6.3 Cardiac Assessment & ECG Interpretation

Electrocardiography is a cornerstone of clinical practice and a prominent focus of MRCP(UK) Part 1 examinations. Candidates are tested on systematic analysis, precise interval calculations, conduction disturbances, bundle branch and fascicular blocks, chamber enlargement criteria, and critical high-risk patterns including Brugada, Wellens, de Winter, and pericarditis signatures.

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1. Systematic ECG Analysis, Axis Determination & Intervals

Standard Calibration & Systematic Approach

A standard diagnostic 12-lead ECG is recorded at a paper speed of $25\text{ mm/s}$ and voltage calibration of $10\text{ mm/mV}$:

• Time calibration: 1 small square ($1\text{ mm}$) = $0.04\text{ seconds}$ ($40\text{ ms}$); 1 large square ($5\text{ mm}$) = $0.20\text{ seconds}$ ($200\text{ ms}$); 5 large squares = $1.0\text{ second}$.
• Voltage calibration: 1 small square = $0.1\text{ mV}$; 1 large square = $0.5\text{ mV}$; 2 large squares ($10\text{ mm}$) = $1.0\text{ mV}$.
• Heart Rate: In regular rhythms, rate equals $300$ divided by the number of large squares between consecutive R waves ($300 / \text{RR}$). In irregular rhythms (e.g., atrial fibrillation), count the number of QRS complexes on the 10-second rhythm strip and multiply by 6.

Mean Electrical Axis in the Frontal Plane

The mean frontal QRS axis is determined by examining limb leads I, II, and aVF:

Systematic Interval Analysis

• PR Interval (Normal: $120\text{–}200\text{ ms}$; 3–5 small squares):
  • Prolonged ($> 200\text{ ms}$): First-degree atrioventricular (AV) block. Causes include degenerative conduction system disease (Lenègre-Lev disease), vagal hypertonia, Lyme carditis, inferior ischaemia, and AV nodal-blocking medications (beta-blockers, non-dihydropyridine CCBs, digoxin).
  • Shortened ($< 120\text{ ms}$): Pre-excitation via an accessory pathway bypass tract (Wolff-Parkinson-White [WPW] syndrome, featuring a delta wave and widened QRS), Lown-Ganong-Levine syndrome, or junctional rhythm.
• QRS Duration (Normal: $< 120\text{ ms}$; $< 3$ small squares):
  • Prolongation ($\ge 120\text{ ms}$) indicates intraventricular conduction delay, bundle branch block, ventricular pacing, pre-excitation, or ventricular origin of depolarisation.
• Corrected QT Interval (QTc):
  • Calculated via Bazett's formula: $\text{QTc} = \text{QT} / \sqrt{\text{RR (in seconds)}}$. Overcorrects at high heart rates; Fridericia's formula ($\text{QT} / \sqrt[3]{\text{RR}}$) is preferred at rates $> 80\text{ bpm}$.
  • Normal values: Men $\le 450\text{ ms}$; Women $\le 460\text{ ms}$.
  • Borderline: Men $450\text{–}470\text{ ms}$; Women $460\text{–}480\text{ ms}$.
  • Prolonged: Men $> 470\text{ ms}$; Women $> 480\text{ ms}$. Values $> 500\text{ ms}$ confer extreme risk for early afterdepolarizations triggering Torsades de Pointes (polymorphic VT).
  • Etiologies:
    • Congenital: Romano-Ward syndrome (autosomal dominant; normal hearing; $KCNQ1, KCNH2, SCN5A$), Jervell and Lange-Nielsen syndrome (autosomal recessive; with sensorineural deafness; $KCNQ1, KCNE1$).
    • Acquired: Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypocalcaemia), hypothermia (Osborn / J waves), severe intracranial hemorrhage (giant negative "cerebral T waves"), and QT-prolonging drugs (antiarrhythmics class Ia [procainamide, quinidine] and class III [amiodarone, sotalol]; psychotropics [citalopram, haloperidol, chlorpromazine, TCAs]; antimicrobials [erythromycin, clarithromycin, ciprofloxacin, moxifloxacin]; and antiemetics [ondansetron]).
  • Emergency Management of Torsades de Pointes: Immediate intravenous magnesium sulphate ($2\text{ g}$ bolus over 10–15 minutes) regardless of baseline serum magnesium; temporary transvenous overdrive pacing ($90\text{–}110\text{ bpm}$) or isoprenaline infusion; unsynchronized electrical defibrillation if haemodynamically unstable.

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2. Conduction Disturbances: Bundle Branch & Fascicular Blocks

Left vs. Right Bundle Branch Block

• Left Bundle Branch Block (LBBB):
  • $\text{QRS duration} \ge 120\text{ ms}$.
  • Broad, notched, or slurred R waves in lateral leads (I, aVL, V5, V6) with absent septal Q waves ("M" pattern in V6).
  • Deep, wide QS or rS complex in lead V1 ("W" pattern in V1). Mnemonic: WiLLiaM ($W$ in V1, $M$ in V6).
  • Secondary repolarisation abnormalities: Appropriate T-wave discordance (ST depression and T-wave inversion opposite the main QRS deflection).
• Right Bundle Branch Block (RBBB):
  • $\text{QRS duration} \ge 120\text{ ms}$.
  • Triphasic $rSR'$, $rsR'$, or notched R wave in right precordial leads V1–V2 ("M" pattern in V1).
  • Wide, slurred S wave in lateral leads I, aVL, V5, and V6 ("W" pattern in V6). Mnemonic: MaRRoW ($M$ in V1, $W$ in V6).
  • Normal septal Q waves are preserved; isolated RBBB does not obscure ischaemic ST deviations.

