EKG/ECG Interpretation — Comprehensive Reference

Electrocardiography (ECG/EKG) — Comprehensive Reference

Based on The Only EKG Deck You'll Ever Need (488 cards)

#### 1. EKG Basics — Paper & Measurement

Standard Settings:

• Speed: 25 mm/s (standard); sometimes 50 mm/s for faster rhythms
• Voltage: 10 mm/mV (standard calibration)
• Time: 1 small square (1 mm) = 0.04 sec; 1 large square (5 mm) = 0.2 sec
• Voltage: 1 small square (1 mm) = 0.1 mV; 1 large square (5 mm) = 0.5 mV

Heart Rate Calculation (Regular Rhythm): | Method | Formula |

--------	---------
Big box method	300 / number of large squares between R-waves

Small box method	1500 / number of small squares between R-waves
6-second method	Number of cycles in 6 sec × 10 (for 60 sec)

Normal Values:

Parameter	Normal Duration	Normal Amplitude

P-wave | <0.12 sec (3 small squares) | <2.5 mm in limb leads |

PR-interval	0.12-0.20 sec (3-5 small squares)	—
QRS-interval	0.06-0.12 sec (1.5-3 small squares)	Variable

QT-interval	<0.44 sec (or <½ of R-R interval)	—
T-wave	Variable	1/3 to 2/3 of R-wave amplitude

#### 2. Wave Morphology

P-Wave (Atrial Depolarization):

• Right atrium depolarizes BEFORE left atrium
• First part of P-wave = right atrial depolarization; second part = left atrial depolarization
• Normally small and positive in left lateral leads (I, aVL, V5-V6) and inferior leads (II, III, aVF)
• Often biphasic in leads III and V1
• Most positive in lead II; most negative in lead aVR
• P-wave axis: normal 0° to 75° (adults); wider in children

QRS Complex (Ventricular Depolarization):

Deflection	Description

Q-wave | First downward deflection |

R-wave	First upward deflection
S-wave	First downward deflection after an upward deflection

R' (R-prime)	Second upward deflection
QS-wave	Entire QRS is one downward deflection

• Septal depolarization produces small initial Q-waves in left lateral leads (I, aVL, V5-V6)
• Normal QRS-interval 0.06-0.12 sec

R-Wave Progression:

• Lead V1 has the smallest R-wave; by V5-V6 R-waves are largest
• Normal transition zone (where R = S) is at V3 or V4
• R-wave progression should be gradual and continuous
• Poor R-wave progression may suggest anterior infarction

T-Wave (Ventricular Repolarization):

• Amplitude normally 1/3 to 2/3 of corresponding R-wave
• Should be upright in most leads except aVR (always inverted)
• Inverted T-waves are normal variants in: V1, V2, V3 (children and young adults), III (isolated), aVR (always)

U-Wave:

• Small deflection following the T-wave
• Prominent in hypokalemia, CNS disease, certain medications
• Best seen in leads V2-V3

#### 3. Leads & Axis Determination

#### Detailed Axis Determination — The Thumb Method

• Lead I Left thumb: Lead I positive → left thumb UP; Lead I negative → left thumb DOWN
• Lead aVF Right thumb: aVF positive → right thumb UP; aVF negative → right thumb DOWN
• Normal axis: Both thumbs UP (or left UP, right UP with some exceptions)
• Left axis deviation: Left UP, Right DOWN (Lead I positive, aVF negative, axis -30 to -90)
• Right axis deviation: Left DOWN, Right UP (Lead I negative, aVF positive, axis +90 to +180)
• Extreme right axis: Both thumbs DOWN (Lead I negative, aVF negative, axis -90 to -180)

Finding Precise Axis:

Find the lead where QRS is most biphasic (isoelectric) — axis is perpendicular to that lead

Check if the axis is toward the positive or negative quadrant using an adjacent lead

Example: Most biphasic in aVL (-30°) → axis could be +60° or -120°. Check lead II (+60°) — if positive, axis is +60°

What is the axis? Practice:

• QRS positive in I, positive in aVF → NORMAL axis (0° to +90°)
• QRS positive in I, negative in aVF → LEFT axis deviation (-30° to -90°)
• QRS negative in I, positive in aVF → RIGHT axis deviation (+90° to +180°)
• QRS negative in I, negative in aVF → EXTREME right axis (-90° to -180°)
• P-wave axis normal: 0° to 75° (P positive in II, negative in aVR, may be biphasic in III and V1)
• T-wave axis should be within 50-60° of the QRS axis

