Can you help me understand most common 10 ecg patterns

Reading File

Finding Sources

Reading File

Finding Sources

Loading Image

Searching the Web

10 most common ECG patterns clinical interpretation guide

I now have comprehensive material from Braunwald's Heart Disease, Tintinalli's Emergency Medicine, Fuster & Hurst's The Heart, plus web sources. Here is the full, detailed guide:

The 10 Most Common ECG Patterns

How to Read Any ECG (Quick Framework First)

Before pattern recognition, always run through 5 steps systematically:

Rate - Count R-R intervals (300/large boxes between R peaks, or complexes x 6 on a 10-sec strip)
Rhythm - Regular or irregular? Regularly irregular or irregularly irregular?
Axis - Look at leads I and aVF: both up = normal, I up/aVF down = left axis, I down/aVF up = right axis
Intervals - PR (0.12-0.20s), QRS (<0.12s), QTc
ST/T waves & morphology - Elevations, depressions, inversions, Q waves

1. Normal Sinus Rhythm (NSR)

The baseline you compare everything else against.

Parameter	Normal Value
Rate	60-100 bpm
P waves	Upright in I, II, aVF; before every QRS
PR interval	0.12-0.20 sec (3-5 small boxes)
QRS duration	≤0.10 sec (≤2.5 small boxes)
Rhythm	Regular

Key teaching point: P wave must precede every QRS with a constant PR interval. If this is present, you have sinus rhythm and can focus on everything else (ST changes, axis, intervals).

2. Sinus Tachycardia

Same as NSR, just fast.

Rate > 100 bpm, all other morphology normal
P wave before every QRS, regular rhythm
Common causes: Pain, fever, hypovolemia, PE, hyperthyroidism, anxiety, drugs (caffeine, stimulants)
Critical point: Sinus tachycardia is a symptom, not a primary arrhythmia. Always treat the underlying cause. Never cardiovert.

3. Sinus Bradycardia

Same as NSR, just slow.

Rate < 60 bpm, all other morphology normal
Common causes: Athletic heart, sleep, increased vagal tone, beta-blockers, hypothyroidism, inferior MI (RCA supplies SA node)
Treatment: Only if symptomatic (dizziness, syncope, hypotension) - atropine 0.5 mg IV, or transcutaneous pacing in severe cases

4. Atrial Fibrillation (AFib)

The most common sustained cardiac arrhythmia.

From Tintinalli's Emergency Medicine:

"Absence of discernible P waves with flat or chaotic isoelectric baseline. QRS complexes narrow unless preexisting bundle branch block or preexcitation syndrome. Irregularly irregular ventricular rhythm."

Feature	Finding
P waves	Absent - replaced by chaotic fibrillatory baseline (f waves)
Rhythm	Irregularly irregular (the hallmark)
QRS	Narrow (unless BBB or WPW)
Rate	Variable (ventricular rate 100-180 bpm if uncontrolled)

Clinical consequences: Loss of atrial kick (up to 30% of cardiac output in some patients), risk of thromboembolism (stroke), and rapid ventricular rates. Risk stratify with CHA₂DS₂-VASc score for anticoagulation decisions.

Atrial flutter ECG examples showing flutter waves in leads II, III, aVF and response to carotid sinus massage

Atrial flutter (a close relative of AFib) - A. Narrow complex tachycardia at 155 bpm. B. Flutter waves best seen in leads II, III, aVF (classic "sawtooth" pattern). C. Carotid sinus massage unmasking flutter waves by transiently increasing AV block.

5. AV Blocks (1st, 2nd, 3rd Degree)

Three distinct patterns with very different clinical urgency:

First-Degree AV Block

PR interval > 0.20 sec (>1 large box), constant
Every P wave conducts - just delayed
Usually benign, often no treatment needed

Second-Degree AV Block - Mobitz Type I (Wenckebach)

PR interval progressively lengthens until a P wave is blocked (no QRS follows)
Then the cycle resets - "group beating" appearance
Mnemonic: "Longer, longer, longer... DROP - then you have a Wenckebach"
Block is at the AV node level - usually benign, rarely needs pacing

Second-Degree AV Block - Mobitz Type II

PR interval constant, then a P wave is suddenly not conducted (no warning)
Block is below the AV node (Bundle of His or bundle branches)
Dangerous - can progress unpredictably to complete block; often requires pacemaker

Third-Degree (Complete) AV Block

Complete dissociation between P waves and QRS complexes
P waves march through at their own rate; QRS at their own (escape) rate
If ventricular escape: wide QRS (20-40 bpm) - medical emergency
If junctional escape: narrow QRS (40-60 bpm) - more stable but still urgent
Requires emergent pacing

