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Explain me 10 common heart diseases with ECG charts and ECG images of those diseases

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common heart diseases ECG patterns with images atrial fibrillation MI heart block

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ECG image STEMI atrial fibrillation ventricular tachycardia heart block site:litfl.com OR site:ecgwaves.com

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ECG images site:litfl.com atrial flutter ventricular fibrillation bradycardia sinus tachycardia WPW Brugada

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ECG electrocardiogram 10 common arrhythmias labeled diagram free medical education

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I now have all the material I need. Let me compile the comprehensive guide:

10 Common Heart Diseases: ECG Patterns & Images

Below is a detailed guide to 10 common cardiac conditions, each with their ECG characteristics and visual references.

Understanding the ECG Baseline

Before diving in, a quick reference on normal ECG components:
  • P wave = atrial depolarization
  • PR interval = AV conduction time (normal: 0.12-0.20 sec)
  • QRS complex = ventricular depolarization (normal: <0.12 sec)
  • ST segment = early ventricular repolarization
  • T wave = ventricular repolarization

1. Atrial Fibrillation (AF)

What it is: The most common sustained cardiac arrhythmia. Chaotic, disorganized electrical activity in the atria replaces the normal coordinated atrial contraction.
Causes: Heart failure, hypertension, coronary artery disease, hyperthyroidism, COPD, alcohol use, mitral valve disease.
Symptoms: Palpitations, fatigue, dyspnea, dizziness; can be asymptomatic. Major risk of stroke from atrial thrombus formation.

ECG Features:

  • No distinct P waves - replaced by fine, irregular fibrillatory baseline (f waves at 300-600 bpm)
  • Irregularly irregular RR intervals (the hallmark)
  • QRS complexes are usually narrow and normal morphology
  • Ventricular rate typically 100-180 bpm if uncontrolled

ECG Image - Atrial Fibrillation (Lead II):

Note the irregularly spaced QRS complexes with no visible P waves - only chaotic baseline activity
Atrial Fibrillation ECG - Lead II showing irregularly irregular QRS complexes with no P waves
Source: Guyton and Hall Textbook of Medical Physiology - Fig. 13.20. The waves visible are ventricular QRS and T waves only; no organized P waves are present.
Treatment: Rate control (beta-blockers, calcium channel blockers), rhythm control (cardioversion, antiarrhythmics), anticoagulation (warfarin or DOACs) to prevent stroke.

2. ST-Elevation Myocardial Infarction (STEMI)

What it is: Complete occlusion of a coronary artery causing full-thickness myocardial necrosis. A medical emergency requiring immediate reperfusion.
Causes: Atherosclerotic plaque rupture with superimposed thrombosis, coronary vasospasm (Prinzmetal angina).
Symptoms: Severe crushing chest pain radiating to arm/jaw, diaphoresis, nausea, shortness of breath.

ECG Features (Rosen's Emergency Medicine):

  • ST segment elevation >1 mm in 2+ contiguous leads (the defining feature)
  • Hyperacute T waves (tall, peaked) - earliest sign
  • Q waves develop over hours (irreversible necrosis)
  • Reciprocal ST depression in opposite leads
  • Location by leads:
    • Anterior STEMI: ST elevation in V1-V4 (LAD territory)
    • Inferior STEMI: ST elevation in II, III, aVF (RCA or LCx territory)
    • Lateral STEMI: ST elevation in I, aVL, V5-V6

ECG Image - Posterior MI (V1-V2 indirect + Posterior leads V8-V9):

Indirect findings in V1-V2 (mirror image of posterior STEMI):
Posterior MI ECG in V1 and V2 showing prominent R waves and ST depression
  • Lead V1: A = tall R wave (mirror of posterior Q), B = ST depression
  • Lead V2: A = tall R wave, B = ST depression, C = upright T wave
Direct posterior leads V8-V9 showing ST elevation:
Posterior MI ECG in leads V8 and V9 showing ST segment elevation
Arrows indicate subtle ST elevation - direct evidence of posterior wall infarction
Source: Rosen's Emergency Medicine - Figs. 64.12 & 64.13
Treatment: Immediate percutaneous coronary intervention (PCI) - "door-to-balloon" time <90 minutes. If PCI unavailable, thrombolysis within 12 hours. Aspirin + P2Y12 inhibitor, heparin, statin.

