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Diagnostic Code Explanations (4)
Diagnoses for this EKG: anterolateral myocardial infarction (ALMI), Wolf-Parkinson-White syndrome (WPW), abnormal QRS (ABQRS), sinus rhythm (SR)
Explanation for anterolateral myocardial infarction (ALMI)
An anterolateral myocardial infarction (MI) is characterized by specific changes on a standard 12-lead ECG that reflect
damage to both the anterior (front) and lateral (side) walls of the left ventricle.
Here are the key signs to look for:
1. Affected Leads
The hallmark of an anterolateral MI is ST-segment elevation in a combination of precordial (chest) and limb leads:
Anterior Leads: V3 and V4 (representing the anterior wall).
Lateral Leads: V5, V6, I, and aVL (representing the lateral wall).
Note: You may often see involvement of leads V1 and V2 as well if the infarction extends to the septum (
anteroseptal-lateral), often referred to simply as an extensive anterior MI.
2. Characteristic Waveform Changes
ST-Segment Elevation: Look for J-point elevation in the leads mentioned above (V3-V6, I, aVL). This is the primary
indicator of acute injury.
Hyperacute T Waves: In the very early stages (minutes after onset), you may see tall, broad, and peaked T waves in
the anterolateral leads before distinct ST elevation develops.
Pathological Q Waves: As the infarction evolves (hours to days), deep and wide Q waves may develop in leads V3-V6,
I, and aVL, indicating necrosis (tissue death).
Poor R-Wave Progression: Normally, the R wave grows larger as you move from V1 to V6. In an anterolateral MI, the
R waves in V3 and V4 may remain very small or disappear entirely.
3. Reciprocal Changes
ECG leads that look at the heart from the opposite angle often show "mirror image" changes. For an anterolateral MI, you
will typically see:
ST-Segment Depression: Most prominent in the inferior leads (II, III, and aVF).
Summary of Diagnostic Criteria
ST Elevation: V3, V4, V5, V6, I, aVL
Reciprocal ST Depression: II, III, aVF
Culprit Artery: Usually the Left Anterior Descending (LAD) artery or a large Diagonal branch (D1). Less
commonly, it can involve the Left Circumflex (LCx) if it supplies the lateral wall.
Visual Tip: If you see ST elevation stretching across the chest leads (V3-V6) and "high lateral" leads (I, aVL),
combined with ST depression in the bottom leads (II, III, aVF), the diagnosis is highly likely an anterolateral STEMI.
Read more:
LITFL (ST segment): https://litfl.com/st-segment-ecg-library/
LITFL (MI
localization): https://litfl.com/mi-localization-ecg-library/
LITFL (anterior
STEMI): https://litfl.com/anterior-myocardial-infarction-ecg-library/
LITFL (high lateral
STEMI): https://litfl.com/high-lateral-stemi-ecg-library/
LITFL (lateral STEMI): https://litfl.com/lateral-stemi-ecg-library/
Explanation for Wolf-Parkinson-White syndrome (WPW)
Wolf-Parkinson-White (WPW) syndrome is a condition where an extra electrical pathway (accessory pathway) connects the
atria and ventricles, bypassing the AV node. This allows electrical signals to arrive at the ventricles earlier than
normal, leading to "pre-excitation."
The three hallmark signs of WPW on a standard 12-lead ECG are often referred to as the WPW Triad:
1. Short PR Interval
Definition: The time from the start of the P wave to the start of the QRS complex is usually less than 120 ms (
0.12 seconds), or less than 3 small squares.
Why it happens: Normally, the AV node holds the electrical signal briefly to allow the ventricles to fill with
blood. In WPW, the signal travels down the accessory pathway (which has no delay mechanism) and activates the
ventricles early, shortening this interval.
2. Delta Wave
Definition: A slurred or slow-rising upstroke at the very beginning of the QRS complex.
Why it happens: This represents the early, slow depolarization of the ventricular muscle tissue via the accessory
pathway (pre-excitation) before the normal signal from the AV node catches up and rapidly depolarizes the rest of the
ventricles.
