10 common ecg findings

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Here are 10 common ECG findings with their key features, clinical significance, and underlying mechanisms - sourced from Harrison's Principles of Internal Medicine 22E, Tintinalli's Emergency Medicine, Roberts and Hedges' Clinical Procedures, and Braunwald's Heart Disease.

1. ST-Segment Elevation

What you see: ST segment raised ≥1 mm above baseline in two or more contiguous leads.

Mechanism: Transmural (full-thickness) ischemia shifts the injury current vector toward the epicardium. This produces ST elevations over the ischemic zone and reciprocal ST depressions in opposite leads.

Localization:

Anterior (V1-V6 + I, aVL) - LAD territory
Inferior (II, III, aVF) - RCA territory
Lateral (I, aVL, V5-V6) - LCx territory
Posterior - reciprocal ST depression in V1-V3

Also caused by: Pericarditis (diffuse, concave-up "saddle-shape" elevation with PR depression), Takotsubo syndrome, early repolarization, LBBB.

Harrison's Principles of Internal Medicine 22E, p. 1915

2. Atrial Fibrillation (AF)

What you see:

Absence of distinct P waves; flat or chaotic isoelectric baseline (fibrillatory f-waves)
Irregularly irregular narrow QRS complexes (unless bundle branch block or pre-excitation is present)
Ventricular rate typically 100-180 bpm if uncontrolled

Mechanism: Multiple chaotic reentrant wavelets in the atria depolarize at 350-600 impulses/min; the AV node filters these, producing an irregularly irregular ventricular response.

Clinical significance: Loss of atrial kick reduces cardiac output by ~20% in compensated hearts (more in stiff ventricles). Major risk of thromboembolism - CHA2DS2-VASc score guides anticoagulation.

Tintinalli's Emergency Medicine, p. 149

3. Left Ventricular Hypertrophy (LVH)

What you see (voltage criteria):

SV1 + RV5 or RV6 ≥ 35 mm (Sokolow-Lyon)
R in aVL ≥ 11 mm (Cornell)
Often accompanied by ST depression + T-wave inversion in lateral leads (the "strain" pattern)
Left atrial abnormality (broad, notched P in II; deep negative terminal P in V1) increases specificity

Caveat: Prominent precordial voltages are a common normal variant in young, athletic individuals. Sensitivity of voltage criteria is low in middle-aged/older adults, obese patients, and those with COPD.

Harrison's Principles of Internal Medicine 22E, p. 1914

4. Bundle Branch Blocks

Comparison of normal, RBBB, and LBBB patterns in V1 and V6 - Harrison's, Figure 247-10

QRS duration ≥120 ms is required for complete block.

Right Bundle Branch Block (RBBB):

rSR' ("M-shaped" or "rabbit ears") in V1
Wide, slurred S wave in V6 and lead I
Secondary T-wave inversion in V1-V3
RBBB alone is often benign; also seen with pulmonary embolism, ASD, RV strain

Left Bundle Branch Block (LBBB):

Wide, predominantly negative (QS) in V1
Broad, tall, entirely positive (R) in V6
Septal activation reversal - no septal Q wave in V6
LBBB is almost always pathological - associated with coronary artery disease, hypertension, dilated cardiomyopathy, valvular disease; a new LBBB in ACS is treated like STEMI (Sgarbossa criteria apply)
Harrison's Principles of Internal Medicine 22E, p. 1914-1915

5. Atrioventricular (AV) Block

1st Degree AV Block:

PR interval >200 ms (>5 small squares); every P conducts
Often benign; can be from increased vagal tone, inferior MI, digoxin

2nd Degree - Mobitz I (Wenckebach):

Progressive PR lengthening until a P wave fails to conduct (dropped QRS)
Usually at the AV node level; often benign

2nd Degree - Mobitz II:

Fixed PR interval with sudden, unpredictable dropped QRS beats
At or below the bundle of His; high risk of progressing to complete heart block

3rd Degree (Complete Heart Block):

No relationship between P waves and QRS complexes (AV dissociation)
Escape rhythm: junctional (narrow, ~40-60 bpm) or ventricular (wide, <40 bpm)
Requires urgent pacing
Harrison's Principles of Internal Medicine 22E; Robbins & Kumar Basic Pathology

6. Prolonged QT Interval

What you see: Corrected QT (QTc) ≥440 ms in men, ≥460 ms in women (Bazett's formula: QTc = QT / √RR).

Mechanism: Delayed ventricular repolarization due to reduced outward K+ currents or increased inward Na+/Ca2+ currents. Creates dispersion of repolarization, predisposing to early afterdepolarizations and Torsades de Pointes (polymorphic VT).

Causes:

Congenital: LQTS1 (KCNQ1), LQTS2 (KCNH2), LQTS3 (SCN5A)
Drugs: antiarrhythmics (sotalol, amiodarone), antipsychotics, macrolides, fluoroquinolones
Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
Hypothyroidism, hypothermia, myocarditis
Fuster and Hurst's The Heart 15E; Harrison's 22E

7. Hyperkalemia

ECG changes in hyperkalemia across severity levels

Sequential ECG changes in hyperkalemia - Harrison's, Figure 247-14

Progressive ECG changes with rising K+:

K+ level	ECG change
5.5-6.5 mEq/L	Tall, peaked ("tented") T waves - earliest sign
6.5-7.5 mEq/L	Widening QRS, PR prolongation, P-wave flattening
>7.5 mEq/L	P waves disappear, sine-wave pattern
>8-9 mEq/L	Ventricular fibrillation or asystole

Emergency: Calcium gluconate stabilizes the myocardium. Sodium bicarbonate, insulin+glucose, and albuterol shift K+ intracellularly.

Harrison's Principles of Internal Medicine 22E, p. 1918

8. Pericarditis / Pericardial Effusion

Pericarditis - 4 evolutionary stages:

Diffuse, concave-up ST elevation with PR segment depression (most leads except aVR/V1)
ST and PR normalization
Diffuse T-wave inversions
T-wave normalization

Pericardial effusion ECG signs:

Sinus tachycardia
PR depression
Low voltage QRS (amplitude ≤5 mm in all limb leads or ≤10 mm in precordial leads)
Electrical alternans - beat-to-beat alternation in QRS amplitude/axis; total (P+QRS+T) alternans with sinus tachycardia is relatively specific for cardiac tamponade

ECG sensitivity for pericardial effusion is only 1-17%, so echo is mandatory for confirmation.

Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 393

9. Sinus Bradycardia and Sinus Tachycardia

Sinus Bradycardia: Rate <60 bpm; normal P morphology (upright in II, inverted in aVR), regular rhythm.

Causes: high vagal tone (athletes, vasovagal), hypothyroidism, hypothermia, sick sinus syndrome, inferior MI, beta-blockers/calcium channel blockers, raised ICP

Sinus Tachycardia: Rate >100 bpm; same P morphology; typically gradual onset/offset.

Causes: pain, fever, hypovolemia, anemia, heart failure, PE, hyperthyroidism, sepsis, sympathomimetics
A reflex sinus tachycardia with a clearly identifiable cause should prompt treatment of the underlying condition, not the rate itself.

10. Pathological Q Waves

What you see: Q wave width ≥40 ms (≥1 small square) or depth ≥25% of the R wave amplitude in the same lead.

Mechanism: Electrically silent infarcted myocardium creates a "window" toward the cavity; leads overlying the infarct record negative (away) vectors as Q waves.

Localization mirrors the ST elevation distribution:

Anterior Q waves (V1-V4): LAD infarction
Inferior Q waves (II, III, aVF): RCA infarction
Lateral Q waves (I, aVL, V5-V6): circumflex infarction

Note: Small septal Q waves (<40 ms, <2 mm) in I, V5, V6 are normal. Q waves in aVR are always normal. Q waves in III alone (without II and aVF) are often positional and non-pathological.

Harrison's Principles of Internal Medicine 22E, p. 1916

Quick Reference Summary

Finding	Key ECG Feature	Primary Concern
ST elevation	≥1 mm elevation in ≥2 contiguous leads	STEMI / pericarditis
Atrial fibrillation	Irregularly irregular, no P waves	Stroke risk, rate control
LVH	Tall R waves (SV1+RV5 ≥35 mm)	Hypertension, HCM
RBBB/LBBB	Wide QRS, specific morphology	LBBB: often pathological
AV block	PR prolongation / dropped beats	3rd degree: urgent pacing
Long QT	QTc ≥440-460 ms	Torsades de Pointes
Hyperkalemia	Peaked T waves → sine wave	Life-threatening arrhythmia
Pericarditis	Diffuse saddle ST + PR depression	Tamponade if effusion
Sinus bradycardia/tachy	Rate <60 or >100, normal P axis	Treat underlying cause
Pathological Q	Wide/deep Q in ≥2 contiguous leads	Old/evolving infarction

Give me images with marked changes compared to normal

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Here are textbook ECG images for each finding, with the key changes explained:

1. ST Elevation - Mechanism

Subendocardial vs transmural ischemia ST changes

A (left): Subendocardial ischemia - ST vector points inward → ST depression in overlying leads. B (right): Transmural/epicardial ischemia - ST vector points outward → ST elevation in overlying leads (the STEMI pattern).

Harrison's 22E, Fig. 247-11

2. Anterior STEMI - Evolving ECG Sequence

Anterior STEMI acute and evolving ECG across all 12 leads

Top row (Acute): ST elevation in I, aVL, V2-V6. Tall, peaked "hyperacute" T waves. Reciprocal ST depression in II, III, aVF. Bottom row (Evolving): Deep Q waves developing in V2-V4. ST elevation resolving. T-wave inversions appearing.

Harrison's 22E, Fig. 247-13A

3. Inferior STEMI - Evolving ECG Sequence

Inferior STEMI acute and evolving ECG across all 12 leads

Top row (Acute): ST elevation in II, III, aVF (RCA territory). Reciprocal ST depression in I, aVL, V1-V4. Bottom row (Evolving): Deep Q waves in II, III, aVF. ST settling. T inversions in inferior leads.

Harrison's 22E, Fig. 247-13B

4. Anterior STEMI - Real 12-Lead Tracing

Real 12-lead ECG showing acute inferior MI with ST elevation in inferior leads

What to see: Marked ST elevation in II, III, aVF with deep reciprocal ST depression in I, aVL, V1-V2. This is a real-patient inferior STEMI tracing.

Textbook of Family Medicine 9E, Fig. 27-12 - "Acute inferior MI with ST elevation in inferior leads"

5. Wellens T-Wave Pattern (Anterior Ischemia / LAD Stenosis)

Deep T-wave inversions V1-V6 Wellens sign precordial leads

Key change: Deep, symmetric T-wave inversions across V1-V6. No ST elevation. No Q waves. Significance: The "Wellens T-wave sign" - almost always indicates critical high-grade LAD stenosis. High risk for impending anterior STEMI. Do NOT stress-test these patients.

Harrison's 22E, Fig. 247-12

6. Bundle Branch Blocks (RBBB vs LBBB)

RBBB vs LBBB morphology in V1 and V6 compared to normal

	V1	V6
Normal	Small r, deep S	Narrow qR, upright T
RBBB	rSR' ("rabbit ears"), inverted T	qRS with wide slurred S
LBBB	Wide, entirely negative (QS)	Broad, monophasic tall R, inverted T

Harrison's 22E, Fig. 247-10

7. Atrial Fibrillation

ECG tracing of atrial fibrillation - no P waves, irregularly irregular QRS

Key changes vs normal:

No P waves - chaotic fibrillatory baseline
Irregularly irregular QRS complexes (note the varying R-R intervals)
Narrow QRS unless BBB is present
Pye's Surgical-Handicraft, Fig. 17.35

8. Complete Heart Block (3rd Degree AV Block)

ECG of complete heart block showing dissociated P waves and slow escape rhythm

Key changes vs normal:

Small P waves (atrial rate ~70-80 bpm) firing independently
Wide, slow QRS complexes (ventricular escape rhythm, ~30-40 bpm)
No relationship between P waves and QRS complexes (AV dissociation)
The long flat stretches after each QRS represent the slow ventricular rate with no conducted beats
Pye's Surgical-Handicraft, Fig. 17.34

9. Hyperkalemia - Progressive Changes

ECG changes in hyperkalemia from mild to very severe - peaked T waves, wide QRS, sine wave

Left (Mild-Moderate ~5.5-6.5 mEq/L): Narrow, tall, peaked ("tented") T waves in V1-V2. Normal QRS. Middle (Moderate-Severe ~6.5-7.5 mEq/L): QRS widens markedly. P waves flattening. T waves remain tall and peaked. Right (Very Severe >7.5 mEq/L): Sine-wave pattern - P waves gone, QRS and T wave merge into a continuous oscillation. Precedes VF/asystole.

