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1. Ventricular Fibrillation (VF)

ECG Features

• Completely chaotic, irregular baseline — no identifiable P waves, QRS, or T waves
• Rapid, disorganized fibrillatory waves of varying amplitude and frequency across all leads
• Coarser fibrillatory waves in precordial leads (V2–V5); finer waves in limb leads
• Fine VF (low amplitude) = prolonged ischemia, worse prognosis for shock success

Management (ACLS)

Reversible causes (4H4T): Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia — Tension pneumothorax, Tamponade, Toxins, Thrombosis (PE/MI)

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2. Ventricular Tachycardia (VT) — Monomorphic

ECG Features

• Wide QRS tachycardia (>120 ms) at rate ≥100 bpm (often 150–200)
• No P waves before QRS (or AV dissociation — P waves "march through" independently)
• Positive or negative concordance across precordial leads
• Capture beats (narrow QRS amid wide complexes) and fusion beats = pathognomonic for VT
• Superior axis (negative in II, III, aVF) suggests VT rather than SVT

Management

• Hemodynamically unstable: Immediate synchronized cardioversion 100–200J biphasic
• Hemodynamically stable:
  • Amiodarone 150 mg IV over 10 min (infusion 1 mg/min × 6 h, then 0.5 mg/min)
  • Lidocaine 1–1.5 mg/kg IV bolus as alternative
  • Correct electrolytes (K⁺ >4.0, Mg²⁺ >2.0 mEq/L)
• Treat underlying cause (ischemia, cardiomyopathy)
• Consider ICD for survivors or recurrent VT

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3. Torsades de Pointes (TdP)

ECG Features

• Polymorphic VT — QRS complexes "twist" around the isoelectric baseline (spindle-shaped)
• QRS amplitude waxes and wanes in a sinusoidal pattern
• Precipitated by long QT (QTc >500 ms is high risk) and triggered by a "short-long-short" RR sequence (pause-dependent)
• No organized P waves; rate 150–300 bpm

Management

Common ICU culprit drugs: Haloperidol, Methadone, Azithromycin, Fluconazole, Sotalol, Amiodarone (less so)

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4. ST-Elevation MI (STEMI)

ECG Features

• ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V1–V3)
• Convex "tombstoning" ST morphology = extensive injury
• Hyperacute T-waves (tall, peaked) — earliest sign
• Reciprocal ST depression in opposing leads (e.g., inferior MI → depression in I, aVL)
• Q waves develop within hours → necrosis

Management

• Door-to-balloon time <90 min — primary PCI is standard of care
• If PCI not available within 120 min → fibrinolysis (tPA/tenecteplase) within 30 min of arrival
• Antiplatelet: Aspirin 325 mg + P2Y12 inhibitor (Ticagrelor 180 mg or Clopidogrel 600 mg)
• Anticoagulation: Heparin UFH or Enoxaparin
• Beta-blocker (if no contraindication), ACE inhibitor, Statin (high-intensity)
• Monitor for complications: Cardiogenic shock, free wall rupture, acute MR, VF/VT

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5. Atrial Fibrillation (AF) with Rapid Ventricular Response

ECG Features

• Irregularly irregular rhythm — no two R-R intervals the same
• Absent P waves — replaced by fine fibrillatory baseline (best seen in V1)
• Narrow QRS (unless aberrant conduction or WPW)
• Rapid ventricular response >100–110 bpm in the ICU setting

Management

• Beta-blockers (Metoprolol 5 mg IV q5 min × 3) — first line if no bronchospasm
• Diltiazem 20 mg IV (0.25 mg/kg) — if beta-blocker contraindicated
• Amiodarone 150–300 mg IV — preferred in hemodynamic compromise/HF

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6. Complete (Third-Degree) AV Block

ECG Features

• Complete AV dissociation — P waves and QRS complexes march at completely independent rates
• Atrial rate faster than ventricular rate (P waves appear before, within, and after QRS)
• Escape rhythm:
  • Junctional escape: narrow QRS (40–60 bpm) — block at/above His bundle
  • Ventricular escape: wide QRS (20–40 bpm) — block below His bundle (worse prognosis)
• No fixed PR interval; P waves "march through" independent of QRS

Management

• Immediate transcutaneous pacing if hemodynamically unstable (bridge)
• IV Atropine 0.5–1 mg (only if junctional/nodal escape rhythm; ineffective for infra-Hisian block)
• Isoproterenol or Dopamine infusion to increase ventricular rate temporarily
• Transvenous temporary pacing — definitive bridge in ICU
• Permanent pacemaker — indications: acquired complete heart block (unless reversible cause)
• Identify/reverse causes: inferior STEMI (RCA), Lyme disease, AV nodal drugs (digoxin, beta-blockers, amiodarone), surgical/procedural trauma

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7. Hyperkalemia

ECG Features (Progressive with Rising K⁺)

Management

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8. Pulmonary Embolism (PE)

