 120 ms. A WIDE QRS — THINK: · Bundle branch block · Ventricular rhythm · Hyperkalemia · WPW pre-excitation · Ventricular pacing narrowwide <120 ms≥120 ms J point The point where the QRS ends and the ST segment begins. It marks the completion of ventricular depolarization, and it is the reference point from which ST elevation or depression is measured. J point ST segment PA CLINICAL BOOTCAMP
Step 4 in practice114-word note
measure the PR interval from the onset of the P wave to the onset of the QRS, not from the end of the P, and measure the QRS from its earliest deflection in any lead to the J point. Both are box counts: 3 to 5 small boxes for a normal PR, under 3 for a normal QRS. Note that the PR segment and the PR interval are different measurements that differ by the width of the P wave itself — a distinction stems exploit. The J point matters beyond anatomy: it is where you place your caliper for ST deviation, and notching at the J point is the signature of benign early repolarization.
Mnemonic Rate → Rhythm → Axis → Intervals → Morphology. Never skip a step, never read out of order.

Practice — run the five steps on a normal tracing

Every abnormal tracing in the practice library is a departure from this one. Work it in order — rate, rhythm, axis, intervals, morphology — and satisfy yourself that all five come back clean before you go hunting for pathology.

✓ Reference · Normal
Normal sinus rhythm — the baseline
Rate 75 · normal axis · PR 160 ms · QRS 90 ms · aVR inverted throughout · R wave grows steadily V1 → V6
Name this tracingRead it before you read about it
Standard 12-lead · 25 mm/s · 10 mm/mV · calibration pulse at the right edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Run all five steps on this tracing. Which statement is correct?
Click to Reveal Answer
Correct answer: E — Every step is within normal limits
What the tracing shows
Normal 12-lead ECG recorded on standard red grid paper, arranged in the conventional four-column by three-row layout — leads I, II and III in the first column, aVR, aVL and aVF in the second, V1 to V3 in the third and V4 to V6 in the fourth — with a continuous rhythm strip along the bottom and a calibration pulse at the right-hand edge of each row.
This is the reference tracing every other one in the syllabus is measured against. Sinus rhythm at a normal rate, one upright P wave in lead II before every QRS, lead I and aVF both upright so the axis is normal, intervals within limits, and orderly R-wave progression from V1 to V6 with aVR negative throughout. Nothing here needs explaining — which is exactly the skill being tested.
Why the other choices are wrong
  • The rhythm is irregular, so the big-box method cannot be used — An irregular rhythm would need the 6-second method. This rhythm is regular, so 300 divided by big boxes works.
  • There is left axis deviation — Left axis deviation requires lead I upright with aVF negative. Both are upright here.
  • The PR interval is prolonged beyond 200 ms — A PR beyond 200 ms would be first-degree AV block — more than 5 small boxes. This PR falls within 3 to 5.
  • There is poor R-wave progression across the precordial leads — Poor R-wave progression means the R fails to grow across the precordium. It grows normally, with the transition around V3 to V4.
Board pearlLearn the normal cold. Every abnormal tracing here is a departure from it, and being unable to leave a normal tracing alone is how normal variants get worked up as disease.
● LIVE RHYTHM STRIP — Normal Sinus RhythmLead II · 25mm/s
"Run all five steps on the normal tracing first — that is how you learn what clean looks like."
Sinus P upright in II, inverted in aVR · one P for every QRS · R grows and S shrinks across V1 → V6 · transition where R = S at V3–V4 · T concordant with the QRS in every lead but aVR
aVR is the built-in error check: if its P wave is upright, suspect limb-lead reversal before you suspect disease.
Rate & Rhythm
75 /min · regular sinus
Axis
Normal — I up, aVF up
Intervals
PR 160 · QRS 90 · QTc 400 ms
Two Quick Checks
aVR all-negative · R progression V1→V6
Why it matters The lower the escape pacemaker that's keeping the patient alive (junctional 40–60 → ventricular 20–40), the sicker they are and the more urgent the pacing.
Don't miss An upright P in aVR or a pattern that "doesn't make sense" → suspect limb-lead reversal before diagnosing pathology.
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START HERE
Rhythm RecognitionSinus · atrial · AV blocks · junctional · SVT · ventricular · arrest
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Before you beginRhythm Recognition6 questions
Read the tracing before you read the module. Missing it is expected — attempting a question first makes the material stick better. The explanation unlocks once you submit.
ECG question 1 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
Elderly woman with a recent syncopal episode. What is the rhythm?
Click to Reveal Answer
Correct answer: D — Atrial fibrillation with a rapid ventricular response
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing a rapid narrow-complex rhythm with irregularly spaced QRS complexes, no discernible P waves, a fine undulating baseline between complexes, and borderline low QRS voltage in the limb leads.
Atrial fibrillation with a very rapid ventricular response. The rhythm is irregular, with subtle fibrillatory waves apparent between the QRS complexes and no organized P waves anywhere. There is borderline low QRS voltage in the limb leads — a non-specific finding. The slight beat-to-beat variation in QRS shape reflects subtle changes in conduction at this very rapid rate, and there are non-specific ST-T changes as well.
Why the other choices are wrong
  • Multifocal atrial tachycardia — Multifocal atrial tachycardia requires at least three distinct P-wave morphologies. There are no discernible P waves here at all — only a fibrillatory baseline — and MAT usually runs slower, around 100–130.
  • Atrial flutter with variable block — Atrial flutter with variable block would show a sawtooth baseline at a fixed atrial rate near 300, and its R–R intervals fall into repeating patterns — regularly irregular. This baseline is fibrillatory, and the irregularity has no pattern to it.
  • Sinus tachycardia with premature atrial complexes — Sinus tachycardia with premature atrial complexes would show discrete upright sinus P waves with occasional early abnormal ones, and the underlying rhythm would be regular between ectopics. No organized atrial activity is present.
  • Paroxysmal supraventricular tachycardia — Paroxysmal supraventricular tachycardia is regular. This rhythm is irregularly irregular, which excludes it.
Board pearlAt very rapid rates atrial fibrillation can look deceptively regular, so measure several R–R intervals rather than judging by eye. And note the history: rapid AF with syncope in an elderly patient should raise tachy-brady syndrome — sinus node dysfunction where the pause following a fast run is what actually drops the blood pressure.
Covered below under Sinus and atrial rhythms · the narrow-complex differential figure sorts every one of these five options by regularity
ECG question 2 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
What AV conduction abnormality is present in this ECG, which shows sinus rhythm with right bundle branch block and left atrial abnormality?
Click to Reveal Answer
Correct answer: E — Mobitz type I AV block (AV Wenckebach)
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing sinus rhythm with a right bundle branch block pattern. The PR interval lengthens progressively across successive beats before a P wave fails to conduct, with some P waves partly buried in the preceding T waves, and the conduction ratio varies through the recording.
The record opens with a long Wenckebach sequence showing 6:5 conduction, followed by a stretch of 2:1 block, and then the beginning of another sequence of progressively prolonging PR intervals. That shifting conduction ratio with lengthening PR intervals is characteristic of Wenckebach and is not seen in Mobitz II or complete block. Watch for the P waves partly hidden inside the preceding T waves — they are easy to lose.
The decisive finding is that the PR after the non-conducted P wave is considerably shorter than the PR before it. That is the hallmark of Wenckebach: the AV node recovers during the dropped beat and conducts the next impulse quickly. And because the sinus P waves arrive on time rather than early, blocked premature atrial depolarisations are excluded.
Why the other choices are wrong
  • Complete heart block — Complete heart block means no fixed relationship between P waves and QRS complexes. Here the PR intervals are plainly related to the P waves and lengthen in an orderly sequence before a beat drops, and conduction then resumes — the AV node is conducting, just failing periodically.
  • Isorhythmic AV dissociation — Isorhythmic AV dissociation has atrial and ventricular rates that are nearly equal, with P waves drifting into and out of the QRS and no beats dropped by block at all. This tracing has clearly non-conducted P waves with progressive PR lengthening.
  • Mobitz type II AV block — Mobitz type II requires a constant PR interval before the sudden dropped beat. Here the PR lengthens progressively — and decisively, the PR after the dropped beat is much shorter than the one before it, which is the Wenckebach signature and does not occur in type II.
  • Sinus rhythm with blocked premature atrial beats — Blocked premature atrial beats would require the non-conducted P waves to arrive early. These sinus P waves come on time at the expected interval, so they are not premature — they are being blocked, not arriving too soon to conduct.
Board pearlDo not diagnose Wenckebach from the lengthening alone — the more reliable sign is the short PR immediately after the dropped beat. One caution here: Mobitz I is usually nodal and benign, but this tracing also carries a right bundle branch block, and coexisting bundle branch disease points to more diffuse conduction-system disease. Wenckebach plus a bundle branch block earns closer follow-up than Wenckebach alone.
Covered below under AV blocks — the four-rungs figure shows the growing PR brackets side by side with the fixed PR of Mobitz II
ECG question 3 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
85-year-old man, no symptoms, on no pertinent cardiac medications. What is the rhythm?
Click to Reveal Answer
Correct answer: B — Sinus rhythm with 2:1 AV block
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing a very slow ventricular rate of about 32 per minute with narrow QRS complexes. Sinus P waves march at about 64 per minute, and every alternate P wave is followed by a QRS at a constant PR interval while the others are not conducted.
A very slow ventricular rate of about 32, with non-conducted sinus P waves alternating with normally conducted ones. The sinus rate is about 64 — exactly double — and the conducted PR intervals are constant at about 200 ms.
The site of block cannot be settled from a single 2:1 tracing. It may be proximal in the AV node or more distal in the His-Purkinje system, and given the narrow QRS here an intra-Hisian location is possible. In general: a narrow QRS with a prolonged PR, or intermittent Wenckebach, favors the AV node; a concomitant bundle branch block, or a PR of 160 ms or less, favors infranodal disease. This patient showed intermittent 3:2 Wenckebach on other tracings and later resumed 1:1 conduction — both consistent with AV nodal disease. The tracing also shows left atrial abnormality, borderline left axis deviation and LVH by voltage with non-specific ST-T changes; that LVH may be hypertensive but always raises the question of aortic stenosis.
Why the other choices are wrong
  • Atrial tachycardia with AV block — Atrial tachycardia with AV block requires an atrial rate above 100. The sinus rate here is about 64 — entirely normal. (That combination is classic for digoxin toxicity, and this patient is on no cardiac medications.)
  • Marked sinus bradycardia consistent with sick sinus syndrome — Marked sinus bradycardia would mean the sinus node is firing slowly. It is not: the P waves march at about 64. What is slow is the ventricular rate at 32, because every second P wave is blocked. The sinus node is healthy and the AV node is the problem.
  • Sinus rhythm with complete (third-degree) AV block — Complete third-degree AV block shows no fixed relationship between P waves and QRS complexes. Here the conducted PR interval is constant at about 200 ms and the atrial rate is exactly double the ventricular rate — a fixed 2:1 relationship, which is second-degree by definition.
  • Sinus rhythm with 3:2 AV Wenckebach — 3:2 AV Wenckebach would show progressive PR lengthening across two conducted beats before a drop, in repeating groups of three P waves. This tracing shows every alternate P blocked with a constant PR. Worth noting though: this patient did show 3:2 Wenckebach on other recordings, which is precisely the clue that his block is nodal.
Board pearlTwo bedside maneuvers localize chronic 2:1 block when there is no active ischemia, and they work in opposite directions. Mild exercise raises the rate and improves nodal conduction but worsens infranodal block. Carotid sinus massage slows the rate and worsens nodal block but may improve infranodal conduction. That matters because pacing is indicated for symptomatic 2:1 block at any site without a reversible cause, and for asymptomatic 2:1 block only when the disease is infranodal.
Covered below under AV blocks — the four-rungs figure and the 2:1 typing note
ECG question 4 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
Tracing source: ECG Wave-Maven, ecg.bidmc.harvard.edu · © 2005 Beth Israel Deaconess Medical Center
Older adult with progressive fatigue and light-headedness on exertion. What is the rhythm?
Click to Reveal Answer
Correct answer: C — Complete AV block with a junctional escape rhythm
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing a slow regular narrow-complex rhythm. P waves are visible marching at a steady rate faster than the QRS complexes, with no consistent interval between any P wave and the following QRS; some P waves fall on T waves and within QRS complexes.
The atria and ventricles are running on separate clocks. P waves march at a steady rate, the QRS complexes march at their own slower rate, and the interval between any P wave and the QRS that follows it keeps changing — some P waves land on T waves, some disappear inside a QRS. That is complete AV dissociation, and the fact that the atrial rate exceeds the ventricular rate is what makes it block rather than an accelerated lower rhythm.
The escape complexes are narrow, which places the escape focus at the AV junction rather than in the ventricle. That matters: a junctional escape sits higher, runs faster (40–60) and is more dependable than a ventricular escape at 20–40. It is still not a rhythm to rely on. With symptoms — and fatigue with exertional light-headedness counts — this patient needs pacing.
Why the other choices are wrong
  • Sinus bradycardia with first-degree AV block — Sinus bradycardia with first-degree AV block conducts every P wave, just slowly — a fixed, prolonged PR before every QRS. Here the PR distance changes from beat to beat because the two chambers are not communicating at all.
  • Second-degree AV block, Mobitz type I (Wenckebach) — Mobitz I (Wenckebach) requires some conducted beats with a PR that lengthens progressively before a drop. That means a demonstrable P-to-QRS relationship, which is exactly what is absent here.
  • Second-degree AV block, Mobitz type II — Mobitz II also requires conducted beats, with a constant PR interval punctuated by sudden dropped beats. Again there is no fixed PR anywhere on this tracing.
  • Sinus arrest with a junctional escape rhythm — Sinus arrest with a junctional escape is the best distractor, because it also produces a slow narrow-complex rhythm from the AV junction. The difference is the atria: in sinus arrest there are no P waves at all, because the sinus node has stopped. Here P waves are present and marching steadily at a rate faster than the QRS — the sinus node is working, the AV node is not conducting.
Board pearlOne question settles third-degree block: does any P wave have a fixed relationship to a QRS? If no — and the atrial rate is the faster of the two — it is complete block. Then read the QRS width to find the escape: narrow means junctional and relatively stable, wide means ventricular, slower and far more precarious. Atropine acts on the AV node, so it often fails when the lesion is infranodal — do not keep redosing it, go to pacing.
Covered below under AV blocks — the four-rungs figure shows the two independent timing rulers
ECG question 5 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
ECG from a young adult with a major bradycardia. The findings are most consistent with which scenario?
Click to Reveal Answer
Correct answer: A — Cape Cod camper
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath. Several non-conducted P waves appear at the start of the recording followed by a long pause without any QRS complex, after which narrow escape complexes resume at about 50 per minute while sinus P waves continue at about 90, dissociated from them.
The option is an epidemiological clue, not an ECG finding: Cape Cod is Lyme endemic, and this patient had documented Lyme carditis. Sinus rhythm is present with advanced AV block and probable paroxysmal complete heart block with transient ventricular asystole. Several non-conducted P waves appear at the beginning of the recording, after an initial partially and artifactually truncated P wave that is likely dissociated from the first QRS as well. After the asystolic pause, sinus P waves continue at about 90 — some almost entirely hidden inside the QRS toward the end of the recording — dissociated from slower narrow-complex junctional escape beats at about 50. Prior and subsequent tracings would be needed to establish when the block began and how long it lasted.
The finding that argues most strongly against a vagal mechanism is the relatively fast sinus rate. Vagal tone would have slowed the sinus node too.
Why the other choices are wrong
  • Severe chest pain — Severe chest pain points at ischemia, and an inferior MI can certainly block the AV node — but that is a story for an older patient with ST-segment changes. Neither is present here, and chest pain is a symptom rather than a mechanism.
  • Sick sinus syndrome — Sick sinus syndrome is disease of the sinus node, so the sinus rate would be slow. It is not: the P waves run at about 90. The sinus node is working perfectly well; the conduction below it is not.
  • Tricyclic antidepressant overdose — Tricyclic overdose blocks sodium channels, producing a wide QRS, a prolonged QT and a terminal R wave in aVR, usually with anticholinergic tachycardia. It does not give advanced AV block with a narrow junctional escape.
  • “Athlete’s heart” with a physiologic increase in vagal tone — Athlete’s heart with high vagal tone is the trap, and the tracing rules it out. Vagal tone slows the sinus node and AV conduction together — so a vagal mechanism would come with a slow sinus rate. A sinus rate of about 90 alongside this degree of block argues strongly against vagus and points to disease in the conduction system itself.
Board pearlAdvanced AV block in a young patient from a Lyme-endemic area is Lyme carditis until proven otherwise — and the reason it matters is that it is usually reversible with antibiotics. Temporary pacing may be needed to get through the acute phase, but a permanent pacemaker should be deferred rather than implanted reflexively. Reversible causes of AV block are the ones worth memorising: Lyme, drug effect, electrolyte derangement and ischemia.
Covered below under AV blocks · further reading: Yeung C, Baranchuk A. Diagnosis and Treatment of Lyme Carditis. JACC Review Topic of the Week
ECG question 6 of 6
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
39-year-old man with a very abnormal ECG. Which ONE of the following is present?
Click to Reveal Answer
Correct answer: E — Wolff-Parkinson-White (WPW) pre-excitation pattern
What the tracing shows
Twelve-lead ECG of a 39-year-old man on pink grid paper with a lead II rhythm strip beneath, showing a short PR interval and a wide QRS with a slurred initial upstroke. The delta wave is negative in II, III and aVF and positive in I and V4 to V6. A calibration pulse appears at the left edge of each row.
The classic WPW pre-excitation triad: a short PR interval, a wide QRS at 140 ms, and delta waves. The delta-wave polarity — negative in II, III and aVF, positive in I, aVL and V2–V6 — is consistent with a posterior bypass tract. There is also marked left atrial abnormality, seen as a prominent biphasic P wave in V1; this patient had severe chronic aortic insufficiency producing left ventricular hypertrophy superimposed on the pre-excitation.
Why the other choices are wrong
  • Sinus rhythm with left bundle branch block (LBBB) — LBBB gives a broad notched R in I, V5 and V6 with a deep QS in V1 — and critically a normal PR interval. Here the PR is short with a slurred delta upstroke.
  • AV sequentially paced rhythm — AV sequentially paced rhythm requires visible pacing spikes before the P wave and before the QRS. None are present.
  • Accelerated idioventricular rhythm (AIVR) — AIVR is a ventricular rhythm at 50–110 with no relationship to preceding P waves. Here every QRS follows a P wave at a short, fixed interval.
  • Inferior wall ST elevation myocardial infarction (STEMI) — Inferior STEMI gives convex ST elevation in II, III and aVF with reciprocal depression in I and aVL. The inferior negativity here is the delta wave and secondary repolarization change of pre-excitation, not injury current.
Board pearlPre-excitation mimics bundle branch block, hypertrophy and infarction, because ventricular activation begins in the wrong place. Before diagnosing any of the three, check the PR interval — a short PR with a slurred upstroke reframes everything else on the tracing.
Relevant tracing in this module: pre-excited AF in WPW · full pre-excitation content in Part 3
Sinus and atrial rhythmsNormal sinus, bradycardia, tachycardia, AF, flutter and MAT.

