Systematic 12-lead ECG analysis: rate, rhythm, axis, intervals, hypertrophy, ischemia, infarction localization, arrhythmias, conduction blocks, electrolyte changes, drug effects, and every diagnostic pattern with the criteria needed to recognize it.
01 Cardiac Electrophysiology
The electrocardiogram (ECG/EKG) is a surface recording of the summed electrical activity of millions of cardiac myocytes as they depolarize and repolarize in sequence. Every wave, interval, and segment on the 12-lead ECG reflects a specific electrical event in the heart. Mastery of ECG interpretation begins with understanding the cellular basis of cardiac electrical activity — the ionic currents that generate the action potential and the anatomic conduction system that propagates it.
Why This Matters
The ECG is the most frequently performed cardiac diagnostic test in the world. It is cheap, fast, non-invasive, and diagnostic for ischemia, arrhythmias, conduction disorders, chamber enlargement, electrolyte disturbances, drug toxicity, and inherited channelopathies. A physician who can read an ECG quickly and systematically will save lives at the bedside — particularly in the recognition of STEMI, dangerous arrhythmias, and lethal channelopathies.
Figure 1 — Cardiac Action Potential. The action potential in the sinoatrial node (pacemaker cell, top) and ventricular contractile myocyte (bottom), showing the five phases and corresponding ionic currents that generate the surface ECG.
Cardiac Action Potential — Ventricular Myocyte
The ventricular (and atrial) action potential has five phases, each driven by specific ion currents. Understanding these phases explains both the surface ECG and the mechanism of every antiarrhythmic drug.
Phase
Event
Ionic Current
ECG Correlate
Phase 0
Rapid depolarization
Fast Na+ influx (INa)
QRS complex (ventricles)
Phase 1
Initial rapid repolarization
Transient K+ efflux (Ito)
J point
Phase 2
Plateau
Ca2+ influx (L-type) balanced by K+ efflux
ST segment
Phase 3
Rapid repolarization
Delayed rectifier K+ efflux (IKr, IKs)
T wave
Phase 4
Resting membrane potential
Inward rectifier K+ (IK1)
TP segment (isoelectric)
The IKr current (rapid delayed rectifier, encoded by hERG/KCNH2) is the most commonly drug-blocked potassium channel. Blocking IKr prolongs phase 3, lengthens the QT interval, and predisposes to torsades de pointes. This is why so many drugs (macrolides, fluoroquinolones, methadone, ondansetron, antipsychotics, class III antiarrhythmics) must be screened for QT prolongation.
Pacemaker (Nodal) Action Potential
SA and AV nodal cells have a distinct four-phase action potential lacking a true resting potential. Phase 4 is a slow spontaneous diastolic depolarization driven by the funny current (If, a mixed Na+/K+ inward current) plus decreasing K+ efflux. Phase 0 upstroke is slow and calcium-mediated (L-type Ca2+ channels), not sodium-mediated. This is why calcium-channel blockers slow the sinus rate and prolong AV nodal conduction while lidocaine (a Na+-channel blocker) has no effect on nodal tissue.
Feature
Nodal Cell
Ventricular Myocyte
Resting potential
Unstable (−60 mV)
Stable (−90 mV)
Phase 0 upstroke
Slow, Ca2+-mediated
Fast, Na+-mediated
Automaticity
Yes (If)
No (normally)
Conduction velocity
0.02–0.1 m/s
0.3–1.0 m/s
Figure 2 — ECG Waves and Cardiac Events. The classical ECG curve showing the P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization) with their corresponding cardiac events.
Vectors & the Surface ECG
At any moment during depolarization, the summed electrical activity of the heart is a three-dimensional vector. Each ECG lead is an oriented "camera" that records the component of this vector along its own axis. A depolarization wave moving toward a positive electrode produces an upward (positive) deflection; a wave moving away produces a downward (negative) deflection; a wave perpendicular to the lead axis produces no (isoelectric) deflection. This single principle explains every ECG finding.
The mean QRS vector normally points down and to the left (toward lead II) because left ventricular mass dominates. When a lead is isoelectric, the mean vector is perpendicular to that lead — the fastest way to find the axis.
Excitation-Contraction Coupling
Action potential propagation into the T-tubule system activates voltage-gated L-type Ca2+ channels (dihydropyridine receptors). The small influx of calcium triggers a much larger release from the sarcoplasmic reticulum via ryanodine receptors (RyR2) — a process called calcium-induced calcium release. The resulting cytosolic calcium surge binds troponin C and initiates cross-bridge cycling. Relaxation requires calcium reuptake into the SR via SERCA2 (inhibited by phospholamban) and extrusion via the Na+/Ca2+ exchanger. Mutations in RyR2 cause catecholaminergic polymorphic VT (CPVT), a dangerous inherited arrhythmia.
Figure 3 — Refractory Periods. The absolute and relative refractory periods during the ventricular action potential. The relative refractory period corresponds to the vulnerable window where a premature stimulus (R-on-T) can trigger arrhythmias.
Refractory Periods
Period
Definition
Significance
Absolute refractory period (ARP)
Phases 0–early 3; no stimulus can initiate AP
Prevents tetany of cardiac muscle
Effective refractory period (ERP)
Slightly longer than ARP; no propagating AP possible
Main antiarrhythmic drug target
Relative refractory period (RRP)
Phase 3 late; a suprathreshold stimulus can fire
The "vulnerable period" for R-on-T
Supernormal period
End of phase 3; subthreshold stimulus can fire
Rarely clinically relevant
R-on-T phenomenon occurs when a premature beat falls during the relative refractory period (the peak of the T wave), which can precipitate polymorphic VT or VF, especially in the setting of long QT. This is why lidocaine was historically used prophylactically in acute MI — but modern trials showed harm and the practice was abandoned.
02 Conduction System & Lead Placement
Figure 4 — Chest Landmarks for ECG Placement. External anatomic landmarks used to locate the intercostal spaces for correct precordial electrode placement. Accurate landmarking at the angle of Louis (sternal angle) is essential to avoid misdiagnosis.
Normal Conduction Pathway
The impulse originates in the sinoatrial (SA) node (upper right atrium, at the junction of the SVC and RA) which has the fastest intrinsic rate (60–100 bpm). The impulse spreads across the atria via internodal tracts (and Bachmann bundle to the left atrium), producing the P wave. It reaches the AV node (floor of the RA, near the coronary sinus), where conduction slows dramatically to allow atrial emptying into the ventricles — this delay creates the PR segment. The impulse then traverses the bundle of His, divides into right and left bundle branches, and terminates in the Purkinje network that depolarizes the ventricular myocardium rapidly and simultaneously (QRS complex).
Structure
Intrinsic Rate
Blood Supply
SA node
60–100 bpm
RCA (60%) / LCx (40%)
AV node
40–60 bpm
RCA (90% — AV nodal branch from PDA)
His-Purkinje
20–40 bpm
LAD (septal) + RCA
Because the RCA supplies both the SA node and AV node in most patients, inferior MI (RCA occlusion) commonly produces sinus bradycardia, AV block, and junctional escape rhythms. These are usually transient and respond to atropine. In contrast, AV block in anterior MI (LAD occlusion) means massive septal necrosis and carries a very poor prognosis — pacemaker required.
Figure 5 — Standard 12-Lead ECG Electrode Placement. Complete electrode placement for a standard 12-lead ECG. The four limb electrodes (RA, LA, RL, LL) record the frontal plane leads, while the six precordial electrodes (V1–V6) record the horizontal plane.
12-Lead Placement — Limb Leads
The six limb leads record the heart's electrical activity in the frontal plane.
Lead
Type
View
Angle
Lead I
Bipolar (LA − RA)
Lateral
0°
Lead II
Bipolar (LL − RA)
Inferior
+60°
Lead III
Bipolar (LL − LA)
Inferior
+120°
aVR
Unipolar (RA)
Right upper / cavity
−150°
aVL
Unipolar (LA)
High lateral
−30°
aVF
Unipolar (LL)
Inferior
+90°
12-Lead Placement — Precordial (Chest) Leads
The six precordial leads record the heart in the horizontal plane.
Lead
Position
View
V1
4th intercostal space, right sternal border
Septal / RV
V2
4th intercostal space, left sternal border
Septal
V3
Between V2 and V4
Anterior
V4
5th intercostal space, midclavicular line
Anterior / apex
V5
Anterior axillary line, level of V4
Lateral
V6
Midaxillary line, level of V4
Lateral
Figure 6 — V4R Lead Placement. The right-sided V4R electrode is placed in the 5th intercostal space at the right midclavicular line, mirroring V4. Essential for diagnosing right ventricular infarction in inferior STEMI.Figure 7 — Posterior Lead Placement (V7–V9). Posterior leads placed at the posterior axillary line (V7), mid-scapular line (V8), and left paraspinal border (V9) at the level of V6. Used to confirm posterior STEMI when V1–V3 show ST depression with tall R waves.