#### Enhanced Chamber Hypertrophy Criteria

RVH Criteria (more specific):

Right axis deviation with QRS axis >+90° (or >+110° for more specificity)

R-wave > S-wave in lead V1 (R/S > 1 in V1)

S-wave > R-wave in lead V6 (R/S < 1 in V6)

Secondary ST depression and T-wave inversion in right precordial leads (V1-V3)

May have right atrial enlargement (P pulmonale) as associated finding

Common causes: Pulmonary disease (COPD, PE), congenital heart disease (ASD, VSD), pulmonary hypertension, mitral stenosis

LVH Criteria (expanded):

Criterion	Measurement	Specificity

Sokolow-Lyon (precordial) | R in V5 or V6 + S in V1 > 35 mm | ~85% |

Cornell (gender-adjusted)	R in aVL + S in V3 > 20 mm (F), >28 mm (M)	~95%
R in aVL	> 11 mm	Moderate

R in aVF	> 20 mm	Moderate
R in I	> 13 mm	Moderate

Left axis deviation	> -15°	Associated
Romhilt-Estes score	Point system	Structural LVH

• LVH criteria are highly specific (~90% when positive) but not sensitive
• Less reliable in patients <35 years (normal variant high voltage)
• Leading causes: Systemic hypertension, aortic stenosis, hypertrophic cardiomyopathy
• Secondary repolarization changes: Asymmetric ST depression + T-wave inversion in left lateral leads (V5-V6, I, aVL)
• Asymmetric T inversion = secondary repolarization (vs symmetric = ischemia)

Limb Leads (Hexaxial System):

Lead	Positive Electrode	Angle

I | Left arm (+) | 0° |

II	Left leg (+)	+60°
III	Left leg (+) vs left arm (-)	+120°

aVR	Right arm (+)	-150° (or +210°)
aVL	Left arm (+)	-30°

| aVF | Left leg (+) | +90° |

Limb Lead Groups:

Lead Group	Leads	View of Heart

Inferior | II, III, aVF | Inferior surface |

Left lateral	I, aVL, V5-V6	Left lateral wall
Right-sided	aVR (the only true right-sided lead)	Right side

Precordial Leads:

Lead	Placement	Views

V1 | Right 4th ICS, sternal border | Right ventricle |

V2	Left 4th ICS, sternal border	Septum
V3	Between V2 and V4	Anterior

V4	Left 5th ICS, midclavicular line	Anterior
V5	Left 5th ICS, anterior axillary line	Left lateral

| V6 | Left 5th ICS, midaxillary line | Left lateral |

Axis Determination Method:

Check leads I and aVF:

- Normal axis: Lead I positive AND aVF positive (0° to +90°) - Left axis deviation: Lead I positive AND aVF negative (-30° to -90°) - Right axis deviation: Lead I negative AND aVF positive (+90° to +180°) - Extreme right axis: Lead I negative AND aVF negative (-90° to -180°)

For precise axis: find the lead with most biphasic (isoelectric) QRS — axis is perpendicular to that lead

Axis Ranges:

Axis Type	Degrees	Clinical Associations

Normal | -30° to +90° | — |

Left axis deviation	-30° to -90°	LVH, left anterior fascicular block, inferior MI
Right axis deviation	+90° to +180°	RVH, COPD, pulmonary embolism, left posterior fascicular block

| Extreme right axis | -90° to -180° | Severe RVH, hyperkalemia, lead reversal |

P-Wave Axis: Normal 0° to 75°; abnormal axis may suggest ectopic atrial focus or retrograde activation T-Wave Axis: Should approximate QRS axis within 50-60°

#### 4. Chamber Hypertrophy & Enlargement

Right Atrial Enlargement (P Pulmonale):

• P-wave amplitude >2.5 mm in inferior leads (II, III, aVF)
• NO change in P-wave duration (normal <0.12 sec)
• Tallest P-wave may be in aVF or III instead of lead II
• Usually caused by pulmonary disease, pulmonary hypertension

Left Atrial Enlargement (P Mitrale):

• Terminal (negative) portion of P-wave in V1: depth ≥1 mm AND width ≥0.04 sec
• Increased P-wave duration (>0.12 sec) — bifid P-wave in lead II
• Usually caused by mitral valve disease (stenosis), LV failure