Harrison's 22E, Fig. 247-14

10. Hypokalemia - Prominent U Wave

ECG of hypokalemia showing flat T wave and prominent U wave in lead II and V3

Key changes vs normal:

Flat or inverted T waves
Prominent U wave (the rounded deflection after the T wave, labeled "U" in V3) - represents delayed Purkinje fiber repolarization
Apparent QT prolongation (actually QU prolongation)
Risk of Torsades de Pointes
Harrison's 22E - Hypokalemia panel

Summary of What to Look for

Finding	Abnormal Feature	Normal comparator
STEMI	ST elevation ≥1 mm, hyperacute T	Flat ST, smooth upright T
Wellens sign	Deep symmetric T inversions V1-V6	Upright T precordially
Inferior STEMI	ST ↑ in II, III, aVF + reciprocal ↓ in I, aVL	Isoelectric ST everywhere
RBBB	rSR' in V1 / wide S in V6	Small r, deep S in V1
LBBB	QS in V1 / monophasic R in V6	rS in V1, qR in V6
AF	No P waves, irregular QRS	Regular rhythm, clear P waves
Complete heart block	P-QRS dissociation, slow escape	1:1 PR relationship
Hyperkalemia	Peaked T → sine wave	Normal T amplitude
Hypokalemia	Flat T + prominent U wave	No U wave visible

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<!-- ══════════════ COVER PAGE ══════════════ -->
<div class="cover">
  <div class="badge">Clinical Reference</div>
  <h1>Quick-Reference<br/><span>ECG Findings</span><br/>Guide</h1>
  <div class="divider"></div>
  <p class="subtitle">10 Common Electrocardiographic Patterns — Mechanisms, Diagnostic Criteria &amp; Clinical Significance</p>
  <div class="findings-list">
    <span class="pill">ST Elevation (STEMI)</span>
    <span class="pill">Atrial Fibrillation</span>
    <span class="pill">LVH</span>
    <span class="pill">RBBB / LBBB</span>
    <span class="pill">AV Block</span>
    <span class="pill">Prolonged QT</span>
    <span class="pill">Hyperkalemia</span>
    <span class="pill">Pericarditis</span>
    <span class="pill">Sinus Arrhythmias</span>
    <span class="pill">Pathological Q Waves</span>
  </div>
  <p class="meta" style="margin-top:40px;">
    Sources: Harrison's Principles of Internal Medicine 22E &nbsp;•&nbsp;
    Tintinalli's Emergency Medicine &nbsp;•&nbsp;<br/>
    Braunwald's Heart Disease &nbsp;•&nbsp; Roberts &amp; Hedges' Clinical Procedures<br/><br/>
    <em>For educational use. Always correlate with clinical context.</em>
  </p>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 1 — ST ELEVATION / STEMI
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">1</div>
  <h2>ST-Segment Elevation (STEMI)</h2>
  <span class="tag">⚠ EMERGENCY</span>
</div>

<div class="two-col">
  <div>
    <div class="card red">
      <h3>Diagnostic Criteria</h3>
      <ul>
        <li>ST elevation <strong>≥1 mm</strong> in ≥2 contiguous leads</li>
        <li>New LBBB with ischaemic symptoms = STEMI equivalent</li>
        <li>Hyperacute (tall, broad) T waves — earliest sign</li>
        <li>Reciprocal ST <em>depression</em> in opposite leads</li>
      </ul>
    </div>
    <div class="key-finding mt8">🔴 Anterior STEMI: <span>ST ↑ in V1–V6, I, aVL → LAD occlusion</span></div>
    <div class="key-finding">🔴 Inferior STEMI: <span>ST ↑ in II, III, aVF → RCA occlusion</span></div>
    <div class="key-finding">🔴 Posterior STEMI: <span>Reciprocal ST ↓ in V1–V3 (mirror image)</span></div>

    <div class="card blue mt8">
      <h3>Mechanism</h3>
      <p>Transmural ischaemia shifts the injury current vector toward the <strong>epicardium</strong>. Overlying leads record ST elevation; opposite leads show reciprocal depression. Subendocardial ischaemia does the reverse (ST depression only).</p>
    </div>
  </div>

  <div>
    <div class="img-block">
      <img src="https://cdn.orris.care/cdss_images/90b2a4e8d8bfd20d740aafeb6a9a46d5110b4355298ab357e1f13d6592fccdef.png"
           alt="ST deviation mechanism diagram"/>
      <div class="caption">A: Subendocardial ischaemia → ST depression (V5).&nbsp; B: Transmural ischaemia → ST elevation (V5).</div>
      <div class="source">Harrison's Principles of Internal Medicine 22E, Fig. 247-11</div>
    </div>

    <div class="card amber">
      <h3>Time to Treatment</h3>
      <ul>
        <li><strong>Door-to-balloon:</strong> &lt;90 min (primary PCI)</li>
        <li><strong>Door-to-needle:</strong> &lt;30 min (thrombolysis if PCI unavailable)</li>
        <li>Repeat ECG every 5–10 min if initial is non-diagnostic</li>
      </ul>
    </div>
  </div>
</div>

<div class="two-col">
  <div class="img-block">
    <img src="https://cdn.orris.care/cdss_images/b2b5c8464b561684b3b8a2cc95393c3af1b8f9ed6381dc7b32369ffca928d62d.png"
         alt="Anterior STEMI evolving ECG"/>
    <div class="caption"><strong>Anterior STEMI sequence.</strong> Top: Acute — ST elevation I, aVL, V2–V6; hyperacute T waves; reciprocal ST ↓ in II, III, aVF.&nbsp; Bottom: Evolving — deep Q waves V2–V4, T-wave inversions.</div>
    <div class="source">Harrison's 22E, Fig. 247-13A</div>
  </div>
  <div class="img-block">
    <img src="https://cdn.orris.care/cdss_images/7efb10c6a3da958c12e7f371fd6a91e0c371475fe60d5407cab75d3f036c4b5e.png"
         alt="Inferior STEMI evolving ECG"/>
    <div class="caption"><strong>Inferior STEMI sequence.</strong> Top: Acute — ST elevation in II, III, aVF; reciprocal ST ↓ in I, aVL, V1–V4.&nbsp; Bottom: Evolving — Q waves II, III, aVF; T-wave inversions.</div>
    <div class="source">Harrison's 22E, Fig. 247-13B</div>
  </div>
</div>