Supraventricular = narrow QRS. The P wave — its shape, count, or absence — is the entire diagnosis.

  • Sinus rhythm — upright P in II, one per QRS, 60–100. Sinus arrhythmia (rate varies with breathing) is normal in the young.
  • AFib — irregularly irregular, no organized P waves, fibrillatory baseline. The #1 board buzzword.
  • Atrial flutter — sawtooth F waves (~300/min), usually 2:1 → ventricular ~150. A regular SVT at exactly 150? Suspect flutter.
  • MAT — ≥3 distinct P-wave morphologies, rate >100, irregular. Classic in COPD/hypoxia.
  • Atrial tach with AV block — think digitalis toxicity.
Narrow-complex tachycardias — sorted by regularity
Regularity splits the list in two before you look at anything else
Narrow-complex tachycardias, a QRS under 120 milliseconds with a rate over 100, sorted by regularity. Regular: sinus tachycardia, atrial flutter with a fixed conduction ratio, AVNRT and orthodromic AVRT. Irregular: atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Four reminders cover checking regularity first, examining P waves, identifying the mechanism, and correlating clinically. Narrow-complex tachycardias QRS < 120 ms · RATE > 100 bpm NARROW FAST REGULAR — RE-ENTRY, OR A DRIVEN SINUS NODE Sinus tachycardia Physiologic response to stress, fever, hypovolemia and similar demands. Atrial flutter with a fixed AV conduction ratio Macro-reentrant circuit, typically around the tricuspid annulus. AV nodal reentrant tachycardia AVNRT The most common paroxysmal SVT. Circuit sits within or beside the AV node. AV reentrant tachycardia AVRT · orthodromic Orthodromic form, using an accessory pathway retrogradely. IRREGULAR — LOOK AT THE BASELINE AND THE P WAVES Atrial fibrillation Irregularly irregular, from chaotic atrial activation. Atrial flutter with variable AV block Regularly irregular — the flutter rate is fixed but conduction varies. Multifocal atrial tachycardia MAT ≥ 3 distinct P-wave morphologies, irregularly irregular. Associated with COPD and hypoxia. CHECK REGULARITY FIRST Regular → the upper block. Irregular → the lower block. P WAVES MATTER Visible? Sawtooth? Absent? Varying in morphology? THINK MECHANISM Re-entry — flutter, AVNRT, AVRT. Automatic — sinus, MAT. ALWAYS CORRELATE With clinical context and the underlying cause. NCT = narrow-complex tachycardia AVNRT = AV nodal re-entry tachycardia AVRT = AV re-entry tachycardia MAT = multifocal atrial tachycardia COPD = chronic obstructive pulmonary disease PA BOOTCAMP · PROPERTY OF PA BOOTCAMP, LLC · FOR EDUCATIONAL USE ONLY
Board move94-word note
regularity is the first branch because it is the one thing you can judge without finding a single P wave. Two entries reward a second look: atrial flutter appears in both halves, regular when the conduction ratio is fixed and irregular when it varies, so flutter can never be excluded on regularity alone; and regularly irregular belongs to flutter with variable block, not to atrial fibrillation, which is irregularly irregular with no organized atrial activity at all. A regular narrow tachycardia sitting at almost exactly 150 is flutter with 2:1 conduction until proven otherwise.
Name this tracingRead it before you read about it
Sawtooth atrial activity · lead II rhythm strip along the bottom · calibration pulse at the right edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Which rhythm is shown?
Click to Reveal Answer
Correct answer: D — Atrial flutter
What the tracing shows
Twelve-lead ECG of atrial flutter on salmon grid paper, in the conventional four-column layout with a lead II rhythm strip along the bottom. A continuous sawtooth baseline of regular atrial activity is visible between the QRS complexes, seen most clearly in the inferior leads and in the lead II rhythm strip. A calibration pulse appears at the right edge of each row.
Atrial flutter. The sawtooth reads most clearly in the inferior leads and in the lead II strip beneath — never judge flutter from a single lead. Then count the conduction ratio: the atrial rate sits near 300, so 2:1 puts the ventricles around 150 and 4:1 around 75.
This is the tracing that settles which half of the figure above flutter belongs to — fixed ratio and it is regular, varying ratio and it is not.
Why the other choices are wrong
  • Sinus tachycardia — Sinus tachycardia shows discrete upright P waves, one per QRS, and rarely reaches this rate at rest in an adult.
  • Atrial fibrillation — Atrial fibrillation is irregularly irregular with a chaotic fibrillatory baseline — not an organized sawtooth at a fixed rate.
  • AV nodal reentrant tachycardia — AVNRT has no organized atrial activity at all; the P wave is buried in the QRS.
  • Multifocal atrial tachycardia — MAT needs at least three distinct P-wave morphologies and is irregularly irregular.
Board pearlFlutter appears in both halves of the regularity split — regular with a fixed conduction ratio, irregular with a varying one. Regularity alone can never exclude it.
Name this tracingRead it before you read about it
12-lead with lead II rhythm strip · calibration pulse at both edges of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
The atrial activity here is the same as on the tracing above, but the ventricular rate is slower. What accounts for the difference?
Click to Reveal Answer
Correct answer: B — The same circuit conducting at a higher fixed ratio
What the tracing shows
Twelve-lead ECG on salmon grid paper in the conventional four-column layout with a lead II rhythm strip along the bottom, standard aVR, aVL and aVF labeling, and a calibration pulse at both the left and right edge of each row. The ventricular rate is slow with narrow QRS complexes, and a regular undulating baseline of atrial activity is visible between the complexes, most clearly in the inferior leads and the lead II rhythm strip.
The flutter circuit is unchanged — the same regular undulating atrial baseline runs between the QRS complexes, seen most clearly in the inferior leads and the lead II strip. What has changed is the AV conduction ratio: more flutter waves are blocked for each one conducted, so the ventricular rate falls. The atrial rate is fixed; the ventricular rate is whatever the AV node lets through.
Why the other choices are wrong
  • A slower atrial rate — the flutter circuit itself has slowed — A slower flutter circuit would show fewer, wider-spaced atrial waves. Count them between QRS complexes — the atrial rate is unchanged.
  • Atrial fibrillation has replaced the flutter — Atrial fibrillation would replace the organized baseline with chaotic fibrillatory activity and make the ventricular response irregularly irregular.
  • A junctional escape rhythm has taken over — A junctional escape rhythm would mean the atria were no longer driving the ventricle, with no relationship between atrial waves and QRS complexes.
  • Second-degree AV block has developed independently of the atrial rhythm — Independent second-degree AV block is not a separate diagnosis here — in flutter the blocked waves are the conduction ratio, so you name the ratio rather than a coexisting block.
Board pearlIn flutter, always report two rates: the atrial rate, fixed near 300, and the ventricular rate, which is 300 divided by the conduction ratio. 2:1 gives about 150, 3:1 about 100, 4:1 about 75 — which is why a flutter at 75 gets mistaken for sinus rhythm when nobody looks at the baseline.
Name this tracingRead it before you read about it
Irregularly irregular · wide QRS changing morphology beat to beat · limb leads labeled VR / VL / VF
Twelve-lead ECG for interpretation
PA Bootcamp Review
The rhythm is irregularly irregular with wide QRS complexes whose shape changes from beat to beat. What is it?
Click to Reveal Answer
Correct answer: A — Pre-excited atrial fibrillation
What the tracing shows
Twelve-lead ECG of pre-excited atrial fibrillation — atrial fibrillation conducting down an accessory pathway in Wolff-Parkinson-White syndrome. The rhythm is irregularly irregular and very rapid, and the QRS complexes are wide and bizarre with morphology that changes from beat to beat, most dramatically in V1 to V3. Limb leads are labeled in the older convention as VR, VL and VF. A calibration pulse appears at the left edge of each row.
Atrial fibrillation conducting down an accessory pathway — pre-excited AF in WPW. Irregular like ordinary AF, but wide, because the impulse bypasses the AV node entirely.
⚑ The exception to the pearl below. Do not rate-control this with AV-nodal blockers — adenosine, verapamil, diltiazem, β-blockers or digoxin can accelerate conduction down the pathway and precipitate VF. Procainamide, or cardioversion if unstable.
Why the other choices are wrong
  • Polymorphic ventricular tachycardia — Polymorphic VT is a ventricular rhythm with continuously changing axis; it does not arise from irregular atrial activity and would not sustain at this rate with preserved consciousness.
  • Atrial fibrillation with a rate-related bundle branch block — Rate-related bundle branch block produces a constant wide morphology once it appears. Beat-to-beat variation in shape is the signature of varying degrees of pre-excitation.
  • Torsades de pointes — Torsades twists around the baseline, arises on a prolonged QT and is usually self-limiting or degenerates to VF.
  • Atrial fibrillation with a ventricular paced rhythm — A paced rhythm would show pacing spikes before the wide complexes. None are present.
Board pearlEvery AV-nodal blocker is dangerous here — adenosine, verapamil, diltiazem, beta blockers, digoxin. Blocking the node pushes more impulses down the pathway. Procainamide, or cardiovert.
12-lead with three rhythm strips — V1, II and V5 · calibration pulse at the left edge of each row
Work this one yourself. Three simultaneous rhythm strips are a gift here — a P wave or flutter wave hidden in one lead is often obvious in another. Compare the atrial baseline across V1, II and V5 before you commit to a rhythm.
Twelve-lead ECG for interpretation
Reveal what the tracing shows
Twelve-lead ECG on pink grid paper with three continuous rhythm strips from V1, II and V5 beneath the standard four-column layout. The ventricular rate is rapid with narrow QRS complexes, and a calibration pulse appears at the left edge of every row. An attribution line reading ecgmadesimple.com, copyright 2008 ECG Made Simple, is printed at the lower right of the tracing.
Tracing source: ecgmadesimple.com · © 2008 ECG Made Simple
PA Bootcamp Review
AV blocksWhere the block sits decides how dangerous it is.

The PR interval and the pattern of dropped beats tell you where the block sits and how dangerous it is. Location decides urgency.