Right Ventricular Hypertrophy (RVH):

Criterion	Finding

Axis | Right axis deviation (>+90°) |

V1 R-wave	R-wave > S-wave in V1
R/S ratio	R/S >1 in V1

Causes	Pulmonary disease, congenital heart disease, PE
Secondary changes	ST depression, T-wave inversion in right precordial leads

Left Ventricular Hypertrophy (LVH):

Criterion	Finding	Specificity

Precordial (Sokolow-Lyon) | R in V5/V6 + S in V1/V2 >35 mm | 85% |

Limb (Cornell)	R in aVL + S in V3 >20 mm (F) or >28 mm (M)	95%
R in aVL	>11 mm	Moderate

R in aVF	>20 mm	Moderate
R in I	>13 mm	Moderate

| Left axis deviation | >-15° | Associated |

• LVH criteria are highly specific (~90%) but poorly sensitive
• Less reliable in patients <35 years (frequent increased voltage normally)
• Leading causes: Systemic hypertension, aortic stenosis
• Secondary repolarization abnormalities (asymmetric T-wave inversion) may accompany severe hypertrophy

Biventricular Hypertrophy:

• May show combination of features (LVH criteria + right axis deviation)
• Often one ventricle dominates the EKG pattern

#### 5. Bundle Branch Blocks

Right Bundle Branch Block (RBBB):

Feature	Description

QRS duration | ≥0.12 sec |

V1	rsR' pattern ("rabbit ears")
V6	Wide S-wave

ST-T	Discordant (opposite to QRS direction)
Causes	PE, ASD, coronary disease, LVH, normal variant

Left Bundle Branch Block (LBBB):

Feature	Description

QRS duration | ≥0.12 sec |

V1	Deep S-wave
V6	Notched/broad R-wave (no Q-wave)

ST-T	Discordant
New LBBB	May signify acute MI — treat as STEMI equivalent

| Causes | Hypertension, CAD, aortic valve disease, cardiomyopathy |

Fascicular Blocks:

• Left Anterior Fascicular Block (LAFB): Left axis deviation (-45° to -90°), qR in I, rS in II/III/aVF
• Left Posterior Fascicular Block (LPFB): Right axis deviation (+90° to +180°), rS in I, qR in II/III/aVF — rare, must exclude RVH

#### 6. Myocardial Ischemia & Infarction

Evolution of STEMI (Typical Progression):

Stage	Timing	EKG Findings

Hyperacute | Minutes to hours | Tall, peaked T-waves ("hyperacute T-waves") |

Acute	Hours to days	ST-segment elevation, evolving Q-waves
Evolving	Days to weeks	Deep Q-waves, T-wave inversion, ST returns to baseline

| Established | Weeks+ | Persistent Q-waves (may ↓ over time), upright T-waves |

Infarction Localization:

Location	Leads with Changes	Culprit Artery

Anterior | V2-V4 | Left anterior descending (LAD) |

Septal	V1-V2	LAD (septal branches)
Lateral	I, aVL, V5-V6	Left circumflex (LCx)

Inferior	II, III, aVF	Right coronary artery (RCA)
Posterior	Tall R in V1-V2 (reciprocal)	RCA or LCx

Anterolateral	Anterior + lateral leads	Left main or LAD + LCx
Right ventricle	V4R (right-sided leads) + inferior	RCA

Posterior MI:

• Tall R-wave in lead V1 (R/S >1) is a key clue
• Must differentiate from RVH: RVH has right axis deviation, posterior MI does not
• Also look for ST depression in V1-V3 suggestive of posterior injury

Reciprocal Changes:

• ST depression in leads opposite to the infarct territory
• e.g., Anterior STEMI → reciprocal ST depression in inferior leads
• Very helpful for confirming STEMI when ST elevation is subtle

NSTEMI:

• Only T-wave inversion and ST-depression (no ST elevation)
• May have deep T-wave inversions in multiple leads
• No new Q-waves (by definition)

Special Patterns:

Pattern	Description	Significance

deWinter T-waves | Upsloping ST depression → tall, symmetric hyperacute T-waves in precordial leads | ~2% of acute LAD occlusions |

Wellens T-waves	Deep, symmetric T-wave inversion in V2-V3	Critical LAD stenosis — high risk
S1Q3T3	S-wave I, Q-wave III, T-inversion III	Acute pulmonary embolism