ECG Features

• Most common finding: Sinus tachycardia (not specific, but most frequent)
• Classic S1Q3T3: Prominent S wave in lead I, Q wave in lead III, T-wave inversion in lead III
• T-wave inversions in V1–V4 — right ventricular strain pattern (most specific)
• Incomplete or complete RBBB — acute cor pulmonale
• P pulmonale (tall P in II >2.5 mm) — right atrial strain
• Right axis deviation and new AF in massive PE
• ECG is non-specific and insensitive — normal ECG does not exclude PE

Management by Severity

• UFH (bolus 80 U/kg IV + infusion) — preferred for massive/unstable (titratable, reversible)
• Rivaroxaban or Apixaban — DOACs for stable patients after initial period

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9. Acute Pericarditis / Cardiac Tamponade

ECG Features — Pericarditis

• Diffuse concave ("saddle-shaped") ST elevation in almost all leads (except aVR, V1)
• PR depression in II, V4–V6 (PR elevation in aVR) — highly specific
• Spodick's sign — downsloping TP segment
• No reciprocal ST depression (unlike STEMI) — key differentiating feature
• Evolves through 4 stages: ST elevation → ST normalization → T inversion → T normalization

ECG Features — Cardiac Tamponade

• Sinus tachycardia — compensatory
• Low voltage (QRS <5 mm all limb leads, <10 mm precordial)
• Electrical alternans — alternating QRS axis/amplitude (pathognomonic for large pericardial effusion with tamponade)

Management

• NSAIDs (Ibuprofen 600–800 mg TID × 2 weeks) + Colchicine 0.5 mg BID × 3 months (reduces recurrence by 50%)
• Avoid anticoagulation if possible
• Restrict activity until symptom-free + CRP normalized

• Emergency pericardiocentesis — definitive treatment (echo-guided preferred)
• IV fluids as temporizing measure (maintain preload)
• Avoid diuretics, vasodilators, PEEP ventilation (all reduce preload → cardiovascular collapse)

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Quick Reference Summary

• VF → unsynchronized shock; VT (unstable) → synchronized cardioversion; TdP → MgSO₄ first

• Hyperkalemia has a predictable ECG progression — calcium gluconate stabilizes the membrane before shifting K⁺
• Tamponade produces electrical alternans — the alternating QRS is almost pathognomonic

• STEMI vs. Pericarditis: reciprocal changes favor STEMI; PR depression + saddle morphology favor pericarditis
• VT vs. SVT with aberrancy: AV dissociation, capture/fusion beats, and concordance all point to VT

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More Critical ICU ECG Cases — Part 2

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10. Inferior STEMI + Right Ventricular (RV) Infarction

ECG Features

• ST elevation in II, III, aVF — inferior territory
• ST III > ST II = strongly suggests RCA (right coronary artery) occlusion over LCx
• Reciprocal ST depression in I and aVL — essential to recognize
• ST elevation in V1 and aVR — flags proximal RCA occlusion with RV involvement
• Confirm RV infarct: Apply right-sided leads → ST elevation ≥1 mm in V3R–V4R is diagnostic
• AV block is a frequent complication (AV node is supplied by RCA in 85% of people)

Why RV Infarction Changes Management Critically

Classic triad of RV infarction: Hypotension + Elevated JVP + Clear lung fields (no pulmonary edema)

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11. Cardiac Tamponade — Electrical Alternans

ECG Features

• Sinus tachycardia — compensatory
• Low voltage — QRS <5 mm in all limb leads AND <10 mm in all precordial leads
• Electrical alternans — beat-to-beat variation in QRS axis/amplitude (heart "swinging" in pericardial fluid)
• Total electrical alternans (P + QRS + T alternating) = pathognomonic for large effusion with tamponade

Beck's Triad (clinical diagnosis)

• Hypotension + Raised JVP + Muffled heart sounds
• Pulsus paradoxus >10 mmHg drop in SBP on inspiration

Management

In the ICU, tamponade is commonly caused by: post-cardiac surgery, aortic dissection, malignancy, uremia, or post-MI (Dressler syndrome)

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12. SVT — Narrow Complex Tachycardia (AVNRT/AVRT)

ECG Features

• Regular, narrow QRS tachycardia (QRS <120 ms) at rate 150–280 bpm
• P waves absent, buried in QRS (AVNRT — "short RP"), or just after QRS as pseudo-S or pseudo-R' in V1
• Perfectly regular R-R intervals (distinguish from AF which is irregular)
• Rate ~150 bpm → always check for atrial flutter with 2:1 block (look for flutter waves in V1, II)
• Rate >200 bpm + wide QRS → consider WPW (antidromic AVRT — treat differently!)

Management

Adenosine terminates re-entry through AV node (AVNRT/AVRT). It does NOT work for atrial flutter/VT — but can unmask flutter waves or reveal VT (AV dissociation). Do NOT give adenosine in WPW with AF (risk of degeneration to VF).