3. Wide QRS Complex
Definition: The total duration of the QRS complex is usually greater than 110–120 ms (typically > 0.11 or 0.12
seconds).
Why it happens: The QRS is widened because it is a "fusion beat"—a combination of the early activation from the
accessory pathway (the Delta wave) and the normal activation from the AV node.
Secondary Signs & Classification
Beyond the classic triad, you may see other specific changes depending on the location of the accessory pathway.
Secondary ST-T Wave Changes
Because the depolarization (activation) of the heart is abnormal, the repolarization (recovery) is also abnormal.
You will often see ST-segment depression or T-wave inversion that is discordant (opposite in direction) to the QRS
complex and Delta wave.
"Pseudo-Infarction" Patterns
The abnormal Delta waves can sometimes be negative (pointing down) in certain leads (often inferior leads II, III,
aVF). This can mimic pathological Q waves, leading to a misdiagnosis of a past heart attack (myocardial infarction).
Type A vs. Type B Pattern
Historically, WPW was classified by the appearance of the QRS in the precordial leads (V1–V6), which helps localize
where the extra pathway is located.
Type A (Left-sided pathway):
Positive Delta wave and QRS complex in lead V1.
Looks similar to a Right Bundle Branch Block (RBBB) pattern.
Indicates the pathway is likely on the left side of the heart.
Type B (Right-sided pathway):
Negative Delta wave and QRS complex in leads V1 and V2.
Looks similar to a Left Bundle Branch Block (LBBB) pattern.
Indicates the pathway is likely on the right side of the heart.
Note: It is clinically important to distinguish "WPW Pattern" from "WPW Syndrome." A patient has the Pattern if
they simply have these ECG findings. They are diagnosed with the Syndrome only if they have the ECG
findings plus symptoms of arrhythmias (such as palpitations or SVT).
Read more on
LITFL: https://litfl.com/pre-excitation-syndromes-ecg-library/
Explanation for abnormal QRS (ABQRS)
An abnormal QRS complex on a 12-lead ECG is typically identified by deviations in three main categories: Duration (
width), Amplitude (height/voltage), and Morphology (shape/contour).
1. Abnormal Duration (Wide QRS)
A normal QRS complex lasts between 0.08 and 0.10 seconds (80–100 ms). A duration of > 0.12 seconds (>120 ms or 3
small squares) is considered abnormally wide.
Bundle Branch Blocks (BBB): A blockage in the electrical conduction system causes one ventricle to depolarize
later than the other, widening the QRS.
Right Bundle Branch Block (RBBB): Characterized by an rSR' ("bunny ears") pattern in leads V1–V2 and a
wide, slurred S wave in leads I and V6.
Left Bundle Branch Block (LBBB): Characterized by a deep, broad S wave in V1 and a broad, notched, or "
M-shaped" R wave in leads I, aVL, V5, and V6.
Ventricular Rhythms: Rhythms originating from the ventricles (rather than the atria) do not use the fast
conduction system, resulting in a wide QRS. Examples include Premature Ventricular Complexes (PVCs), Ventricular
Tachycardia (VT), and Idioventricular rhythms.
Hyperkalemia: High potassium levels can slow conduction, leading to a bizarrely wide QRS that may merge with the T
wave (sine-wave pattern).
Wolff-Parkinson-White (WPW) Syndrome: An accessory pathway allows early activation of the ventricles (
pre-excitation), causing a Delta wave (slurring of the initial upstroke) and a widened QRS.
2. Abnormal Amplitude (Voltage)
The height of the QRS complex represents the electrical force generated by the ventricular muscle mass.
High Voltage (Hypertrophy):
Left Ventricular Hypertrophy (LVH): The muscle wall is thickened, generating stronger electrical forces. A
common sign is the Sokolow-Lyon criteria: Depth of S wave in V1 + Height of R wave in V5 or V6 > 35 mm.