3. Ventricular Fibrillation (VF)

What it is: Completely chaotic ventricular electrical activity with no coordinated contraction - no cardiac output. The most common cause of sudden cardiac death.
Causes: Ischemic heart disease (most common), electrolyte imbalances (hypokalemia, hypomagnesemia), drug toxicity, cardiomyopathy, Brugada syndrome.
Symptoms: Sudden cardiac arrest - loss of consciousness, no pulse.

ECG Features:

  • Completely chaotic, irregular waveforms with no identifiable P waves, QRS complexes, or T waves
  • Variable amplitude and frequency oscillations
  • No organized rhythm whatsoever
  • Coarse VF = higher amplitude (more likely to respond to defibrillation)
  • Fine VF = low amplitude (longer duration, harder to convert)

ECG Pattern Reference:

From the physiology comparison chart above (panel d), the ECG shows chaotic irregular oscillations with total lack of normal electrical activity - the classic "bag of worms" appearance.
ECG Arrhythmia comparison chart showing VF (d) and other arrhythmias
Panel (d) = Ventricular fibrillation: chaotic, irregular oscillations with no organized waveforms
Treatment: Immediate CPR + defibrillation (unsynchronized DC shock). ACLS protocol: adrenaline 1 mg IV, amiodarone 300 mg IV after 3rd shock. Treat reversible causes (4 H's and 4 T's).

4. Ventricular Tachycardia (VT)

What it is: A rapid, potentially life-threatening arrhythmia originating in the ventricles at rate >100 bpm (usually 150-250 bpm).
Causes: Coronary artery disease (most common in adults), cardiomyopathy, electrolyte abnormalities, drug toxicity, channelopathies (Long QT, Brugada).
Symptoms: Palpitations, dizziness, syncope, chest pain. Hemodynamic collapse if sustained.

ECG Features (Goldman-Cecil Medicine):

  • Wide QRS complexes (>0.12 sec, usually >0.14 sec)
  • Monomorphic VT: All QRS complexes have the same morphology
  • Rate typically 150-250 bpm
  • AV dissociation (P waves independent of QRS) - pathognomonic when seen
  • Fusion beats and capture beats - highly specific for VT
  • Concordance in precordial leads (all positive or all negative)
Panel (c) in the arrhythmia chart above shows the unusual wide, rapid QRS complexes of ventricular tachycardia with increased frequency.
Treatment: If pulseless - CPR + defibrillation. If with pulse - cardioversion (synchronized) if unstable; amiodarone or procainamide if stable. Long-term: ICD implantation, catheter ablation.

5. Second-Degree AV Block (Heart Block)

What it is: Intermittent failure of conduction from the atria to the ventricles. Two main types:
  • Mobitz Type I (Wenckebach): Progressive PR prolongation until a P wave is blocked
  • Mobitz Type II: Sudden non-conducted P waves without PR prolongation - more dangerous
Causes: Inferior MI (Mobitz I - usually reversible), anterior MI (Mobitz II - often requires pacing), myocarditis, drug toxicity (digoxin, beta-blockers), degenerative conduction disease.

ECG Features:

  • Mobitz I: PR interval gets progressively longer until one P wave is not followed by QRS; then cycle repeats (group beating pattern)
  • Mobitz II: Constant PR interval, then sudden dropped beat (P wave with no QRS); often with bundle branch block
Panel (a) in the physiology chart shows second-degree (partial) block - note how half of the P waves are not followed by QRS complexes.
Treatment: Mobitz I - usually monitor, treat underlying cause, atropine if symptomatic. Mobitz II - urgent pacing (temporary then permanent pacemaker).

6. Third-Degree (Complete) AV Block

What it is: Complete failure of conduction between atria and ventricles. The atria and ventricles beat completely independently, maintained by a slow escape rhythm.
Causes: Degenerative conduction disease (most common in elderly), inferior or anterior MI, myocarditis, Lyme disease, drug toxicity, congenital.
Symptoms: Bradycardia, syncope (Stokes-Adams attacks), heart failure, sudden death risk.

