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Diagnostic Code Explanations (5)
Diagnoses for this EKG: inferior myocardial infarction (IMI), left ventricular hypertrophy (LVH), atrial premature complex (PAC), Q waves present (QWAVE), sinus tachycardia (STACH)
Explanation for inferior myocardial infarction (IMI)
An inferior myocardial infarction (MI) is a heart attack affecting the inferior wall of the heart, which rests on the
diaphragm. It is most commonly caused by an occlusion of the Right Coronary Artery (RCA), though it can also result
from a blockage in the Left Circumflex Artery (LCx).
On a standard 12-lead ECG, you can identify an inferior MI by looking for specific changes in the "inferior leads" (II,
III, and aVF).
1. Primary Diagnostic Signs
The hallmark of an acute inferior MI is ST-segment elevation in the leads that view the bottom of the heart:
Lead II
Lead III
Lead aVF
Diagnostic Criteria: Significant ST-elevation (usually ≥1 mm) in at least two of these contiguous leads.
2. Reciprocal Changes
Reciprocal changes are "mirror images" of the injury that appear in leads on the opposite side of the heart. These are
critical for confirming the diagnosis and ruling out mimics like pericarditis.
Lead aVL: This is the most sensitive lead for reciprocal changes in an inferior MI. You will typically see *
ST-segment depression* here.
Lead I: Often shows ST-depression as well, though usually less pronounced than in aVL.
3. Identifying the Culprit Artery (RCA vs. LCx)
While an angiogram is definitive, the ECG can offer clues about which artery is blocked:
RCA Occlusion (Most Common):
ST elevation in Lead III > Lead II.
Reciprocal ST depression in Lead I and aVL.
LCx Occlusion:
ST elevation in Lead II ≥ Lead III.
May have ST elevation in lateral leads (I, aVL, V5, V6) or absence of reciprocal depression in Lead I.
4. Associated "Danger" Signs
Inferior MIs are unique because they often extend to other areas of the heart. You must check for these two common
complications immediately, as they change treatment:
A. Right Ventricular (RV) Infarction
Because the RCA supplies the right ventricle in most people, roughly 40% of inferior MIs involve the RV.
ECG Clue: Look at lead V1. If you see ST elevation in V1 (or if V1 is isoelectric while V2 is
significantly depressed), suspect RV involvement.
Action: Perform a Right-Sided ECG. Look for ST elevation in V4R.
Clinical Relevance: These patients are very sensitive to preload-reducing medications (like
nitrates/nitroglycerin), which can cause severe hypotension.
B. Posterior Extension
The infarction may extend to the back of the heart (posterior wall).
ECG Clue: Look at the anterior leads (V1, V2, V3). Instead of ST elevation, you will see the "mirror image":
Horizontal ST depression
Tall, dominant R waves (the mirror of a Q wave)
Upright, prominent T waves (the mirror of T-wave inversion)
Action: Perform a Posterior ECG (leads V7, V8, V9) to confirm ST elevation.
5. Rhythm Disturbances
The RCA supplies the AV node in ~90% of people. Consequently, inferior MIs are frequently associated with:
Bradycardia (slow heart rate).
AV Blocks (First-degree, Wenckebach/Type I, or even Complete Heart Block).
Read more:
LITFL (ST segment): https://litfl.com/st-segment-ecg-library/
LITFL (MI
localization): https://litfl.com/mi-localization-ecg-library/
LITFL (inferior STEMI): https://litfl.com/inferior-stemi-ecg-library/
Explanation for left ventricular hypertrophy (LVH)
The signs of left ventricular hypertrophy (LVH) on a 12-lead ECG generally fall into two categories: **voltage criteria
** (increased amplitude of electrical signals) and non-voltage criteria (changes in wave shape, timing, or axis).
Because the left ventricle is the largest and thickest chamber of the heart, its hypertrophy (thickening) generates
stronger electrical forces that take longer to conduct. This results in taller R waves, deeper S waves, and specific
repolarization abnormalities.
1. Voltage Criteria
These are the most commonly cited signs. While there are many different formulas, the following are the most widely used
in clinical practice.
A. Sokolow-Lyon Criteria
This is the classic "quick check" for LVH.
