What are the characteristic ECG (electrocardiogram) findings for premature ventricular beats, hypokalemia (low potassium levels), hyperkalemia (high potassium levels), atrial fibrillation, hypermagnesemia (elevated magnesium levels), hypomagnesemia (low magnesium levels), acute pericarditis, Brugada's syndrome, STEMI (ST-elevation myocardial infarction), hypertrophic obstructive cardiomyopathy, and bundle branch blocks?

ECG Characteristics for Diagnosing Cardiac Conditions

Premature Ventricular Beats (PVCs)

Look for wide QRS complexes (>120 ms) occurring earlier than expected, without preceding P waves, followed by a compensatory pause. 1

• Focus on all leads to identify the wide, bizarre QRS morphology that distinguishes PVCs from normal beats 1
• The QRS complex will be >120 ms in duration and appear premature relative to the expected sinus rhythm 1
• A full compensatory pause typically follows the PVC (the interval from the beat before the PVC to the beat after equals two normal RR intervals) 1
• If you detect >2,000 PVCs in 24 hours on monitoring, this warrants comprehensive cardiac evaluation including echocardiography and cardiac MRI to exclude cardiomyopathy 1

Hypokalemia

Hypokalemia produces prominent U waves, QT prolongation, and flattened T waves, most evident in precordial leads. 1

• Focus on precordial leads (V2-V6) where U waves are most prominent 1
• Progressive changes occur as potassium drops: T wave flattening → U wave appearance → ST depression → QT prolongation 1
• U waves become increasingly prominent and may exceed T wave amplitude in severe hypokalemia 1
• Predisposes to torsades de pointes due to QT prolongation 1
• Important caveat: Severe hypokalemia (around 2.9 mmol/L) can unmask Type 1 Brugada pattern with coved ST elevation in V1-V2, which resolves with potassium correction 2

Hyperkalemia

Hyperkalemia creates peaked, narrow-based "tented" T waves initially, progressing to widened QRS, flattened P waves, and potentially Brugada-like patterns in severe cases. 1

• Focus on precordial leads for the earliest changes, though peaked T waves appear diffusely 1
• Progressive ECG changes correlate with potassium levels:
  • Mild (5.5-6.5 mEq/L): Peaked, narrow T waves 1
  • Moderate (6.5-8.0 mEq/L): Prolonged PR interval, flattened/absent P waves, widened QRS 1
  • Severe (>8.0 mEq/L): Sine wave pattern, ventricular arrhythmias, cardiac arrest 1
• Critical pitfall: Severe hyperkalemia can produce ST elevation mimicking Brugada syndrome or STEMI, which resolves with potassium correction 3, 4
• Hyperkalemia-induced Brugada-like pattern shows coved ST elevation in right precordial leads (V1-V2) that disappears after normalizing potassium 3, 4

Atrial Fibrillation

Atrial fibrillation shows irregularly irregular RR intervals with absent P waves, replaced by chaotic fibrillatory waves best seen in leads V1, II, III, and aVF. 1

• Focus on leads V1, II, III, and aVF where fibrillatory waves are most visible 1
• The hallmark is irregularly irregular ventricular response with no discernible P waves 1
• Fibrillatory waves appear as chaotic baseline undulations with varying amplitude and frequency 1
• Measure ventricular rate over 6 seconds and multiply by 10 for average rate 1
• QRS complexes are typically narrow unless there is concurrent bundle branch block or aberrant conduction 1

Hypermagnesemia

Hypermagnesemia produces prolonged PR and QT intervals with widened QRS, though ECG changes are less specific than other electrolyte disorders. 1

• Monitor all intervals across multiple leads as changes are diffuse and nonspecific 1
• Progressive changes include: PR prolongation → QRS widening → QT prolongation 1
• Severe hypermagnesemia can lead to complete heart block and cardiac arrest 1
• ECG findings are less diagnostically specific compared to potassium or calcium abnormalities 1

Hypomagnesemia

Hypomagnesemia causes QT prolongation, prominent U waves, and predisposes to torsades de pointes, with changes most evident in precordial leads. 1

• Focus on precordial leads (V2-V6) for U waves and QT measurement 1
• ECG findings overlap significantly with hypokalemia: flattened T waves, prominent U waves, QT prolongation 1
• The primary danger is predisposition to torsades de pointes due to QT prolongation 1
• Often coexists with hypokalemia, making ECG interpretation challenging 1

Acute Pericarditis

Acute pericarditis shows diffuse ST elevation with upward concavity (saddle-shaped) in multiple leads, accompanied by PR depression, without reciprocal ST depression. 1

• Focus on leads I, II, aVL, aVF, V2-V6 for widespread ST elevation with upward concavity 1
• Key distinguishing features from STEMI:
  • ST elevation has upward concavity ("saddle-shaped") rather than convex morphology 1
  • ST elevation is widespread across multiple territories, not confined to contiguous leads of one coronary distribution 1
  • PR depression is present in most leads (except aVR which shows PR elevation) 1
  • No reciprocal ST depression (except in aVR) 1
• The PR depression is highly specific for pericarditis and helps differentiate from MI 1