BlockSignatureLevel / Risk
1st degreePR >200 ms, every P conductsBenign
Mobitz IPR lengthens → drop (PR after drop is shortest)AV-nodal · benign
Mobitz IIConstant PR → sudden drop, often wide QRSInfranodal · pace
3rd degreeP's and QRS's independent, atrial > ventricularPace
AV Block — the four rungs
One question decides it: what is each P wave doing to the QRS?
Comparison of first-degree AV block, Mobitz I, Mobitz II and third-degree AV block. Each row shows a rhythm strip with the P wave to QRS relationship and whether pacing is required. BLOCK WHAT THE STRIP SHOWS PACE? First degree Mobitz I Mobitz II Third degree PR >200 ms andevery P conducts PR lengthens beatto beat, then drops PR constant, thena QRS drops out P and QRS marchindependently PR >200 ms · constant P, no QRS PR grows → P, no QRS — no warning PR identical P–P regular QRS–QRS regular but slower — no relationship between them No Usually no Yes Yes
Board move65-word note
Mobitz II and third-degree block are the pacing pair: both are infranodal, both are unpredictable, and neither responds reliably to atropine. Mobitz I sits in the AV node itself, is often vagal or drug-related, and usually needs nothing more than a medication review. If a stem gives you a 2:1 ratio alone, you cannot classify it — there is no second PR interval to compare.
AV block — the ladder diagram
Conduction through the AV node · steeper slope = longer PR
Dashed line = conduction through the AV node. Steeper slope = longer PR. Bracket below baseline = PR interval. 1st Degree AV Block Level: AV node · every P conducts NO pacemaker PR is long but never changes — nothing is ever dropped PR 240 Constant PR > 200 ms · 1:1 conduction 2nd Degree — Mobitz I (Wenckebach) Level: AV node (supranodal) USUALLY NO pacemaker PR stretches beat by beat, then one drops — and the cycle resets PR 160 PR 220 PR 300 DROPPED no QRS PR 160 Progressive PR lengthening → grouped beating cycle resets 2nd Degree — Mobitz II Level: infranodal (His-Purkinje) PACEMAKER — Class I PR never changes — the drop arrives without any warning PR 180 PR 180 PR 180 DROPPED no QRS PR 180 PR 180 Fixed PR → sudden dropped QRS · no warning 3rd Degree (Complete) AV Block Level: infranodal · complete AV dissociation PACEMAKER — Class I Atria and ventricles are on separate clocks — no PR exists P–P regular (atrial rate ~85) R–R regular (escape ~38, WIDE) No relationship · P waves march through the QRS Wide escape = unreliable, risk of asystole ⚑ The whole exam question is Mobitz I vs Mobitz II — look at the PR before the dropped beat PR was lengthening → Mobitz I → observe. PR was unchanged → Mobitz II → pacemaker, even if the patient feels fine.
How to read it62-word note
Each dashed line traces one P wave down through the AV node to its QRS, so a steeper line simply means a longer PR, and the bracket beneath the baseline gives you that interval in milliseconds. A red cross marks a P that conducts nowhere. The whole diagnosis rests on the beats before the dropped one: PR lengthening beat to beat is Mobitz I, PR identical is Mobitz II.

2:1 block can't be typed from one strip: narrow QRS → likely nodal (I); wide QRS → likely infranodal (II). 3rd-degree escape sets survival — junctional (narrow, 40–60) vs ventricular (wide, 20–40).

Mnemonic "Longer, longer, longer, drop — then you have a Wenckebach." Fixed PR with a sudden vanished beat = Mobitz II.
Junctional rhythms and re-entrant SVTAVNRT, AVRT, and the narrow-complex workup.
Name this tracingJunctional rhythms
12-lead with V1, II and V5 rhythm strips · reproduced unmodified
Twelve-lead ECG for interpretation
PA Bootcamp Review
A 65-year-old man undergoes routine ECG monitoring and the tracing above is obtained. Which of the following is the most likely rhythm?
Click to Reveal Answer
Correct answer: E — Accelerated junctional rhythm
What the tracing shows
Twelve-lead ECG on pink grid paper with three continuous rhythm strips from V1, II and V5 beneath. The rhythm is regular with narrow QRS complexes at a rate within the normal range, and no upright sinus P wave precedes the QRS complexes in lead II.
A regular narrow-complex rhythm at a rate in the 60–100 range with no upright sinus P wave before the QRS complexes. Narrow complexes place the origin at or above the AV junction, and the absence of an antegrade sinus P wave places it at the junction rather than in the sinus node. When a junctional focus runs at 60–100 it is by definition accelerated — faster than the junction’s own intrinsic rate of 40–60.
The junctional family is defined purely by rate: escape at 40–60, accelerated at 60–100, junctional tachycardia above 100. All three share a narrow QRS with P waves that are absent, inverted or retrograde.
Why the other choices are wrong
  • Sinus bradycardia — Sinus bradycardia fails on two counts. It requires an upright sinus P wave before every QRS in lead II — absent here — and a rate below 60. This rate sits in the normal range, so even if the P waves were sinus the label would be wrong.
  • First-degree AV block — First-degree AV block cannot be diagnosed without a conducted P wave to measure from. The definition is a PR interval above 200 ms, and there is no antegrade P wave preceding these complexes to give a PR at all.
  • Ectopic atrial rhythm — Ectopic atrial rhythm is the best distractor, because a low atrial focus also produces an abnormal — often inverted — P wave in the inferior leads. The distinction is timing: in an ectopic atrial rhythm the inverted P still precedes the QRS with a measurable PR interval, whereas in a junctional rhythm the P is absent, buried inside the QRS, or appears after it as a retrograde deflection.
  • Junctional escape rhythm — Incorrect — and this is the closest call on the tracing. Escape and accelerated junctional rhythms share the same morphology; only the rate separates them. The intrinsic junctional pacemaker fires at 40–60, so a junctional rhythm faster than 60 is accelerated, not escape.
Board pearlThe word accelerated is the clue to look further. A junctional focus firing faster than its own intrinsic rate means either enhanced junctional automaticity — classically digoxin toxicity, and also ischemia, myocarditis or the post-cardiac-surgery state — or a sinus node that has slowed enough to let the junction take over. Check a digoxin level and review the rate-limiting drugs before calling it benign.

When the SA node fails or a re-entry circuit fires, the junction runs the show: narrow QRS with P waves absent, inverted, or retrograde.

Junctional rhythms — when the junction is the pacemaker

Junctional escape 40–60Accelerated junctional 60–100Junctional tach >100
AV junction arrhythmias — two mechanisms, one junction
Is the junction driving the rhythm, or merely carrying it?
The AV junction produces arrhythmias by two mechanisms. As a pacemaker through automaticity or escape it gives junctional escape at 40 to 60, accelerated junctional at 60 to 100, and junctional tachycardia above 100, all with a narrow QRS and absent, inverted or retrograde P waves. As part of a re-entry circuit it gives AVNRT, with dual pathways within or near the node, and AVRT in Wolff-Parkinson-White, which uses an accessory pathway and is narrow when orthodromic and wide when antidromic. AV junction arrhythmias Two mechanisms. One junction. HIGH-YIELD · BOARD-FOCUSED · CLINICALLY RELEVANT THE AV JUNCTION AV NODE + HIS BUNDLE AUTOMATICITY / ESCAPE The junction is the pacemaker It generates the impulse because the SA node is slow or has failed. 1 Junctional escape 40–60 bpm Backup pacemaker when the SA node fails or runs too slowly. 2 Accelerated junctional 60–100 bpm The junction fires faster than the SA node and takes over. 3 Junctional tachycardia > 100 bpm Abnormal automaticity of the AV junction itself. RE-ENTRY The junction is part of the circuit The impulse does NOT start here. It re-enters and keeps circulating. A AVNRT AV nodal re-entrant tachycardia. Circuit sits within or very near the AV node — dual pathways, fast and slow. The most common regular narrow-complex SVT. B AVRT — WPW AV re-entrant tachycardia. Circuit uses the AV node plus an accessory pathway (the bundle of Kent). Orthodromic → narrow QRS. Antidromic → wide QRS. KEY FEATURES · ALL THREE Narrow QRS · absent, inverted or retrograde P · usually regular KEY FEATURES · BOTH Narrow QRS (usually) · abnormal or hidden P · regular tachycardia PA CARDIOLOGY BOOTCAMP @paclinicalbootcamp
Why the split matters80-word note
it decides your treatment. When the junction is the pacemaker, it is a rescuer: the rhythm is a symptom of sinus node failure or AV block, and suppressing it removes the only thing maintaining output. When the junction is part of a circuit, it is the culprit, and interrupting it at the AV node with adenosine or a vagal maneuver terminates the arrhythmia. Same anatomy, opposite response — which is why identifying the mechanism comes before reaching for a drug.

Re-entrant SVT — AVNRT versus AVRT

AVNRTAVRT
Circuitwithin AV nodeaccessory pathway (WPW)
Frequencymost common SVT (~60%)orthodromic 90% (narrow) / antidromic 10% (wide, mimics VT)
Cluepseudo-r′ in V1, pseudo-S inferiorlyretrograde P after QRS (short RP)
AVRT versus AVNRT — side by side
One road or two: where the circuit runs decides everything else
A side-by-side comparison of AVNRT and AVRT across re-entry location, presence of an extra pathway, association with Wolff-Parkinson-White, typical QRS width and P-wave behavior, with circuit schematics showing dual pathways inside the AV node for AVNRT and a macro circuit using the node plus the bundle of Kent for AVRT. AVRT vs AVNRT Two common re-entry SVTs. Know the difference. HIGH-YIELD · BOARD-FOCUSED · CLINICALLY RELEVANT FEATURE AVNRT AVRT Re-entry location Within or near the AV node AV node + accessory pathway Extra pathway? ✕ No ✓ Yes — the bundle of Kent Associated with WPW? ✕ No ✓ Yes Typical QRS Narrow Narrow (orthodromic) · wide (antidromic) P waves Usually hidden Often visible after the QRS, usually retrograde AVNRT Re-entry within or near the AV node ATRIA VENTRICLES AV NODE slow fast Dual pathways inside or beside the node form a self-sustaining loop. P waves usually hidden. AVRT Re-entry using the AV node + accessory pathway ATRIA VENTRICLES AV NODE KENT Down one limb and back up the other — a macro loop through the ventricle. ORTHODROMIC → narrow ANTIDROMIC → wide Pearl — AVNRT is one road, inside the AV node. AVRT is two roads: the AV node plus an accessory pathway. MASTER THE TEST. IMPACT THE PATIENT. PA CARDIOLOGY BOOTCAMP · @paclinicalbootcamp
The trap83-word note
antidromic AVRT conducts down the accessory pathway, so the QRS is wide and the tracing is indistinguishable from ventricular tachycardia on morphology alone. It is only about 10% of AVRT, but it is the reason a wide regular tachycardia is treated as VT until proven otherwise. The related danger sits one step further: if that same pathway is fed by atrial fibrillation rather than a re-entry circuit, AV-nodal blockade can accelerate conduction down it into VF — the pre-excited AF tracing in Part 2.
Name this tracingRead it before you read about it
Regular narrow-complex tachycardia · limb leads labeled VR / VL / VF in the older convention (= aVR / aVL / aVF)
Twelve-lead ECG for interpretation
Regular narrow-complex tachycardia with no discernible P waves. Which is most likely?
Click to Reveal Answer
Correct answer: D — AV nodal reentrant tachycardia
What the tracing shows
Twelve-lead ECG of a regular narrow-complex tachycardia consistent with AVNRT, recorded on pink grid paper. The limb leads are labeled in the older convention as VR, VL and VF rather than aVR, aVL and aVF. Every lead shows rapid, uniformly spaced narrow QRS complexes with no clearly visible preceding P waves, and a calibration pulse appears at the left edge of each row. A navy banner across the bottom of the tracing reads PAClinical Bootcamp.
Apply the comparison above. This is the one-road case — a circuit confined to the AV node, so there is no accessory pathway and nothing pre-excites the ventricle. The P wave is the giveaway: usually buried inside the QRS, and when it does surface it appears as a pseudo-r′ in V1 or a pseudo-S in the inferior leads rather than as a discrete wave after the QRS.
Why the other choices are wrong
  • Sinus tachycardia — Sinus tachycardia would show a discrete upright P wave before every QRS in lead II.
  • Atrial flutter with 2:1 conduction — Flutter with 2:1 conduction sits near 150 and shows a sawtooth baseline, best seen in II, III, aVF and V1.
  • Atrial fibrillation with a rapid ventricular response — Atrial fibrillation is irregularly irregular by definition; this rhythm is regular.
  • Junctional tachycardia — Junctional tachycardia is an automatic rhythm that tends to warm up and slow down gradually rather than start and stop abruptly, and it does not terminate with adenosine.
Board pearlIn AVNRT the P wave is not absent, it is hidden — look for a pseudo-r′ in V1 or a pseudo-S inferiorly rather than a discrete wave.

The narrow-complex workup

Narrow-complex workup: regular or irregular first (irregular → AFib / MAT / flutter with variable block). For regular SVT, vagal maneuvers / adenosine either break AVNRT/AVRT or transiently block the node to unmask flutter.

Narrow-complex tachycardia — differentiation algorithm
Three questions, four destinations
A differentiation algorithm for regular narrow-complex tachycardia. Step one: can you identify atrial activity? If not, think AVNRT or AVRT. If yes, step two: are they sawtooth flutter waves? If yes, atrial flutter. If not, step three: P waves are visible, so judge their timing — an abnormal P before the QRS indicates atrial tachycardia, while a retrograde P after the QRS indicates AVRT. Narrow-complex tachycardia — differentiation algorithm Once you know it is regular, the P wave decides the diagnosis REGULAR NARROW-COMPLEX TACHYCARDIA 1 Can you identify atrial activity? NO — none visible Think AVNRT or AVRT 2 Are they sawtooth (F) waves? YES — sawtooth baseline Atrial flutter IF YES IF NO 3 P waves visible — where are they? Timing relative to the QRS separates the last two possibilities. ABNORMAL P BEFORE QRS Atrial tachycardia RETROGRADE P AFTER QRS AVRT PA BOOTCAMP PROPERTY OF PA BOOTCAMP, LLC · FOR EDUCATIONAL USE ONLY
Where this fits105-word note
the regularity figure earlier in this part sorts every narrow-complex tachycardia. This one picks up the regular branch and works it to a diagnosis, which is why it opens where that figure leaves off. Two practical notes: absent atrial activity is not the same as absent P waves — in AVNRT the P is usually buried inside the QRS and may surface only as a pseudo-r′ in V1 or a pseudo-S inferiorly, so look for distortion rather than a discrete wave. And adenosine belongs at every branch point, because slowing the node either terminates a re-entrant circuit or unmasks the flutter waves that were hiding.
Ventricular rhythms and arrestVT, VF, torsades, asystole and PEA.

Wide QRS (≥120 ms) from a ventricular focus. The safe default: assume VT until proven otherwise.

