ECG Reference Guide For Medical Trainees

A quick reference guide for diagnostic ECG criteria with examples. Will continue to update regularly.


P-Wave Abnormalities

Right atrial enlargement (RAE)

  • 2 things help me remember RAE. First, the normal P-wave on an ECG typically represents the left atrium because the right atrium is typically smaller and it’s electrical current is typically hidden in the left atrium’s electrical signal. Second, the SA node sits in the right atrium. So when the right atrium gets enlarged we start to see it on the ECG. The P-wave gets BIGGER! I think of it similar to what we see in left ventricular hypertrophy. Typically, in a normal QRS complex we only see the left ventricle because it’s size and electrical signal is so much larger than the right atrium (similar to our atria). However, in LVH the left ventricle gets even larger. So the electrical signal it puts out is even bigger too. This is just like what happens in RAE. The right atrium is able to be seen in the P-wave which manifests with TALL P-waves. Thus, the diagnostic criterion are:
  • Inferior lead P-waves: >2.5 mm in height (tall positive P-wave because the SA node is superior in the heart so the electrical signal in the inferior leads, the direction the electrical impulse goes toward, will be larger in size)
  • >1.5mm in V1, V2
  • Clinically can be seen in RVH, COPD, pHTN > CHD >>tricuspid stenosis

Left atrial enlargement (LAE)

  • Back to our discussion about P-waves. In normal physiology the SA node in the right atrium fires and then the signal has to travel all the way over the left atrium. We already know that on normal ECG’s that the P-wave represents the left atrium. Thus, if the left atrium gets enlarged you will see LONGER P-waves because it will take more time for that signal to reach the entirety of the left atrium. Or at least that’s how I remember it in my head. Thus, for LAE think “1 box deep, 1 box wide”. If you can fit 1 small box inside the negatively deflected P-wave you should be thinking about LAE. The diagnostic criterion are:
  • Terminal portion V1 > 1mm deep, >40ms duration
  • Inferior leads: notched P-wave > 120ms

Biatrial enlargement (BAE)

You can also have both diagnostic criterion met for both left and right atrial enlargement. In these cases we simply call it biatrial enlargement. Here’s a quick and dirty reference for atrial enlargement:


Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

There are a LOT of criterion for LVH but the most frequent ones that I use in clinical practice are:

  • aVL >11 (Sokolow-Lyon ‘stand alone‘ criteria)
  • Cornell Criteria: R wave in avL + S wave in V3 > 28mm in men/> 20mm in women (Easy way to remember: CorneLL has 2 L’s, aVL has 1 L. Add them together to remember you use lead V3)
  • Sokolow-Lyon Criteria: S wave in V1 + R wave in V5 or V6 > 35mm
  • Delayed intrinsicoid deflection in V5, V6 >50ms (interestingly this is the only non-voltage criteria for LVH)

LVH can also have a ‘strain pattern’ with T-wave inversions (TWI) as seen in the ECG below.

LVH with strain pattern in I, II, V5, V6

Right Ventricular Hypertrophy (RVH)

  1. RAD: mean QRS axis ≥ 100 degrees
  2. Secondary ST-T segment changes (STD, TWI) in right precordial leads
  3. (R/S ratio in V1 > R/S ratio in V5, V6) or (R/S ration in V6 <1) or (R wave > 7mm in V1)

Clinically, Posterior MI can mimic RVH

  • Factors that favor RVH diagnosis: concomitant RAD, TWI in V1-V2
  • Factors that favor posterior MI: presence of inferior Q-waves

Combined Ventricular Hypertrophy

  • Exists when criteria for both isoloated LVH) and RVH are met
  • Should be suspected when criteria for LVH is present but QRS axis is > 90 degrees or criteria for right atrial enlargement exist
  • R/S ratio approximately equal to 1 in both V3 and V4 (Kutz-Wachtel phenomenon)
Diagnosis: Atrial flutter, LAD, LVH, RVH, iRBBB