<div class="img-block">
  <img src="https://cdn.orris.care/cdss_images/adead81bbf6a6b405ebe5fcb2d8a38aaf43371d3988355961a3824c62a1d50b9.png"
       alt="Real 12-lead inferior STEMI ECG"/>
  <div class="caption"><strong>Real 12-lead ECG — Acute Inferior STEMI.</strong> Marked ST elevation in II, III, aVF with deep reciprocal ST depression in I, aVL, V1–V2. Right ventricular leads would show ST elevation in V3R–V4R confirming RV involvement.</div>
  <div class="source">Textbook of Family Medicine 9E, Fig. 27-12</div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 2 — Wellens Sign (bonus, grouped with STEMI)
══════════════════════════════════════════════ -->
<div class="card purple mt12" style="page-break-inside:avoid;">
  <h3>⚠ Wellens T-Wave Sign — Critical LAD Stenosis</h3>
  <div class="two-col" style="margin-bottom:0;">
    <div>
      <p>Deep, symmetric T-wave inversions in V1–V4 (sometimes V6) <em>without</em> ST elevation and <em>without</em> Q waves. Seen in pain-free window after LAD ischaemia.</p>
      <ul class="mt8">
        <li><strong>Type A:</strong> Biphasic T waves (V2–V3) — earlier pattern</li>
        <li><strong>Type B:</strong> Deep symmetric T inversions — more common</li>
        <li>Indicates <strong>≥70% LAD stenosis</strong> — impending anterior STEMI</li>
        <li><strong>Do NOT stress-test</strong> these patients</li>
      </ul>
    </div>
    <div class="img-block" style="margin:0;">
      <img src="https://cdn.orris.care/cdss_images/f3e984a53a0a64a9ac96e6035acfa4f3e60f0b0b4f43f8a50327252b01f9f891.png"
           alt="Wellens T-wave sign V1-V6"/>
      <div class="caption">Deep symmetric T inversions V1–V6. No Q waves. No ST elevation.</div>
      <div class="source">Harrison's 22E, Fig. 247-12</div>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 3 — ATRIAL FIBRILLATION
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">2</div>
  <h2>Atrial Fibrillation (AF)</h2>
  <span class="tag">Common Arrhythmia</span>
</div>

<div class="two-col">
  <div>
    <div class="card red">
      <h3>ECG Criteria (all 3 required)</h3>
      <ul>
        <li><strong>No distinct P waves</strong> — flat or chaotic fibrillatory baseline (f-waves 350–600/min)</li>
        <li><strong>Irregularly irregular</strong> QRS rhythm (varying R-R intervals)</li>
        <li><strong>Narrow QRS</strong> — unless pre-existing BBB or pre-excitation (WPW)</li>
      </ul>
    </div>

    <div class="mech-box mt8">
      <strong>Mechanism:</strong> Multiple chaotic re-entrant wavelets in both atria fire at 350–600/min. The AV node cannot conduct all impulses — it filters them, producing a randomly irregular ventricular response.
    </div>

    <div class="card amber mt8">
      <h3>Clinical Consequences</h3>
      <ul>
        <li>Loss of atrial "kick" → ↓CO by ~20% (more in stiff LV)</li>
        <li>Rapid ventricular rate → angina, HF</li>
        <li><strong>Thromboembolism risk</strong> — use CHA₂DS₂-VASc score</li>
        <li>Conversion risk if &gt;48 h — anticoagulate ≥3 weeks first</li>
      </ul>
    </div>
  </div>

  <div>
    <div class="img-block">
      <img src="https://cdn.orris.care/cdss_images/fe540927466023e89897808fc74499319d5538d36547710049c60da77a0ffea7.png"
           alt="Atrial fibrillation ECG tracing"/>
      <div class="caption"><strong>Atrial Fibrillation.</strong> Note: no discernible P waves, chaotic baseline, and irregularly irregular QRS complexes with varying R-R intervals.</div>
      <div class="source">Pye's Surgical-Handicraft, Fig. 17.35</div>
    </div>

    <table class="mt8">
      <thead>
        <tr><th>Type</th><th>Duration</th><th>Key Point</th></tr>
      </thead>
      <tbody>
        <tr><td>Paroxysmal</td><td>&lt;7 days</td><td>Terminates spontaneously</td></tr>
        <tr><td>Persistent</td><td>&gt;7 days</td><td>Requires cardioversion</td></tr>
        <tr><td>Long-standing</td><td>&gt;1 year</td><td>Structural remodelling</td></tr>
        <tr><td>Permanent</td><td>Ongoing</td><td>Rhythm control abandoned</td></tr>
      </tbody>
    </table>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 4 — BUNDLE BRANCH BLOCKS
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">3</div>
  <h2>Bundle Branch Blocks</h2>
  <span class="tag">Conduction Defect</span>
</div>

<div class="img-block full-col">
  <img src="https://cdn.orris.care/cdss_images/ad352bb18c8368864e520ff78d27c0ceb0cb0271df10661e01be29f6d32f38b3.png"
       alt="RBBB and LBBB compared to normal in V1 and V6" style="max-height:250px;"/>
  <div class="caption"><strong>Comparison of Normal, RBBB, and LBBB in leads V1 and V6.</strong> Normal (top) → rS in V1, qR in V6. RBBB (middle) → rSR' in V1, slurred S in V6. LBBB (bottom) → QS in V1, broad monophasic R in V6.</div>
  <div class="source">Harrison's Principles of Internal Medicine 22E, Fig. 247-10</div>
</div>

<div class="two-col">
  <div class="card red">
    <h3>Right Bundle Branch Block (RBBB)</h3>
    <ul>
      <li><strong>QRS ≥120 ms</strong></li>
      <li>V1: <strong>rSR'</strong> ("rabbit ears" / M-shaped)</li>
      <li>V6 + Lead I: wide, slurred <strong>S wave</strong></li>
      <li>Secondary T-wave inversions in V1–V3</li>
    </ul>
    <div class="mech-box mt8">
      RV depolarisation delayed → terminal QRS vector rightward + anterior
    </div>
    <p class="mt8 small"><strong>Causes:</strong> Benign (normal variant), PE, ASD, RV strain, ischaemia</p>
  </div>