6. Right Bundle Branch Block (RBBB)

Classic mnemonic: "William MaRRow" - WiRRoW for RBBB

Feature	Finding
QRS duration	≥ 0.12 sec (≥3 small boxes) - wide complex
V1	rSR' pattern ("rabbit ears" or "M" shaped)
V5/V6	Wide, slurred S wave
T waves	Inverted in V1-V2 (right "strain" pattern)

Cause: RCA disease, PE (acute RBBB + S1Q3T3), congenital heart disease, normal variant in athletes
Isolated RBBB rarely progresses to complete heart block - Fuster & Hurst's, p.1233

7. Left Bundle Branch Block (LBBB)

Classic mnemonic: "WiLLiaM" - W in V1, M in V5/V6

Feature	Finding
QRS duration	≥ 0.12 sec - wide complex
V1	Broad, deep QS or rS wave
V5/V6	Tall, broad, notched R wave - no septal Q
Lateral leads	Discordant ST-T changes (ST opposite to QRS direction)

New LBBB in a patient with chest pain = STEMI equivalent until proven otherwise (Sgarbossa criteria apply)
Associated with dilated cardiomyopathy, severe LV disease, worse prognosis
Fuster & Hurst's: "LBBB in patients with cardiomyopathy is associated with significant ventricular dyssynchrony, worsening HF, and increased mortality."

Complete AV block and RV pacing ECG from Fuster and Hurst's The Heart

A. Complete AV nodal block - note the independent P waves and escape QRS complexes. B. Post RV pacing showing typical LBBB-like paced morphology.

8. ST-Elevation - STEMI

The most time-critical pattern you will ever see.

ST elevation ≥ 1 mm in ≥2 contiguous limb leads, or ≥ 2 mm in contiguous precordial leads
New LBBB counts as STEMI equivalent
Reciprocal ST depression in opposite leads (confirms true elevation)

Localization by territory:

Leads with ST Elevation	Territory	Artery
V1-V4	Anterior	LAD
II, III, aVF	Inferior	RCA (or LCx)
I, aVL, V5-V6	Lateral	LCx
V1-V3 (posterior: tall R in V1-V2)	Posterior	RCA/LCx
V4R-V5R	Right ventricle	RCA proximal

From Textbook of Family Medicine: "STEMI occurs secondary to a sudden interruption of coronary blood supply to a part of the myocardium as a result of a complete thrombotic occlusion of a coronary artery. Emergent and complete revascularization is the most important goal - primary angioplasty within 90 minutes (door-to-balloon time)."

Evolutionary changes: Hyperacute T waves → ST elevation → Q wave formation → T inversion → Q waves persist permanently

9. ST Depression and T-Wave Inversions (Ischemia/NSTEMI)

Subendocardial ischemia or NSTEMI pattern:

ST depression ≥ 0.5 mm in ≥2 contiguous leads
T-wave inversions (symmetrical, deep T inversions = Wellens' syndrome in V2-V3 = critical LAD stenosis)
Horizontal or downsloping ST depression is more specific for ischemia than upsloping

Key patterns to know:

Wellens' A: Biphasic T waves in V2-V3 (deeply ominous - proximal LAD lesion)
Wellens' B: Deep symmetrical T inversions in V2-V3
De Winter T waves: Upsloping ST depression + tall peaked T waves in precordial leads = LAD occlusion STEMI equivalent (no ST elevation!)
Diffuse ST depression + ST elevation in aVR: Left main or proximal LAD occlusion

Strain pattern: Down-sloping ST depression + T inversion in lateral leads (I, aVL, V5-V6) with LVH = "LV strain," not necessarily ischemia

10. Left Ventricular Hypertrophy (LVH)

Very common - seen in hypertension, aortic stenosis, HCM.