Formula: Amplitude of S wave in V1 + Amplitude of R wave in V5 or V6 (whichever is taller).
Threshold: A sum ≥ 35 mm (3.5 mV) indicates LVH.
Note: A separate criterion is an R wave in aVL ≥ 11 mm.
B. Cornell Voltage Criteria
This criterion is often considered more accurate (higher sensitivity) than Sokolow-Lyon because it accounts for gender
differences.
Formula: Amplitude of S wave in V3 + Amplitude of R wave in aVL.
Threshold (Men): > 28 mm.
Threshold (Women): > 20 mm.
C. Limb Lead Voltage Criteria
High voltage in the limb leads alone can also indicate LVH.
Lead aVL: R wave ≥ 11 mm.
Lead I: R wave ≥ 14 mm.
Lead aVR: S wave ≥ 14 mm.
2. Non-Voltage Criteria (Supporting Signs)
Voltage criteria alone can sometimes be misleading (e.g., in very thin young patients). The presence of these
non-voltage signs significantly increases the likelihood of true pathological hypertrophy.
A. "Strain" Pattern (ST-T Wave Abnormalities)
This is a sign of repolarization abnormality due to the thickened muscle.
Appearance: You will see ST-segment depression and T-wave inversion in the lateral leads (I, aVL, V5, V6).
Morphology: The depression is often down-sloping with an asymmetric T-wave inversion (the downslope is gradual,
the return to baseline is steep).
Discordance: The ST-T changes are usually "discordant" to the QRS complex (if the QRS is predominantly positive,
the ST/T is negative).
B. Left Axis Deviation (LAD)
The QRS axis is shifted to the left (between -30° and -90°).
On a standard trace: Positive QRS in Lead I, Negative QRS in leads II and aVF.
C. Left Atrial Enlargement (LAE)
Because a stiff, hypertrophied ventricle is harder to fill, the left atrium often enlarges.
Lead II: A "P-mitrale" pattern (a broad, notched M-shaped P wave).
Lead V1: A deep, wide terminal negative portion of the P wave (at least 1mm deep and 1 small box wide).
D. Prolonged R-Wave Peak Time (Intrinsicoid Deflection)
It takes longer for the electrical impulse to travel through the thickened ventricular wall.
Measurement: Time from the onset of the QRS to the peak of the R wave in leads V5 or V6.
Threshold: > 50 ms (more than 1.25 small boxes).
3. The Romhilt-Estes Score
This is a point-scoring system that combines the above features to estimate the probability of LVH.
Definite LVH: 5 or more points.
Probable LVH: 4 points.
Voltage Criteria (Any of: Limb R or S ≥20mm, V1/V2 S ≥30mm, V5/V6 R ≥30mm): 3 points
ST-T Abnormalities (Strain pattern without digoxin): 3 points
Left Atrial Enlargement (Terminal P in V1 ≥1mm deep/wide): 3 points
Left Axis Deviation (≥ -30°): 2 points
QRS Duration (≥ 90 ms): 1 point
Delayed Intrinsicoid Deflection (V5/V6 ≥ 50 ms): 1 point
Summary Checklist
If you suspect LVH, scan the ECG for:
Big Voltages: Deep S in V1/V2 + Tall R in V5/V6.
Strain: Inverted T waves and depressed ST segments in V5, V6, I, and aVL.
Left Axis: Negative QRS in aVF.
Atrial Issues: M-shaped or biphasic P waves.
Note: ECG has high specificity but low sensitivity for LVH. This means if the signs are present, the patient likely has
LVH; however, a normal ECG does not rule out LVH. Echocardiography is the gold standard for confirmation.
Read more on
LITFL: https://litfl.com/left-ventricular-hypertrophy-lvh-ecg-library/
Explanation for atrial premature complex (PAC)
Premature Atrial Complexes (PACs), also known as Premature Atrial Contractions, are early heartbeats originating from an
ectopic focus within the atria (upper chambers) rather than the normal sinus node.
On a standard 12-lead ECG, you can identify them by looking for a specific set of signs involving timing, P-wave
morphology, and the post-beat pause.
1. Timing (Prematurity)
The most defining feature is that the beat occurs earlier than the next expected sinus beat.
If you measure the distance between the two previous R-waves (the R-R interval), the PAC will arrive sooner than that
interval would predict.