Special Lead Placements
Two right-sided leads (V4R) and posterior leads (V7–V9) are essential in specific clinical scenarios:
V4R (5th intercostal space, right midclavicular line): diagnoses RV infarction in the setting of inferior STEMI — any ST elevation ≥ 0.5 mm is diagnostic.
V7–V9 (posterior axillary, mid-scapular, paraspinal lines at level of V6): diagnose posterior STEMI when V1–V3 show ST depression & tall R waves. ST elevation ≥ 0.5 mm in V7–V9 is diagnostic.
Lead Grouping Mnemonic
Inferior = II, III, aVF. Lateral = I, aVL, V5, V6. Septal = V1, V2. Anterior = V3, V4. High lateral = I, aVL. Posterior = V7–V9 (mirror in V1–V3). RV = V4R.
03 Paper Speed, Calibration & Normal Intervals
Figure 8 — Normal ECG Waveform Components. A labeled diagram of the normal ECG tracing showing the P wave, PR interval, QRS complex, J point, ST segment, T wave, QT interval, and U wave. Each wave and interval corresponds to a specific phase of cardiac electrical activity.
Paper Speed & Calibration Standards
Standard ECG paper moves at 25 mm/s with voltage calibration of 10 mm/mV. Each small box is 1 mm (0.04 s horizontally, 0.1 mV vertically). Each large box is 5 mm (0.20 s, 0.5 mV). Always confirm the calibration pulse at the start of the tracing — half-standard calibration (5 mm/mV) can mimic low voltage, and doubled calibration (20 mm/mV) can falsely suggest LVH.
Measurement
Small Box
Large Box
Time (horizontal)
0.04 s (40 ms)
0.20 s (200 ms)
Voltage (vertical)
0.1 mV (1 mm)
0.5 mV (5 mm)
Normal ECG Intervals & Durations
Interval
Normal Range
Represents
P wave duration
< 0.12 s (< 3 small boxes)
Atrial depolarization
P wave amplitude
< 2.5 mm in II; < 1.5 mm in V1
Atrial mass
PR interval
0.12–0.20 s (3–5 small boxes)
Atrial depolarization + AV nodal delay
QRS duration
< 0.12 s (usually < 0.10 s)
Ventricular depolarization
QT interval
< 0.44 s (M), < 0.46 s (F) corrected
Ventricular depolarization + repolarization
R wave in V1
< 7 mm
Initial septal activation
ST segment
Isoelectric
Early repolarization plateau
T wave
Upright in I, II, V3–V6; inverted in aVR
Ventricular repolarization
The J point is the junction between the end of the QRS and the start of the ST segment. It is the reference point for measuring ST elevation or depression. Always measure ST shift at the J point, not later in the ST segment — T-wave slope can fool you.
04 The 10-Step Approach
Every ECG should be interpreted in the same order, every time. A systematic approach prevents the most common error in ECG reading: seeing the obvious abnormality and missing the subtle one. The ten-step approach below forms the backbone of any formal ECG read.
Step
What to Check
Key Questions
1. Rate
Atrial & ventricular rate
Brady, normal, or tachy? Same rate?
2. Rhythm
Regularity and origin
Sinus? P before every QRS? Regular?
3. Axis
Mean QRS vector in frontal plane
Normal, LAD, RAD, extreme?
4. Intervals
PR, QRS, QT/QTc
Short PR? Wide QRS? Long QT?
5. P wave
Morphology in II & V1
RAE? LAE? Ectopic?
6. QRS
Voltage, morphology, transition
LVH? RVH? BBB? Poor R progression?
7. ST segment
J-point position
Elevation? Depression? Reciprocal?
8. T wave
Polarity & symmetry
Inverted? Peaked? Flattened?
9. U wave
Presence & size
Hypokalemia? Bradycardia?
10. Comparison
Prior ECG
New change vs chronic finding?
Discipline = Diagnosis
The single most valuable habit in ECG reading is comparing the current tracing to a prior one. A new RBBB, a new T-wave inversion, a new Q wave — any of these can represent an acute process that would be missed if the tracing is read in isolation. Always ask for the prior ECG.
05 Rate Calculation Methods
Figure 9a — Rate Calculation on a Rhythm Strip. A rhythm strip in normal sinus rhythm. Rate can be calculated by the 300 method (300 divided by the number of large boxes between consecutive R waves) or the 1500 method (1500 divided by small boxes between R waves).
Three Standard Methods
Method
Formula
Best Used When
300 Rule (large box)
300 ÷ (# large boxes between R waves)
Regular rhythm
1500 Rule (small box)
1500 ÷ (# small boxes between R waves)
Regular rhythm; more precise
6-Second Rule
(# QRS in 6 s) × 10
Irregular rhythm (e.g., AF)
The 300 Sequence
Memorize the landmark sequence: 1 large box = 300, 2 = 150, 3 = 100, 4 = 75, 5 = 60, 6 = 50. Find an R wave that lands on a heavy line, count large boxes to the next R, and recite the sequence.
Always calculate both atrial and ventricular rates. They are different in AV block (atrial faster), ventricular tachycardia with AV dissociation, and during paced rhythms. A discrepancy between atrial and ventricular rates is one of the most important diagnostic clues on the ECG.
06 Sinus Rhythms & Variants
Figure 9 — Normal Sinus Rhythm (12-Lead). A 12-lead ECG demonstrating normal sinus rhythm. Note the regular rhythm, upright P waves in leads I, II, and aVF, consistent PR intervals, narrow QRS complexes, and normal ST segments.
Criteria for Normal Sinus Rhythm
Rate 60–100 bpm
Upright P wave in leads I, II, aVF (inverted in aVR)
One P wave before every QRS; one QRS after every P
An isolated sinus pause > 3 seconds in an awake patient is pathologic. During sleep, pauses up to 2 seconds may be normal. Pauses associated with syncope require permanent pacemaker placement regardless of duration.
Ectopic Beats
Beat
Features
Significance
Premature atrial complex (PAC)
Early P wave of different morphology, usually followed by narrow QRS; non-compensatory pause
Benign in most; can trigger AF
Premature junctional complex (PJC)
Narrow QRS without preceding P (or retrograde P)
Usually benign
Premature ventricular complex (PVC)
Wide QRS without preceding P; compensatory pause; T wave opposite QRS
Benign if rare; > 10% burden can cause cardiomyopathy
Interpolated PVC
Falls between two sinus beats without a pause
Indicates slow underlying rate
Bigeminy / trigeminy
PVC after every 1 / every 2 sinus beats
Pattern of ectopy, not pathognomonic
Couplet / triplet
2 or 3 consecutive PVCs
≥ 3 at > 100 bpm = nonsustained VT
07 Electrical Axis Determination
Figure 10 — Hexaxial Reference System. The six frontal plane leads arranged in the hexaxial reference system. Each lead has a defined angle, and the mean QRS vector can be plotted using these axes to determine the electrical axis of the heart.
Normal Axis Range
The normal mean QRS axis in adults is −30° to +90°. Axis deviation is classified as left (−30° to −90°), right (+90° to +180°), or extreme/northwest (−90° to −180° / +180° to +270°).
The Quadrant Method (Leads I & aVF)
Lead I
Lead aVF
Axis
Range
Positive
Positive
Normal
0° to +90°
Positive
Negative
Possible LAD (check II)
0° to −90°
Negative
Positive
Right axis deviation
+90° to +180°
Negative
Negative
Extreme axis / northwest
−90° to −180°
To distinguish physiologic leftward axis (0 to −30°, still normal) from true left axis deviation (−30 to −90°), look at lead II. If lead II is net positive, the axis is > −30° (normal). If lead II is net negative, the axis is < −30° (true LAD).
The 30-Degree (Equiphasic) Method
More precise than the quadrant method. Find the limb lead with the most equiphasic (isoelectric) QRS — the mean axis is perpendicular to it. Then determine polarity in the perpendicular lead to select between the two possible perpendicular directions.
Isoelectric Lead
Perpendicular Lead
Axis if Perp Positive
Axis if Perp Negative
I
aVF
+90°
−90°
II
aVL
−30°
+150°
III
aVR
−150°
+30°
aVR
III
+120°
−60°
aVL
II
+60°
−120°
aVF
I
0°
+180°
Figure 11 — Quadrant Method for Axis Determination. A summary of the quadrant method using leads I and aVF. The polarity of the QRS complex in these two leads places the axis into one of four quadrants: normal, left axis deviation, right axis deviation, or extreme axis.
RVH, LPFB, lateral MI, PE/acute cor pulmonale, COPD, dextrocardia, WPW, normal in children/tall thin adults
Extreme axis
VT, hyperkalemia, paced rhythm, lead misplacement
Quick Axis Rule
Lead I up + aVF up = normal (both leaving the "+" quadrant). Reach for each other (I up, aVF down) = left axis. Reach away (I down, aVF up) = right axis. Both down = extreme (bad news).
A QRS ≥ 0.12 s is "wide." Wide-QRS rhythms originate in, or are conducted abnormally through, the ventricles.