ECG Features (LITFL):

  • Complete AV dissociation - P waves and QRS complexes have NO relationship
  • P waves at atrial rate (usually 60-100 bpm)
  • QRS complexes at escape rate (40-60 bpm if junctional; 20-40 bpm if ventricular)
  • Ventricular escape rhythm - wide QRS if below His bundle
  • Junctional escape rhythm - narrow QRS (faster, more stable)
  • PP intervals regular; RR intervals regular - but completely independent of each other
Panel (e) in the physiology chart shows third-degree block - impulses from SA node do not reach AV node for some beats, P waves are not followed by QRS.
Treatment: Emergency transcutaneous pacing or temporary transvenous pacing, followed by permanent pacemaker implantation.

7. Atrial Flutter

What it is: A rapid, organized atrial arrhythmia caused by a single reentrant circuit in the right atrium, producing atrial rates of 250-350 bpm.
Causes: Heart failure, mitral/tricuspid valve disease, COPD, pulmonary embolism, hyperthyroidism, post-cardiac surgery.
Symptoms: Palpitations, dyspnea, fatigue; can degenerate into AF.

ECG Features (Guyton and Hall):

  • Classic "sawtooth" flutter waves (F waves) at 250-350 bpm - best seen in leads II, III, aVF, V1
  • Regular atrial activity (unlike AF)
  • Fixed AV conduction ratio - usually 2:1 (ventricular rate ~150 bpm), 3:1, or 4:1
  • QRS complexes are normal/narrow (unless aberrant conduction)
  • No isoelectric baseline between flutter waves
The EKG cheat sheet above shows atrial flutter with the characteristic sawtooth pattern and regular QRS response.
Treatment: Rate control with AV nodal blocking agents, cardioversion (electrical or chemical with ibutilide), radiofrequency ablation of the cavotricuspid isthmus (highly effective, ~95% cure rate).

8. Left Ventricular Hypertrophy (LVH)

What it is: Thickening of the left ventricular myocardium in response to chronic pressure or volume overload. A major risk factor for heart failure, arrhythmias, and sudden death.
Causes: Long-standing hypertension (most common), aortic stenosis, hypertrophic cardiomyopathy, aortic regurgitation.
Symptoms: Often asymptomatic until complications develop. Can cause dyspnea, chest pain, palpitations.

ECG Features:

  • High-voltage QRS complexes:
    • Sokolow-Lyon criteria: S in V1 + R in V5 or V6 >35 mm
    • Cornell criteria: R in aVL + S in V3 >28 mm (men) or >20 mm (women)
  • Left axis deviation
  • ST depression and T wave inversion in lateral leads (V5-V6, I, aVL) - "strain pattern"
  • Prolonged QRS duration (often 0.10-0.12 sec)
  • Left atrial enlargement - broad, notched P waves in II ("P mitrale")
Treatment: Address underlying cause - aggressive blood pressure control (target <130/80 mmHg), treat aortic stenosis/regurgitation, ACE inhibitors/ARBs can promote LVH regression.

9. Wolff-Parkinson-White Syndrome (WPW)

What it is: Pre-excitation syndrome caused by an accessory pathway (Bundle of Kent) that bypasses the AV node, allowing direct electrical conduction from atria to ventricles. Predisposes to dangerous tachyarrhythmias.
Causes: Congenital. Can be associated with Ebstein's anomaly.
Symptoms: Palpitations, syncope, sudden cardiac death risk (especially if AF develops with rapid conduction down the accessory pathway).