Voltage criteria (any one sufficient for diagnosis):

Criterion	Threshold
Sokolow-Lyon	S in V1 + R in V5 or V6 > 35 mm
Cornell	R in aVL + S in V3 > 28 mm (men) or > 20 mm (women)
R in aVL alone	> 11 mm
R in V5 or V6	> 26 mm

LV "strain" pattern: ST depression + T-wave inversion in I, aVL, V4-V6 (opposite direction to QRS)

Left axis deviation commonly present
LAE (left atrial enlargement): Notched P wave ("P mitrale") in lead II, biphasic P in V1

Bonus: Quick Reference Table

Pattern	Rate	Rhythm	P Wave	QRS	Key Finding
NSR	60-100	Regular	Before every QRS	Narrow	Baseline normal
Sinus Tach	>100	Regular	Before every QRS	Narrow	Treat the cause
AFib	Variable	Irregularly irregular	Absent/chaotic	Narrow*	"Irregularly irregular"
Atrial Flutter	~150	Regular (2:1)	Sawtooth waves	Narrow*	300 atrial / 150 ventricular
1° AVB	60-100	Regular	Before every QRS	Narrow	PR > 0.20s
2° AVB Mobitz I	Variable	Regularly irreg.	Progressively longer PR then dropped	Narrow	Wenckebach
3° AVB	~30-60	Regular but dissociated	March through independently	Wide or narrow	Complete dissociation
RBBB	Normal	Regular	Normal	Wide ≥0.12s	rSR' in V1
LBBB	Normal	Regular	Normal	Wide ≥0.12s	Broad R in V5/V6, no septal Q
STEMI	Variable	Variable	Variable	Variable	ST elevation ≥1-2mm in contiguous leads
LVH	Normal	Regular	± wide/notched	± wide	Voltage criteria + strain pattern

*Wide QRS with AFib/flutter if BBB or WPW present

Sources:

Tintinalli's Emergency Medicine: A Comprehensive Study Guide
Fuster and Hurst's The Heart, 15th Edition
Textbook of Family Medicine, 9e
Roberts and Hedges' Clinical Procedures in Emergency Medicine

Can you summarize every ecg with visual presentation

Finding Sources

Reading File

Finding Sources

Reading File

Loading Image

Reading File

Loading Image

Reading File

Loading Image

Reading File

I now have a rich set of textbook ECG images. Let me compile the full visual guide:

10 Common ECG Patterns - Visual Reference Guide

1. Normal Sinus Rhythm (NSR)

What to look for: Regular P before every QRS, PR 0.12-0.20s, QRS <0.12s, rate 60-100 bpm, upright P in leads I, II, aVF.

Feature	Normal Value
Rate	60-100 bpm
Rhythm	Regular
P waves	Upright in I, II, aVF - before every QRS
PR interval	0.12-0.20 sec
QRS	Narrow ≤0.10 sec

Clinical tip: This is your baseline. Every abnormal pattern is a deviation from this.

2. Sinus Tachycardia / Sinus Bradycardia

Same morphology as NSR - just the rate is different.

Tachycardia: Rate > 100 bpm. All complexes identical to NSR. Always treat the underlying cause (pain, fever, PE, bleeding, drugs).
Bradycardia: Rate < 50 bpm (Braunwald's defines pathologic threshold at 50 bpm). Normal P wave contour, upright in I, II, aVF. Often physiologic in athletes. Treat only if symptomatic.

3. Atrial Fibrillation (AFib) - Three Real Examples

The three strips below show three actual patients with AFib - each looks slightly different, but all share the cardinal features:

Three examples of atrial fibrillation from Tintinalli's Emergency Medicine showing irregularly irregular ventricular rhythm with absent P waves across all three strips

Three examples of AFib (Tintinalli's Emergency Medicine). A. Rapid ventricular rate with chaotic baseline. B. Controlled ventricular rate, clearly irregular rhythm. C. Slower response, irregular rhythm remains.

Key features (ALL must be present):

No P waves - replaced by chaotic fibrillatory (f) waves
Irregularly irregular ventricular rhythm - the hallmark
QRS narrow (unless BBB or WPW coexist)
Atrial rate > 400-600 bpm, ventricular rate depends on AV node

Atrial flutter (close relative): Regular "sawtooth" flutter waves at ~300 bpm, most visible in II, III, aVF and V1. Usually conducts with 2:1 block → ventricular rate ~150 bpm.

Atrial flutter with sawtooth flutter waves - three panels showing A regular tachycardia at 155 bpm B 12-lead ECG showing classic flutter waves C carotid sinus massage response unmasking flutter waves

Atrial Flutter (Tintinalli's). A. Regular narrow tachycardia at 155 bpm. B. 12-lead showing sawtooth flutter waves best in II, III, aVF. C. Carotid sinus massage slows conduction and unmasks flutter waves.

4. AV Blocks

Idioventricular Escape Rhythm (seen in 3rd degree block)

Idioventricular rhythm at approximately 30 bpm showing slow wide QRS complexes on a flat baseline - a ventricular escape rhythm

Idioventricular escape rhythm at ~30 bpm (Tintinalli's). Wide, slow QRS complexes - a ventricular escape rhythm seen in complete (3rd degree) AV block or severe bradycardia.