Intraventricular Conduction

Left Bundle Branch Block (LBBB)

  1. QRS ≥120 ms
  2. Terminal S-wave in V1 (late forces of QRS should be negative)
  3. I, aVL, V5, V6: Broad notched or slurred R-wave. Occasional RS pattern in V5, V6 may be attributed to displaced transition of QRS complex)
  4. No Q-waves in I, V5, V6 but in aVL a narrow Q-wave may be present without myocardial pathology
  5. Delayed onset of intrinsicoid deflection >60 ms from beginning of QRS to peak of R-wave in V5, V6 but normal in V1-V3 when small initial R-wave can be discerned

Left Anterior Fascicular Block (LAFB)

  1. LAD (QRS axis between -45 to -90 degrees) and mean QRS duration < 120 ms
  2. qR complexes in I, aVL
  3. rS complexes in II, III, aVF
  4. Prolonged R wave peak time in aVL > 45ms (from beginning of QRS complex to peak of R wave)
  5. *Absence of other causes of marked LAD such as inferior MI or LVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle. The above criteria of left anterior fascicular block do not apply to patients with congenital heart disease in whom left-axis deviation is present in infancy.

Left Anterior Fascicular Block (LAFB)

Left Posterior Fascicular Block (LPFB)

  1. RAD (QRS axis 90 to 180 degrees in adults) with mean QRS duration < 120 ms
  2. rS complexes in leads I and aVL
  3. qR complexes in leads II, III and aVF
  4. *Absence of other causes of right axis deviation including lateral MI, dextrocardia, or RVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left posterior fascicle is shorter and thicker than the left anterior, and receives dual blood supply from both the left and right coronary arteries. Multivessel coronary artery disease is the most common cause of left posterior fascicular block.

Right Bundle Branch Block (RBBB)

  1. QRS ≥ 120 ms
  2. V1, V2: RSR’ with secondary R-wave usually wider than initial R-wave
  3. Minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
  4. S wave duration > than R wave or > 40 ms in leads I and V6
  5. Normal R peak time in leads V5 and V6 but > 50 ms in lead V1

Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied

ECG Right Bundle Branch Block RBBB 5

Incomplete Right Bundle Branch Block (iRBBB)

  1. Same criteria for RBBB but QRS < 120ms but > 100ms

Non-specific inter-ventricular conduction delay

  1. QRS ≥ 110 ms
  2. Specific criteria for RBBB, LBBB not met

Quick and dirty reference to compare LBBB and RBBB:

Bundle Branch Block : Mnemonic | Epomedicine

Atrial Rhythms

Sinus Rhythm

In medical school we are taught this incorrectly. The correct way to tell that a P-wave is of sinus origin is that they are:

  1. Upright in the inferior leads (remember the sinus node is in the right atrium so the electrical wave will go from the top down and thus be positive inferiorly)
  2. Biphasic in V1
  3. Axis between 0 to 75 degrees (i.e. upright in the inferior leads)

The number of P-waves before every QRS complex is irrelevant. You can have sinus rhythm but be in complete heart block. Or have sinus rhythm but have second degree type I or type II heart block. Generally however they should have the same morphology. A single P-wave with a different morphology can indicate a premature atrial complex (PAC) but if you have multiple different P-wave morphologies then you might be dealing with wandering atrial pacemaker (WAP) or multifocal atrial tachycardia (MAT). I think of WAP and MAT as the same rhythm across a spectrum ranging from a normal heart rate (WAP) to a fast heart rate (MAT).

Sinus Arrhythmia

Diagnostic criteria:

  • Normal P wave axis (0 to 75 degrees; i.e. upright in leads I and II)
  • P-P interval varies by > 10% or 0.16 seconds

tl;dr normal sinus P-waves (as above) but P-P interval varies by >10% or 160ms (4 little boxes). ECG intervals can vary with respiration but they shouldn’t vary by more than 10%. Often incidental without major clinical significance