  • PVCs — wide, bizarre, early, no preceding P, usually a full compensatory pause. Bigeminy / trigeminy / couplets; unifocal vs multifocal.
  • AIVR — regular wide rhythm at 50–100; classic during reperfusion after MI — benign and self-limited.
  • VT — ≥3 consecutive ventricular beats >100. Monomorphic (scar) vs polymorphic (ischemia/channelopathy). Sustained ≥30 s or unstable.
  • Torsades — polymorphic VT on a long QT, twisting around baseline → magnesium.
  • VF — chaotic, no QRS → defibrillate.
Don't miss New AFib → score stroke risk (CHA₂DS₂-VASc) and decide rate vs. rhythm. A regular narrow tachy at ~150 is flutter until proven otherwise.
Don't miss Mobitz II and complete block need pacing — don't be reassured by the normal beats between drops.
Board tip Adenosine is diagnostic and therapeutic in regular narrow SVT — it won't hurt and it reveals what's underneath.
Don't miss Wide-complex tachycardia in an older patient with heart disease is VT until proven otherwise — treat as VT.
Name this tracingRhythm Recognition — Day 1 drill7 questions
Drill question 1 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A 30-year-old endurance cyclist has this ECG at a pre-participation physical. He is asymptomatic and takes no medication. What is the rhythm?
Click to Reveal Answer
Correct answer: A — Sinus bradycardia
Rate is about 44. Every QRS is preceded by a P wave at a constant, normal PR interval, and the P waves are upright in II and aVF and inverted in aVR — the signature of a sinus origin. The QRS complexes are narrow. In an asymptomatic trained athlete this is physiologic, driven by high resting vagal tone, and needs no treatment or workup.
Why the other choices are wrong
  • Complete AV block — in third-degree block the P waves and QRS complexes are dissociated, so the PR interval varies continuously. This PR is fixed.
  • Junctional bradycardia — a junctional focus produces either no visible P wave or a retrograde P that is inverted in II and may fall after the QRS. Here upright sinus P waves precede every complex.
  • Sinus arrest with a junctional escape rhythm — sinus arrest means a pause with absent P waves followed by an escape beat. The rhythm here is regular with no dropped P.
  • Second-degree AV block with 2:1 conduction — 2:1 block shows twice as many P waves as QRS complexes, with the non-conducted P hiding in the T wave. Count them: the P:QRS ratio here is 1:1.
Board pearlRate alone never makes a rhythm pathological. Asymptomatic sinus bradycardia in a trained athlete needs nothing at all. Go looking for a cause only when there are symptoms — and then think drugs first (beta-blocker, non-dihydropyridine CCB, digoxin, amiodarone), then hypothyroidism, sinus node dysfunction, and inferior ischemia.
Drill question 2 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A 24-year-old woman presents with a temperature of 39.1°C and clinical dehydration. Her rate is 125. What is the rhythm, and what is the correct priority?
Click to Reveal Answer
Correct answer: B — Sinus tachycardia — treat the underlying cause
A discrete P wave precedes every QRS, upright in II with a constant PR, and the rate sits comfortably inside the sinus range for her age (roughly 220 minus age). Sinus tachycardia is almost always a response rather than a primary arrhythmia. The treatment is the cause: antipyretics and volume here. Rate-slowing the compensation is the error.
Why the other choices are wrong
  • AV nodal reentrant tachycardia — give adenosine — AVNRT is typically 150–250, starts and stops abruptly, and the P wave is buried in or just after the QRS rather than clearly in front of it.
  • Inappropriate sinus tachycardia — start a beta-blocker — that diagnosis requires a persistently elevated sinus rate without an identifiable trigger. She has two obvious triggers. Giving a beta-blocker to a febrile hypovolemic patient removes the compensation keeping her cardiac output up.
  • Focal atrial tachycardia — synchronized cardioversion — would show an abnormal P morphology different from sinus, and cardioverting a physiologic sinus tachycardia is both futile and harmful.
  • Atrial flutter with 2:1 conduction — rate control — flutter conducting 2:1 lands near 150 and shows uniform sawtooth F waves, best seen in II, III, aVF and V1. There is no sawtooth here.
Board pearlA rate near 150 is the ambiguity zone: sinus tachycardia, atrial flutter with 2:1 conduction, and AVNRT all live there. Hunt for flutter waves in II, III, aVF and V1 before you commit. And remember the general rule — sinus tachycardia is a symptom, so find what is driving it rather than treating the number.
Drill question 3 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
This tracing shows a PR interval of 300 ms with a QRS following every P wave. Which statement is correct?
Click to Reveal Answer
Correct answer: C — First-degree AV block — no pacing, and no treatment if asymptomatic
A PR interval above 200 ms with every P wave conducted defines first-degree AV block. The delay is almost always within the AV node itself, it is usually benign, and it does not require a pacemaker. The useful clinical move is to review rate-slowing medication and check for the reversible contributors — and in a young patient with new AV conduction delay, to think about Lyme carditis.
Why the other choices are wrong
  • A normal PR interval for this heart rate — the upper limit of normal is 200 ms and does not widen because the rate is slow.
  • Mobitz type I second-degree block — expect intermittent dropped beats — Wenckebach shows progressive PR lengthening ending in a dropped QRS. Nothing is dropped here; the PR is long but constant.
  • Mobitz type II second-degree block — pacing is indicated — Mobitz II shows a fixed PR with a sudden non-conducted P wave and carries a real risk of progression to complete block. Again, no beat is dropped here.
  • Complete AV block — pacing is indicated — third-degree block means no relationship at all between P waves and QRS complexes, with a varying PR and an escape rhythm. This PR is fixed and every P conducts.
Board pearlSort the AV blocks by whether beats drop and whether the PR is constant. Nothing drops and PR is long → first degree. PR lengthens progressively then a beat drops → Mobitz I. PR is fixed and a beat drops without warning → Mobitz II. No relationship at all → complete block. Only the bottom two rungs need a pacemaker.
Drill question 4 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A 71-year-old man with severe COPD, currently on theophylline, has this irregular tachycardia. What is the rhythm?
Click to Reveal Answer
Correct answer: A — Multifocal atrial tachycardia
The rate is above 100, the RR intervals are irregular, and there are discrete P waves of at least three different morphologies with varying PR intervals. That combination is multifocal atrial tachycardia, and it is strongly associated with decompensated COPD, hypoxia, and theophylline toxicity. Treatment is directed at the lung disease and oxygenation; when rate control is genuinely needed, verapamil or diltiazem is preferred because nonselective beta-blockade risks bronchospasm.
Why the other choices are wrong
  • Atrial flutter with variable block — flutter produces a uniform sawtooth at a fixed atrial rate near 300. These atrial waves differ from one another in shape.
  • Sinus tachycardia with frequent premature atrial contractions — PACs interrupt an otherwise regular sinus rhythm with an identifiable dominant sinus P. Here no single P morphology dominates.
  • Atrial fibrillation — AF has no organized P waves at all, only a fibrillatory baseline. The presence of discrete, countable P waves excludes it, and this is the single most commonly missed distinction on this pair.
  • Wandering atrial pacemaker — the same phenomenon, multiple atrial foci with shifting P morphology, but by definition at a rate below 100. This rate is above 100.
Board pearlMAT is wandering atrial pacemaker with a rate over 100 — the mechanism is identical and only the rate separates them. Clinically it is a marker of lung disease severity, so the answer to "how do I treat the rhythm" is usually "treat the hypoxia." Cardioversion does not work, because there is no single circuit to break.
Drill question 5 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
Every second beat on this tracing is early, wide and not preceded by a P wave. What is the rhythm?
Click to Reveal Answer
Correct answer: C — Ventricular bigeminy
A normal sinus beat alternates with a wide, early complex that has no preceding P wave, a T wave pointing opposite to the QRS, and a full compensatory pause after it. That is ventricular bigeminy — a PVC every other beat. The positive complex in V1 places the origin in the left ventricle. Note that the palpable pulse rate will be roughly half the complex count, because many PVCs generate too little stroke volume to be felt.
Why the other choices are wrong
  • Atrial bigeminy with aberrant conduction — a premature atrial beat is preceded by an ectopic P wave and typically followed by an incomplete pause. There is no premature P wave in front of these wide complexes.
  • Ventricular tachycardia — VT requires three or more consecutive ventricular beats. Here every ventricular beat is separated by a sinus beat, so consecutive ventricular activity never occurs.
  • Accelerated junctional rhythm with fusion beats — a junctional rhythm is regular with narrow complexes and is not premature. These complexes are both wide and early.
  • Second-degree AV block with 2:1 conduction — 2:1 block drops a QRS rather than adding an early one, and the conducted complexes stay narrow.
Board pearlPVCs in a structurally normal heart are common and usually benign, and suppressing them with antiarrhythmics causes more harm than the ectopy does. The features that should prompt investigation are a high burden (roughly above 10–15% of beats, which can cause a reversible cardiomyopathy), polymorphic PVCs, ectopy that increases with exercise, or any association with syncope or known structural disease.
Drill question 6 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A patient collapses and is unresponsive with no palpable pulse. This is the tracing. What is the immediate next step?
Click to Reveal Answer
Correct answer: E — Unsynchronized defibrillation
There is chaotic electrical activity with no identifiable P wave, QRS complex or T wave. In a pulseless patient this is ventricular fibrillation, and it is a shockable rhythm. Defibrillate as early as possible and resume high-quality compressions immediately afterwards without pausing to reassess the rhythm. Every interruption in compressions costs coronary perfusion pressure.
Why the other choices are wrong
  • Transcutaneous pacing — pacing treats bradycardia. It has no role in a fibrillating ventricle, which has too much electrical activity rather than too little.
  • IV magnesium sulfate 2 g — magnesium is for torsades de pointes, meaning polymorphic VT on a prolonged QT. It is not a routine VF drug.
  • IV amiodarone 300 mg — amiodarone has a role in VF, but only after defibrillation and epinephrine. Giving a drug before the first shock delays the only intervention that reliably terminates VF.
  • Synchronized cardioversion at 100 J — synchronization requires a QRS complex for the defibrillator to time the shock to. There is no organized QRS here, so the machine cannot synchronize and the shock would never be delivered.
Board pearlTwo rhythms are shockable in arrest: VF and pulseless VT. Two are not: asystole and PEA, which get compressions and epinephrine. Keep the vocabulary straight, because it encodes the physiology — defibrillation is unsynchronized and used when there is no usable QRS, while cardioversion is synchronized and requires one.
Drill question 7 of 7
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A patient is unresponsive with no pulse, and this appearance is present in every lead. What is the immediate next step?
Click to Reveal Answer
Correct answer: D — High-quality CPR with IV epinephrine
There is no organized electrical activity. Asystole is a non-shockable rhythm: the treatment is uninterrupted high-quality compressions plus epinephrine every 3–5 minutes, with a deliberate search for reversible causes. Before accepting a flat line as real, confirm it — check that the leads are attached, turn up the gain, and look in a second lead, because a disconnected lead and fine ventricular fibrillation can both masquerade as asystole, and one of those is shockable.
Why the other choices are wrong
  • Immediate unsynchronized defibrillation — shocking asystole does not help and interrupts compressions. Defibrillation only benefits VF and pulseless VT.
  • Synchronized cardioversion — there is no QRS to synchronize to, and no tachyarrhythmia to convert.
  • IV atropine 1 mg — atropine was removed from the asystole and PEA algorithm because it showed no benefit. It remains a drug for symptomatic bradycardia with a pulse.
  • Transcutaneous pacing — pacing has not been shown to improve outcomes in asystolic cardiac arrest and is not recommended in the arrest algorithm.
Board pearlConfirm the flat line before you believe it: leads, gain, second lead. Then run the non-shockable pathway — compressions and epinephrine — while working the reversible causes. Note the asymmetry worth memorising: atropine is out for asystole and PEA, but still in for symptomatic bradycardia in a patient who has a pulse.
3
THEN THESE
Conduction Abnormalities & Bundle Branch BlocksRBBB · LBBB · fascicular · bifascicular · WPW · pacemakers
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Before you beginConduction Abnormalities & Bundle Branch Blocks2 questions
Read the tracing before you read the part. Missing it is expected — attempting a question first makes the material stick better. The explanation unlocks once you submit.
ECG question 1 of 2
12-lead with lead II rhythm strip · 25 mm/s · 1 cm/mV · reproduced unmodified
Twelve-lead ECG for interpretation
PA Bootcamp Review
Which conduction abnormality is present on this tracing?
Click to Reveal Answer
Correct answer: C — Left bundle branch block
What the tracing shows
Twelve-lead ECG on red grid paper with a lead II rhythm strip beneath, annotated 25 millimetres per second and 1 centimetre per millivolt. The QRS complexes are broad. V1, V2 and V3 show deep predominantly negative complexes with ST elevation, while leads I and aVL show upright complexes with a broad contour.
A broad QRS of 120 ms or more with the LBBB pattern: a deep QS or rS in V1–V3 and a broad, notched or monophasic R wave in I, aVL, V5 and V6. The mnemonic is WiLLiaM — a W in V1 and an M in V6.
The ST-T changes here are secondary and expected, not ischemic. Where the QRS is predominantly negative the ST segment normally points the other way, which is why V1–V3 show elevation. Discordance is the rule in LBBB — and it is why judging ischemia on such a tracing needs the modified Sgarbossa criteria rather than the usual STEMI thresholds.
Why the other choices are wrong
  • Right bundle branch block — Right bundle branch block is the mirror of this. RBBB gives an rSR′ in V1 — the “rabbit ears”, an M shape — with a wide slurred S wave in I and V6. Here V1 carries a deep negative complex, the opposite pattern. MaRRoW for RBBB, WiLLiaM for LBBB.
  • Left anterior fascicular block — Left anterior fascicular block shifts the axis leftward to between −45° and −90°, with a qR in aVL and rS inferiorly — but it keeps the QRS under 120 ms. Only one fascicle is out, so the ventricle still activates quickly. A QRS this wide means a whole bundle is blocked, not a fascicle.
  • Ventricular paced rhythm — a sharp narrow deflection immediately before each QRS. There are none here.
  • Nonspecific intraventricular conduction delay — Incorrect. NSIVCD is the label for a QRS wider than 120 ms that fits neither bundle pattern — no broad monophasic R in V6 and I, no rSR′ in V1. This tracing shows the full left-sided pattern, so it earns the specific name.
Board pearlThe two blocks are not clinical equals. Isolated RBBB occurs in structurally normal hearts and is often incidental. LBBB is essentially always pathologic — it implies underlying structural disease and it makes ischemia uninterpretable by standard criteria. Note the guideline change here, because older sources still teach the old rule: a new LBBB is no longer a STEMI equivalent on its own. It raises the probability of coronary disease, but the decision to activate the cath lab rests on the Smith-modified Sgarbossa criteria (see the next question), not on the block itself. One habit worth building: any LBBB-looking QRS should prompt a scan for pacing spikes before you name the block.
Covered below under Bundle branch block — name it from V1 and V6 · pacing in the Pacemakers group · Sgarbossa in Part 5
ECG question 2 of 2
12-lead with lead II rhythm strip · reproduced unmodified
Twelve-lead ECG for interpretation
PA Bootcamp Review
This patient has a left bundle branch block. Which finding on this tracing indicates a superimposed acute anterior myocardial infarction?
Click to Reveal Answer
Correct answer: B — Disproportionate convex ST elevation in V4
What the tracing shows
Twelve-lead ECG on pink grid paper with a lead II rhythm strip beneath, showing a wide-complex rhythm with a left bundle branch block pattern. The right precordial leads carry deep negative complexes with marked ST elevation, and the ST segments in V3 and V4 are elevated with an upwardly convex contour.
Three of the four options are simply features of the bundle branch block itself. Only one breaks the rules that LBBB is allowed to break.
Look at how convex the ST segments are in V4. Normal discordant elevation in LBBB is concave — it scoops. A convex, domed contour is specific, though insensitive, for a large anterior infarction. It will not be present in every case, but when it is present it means something.
The infarction can also be called from V3, where the ST elevation is disproportionate to the depth of the preceding S wave. That is modified Sgarbossa criterion 3: an ST elevation to S-wave-depth ratio of 25 per cent or more. Small absolute elevation still counts when the S wave it accompanies is also small — which is exactly why the proportional rule replaced the old flat 5 mm threshold and lifted sensitivity from roughly 52 to 91 per cent.
Why the other choices are wrong
  • A QRS duration of 140 ms — A QRS of 140 ms is what defines the bundle branch block. It tells you conduction is abnormal and nothing whatever about ischemia.
  • Discordant ST elevation across V1 to V3 — Discordant ST elevation in V1–V3 is expected in LBBB. Where the QRS is predominantly negative the ST segment normally points the opposite way, so elevation in those leads on its own proves nothing. This is the single commonest reason LBBB tracings get over-called.
  • Deep S waves in V1 and V2 — Deep S waves in V1 and V2 are part of the normal LBBB pattern — the QS or rS complex in the right precordial leads. Again a feature of the block, not of infarction.
  • Left axis deviation with a wide QRS — Incorrect. Axis and QRS width are properties of the block, not of ischemia. Neither appears in any Sgarbossa criterion, and reading them as infarction is how LBBB tracings get over-called.
Board pearlIn LBBB, never ask “is there ST elevation?” — there always is. Ask two different questions instead. Is any elevation concordant, running the same way as a positive QRS? That is Sgarbossa criterion 1 and the most specific finding there is. If it is discordant, is it disproportionate at ST ÷ S of 25 per cent or more? Then add shape as a third check, because normal LBBB discordance is concave and convexity is a warning even when the ratios sit borderline. And remember the criteria are rule-in only — a negative result never excludes occlusion in a patient with ongoing pain.
Bundle branch morphology is covered below · the Sgarbossa criteria and the shape of ST elevation are both in Part 5 — Ischemia & Infarction

