ECG Analysis - 28-Year-Old African Male, Chest + Back Pain x 2 Days

Machine Measurements (from ECG header)

• Heart rate: ~58 bpm (RR 1036 ms) - sinus bradycardia
• PR interval: 55 ms (short - likely machine artifact or measurement at fast segment)
• QRS duration: 74 ms (normal)
• QT/QTc: 40 degrees axis (normal)
• Speed: 25 mm/s | Gain: 10 mm/mV

Key ECG Findings

• ST elevation is present across multiple leads: I, II, aVF, V2-V6
• The morphology appears concave (saddle-shaped/upward concavity) - the ST segment curves upward rather than the convex "tombstone" pattern of STEMI
• Elevation appears most prominent in the mid-precordial leads (V3-V5)
• No reciprocal ST depression in opposing leads (e.g., no depression in aVL or V1) - which would be expected in true STEMI

• There appears to be PR depression visible, particularly in inferior leads - a specific (though insensitive) marker of pericarditis

• T waves are tall, peaked, and concordant with the ST elevation - upright and prominent
• No T-wave inversion

• Notching at the J point (junction of QRS and ST segment) is visible in precordial leads - characteristic of early repolarization
• No pathological Q waves

• The ST elevation is diffuse (multiple non-contiguous territories), not localized to a single coronary territory

Differential Diagnosis

Critical Point on Aortic Dissection

"Aortic dissection can be manifested with chest pain radiating to the back." - Goldman-Cecil Medicine

Pericarditis ECG Interpretation (Textbook)

• Diffuse ST elevation (concave morphology)
• PR segment depression
• No Q waves
• No reciprocal changes

Recommended Workup (Urgent)

1. Immediate: CT angiography of the chest/aorta to rule out aortic dissection - given the back pain, this is non-negotiable
2. Troponin, CK-MB - to assess for myocardial injury (myopericarditis)
3. CRP, ESR, FBC - inflammatory markers
4. Chest X-ray - cardiac silhouette (>300 mL effusion enlarges it), mediastinal widening (dissection)
5. Echocardiography - pericardial effusion assessment (present in ~60% of pericarditis cases)
6. TB workup - Quantiferon/TST, sputum AFB, HIV status (critical in African context)
7. Repeat ECG - serial ECGs to track evolution

Bottom Line

Do not discharge this patient based on ECG alone. CT aorta and echo are the next immediate steps.

ECG Interpretation

Machine Measurements (from header)

Systematic Analysis

1. Rate & Rhythm

• Rate is 96 bpm - normal sinus rhythm, at the upper end of normal
• Rhythm appears regular with upright P waves preceding each QRS in lead II
• Normal sinus rhythm

2. Axis

• P axis: 71° - normal
• QRS axis: 53° - normal (no axis deviation)
• T axis: 43° - normal

3. P Waves

• P waves appear present and upright in I, II, aVF
• Normal morphology - no evidence of atrial enlargement visible

4. PR Interval

• Appears normal (~160-180 ms)

5. QRS Complex - KEY FINDING

• QRS duration 102 ms - borderline (normal <100 ms; this is at the threshold)
• Very high voltage in precordial leads, particularly V2-V5
• The precordial gain is marked at 5 mm/mV (half standard). This means the actual QRS amplitudes are DOUBLE what appears on the trace
• Machine reports RV5 + SV1 = 3.48 mV = 34.8 mm - this already meets Sokolow-Lyon criteria for LVH (>3.5 mV = 35 mm). At full gain, the apparent precordial voltages would be even more striking
• Tall R waves in V4-V6, deep S waves in V1-V2

6. ST Segments & T Waves - KEY FINDING

• In the lateral leads (V5, V6, I, aVL): there is ST depression with asymmetric T-wave inversion
• This is the classic LVH strain pattern (formerly "left ventricular strain")
• The ST depression is downsloping with negative T waves in leads with the tallest R waves - hallmark of pressure-overload repolarization abnormality
• No focal ST elevation suggesting acute infarction

7. QT Interval

• QTc 377 ms - normal (normal <440 ms in males)

