STEMI
ST-Elevation Myocardial Infarction
Pattern: ST elevation โฅ 1mm in โฅ 2 contiguous leads (โฅ 2mm in V1-V3 for men)
Morphology: Concave-up ("tombstone") or convex-up ST elevation with reciprocal ST depression in opposite leads
Localisation:
โข II, III, aVF โ Inferior (RCA)
โข V1-V4 โ Anterior (LAD)
โข I, aVL, V5-V6 โ Lateral (LCx)
โข V1-V2 depression โ Posterior (get V7-V9)
โข V3R-V4R elevation โ RV infarct (avoid nitrates/volume depletion)
Action: Activate cath lab. ASA 325mg chewed. Heparin. Door-to-balloon < 90 min.
Ventricular Tachycardia (VT)
Wide complex, regular, โฅ 3 consecutive beats
Pattern: Wide QRS (> 120ms), regular, rate 150-250 bpm
Features favouring VT over SVT with aberrancy:
โข AV dissociation (P waves marching independently)
โข Capture/fusion beats
โข Concordance (all precordial QRS same direction)
โข Very wide QRS (> 160ms)
โข Northwest axis (extreme right axis deviation)
Rule: Wide complex tachycardia = VT until proven otherwise, especially if age > 50 or structural heart disease.
Action: Stable โ amiodarone (Cordarone) 150mg IV. Unstable โ synchronized cardioversion. Pulseless โ defibrillate.
Hyperkalemia
Progressive changes as Kโบ rises
Progression:
โข Kโบ 5.5-6.5: Peaked T waves (tall, narrow, symmetric -earliest sign)
โข Kโบ 6.5-7.5: Prolonged PR โ flattened P waves โ widened QRS
โข Kโบ 7.5-8.0: Sine wave pattern (QRS merges with T wave)
โข Kโบ > 8.0: VF โ asystole
Action: Calcium gluconate 1g IV immediately (stabilises membrane). Then insulin + D50 to shift Kโบ. See Hyperkalemia topic for full protocol.
Complete Heart Block (3rd Degree)
No atrial impulses conduct to ventricles
Pattern: P waves and QRS complexes completely independent (AV dissociation). Regular P-P intervals. Regular R-R intervals. But NO relationship between them.
Escape rhythm:
โข Junctional escape (narrow QRS, 40-60 bpm) โ more stable
โข Ventricular escape (wide QRS, 20-40 bpm) โ unstable, high risk of asystole
Action: Atropine 1mg IV (may not work if infranodal). Transcutaneous pacing. Cardiology for transvenous pacer. Dopamine or epinephrine drip as bridge.
Wellens Syndrome
Critical LAD stenosis -will STEMI if missed
Pattern: Deep symmetric T-wave inversions (Type A, more common) or biphasic T waves (Type B) in V2-V3 (ยฑ V1, V4-V6)
Key: Seen during pain-FREE interval (not during active chest pain). During pain, ST may be elevated.
Critical point: Do NOT stress test -will STEMI on the treadmill. Needs cath.
Action: Admit, anticoagulate, cardiology consult for cath. Medical management until intervention.
Brugada Syndrome
Risk of sudden cardiac death in structurally normal heart
Type 1 (diagnostic): Coved ST elevation โฅ 2mm in V1-V3 with T-wave inversion. "Shark fin" morphology.
Type 2 (suggestive): Saddleback ST elevation in V1-V3. Not diagnostic alone -needs provocation test (ajmaline/procainamide).
Key features: Young male, Asian descent, family history of sudden death, syncope, nocturnal agonal breathing.
Action: EP consult. ICD is the only proven therapy (no drug prevents VF in Brugada). Avoid fever (unmasks pattern), avoid Class I antiarrhythmics.
Prolonged QTc
Risk of Torsades de Pointes
Normal: < 440ms (men), < 460ms (women)
Concerning: > 480ms
Dangerous: > 500ms โ high risk for Torsades de Pointes (TdP)
Common offenders: Haloperidol (Haldol), ondansetron (Zofran), fluoroquinolones, azithromycin (Zithromax), methadone, amiodarone (Cordarone), antipsychotics, hypoK, hypoMg
Action: Stop offending drug. Replete Kโบ > 4.0, Mgยฒโบ > 2.0. If TdP occurs: IV magnesium 2g bolus + overdrive pacing (โ HR shortens QT).
PE / Right Heart Strain
Acute right ventricular pressure overload
Classic (but uncommon): S1Q3T3 -deep S in lead I, Q wave + T inversion in lead III. Present in only ~20% of PE.