Cause
Clue
LBBB
Broad monophasic R in I/V6; deep S in V1
RBBB
rSR' ("rabbit ear") in V1; wide S in I/V6
Nonspecific IVCD
Wide QRS without typical BBB morphology
WPW
Short PR + delta wave
Ventricular rhythm
No P, AV dissociation, fusion/capture beats
Hyperkalemia
Peaked T, wide QRS, eventual sine wave
Na-channel blockade
TCA overdose, class IA/IC antiarrhythmics
Paced rhythm
Pacing spike before QRS
QT Interval & Correction Formulas
The QT interval is rate-dependent — it shortens at faster rates and lengthens at slower rates. The corrected QT (QTc) normalizes for heart rate.
Formula
Equation
Use
Bazett (most common)
QTc = QT / √RR
Standard; overcorrects at fast rates
Fridericia
QTc = QT / ∛RR
Better at extremes of rate
Framingham (linear)
QTc = QT + 0.154(1−RR)
Epidemiologic studies
Hodges
QTc = QT + 1.75(HR−60)
Alternative
Upper limits: QTc > 0.44 s (men), > 0.46 s (women) is prolonged. QTc > 0.50 s is dangerous and carries substantial torsades risk. A rough bedside rule: the QT should be less than half the preceding RR interval at normal rates.
The most common causes of acquired long QT are drugs (antipsychotics, macrolides, fluoroquinolones, methadone, ondansetron, antiemetics), hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, and hypothermia. Congenital long QT syndromes (LQT1–15) are channelopathies caused by mutations in KCNQ1, KCNH2, SCN5A, and others.
09 P Wave Morphology & Atrial Enlargement
Figure 12 — P Wave Morphology: Normal and Abnormal. Comparison of the normal P wave with P pulmonale (tall, peaked P wave in right atrial enlargement) and P mitrale (broad, notched P wave in left atrial enlargement). The terminal negative deflection in V1 is key for diagnosing LAE.
Normal P Wave
The first half of the P wave represents right atrial depolarization; the second half represents left atrial depolarization. Normally upright in I, II, aVF and biphasic (initially positive, then negative) in V1. Duration < 0.12 s; amplitude < 2.5 mm in lead II.
Biatrial enlargement = meets criteria for both RAE and LAE. The classic finding is a large initial positive deflection in V1 (RAE) followed by a deep negative terminal deflection (LAE), producing a large biphasic P wave.
10 Left Ventricular Hypertrophy
LVH on ECG is diagnosed by voltage criteria (increased QRS amplitude) often accompanied by repolarization abnormalities ("strain pattern"). Multiple scoring systems exist — all are specific but insensitive.
Figure 13 — Left Ventricular Hypertrophy. A 12-lead ECG demonstrating LVH with markedly increased QRS voltages meeting Sokolow-Lyon criteria. Note the lateral strain pattern with asymmetric ST depression and T-wave inversion in the lateral leads.
LVH Criteria
System
Criterion
Sokolow-Lyon
S in V1 + R in V5 or V6 > 35 mm; or R in aVL > 11 mm
Cornell voltage
R in aVL + S in V3 > 28 mm (M) or > 20 mm (F)
Cornell product
(R aVL + S V3) × QRS duration > 2440 mm·ms
Romhilt-Estes score
Point score: ≥ 5 = definite LVH, 4 = probable
R in aVL alone
> 11 mm
R in I + S in III
> 25 mm
Figure 13a — LVH Voltage Criteria (Sokolow-Lyon). Close-up of leads V2 and V5 demonstrating LVH by Sokolow-Lyon criteria: the sum of the S wave depth in V1 (or V2) and R wave height in V5 (or V6) exceeds 35 mm.
LVH with Strain Pattern
"Strain" = asymmetric downsloping ST depression with T-wave inversion in the lateral leads (I, aVL, V5, V6). The strain pattern signals advanced LVH and is associated with worse prognosis. In V1–V3, LVH typically shows deep symmetric S waves with upright or tall T waves (reciprocal).
LVH is the single most common STEMI mimic. Deep S waves in V1–V3 produce reciprocal ST elevation, and the strain T waves can be confused with ischemia. The key: LVH ST changes are proportional to QRS voltage (ST/S ratio < 25%), while STEMI ST elevation is disproportionately large.
11 Right Ventricular Hypertrophy
RVH Criteria
The normal adult RV is too thin to dominate the ECG. RVH is diagnosed when the R wave in V1 is abnormally large and the ECG shows right-sided dominance.
Criterion
Value
R wave in V1
> 7 mm
R/S ratio in V1
> 1
R/S ratio in V6
< 1
Right axis deviation
> +100°
RV strain
ST depression / T inversion V1–V3
RAE
Often coexists
Causes of RVH
Category
Examples
Pressure overload
Pulmonary HTN, pulmonic stenosis, chronic PE, COPD, OSA
Volume overload
ASD, TR, pulmonary regurgitation
Congenital
Tetralogy of Fallot, Ebstein anomaly
Infiltrative
Amyloid, sarcoid (biventricular)
Differential for Tall R in V1
Cause
Distinguishing Feature
RVH
RAD, RAE, RV strain pattern
Posterior MI
Tall R + ST depression in V1–V3; inferior Q waves
RBBB
rSR' pattern, wide QRS
WPW (type A)
Short PR, delta wave
Dextrocardia
Inverted P in I; R wave progression reverses
Duchenne muscular dystrophy
Characteristic finding
Lead misplacement
V1–V2 placed too high
12 ST-Segment Morphology
The ST segment is the interval from the J point to the onset of the T wave and represents phase 2 of the action potential. Any deviation from the isoelectric baseline raises concern for ischemia — but ST shifts have many causes, and morphology matters.
Figure 14 — ST Elevation Morphologies. The different patterns of ST segment elevation and their associated diagnoses. Convex-upward (tombstone) morphology is highly specific for STEMI, while concave-upward patterns suggest benign early repolarization or pericarditis.
Patterns of ST Elevation
Morphology
Typical Cause
Convex upward ("tombstone")
STEMI (high specificity)
Concave upward ("smiley")
Early repolarization, pericarditis, benign
Horizontal / straight
STEMI (concerning)
Downsloping from peaked R
Very acute STEMI with reciprocal changes
Coved ("shark fin")
Massive occlusion, often left main or proximal LAD
"Saddleback"
Brugada type 2/3
Figure 15 — ST Depression Patterns. The morphologic subtypes of ST segment depression: horizontal and downsloping (ischemia), upsloping (less specific), and scooped (digitalis effect). Horizontal or downsloping depression is the most concerning for subendocardial ischemia.
Patterns of ST Depression
Morphology
Significance
Horizontal / downsloping ≥ 0.5 mm
Subendocardial ischemia, NSTEMI
Upsloping
Less specific (physiologic, rate-related)
"Scooped" (digitalis effect)
Chronic digoxin use, not toxicity
Reciprocal (mirror of ST elevation)
Confirms STEMI territory
V1–V3 with tall R wave
Posterior STEMI (mirror image)
Diffuse with ST elevation in aVR
Left main / proximal LAD / 3VD
13 STEMI Criteria & Localization
Fourth Universal Definition of MI — STEMI Criteria
New ST elevation at the J point in at least two contiguous leads:
≥ 1 mm in any lead other than V2–V3
In V2–V3: ≥ 2 mm (men ≥ 40 y), ≥ 2.5 mm (men < 40 y), ≥ 1.5 mm (women)
Posterior STEMI: ST depression ≥ 0.5 mm V1–V3 with posterior ST elevation in V7–V9
RV STEMI: ST elevation ≥ 0.5 mm in V4R
Figure 16 — Anterior STEMI. A 12-lead ECG demonstrating anterolateral STEMI with prominent ST elevation in the precordial leads (V1–V6) and lateral leads (I, aVL), with reciprocal ST depression in the inferior leads (II, III, aVF). This pattern indicates proximal LAD occlusion.
MI Localization Table
Territory
ST Elevation Leads
Reciprocal ST Depression
Artery
Septal
V1, V2
—
LAD (proximal septal branches)
Anterior
V3, V4
Sometimes II, III, aVF
LAD
Anteroseptal
V1–V4
II, III, aVF
LAD
Extensive anterior
V1–V6, I, aVL
II, III, aVF
Proximal LAD / left main
Lateral
I, aVL, V5, V6
II, III, aVF
LCx or diagonal
High lateral
I, aVL
III (often sensitive)
D1 (first diagonal)
Inferior
II, III, aVF
I, aVL (specific)
RCA (90%) or LCx (10%)
Posterior
V7–V9 (ST dep V1–V3)
—
LCx or RCA (PDA)
Right ventricular
V4R (with inferior)
—
Proximal RCA
Figure 17 — Inferior STEMI. A 12-lead ECG demonstrating inferior STEMI with ST elevation in leads II, III, and aVF, and reciprocal ST depression in leads I and aVL. This pattern most commonly results from RCA occlusion.
