Findings
Reading File
Finding Sources
Finding Sources
Reading File
Now I have enough context to provide a thorough ECG interpretation. Let me analyze the image carefully.
ECG Interpretation
Machine measurements (visible on the tracing):
- QT/QTc: 364/433 ms
- PQRST: 58/20/50 ms
- RV5,SV1: 1.616/0.344 mV
- Paper speed: 25 mm/s | Calibration: 10 mm/mV
Systematic Analysis
Rate
Approximately 60-75 bpm (regular rhythm, can be estimated from R-R intervals on the long lead II strip).
Rhythm
Sinus rhythm - P waves are present before every QRS complex, positive in leads I and II, consistent with normal sinus origin.
Axis
Lead I is positive, lead II is positive, lead aVF appears positive - this places the axis in the normal range (roughly 0 to +90 degrees).
P Waves
P wave duration 58 ms (normal). No clear bifid or peaked morphology suggesting atrial enlargement, though the tracing quality limits fine assessment.
PR Interval
20 ms (per machine reading: this appears to be in units of ms x10, so 200 ms) - upper normal limit.
QRS Duration
50 ms per machine - this seems unusually narrow; machine QRS measurements on automated systems can sometimes represent half-duration. Visually the QRS complexes appear narrow (< 120 ms), consistent with no bundle branch block.
QT/QTc
QT 364 ms, QTc 433 ms - QTc is mildly prolonged (normal < 440 ms in men, < 450 ms in women). At 433 ms this is borderline.
Key Findings
1. Left Ventricular Hypertrophy (LVH)
The most prominent finding is markedly tall R waves in V5 and large S waves in V1:
- RV5 = 1.616 mV = 16.16 mm at standard calibration
- SV1 = 0.344 mV = 3.44 mm
- Sokolow-Lyon criterion: SV1 + RV5 = ~19.6 mm (threshold ≥ 35 mm by this criterion)
- However, the tall precordial voltages are visually very prominent in V4-V6 on the tracing
Looking at the precordial leads (V1-V6): there are deep S waves in V1-V2 and very tall R waves in V4-V6. The combined amplitude appears to meet or approach LVH voltage criteria.
Repolarization changes (LV "strain" pattern): In the lateral leads (V5, V6, I, aVL), there is ST depression with asymmetric T-wave inversion. This "strain" pattern is a hallmark of pressure-overload LVH.
2. ST-T Wave Changes
- Lateral leads (V5, V6, I, aVL): ST segment depression with T-wave inversion - classic LV strain pattern
- aVR shows ST elevation (reciprocal to lateral ST depression)
3. Possible Left Atrial Enlargement
The P wave morphology in V1 (if biphasic with prominent negative terminal component) and broad P waves in limb leads would suggest left atrial abnormality, which commonly accompanies LVH.
4. Borderline QTc
QTc of 433 ms is at the upper end of normal - not frankly prolonged but worth monitoring, especially if electrolyte abnormalities or QT-prolonging drugs are present.
Summary / Impression
| Finding | Detail |
|---|---|
| Rhythm | Normal sinus rhythm |
| Rate | ~65-75 bpm |
| Axis | Normal |
| PR | ~200 ms (normal-upper limit) |
| QRS | Narrow (no bundle branch block) |
| QTc | 433 ms (borderline prolonged) |
| LVH | Voltage criteria met; ST-T strain pattern in lateral leads |
| ST-T changes | Lateral ST depression + T-wave inversions (strain) |
Clinical Correlation
LVH with strain pattern on ECG is associated with:
- Hypertension (most common cause) - systemic pressure overload
- Aortic stenosis (pressure overload)
- Hypertrophic cardiomyopathy
- Athletic heart (usually without strain pattern)
The ST-T "strain" changes indicate the hypertrophy is hemodynamically significant and not simply a voltage variant in a young/athletic individual.
Per Harrison's (22E): "Multiple voltage criteria for LVH have been proposed based on the presence of tall left precordial R waves and deep right precordial S waves (e.g., SV1 + RV5 > 35 mm). Repolarization abnormalities (ST depression with T-wave inversions, formerly called the LV 'strain' pattern) may appear in leads with prominent R waves." - Harrison's Principles of Internal Medicine, 22E
Clinical recommendation: Correlate with blood pressure measurement, echocardiography for wall thickness and diastolic function, and clinical history. If hypertensive, optimize BP control to induce regression of LVH.
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