More common findings:
โข Sinus tachycardia (#1 finding -most sensitive)
โข Right axis deviation
โข T-wave inversions in V1-V4 (RV strain pattern)
โข New RBBB or incomplete RBBB
โข Atrial fibrillation (new onset)
Remember: A normal ECG does NOT rule out PE. ECG is often normal in PE.
Action: If PE suspected โ Wells score โ D-dimer or CT-PA. See PE topic.
Atrial Fibrillation
Irregularly irregular -most common sustained arrhythmia
Pattern: No P waves (fibrillatory baseline), irregularly irregular R-R intervals, narrow QRS (unless aberrancy/BBB)
Distinguish from:
โข Atrial flutter: Regular, sawtooth P waves (especially II, III, aVF), often 150 bpm (2:1 block)
โข MAT: โฅ 3 different P-wave morphologies, irregular, associated with COPD/hypoxia
Action: Rate control (metoprolol (Lopressor) or diltiazem (Cardizem)). CHAโDSโ-VASc for anticoagulation. See Afib topic.
Pericarditis
Diffuse ST elevation -NOT a STEMI
Pattern: Diffuse concave-up ST elevation in nearly ALL leads + PR depression (especially II) + ST depression in aVR
Distinguish from STEMI:
โข Pericarditis: diffuse (many territories), NO reciprocal changes, PR depression, concave-up
โข STEMI: localised (one territory), reciprocal changes present, often convex-up
Key: PR depression in lead II is nearly pathognomonic for pericarditis.
Action: NSAIDs + colchicine (Colcrys). Echo to rule out effusion/tamponade. Do NOT give thrombolytics (not a STEMI!).
Heart Blocks (1st, 2nd degree)
AV conduction delays
1st degree: Prolonged PR > 200ms. Every P conducts. Usually benign -no treatment.
2nd degree Type I (Wenckebach): Progressive PR prolongation โ dropped beat โ cycle repeats. Usually nodal. Often benign.
2nd degree Type II (Mobitz II): Constant PR interval with sudden dropped QRS (no warning). Infranodal. High risk of progressing to complete heart block. Needs pacemaker.
Key rule: Wenckebach = watch. Mobitz II = pacer.
Bundle Branch Blocks
QRS > 120ms -which bundle is blocked?
RBBB: rsR' ("bunny ears") in V1-V2, wide S in I/V6. Mnemonic: "MaRRoW" -V1 has R (tall R'), V6 has W (wide S).
LBBB: Broad notched R in I/V6, deep QS or rS in V1. Mnemonic: "WiLLiaM" -V1 has W (QS), V6 has M (notched R).
Clinical significance:
โข RBBB: Can be normal. New RBBB in ACS/PE โ concerning.
โข LBBB: Almost always pathological. New LBBB + chest pain โ treat as STEMI equivalent (Sgarbossa criteria). Old LBBB makes STEMI diagnosis difficult.
Sgarbossa criteria (STEMI in LBBB): Concordant ST elevation โฅ 1mm (5 pts), concordant ST depression โฅ 1mm in V1-V3 (3 pts), discordant ST elevation โฅ 5mm (2 pts). โฅ 3 pts โ STEMI.
Digoxin Effect vs Toxicity
Know the difference -one is expected, one is dangerous
Digoxin effect (therapeutic): "Salvador Dali moustache" -downsloping ST depression with scooped/sagging morphology. Shortened QT. This is expected and NOT toxic.
Digoxin toxicity:
โข Virtually ANY arrhythmia (classic: regularised Afib, bidirectional VT, accelerated junctional rhythm, PAT with block)
โข Nausea, vomiting, visual disturbances (yellow halos)
โข Risk factors: hypoK, hypoMg, renal failure, advanced age
Action for toxicity: Hold digoxin. Check level + Kโบ + Mgยฒโบ. Digoxin-specific antibody (Digibind/DigiFab) if haemodynamically unstable, life-threatening arrhythmia, or Kโบ > 5.0.
Hypothermia (Osborn/J Waves)
Pathognomonic for hypothermia
Pattern: Positive deflection at the J-point (junction of QRS and ST segment). Amplitude increases as temperature drops.
Other findings: Bradycardia, prolonged intervals (PR, QRS, QT), atrial fibrillation, muscle tremor artifact (shivering)
Key: At core temp < 28ยฐC โ high risk of VF. Osborn waves resolve with rewarming. NOT an indication for antiarrhythmics.
Action: Rewarm. See Hypothermia topic. "No one is dead until warm and dead."