RCA vs LCx in Inferior STEMI
Finding
RCA
LCx
ST elevation III > II
Yes
No
ST depression I & aVL
Yes
Variable
ST elevation in V4R
Yes (proximal RCA)
No
ST elevation II ≥ III
No
Yes
Lateral ST elevation (I, V5–V6)
No
Yes
Critical Pattern — Left Main Occlusion
ST elevation in aVR > 1 mm, often > ST elevation in V1, with diffuse ST depression (≥ 6 leads) signals left main coronary artery occlusion, proximal LAD occlusion, or severe three-vessel disease. Mortality is extremely high — emergent catheterization and often CABG rather than PCI.
Every inferior STEMI needs a right-sided ECG. RV infarction is present in 30–50% of inferior STEMIs and mandates volume loading rather than nitrates — nitroglycerin can cause catastrophic hypotension in RV infarct because the RV is preload-dependent.
Preload-dependent: hypotension with nitrates, give fluids
Figure 18 — Hyperacute STEMI. A 12-lead ECG capturing the hyperacute phase of anterior STEMI. Note the tall, broad, hyperacute T waves in the precordial leads with early ST elevation — a pattern that precedes full ST elevation and can be easily missed if not recognized.Figure 19 — Tombstoning STEMI Pattern. Extensive anterior STEMI demonstrating the ominous tombstoning pattern where massive ST elevation merges with the T wave, producing a rectangular monophasic deflection. This pattern indicates very large infarction territory and carries high mortality.
Evolution of STEMI Over Time
Phase
Time
ECG Findings
Hyperacute
Minutes
Tall, broad ("hyperacute") T waves; subtle ST elevation; tall R waves
Acute
Hours
Marked ST elevation, beginning Q waves, reciprocal depression
Subacute (evolved)
Hours–days
Deep Q waves, decreasing ST elevation, T-wave inversion
Chronic (old)
Weeks–years
Persistent Q waves, normalizing ST and T waves
LV aneurysm
Weeks+
Persistent ST elevation with Q waves (fails to normalize)
14 STEMI Mimics & Sgarbossa Criteria
Differential for ST Elevation
Mimic
Distinguishing Features
Early repolarization
Concave ST, J-point notch/slur, young healthy patient, most prominent V2–V5
Pericarditis
Diffuse concave ST elevation, PR depression, PR elevation in aVR, no reciprocal changes
LVH
Discordant ST opposite deep S wave; proportional to QRS
LBBB
Discordant ST opposite QRS; use Sgarbossa
Brugada syndrome
Coved ST in V1–V2 > 2 mm with inverted T
Hyperkalemia
Peaked T, wide QRS, long PR, brady
Takotsubo cardiomyopathy
Apical ballooning; mimics anterior STEMI but no coronary occlusion
Ventricular aneurysm
Persistent ST elevation with Q waves weeks-months post-MI
PE
S1Q3T3, RV strain, T inversion V1–V4
Acute aortic dissection
May extend into RCA ostium → inferior STEMI
Figure 20 — Acute Pericarditis. A 12-lead ECG demonstrating acute pericarditis (Stage I) with diffuse concave-upward ST elevation across multiple vascular territories, PR depression in limb leads, and PR elevation in aVR. The absence of reciprocal changes and territorial distribution distinguishes pericarditis from STEMI.
Sgarbossa Criteria (STEMI in LBBB or Paced Rhythm)
Because LBBB obscures repolarization, standard STEMI criteria don't apply. The original Sgarbossa score ≥ 3 is 98% specific for STEMI:
Criterion
Points
Concordant ST elevation ≥ 1 mm (ST in same direction as QRS)
5
Concordant ST depression ≥ 1 mm in V1, V2, or V3
3
Discordant ST elevation ≥ 5 mm (opposite direction to QRS)
2
Modified (Smith) Sgarbossa
The Smith-modified rule replaces the third criterion with the ratio of ST elevation to preceding S-wave depth: if ST/S ≤ −0.25 (i.e., disproportionate discordant ST elevation), STEMI is likely. This modification improves sensitivity substantially while retaining high specificity.
15 Q Waves, T Inversion & Wellens
Pathologic Q Waves
A Q wave is pathologic if it is ≥ 0.04 s wide or > 25% of the R-wave amplitude in the same lead. Pathologic Q waves in contiguous leads indicate completed transmural infarction (usually > 6 hours after onset). Small "septal" q waves in I, aVL, V5, V6 are normal and reflect left-to-right septal depolarization.
Figure 21 — T-Wave Morphology Patterns. A visual guide to the different T-wave morphologies and their clinical significance: normal upright T waves, hyperacute T waves (early STEMI), deep symmetric inversions (ischemia), biphasic T waves (Wellens), and other pathologic patterns.
T-Wave Inversion Patterns
Pattern
Significance
Deep symmetric ("coronary T")
Ischemia / NSTEMI
Shallow asymmetric
Nonspecific
Biphasic V2–V3
Wellens type A (proximal LAD critical stenosis)
Deep symmetric V2–V3
Wellens type B
Global deep T inversion (“cerebral T”)
↑ICP, SAH, post-ictal, pheo
Strain pattern (lateral)
LVH, RVH
Juvenile pattern (V1–V3)
Normal in children, young adults
Figure 22 — Wellens Syndrome Type A (Biphasic T Waves). Biphasic T waves in V2–V3, characteristic of Wellens type A pattern (25% of cases). This pattern in a pain-free patient after recent angina signifies critical proximal LAD stenosis requiring urgent catheterization.Figure 23 — Wellens Syndrome Type B (Deep T-Wave Inversion). Deep symmetric T-wave inversions in the precordial leads, characteristic of Wellens type B pattern (75% of cases). The isoelectric ST segment and preserved R waves distinguish this from evolved MI.
Wellens Syndrome
Wellens syndrome is a high-risk pre-infarction ECG pattern signaling critical proximal LAD stenosis. Found in pain-free patients after an angina episode with:
Biphasic (type A, 25%) or deep symmetric (type B, 75%) T-wave inversions in V2–V3
Isoelectric or minimally elevated ST (< 1 mm)
No pathologic Q waves, preserved R waves
Recent angina but currently pain-free
Normal or only slightly elevated troponin
High-Risk Pattern Alert
Wellens pattern demands urgent cardiac catheterization even if symptoms have resolved. Up to 75% of untreated patients progress to anterior STEMI within weeks. Stress testing is contraindicated — it can precipitate acute infarction.
Figure 24 — De Winter T Waves. A 12-lead ECG demonstrating the De Winter pattern: upsloping ST depression at the J point with tall, symmetric, peaked T waves in the precordial leads. This STEMI-equivalent pattern indicates proximal LAD occlusion and requires emergent catheterization.
De Winter T Waves
De Winter ST/T changes are a STEMI-equivalent pattern of proximal LAD occlusion:
Upsloping ST depression > 1 mm at J point in V1–V6
Tall, symmetric, "pulled-up" T waves
Often slight ST elevation in aVR
Present in ~2% of proximal LAD occlusions
De Winter pattern is technically not a STEMI on standard criteria but represents a complete proximal LAD occlusion and must be treated as a STEMI equivalent — immediate cath lab activation.
16 Narrow Complex Tachycardias
A narrow-complex tachycardia (QRS < 0.12 s) originates at or above the His bundle. The first question is whether the rhythm is regular or irregular.
Figure 25 — Atrial Fibrillation. A rhythm strip demonstrating atrial fibrillation with its hallmark features: irregularly irregular R-R intervals, absence of discrete P waves, and fibrillatory baseline. This is the most common sustained arrhythmia.
Regular Narrow-Complex Tachycardias
Rhythm
Rate
Key Features
Sinus tachycardia
100–180
Upright P in II, gradual onset/termination, rate responds to physiology
Atrial flutter (typical)
Atrial 300; ventricular usually 150
Sawtooth F waves (inverted in II, III, aVF); 2:1 most common
AVNRT
150–250
Sudden onset/termination; retrograde P buried in or just after QRS (pseudo-R' in V1)
AVRT (orthodromic)
150–250
Accessory pathway; retrograde P after QRS; underlying WPW
Atrial tachycardia
150–250
Non-sinus P-wave morphology; "warm-up" phenomenon
Junctional tachycardia
60–130
No P or retrograde P; narrow QRS; digoxin toxicity, post-op
Irregular Narrow-Complex Tachycardias
Rhythm
Key Features
Atrial fibrillation
Irregularly irregular, no discernible P waves, fibrillatory baseline
≥ 3 distinct P morphologies, rate > 100; classic in COPD exacerbation
Wandering atrial pacemaker
Like MAT but rate < 100
AVNRT is the most common paroxysmal SVT. It uses a dual-pathway reentry circuit within the AV node (slow and fast pathways). Adenosine terminates it by transient AV nodal block. Vagal maneuvers (Valsalva, carotid sinus massage) can also break the circuit.