A wide QRS (≥120 ms) from a slow detour through the ventricle. Look at V1 and V6 to name the block.

Bundle branch block — name it from V1 and V6

RBBB — MaRRoWLBBB — WiLLiaM
V1rSR′ "rabbit ears" (M)deep QS (W)
V6wide slurred S (W)broad notched R, no septal Q (M)
Meaningoften benignalways pathologic; discordant ST-T
Bundle branches — RBBB versus LBBB
Two leads name the block: look at V1, confirm in V6
The bundle branches descend either side of the interventricular septum from the bundle of His, conducting rapidly so that both ventricles activate almost simultaneously, which keeps the QRS under 120 milliseconds. Right bundle branch block produces an rSR prime pattern in V1 and a wide slurred S in V6 and is often benign; left bundle branch block produces a deep QS in V1 and a broad notched R in V6 and is always pathologic. Bundle branches They carry the impulse from the bundle of His to each ventricle ANATOMY SEPTUM BUNDLE OF HIS RIGHT BUNDLE LEFT BUNDLE FUNCTION 1 Conduct to each ventricle Right branch → right ventricle. Left branch → left ventricle. 2 Rapid conduction Deliver the impulse quickly onward into the Purkinje fibers. 3 Coordinated activation Both ventricles activate almost simultaneously. ON THE ECG Conduction through the bundle branches is part of the QRS complex. Normal conduction → a narrow QRS, under 120 ms. CLINICAL CORRELATIONS — NAME IT FROM V1 AND V6 RIGHT BUNDLE BRANCH BLOCK — RBBB Delay in the right bundle branch. V1 rSR′ — “rabbit ears” V6 wide, slurred S Often benign in isolation. LEFT BUNDLE BRANCH BLOCK — LBBB Delay in the left bundle branch. V1 deep QS or rS V6 broad, notched R Always pathologic; ST-T discordant. BOARD PEARL The bundle branches are the high-speed highways from the bundle of His to the ventricles.
The mnemonic, and why it works80-word note
MaRRoW for RBBB: an M in V1 (the rSR′ rabbit ears) and a W in V6. WiLLiaM for LBBB: a W in V1 and an M in V6. The shapes follow the physiology — the blocked ventricle depolarizes late, so its wall pulls the terminal QRS toward whichever lead overlies it. Clinically the two are not equals: isolated RBBB is common in healthy hearts, while LBBB implies structural disease, obscures ischemia, and when new alongside ischemic symptoms is a STEMI-equivalent.

Fascicular blocks

Fascicular blocks: LAFB → left axis (−45° to −90°), qR in aVL, rS inferiorly, QRS <120; LPFB → right axis (rarer).

Pre-excitation — WPW

WPW: short PR (<120 ms), delta wave, wide QRS, secondary ST-T changes.

Bifascicular and trifascicular block

Bifascicular = RBBB plus one fascicular block. RBBB with LAFB (left axis) is much the commoner pair; RBBB with LPFB (right axis) is rare and implies more extensive disease. Trifascicular is a loose term — strictly it means bifascicular block plus a delay in the remaining fascicle, most often reported as bifascicular block with first-degree AV block. It is not the same as complete heart block, and the label alone does not mandate pacing; symptoms and documented higher-grade block do.

RBBB + LAFB commonest bifascicular pairRBBB + LPFB rare, more disease+ 1° AV block often called trifascicular
PacemakersFind the spikes, then ask about capture and sensing.

Find the pacing spikes, then ask two questions: is each spike producing a beat (capture), and is the device seeing the heart (sensing)?

NBG code

Position 1 chamber Paced · 2 chamber Sensed · 3 Response (I/T/D) · 4 rate modulation (R). VVI = ventricle paced+sensed, inhibited. DDD = dual everything. CRT/BiV = biventricular for HF with LBBB. A paced ventricular beat looks like LBBB (RV apical pacing).

Malfunction

  • Failure to capture — spike present, no complex follows.
  • Undersensing — spikes fire despite native beats (doesn't "see" them).
  • Oversensing — inappropriately inhibited by T waves / myopotentials → pauses.
  • Failure to pace — no spike when one is needed.

Ambulatory monitoring (match duration to symptom frequency)

Holter 24–48 hEvent recorder 2–4 wkMCT ~30 dLoop recorder up to 3 yr
Don't miss New LBBB + ischemic symptoms = STEMI-equivalent → Sgarbossa. And AFib in WPW: avoid AV-nodal blockers (adenosine, verapamil, β-blockers, digoxin) — they can accelerate conduction down the pathway into VF. Use procainamide or cardioversion.
Board tip A paced rhythm looks like LBBB — use modified Sgarbossa to find a STEMI hiding inside it. Treat computer/AI reads as a first pass: they miss subtle STEMI and over-call artifact.
Name this tracingBundle Branch Blocks — Day 1 drill1 question
Drill question 1 of 1
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
The QRS duration on this tracing is 140 ms. Which conduction abnormality is present, and what does it imply?
Click to Reveal Answer
Correct answer: C — Right bundle branch block — it does not obscure STEMI
The QRS is at or above 120 ms, V1 and V2 show an rSR′ with the tall terminal R′, and I, aVL, V5 and V6 show a broad slurred terminal S wave. That is right bundle branch block. RBBB can be an incidental finding in a structurally normal heart, but it is also seen with right heart strain including pulmonary embolism, with ischemia, and with degenerative conduction disease. Clinically the most important point is that RBBB preserves your ability to read ST elevation, so a STEMI is still diagnosable.
Why the other choices are wrong
  • A ventricular paced rhythm — a paced beat is preceded by a sharp pacing spike and typically produces an LBBB-like morphology from a right ventricular lead. There are no spikes here.
  • Wolff-Parkinson-White pre-excitation — WPW shows a short PR interval with a slurred delta wave on the QRS upstroke. The PR interval here is normal and there is no delta wave.
  • Left anterior fascicular block — LAFB produces a leftward axis shift with qR in I and aVL and rS in II, III and aVF, and the QRS stays under 120 ms.
  • Left bundle branch block — it obscures the diagnosis of STEMI — LBBB gives a broad monophasic R in V5–V6 and a deep QS or rS in V1 with no terminal R′. It is the block that obscures STEMI diagnosis and requires the modified Sgarbossa criteria.
Board pearlThe shape mnemonic is WiLLiaM MaRRoW: a W in V1 with an M in V6 is LBBB; an M in V1 with a W in V6 is RBBB. Then hold on to the difference that changes management — new LBBB can hide an infarct and needs Sgarbossa, whereas RBBB leaves the ST segments readable.
4
THEN THESE
Hypertrophy & Chamber EnlargementAtrial abnormality · LVH voltage criteria · RVH · low voltage
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A bigger chamber writes a bigger, odder deflection. Read the P wave in II and V1 for the atria; read QRS voltage for the ventricles.

Atrial abnormality

  • Left (LAA) — wide notched "M" P ≥120 ms in II = P mitrale; deep, wide (≥1 mm, ≥40 ms) negative terminal in V1.
  • Right (RAA) — tall peaked P >2.5 mm in II = P pulmonale; initial positive >1.5 mm in V1.
Atrial abnormality — P mitrale and P pulmonale
Left atrium widens the P wave; right atrium heightens it
Three P-wave morphologies compared in lead II and V1: the normal P wave under 2.5 millimetres tall and under 120 milliseconds wide; left atrial abnormality or P mitrale, a wide notched M-shaped P of 120 milliseconds or more with a deep wide negative terminal component in V1; and right atrial abnormality or P pulmonale, a tall peaked P above 2.5 millimetres of normal width with a tall initial positive component in V1. READ THE P WAVE IN LEAD II FOR WIDTH AND HEIGHT · IN V1 FOR ITS TWO COMPONENTS NORMAL P WAVE Reference LEAD II V1 < 2.5 mm tall in II < 120 ms wide (< 3 small boxes) V1 may be slightly biphasic LEFT ATRIAL ABNORMALITY P mitrale LEAD II V1 Wide, notched “M” P ≥ 120 ms in II Deep, wide negative terminal in V1 ≥ 1 mm deep and ≥ 40 ms wide RIGHT ATRIAL ABNORMALITY P pulmonale LEAD II V1 Tall, peaked P > 2.5 mm in II Width stays normal (< 120 ms) Initial positive > 1.5 mm in V1
The one-line rule83-word note
the left atrium depolarizes last, so enlarging it stretches the tail of the P wave: wider, notched, with a deep terminal negative deflection in V1, which sits closest to the left atrium. The right atrium depolarizes first, so enlarging it builds the front of the P wave taller without making it longer. Hence left widens, right heightens. Note the modern terminology: these are called atrial abnormality rather than enlargement, because the ECG cannot separate true enlargement from pressure overload or a conduction delay.

Left ventricular hypertrophy — voltage criteria

Sokolow-Lyon S(V1)+R(V5/6) ≥35 mmCornell R(aVL)+S(V3) >28 M / >20 F
Sokolow-Lyon Criteria
Voltage-based — the easy screening tool for LVH.
Sokolow-Lyon voltage criteria for left ventricular hypertrophy: the depth of the S wave in V1 added to the height of the R wave in V5 or V6, positive at 35 mm or more. Worked example: 18 mm plus 20 mm equals 38 mm, positive. SOKOLOW-LYON CRITERIA S in V1 + R in V5 or V6 ≥ 35 mm Voltage-based — the easy screening tool for LVH. DEEP S IN V1 18 mm TALL R IN V5 OR V6 20 mm TOTAL 18 mm + 20 mm 38 mm POSITIVE If the sum is ≥ 35 mm → LVH by Sokolow-Lyon
Using it66-word note
measure the deepest S in V1 and the tallest R in either V5 or V6, whichever is larger, and add the two. It is a screening tool: sensitive enough to raise the question but prone to false positives in thin young patients with a narrow chest, and to false negatives in obesity, COPD and anything else that puts insulating tissue between the heart and the electrode.
Cornell Criteria
More specific for LVH than Sokolow-Lyon — and sex-adjusted.
Cornell voltage criteria for left ventricular hypertrophy: the height of the R wave in aVL added to the depth of the S wave in V3, positive above 28 mm in men and above 20 mm in women. Worked example: 16 mm plus 15 mm equals 31 mm, positive in both sexes. CORNELL CRITERIA R in aVL + S in V3 > 28 mm (men) · > 20 mm (women) More specific for LVH than Sokolow-Lyon — and sex-adjusted. R IN aVL 16 mm S IN V3 15 mm TOTAL 16 mm + 15 mm 31 mm POSITIVE — men and women If > 28 mm in men or > 20 mm in women → LVH by Cornell
Using it53-word note
Cornell trades a little sensitivity for meaningfully better specificity than Sokolow-Lyon, and it is the only common criterion with a separate female threshold, which matters because women generate lower QRS voltage at any given ventricular mass. When the two criteria disagree, Cornell is the more trustworthy positive and Sokolow-Lyon the more trustworthy negative.

Right ventricular hypertrophy

RVH: R>S in V1, right axis deviation, RAA, ± RV strain (V1–3) — think pulmonary HTN / cor pulmonale.

Low voltage

Low voltage <5 mm limb / <10 mm precordial

Low-voltage differential — "fat, fluid, air, infiltrate": obesity, pericardial effusion, COPD, hypothyroidism, amyloid.

Board tip LVH strain mimics ischemia — clinical context, not the tracing alone, makes the call.
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Ischemia & InfarctionCascade · STEMI criteria · localization · equivalents · Sgarbossa
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The ST segment is the headline: elevation = injury/occlusion, depression and T-inversion = ischemia. Localize by lead group and always hunt for reciprocal change.

Ischemic cascade

Hyperacute T (tall, broad, symmetric) → ST elevation (convex / "tombstone") → T-wave inversion → pathologic Q (>40 ms wide or >25% of R height).