Brugada Syndrome

Brugada syndrome Type 1 pattern shows coved ST elevation ≥2 mm in V1-V2 with downsloping ST segment and inverted T wave, often with right bundle branch block. 1

• Focus exclusively on leads V1-V2 recorded in the 4th intercostal space 1
• Type 1 pattern (diagnostic): Coved ST elevation ≥2 mm with downsloping ST segment and inverted T wave in V1-V2 1
• Consider recording V1-V2 in the 2nd intercostal space to unmask the Brugada pattern if initial ECG is non-diagnostic 1
• Often accompanied by right bundle branch block pattern 1
• Critical pitfall: Hypokalemia and hyperkalemia can both induce reversible Brugada-like patterns that disappear with electrolyte correction 2, 3, 4
• Brugada syndrome is predominantly seen in males (8-10:1 male to female ratio) and is caused by SCN5A gene mutations affecting cardiac sodium channels 5

STEMI (ST-Elevation Myocardial Infarction)

STEMI requires ST elevation at the J-point in two or more contiguous leads: ≥0.1 mV in all leads except V2-V3, where thresholds are higher and age/sex-dependent. 1

General STEMI Criteria

• Measure ST elevation at the J-point in two or more contiguous leads 1, 6
• Standard leads (other than V2-V3): ≥0.1 mV (1 mm) elevation 1, 6
• Leads V2-V3 have higher thresholds 1, 6:
  • Men <40 years: ≥0.25 mV (2.5 mm)
  • Men ≥40 years: ≥0.2 mV (2 mm)
  • Women (all ages): ≥0.15 mV (1.5 mm)
• Obtain ECG within 10 minutes of presentation and repeat every 15-30 minutes if initially non-diagnostic 1, 6

Territory-Specific STEMI Patterns

Inferior STEMI:

• Focus on leads II, III, aVF for ST elevation 6
• Look for reciprocal ST depression in anterior leads (V1-V4, aVL) 6
• Always record right precordial leads V3R and V4R to detect right ventricular involvement 6
• ST elevation ≥0.05 mV in V3R-V4R (≥0.1 mV in men <30 years) indicates RV infarction 6

Lateral STEMI:

• Focus on leads I, aVL, V5, V6 for ST elevation 6
• May occur in isolation or with inferior/anterior MI 6

Anterior STEMI:

• Focus on leads V1-V4 for ST elevation 6
• Hyperacute T waves may precede ST elevation 6
• Increased R-wave amplitude and width may accompany ST elevation 6

Posterior STEMI:

• Focus on leads V1-V3 for ST depression with positive terminal T waves (ST elevation equivalent) 6
• Confirm with posterior leads V7-V9 at the fifth intercostal space showing ST elevation ≥0.05 mV (≥0.1 mV in men <40 years) 6
• Posterior MI is often missed without recording posterior leads 6

Special STEMI Considerations

• Prolonged ST elevation (>20 minutes) with reciprocal ST depression indicates acute coronary occlusion 1, 6
• ST depression in eight or more leads with ST elevation in aVR indicates left main or multivessel disease 6
• In left bundle branch block, concordant ST elevation strongly suggests acute MI 6

Hypertrophic Obstructive Cardiomyopathy (HOCM)

HOCM shows deep, narrow Q waves in lateral and inferior leads, giant inverted T waves in precordial leads, and voltage criteria for left ventricular hypertrophy. 1

• Focus on lateral leads (I, aVL, V5-V6) for deep, narrow Q waves and ST-T changes 1
• Focus on V2-V4 for giant T wave inversion (often >10 mm deep) 1
• Look for voltage criteria for left ventricular hypertrophy across precordial leads 1
• The Q waves in HOCM are typically narrow (<0.04 seconds) and deep, distinguishing them from MI Q waves 1
• Giant negative T waves in precordial leads are highly characteristic of apical HOCM 1

Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

RBBB shows QRS ≥120 ms with RSR' pattern ("M-shaped") in V1-V2 and wide S waves in lateral leads I, aVL, V5-V6. 1

• Focus on lead V1-V2 for the characteristic RSR' ("M-shaped") pattern 1
• Focus on lateral leads (I, aVL, V5-V6) for wide, deep S waves 1
• QRS duration must be ≥120 ms 1
• Secondary ST-T abnormalities are common in V1-V3 and should not be mistaken for ischemia 6
• Pitfall: New ST elevation or Q waves in the setting of RBBB should raise suspicion for acute MI despite the expected ST-T abnormalities 6

Left Bundle Branch Block (LBBB)

LBBB shows QRS ≥120 ms with broad, notched R waves in lateral leads (I, aVL, V5-V6) and deep S waves in V1-V2, without Q waves in lateral leads. 1

• Focus on lateral leads (I, aVL, V5-V6) for broad, notched (or "M-shaped") R waves 1
• Focus on V1-V2 for deep S waves (often QS or rS pattern) 1
• Absence of Q waves in lateral leads is characteristic (Q waves suggest prior MI) 1
• QRS duration must be ≥120 ms 1
• Critical pitfall: LBBB makes STEMI diagnosis challenging; concordant ST elevation (ST elevation in leads with positive QRS) strongly suggests acute MI 6
• Compare with previous ECG when available, as new or presumed new LBBB with clinical suspicion warrants immediate reperfusion therapy 6