Summary of all AV blocks:

Block	PR Interval	P:QRS Ratio	Key Feature	Urgency
1st degree	Prolonged (>0.20s), constant	1:1	All P waves conduct	Benign
2nd degree Mobitz I	Progressive lengthening then dropped beat	>1:1	Wenckebach - "longer, longer, drop"	Usually benign
2nd degree Mobitz II	Constant PR, then sudden non-conducted P	>1:1	Sudden drop, no warning	Dangerous - needs pacer
3rd degree (complete)	No relationship	Independent	Full AV dissociation	Emergency

From Morgan & Mikhail's Clinical Anesthesiology: "Mobitz type II... conduction block is nearly always in or below the His bundle and frequently progresses to complete (third-degree) AV block."

5. Right Bundle Branch Block (RBBB)

Complete AV block and paced rhythm - the ECG below shows complete AV block (Panel A) and RV pacing producing a LBBB-like pattern (Panel B):

Complete AV nodal block and RV pacing ECG - Panel A shows complete heart block with independent P waves and escape QRS complexes Panel B shows RV paced rhythm with LBBB-like wide QRS morphology

Fuster & Hurst's The Heart - A. Complete AV nodal block: P waves march independently, slow escape rhythm. B. RV pacing: Wide QRS complexes with LBBB-like morphology (RV pacing mimics LBBB because activation starts from the right ventricle).

RBBB - Key ECG features:

QRS ≥ 0.12 sec (wide complex)
rSR' pattern in V1 ("rabbit ears" or M shape)
Wide, slurred S wave in I, V5, V6
T-wave inversion in V1-V3 (right "strain")
Mnemonic: WiRRoW - W in V1, M in V6 for RBBB... or remember "MaRRoW" = M in V1 for RBBB

Morgan & Mikhail: "A conduction delay or block in the right bundle-branch results in a typical RBBB QRS pattern on the surface ECG (M-shape or rSR' in V1)."

6. Left Bundle Branch Block (LBBB)

LBBB - Key ECG features:

QRS ≥ 0.12 sec (wide complex)
Broad, deep QS or rS in V1 (W shape)
Tall, broad, notched R in V5/V6 (M shape) - no septal Q waves in lateral leads
Discordant ST-T changes (ST depression/T inversion OPPOSITE to main QRS direction)
Mnemonic: WiLLiaM - W in V1, M in V6 for LBBB

Critical clinical point: New LBBB + chest pain = treat as STEMI equivalent. Apply Sgarbossa criteria to detect superimposed MI.

7. ST-Elevation Myocardial Infarction (STEMI) - Multiple Territories

Anterior STEMI (LAD territory - V1 to V4)

Anterior wall STEMI showing ST segment elevation in leads V1 to V4 with obliquely straight morphology - due to 90% LAD stenosis

Anterior wall STEMI (Rosen's Emergency Medicine). ST elevation in V1-V4, obliquely straight morphology. LAD 90% stenosis confirmed on catheterization.

Anterolateral STEMI (LAD + LCx - V2-V6, I, aVL)

Anterolateral STEMI showing massive ST elevation in V2 to V6 and leads I and aVL - due to 100 percent in-stent thrombosis of LAD

Anterolateral STEMI (Rosen's). Massive STE in V2-V6, I, aVL. Patient had prior LAD stent - emergency cath revealed 100% in-stent thrombosis.

ST Elevation in aVR = Left Main / Proximal LAD Occlusion

ST elevation in aVR with widespread ST depression in other leads indicating left main coronary artery 80 percent stenosis

ST elevation in aVR + diffuse ST depression (Rosen's). ST elevation >1 mV in aVR plus widespread ST depression → left main coronary artery 80% stenosis found on catheterization.

Right Ventricular Infarction (Inferior STEMI + RV involvement)

Right ventricular infarction ECG using right-sided precordial leads showing ST elevation from RV1 to RV6 alongside inferior STEMI in leads II III and aVF

Right ventricular infarction (Rosen's). Right-sided leads (RV1-RV6). Standard limb leads show inferior STEMI (II, III, aVF) + reciprocal depression in I and aVL. Right-sided leads confirm RV infarction with STE in RV3-RV6.