The evolving infarct — reading the age of an occlusion
One territory, five appearances, depending on when you catch it
The five appearances of an infarcting territory over time, each drawn on ECG paper. Baseline shows a small q, dominant R and concordant T. Within minutes the T wave becomes tall, broad and symmetric — the hyperacute T, the earliest and most missed change. Over minutes to hours convex tombstone ST elevation develops, which must meet criteria in at least two contiguous leads. Over hours to days the T wave inverts deeply and symmetrically as the ST settles. Over days and permanently a pathologic Q wave remains, at least 40 milliseconds wide or a quarter of the R-wave height, marking completed necrosis. The evolving infarct The stage of the tracing tells you the age of the occlusion TIME IS MYOCARDIUM 0 Normal BASELINE Small q, dominant R, flat ST, T concordant with the QRS. 1 Hyperacute T MINUTES Tall, broad and symmetric. The earliest change — and the most missed. 2 ST elevation MIN – HOURS Convex, "tombstone". Must meet criteria in ≥ 2 contiguous leads. 3 T inversion HOURS – DAYS Deep and symmetric as the ST segment settles back toward baseline. 4 Pathologic Q DAYS – PERMANENT ≥ 40 ms wide or ≥ 25% of R height. Marks completed necrosis. OCCLUSION WEEKS LATER WHERE THE DECISION LIVES Stages 1 and 2 are the reperfusion window. A hyperacute T with the right story is an occlusion — do not wait for the ST segment to declare itself.
The stages overlap — read the combination173-word note
The five stages are a continuum, not a queue — Q waves begin forming while the ST segment is still elevated, and T inversion often overlaps both. What matters is the combination in front of you: hyperacute T with a flat ST is minutes old, ST elevation with a clean R wave is early and salvageable, and ST elevation alongside a fully formed Q wave is hours in with muscle already lost. Three practical consequences. A hyperacute T is the highest-value catch on this figure, because it is the one stage where the ECG is abnormal before criteria are met — compare with a prior tracing rather than waiting to repeat. Q waves do not close the door: ongoing pain with persistent elevation still means viable myocardium and still means the cath lab. And the reverse trap is a tracing that has moved on — deep symmetric T inversion with Q waves and no elevation is a completed infarct presenting late, which changes urgency but not the need for admission and risk stratification.

STEMI criteria (4th Universal Definition) — STE in ≥2 contiguous leads

All leads ≥1 mmV2–V3 men ≥40: ≥2 mmmen <40: ≥2.5 mmwomen: ≥1.5 mm
The shape of ST elevation
Four morphologies that suggest ischemia, and the one that argues against it
Four shapes of ST elevation that suggest ischemia, each drawn from an elevated J point: convex or domed, the classic tombstone and the most specific for acute occlusion; straight upsloping; straight horizontal; and straight downsloping. Contrasted below with concave upward elevation, the scooped shape typical of benign early repolarization and pericarditis, which lowers but does not eliminate the probability of infarction. The shape of ST elevation How much it is elevated meets criteria — what shape it takes tells you whether to believe it FOUR SHAPES THAT SUGGEST ISCHEMIA — ANY ONE OF THEM COUNTS Convex Domed, bulging upward — the classic "tombstone". The most specific shape for acute coronary occlusion. Straight upsloping A straight line climbing from the J point into the T wave. No concavity anywhere along the segment. Straight horizontal A flat plateau sitting above the baseline before the T. Rigidly straight rather than scooped. Straight downsloping A straight line descending from an elevated J point. Elevation that falls away is still elevation. THE SHAPE THAT ARGUES AGAINST IT Concave upward Scooped, "smiley" — the segment sags below a line drawn from the J point to the top of the T. Typical of benign early repolarization and of pericarditis, where the elevation is diffuse and accompanied by PR depression rather than confined to a coronary territory. Concave does not exclude infarction — it lowers the odds. Shape supports the read; it never overrides the story.
Draw a line from the J point to the top of the T148-word note
The rule of thumb is that anything other than concave should worry you, and the reason is geometric rather than arbitrary. Draw a straight line from the J point to the peak of the T wave: in benign early repolarization the ST segment sags below that line, while in occlusion it bulges above it or runs straight along it. That single construction separates the five shapes on this figure without measuring anything. Two cautions. Shape is a probability shifter, not a rule-out — a genuine occlusion can begin with concave elevation and only dome later, which is why a concave tracing in a patient with ongoing pain earns a repeat ECG rather than reassurance. And shape says nothing about distribution: elevation confined to a coronary territory with reciprocal depression elsewhere outranks any morphological impression, whereas diffuse elevation with PR depression points at pericarditis whatever the curve looks like.
TerritoryLeadsArtery
Anterior/septalV1–V4LAD
LateralI, aVL, V5–V6LCx / diagonal
InferiorII, III, aVFRCA (85%) / LCx
PosteriorST↓ V1–V3 (mirror); STE V7–9 ≥0.5 mmRCA / LCx
Right ventricleSTE in V4Rproximal RCA
Name this tracingRead it before you read about it
12-lead with V1, II and V5 rhythm strips · calibration pulse at the left edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Which territory is infarcting, and which artery is responsible?
Click to Reveal Answer
Correct answer: D — Anterior — left anterior descending
What the tracing shows
Twelve-lead ECG of an anterior ST-elevation myocardial infarction on pink grid paper with V1, II and V5 rhythm strips beneath. Leads V2, V3 and V4 show marked convex ST elevation merging into broad T waves, while the limb leads show comparatively small complexes. A calibration pulse appears at the left edge of each row.
Anterior STEMI. Work the territory table above: elevation across V2–V4 is the LAD. Then check the shape against the figure above it — this is domed, convex elevation merging into the T wave, not a scooped concave curve.
Why the other choices are wrong
  • Inferior — right coronary artery — Inferior infarction elevates II, III and aVF.
  • Lateral — left circumflex — Lateral infarction elevates I, aVL, V5 and V6.
  • Posterior — circumflex or RCA — Posterior infarction shows ST depression in V1–V3 with tall R waves, not elevation.
  • Right ventricular — proximal RCA — RV infarction is suggested by elevation in V1 with inferior changes and is confirmed on a right-sided V4R.
Board pearlContiguous means anatomically adjacent, not adjacent on the printed page. V1–V2 are contiguous; III and V3 are not.
Name this tracingRead it before you read about it
12-lead with lead II rhythm strip · 25 mm/s · 10 mm/mV · calibration pulse at the right edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Which territory is involved, and what should you obtain before giving nitrates?
Click to Reveal Answer
Correct answer: A — Inferior — obtain a right-sided V4R
What the tracing shows
Twelve-lead ECG of an inferior ST-elevation myocardial infarction printed on blue grid paper with a lead II rhythm strip beneath. Leads II, III and aVF show ST elevation, with reciprocal ST depression in the high lateral leads. A footer reads paper speed 25 mm per second, voltage gain 10 mm per millivolt, and a calibration pulse appears at the right edge of each row.
Inferior STEMI. Elevation in II, III and aVF — the RCA in the large majority of people. Now look at I and aVL for the mirror: reciprocal depression in the high lateral leads is what separates a true inferior infarct from a look-alike.
⚑ Before nitrates, get a right-sided V4R. Inferior infarcts frequently involve the RV, which is preload-dependent — nitroglycerin can drop the pressure precipitously.
Why the other choices are wrong
  • Anterior — obtain posterior leads V7–V9 — Anterior involvement would elevate V1–V4, and posterior leads are for suspected posterior infarction.
  • Lateral — no additional leads needed — Lateral infarction elevates I, aVL, V5 and V6 — not the inferior leads.
  • Posterior — obtain V7–V9 — Posterior infarction shows ST depression in V1–V3; V7–V9 confirm it, but that is not this pattern.
  • Septal — no additional leads needed — Septal infarction elevates V1–V2.
Board pearlInferior infarcts frequently involve the right ventricle, which is preload-dependent. Nitroglycerin can drop the pressure precipitously — get V4R first, and give fluid rather than diuretics if the RV is involved.
Name this tracingRead it before you read about it
12-lead · standard labeling · calibration pulse at the left edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Tall R waves with horizontal ST depression and upright T waves in V1–V3. What is the diagnosis and disposition?
Click to Reveal Answer
Correct answer: B — Posterior MI — a STEMI-equivalent needing the cath lab
What the tracing shows
Twelve-lead ECG of posterior myocardial infarction on pink grid paper with standard lead labeling. The right precordial leads V1 to V3 show tall R waves with horizontal ST depression and upright T waves, the mirror image of ST elevation on the posterior wall, while the inferior leads show small complexes. A calibration pulse appears at the left edge of each row.
Posterior MI — the mirror image. Read the Posterior row of the table above against V1–V3: tall R waves, horizontal ST depression and upright T waves. Turn the tracing upside down and it becomes the ST elevation you were looking for. Confirm with posterior leads V7–V9, where ≥ 0.5 mm of elevation is diagnostic.
⚑ This is a STEMI-equivalent, not an NSTEMI. It belongs in the cath lab. Posterior infarction is the most commonly missed of all, because no lead on a standard 12-lead faces the posterior wall — you only ever see its reflection.
Why the other choices are wrong
  • Anterior ischemia — medical management — Anterior ischemia produces depression or T inversion without tall R waves and without upright T waves.
  • Right ventricular hypertrophy — no acute intervention — RVH gives R taller than S in V1 with right axis deviation, and it is not an acute finding.
  • NSTEMI — medical management and serial troponins — Treating this as an NSTEMI is the classic and dangerous error — it is an occlusion, and medical management delays reperfusion.
  • Benign early repolarization — reassurance — Benign early repolarization produces concave ST elevation with a notched J point, not depression.
Board pearlPosterior infarction is the most commonly missed of all, because no lead on a standard 12-lead faces the posterior wall — you only ever see its reflection. Confirm with V7–V9, where 0.5 mm of elevation is diagnostic.

Ischemia without ST elevation — NSTEMI

Name this tracingRead it before you read about it
12-lead with lead II rhythm strip · calibration pulse at the right edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
ST depression and T-wave change with no ST elevation anywhere. What establishes the diagnosis of infarction?
Click to Reveal Answer
Correct answer: C — A rise in troponin
What the tracing shows
Twelve-lead monochrome ECG of non-ST-elevation myocardial infarction with a lead II rhythm strip along the bottom. The rhythm is regular and narrow-complex, and widespread ST depression with T-wave changes is present across multiple lead groups without any ST elevation. A calibration pulse appears at the right edge of each row.
NSTEMI. ST depression and T-wave change without ST elevation anywhere. Note what the ECG cannot do here: it establishes ischemia, but troponin completes the diagnosis and separates NSTEMI from unstable angina. Compare the ST shape with the pericarditis table below — depression here is flat or downsloping, not concave.
⚑ One pattern that is not a routine NSTEMI. Widespread ST depression accompanied by ST elevation in aVR points to left main or proximal three-vessel disease. That combination is a cath-lab call, not a medical-management call.
Why the other choices are wrong
  • The ECG alone is diagnostic — The ECG alone establishes ischemia but cannot distinguish NSTEMI from unstable angina.
  • An echocardiogram — Echocardiography may show regional dysfunction but does not define infarction.
  • An exercise stress test — A stress test is contraindicated in the acute setting.
  • A repeat ECG at six hours — A repeat ECG is appropriate to track evolution but does not itself confirm infarction.
Board pearlWidespread ST depression with ST elevation in aVR is a different animal — it points to left main or proximal three-vessel disease and is a cath-lab call, not medical management.

Equivalents not to miss

  • Wellens — biphasic (Type A) or deep symmetric (Type B) T inversions in V2–V3 while pain-free → critical proximal LAD. Do NOT stress test; cath.
  • de Winter — upsloping ST depression >1 mm with tall symmetric T waves (± STE in aVR) → acute LAD occlusion. Treat as STEMI.
  • Posterior MI — isolated ST↓ V1–V3; get V7–V9.
Name this tracingRead it before you read about it
12-lead with lead II rhythm strip · calibration pulse at the left edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
A currently pain-free patient with these precordial T-wave changes, preserved R waves and no Q waves. What must you avoid?
Click to Reveal Answer
Correct answer: B — An exercise stress test
What the tracing shows
Twelve-lead ECG of Wellens syndrome on pink grid paper with a lead II rhythm strip beneath. The precordial leads show inverted and biphasic T waves while the R waves remain preserved, with no pathological Q waves and no ST elevation. A calibration pulse appears at the left edge of each row.
Wellens syndrome. Check the three things that make the diagnosis besides the T waves: R waves preserved, no pathological Q waves, and no meaningful ST elevation. Then decide the type — biphasic is Type A, deep and symmetric is Type B.
⚑ The trap is that it looks reassuring. This pattern appears after the pain resolves, so the patient is comfortable and the ST segments have normalized — yet the proximal LAD is critically stenosed. Do not stress test: provoking ischemia here can complete the infarct. It goes to the cath lab.
Why the other choices are wrong
  • Urgent coronary angiography — Angiography is the definitive and correct step.
  • Serial troponin measurement — Serial troponins are appropriate, and are often normal — part of what makes the pattern deceptive.
  • Admission for monitoring — Admission is mandatory, not something to avoid.
  • Aspirin — Aspirin is appropriate antiplatelet therapy.
Board pearlThe trap is that the patient looks well: the pattern appears after the pain resolves and the ST segments have normalized, while the proximal LAD remains critically stenosed. Provoking ischemia can complete the infarct.
Name this tracingRead it before you read about it
12-lead with lead II, V1 and V5 rhythm strips · calibration pulse at the left edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Upsloping ST depression rising into tall, broad, symmetric T waves across the precordial leads. How should this be managed?
Click to Reveal Answer
Correct answer: A — Treat as a STEMI — activate the cath lab
What the tracing shows
Twelve-lead ECG of the de Winter pattern on pink grid paper with lead II, V1 and V5 rhythm strips beneath. The precordial leads show upsloping ST depression beginning at the J point and rising into tall, broad, symmetric T waves, without ST elevation in those leads. A calibration pulse appears at the left edge of each row.
The de Winter pattern. Follow the ST segment out of the J point in the precordial leads: it depresses, then sweeps upward into a tall, broad, symmetric T wave. Depression plus a giant T, with no elevation where you are looking for it.
⚑ Treat as a STEMI. This is proximal LAD occlusion wearing a different face, and in roughly half of cases it never evolves into recognisable ST elevation — so waiting for a "real" STEMI to appear is how the diagnosis gets missed. Look for slight ST elevation in aVR as the supporting clue.
Why the other choices are wrong
  • Medical management as an NSTEMI — Medical management misses an acute occlusion; this is a STEMI-equivalent.
  • Discharge with outpatient follow-up — Discharge would be catastrophic in an acute LAD occlusion.
  • Exercise stress testing — Stress testing is contraindicated with an active occlusion.
  • Observe and repeat the ECG in six hours — Waiting for evolution is the specific trap: in roughly half of cases the pattern never evolves into recognisable ST elevation.
Board pearlLook for slight ST elevation in aVR as the supporting clue. And remember why waiting fails — de Winter frequently never becomes a “real” STEMI on the tracing, while the artery stays shut.

Sgarbossa (MI in LBBB / paced)

Concordant STE ≥1 mm (most specific) · concordant ST↓ ≥1 mm V1–3 · discordant STE ≥5 mm. Modified: replace the 5 mm rule with ST/S ratio ≥25% (sensitivity 52% → 91%).