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13. Wolff-Parkinson-White (WPW) Syndrome

ECG Features (Sinus Rhythm)

• Short PR interval (<120 ms) — bypass of AV node delay
• Delta wave — slurred, upsloping initial QRS deflection
• Wide QRS (>120 ms) — combined normal + accessory pathway conduction
• Discordant ST-T changes — secondary to abnormal depolarization

The ICU Emergency: WPW + Atrial Fibrillation

• If AF occurs in WPW, impulses conduct via accessory pathway at full rate (no AV node protection)
• Results in extremely rapid, irregular, wide-complex tachycardia (can approach 300 bpm)
• Can degenerate to VF and sudden cardiac death
• ECG shows: irregular, wide, bizarre-looking QRS at very rapid rate

Management

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14. Hypokalemia

ECG Features (K⁺ <3.5 mEq/L)

U wave = deflection after T wave, same polarity as T, best seen in V2–V4. When U > T amplitude = significant hypokalemia.

Management

• Oral KCl if mild and patient can take PO
• IV KCl (central line preferred for concentrated solutions):
  • Rate: max 20 mEq/h via central line (10 mEq/h via peripheral)
  • Monitor ECG continuously during infusion
• Replenish Magnesium simultaneously (hypoMg drives renal K⁺ wasting — refractory hypokalemia until Mg corrected)
  • MgSO₄ 1–2 g IV over 15–30 min
• Identify cause: diuretics, vomiting, NGT losses, mineralocorticoid excess, RTA

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15. New Left Bundle Branch Block (LBBB) — STEMI Equivalent

ECG Features

• Wide QRS >120 ms
• Broad, notched "M-shaped" R waves in lateral leads (I, aVL, V5, V6)
• Deep QS pattern in right precordial leads (V1–V3)
• Discordant ST-T changes — ST and T wave go opposite to the main QRS deflection (NORMAL in LBBB)

Sgarbossa Criteria — Diagnosing MI in LBBB

Modified Sgarbossa (Smith criteria): ST/S ratio < −0.25 in any lead (excessive discordant STE) is more sensitive and has largely replaced the original ≥5 mm criterion.

Management

• New LBBB + ischemic symptoms = treat as STEMI (activate cath lab, primary PCI)
• Pre-existing LBBB: apply Sgarbossa/modified Sgarbossa criteria

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16. Hypothermia — Osborn (J) Waves

ECG Features (Progressive with Falling Temperature)

Osborn wave amplitude correlates inversely with temperature — larger waves = colder patient

Management

Golden rule: "Not dead until warm and dead" — CPR must continue until core temperature ≥32°C. VF in hypothermia is resistant to defibrillation until temperature >30°C.

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17. Digoxin Toxicity

ECG Features

• Sagging/scooped "reverse tick" or "hockey stick" ST depression in V4–V6 and inferior leads
• Shortened QT interval
• T-wave flattening/inversion
• Prolonged PR interval (slows AV conduction)

• Bradyarrhythmias: Sinus bradycardia, all degrees of AV block, junctional escape rhythms
• Tachyarrhythmias: PAT (paroxysmal atrial tachycardia) with block is classic; accelerated junctional rhythm; bidirectional VT (pathognomonic — alternating QRS axis, seen with severe toxicity)
• "Regularization" of AF (junctional rhythm emerges) — sign of toxicity

Management

Digibind indication: VT/VF, complete heart block, K⁺ >5.5 mEq/L in acute toxicity, hemodynamic instability

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18. Brugada Syndrome — Type 1 Pattern

ECG Features

• "Coved" ST elevation ≥2 mm in V1–V2 (or V1–V3 when leads placed in 2nd–3rd intercostal space)
• Convex downsloping ST segment → inverted T wave
• No ischemic symptoms needed for diagnosis
• Type 2 = "saddleback" pattern (≥2 mm STE with saddle shape) — not diagnostic alone, may unmask Type 1 with fever/sodium channel blockers

ICU Significance

• Often presents as resuscitated VF/VT or unexplained syncope
• Triggers in ICU: Fever (unmasks pattern), hyponatremia, vagotonia, TCA overdose, cocaine, class Ic drugs

Management

• Acute VF/VT: Unsynchronized defibrillation + Isoproterenol infusion (increases HR, suppresses early repolarization)
• Quinidine — only oral drug shown to suppress VF in Brugada (blocks Ito channel)
• ICD — definitive therapy for symptomatic patients (aborted SCA, syncope with documented VT/VF)
• Avoid: Sodium channel blockers (flecainide, procainamide), beta-blockers, excess alcohol, treat fever aggressively

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19. De Winter T-Waves — STEMI Equivalent (Proximal LAD)

ECG Features

• J-point (ST) depression 1–3 mm at takeoff of QRS in V1–V6 (upsloping ST depression)
• Transitions into tall, symmetrical, hyperacute T waves in precordial leads
• Mild ST elevation in aVR (~0.5–1 mm)
• No classic ST elevation in anterior leads — does NOT meet STEMI criteria but IS a STEMI equivalent
• Represents ~2% of LAD occlusions — static pattern (doesn't evolve to STE)

Clinical Significance

• Indicates acute proximal LAD occlusion with extensive anterior wall ischemia
• Carry same urgency as anterior STEMI
• Commonly missed because no ST elevation — high-yield exam and clinical pearl

Management

• Activate cath lab immediately — treat as anterior STEMI
• Same antiplatelet, anticoagulation, and PCI protocol as STEMI
• Do NOT wait for troponin results

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Expanded Quick Reference Table