This disrupts the regular rhythm, making the heart rate appear irregular.
2. Abnormal P Wave Morphology
Because the electrical impulse originates from a different location in the atria than the sinus node, the path of
depolarization is different. This results in a P wave that looks different from the normal sinus P waves.
Shape: The P wave may be flattened, peaked, notched, biphasic (part positive, part negative), or inverted,
depending on where the ectopic focus is located.
Axis: The axis of the P wave may change (e.g., becoming negative in leads where it is usually positive, like II,
III, and aVF).
"Buried" P Waves: If the PAC is very premature, the P wave may be hidden within the T wave of the preceding beat.
This often creates a "camel hump" appearance or makes the T wave look taller and more pointed than usual. Always
scrutinize the T wave of the preceding beat if you see a pause.
3. PR Interval
The PR interval of a PAC is often different from the normal sinus PR interval.
Normal or Prolonged: It is usually normal (0.12–0.20s) but can be prolonged if the AV node is still partially
refractory (recovering) from the previous beat.
Shortened: It may be shorter than the sinus PR interval if the ectopic focus is located closer to the AV node (low
atrial origin).
4. QRS Complex Characteristics
The QRS complex usually follows the P wave and typically looks identical to the patient’s normal sinus QRS complex (
narrow, <0.12s). This is because the impulse travels down the normal conduction pathways (His-Purkinje system) once it
passes the AV node.
However, there are two important variations:
Aberrant Conduction: If the PAC arrives very early, one of the bundle branches (usually the right) may still be
refractory. This forces the impulse to travel down the other bundle, resulting in a wide QRS complex that
resembles a Bundle Branch Block pattern.
Non-Conducted (Blocked) PAC: If the PAC arrives so early that the AV node is completely refractory, the impulse is
blocked entirely. You will see a premature, abnormal P wave (often deforming the preceding T wave) followed by a *
pause* with no QRS complex.
5. Non-Compensatory Pause
Following the PAC, there is usually a pause before the next normal sinus beat occurs.
Resetting the SA Node: PACs typically depolarize the sinus node prematurely, "resetting" its internal clock.
Because of this reset, the pause is usually non-compensatory (or incomplete).
Measurement: The interval between the beat before the PAC and the beat after the PAC is less than two full
normal cardiac cycles (2x P-P interval).
Read more on LITFL: https://litfl.com/premature-atrial-complex-pac/
Explanation for Q waves present (QWAVE)
In a standard 12-lead ECG, a Q wave is defined as the first negative deflection of the QRS complex that is not
preceded by any positive deflection (R wave). If there is any positive wave before the dip, that dip is an S wave, not a
Q wave.
While small Q waves can be normal in certain leads, "pathological" Q waves are a key sign of myocardial infarction (
heart attack) or other structural heart issues.
The following breakdown details how to identify Q waves and distinguish normal from abnormal.
1. Identifying a Q Wave
Visual Check: Look at the QRS complex. Does it start immediately with a downward line? That is a Q wave.
QS Complex: If the entire QRS complex is just one deep downward stroke with no upward R wave at all, this is
called a QS complex and is considered a Q wave equivalent.
2. Normal (Physiological) Q Waves
Not all Q waves are bad. Normal "septal" Q waves represent the normal depolarization of the interventricular septum (
from left to right).
Appearance: Narrow (short duration) and shallow.
Duration: Less than 0.03 seconds (less than 1 small box).
Amplitude: Less than 25% of the height of the following R wave.
Location: Commonly seen in the lateral leads (I, aVL, V5, V6).
Note: Deep Q waves can be normal in lead aVR (because it looks at the heart from the opposite angle) and
sometimes in lead III (especially if they disappear when the patient takes a deep breath).
3. Pathological (Abnormal) Q Waves
Pathological Q waves usually indicate that there is an electrical "hole" in the heart tissue, often scar tissue from a
previous myocardial infarction (MI). Since dead tissue cannot conduct electricity, the electrode "looks through" the
dead patch and records the electrical forces moving away from it on the opposite side of the heart, resulting in a deep
negative deflection.
Criteria for Pathological Q Waves:
Duration (Width): ≥ 0.04 seconds (1 small box or wider). This is the most specific sign of pathology.