Primary Diagnosis

Left Ventricular Hypertrophy (LVH) with Strain Pattern

• Sokolow-Lyon: RV5 + SV1 = 3.48 mV (threshold >3.5 mV - borderline, but note the 5 mm/mV precordial gain means actual voltage is higher)
• Cornell voltage: RaVL + SV3 - would need to measure precisely, but high voltages throughout suggest this is exceeded
• Strain pattern: ST depression + T-wave inversion in lateral leads (I, aVL, V5-V6)

LVH: deep S in V1, tall R in V6, with strain-pattern ST-T changes (Harrison's)

Summary Table

Clinical Implications

1. LVH with strain strongly suggests chronic pressure or volume overload - the most common cause is systemic hypertension. Other causes include aortic stenosis, hypertrophic cardiomyopathy (HCM), and coarctation of the aorta
2. LVH with strain is an independent cardiovascular risk factor - associated with increased risk of heart failure, ventricular arrhythmias, and sudden cardiac death
3. Workup recommended:
   • Blood pressure measurement (both arms)
   • Echocardiogram - to confirm LVH, assess wall thickness, EF, valves, and rule out HCM
   • Renal function (hypertensive nephropathy)
   • Urinalysis for proteinuria
   • Fasting lipids and glucose

No patient context was provided (age, sex, symptoms, BP). Please correlate these ECG findings with the clinical picture to guide management.

ECG Interpretation - Aster Medical Center

Technical Parameters

Systematic Analysis

1. Rate & Rhythm - PRIMARY FINDING

• No clearly discernible P waves in any lead - the baseline is flat to finely undulating without organized atrial activity
• Irregularly irregular R-R intervals - the QRS complexes occur at varying intervals with no consistent pattern
• This combination is the hallmark of Atrial Fibrillation (AF)

Rhythm: Atrial Fibrillation with a controlled ventricular rate

2. QRS Complex - SECOND KEY FINDING

• rSR' (RSR-prime) pattern in V1 - a notched, broad, or bifid R wave pattern
• Wide, slurred S waves in leads I and aVL (left lateral leads)
• QRS duration appears >120 ms (≥3 small squares at 25 mm/s)

3. ST Segments & T Waves

• V1-V2: ST depression with T-wave inversion - this is expected secondary to RBBB (discordant repolarization), not a primary ischemic finding
• Lateral leads (I, aVL, V5-V6): Appropriate for RBBB morphology
• No primary ischemic ST elevation is identified
• Inferior leads (II, III, aVF): Relatively flat, small complexes - no significant ST changes

4. Voltage

• RV5 + SV1 = 1.98 mV (19.8 mm) - this is below the Sokolow-Lyon threshold of 3.5 mV for LVH
• No voltage criteria for LVH met
• Overall QRS amplitude is somewhat low to moderate in limb leads

5. QT Interval

• Difficult to measure accurately in AF (no fixed R-R interval), but T-wave morphology does not suggest gross QT prolongation

Summary of Findings

Primary Diagnosis

Atrial Fibrillation with Right Bundle Branch Block (RBBB)

Clinical Implications

• Requires assessment of stroke risk (CHA₂DS₂-VASc score) - most patients will need anticoagulation
• Rate vs. rhythm control strategy decision based on clinical context (symptom burden, duration of AF, hemodynamic stability)
• Thyroid function, echocardiogram, and renal function are standard workup

• RBBB can be a normal variant (isolated RBBB without structural disease) OR secondary to:
  • Right heart pressure overload (pulmonary hypertension, PE)
  • Ischemic heart disease
  • Atrial septal defect
  • Cardiomyopathy
• New RBBB in the context of AF deserves investigation with echocardiogram and consideration of coronary artery disease
• If acute presentation: pulmonary embolism must be excluded (PE can cause both AF and new RBBB)

1. Echocardiogram (structural heart disease, RV size/function, atrial size)
2. Thyroid function tests
3. If new RBBB: CT pulmonary angiogram to rule out PE
4. Electrolytes, renal function
5. Holter/event monitor if paroxysmal AF suspected

No patient demographics were provided. Please correlate with clinical context (age, symptoms, hemodynamic status, prior ECGs) for complete management decisions.