Figure 26 — Atrial Flutter (Sawtooth Pattern). Atrial flutter with clearly visible sawtooth F waves (inverted in inferior leads) and 3:1 AV block. The regular sawtooth baseline between QRS complexes is the hallmark of flutter, best seen in leads II, III, aVF, and V1.Figure 27 — Atrial Flutter with 2:1 Block. Atrial flutter with 2:1 conduction producing a regular ventricular rate near 150 bpm. Every other flutter wave is hidden within the QRS or T wave, making this pattern commonly misdiagnosed. A rate of exactly 150 should always prompt consideration of flutter.
Atrial Flutter — Detailed Features
Feature
Typical (Type I)
Atypical (Type II)
Atrial rate
250–350 (usually 300)
350–450
Circuit
Cavotricuspid isthmus, counterclockwise
Variable, often left atrial
Flutter waves
Sawtooth, negative in II/III/aVF
Variable morphology
Block ratio
2:1 (most), 3:1, 4:1, or variable
Variable
Treatment
Rate control, cardioversion, isthmus ablation
Cardioversion, ablation more complex
AVNRT vs AVRT
Feature
AVNRT
Orthodromic AVRT
Circuit
Dual AV-nodal pathways
AV node (antegrade) + accessory pathway (retrograde)
Retrograde P
Buried in/just after QRS (RP < 70 ms)
After QRS (RP > 70 ms)
QRS alternans
Uncommon
Common at high rates
Baseline ECG
Normal
May show delta wave (WPW)
Most common age
Middle-aged women
Younger patients
17 Wide Complex Tachycardias
A wide-complex tachycardia (QRS ≥ 0.12 s, rate > 100) is VT until proven otherwise. In patients with coronary disease, > 90% of wide-complex tachycardias are VT. Treat hemodynamic instability with synchronized cardioversion.
Figure 28 — Monomorphic Ventricular Tachycardia. A rhythm strip demonstrating monomorphic VT with wide, uniform QRS complexes at a rapid rate. All complexes have the same morphology, indicating a single reentrant circuit or focus, typically scar-related in post-MI patients.
Types of Wide-Complex Tachycardia
Rhythm
Features
Monomorphic VT
Uniform QRS shape; scar-related reentry, post-MI
Polymorphic VT (normal QT)
Ischemic, often during acute MI
Torsades de pointes
Polymorphic VT with long QT; twisting QRS around baseline
Ventricular fibrillation
Chaotic, no discernible QRS; unsynchronized defibrillation
Accelerated idioventricular (AIVR)
40–120 bpm; reperfusion marker post-fibrinolysis
SVT with aberrancy
Rate-related BBB; RBBB morphology most common
Antidromic AVRT
Preexcited tachycardia using accessory pathway antegrade
In a WPW patient with AF, AV nodal blockers (adenosine, β-blockers, calcium-channel blockers, digoxin) can accelerate conduction down the accessory pathway and precipitate VF. Use procainamide or ibutilide, or cardiovert. Clue: irregular wide-complex tachycardia with rates > 200 bpm and varying QRS morphology.
Torsades de Pointes
Polymorphic VT in the setting of prolonged QT. "Twisting of the points" describes the undulating QRS axis around the baseline. Treat with IV magnesium (first-line regardless of serum Mg), withdraw offending drugs, correct K+, temporary overdrive pacing or isoproterenol if recurrent (bradycardia-dependent). Never give class IA or III antiarrhythmics — they worsen it.
Figure 29 — Ventricular Fibrillation. A rhythm strip demonstrating ventricular fibrillation with completely chaotic, disorganized electrical activity and no identifiable P waves, QRS complexes, or T waves. This is a non-perfusing rhythm requiring immediate unsynchronized defibrillation.
VT Morphology Clues to Origin
Morphology
Origin
Clinical Context
LBBB-like with inferior axis
RVOT
Idiopathic RVOT VT in structurally normal heart; responds to adenosine/β-blocker
RBBB-like with superior axis
Left posterior fascicle
Idiopathic fascicular VT; responds to verapamil
LBBB-like, scar pattern
Prior MI (usually inferior wall)
Scar-related reentry; often needs ablation or ICD
Bidirectional VT
Purkinje fibers
Digoxin toxicity, CPVT, Andersen-Tawil syndrome
18 SVT vs VT Differentiation
Classic Clues Favoring VT
AV dissociation (pathognomonic) — independent P waves marching through
Capture beats (fusion of sinus conducted beat with VT)
Fusion beats (hybrid morphology)
QRS > 0.14 s (RBBB pattern) or > 0.16 s (LBBB pattern)
Extreme axis (−90 to ±180°, "northwest")
Concordance across all precordial leads (all positive or all negative)
Age > 35 or history of CAD/MI/cardiomyopathy
Figure 30 — VT with AV Dissociation. A 12-lead ECG demonstrating ventricular tachycardia with AV dissociation — independent P waves marching through the wide QRS complexes at a slower rate. AV dissociation is pathognomonic for VT and one of the most reliable differentiating features from SVT with aberrancy.
Brugada Algorithm (Stepwise)
Step
Question
If Yes
1
Absence of RS complex in all precordial leads?
VT
2
R to S interval > 100 ms in any precordial lead?
VT
3
AV dissociation present?
VT
4
Morphology criteria for VT in V1 & V6?
VT
—
None of the above
SVT with aberrancy
Vereckei aVR Algorithm
A simpler alternative that uses only lead aVR: an initial R wave in aVR (reversed ventricular activation) favors VT. Four stepwise criteria: (1) initial R in aVR → VT; (2) initial r or q > 40 ms → VT; (3) notch on descending limb of negative QRS → VT; (4) Vi/Vt ratio ≤ 1 → VT.
When in doubt, treat wide-complex tachycardia as VT. Giving adenosine to a true VT does no harm (most times), but giving a calcium-channel blocker to a VT thought to be SVT can precipitate cardiac arrest. The safer default is always VT.
19 SA & AV Blocks
SA Blocks
Type
Features
1° SA block
Cannot diagnose on surface ECG (SA node firing is not visible)
2° SA block (Wenckebach)
Progressive shortening of P-P intervals then dropped P wave
2° SA block (Mobitz II)
Constant P-P then sudden dropped P
3° SA block / arrest
No P waves; escape rhythm (junctional or ventricular)
Figure 31 — Mobitz Type I (Wenckebach) AV Block. A rhythm strip demonstrating classic Wenckebach phenomenon with progressive PR interval prolongation until a P wave is not conducted (dropped QRS), followed by a shorter PR interval as the cycle resets. Note the grouped beating pattern.Figure 32 — Complete (Third-Degree) Heart Block. A rhythm strip demonstrating complete heart block with AV dissociation. The P waves (atrial rate) march through independently at a faster rate, while the QRS complexes (ventricular escape rhythm) fire at a regular, slower rate with no relationship to the P waves.
AV Blocks
Degree
Criteria
Site
Pacemaker?
1° AV block
PR > 0.20 s, every P conducted
AV node
No
2° Mobitz I (Wenckebach)
Progressive PR prolongation until dropped QRS; grouped beating
AV node
Only if symptomatic
2° Mobitz II
Constant PR then sudden dropped QRS; often wide QRS
Infra-Hisian
Yes (high risk of complete block)
2:1 AV block
Every other P conducted; can be I or II — look at PR of conducted beats & QRS width
Either
Depends
High-grade AV block
≥ 2 consecutive non-conducted P waves
Infra-Hisian
Yes
3° (complete) AV block
AV dissociation; atrial rate > ventricular rate; regular R-R
AV node or below
Yes
Wenckebach Footprints
Mobitz I ("Wenckebach") shows: (1) progressive PR lengthening, (2) progressive R-R shortening (because each PR increment is smaller than the last), (3) a dropped QRS, (4) the pause is less than twice the shortest R-R. Grouped beating is the clinical footprint.
Mobitz II and complete heart block usually reflect disease below the AV node (His-Purkinje) with unreliable ventricular escape rates (20–40 bpm). Both require permanent pacemaker. Mobitz I is usually benign, within the AV node, and atropine-responsive.
20 Escape Rhythms & AV Dissociation
Intrinsic Rates of Escape Pacemakers
Site
Intrinsic Rate
QRS Width
SA node
60–100
Narrow
Atrial ectopic
60–80
Narrow (abnormal P)
Junctional
40–60
Narrow (no P or retrograde)
Ventricular
20–40
Wide
Types of AV Dissociation
Type
Mechanism
Complete (3° AV block)
Atrial impulses cannot conduct; ventricular escape takes over
Isorhythmic
Sinus and junctional/ventricular rates nearly equal; P waves drift through QRS
VT with AV dissociation
Ventricles firing faster than sinus; pathognomonic for VT
21 RBBB & LBBB
Figure 33 — Right Bundle Branch Block (RBBB). A 12-lead ECG demonstrating RBBB with the classic rSR' (rabbit ears) pattern in V1, broad terminal S wave in leads I and V6, and discordant T-wave changes in V1–V3. QRS duration is ≥ 0.12 s.