Diagnosing Acute MI in the Presence of LBBB: Sgarbossa Criteria

LBBB normally masks acute transmural STEMI due to altered initial septal and ventricular depolarisation. The Sgarbossa criteria restore diagnostic accuracy:

1. Concordant ST-segment elevation $\ge 1\text{ mm}$ ($0.1\text{ mV}$) in any lead with a positive QRS complex (5 points).
2. Concordant ST-segment depression $\ge 1\text{ mm}$ ($0.1\text{ mV}$) in leads V1, V2, or V3 (3 points).
3. Modified Smith-Sgarbossa Criterion (Excessive Discordance): Discordant ST-segment elevation $\ge 1\text{ mm}$ with an $\text{ST}/\text{S ratio} \ge 0.25$ ($25%$) (measured as ST elevation at the J-point divided by the preceding negative S-wave amplitude). This replaces the original rule of discordant ST elevation $\ge 5\text{ mm}$.

• A score of $\ge 3$ points carries a specificity $> 98%$ for acute coronary occlusion, mandating emergent primary PCI pathway activation.

Fascicular, Bifascicular & Trifascicular Blocks

The left bundle branch bifurcates into a thin left anterior fascicle and a broad left posterior fascicle:

• Left Anterior Fascicular Block (LAFB): LAD ($-45^\circ\text{ to }-90^\circ$), small $q$ in I and aVL, small $r$ in II, III, aVF, and normal QRS duration ($< 120\text{ ms}$).
• Left Posterior Fascicular Block (LPFB): RAD ($+90^\circ\text{ to }+180^\circ$), small $r$ in I and aVL, small $q$ in II, III, aVF, normal QRS duration ($< 120\text{ ms}$), with exclusion of RVH or lateral MI.
• Bifascicular Block: Combination of RBBB plus either LAFB (commonest) or RBBB plus LPFB.
• Trifascicular Block: Bifascicular block plus first-degree AV block (prolonged PR interval), or alternating RBBB and LBBB. When accompanied by syncope, it carries high risk of complete heart block and warrants permanent pacemaker implantation.

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3. Chamber Enlargement Criteria

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4. High-Yield Non-Ischaemic & Diagnostic Ischaemic ECG Signatures

Brugada Syndrome

An autosomal dominant cardiac channelopathy primarily caused by loss-of-function mutations in the $SCN5A$ gene (encoding the cardiac Nav1.5 voltage-gated sodium channel alpha-subunit).

• Type 1 Pattern (Diagnostic): Coved-type ST-segment elevation $\ge 2.0\text{ mm}$ ($0.2\text{ mV}$) followed by a negative T wave in one or more right precordial leads (V1–V2, placed in the 4th, 3rd, or 2nd intercostal space).
• Type 2 (Saddleback): ST elevation $\ge 2.0\text{ mm}$ with a trough $\ge 1.0\text{ mm}$ and positive or biphasic T wave.
• Triggers & Risk: Unmasked by fever, high ambient temperature, alcohol, or sodium channel blockers (ajmaline, flecainide, procainamide). High risk of polymorphic VT, VF, and nocturnal sudden cardiac death; definitive management is an implantable cardioverter-defibrillator (ICD).

Wellens Syndrome

Characterizes severe, critical ($> 90%$) stenosis of the proximal left anterior descending (LAD) coronary artery:

• Diagnostic Criteria:
  1. Deeply inverted or biphasic T waves in leads V2 and V3 (often extending V1–V6).
  2. Recorded during a pain-free interval in a patient with recent typical angina.
  3. Normal or minimally elevated cardiac enzymes.
  4. Absence of pathological precordial Q waves and preserved R-wave progression.
  5. Minimal or absent ST-segment elevation ($< 1\text{ mm}$).
• Variants: Type A (~25%): Biphasic T waves in V2–V3. Type B (~75%): Deep, symmetrical, sharply inverted T waves in V2–V3.
• Critical Management Pearl: Provocative exercise stress testing is strictly contraindicated (precipitates massive transmural anterior MI or fatal ventricular arrhythmias). Patients require urgent invasive coronary angiography.

de Winter T Waves

An acute STEMI equivalent identified in ~2% of acute proximal LAD occlusions:

• Diagnostic ECG Features:
  1. Upsloping ST-segment depression ($1\text{–}3\text{ mm}$) at the J-point in precordial leads V1–V6.
  2. Tall, prominent, symmetrical T waves with a sharp take-off in leads V1–V6.
  3. ST-segment elevation ($0.5\text{–}1.0\text{ mm}$) in lead aVR.
  4. Absence of classic convex ST elevation across anterior chest leads.
• Mandates immediate catheterization laboratory activation for primary PCI.

Acute Pericarditis vs. Acute STEMI

Pericardial inflammation alters ventricular and atrial epicardial repolarisation through 4 classical stages:

• Stage 1 ECG Features:
  • Widespread, concave ("saddle-shaped") ST elevation in almost all limb and precordial leads (I, II, III, aVF, aVL, V2–V6).
  • Widespread PR-segment depression (reflects atrial subepicardial injury).
  • Reciprocal changes isolated strictly to lead aVR: Reciprocal ST-segment depression and PR-segment elevation in lead aVR (and occasionally lead V1).
  • Spodick's Sign: Downsloping of the TP segment, present in ~80% of cases.
• Distinguishing from STEMI: Pericarditis does not follow a regional coronary vascular territory, lacks convex ("tombstone") ST morphology, exhibits widespread PR depression, lacks reciprocal ST depression in opposing vascular territories (e.g., lead III vs lead aVL), and never generates pathological Q waves. First-line therapy is high-dose NSAIDs (e.g., ibuprofen 600 mg tds or aspirin 750–1000 mg tds) plus colchicine (0.5 mg od or bd for 3 months) to prevent recurrences.