Finding infarction behind an LBBB or paced rhythm

Modified Sgarbossa criteria
Finding an occlusion hidden behind LBBB or a paced rhythm
The modified Sgarbossa criteria, used only when acute MI is suspected in left bundle branch block or a ventricular paced rhythm. Because depolarization and repolarization are both abnormal in these rhythms, the ST-T normally points opposite to the QRS, so concordance is the abnormal finding. Any one of three criteria is positive: concordant ST elevation of at least 1 millimetre in any lead, which is the most specific; concordant ST depression of at least 1 millimetre in V1 to V3; or excessively discordant ST elevation where ST elevation divided by the depth of the preceding S wave is 25 percent or more. Modified Sgarbossa criteria For suspected acute MI in LBBB or a ventricular paced rhythm HIGH-YIELD · BOARD-FOCUSED · CLINICALLY RELEVANT WHEN TO USE Only when you suspect acute MI in a patient who has: Left bundle branch block Ventricular paced rhythm Both produce secondary ST-T changes that mimic ischemia, which is what makes these tracings so hard to read. THE CONCEPT — DISCORDANCE IS NORMAL In LBBB and paced rhythms both depolarization and repolarization are abnormal, so the ST-T normally points opposite to the QRS. NORMAL — DISCORDANT Positive QRS (I, V6) → ST depression Negative QRS (V1) → ST elevation ABNORMAL — CONCORDANT Positive QRS (I, V6) → ST elevation Negative QRS (V1) → ST depression → Concordant ST change is abnormal, and raises concern for acute MI. Criterion 3 is the exception: discordance that is excessive also counts. THE THREE CRITERIA — SMITH MODIFICATION · ANY ONE IS POSITIVE 1 Concordant ST elevation ≥ 1 mm in any lead — ST shifted in the SAME direction as the QRS MOST SPECIFIC 2 Concordant ST depression ≥ 1 mm in V1–V3 — ST shifted in the SAME direction as the QRS MODERATE SPECIFICITY 3 Excessively discordant ST elevation ST elevation ÷ depth of the preceding S wave ≥ 25% FEWER FALSE POSITIVES KEY TAKEAWAYS 1 Apply these criteria ONLY in LBBB or a ventricular paced rhythm. 2 Hunt for CONCORDANT change — ST in the same direction as the QRS. 3 Criterion 3 is a ratio: ST ÷ S ≥ 25% catches true occlusions. 4 Always integrate with symptoms, troponin and bedside echo. PA CARDIOLOGY BOOTCAMP · MASTER THE TEST. IMPACT THE PATIENT. @paclinicalbootcamp
Why the modification matters92-word note
the original Sgarbossa rule used a flat threshold of 5 mm of discordant elevation, which almost never occurs, so sensitivity sat near 52%. Replacing it with the proportional ST ÷ S ratio of 25% raised sensitivity to roughly 91% without giving up specificity, because a small absolute elevation is significant when the S wave it accompanies is also small. Two cautions: the criteria are rule-in only — a negative result never excludes occlusion — and they apply equally to a ventricular paced rhythm, since RV apical pacing produces the same LBBB-like morphology.
Don't miss Inferior STEMI → get a right-sided V4R before nitrates. RV infarct is preload-dependent and nitroglycerin can drop the pressure out from under them.
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Electrolytes & Metabolic ECGsPotassium · calcium · magnesium · digoxin
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The ECG is a window onto chemistry and drug levels. A handful of these patterns are genuinely can't-miss.

Electrolytes

  • Hyperkalemia (progressive): peaked narrow T (5.5–6.5) → PR prolongation, P flattening, QRS widening (6.5–7.5) → loss of P, sine wave (7+) → VF/asystole. QRS widens at both ends (unlike BBB).
  • Hypokalemia — ST depression, flat T, prominent U waves (V2–3), long QU; risk of torsades.
  • Calcium — high Ca → short QT; low Ca → long QT. Calcium tweaks the ST segment; potassium tweaks the T wave.
Hyperkalemia — the four-stage escalation
The tracing tells you how urgent the potassium is
Four stages of hyperkalemia on the ECG, from peaked T waves through P wave loss, QRS widening, and finally a sine wave, with the treatment sequence beneath. RISING SERUM POTASSIUM STAGE 1 STAGE 2 STAGE 3 STAGE 4 K⁺ 5.5–6.5 K⁺ 6.5–7.5 K⁺ 7.5–8.5 K⁺ >8.5 Tall, peaked, narrow “tented” T waves Shortened QT Earliest change P waves flatten, PR prolongs QRS begins to widen Conduction failing P waves gone QRS very wide, merging into the T wave Pre-terminal Sine wave — QRS and T indistinguishable VF or asystole next Cardiac arrest imminent Any ECG change = a rhythm emergency, not a lab result. 1. Stabilize — IV calcium gluconate or chloride first. It protects the membrane within minutes and does not lower the potassium. 2. Shift insulin + glucose, albuterol, bicarbonate if acidotic. 3. Remove dialysis, loop diuretic, potassium binder.
Board move58-word note
peaked T waves in a dialysis or renal-failure patient are hyperkalemia until proven otherwise. The distinguishing feature is that the QRS widens at both ends: in a bundle branch block only the terminal portion is delayed. Note also that the ECG correlates poorly with the absolute number in chronic kidney disease, so treat the tracing, not the value.
Name this tracingRead it before you read about it
12-lead with V1, II and V5 rhythm strips · calibration pulse at the left edge of each row
Twelve-lead ECG for interpretation
PA Bootcamp Review
Tall, sharply peaked T waves across the inferior and lateral leads. Which is most likely?
Click to Reveal Answer
Correct answer: D — Hyperkalemia
What the tracing shows
Twelve-lead ECG showing hyperkalemia on pink grid paper, with V1, II and V5 rhythm strips beneath the standard four-column layout. Tall, narrow-based, sharply peaked T waves are present across the inferior and lateral leads and the mid-precordial leads, while the QRS complexes remain narrow and P waves are still discernible. A calibration pulse appears at the left edge of each row.
Hyperkalemia. Look at the T waves in the inferior and lateral leads: tall, narrow-based and sharply peaked — tented rather than broad. Then place it on the escalation above by asking two questions: are the P waves still there, and is the QRS still narrow? Both preserved here, which puts it at the early end of the sequence.
⚑ Do not wait for the QRS to widen. Peaked T waves in a renal or dialysis patient are hyperkalemia until proven otherwise, and the treatment order is IV calcium first to stabilise the membrane, then insulin with dextrose to shift, then dialysis to remove.
Why the other choices are wrong
  • Hyperacute T waves of early STEMI — Hyperacute T waves of early infarction are tall but broad, and are confined to a coronary territory rather than appearing diffusely.
  • Benign early repolarization — Benign early repolarization gives concave ST elevation with a notched J point, not tented T waves.
  • Hypokalemia — Hypokalemia does the opposite: flattened T waves, ST sagging, prominent U waves and a long QT–U.
  • Normal variant in a young athlete — A normal athletic variant would not produce narrow-based tented T waves across multiple lead groups.
Board pearlHyperkalemic T waves are tall and narrow-based — tented rather than broad. That single feature separates them from the hyperacute T of early infarction, and it is the earliest change of the four-stage escalation.

Drugs

Digitalis effect = scooped "Salvador Dalí" ST sagging (therapeutic); toxicity = atrial tach with block, bidirectional VT, accelerated junctional. QT-prolongers (class IA/III, macrolides, fluoroquinolones, antipsychotics, methadone) → torsades. TCA overdose → sinus tach, wide QRS, terminal R in aVR >3 mm.

Don't miss Peaked T waves in a renal/dialysis patient = hyperkalemia until proven otherwise. Give IV calcium first (membrane stabilizer) before the QRS widens into a sine wave.
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ECG Mimics — Don’t Be FooledThe look-alikes that cost marks and patients
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Every pattern here has a benign twin or a dangerous doppelgänger. Grouping them in one place is deliberate: the discriminators only make sense side by side, and on the exam the distractor is almost always the mimic.

LVH strain versus ischemia

LVH strain: asymmetric ST depression / T inversion in lateral leads (I, aVL, V5–6).

Name this tracingRead it before you read about it
Standard 12-lead · 25 mm/s · 10 mm/mV · 100 Hz · rhythm strips V1, II and V5
Twelve-lead ECG for interpretation
PA Bootcamp Review
High QRS voltage with ST depression and asymmetric T inversion confined to I, aVL, V5 and V6. What is this?
Click to Reveal Answer
Correct answer: E — Left ventricular hypertrophy with strain
What the tracing shows
Twelve-lead ECG showing left ventricular hypertrophy with a strain pattern. Recorded on pink grid paper at 25 mm per second and 10 mm per millivolt with a 100 Hz filter, in the conventional four-column layout with blue lead labels, followed by three continuous rhythm strips from V1, II and V5. Very tall R waves dominate the lateral precordial leads and deep S waves the right precordial leads, with ST-segment and T-wave changes in the lateral leads.
Work the lateral leads — I, aVL, V5, V6 — then ask the question the figure below answers: do the ST/T changes appear only in leads with tall R waves?
Why the other choices are wrong
  • Lateral wall NSTEMI with reciprocal change — Lateral NSTEMI produces symmetric T inversion with flat or downsloping ST depression, and is not restricted to leads with tall R waves.
  • Left bundle branch block — LBBB requires a QRS of 120 ms or more with a broad notched R in V6 and a deep QS in V1.
  • Digoxin effect — Digoxin effect gives scooped, sagging ST segments rather than convex depression with asymmetric T inversion.
  • Hypokalemia — Hypokalemia gives flat T waves with prominent U waves, not high voltage with discordant strain.
Board pearlStrain is a voltage phenomenon: it can only appear in leads that already carry a tall R wave, and it is strictly discordant with them. Ischemia follows a coronary territory regardless of QRS polarity.
LVH strain versus true ischemia
Four features that separate two patterns that look alike
A four-feature comparison of the LVH strain pattern against true myocardial ischemia, covering T-wave symmetry and shape, ST-segment morphology, the relationship to QRS direction, and co-existing QRS voltage, with summary panels for when to favor each and a reminder that clinical correlation decides. LVH strain pattern vs true myocardial ischemia Both produce ST depression and T-wave inversion — these four features separate them FEATURE LVH STRAIN PATTERN TRUE MYOCARDIAL ISCHEMIA 1 T-wave symmetry and shape Asymmetrical. The initial downslope is gradual and prolonged; the terminal upslope is steep and quick. Symmetrical — the deep, sharp, pointed “coronary” T inversion, with both limbs of the T wave equal. 2 ST-segment morphology Upwardly convex, or “bowed”. The ST curves gently downward from the J point before blending into the inverted T. Flat, horizontal or downsloping, with the J point often depressed horizontally. No gentle convex curve. 3 Relationship to QRS direction Strict QRS–T discordance. ST depression and T inversion appear ONLY in leads with tall R waves — typically I, aVL, V5, V6. Often concordant, or distributed independently. Changes follow a coronary territory, not QRS polarity. 4 Co-existing QRS voltage Very high voltage in V5–V6: a deep S in V1 plus a tall R that together satisfy an LVH voltage criterion. Normal or low QRS voltage — unless chronic LVH and a new ischemic event happen to coexist in the same patient. THINK LVH STRAIN WHEN · Very high QRS voltage that meets an LVH criterion · ST depression and T inversion only in leads with tall R waves · Asymmetrical T waves with convex ST segments · Findings stable on prior tracings CLINICAL CORRELATION IS KEY Assess symptoms, risk factors, troponin, echo and prior tracings. When in doubt, treat for possible ischemia until it is proven otherwise. THINK TRUE ISCHEMIA WHEN · ST/T changes in leads without tall R waves · Symmetrical “coronary” T wave inversion · Flat or downsloping ST depression · New changes, or dynamic evolution
Board move94-word note
the discriminator that carries the most weight is the third one. Strain is a voltage phenomenon: it can only appear in leads that already have a tall R wave, and it is strictly discordant with them. Ischemia has no such constraint — it follows a coronary territory, so ST/T changes in a lead with a small or negative QRS argue strongly against strain. Two supporting habits: strain is stable across old tracings while ischemia evolves, and the two can coexist, which is why the safe move in genuine doubt is to treat for ischemia.

Normal variants that fake disease

Early repolarization (concave ST elevation, notched J point, young/healthy), persistent juvenile T inversions, vagal effects.

Pericarditis vs STEMI

PericarditisSTEMI
ST shapeconcave "smiley"convex / straight
Distributiondiffuseregional (territory)
Reciprocalabsent (except aVR)present
PR segmentdepressednormal

Hyperkalemia — the three patterns it imitates

Rising potassium widens the QRS and distorts repolarization, so severe hyperkalemia can be mistaken for three entirely different emergencies. In every case the tell is the same: look for the peaked, narrow-based T wave and the loss of P waves, and check a potassium before you commit.

Mistaken forWhy it fools youWhat gives hyperkalemia away
STEMITall T waves resemble hyperacute T waves; severe cases can produce genuine ST elevation, classically in V1–V2 (the “dialysis Brugada” pattern)Hyperkalemic T waves are narrow-based and tented, not broad; changes are diffuse rather than confined to a coronary territory, and there are no reciprocal changes
LBBBThe QRS widens diffusely and can exceed 120 ms with a bizarre, LBBB-like shapeTrue LBBB preserves discrete P waves and has a reproducible morphology; hyperkalemic widening comes with flattened or absent P waves and peaked T waves, and it reverses within minutes of calcium
VTExtreme widening blurs into a sine wave that looks like a slow, wide monomorphic tachycardiaThe rate is usually not fast — hyperkalemic sine wave is typically 60–120, whereas VT runs 140–200; and no P waves were ever visible on the preceding tracing
Don't miss A wide-complex rhythm in a dialysis patient is hyperkalemia until the potassium comes back. Give IV calcium empirically — it is diagnostic as well as therapeutic, because the QRS narrows within minutes if potassium was the cause.

VT vs SVT-with-aberrancy → favors VT

AV dissociation, capture beats, fusion beats, precordial concordance, QRS >160 ms, prior MI. Vereckei: an initial R wave in aVR → VT.