Right Bundle Branch Block (RBBB)
Criterion
Value
QRS duration
≥ 0.12 s
V1
rSR' ("rabbit ears") or broad R
I, V6
Broad terminal S wave
T wave
Discordant (opposite QRS) in V1–V3
Causes
Normal variant, RV strain, PE, ASD, cardiomyopathy, ischemia, age
Figure 34 — Left Bundle Branch Block (LBBB). A 12-lead ECG demonstrating LBBB with broad monophasic (often notched) R waves in I, aVL, V5, V6, deep broad S waves in V1–V2, absent septal Q waves, and discordant ST/T changes throughout. QRS duration is ≥ 0.12 s.
New LBBB in a patient with chest pain is a STEMI equivalent and must be managed with urgent cath activation (apply Sgarbossa to confirm). Isolated chronic LBBB is not itself an indication for emergent reperfusion but is rarely benign.
Figure 35 — RBBB V1 Morphology (rSR'). Close-up of the V1 lead demonstrating the classic rSR' pattern of RBBB. The initial small r wave (septal depolarization), deep S wave (LV depolarization), and terminal R' (delayed RV depolarization) create the characteristic "rabbit ears" morphology.Figure 36 — LBBB Precordial Lead Progression. The precordial leads in LBBB showing the characteristic pattern: deep, broad QS or rS complexes in V1–V2, transitioning to tall, broad, monophasic R waves in V5–V6. Note the discordant ST/T changes throughout.
WiLLiaM MaRRoW Mnemonic
WiLLiaM: LBBB — "W" in V1 and "M" in V6. MaRRoW: RBBB — "M" in V1 (rSR') and "W" in V6 (broad S).
RBBB vs LBBB Comparison
Feature
RBBB
LBBB
QRS duration
≥ 0.12 s
≥ 0.12 s
V1 morphology
rSR' or M-shape
QS or deep, broad S
V6 morphology
qRS with broad terminal S
Broad monophasic R, often notched
Axis
Usually normal (unless fascicular block)
Usually normal or leftward
ST/T
Discordant in V1–V3 only
Discordant throughout
Pathology
Often benign; can be rate-related
Nearly always pathologic
STEMI detection
Not obscured (interpret normally)
Obscured (Sgarbossa required)
Intermittent / Rate-Related BBB
A bundle branch block that appears only at faster heart rates ("rate-related" or "tachycardia-dependent") is a common cause of diagnostic confusion during SVT. It can also appear paradoxically at slow rates (bradycardia-dependent BBB, phase 4 block), reflecting His-Purkinje disease.
QRS duration normal or only slightly prolonged (< 0.12 s)
No other cause of LAD
Left Posterior Fascicular Block (LPFB)
Right axis deviation (+90° to +180°)
rS in I, aVL; qR in II, III, aVF
QRS normal or slightly prolonged
No RVH or other cause of RAD (diagnosis of exclusion)
LAFB vs Inferior MI
Both can produce left axis deviation and q waves in inferior leads. Key differences: in LAFB the q waves in II, III, aVF are small and part of an rS pattern, the R wave is preserved in aVL, and there are no repolarization abnormalities. In inferior MI, the Q waves are pathologic (> 0.04 s wide), loss of R wave progression, and ST/T changes reflect ischemia or prior infarction.
Bifascicular & Trifascicular Blocks
Pattern
Criteria
Bifascicular block
RBBB + LAFB (common) or RBBB + LPFB (rare)
"Trifascicular" block
Bifascicular block + 1° AV block (incomplete trifascicular); or bifascicular + alternating BBB (complete trifascicular)
Nonspecific IVCD
QRS > 0.11 s without typical LBBB or RBBB morphology
Alternating bundle branch block (RBBB on one beat, LBBB on the next) is a true trifascicular block and mandates emergent pacemaker — the next beat may be complete heart block with no escape.
23 Preexcitation & Paced Rhythms
Figure 37 — Wolff-Parkinson-White (WPW) Pattern. A 12-lead ECG demonstrating the WPW triad in sinus rhythm: short PR interval (< 0.12 s), delta waves (slurred QRS upstroke), and widened QRS complex due to ventricular preexcitation via an accessory pathway.
Wolff-Parkinson-White (WPW)
Criterion
Value
PR interval
< 0.12 s
Delta wave
Slurred upstroke on QRS
QRS duration
> 0.10 s (fused conduction)
ST/T changes
Secondary repolarization abnormalities
Pathway location
Type A: left-sided (positive delta V1); Type B: right-sided (negative delta V1)
WPW risks include orthodromic AVRT (narrow QRS), antidromic AVRT (wide QRS), and, most dangerously, AF with rapid antegrade conduction down the accessory pathway → VF.
Lown-Ganong-Levine (LGL)
Short PR with normal QRS and no delta wave; thought to represent enhanced AV-nodal conduction. Controversial entity.
Electronic Pacemakers
Letter
Position 1 (Paced)
Position 2 (Sensed)
Position 3 (Response)
A
Atrium
Atrium
—
V
Ventricle
Ventricle
—
D
Dual
Dual
Dual (trigger + inhibit)
I
—
—
Inhibited
T
—
—
Triggered
O
None
None
None
Common modes: VVI (ventricular demand), DDD (dual chamber, most physiologic), AAI (atrial demand, used in SSS with intact AV conduction). A pacing spike precedes the paced chamber; RV pacing produces an LBBB morphology.
A paced RV complex has LBBB morphology. When diagnosing STEMI in a patient with a V-paced rhythm, apply the Sgarbossa criteria just as for native LBBB.
24 Channelopathies & Inherited Syndromes
Figure 38 — Brugada Syndrome ECG Types. Comparison of the three Brugada patterns in leads V1–V2. Type 1 (coved) with ≥ 2 mm ST elevation and descending T-wave inversion is diagnostic. Types 2 and 3 (saddleback) are suggestive but require provocation testing for confirmation.
Brugada Syndrome
Autosomal dominant sodium channelopathy (SCN5A mutations in ~20%) with characteristic RBBB-like pattern in V1–V2 and increased risk of polymorphic VT/sudden cardiac death. Three patterns:
Type
V1–V2 Pattern
Diagnostic?
Type 1 ("coved")
ST elevation ≥ 2 mm with descending ST and inverted T
Yes (definitive)
Type 2 ("saddleback")
ST elevation ≥ 2 mm with saddleback morphology, positive/biphasic T
Suggestive; drug challenge needed
Type 3
Either pattern but ST elevation < 2 mm
Suggestive; drug challenge needed
The pattern is unmasked by fever, sodium-channel blockers, vagal tone. Diagnostic testing: procainamide/ajmaline challenge. Management: ICD for symptomatic patients.
Figure 39 — Brugada Type 1 (Coved Pattern). A 12-lead ECG demonstrating the diagnostic Brugada type 1 pattern with coved ST elevation ≥ 2 mm followed by a descending ST segment and inverted T wave in V1–V2. This pattern carries significant risk of polymorphic VT and sudden cardiac death.
Long QT Syndromes (LQTS)
Type
Gene
Channel
Trigger
LQT1
KCNQ1
IKs
Exercise, swimming
LQT2
KCNH2 (hERG)
IKr
Auditory (alarm, phone)
LQT3
SCN5A
INa
Sleep, rest
Jervell-Lange-Nielsen syndrome: autosomal recessive LQT with congenital deafness. Romano-Ward: autosomal dominant without deafness. Management: β-blockers (first-line), ICD in high-risk patients, avoid QT-prolonging drugs.
Short QT Syndrome
QTc < 0.34 s with peaked T waves; risk of AF and sudden death. Caused by gain-of-function K+-channel mutations. ICD for symptomatic patients.
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Fibrofatty replacement of RV myocardium, primarily affecting young athletes. ECG features:
Epsilon wave (small deflection at the end of QRS in V1–V3)
T-wave inversion in V1–V3
Prolonged terminal activation duration in V1
LBBB-morphology VT (arising in RV)
Hypertrophic Cardiomyopathy (HCM)
ECG shows LVH voltage criteria, deep narrow ("dagger-like") Q waves in lateral leads (I, aVL, V5, V6), giant inverted T waves (apical HCM — Yamaguchi syndrome). LAE is common. QRS may be widened. Careful: HCM with Q waves is a common STEMI mimic in young patients.
Catecholaminergic Polymorphic VT (CPVT)
Normal baseline ECG. Bidirectional VT or polymorphic VT provoked by exercise or emotional stress. Caused by RyR2 or calsequestrin (CASQ2) mutations causing calcium leak from SR. Management: β-blockers, flecainide, ICD, left cardiac sympathetic denervation.