STEMI territory summary from Rosen's Emergency Medicine:

Location	Leads with STE	Artery
Anterior	V1-V4	LAD
Lateral	I, aVL, V5, V6	LCx
Inferior	II, III, aVF	RCA
RV	V6R (right-sided)	Proximal RCA
Posterior	V8, V9 elevation; V1-V3 depression	RCA/LCx

8. ST Depression / Ischemia Pattern (NSTEMI/Unstable Angina)

Horizontal or downsloping ST depression ≥ 0.5 mm in ≥2 contiguous leads = subendocardial ischemia
Symmetrical deep T inversions in precordial leads (especially V2-V3) = Wellens' syndrome (critical proximal LAD stenosis)
De Winter T waves: Upsloping ST depression + tall peaked T waves in precordial leads = LAD occlusion without classic STE

9. Left Ventricular Hypertrophy (LVH) with Strain Pattern

LVH with strain pattern showing large R waves in left-sided leads V4 to V6 with asymmetric T wave inversions and ST depression plus ST elevation in V1 to V3 with concave contour

LVH with repolarization/strain pattern (Rosen's). Large amplitude R waves in V4-V6 + asymmetric T inversions (strain) in lateral leads. V1-V3 show concave ST elevation - the RIGHT precordial mirror of LV strain. This pattern is seen in ~75% of voltage-positive LVH. Do NOT confuse with ischemia.

Voltage criteria (any one is sufficient):

S in V1 + R in V5 or V6 > 35 mm (Sokolow-Lyon)
R in aVL > 11 mm
Cornell criteria: R aVL + S V3 > 28 mm (men) / > 20 mm (women)

LV strain pattern: Asymmetric ST depression + T inversion in I, aVL, V4-V6 (concave morphology, opposite to QRS direction)

Common causes: Hypertension (most common), aortic stenosis, hypertrophic cardiomyopathy, coarctation of aorta.

10. Ventricular Tachycardia (VT) / Ventricular Fibrillation (VF)

VT - Key ECG features:

Rate > 100 bpm (often 150-250 bpm)
Wide QRS ≥ 0.12 sec - all complexes look the same (monomorphic)
AV dissociation (P waves independent of QRS) - pathognomonic when visible
Fusion beats and capture beats (diagnostic when present)
Concordance in precordial leads (all positive or all negative) strongly favors VT over SVT with aberrancy

Torsades de Pointes (polymorphic VT):

QRS complexes continuously shift axis, appearing to "twist" around the baseline
Occurs in setting of prolonged QTc (drugs, electrolyte abnormalities, congenital LQTS)

VF - Key ECG features (from Fuster & Hurst's):

"Rapid, irregular, dysmorphic pattern with no clearly defined QRS complex"
Chaotic, disorganized waveforms
No cardiac output - immediate defibrillation required
Survival decreases 7-10% for every minute of delay in defibrillation

Quick Visual Identification Cheat Sheet

Pattern	Rate	Rhythm	P Wave	QRS Width	Signature Finding
NSR	60-100	Regular	Before every QRS	Narrow	Textbook normal
Sinus Tach	>100	Regular	Normal	Narrow	Fast NSR
Sinus Brady	<60	Regular	Normal	Narrow	Slow NSR
AFib	Variable	Irregularly irregular	Absent	Narrow*	No P waves + chaos
A-Flutter	~150	Regular	Sawtooth	Narrow*	300 atrial / 150 ventricular
1° AVB	60-100	Regular	Normal	Narrow	PR > 0.20s
Mobitz I	Variable	Group beating	Progressive PR	Narrow	Wenckebach drop
Mobitz II	Variable	Regular then pause	Constant PR	Wide	Sudden non-conducted P
3° AVB	~30-60	Dissociated	March through independently	Wide	Complete dissociation
RBBB	Normal	Regular	Normal	≥ 0.12s	rSR' in V1 + slurred S in I/V6
LBBB	Normal	Regular	Normal	≥ 0.12s	Broad R in V5/V6, no septal Q
STEMI	Variable	Variable	Variable	Variable	STE ≥ 1-2 mm in contiguous leads
NSTEMI/UA	Variable	Variable	Variable	Narrow	ST depression / T inversions
LVH	60-100	Regular	± wide/notched	Narrow-wide	Voltage criteria + lateral strain
VT	150-250	Regular (wide)	Dissociated	Wide	Wide complex tachycardia + AV dissociation
VF	-	Chaotic	None	None	No QRS - immediate shock

*Narrow unless BBB or WPW coexist

Sources: Rosen's Emergency Medicine, Tintinalli's Emergency Medicine, Fuster & Hurst's The Heart 15th Ed, Braunwald's Heart Disease, Morgan & Mikhail's Clinical Anesthesiology

This is a shared conversation. Sign in to Orris to start your own chat.