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Diagnostic Code Explanations (4)
Diagnoses for this EKG: anteroseptal myocardial infarction (ASMI), anterolateral myocardial infarction (ALMI), abnormal QRS (ABQRS), sinus rhythm (SR)
Explanation for anteroseptal myocardial infarction (ASMI)
An anteroseptal myocardial infarction (MI) is characterized by ischemia and necrosis affecting the anterior wall of the
left ventricle and the interventricular septum. It typically results from an occlusion of the Left Anterior
Descending (LAD) coronary artery.
On a standard 12-lead ECG, the signs of an anteroseptal MI are primarily observed in the precordial leads V1 through
V4.
Key ECG Findings
ST-Segment Elevation
Leads: The hallmark sign is ST-segment elevation in leads V1, V2, V3, and V4.
Morphology: The elevation is often significant and may evolve into a "tombstone" pattern in severe cases.
Specifics:
Septal leads: V1 and V2.
Anterior leads: V3 and V4.
The involvement of both groups defines the "anteroseptal" pattern.
Q Waves (Pathological)
As the infarction evolves (or if it is age-indeterminate), pathological Q waves will develop in leads V1–V4.
A QS complex (a deep negative deflection with no preceding positive R wave) is commonly seen in V1 and V2.
Poor R-Wave Progression (PRWP)
In a healthy heart, the R wave (the first positive spike of the QRS complex) should get progressively taller as
you move from lead V1 to V6.
In an anteroseptal MI, the destruction of heart muscle in the anterior wall leads to a loss of these positive
forces. Consequently, you will see small or absent R waves in leads V1–V3 (or even up to V4).
T-Wave Changes
Hyperacute Phase: Immediately after occlusion, you may see tall, peaked "hyperacute" T waves in V1–V4 before
ST elevation becomes obvious.
Evolving/Subacute Phase: As the MI progresses, the T waves typically become inverted (negative) in the same
leads (V1–V4).
Reciprocal Changes
Unlike inferior or lateral MIs, pure anteroseptal MIs often lack distinct reciprocal changes (ST depression) in the
standard limb leads.
Why? The electrical "opposite" of the anterior wall is the posterior wall. Standard 12-lead ECGs do not have leads
on the patient's back to record this directly.
Exception: If the infarction extends to the high lateral wall (leads I and aVL), you may see reciprocal ST
depression in the inferior leads (II, III, aVF).
Summary Checklist for Anteroseptal MI
ST Elevation: Leads V1, V2, V3, V4
Q Waves: Developing in V1–V4
R Waves: Loss of height in V1–V3 (Poor R-wave progression)
Reciprocal Changes: usually absent (unless lateral extension is present)
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/
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 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/