Early Repolarization — Benign vs Malignant
Feature
Benign Early Repolarization
Malignant (J-wave syndrome)
Leads involved
V2–V5 (anterolateral)
Inferior or inferolateral
J-point elevation
< 2 mm
> 2 mm, especially horizontal/descending ST
T waves
Upright, concordant with ST
Can be flat or inverted
History
Young, healthy, male, athletes
Unexplained syncope, family history of SCD
25 Electrolyte & Drug Effects
Electrolyte Summary Table
Electrolyte
Key ECG Findings
Progression
↑K+
Peaked T → long PR → wide QRS → sine wave
Progressive with level
↓K+
Flat T, U waves, ST depression, long QU
Torsades risk
↑Ca2+
Short QT (short ST); Osborn wave possible
Arrest at severe levels
↓Ca2+
Long QT (long ST, normal T)
Tetany, torsades uncommon
↑Mg2+
Long PR, long QT, wide QRS, AV block
Arrest at very high levels
↓Mg2+
Like hypokalemia; torsades risk
Must replete with K
Figure 40 — Hyperkalemia: Peaked T Waves. A 12-lead ECG showing the earliest and most recognizable sign of hyperkalemia: tall, narrow-based, symmetric ("tented") T waves, most prominent in the precordial leads. This pattern typically appears at serum potassium levels of 5.5–6.5 mEq/L.
Hyperkalemia — Sequential ECG Changes
Serum K+ (mEq/L)
ECG Finding
5.5–6.5
Peaked, narrow-based, symmetric T waves ("tented")
6.5–7.5
Prolonged PR, flattened P
7.0–8.0
Loss of P wave, widened QRS
> 8.0
Sine wave, VF, asystole
Figure 41 — Hyperkalemia: Sine Wave Pattern. A 12-lead ECG demonstrating severe hyperkalemia (K+ 9.9 mEq/L) with the terminal sine wave pattern. The QRS has merged with the T wave to form a sinusoidal waveform. This is a pre-arrest rhythm requiring emergent IV calcium and dialysis.
Hyperkalemia Treatment Priority
Calcium first (membrane stabilization) → shift (insulin + glucose, β2-agonist, bicarbonate if acidotic) → eliminate (loop diuretic, K-binder, dialysis). Calcium works in minutes and buys time for definitive therapy.
Hypokalemia
Finding
Details
U waves
Prominent after T; classic finding
T-wave flattening
Progresses with severity
ST depression
Diffuse
Prolonged QT (QU)
Predisposes to torsades
Increased arrhythmia risk
Especially with digoxin, long-QT drugs
Calcium Abnormalities
Abnormality
ECG Effect
Hypercalcemia
Shortened QT (shortened ST segment)
Hypocalcemia
Prolonged QT (prolonged ST segment, normal T)
Hypermagnesemia
AV block, QRS widening
Hypomagnesemia
Like hypokalemia; torsades risk
Digitalis Effect vs Toxicity
Effect (therapeutic)
Toxicity
Scooped ("Salvador Dali") ST depression
Atrial tachycardia with AV block (pathognomonic)
T-wave flattening/inversion
Junctional rhythms, VT, bidirectional VT
Shortened QT
Any new arrhythmia in a dig patient is toxicity until proven otherwise
Prolonged PR
Hyperkalemia is a marker of acute toxicity
Mixed Electrolyte Disturbances
Combination
ECG Clue
Hypokalemia + hypomagnesemia
Markedly prolonged QT, U waves, torsades risk — always replete Mg when correcting K
Hyperkalemia + hypocalcemia
Peaked T waves with prolonged ST (dialysis patients)
Enhanced digoxin toxicity (compete for Na/K-ATPase site)
Other Drug Effects
Drug
ECG Finding
Class IA (quinidine, procainamide)
Wide QRS, long QT
Class IC (flecainide, propafenone)
Wide QRS, PR prolongation
Class III (sotalol, amiodarone, dofetilide)
Long QT (amiodarone rarely causes torsades)
TCA overdose
Wide QRS, RAD (R in aVR > 3 mm), long QT → treat with NaHCO3
Lithium
T-wave flattening, QT prolongation, brady
Cocaine
Vasospasm STEMI, Brugada unmasking, long QT
26 Miscellaneous Patterns
Figure 42 — Normal R-Wave Progression. The normal progression of R-wave amplitude across the precordial leads V1 through V6. The R wave grows progressively taller while the S wave becomes smaller, with the transition zone (R = S) normally between V3 and V4.
R-Wave Progression
Normally, the R wave grows across the precordial leads with the transition zone (R = S) between V3 and V4. Abnormalities:
Finding
Meaning
Poor R-wave progression (R < 3 mm in V3)
Prior anterior MI, LVH, LBBB, COPD, lead misplacement
Early transition (R > S in V1–V2)
RVH, posterior MI, WPW type A, dextrocardia, lead misplacement
Late transition (R < S through V5)
LVH, LBBB, clockwise rotation, COPD
Reverse R progression
Dextrocardia, lead reversal
Pulmonary Embolism
Finding
Frequency
Sinus tachycardia
Most common (40%)
S1Q3T3
Classic but insensitive (~20%)
New RBBB (complete or incomplete)
RV strain
T-wave inversion V1–V4
RV strain pattern; poor prognosis
Right axis deviation
Acute cor pulmonale
Atrial tachyarrhythmias
AF, flutter
Pericarditis vs STEMI vs Early Repolarization
Feature
Pericarditis
STEMI
Early Repolarization
ST elevation distribution
Diffuse, multiple territories
Territorial (one vascular bed)
Predominantly V2–V5
ST morphology
Concave up
Convex up / straight
Concave up
PR segment
Depressed (elevated in aVR)
Normal
Normal
Reciprocal changes
None (except aVR)
Present
None
Q waves
Absent
Develop over hours
Absent
T wave
Upright initially; inverts later
Inverts after hours
Upright, tall
Patient
Pleuritic pain, positional
Crushing substernal pain
Young, asymptomatic
Pericarditis — 4 Stages
Stage
Findings
I (hours–days)
Diffuse concave ST elevation, PR depression, PR elevation in aVR
II (days)
ST and PR normalize; T waves flatten
III (weeks)
Diffuse T-wave inversion
IV (weeks–months)
Normalization
Hypothermia — Osborn (J) Waves
Slow positive deflection at the J point, most prominent in lateral leads. Appears when core temp < 32°C, proportional to degree of hypothermia. Other findings: bradycardia, prolonged intervals, shivering artifact, AF.
Pre-Participation Screening — Normal vs Abnormal in Athletes
Normal (training-related)
Abnormal (requires evaluation)
Sinus bradycardia ≥ 30 bpm
T-wave inversion (except V1–V2)
Sinus arrhythmia
ST depression
1° AV block (PR ≤ 0.40 s)
Pathologic Q waves
Mobitz I (Wenckebach)
Complete LBBB or any Mobitz II
Incomplete RBBB
Long or short QT
Early repolarization
Brugada, WPW, epsilon wave
Isolated LVH voltage
LVH with strain, LAE, RAE
Athlete's Heart
Sinus bradycardia, sinus arrhythmia
1° AV block, Wenckebach (vagal tone)
Voltage criteria for LVH without strain
Early repolarization, J-point elevation
Incomplete RBBB
Hypothyroidism vs Hyperthyroidism
Condition
ECG Findings
Hypothyroidism / myxedema
Sinus bradycardia, low voltage (pericardial effusion), long QT, T-wave flattening
Hyperthyroidism
Sinus tachycardia, AF (classic in older patients), increased QRS voltage
Increased Intracranial Pressure
"Cerebral T waves" — deep symmetric T-wave inversion with long QT, often after SAH or massive stroke. Can mimic ischemia.
Takotsubo (Stress) Cardiomyopathy
Apical ballooning after emotional or physical stress. ECG shows anterior ST elevation and/or deep T-wave inversion mimicking anterior STEMI, with mildly elevated troponin but clean coronaries on catheterization. More common in post-menopausal women.
Dextrocardia
Inverted (negative) P wave, QRS, and T wave in lead I
Absent R-wave progression across the precordial leads (reversed)
Right axis deviation
Can be mistaken for limb-lead reversal — confirm by placing precordial leads on the right side
Limb Lead Reversal
Reversal
Finding
LA-RA reversal
Inverted P/QRS/T in I; normal V leads (differentiates from dextrocardia)
LA-LL reversal
P wave in I taller than II (subtle)
RA-LL reversal
Inverted complexes in II, III; upright in aVR
RA-limb reversal (any)
Flat line in one lead (disconnection)
Low Voltage QRS
QRS amplitude < 5 mm in all limb leads or < 10 mm in all precordial leads. Causes: pericardial effusion (especially with electrical alternans in tamponade), obesity, COPD, myxedema, amyloidosis, massive pleural effusion, constrictive pericarditis, restrictive cardiomyopathy, extensive MI with loss of myocardium.
Electrical Alternans
Beat-to-beat alternation of QRS amplitude. Classic for large pericardial effusion with tamponade (heart "swinging" in the effusion). Also seen in AVRT, severe LV dysfunction, and rarely in ischemia.