  <div class="card blue">
    <h3>Left Bundle Branch Block (LBBB)</h3>
    <ul>
      <li><strong>QRS ≥120 ms</strong></li>
      <li>V1: wide, entirely negative (<strong>QS complex</strong>)</li>
      <li>V6: broad, tall, entirely positive (<strong>R wave</strong>)</li>
      <li>No septal Q wave in V6 (reversed septal activation)</li>
      <li>Secondary T-wave inversion where R is dominant</li>
    </ul>
    <div class="mech-box mt8">
      LV depolarisation delayed; septal activation reversed (R→L instead of L→R)
    </div>
    <p class="mt8 small"><strong>Causes (almost always pathological):</strong> CAD, hypertension, dilated CMP, valvular disease.&nbsp; New LBBB + chest pain → treat as STEMI equivalent (Sgarbossa criteria)</p>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 5 — LVH
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">4</div>
  <h2>Left Ventricular Hypertrophy (LVH)</h2>
  <span class="tag">Structural Change</span>
</div>

<div class="two-col">
  <div class="card red">
    <h3>Voltage Criteria (any one = LVH)</h3>
    <table>
      <thead><tr><th>Criterion</th><th>Threshold</th></tr></thead>
      <tbody>
        <tr><td><strong>Sokolow-Lyon</strong></td><td>SV1 + RV5 or RV6 ≥ 35 mm</td></tr>
        <tr><td><strong>Cornell (men)</strong></td><td>R aVL &gt; 28 mm</td></tr>
        <tr><td><strong>Cornell (women)</strong></td><td>R aVL &gt; 20 mm</td></tr>
        <tr><td><strong>R aVL alone</strong></td><td>≥ 11 mm (simple screen)</td></tr>
      </tbody>
    </table>
  </div>
  <div>
    <div class="card blue">
      <h3>Associated Features</h3>
      <ul>
        <li><strong>"Strain" pattern:</strong> ST depression + T-wave inversion in lateral leads (I, aVL, V5–V6) where R is tall</li>
        <li><strong>Left atrial abnormality:</strong> broad notched P in II; deep negative terminal P in V1 — increases specificity</li>
        <li>May progress to LBBB</li>
      </ul>
    </div>
    <div class="card amber mt8">
      <h3>Pitfalls</h3>
      <ul>
        <li>High voltage is a <strong>normal variant</strong> in young/athletic individuals</li>
        <li>Sensitivity low in obese, COPD, older adults</li>
        <li>Echo/MRI provides definitive anatomic assessment</li>
        <li>LVH on ECG = independent cardiovascular risk marker</li>
      </ul>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 6 — AV BLOCK
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">5</div>
  <h2>Atrioventricular (AV) Block</h2>
  <span class="tag">Conduction Defect</span>
</div>

<div class="img-block">
  <img src="https://cdn.orris.care/cdss_images/1b7cd0186cf60b18a2a29dd04908ddeac5265c3fadc40a2a02cf2f87bf522be7.png"
       alt="Complete heart block ECG tracing"/>
  <div class="caption"><strong>Complete (3rd-degree) Heart Block.</strong> Small independent P waves fire at ~75/min (atrial rate). Wide, slow QRS complexes represent ventricular escape rhythm at ~35/min. No relationship between P and QRS.</div>
  <div class="source">Pye's Surgical-Handicraft, Fig. 17.34</div>
</div>

<table>
  <thead>
    <tr>
      <th>Type</th><th>PR Interval</th><th>QRS Dropped?</th><th>Site of Block</th><th>Urgency</th>
    </tr>
  </thead>
  <tbody>
    <tr>
      <td><strong>1st Degree</strong></td>
      <td>&gt;200 ms (constant)</td>
      <td>Never</td>
      <td>AV node</td>
      <td><span class="badge-g">Benign</span></td>
    </tr>
    <tr>
      <td><strong>2nd Degree Mobitz I</strong> (Wenckebach)</td>
      <td>Progressive lengthening until dropped beat</td>
      <td>Yes, periodically</td>
      <td>AV node</td>
      <td><span class="badge-o">Monitor</span></td>
    </tr>
    <tr>
      <td><strong>2nd Degree Mobitz II</strong></td>
      <td>Fixed, sudden dropped QRS</td>
      <td>Yes, unpredictably</td>
      <td>Bundle of His / below</td>
      <td><span class="badge-r">Pace risk</span></td>
    </tr>
    <tr>
      <td><strong>3rd Degree (Complete)</strong></td>
      <td>No relationship (AV dissociation)</td>
      <td>Total dissociation</td>
      <td>Any level</td>
      <td><span class="badge-r">Urgent pacing</span></td>
    </tr>
  </tbody>
</table>

<div class="card amber mt8">
  <h3>Common Causes of AV Block</h3>
  <p>Inferior MI (RCA supplies AV node) • Digoxin toxicity • Beta-blockers / CCBs • Lyme disease • Sarcoidosis • Congenital • Post-cardiac surgery • Age-related fibrosis (Lenègre disease)</p>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 7 — PROLONGED QT
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">6</div>
  <h2>Prolonged QT Interval</h2>
  <span class="tag">Arrhythmia Risk</span>
</div>

<div class="two-col">
  <div class="card red">
    <h3>Diagnostic Criteria</h3>
    <ul>
      <li>QTc (Bazett) = QT ÷ √RR interval</li>
      <li><strong>Men: QTc ≥ 440 ms</strong></li>
      <li><strong>Women: QTc ≥ 460 ms</strong></li>
      <li>Symptomatic LQTS diagnosis: QTc ≥ 480 ms</li>
    </ul>
    <div class="key-finding mt8">Risk of Torsades de Pointes → polymorphic VT → VF</div>

    <div class="card green mt8">
      <h3>Congenital LQTS Subtypes</h3>
      <table>
        <thead><tr><th>Subtype</th><th>Gene</th><th>Trigger</th></tr></thead>
        <tbody>
          <tr><td>LQTS1</td><td>KCNQ1 (IKs ↓)</td><td>Exercise / swimming</td></tr>
          <tr><td>LQTS2</td><td>KCNH2 (IKr ↓)</td><td>Sudden noise, emotion</td></tr>
          <tr><td>LQTS3</td><td>SCN5A (INa ↑)</td><td>Sleep / bradycardia</td></tr>
        </tbody>
      </table>
    </div>
  </div>

