Clinical Skill

EKG Interpretation

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.

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 (I_Na)	QRS complex (ventricles)
Phase 1	Initial rapid repolarization	Transient K⁺ efflux (I_to)	J point
Phase 2	Plateau	Ca²⁺ influx (L-type) balanced by K⁺ efflux	ST segment
Phase 3	Rapid repolarization	Delayed rectifier K⁺ efflux (I_Kr, I_Ks)	T wave
Phase 4	Resting membrane potential	Inward rectifier K⁺ (I_K1)	TP segment (isoelectric)

The I_Kr current (rapid delayed rectifier, encoded by hERG/KCNH2) is the most commonly drug-blocked potassium channel. Blocking I_Kr 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 (I_f, 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 (I_f)	No (normally)
Conduction velocity	0.02–0.1 m/s	0.3–1.0 m/s

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.

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

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.

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

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

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

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

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
Constant PR interval (0.12–0.20 s)
Regular R-R intervals (variation < 10%)

Sinus Variants

Rhythm	Rate	Key Features	Causes
Sinus bradycardia	< 60	Otherwise normal sinus	Athletes, sleep, vagal, β-blockers, SSS, inferior MI, hypothyroid, ↑ICP
Sinus tachycardia	> 100	Otherwise normal sinus	Pain, fever, hypovolemia, anemia, PE, thyrotoxicosis, sepsis, sympathomimetics
Sinus arrhythmia	Variable	Respirophasic R-R variation	Normal in young; high vagal tone
Sinus pause / arrest	Variable	Absent P-QRS-T for > 2 s; no reset	SSS, vagal, drugs, ischemia
Sick sinus syndrome	Variable	Alternating brady/tachy ("tachy-brady")	Sinus node dysfunction in elderly

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

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°

Causes of Axis Deviation

Axis	Common Causes
Left axis deviation	LVH, LAFB, inferior MI, WPW, hyperkalemia, mechanical shift (pregnancy, ascites, obesity)
Right axis deviation	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).

08 PR, QRS & QT Intervals

PR Interval

PR Interval	Interpretation	Causes
Short (< 0.12 s)	Preexcitation or junctional	WPW, LGL, low atrial/junctional rhythm
Normal (0.12–0.20 s)	Normal AV conduction	—
Long (> 0.20 s)	1° AV block	↑Vagal tone, AV node disease, drugs (digoxin, β-blocker, CCB), ischemia, Lyme carditis
Variable (progressively longer)	Mobitz I (Wenckebach)	AV nodal disease, inferior MI
Variable (random)	3° AV block / AV dissociation	AV node / His failure

QRS Width

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

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.

Right Atrial Enlargement (RAE / "P Pulmonale")

Criterion	Value
P-wave amplitude in II	> 2.5 mm (tall, peaked)
Initial deflection in V₁	> 1.5 mm positive
Duration	Normal (< 0.12 s)
Common causes	COPD, pulmonary HTN, tricuspid stenosis, congenital heart disease

Left Atrial Enlargement (LAE / "P Mitrale")

Criterion	Value
P-wave duration in II	> 0.12 s, often notched ("bifid M-shape")
Terminal deflection in V₁	Negative, ≥ 1 mm deep & ≥ 0.04 s wide (Morris criterion)
Common causes	Mitral stenosis/regurgitation, LVH, HTN, aortic valve disease, HFrEF

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.

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

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.

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

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

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

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.

Territory Summary by Wall

Wall	Leads	Artery	Complications
Anterior (LAD)	V₁–V₆, I, aVL	LAD	Cardiogenic shock, VSD, LV aneurysm, heart block (infra-Hisian), mural thrombus
Inferior (RCA)	II, III, aVF	RCA (90%) / LCx (10%)	Sinus brady, AV block (AV-nodal, atropine-responsive), RV infarct, papillary muscle rupture, pericarditis
Lateral (LCx)	I, aVL, V₅–V₆	LCx or diagonal	Often silent; missed on standard leads
Posterior	V₇–V₉ (mirror V₁–V₃)	LCx or RCA	Usually with inferior or lateral MI
RV	V₄R	Proximal RCA	Preload-dependent: hypotension with nitrates, give fluids

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

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.

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

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.

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.

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
Atrial flutter with variable block	Flutter waves visible, irregular ventricular response
Multifocal atrial tachycardia (MAT)	≥ 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.

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.

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
Preexcited AF	Irregularly irregular wide QRS, rate > 200 — avoid AV-nodal blockers

Critical — Preexcited Atrial Fibrillation

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.

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

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) V_i/V_t 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)

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

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

Left Bundle Branch Block (LBBB)

Criterion	Value
QRS duration	≥ 0.12 s
I, aVL, V₅, V₆	Broad monophasic R (often notched)
V₁, V₂	Deep broad S wave (QS or rS)
Septal Q waves	Absent in I, V₆ (reversed septal depolarization)
ST/T	Discordant (opposite QRS main vector)
Causes	Nearly always pathologic: HTN, LVH, CAD, cardiomyopathy, aortic stenosis

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.

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.

22 Fascicular, Bifascicular & Trifascicular Blocks

Left Anterior Fascicular Block (LAFB)

Left axis deviation (−45° to −90°)
qR in I, aVL; rS in II, III, aVF
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

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

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.

Long QT Syndromes (LQTS)

Type	Gene	Channel	Trigger
LQT1	KCNQ1	I_Ks	Exercise, swimming
LQT2	KCNH2 (hERG)	I_Kr	Auditory (alarm, phone)
LQT3	SCN5A	I_Na	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

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

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)
Hypercalcemia + digitalis	Synergistic: hypercalcemia worsens digoxin toxicity
Hypokalemia + digitalis	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

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 V_5/6 > 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
Symptomatic bradycardia	Atropine 1 mg; transcutaneous pacing; epinephrine/dopamine infusion
Complete heart block	Transcutaneous → transvenous → permanent pacemaker
STEMI	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.