Amplitude (Depth): ≥ 2 mm deep OR > 25% of the height of the subsequent R wave.
Location:
Leads V1–V3: Any Q wave in these leads (except a QS complex in V1) is generally considered abnormal.
Contiguity: To be significant, Q waves must appear in two or more contiguous leads (leads that look at the
same area of the heart).
4. Locating the Damage (Infarct Localization)
The leads where pathological Q waves appear tell you which part of the heart has scarring:
Inferior: II, III, aVF (Right Coronary Artery - RCA)
Lateral: I, aVL, V5, V6 (Left Circumflex - LCx)
Anterior: V3, V4 (Left Anterior Descending - LAD)
Septal: V1, V2 (Left Anterior Descending - LAD)
Posterior: Tall R wave in V1, V2* (RCA or LCx)
(Note: Posterior MI is often indicated by a "reciprocal" change: a tall, wide R wave in V1 or V2, which is
essentially an upside-down Q wave.)
5. Other Causes of Q Waves (Mimics)
While a prior heart attack is the most common cause, other conditions can create Q waves or Q-wave-like patterns:
Lead Placement Errors: Switching limb leads can create fake Q waves.
Left Bundle Branch Block (LBBB): Can cause QS complexes in leads V1–V3.
Ventricular Hypertrophy (LVH/RVH): Enlarged heart muscle can distort electrical forces, creating deep Q waves in
certain leads.
Wolff-Parkinson-White (WPW) Syndrome: The delta wave (pre-excitation) can sometimes be negative, mimicking a Q
wave (pseudo-Q wave).
Pulmonary Embolism: Classic "S1Q3T3" pattern includes a Q wave in lead III.
Read more on LITFL: https://litfl.com/q-wave-ecg-library/
Explanation for sinus tachycardia (STACH)
To identify sinus tachycardia on a standard 12-lead ECG, you must confirm that the rhythm originates from the sinus
node (normal P-wave morphology) but fires at a rate faster than 100 beats per minute.
The following is a breakdown of the specific signs and criteria.
1. Heart Rate
Rate: > 100 beats per minute (bpm).
Typical Range: Usually between 100 and 160 bpm.
Note: In extreme physical stress or younger patients, it can exceed 160 bpm. If the rate is resting and >140-150
bpm, clinicians often consider other tachyarrhythmias (like atrial flutter or SVT) until P waves are clearly
identified.
2. Rhythm
Regularity: The rhythm is regular. The R-R intervals (distance between consecutive QRS complexes) are constant.
Onset/Termination: unlike other supraventricular tachycardias (which start/stop abruptly), sinus tachycardia
typically has a gradual onset ("warm-up") and gradual termination ("cool-down").
3. P-Wave Morphology (The Key Identifier)
To confirm the rhythm is "Sinus," the P waves must show that depolarization is starting in the Sinoatrial (SA) node and
moving downward and to the left.
Lead II: Upright (positive) P wave. This is the most important lead to check.
Lead aVR: Inverted (negative) P wave.
Leads I and aVF: Typically upright (positive).
Consistency: All P waves look identical (monomorphic) and clearly precede every QRS complex.
4. Intervals
PR Interval: Normal duration (0.12 – 0.20 seconds) and constant.
Note: As the heart rate increases, the PR interval naturally shortens slightly but usually remains within the
normal range.
QRS Complex: Narrow (< 0.12 seconds), assuming there is no pre-existing bundle branch block.
QT Interval: Shortens as the heart rate increases (rate-related shortening).
5. Visual Challenges at High Rates
"Camel Hump" Appearance: At very fast rates (>140 bpm), the P wave may occur so early that it falls on top of the
preceding T wave. This creates a fused "camel hump" look between the T wave and P wave. If the P wave becomes
completely buried in the T wave, it can be difficult to distinguish sinus tachycardia from a re-entrant SVT.
Clinical Context Note: Sinus tachycardia is usually a symptom of an underlying physiological stressor (e.g.,
fever, pain, dehydration, anxiety, exercise, PE) rather than a primary cardiac arrhythmia. Treatment focuses on the
underlying cause, not the rhythm itself.
Read more on LITFL: https://litfl.com/sinus-tachycardia-ecg-library/