27 ECG Criteria Summary & Pitfalls
Essential Criteria at a Glance
Finding
Criterion
1° AV block
PR > 0.20 s
LAE
P wave > 0.12 s in II, terminal negative V1 ≥ 1 mm × 0.04 s
RAE
P wave > 2.5 mm in II
LVH (Sokolow-Lyon)
S V1 + R V5/6 > 35 mm
RVH
R V1 > 7 mm, R/S V1 > 1
LBBB
QRS ≥ 0.12, broad R in I/V6, deep S V1
RBBB
QRS ≥ 0.12, rSR' V1, broad S I/V6
LAFB
LAD, qR I/aVL, rS II/III/aVF
LPFB
RAD, rS I/aVL, qR II/III/aVF
STEMI
ST elevation ≥ 1 mm (2 contiguous leads; ≥ 2 mm in V2–V3)
WPW
PR < 0.12, delta wave, QRS > 0.10
Long QT
QTc > 0.44 (M), > 0.46 (F)
Brugada type 1
Coved ST elevation ≥ 2 mm with T inversion V1–V2
Common Pitfalls
Pitfall
Correction
Missing lead misplacement
Check for negative P in I (limb reversal) and R-wave progression
Calling LVH "STEMI"
Proportional ST/S rule; compare to prior ECG
Calling "SVT with aberrancy"
Default to VT in older patients with CAD
Ignoring aVR
ST elevation in aVR = left main / 3VD
Missing posterior MI
ST depression in V1–V3 with tall R — order V7–V9
Missing RV infarct
Always get V4R in inferior STEMI
Missing Wellens
Pain-free patient with biphasic T in V2–V3
Treating preexcited AF with AV blocker
Use procainamide or cardioversion
Calling hyperkalemia "ischemia"
Peaked T + wide QRS = check K+ immediately
Giving nitrates in RV infarct
Fluid bolus first; avoid preload reduction
28 High-Yield Review
Indications for Permanent Pacemaker
Indication
Detail
Symptomatic sinus node dysfunction
Bradycardia or pauses with symptoms
Symptomatic 2° Mobitz I
Only if symptomatic
2° Mobitz II
Symptomatic or not
High-grade or complete AV block
All patients
Alternating BBB
True trifascicular — emergent pacing
Persistent AV block after MI
Class I indication
Carotid sinus hypersensitivity with syncope
Cardioinhibitory type
Rapid-Fire ECG Pearls
Every ECG interpretation must follow the same 10-step sequence every time. Rate, rhythm, axis, intervals, P morphology, QRS morphology, ST segment, T waves, U waves, comparison. Discipline is what separates a good ECG reader from a great one.
Inferior STEMI always requires a right-sided lead (V4R) to look for RV infarction and posterior leads (V7–V9) if there is ST depression in V1–V3. Missing an RV infarct and giving nitroglycerin can cause fatal hypotension.
ST elevation in aVR with diffuse ST depression in ≥ 6 leads is the signature of left main coronary artery occlusion, proximal LAD occlusion, or severe three-vessel disease. This pattern has the highest mortality of any ECG finding and usually needs CABG rather than PCI.
Wellens syndrome is the easiest life-threatening ECG pattern to miss because patients are pain-free. Biphasic or deeply inverted T waves in V2–V3 after resolution of chest pain signals critical proximal LAD stenosis and requires urgent angiography, not stress testing.
De Winter T waves — upsloping ST depression with tall symmetric T waves in the precordial leads — are a STEMI equivalent for proximal LAD occlusion. They are underrecognized because they don't meet classic STEMI criteria.
New LBBB with chest pain should be treated as a STEMI equivalent. Apply Sgarbossa criteria: concordant ST elevation ≥ 1 mm (5 points), concordant ST depression in V1–V3 (3 points), or disproportionate discordant ST elevation (Smith-modified).
In a wide-complex tachycardia, AV dissociation, capture beats, and fusion beats are pathognomonic for ventricular tachycardia. When in doubt, treat as VT — the default that saves lives.
Preexcited atrial fibrillation (WPW + AF) is a medical emergency. AV nodal blockers can precipitate VF by enhancing accessory pathway conduction. Use procainamide or ibutilide, or synchronized cardioversion.
Mobitz II and complete heart block reflect disease below the AV node. Both have unreliable escape rhythms and both require permanent pacing. Mobitz I (Wenckebach) is usually benign and atropine-responsive.
Hyperkalemia progresses through predictable ECG stages: peaked T waves → PR prolongation → P-wave loss → QRS widening → sine wave → asystole. Give IV calcium first (membrane stabilization) in any ECG abnormality suggestive of hyperkalemia.
Torsades de pointes is polymorphic VT with prolonged QT. First-line therapy is IV magnesium sulfate regardless of serum magnesium level. Correct potassium, withdraw offending drugs, and consider isoproterenol or overdrive pacing for bradycardia-dependent torsades.
The Brugada type 1 pattern (coved ST elevation in V1–V2) is diagnostic by itself. Types 2 and 3 (saddleback) require provocative drug testing with a sodium-channel blocker. Fever, alcohol, vagal tone, and sodium-channel blockers can unmask the pattern.
Digoxin toxicity should be suspected in any patient on digoxin with new arrhythmias. The most specific finding is atrial tachycardia with AV block. Hyperkalemia is a marker of acute toxicity. Treatment: digoxin-specific Fab fragments.
Tricyclic antidepressant overdose produces wide QRS (> 100 ms), terminal R wave in aVR (> 3 mm), and QT prolongation. Treatment is IV sodium bicarbonate, which overcomes the sodium-channel blockade and narrows the QRS.
The most common STEMI mimic is LVH. Use the proportionality rule: the ST elevation should be proportional to the S-wave depth (< 25%) in LVH. Disproportionate ST elevation suggests true STEMI on top of LVH.
Pericarditis classically produces diffuse concave ST elevation with PR depression and PR elevation in aVR. There are no reciprocal changes (except in aVR), no Q waves, and the patient typically has positional or pleuritic pain. The ECG evolves through four stages over weeks.
Posterior MI is easy to miss because there is no "posterior" standard lead. Look for ST depression in V1–V3 with tall R waves (mirror image of posterior ST elevation and Q waves). Confirm by placing posterior leads V7–V9 — any ST elevation ≥ 0.5 mm is diagnostic.
The Brugada algorithm for wide-complex tachycardia identifies VT with > 95% sensitivity: (1) absence of RS in any precordial lead, (2) R-to-S interval > 100 ms, (3) AV dissociation, (4) VT morphology criteria in V1 and V6. Any single "yes" answer = VT.
U waves are small deflections after the T wave, best seen in V2–V3 at slow rates. Prominent U waves suggest hypokalemia, hypomagnesemia, or LVH. Inverted U waves suggest ischemia or LV strain.
Hypothermia produces a distinctive J wave (Osborn wave) at the end of the QRS complex, most prominent in the lateral leads. It appears below 32°C core temperature and its size is roughly proportional to the severity. Treat the underlying hypothermia rather than the ECG finding.
Fragmented QRS (notching or additional R waves within the QRS in two contiguous leads) is a marker of myocardial scar and is associated with adverse cardiac outcomes. Often seen in prior MI, cardiomyopathy, and Brugada syndrome.
Epsilon waves — small positive deflections at the end of the QRS in V1–V3 — are a major diagnostic criterion for arrhythmogenic right ventricular cardiomyopathy (ARVC). They reflect delayed RV activation from fibrofatty replacement of the RV free wall.
The S1Q3T3 pattern (large S in I, Q and inverted T in III) is the textbook finding in pulmonary embolism but appears in only ~20% of cases. Sinus tachycardia, incomplete RBBB, and T-wave inversions in V1–V4 (RV strain) are more common. Most PEs produce only sinus tachycardia.
Always compare the current ECG to the patient's previous tracing. A "new" abnormality can be decades old, and a "normal" tracing can represent improvement over a prior abnormal one. The prior ECG is the most valuable piece of data after the current tracing itself.
ECG in isolation is not enough. Every finding must be interpreted in the clinical context. Peaked T waves in a dialysis patient are hyperkalemia until proven otherwise; the same waves in a young athlete may be normal early repolarization. Always integrate the tracing with the patient in front of you.
Arrhythmia Quick Reference
Situation
First-Line Response
Stable narrow-complex regular SVT
Vagal maneuvers → adenosine 6 mg IV → 12 mg
Stable narrow-complex irregular (AF)
Rate control with β-blocker or CCB; anticoagulate per CHA2DS2-VASc
Stable wide-complex regular
Assume VT; amiodarone 150 mg IV
Stable wide-complex irregular
Consider polymorphic VT, preexcited AF; avoid AV blockers in WPW+AF
Unstable any tachycardia
Synchronized cardioversion (unsynced for VF/pulseless VT)
Torsades de pointes
IV magnesium 2 g, correct K, withdraw offending drug
PCI within 90 min (door-to-balloon); fibrinolytics if not available
Hyperkalemia with ECG changes
IV calcium gluconate → insulin/glucose → β2-agonist → dialysis
Final Exam Strategy
When reading any ECG under time pressure: (1) Start with rate and rhythm to rule out immediate threats. (2) Scan the ST segments across all leads for elevation or depression — the single highest-yield step. (3) Check aVR — don't ignore it. (4) Measure the QT and look for U waves. (5) Compare to the prior ECG. (6) When you see something unusual, form a differential diagnosis rather than stopping at the first plausible answer. These habits will correctly read the great majority of ECGs encountered in clinical practice and on any examination.