Right Ventricular Hypertrophy (RVH): Often causes a dominant R wave in lead V1 (height > 7 mm) and a deep S
wave in V5 or V6.
Low Voltage:
Defined as QRS amplitude < 5 mm in all limb leads and < 10 mm in all precordial (chest) leads.
Causes: Anything that insulates the heart or dampens the signal, such as pericardial effusion (fluid
around the heart), COPD (air trapping), obesity, or hypothyroidism (myxedema).
3. Abnormal Morphology (Shape)
Even if the width and height are normal, the shape of the wave can indicate pathology.
Pathological Q Waves:
Q waves are the first downward deflection of the QRS. While small "septal" Q waves are normal in some leads, *
pathological* Q waves indicate dead myocardial tissue (previous Myocardial Infarction).
Signs: Duration > 0.04 s (40 ms) or depth > 25% of the following R wave height.
Poor R Wave Progression:
Normally, the R wave grows larger as you move from lead V1 to V6. If the R wave remains small or absent in leads
V1–V3, it is termed "poor progression."
Causes: Anterior Myocardial Infarction (old or new), LBBB, or lead misplacement.
Fragmented QRS:
Presence of additional spikes, notches, or slurs within the QRS complex (not fitting a typical BBB pattern). This
often represents myocardial scarring or fibrosis.
Electrical Alternans:
The height of the QRS complex alternates between beats (large, small, large, small). This is a specific sign of a
large pericardial effusion (cardiac tamponade) as the heart swings back and forth in the fluid.
Read more:
LITFL (interventricular conduction
delay): https://litfl.com/intraventricular-conduction-delay-qrs-widening/
LITFL (low QRS
voltage): https://litfl.com/low-qrs-voltage-ecg-library/
Explanation for sinus rhythm (SR)
Identifying Sinus Rhythm on a standard 12-lead ECG is the foundational skill of ECG interpretation. It essentially
means the heart's electrical impulse is originating correctly from the Sinoatrial (SA) node.
To confirm sinus rhythm, you must look for specific signs related to the P wave, the rhythm regularity, and the
conduction intervals.
1. The P Wave (The most critical sign)
The definitive sign of sinus rhythm is the "P wave axis." Because the SA node is located in the top right of the heart,
the electrical current should flow down and to the left.
Lead II: The P wave must be upright (positive). This is the most important lead to check.
Lead aVR: The P wave must be inverted (negative). If the P wave is upright in aVR, the rhythm is likely not
sinus (e.g., it may be a low atrial or junctional rhythm).
Leads I and aVF: P waves are typically upright.
Consistency: The P waves should all look the same (consistent morphology) within a single lead.
2. The Relationship Between P and QRS
The SA node should be driving the ventricles.
1:1 Ratio: Every P wave must be followed by a QRS complex, and every QRS complex must be preceded by a P wave.
PR Interval: The time between the start of the P wave and the start of the QRS complex should be constant and
within normal limits (0.12 to 0.20 seconds, or 3–5 small squares).
3. Rhythm Regularity
Regularity: The distance between R waves (R-R interval) and P waves (P-P interval) should be consistent.
Note: Minor variation is normal due to breathing (called respiratory sinus arrhythmia), but the rhythm should look
visibly regular to the naked eye.
4. Heart Rate
While "Sinus Rhythm" describes the origin of the beat, the rate determines the specific diagnosis:
Normal Sinus Rhythm (NSR): Rate between 60 and 100 bpm.
Sinus Bradycardia: All sinus criteria met, but rate is < 60 bpm.
Sinus Tachycardia: All sinus criteria met, but rate is > 100 bpm.
Summary Checklist
When looking at a 12-lead ECG, you can confidently state "Sinus Rhythm" if:
P waves are upright in Lead II.
P waves are inverted in aVR.
There is a P wave before every QRS.
The rhythm is regular.
Read more on
LITFL: https://litfl.com/normal-sinus-rhythm-ecg-library/