  <div class="card blue">
    <h3>Acquired Causes (DRUGS most common)</h3>
    <table>
      <thead><tr><th>Category</th><th>Examples</th></tr></thead>
      <tbody>
        <tr><td>Antiarrhythmics</td><td>Sotalol, amiodarone, quinidine</td></tr>
        <tr><td>Antibiotics</td><td>Azithromycin, fluoroquinolones</td></tr>
        <tr><td>Antipsychotics</td><td>Haloperidol, quetiapine</td></tr>
        <tr><td>Antifungals</td><td>Fluconazole</td></tr>
        <tr><td>Electrolytes</td><td>Hypokalaemia, hypomagnesaemia, hypocalcaemia</td></tr>
        <tr><td>Other</td><td>Hypothyroidism, hypothermia, myocarditis</td></tr>
      </tbody>
    </table>

    <div class="mech-box mt8">
      <strong>Mechanism:</strong> Reduced outward K⁺ current or increased inward Na⁺/Ca²⁺ current → delayed ventricular repolarisation → dispersion of refractoriness → susceptibility to early afterdepolarisations (EADs) → Torsades.
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 8 — HYPERKALEMIA
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">7</div>
  <h2>Hyperkalemia — ECG Changes</h2>
  <span class="tag">⚠ LIFE-THREATENING</span>
</div>

<div class="img-block">
  <img src="https://cdn.orris.care/cdss_images/35643c9e9ee1c957d7778234b0449dd100bef8f320fa17fe7fdb50e2cc3d6f38.png"
       alt="Sequential ECG changes in hyperkalemia" style="max-height:220px;"/>
  <div class="caption"><strong>Hyperkalemia — Progressive ECG Changes.</strong> Left: Mild-moderate — narrow, tall peaked ("tented") T waves in V1–V2. Middle: Moderate-severe — QRS widening, P-wave flattening, tall peaked T persists. Right: Very severe — sine-wave pattern; imminent VF / asystole.</div>
  <div class="source">Harrison's Principles of Internal Medicine 22E, Fig. 247-14</div>
</div>

<table>
  <thead>
    <tr><th>K⁺ Level</th><th>ECG Change</th><th>Action</th></tr>
  </thead>
  <tbody>
    <tr><td>5.5–6.5 mEq/L</td><td>Tall, narrow, peaked ("tented") T waves — <em>earliest change</em></td><td><span class="badge-o">Monitor</span></td></tr>
    <tr><td>6.5–7.5 mEq/L</td><td>PR prolongation, QRS widening, P-wave flattening</td><td><span class="badge-o">Treat urgently</span></td></tr>
    <tr><td>&gt;7.5 mEq/L</td><td>P waves disappear; sine-wave QRS-T fusion</td><td><span class="badge-r">Emergency</span></td></tr>
    <tr><td>&gt;8–9 mEq/L</td><td>VF or asystole</td><td><span class="badge-r">Resuscitation</span></td></tr>
  </tbody>
</table>

<div class="card red mt8">
  <h3>Emergency Management</h3>
  <p><strong>1. Membrane stabilisation:</strong> IV Calcium gluconate 10 ml 10% (immediate, 30-min effect) &nbsp;|&nbsp; <strong>2. Shift K⁺ intracellularly:</strong> Insulin 10 U + Glucose 50% 50 ml IV; Nebulised salbutamol 10–20 mg; IV Sodium bicarbonate (if acidotic) &nbsp;|&nbsp; <strong>3. Eliminate K⁺:</strong> Furosemide (if urine output adequate); Calcium resonium; Dialysis (definitive in renal failure)</p>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 9 — HYPOKALEMIA
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">8</div>
  <h2>Hypokalemia — U Waves &amp; QT Prolongation</h2>
  <span class="tag">Electrolyte</span>
</div>

<div class="two-col">
  <div class="img-block">
    <img src="https://cdn.orris.care/cdss_images/ec713da1bee437018189466a17d21250e796dea97ac8a54750c9cd42ebde487f.png"
         alt="Hypokalemia ECG showing U waves in lead II and V3"/>
    <div class="caption"><strong>Hypokalemia.</strong> Lead II: flat T wave, low amplitude. Lead V3: Prominent U wave (labeled "U") after the T wave — represents delayed Purkinje repolarisation. The apparent long QT is actually QU prolongation.</div>
    <div class="source">Harrison's 22E — Hypokalemia panel</div>
  </div>

  <div>
    <div class="card red">
      <h3>Key ECG Features</h3>
      <ul>
        <li><strong>Flat or inverted T waves</strong></li>
        <li><strong>Prominent U wave</strong> — most visible in V2–V4 (rounded deflection <em>after</em> T wave, same polarity)</li>
        <li>Apparent QT prolongation (actually QU interval)</li>
        <li>ST depression</li>
        <li>Risk of <strong>Torsades de Pointes</strong></li>
      </ul>
    </div>
    <div class="mech-box mt8">
      <strong>U wave origin:</strong> Delayed repolarisation of Purkinje fibres and mid-myocardial (M) cells when extracellular K⁺ is low → prolonged phase 3 of action potential
    </div>
    <div class="card amber mt8">
      <h3>Causes</h3>
      <p>Diuretics (most common) • Vomiting / diarrhoea • Hyperaldosteronism • Renal tubular acidosis • Magnesium depletion (co-correct) • Insulin / catecholamines</p>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 10 — PERICARDITIS
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">9</div>
  <h2>Acute Pericarditis &amp; Pericardial Effusion</h2>
  <span class="tag">Inflammatory</span>
</div>

