Interpreting an #ECG can seem overwhelming at first, but with a structured approach, it becomes far more manageable.
In this thread, I’ll walk you through how to analyze an ECG like a professional, step by step.
Let’s begin.🧵
Step 0: Initial Checks 1. Paper Speed
The standard ECG paper speed is 25 mm/s, meaning:
◾1 small square = 0.04 s
◾1 large square = 0.20 s (5 small squares) 2. Calibration
This determines the amplitude of the waves:
⏺️ 1 mV = 10 mm (i.e., 2 large squares vertically
Step 1: Heart Rate (HR)
If rhythm is regular:
Use the formula
Heart Rate = 300 / number of large squares between R waves
Alternatively, memorize the sequence:
300 → 150 → 100 → 75 → 60 → 50
Estimate HR by seeing where the next R wave falls in this pattern.
....If rhythm is irregular:
🔹Count 30 large squares (which equals 6 seconds)
🔹Count the number of QRS complexes in that span
🔹Multiply the count by 10 to estimate the HR (beats per minute
Step 2: Rhythm Assessment
Determine whether the rhythm is regular or irregular.
◾Regular rhythm: Fixed R–R intervals
Proceed to examine P waves and confirm if it's sinus rhythm
◽Irregular rhythm: Consider
🔸Atrial fibrillation
🔸Ectopic beats
🔸Heart blocks
Step 3: P Waves
Evaluate the presence, morphology, and relationship to QRS.
✳️Present and upright in leads I, II, and aVF
→ Suggests sinus rhythm (if criteria below are met):
🔹Heart rate between 50–120 bpm
🔹Every P wave is followed by a QRS
🔹Consistent PR interval
....Absent P waves: Think of atrial fibrillation
More P waves than QRS complexes: Suspect atrial flutter or atrial tachycardia
Step 4: PR Interval
Normal range: 120–200 ms (3–5 small squares)
◾Short PR interval (<120 ms): Suggests pre-excitation (e.g., Wolff–Parkinson–White syndrome)
◾Prolonged PR interval (>200 ms): Indicates 1st-degree AV block
Step 5: QRS Complex
Normal duration: <120 ms (3 small squares)
Electrical axis refers to the overall direction of ventricular depolarization in the frontal plane.
Quick method: 1. Look at Lead I and aVF:
✳️ Both positive → Normal axis (–30° to +90°)
👉I positive, aVF negative → Go to Step 2.... 👇
...2. Look at Lead II:
🔺Positive → Still normal
🔻Negative → Left axis deviation
Interpretation ranges:
- Normal axis: –30° to +90°
- Left axis deviation: –30° to –90° (e.g., LBBB, left anterior fascicular block)
- Right axis deviation: +90° to +180° (e.g., RBBB, RVH, PE)
Step 7: ST Segment and T Waves
🔺ST elevation: Think STEMI, pericarditis, early repolarization, or ventricular aneurysm
🔻ST depression: Indicates subendocardial ischemia or reciprocal change
◾T wave inversion: Causes include ischemia, strain, Takotsubo, electrolyte disorders
Step 8: QT Interval
How to measure:
🔸Use leads II, V5, or V6
🔸From beginning of Q wave to end of T wave (tangent method)
🔹Corrected QT (QTc) using Bazett’s formula: QTc = QT / √RR
Prolonged QTc:
🔹Men: >440 ms
🔹Women: >460 ms
Prolongation increases the risk of torsades
Final Checklist for ECG Interpretation 1. Confirm paper speed and calibration 2. Determine heart rate 3. Assess rhythm 4. Examine P waves 5. Measure PR interval 6. Evaluate QRS duration 7. Determine QRS axis 8. Analyze ST segments and T wave
Suggested References:
- ECG Step by Step by Garamendi & Lip
- Life in the Fast Lane (LITFL)
-
- Mayo Clinic ECG Curriculum
- Dr Smith's ECG blogspot.
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🧵 Thread: Brugada-type ECG, beyond the classic Type 1 pattern 1/ Brugada syndrome is defined by dynamic ECG changes in the right precordial leads (V1–V3), not a single static pattern.