Wide-complex tachycardia — VT or SVT with aberrancy?
The default answer is VT, and the burden of proof runs the other way
Features favouring ventricular tachycardia versus SVT with aberrant conduction in a wide-complex tachycardia, with management guidance beneath. QRS ≥120 ms + rate >100 → assume VT until proven otherwise VT causes roughly 80% of wide-complex tachycardia overall, and about 95% when there is a prior myocardial infarction. FAVORS VT FAVORS SVT WITH ABERRANCY Prior MI, cardiomyopathy, or an ICD QRS >140 ms RBBB-like, >160 ms LBBB-like AV dissociation, fusion or capture beats Concordance across all of V1–V6 Extreme “northwest” axis deviation R-to-S >100 ms in any precordial lead strongest single predictor Known BBB, identical baseline morphology Textbook rSR′ in V1, or a classic LBBB shape Onset triggered by a premature P wave Breaks with adenosine or a vagal maneuver Young patient, structurally normal heart rS with R-to-S <100 ms precordially an old tracing is worth more than any criterion Unstable synchronized cardioversion. Stable and uncertain treat as VT — amiodarone or procainamide. Never give verapamil or diltiazem for an undifferentiated wide-complex tachycardia — it can precipitate hemodynamic collapse.
Board move53-word note
history beats morphology. A regular wide-complex tachycardia in a 68-year-old with a prior anterior MI is VT, and no amount of QRS-shape analysis should talk you out of it. The classic distractor is a stem that offers a calcium channel blocker for a “probable SVT”; the safe answer treats the rhythm as ventricular.
Name this tracingRead it before you read about it
12-lead · 4 × 2.5 s + one rhythm lead (V1) · 25.0 mm/s · 10.0 mm/mV · 100 Hz filter
Twelve-lead ECG for interpretation
PA Bootcamp Review
Regular wide-complex tachycardia with uniform QRS morphology in a patient with a previous myocardial infarction. What is it, and how should it be treated?
Click to Reveal Answer
Correct answer: D — Monomorphic VT — treat as ventricular tachycardia
What the tracing shows
Twelve-lead ECG of monomorphic ventricular tachycardia on pink grid paper, recorded in a four-by-2.5-second layout with a single V1 rhythm lead beneath. Every lead shows a rapid, regular, very broad and uniform QRS complex with no discernible preceding P waves, and the complexes are similarly directed across the precordial leads. Machine settings printed along the bottom read 100 Hz, 25.0 mm per second and 10.0 mm per millivolt.
Monomorphic ventricular tachycardia. Run the discriminators from the figure above against it: QRS width, whether the precordial leads are concordant, the axis, and whether any beat betrays fusion or capture. Note how uniform the complexes are — monomorphic means one morphology, which points to a fixed scar circuit rather than acute ischemia.
Why the other choices are wrong
  • SVT with aberrancy — give adenosine — Assuming SVT risks giving an AV-nodal blocker to a patient in VT, which can cause haemodynamic collapse.
  • Sinus tachycardia with bundle branch block — treat the underlying cause — Sinus tachycardia would show P waves at a matching rate.
  • Atrial fibrillation with aberrancy — rate control — Atrial fibrillation is irregularly irregular; this rhythm is regular.
  • Artefact — repeat the tracing — Calling it artefact delays treatment of a lethal rhythm.
Board pearlPrior MI plus a wide regular tachycardia carries a positive predictive value for VT above 95 per cent. Uniform morphology means one fixed circuit — usually old scar rather than acute ischemia.
Name this tracingRead it before you read about it
Wide-complex tachycardia · six-row by two-column layout · 25 mm/s · 10 mm/mV · 150 Hz filter
Twelve-lead ECG for interpretation
PA Bootcamp Review
This wide regular tachycardia is supraventricular with aberrant conduction, yet it is very hard to separate from the VT above by eye. Which factor separates them most reliably?
Click to Reveal Answer
Correct answer: E — Structural heart disease or prior MI
What the tracing shows
Twelve-lead ECG of a regular wide-complex tachycardia attributed to supraventricular tachycardia with aberrant conduction, printed on pink grid paper in an unusual six-row by two-column layout: leads I, II, III, aVR, aVL and aVF down the left, V1 to V6 down the right. Every lead shows rapid, regular, broad QRS complexes of uniform morphology with no discernible preceding P waves. Machine settings along the bottom read 25 mm per second, 10 mm per millivolt and a 150 Hz filter.
SVT with aberrant conduction — supraventricular in origin, wide only because it is conducting down a diseased or refractory bundle. Compare it directly against the VT tracing above: both are regular, both are broad, both lack visible P waves.
If you cannot separate these two by eye, that is the correct reaction. Morphology alone is unreliable, which is exactly why the discriminators in the figure above lean on history and structure — prior MI, cardiomyopathy, an ICD — over QRS shape, and why an undifferentiated wide regular tachycardia is treated as VT.
Why the other choices are wrong
  • QRS duration — QRS duration overlaps substantially between the two; a QRS above 160 ms favors VT but does not settle it.
  • QRS morphology in V1 — V1 morphology is suggestive at best — both rhythms can produce right or left bundle patterns.
  • The ventricular rate — Rate does not discriminate; both commonly run 150–200.
  • Whether it responds to a vagal maneuver — Vagal maneuvers may terminate a nodal-dependent SVT, but failure proves nothing and delays treatment in VT.
Board pearlIf you cannot separate these two by eye, that is the correct reaction. History and structure outrank morphology — which is why an undifferentiated wide regular tachycardia is treated as VT until proven otherwise.
Name this tracingST-Elevation Mimics — Day 1 drill2 questions
Drill question 1 of 2
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A 28-year-old man has sharp pleuritic chest pain that is worse lying flat and better sitting forward, five days after a viral illness. Which finding on this tracing best distinguishes his diagnosis from an acute STEMI?
Click to Reveal Answer
Correct answer: D — PR depression with diffuse concave ST elevation
Three features here point to pericarditis rather than infarction. The ST elevation is diffuse, crossing territories that no single coronary artery supplies. Its shape is concave or saddle-shaped rather than domed. And the PR segment is depressed, with the mirror finding in aVR of PR elevation and ST depression. There is no reciprocal depression and no Q-wave formation. PR-segment depression is close to specific for pericardial inflammation.
Why the other choices are wrong
  • ST depression in the reciprocal territory — reciprocal change is a hallmark of STEMI. Its absence is what supports pericarditis, so its presence would argue the other way.
  • Convex ST elevation confined to contiguous leads — that describes a STEMI. Territorial distribution and a domed upward-convex ST segment are the infarct pattern.
  • Terminal T-wave inversion in the leads with ST elevation — this is part of the evolving infarct sequence. In pericarditis T-wave inversion appears only later, after the ST segments have returned to baseline.
  • Q waves in the leads showing ST elevation — Q waves indicate established myocardial necrosis and point toward infarction. Pericarditis does not produce them.
Board pearlThree discriminators, in order of usefulness: territory (diffuse versus regional), PR segment (depressed in pericarditis), and ST morphology (concave versus convex). Read aVR as the confirmatory lead — PR elevation with ST depression there is the reciprocal of diffuse pericardial injury. Spodick sign, a downsloping TP segment, supports the diagnosis when present.
Drill question 2 of 2
12-lead with lead II rhythm strip · 25 mm/s, 10 mm/mV · Bootcamp-generated tracing
Twelve-lead ECG with a lead II rhythm strip, for interpretation
A 22-year-old asymptomatic man has this ECG during pre-participation screening. He has no chest pain and no family history of sudden death. What is the most likely explanation for the precordial ST elevation?
Click to Reveal Answer
Correct answer: C — Benign early repolarization
The ST elevation is confined to V2–V5, concave upward, and begins from a notched or slurred J point — the classic fish-hook. The R waves are preserved, the T waves are tall and concordant, there is no reciprocal depression, and the PR segment is flat. In an asymptomatic young man this is benign early repolarization, a normal variant that is more common in young males and in patients of African descent, and it is stable across years of tracings.
Why the other choices are wrong
  • Left ventricular hypertrophy with a strain pattern — LVH strain gives high QRS voltage with ST depression and asymmetric T-wave inversion in the lateral leads, which is close to the opposite of this picture.
  • Acute anterior STEMI — infarction produces convex domed ST elevation in a coronary territory, usually with reciprocal depression, and it evolves over hours with Q-wave formation and T-wave inversion. It would also not occur in a well, pain-free 22-year-old at a screening visit.
  • Brugada type 1 pattern — Brugada shows coved ST elevation of 2 mm or more in V1–V3 that descends into an inverted T wave. Here the elevation is concave and the T waves are upright.
  • Acute pericarditis — pericarditis is diffuse rather than confined to the mid-precordial leads and characteristically depresses the PR segment. The PR segment here is flat.
Board pearlThe triad is a notched J point, elevation limited to the mid-precordial leads, and a well patient. When you are genuinely unsure, the single most valuable next step is a prior ECG: early repolarization looks identical years apart, and an infarct does not.
8
THEN THESE
High-Yield Special PatternsBrugada · ARVC · long & short QT · torsades · Osborn · PE · HCM · alternans
▼

Named patterns worth recognizing on sight. Each is a single visual association carrying a disproportionate amount of exam weight — and several are the reason a young patient with a normal-looking heart is at risk of sudden death.

Disease patterns

Pericarditis: diffuse concave STE + PR depression, Spodick sign (downsloping TP). PE / cor pulmonale: sinus tach is most common; classic S1Q3T3, RV strain (TWI V1–4). Brugada: Type 1 coved STE ≥2 mm V1–3. Long QT: QTc >500 = high torsades risk (LQT1 exercise, LQT2 auditory, LQT3 sleep). HCM: LVH + deep narrow "dagger" Q waves. Hypothermia: Osborn (J) waves. CNS/SAH: deep "cerebral" T inversions + long QT. Dextrocardia: inverted P/QRS in I, reverse R progression.

ARVC — arrhythmogenic right ventricular cardiomyopathy

Fibro-fatty replacement of RV myocardium in a young patient, and a cause of exercise-related sudden death that the resting ECG can flag. Look for T-wave inversion in V1–V3 beyond age 14 with no RBBB, an epsilon wave (a small discrete deflection in the terminal QRS in V1–V3), prolonged terminal activation duration, and ventricular ectopy or VT with a left bundle morphology and inferior axis — the signature of an RV origin.

T inversion V1–V3, age >14, no RBBBEpsilon wave terminal QRS notchVT LBBB morphology, inferior axis

The nine patterns, side by side

PatternECG signatureWhy it matters
BrugadaCoved ST elevation with RBBB-like morphology in V1–V3 (type 1)Sodium channelopathy; sudden-death risk. Ask about syncope and family history
ARVCT inversion V1–V3 without RBBB, epsilon wave, VT with LBBB morphology and inferior axisExercise-related sudden death in the young
Long QTQTc >460 ms (women) / >450 ms (men); often drug-induced or electrolyte-drivenSubstrate for torsades — check the medication list
Short QTQTc <340 ms with tall peaked T waves and no ST segmentRare channelopathy with AF and sudden death; also hypercalcemia and digoxin
Torsades de pointesPolymorphic VT with a QRS axis that twists around the baselineIV magnesium first, then correct the QT and stop the offending drug
Osborn (J) wavesNotched, dome-shaped J point with bradycardiaHypothermia — resolves with rewarming
Pulmonary embolismS1Q3T3, sinus tachycardia, RBBB, right axis, T inversion V1–V4Suggestive but neither sensitive nor specific; sinus tachycardia is commoner than the triad
HCMHigh LV voltage with deep narrow “dagger” Q waves laterally and inferiorlyCommonest cause of sudden cardiac death in young athletes
Electrical alternansBeat-to-beat variation in QRS amplitude with sinus tachycardiaLarge effusion with tamponade — echo and pericardiocentesis, never diurese
Don't miss Four of these nine — Brugada, ARVC, long QT and HCM — are causes of sudden death in a young person whose heart looks structurally normal on examination. In a syncope history with a family history of early sudden death, the ECG is the screening test.
The night-before rules
High-Yield Pearls

The reflex reads, the can't-miss moves, and the buzzword associations — the points-per-minute payoff of any ECG review, pulled into one place.

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Reflex reads
…until proven otherwise
  • Irregularly irregular, no P waves → atrial fibrillation
  • Regular narrow tachy at ~150 → atrial flutter (2:1)
  • Regular narrow tachy 150–250, abrupt → AVNRT
  • Wide-complex tachycardia → VT (esp. prior MI / structural disease)
  • Peaked T waves in a renal patient → hyperkalemia
  • Electrical alternans + sinus tach → effusion / tamponade
Can't-miss moves
Pattern → the action
  • Inferior STEMI → V4R before nitrates (RV infarct)
  • New LBBB + ischemic pain → Sgarbossa; STEMI-equivalent
  • AFib + WPW → procainamide / cardiovert; no AV-nodal blockers
  • Torsades → IV magnesium
  • Mobitz II / complete block → pacing
  • Wellens → no stress test, urgent cath
  • de Winter → treat as acute LAD occlusion
  • Hyperkalemia w/ ECG changes → IV calcium first
Buzzword → diagnosis
Instant associations
  • Sawtooth waves → atrial flutter
  • Short PR + delta wave → WPW
  • S1Q3T3 → pulmonary embolism
  • Osborn (J) waves → hypothermia
  • Scooped "Salvador Dalí" ST → digitalis effect
  • Deep narrow "dagger" Q waves → HCM
  • Coved ST elevation V1–V3 → Brugada
  • Prominent U waves → hypokalemia
Expert consensus · Priority list
The Must-Know 23

The highest-priority patterns every PA/MD student must recognize on sight. The ones in red are the can't-miss, time-critical reads.

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01
Normal sinus rhythm
Rate 60–100, upright P in II, constant PR, 1:1
02
Sinus tachycardia
Rate >100, normal P waves, gradual on/off
03
Sinus bradycardia
Rate <60, normal P waves; find the cause
04
Atrial fibrillation
Irregularly irregular, no P waves, fibrillatory baseline
05
Atrial flutter
Sawtooth F waves (~300), often 2:1 → ~150
06
SVT (AVNRT / AVRT)
Regular narrow, 150–250, abrupt onset/offset
07
PACs
Early P (different morphology), narrow QRS
08
PVCs
Wide bizarre QRS, no preceding P, compensatory pause
09
Monomorphic VT
Wide (>120), regular, >100, uniform morphology
10
Ventricular fibrillation
Chaotic, no QRS — defibrillate immediately
11
1st-degree AV block
PR >200 ms, all P waves conduct
12
2nd-degree AV block (I & II)
I: PR lengthens → drop · II: constant PR → sudden drop (high risk)
13
3rd-degree AV block
Complete dissociation, atrial > ventricular rate
14
RBBB
QRS ≥120, rSR′ in V1, wide S in I/V6 (MaRRoW)
15
LBBB
QRS ≥120, notched R I/V5–6, QS in V1 (WiLLiaM)
16
LAFB
LAD, qR in aVL, rS inferiorly, QRS <120
17
LVH
Sokolow ≥35 mm or Cornell ± strain
18
RVH
R>S in V1, right axis deviation, ± RV strain
19
Acute STEMI
STE meeting criteria + reciprocals → localize
20
Acute pericarditis
Diffuse concave STE + PR depression, no reciprocals
21
Hyperkalemia
Peaked T → wide QRS → loss of P → sine wave
22
Hypokalemia
ST depression, flat T, prominent U waves
23
WPW pattern
Short PR <120, delta wave, wide QRS
PA Clinical Bootcamp — ECG Interpretation
Rajiv Choudhary, MD, MPH · Curriculum & visual tracing library for PANCE/PANRE preparation

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