<div class="two-col">
  <div class="card red">
    <h3>4 Evolutionary ECG Stages</h3>
    <table>
      <thead><tr><th>Stage</th><th>Timeframe</th><th>ECG Change</th></tr></thead>
      <tbody>
        <tr><td><strong>1</strong></td><td>Hours–days</td><td>Diffuse <em>concave-up</em> ("saddle") ST elevation + PR depression (most leads except aVR/V1 which show opposite)</td></tr>
        <tr><td><strong>2</strong></td><td>Days 1–3</td><td>ST &amp; PR normalise</td></tr>
        <tr><td><strong>3</strong></td><td>Days 3–14</td><td>Diffuse T-wave inversions</td></tr>
        <tr><td><strong>4</strong></td><td>Weeks</td><td>T waves normalise</td></tr>
      </tbody>
    </table>
    <div class="key-finding mt8">Key distinguisher from STEMI: <span>Concave (smiley-face) ST elevation is diffuse across multiple territories; STEMI is focal + reciprocal changes</span></div>
  </div>
  <div>
    <div class="card blue">
      <h3>Pericardial Effusion / Tamponade ECG Signs</h3>
      <ul>
        <li><strong>Sinus tachycardia</strong> — usually first finding</li>
        <li><strong>Low QRS voltage</strong> — ≤5 mm in all limb leads <em>or</em> ≤10 mm in all precordial leads</li>
        <li><strong>PR depression</strong> — ≥1 mm in ≥1 lead (not aVR)</li>
        <li><strong>Electrical alternans</strong> — beat-to-beat alternation in QRS amplitude (heart "swinging" in fluid). Total P+QRS+T alternans with tachycardia = relatively specific for <strong>cardiac tamponade</strong></li>
      </ul>
    </div>
    <div class="card amber mt8">
      <h3>Important Caveat</h3>
      <p>ECG sensitivity for pericardial effusion is only <strong>1–17%</strong>. A normal ECG does <strong>not</strong> exclude tamponade. <strong>Bedside echo is mandatory</strong> for confirmation (look for RA/RV collapse in diastole).</p>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     FINDING 11 — PATHOLOGICAL Q WAVES
══════════════════════════════════════════════ -->
<div class="section-header">
  <div class="num">10</div>
  <h2>Pathological Q Waves (Old/Evolving Infarction)</h2>
  <span class="tag">Infarction Marker</span>
</div>

<div class="two-col">
  <div class="card red">
    <h3>Diagnostic Criteria</h3>
    <ul>
      <li>Width <strong>≥40 ms</strong> (≥1 small square at 25 mm/s) <strong>OR</strong></li>
      <li>Depth <strong>≥25%</strong> of the R-wave amplitude in the same lead</li>
      <li>Present in ≥2 contiguous leads in the same territory</li>
    </ul>
    <div class="mech-box mt8">
      <strong>Mechanism:</strong> Infarcted myocardium is electrically silent. The "window" created faces the ventricular cavity. Leads overlying the infarct record the opposing cavity's negative vector → deep Q wave.
    </div>
  </div>
  <div>
    <div class="card blue">
      <h3>Localisation by Lead Group</h3>
      <table>
        <thead><tr><th>Leads with Q waves</th><th>Territory</th><th>Artery</th></tr></thead>
        <tbody>
          <tr><td>V1–V4</td><td>Anterior</td><td>LAD</td></tr>
          <tr><td>II, III, aVF</td><td>Inferior</td><td>RCA (85%)</td></tr>
          <tr><td>I, aVL, V5–V6</td><td>Lateral</td><td>LCx</td></tr>
          <tr><td>V1–V2 (tall R)</td><td>Posterior</td><td>RCA/LCx</td></tr>
        </tbody>
      </table>
    </div>
    <div class="card green mt8">
      <h3>Normal Q Waves (do NOT over-diagnose)</h3>
      <ul>
        <li>Small septal Q waves (&lt;40 ms, &lt;2 mm) in I, V5, V6 — normal septal activation</li>
        <li>Q in aVR — always normal</li>
        <li>Q in III alone (without II + aVF) — often positional</li>
        <li>Q in V1 — normal variant</li>
      </ul>
    </div>
  </div>
</div>

<!-- ══════════════════════════════════════════════
     QUICK-REFERENCE SUMMARY TABLE (final page)
══════════════════════════════════════════════ -->
<div class="summary-page">
  <div class="summary-header">⚡ QUICK-REFERENCE SUMMARY — 10 Common ECG Findings</div>
  <div class="summary-table">
    <table>
      <thead>
        <tr>
          <th>#</th>
          <th>Finding</th>
          <th>Key ECG Feature</th>
          <th>Normal Comparator</th>
          <th>Primary Concern</th>
          <th>Urgency</th>
        </tr>
      </thead>
      <tbody>
        <tr>
          <td>1</td>
          <td><strong>ST Elevation (STEMI)</strong></td>
          <td>≥1 mm ST ↑ in ≥2 contiguous leads; hyperacute T</td>
          <td>Isoelectric ST segment</td>
          <td>Total coronary occlusion</td>
          <td><span class="badge-r">Emergency</span></td>
        </tr>
        <tr>
          <td>2</td>
          <td><strong>Wellens Sign</strong></td>
          <td>Deep symmetric T inversions V1–V4, no Q, no ST ↑</td>
          <td>Upright T waves precordially</td>
          <td>Critical LAD stenosis; impending STEMI</td>
          <td><span class="badge-r">Urgent</span></td>
        </tr>
        <tr>
          <td>3</td>
          <td><strong>Atrial Fibrillation</strong></td>
          <td>No P waves; irregularly irregular narrow QRS</td>
          <td>Regular rhythm; clear P waves</td>
          <td>Stroke risk; rate/rhythm control</td>
          <td><span class="badge-o">Manage</span></td>
        </tr>
        <tr>
          <td>4</td>
          <td><strong>RBBB</strong></td>
          <td>rSR' in V1; wide slurred S in V6; QRS ≥120 ms</td>
          <td>rS in V1; narrow QRS</td>
          <td>Can be benign; check for PE/ASD</td>
          <td><span class="badge-g">Context</span></td>
        </tr>
        <tr>
          <td>5</td>
          <td><strong>LBBB</strong></td>
          <td>QS in V1; monophasic R in V6; QRS ≥120 ms</td>
          <td>rS in V1; narrow QRS</td>
          <td>Usually pathological; new LBBB = STEMI equivalent</td>
          <td><span class="badge-r">Urgent</span></td>
        </tr>
        <tr>
          <td>6</td>
          <td><strong>LVH</strong></td>
          <td>SV1 + RV5/V6 ≥35 mm; lateral ST depression/T inversions</td>
          <td>Normal QRS amplitude</td>
          <td>Hypertension; HCM; increased CV risk</td>
          <td><span class="badge-o">Investigate</span></td>
        </tr>
        <tr>
          <td>7</td>
          <td><strong>Complete Heart Block</strong></td>
          <td>P-QRS dissociation; slow escape rhythm</td>
          <td>1:1 PR relationship; regular rhythm</td>
          <td>Haemodynamic compromise; syncope</td>
          <td><span class="badge-r">Urgent pacing</span></td>
        </tr>
        <tr>
          <td>8</td>
          <td><strong>Prolonged QT</strong></td>
          <td>QTc ≥440 ms (M) / ≥460 ms (F)</td>
          <td>QTc &lt;440 ms (M) &lt;460 ms (F)</td>
          <td>Torsades de Pointes; VF</td>
          <td><span class="badge-r">Urgent</span></td>
        </tr>
        <tr>
          <td>9</td>
          <td><strong>Hyperkalemia</strong></td>
          <td>Peaked T → QRS widening → sine wave</td>
          <td>Normal T amplitude; narrow QRS</td>
          <td>VF / asystole</td>
          <td><span class="badge-r">Emergency</span></td>
        </tr>
        <tr>
          <td>10</td>
          <td><strong>Hypokalemia</strong></td>
          <td>Flat T; prominent U wave; apparent long QT</td>
          <td>No U wave; normal T amplitude</td>
          <td>Torsades de Pointes</td>
          <td><span class="badge-o">Correct</span></td>
        </tr>
        <tr>
          <td>11</td>
          <td><strong>Pericarditis</strong></td>
          <td>Diffuse concave ST ↑ + PR depression (Stage 1)</td>
          <td>Isoelectric ST/PR</td>
          <td>Tamponade if effusion (look for electrical alternans)</td>
          <td><span class="badge-o">Monitor</span></td>
        </tr>
        <tr>
          <td>12</td>
          <td><strong>Pathological Q Waves</strong></td>
          <td>Q ≥40 ms wide or ≥25% R amplitude in ≥2 contiguous leads</td>
          <td>No Q or small septal Q &lt;40 ms</td>
          <td>Old or evolving myocardial infarction</td>
          <td><span class="badge-o">Investigate</span></td>
        </tr>
      </tbody>
    </table>
  </div>