ECG Features:

  • Short PR interval (<0.12 sec) - accessory pathway bypasses AV node delay
  • Delta wave - slurred, slow upstroke at the beginning of QRS (slow conduction through ventricular myocardium via accessory pathway)
  • Widened QRS complex (>0.12 sec) due to delta wave
  • Discordant ST-T changes (secondary to abnormal ventricular activation)
  • During tachycardia: can be narrow complex (orthodromic AVRT) or wide complex (antidromic AVRT, or AF with rapid accessory pathway conduction)
Danger: AF in WPW can conduct at very rapid rates (>300 bpm) down the accessory pathway, potentially triggering VF and sudden death. Never use AV nodal blocking agents (digoxin, verapamil, adenosine) in AF with WPW.
Treatment: Radiofrequency catheter ablation of the accessory pathway (definitive, >95% success). Acute AVRT: adenosine (if narrow complex, no AF). Acute AF with WPW: procainamide or electrical cardioversion.

10. Long QT Syndrome

What it is: Prolongation of the QT interval representing delayed ventricular repolarization. Predisposes to a specific polymorphic VT called Torsades de Pointes (TdP), which can degenerate into VF and cause sudden death.
Causes:
  • Congenital: Romano-Ward syndrome (autosomal dominant), Jervell and Lange-Nielsen syndrome (with deafness)
  • Acquired (more common): Drugs (antiarrhythmics, antibiotics like azithromycin/fluoroquinolones, antipsychotics, antihistamines), hypokalemia, hypomagnesemia, hypothyroidism, bradycardia, myocarditis

ECG Features:

  • Prolonged QT interval - corrected QT (QTc) using Bazett formula: QTc = QT / √RR
    • Normal QTc: <440 ms (men), <460 ms (women)
    • Borderline: 440-470 ms
    • Prolonged: >470 ms (men), >480 ms (women)
    • Very high risk: >500 ms
  • T wave abnormalities - broad-based, notched, or biphasic T waves
  • U waves may be prominent (especially in hypokalemia)
  • Torsades de Pointes: Polymorphic VT with characteristic twisting of QRS axis around the isoelectric line ("twisting of the points")
Treatment: Remove offending drugs/correct electrolytes. Congenital LQTS: beta-blockers (especially nadolol), ICD in high-risk patients, left cardiac sympathetic denervation. Acquired TdP: IV magnesium sulfate 2g, increase heart rate (overdrive pacing or isoproterenol).

ECG Reference Charts

Comprehensive Arrhythmia Comparison:

The image below shows ECG strip comparisons of multiple arrhythmias side-by-side:
ECG comparison chart showing second-degree block, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and third-degree block

EKG Interpretation Quick Reference (Arrhythmias with ECG Strips):

EKG Interpretation Cheat Sheet for Heart Arrhythmias - showing PSVT, atrial flutter, atrial fibrillation, junctional rhythm, PJCs, and first-degree AV block with ECG strips, descriptions, causes, and treatments

Quick Summary Table

#ConditionKey ECG FindingRateRhythm
1Atrial FibrillationNo P waves, fibrillatory baseline100-180 bpmIrregularly irregular
2STEMIST elevation ≥1mm in 2+ leadsVariableRegular
3Ventricular FibrillationChaotic oscillations, no organized waveformsUndetectableChaotic
4Ventricular TachycardiaWide QRS (>0.12s), AV dissociation150-250 bpmRegular
52nd-Degree AV BlockDropped beats (Mobitz I: progressive PR; Mobitz II: sudden block)VariableIrregular
6Complete Heart BlockP waves & QRS completely independentAtria 60-100; Ventricles 20-60Two independent regular rhythms
7Atrial FlutterSawtooth F waves 250-350 bpm, 2:1 AV block~150 bpmRegular
8LVHTall QRS voltage (S V1 + R V5 >35mm), lateral strain patternNormalNormal sinus
9WPW SyndromeShort PR, delta wave, wide QRSNormal (or tachycardia)Variable
10Long QT SyndromeQTc >470 ms, abnormal T waves; TdP if arrhythmiaNormal baseline; TdP rapidNormal baseline; TdP polymorphic
Sources:
  • Guyton and Hall Textbook of Medical Physiology, Fig. 13.20
  • Rosen's Emergency Medicine, Figs. 64.12-64.13
  • Goldman-Cecil Medicine, Chapter 53 (Ventricular Arrhythmias)
  • Harrison's Principles of Internal Medicine 22E
  • LITFL ECG Library (litfl.com)
  • Nurseslabs EKG Interpretation Reference
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