Understanding when and why these patterns appear is as important as recognizing them.
2/ Consensus classification describes three Brugada-type ECG patterns based on ST-segment morphology and J-point amplitude:
🟢 Type 1 (coved)
🟢 Type 2/3 (saddleback spectrum)
🟢Type S (mild coved, “suggestive”)
📌 Only Type 1 is diagnostic.
3/ Type 1 pattern
- Coved ST elevation ≥2 mm
- Gradual downsloping ST
- Negative or isoelectric T wave
This pattern may be spontaneous or unmasked under specific conditions
2026 Stroke Guideline: 10 Updates You MUST Know
The 2026 AHA/ASA Acute Ischemic Stroke Guideline just dropped and it changes practice.
Here are the 10 most important updates 🧵⬇️
1️⃣ Mobile Stroke Units (MSUs)
MSUs are recommended where available because they significantly reduce onset-to-thrombolysis time and improve outcomes.
Speed still saves brain 🧠
2️⃣ EMS Destination Strategy Changed
Instead of always going to the nearest thrombolysis center, direct transport to EVT-capable hospitals is supported when systems of care allow.
🧵 Why can oxygen worsen respiratory failure in COPD?
Many clinicians still fear giving oxygen to COPD patients.
The reason they’re taught?
"Loss of hypoxic drive"
But this is mostly a myth.
Here’s what really causes oxygen-induced hypercapnia 👇
Oxygen does NOT usually cause dangerous hypercapnia by stopping breathing.
Studies show:
- Ventilatory drive remains high
- Minute ventilation recovers quickly
- CO₂ continues to rise anyway
So what’s the real mechanism?
1️⃣ Worsened ventilation–perfusion (V/Q) mismatch, the BIGGEST factor
High FiO₂ reverses hypoxic pulmonary vasoconstriction, sending blood to poorly ventilated alveoli → ↑ dead space → ↑ PaCO₂
This explains most of the CO₂ rise
The liver rarely complains out loud but it leaves clues everywhere. From yellowing eyes and reddened palms to distended abdomens and subtle nail changes, liver disease tells its story on the skin, breath, and body.
A 🧵
🔵Icterus
Yellow discoloration of the sclera caused by elevated serum bilirubin. It reflects impaired bilirubin metabolism or excretion and is often the earliest visible sign of liver dysfunction.
🔵Spider nevi (spider angiomas)
Dilated superficial blood vessels with a central arteriole and radiating branches that blanch on pressure and refill from the center outward. They occur due to hyperestrogenism and are typical of chronic liver disease.
Activate the Cath Lab: ECG patterns that matter even without classic STEMI
Not every coronary occlusion announces itself with obvious ST-segment elevation.
Some ECG patterns are quieter, atypical, and easy to miss, yet they represent the same emergency.
Thread below ⬇️
🔵 Posterior MI & Right Ventricular MI
Posterior infarction often presents as ST depression in V1–V3 with tall R waves.
Posterior leads (V7–V9) may reveal the missing ST ⬆️.
RV infarction shows ST⬆️ in right-sided leads (V3R–V4R)
Both require urgent reperfusion.
🔵 Early anterior occlusion (V1–V3 changes)
Hyperacute, tall symmetric T waves or subtle ST elevation in V1–V3 may be the earliest sign of LAD occlusion.
This is often the window before a full STEMI develops.
Waiting for “textbook” changes risks losing myocardium.
What Makes V1–V3 Unique?
Although every ECG should be read systematically, V1–V3 deserve special attention because they capture patterns that may remain subtle or even invisible in other leads. Their position over the RV, septum, and RVOT gives them unique diagnostic value
A 🧵
🔵Early Anterior Ischemia
These leads are the earliest to show anterior ischemia. Subtle hyperacute T waves, loss of R-wave progression, ST elevation, and the de Winter pattern often appear in V2–V3 long before other leads show convincing changes.
🔵Wellens Syndrome
V2–V3 are where Wellens syndrome becomes unmistakable. Deeply inverted or biphasic T waves during a pain-free interval signal critical LAD stenosis. Missing this pattern risks sending the patient to stress testing with catastrophic consequences.