  <div class="card amber" style="margin-top:16px; page-break-inside:avoid;">
    <h3>ECG Interpretation Checklist (Systematic Approach)</h3>
    <div class="three-col" style="margin:8px 0 0 0;">
      <div>
        <p class="bold">1. Rate</p>
        <p class="small">300 ÷ large squares between R-R. Normal 60–100 bpm.</p>
        <p class="bold mt8">2. Rhythm</p>
        <p class="small">Regular? P before every QRS? QRS after every P?</p>
        <p class="bold mt8">3. Axis</p>
        <p class="small">Normal –30° to +90°. LAD if negative in aVF. RAD if positive in aVF + negative in I.</p>
      </div>
      <div>
        <p class="bold">4. P Wave</p>
        <p class="small">Upright in II, inverted in aVR. Duration &lt;120 ms. Amplitude &lt;2.5 mm.</p>
        <p class="bold mt8">5. PR Interval</p>
        <p class="small">Normal 120–200 ms. Short → WPW/junctional. Long → AV block.</p>
        <p class="bold mt8">6. QRS Complex</p>
        <p class="small">Duration &lt;120 ms. Check for Q waves, R progression (V1→V6), voltage.</p>
      </div>
      <div>
        <p class="bold">7. ST Segment</p>
        <p class="small">Isoelectric at J-point. Elevation or depression ≥1 mm = abnormal until proved otherwise.</p>
        <p class="bold mt8">8. T Wave</p>
        <p class="small">Upright in I, II, V4–V6. Inversion = ischaemia, strain, BBB, PE.</p>
        <p class="bold mt8">9. QT Interval</p>
        <p class="small">Correct for rate (Bazett). QTc ≥500 ms = very high TdP risk.</p>
      </div>
    </div>
  </div>

  <p style="text-align:center; margin-top:14px; font-size:7pt; color:#8892b0;">
    Sources: Harrison's Principles of Internal Medicine 22E (2025) &nbsp;•&nbsp; Tintinalli's Emergency Medicine &nbsp;•&nbsp; Braunwald's Heart Disease &nbsp;•&nbsp; Roberts &amp; Hedges' Clinical Procedures in Emergency Medicine &nbsp;•&nbsp; Textbook of Family Medicine 9E &nbsp;•&nbsp; Pye's Surgical-Handicraft<br/>
    <em>This guide is for educational purposes only. Clinical decisions should always incorporate full patient context, serial ECGs, and senior clinical review.</em>
  </p>
</div>

</body>
</html>

Running Command

cd /home/daytona/workspace/ecg-guide && python3 -c "import weasyprint; print(weasyprint.__version__)"

Running Command

which wkhtmltopdf && wkhtmltopdf --version 2>/dev/null; which chromium-browser 2>/dev/null; which google-chrome 2>/dev/null; which chromium 2>/dev/null; python3 -c "import pdfkit; print('pdfkit ok')" 2>/dev/null; python3 -c "from reportlab.lib import pagesizes; print('reportlab ok')" 2>/dev/null; python3 -c "import playwright; print('playwright ok')" 2>/dev/null

Running Command

chromium --headless --no-sandbox --disable-gpu --print-to-pdf=/home/daytona/workspace/ecg-guide/ECG_Quick_Reference_Guide.pdf --print-to-pdf-no-header "file:///home/daytona/workspace/ecg-guide/ecg_guide.html" 2>&1 | tail -5

Running Command

ls -lh /home/daytona/workspace/ecg-guide/ECG_Quick_Reference_Guide.pdf

Your guide is ready - 2.5 MB, fully formatted with all images and annotations:

ECG Quick Reference Guide
PDF Document · PDF

What's inside the guide:

Section	Content
Cover page	Styled title page listing all 10 findings
Findings 1–10	Each on its own section with colour-coded cards
Textbook ECG images	Anterior STEMI, Inferior STEMI, Wellens sign, RBBB/LBBB comparison, AF, Complete heart block, Hyperkalemia progression, Hypokalemia U waves, ST deviation mechanism diagram
Mechanism boxes	Brief pathophysiology for each finding
Urgency badges	Emergency / Urgent / Monitor / Benign colour coding
Quick-reference summary table	All 12 findings in one table with key ECG features, normal comparators, and urgency
ECG interpretation checklist	9-step systematic approach (Rate → Rhythm → Axis → P → PR → QRS → ST → T → QT)

Sources cited throughout: Harrison's 22E, Tintinalli's Emergency Medicine, Braunwald's Heart Disease, Roberts & Hedges, Textbook of Family Medicine 9E.

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