LVH with strain	Asymmetric T-inversion + ST depression	LV "strain" pattern
Takotsubo	Mimics acute STEMI exactly (no distinction)	Broken heart syndrome, stress-induced

STEMI vs Early Repolarization (J point elevation):

• STEMI: ST elevation has upward convexity, reciprocal changes, evolves over time
• J point elevation: Concave upward ST elevation, no reciprocal changes, stable pattern
• J point elevation common in young, healthy individuals (especially V1-V3)

STEMI Diagnosis Criteria:

#### Detailed MI Localization & Specific Patterns

Infarct Localization with Lead-Specific Changes:

Location	ST Elevation In	Reciprocal ST Depression In	Culprit Artery

Anterior | V2-V4 | II, III, aVF | LAD |

Extensive anterior	V1-V6, I, aVL	II, III, aVF	Left main or proximal LAD
Septal	V1-V2	None specific	LAD (septal)

Anteroseptal	V1-V4	II, III, aVF	LAD
Anterolateral	V3-V6, I, aVL	II, III, aVF	LAD + LCx or left main

Lateral	I, aVL, V5-V6	II, III, aVF	LCx or diagonal branch
High lateral	I, aVL	II, III, aVF	Diagonal branch

Inferior	II, III, aVF	I, aVL	RCA (80%) or LCx (20%)
Posterior	Tall R in V1-V2, ST↓ V1-V3	Anterior leads	RCA or LCx

| Right ventricle | V4R, ST↑ V1 + inferior | — | RCA (proximal) |

Posterior MI — Key Differentiating Points:

• Tall R-wave in V1 (R/S > 1) is hallmark
• ST depression in V1-V3 (reciprocal of posterior ST elevation)
• Distinguish from RVH: RVH has right axis deviation (>+90°), posterior MI has normal axis

Right Ventricle Infarction:

• Always accompanies inferior MI (RCA proximal occlusion)
• ST elevation in V1 plus inferior leads
• Use right-sided leads (V4R) for best sensitivity
• Key clinical clue: Hypotension with inferior MI → suspect RV involvement
• Avoid nitrates and diuretics — they reduce preload and worsen hypotension

Wellens T-Waves:

• Deep, symmetric T-wave inversion in V2-V3 (may extend to V1, V4-V6)
• Usually biphasic or deeply inverted
• Indicates critical proximal LAD stenosis
• High risk for anterior MI — requires urgent catheterization
• Pain-free interval with T-wave changes

deWinter T-Waves:

• Upsloping ST depression at J point → tall, symmetric, hyperacute T-waves in precordial leads
• Represents ~2% of acute LAD occlusions
• No ST elevation! Easy to miss

Takotsubo Cardiomyopathy (Broken Heart Syndrome):

• EKG indistinguishable from acute anterior STEMI
• ST elevation, T-wave inversions, sometimes Q-waves
• Caused by emotional or psychological stress
• Usually resolves with transient heart failure
• More common in postmenopausal women
• No obstructive coronary artery disease on angiography

S1Q3T3 Pattern (Acute PE):

• S-wave in lead I, Q-wave in lead III, T-wave inversion in lead III
• May also have: Right axis deviation, RVH pattern, RBBB (transient), sinus tachycardia
• Low voltage in all leads with pericardial effusion

Age/Gender	ST Elevation in V2-V3	All Other Leads

Men ≤40 | ≥2.5 mm | ≥1 mm |

Men >40	≥2.0 mm	≥1 mm
Women	≥1.5 mm	≥1 mm

#### 7. Arrhythmias — Systematic Approach

4 Questions for Rhythm Assessment:

#### Rhythm Differentiation — Key Pearls

Narrow Complex Tachycardia (QRS < 0.12 sec):

Regularity	Likely Rhythm	Key Features

Regular | Sinus tachycardia | P-waves present, normal axis, gradual onset/offset |

Regular	AVNRT (PSVT)	P-waves buried/pseudo-R'/retrograde, sudden onset
Regular	Atrial flutter	Saw-tooth flutter waves, 2:1, 3:1, 4:1 conduction

Regular	Atrial tachycardia	Abnormal P-waves, may have variable block
Irregularly irregular	Atrial fibrillation	No P-waves, chaotic baseline

| Irregular | Multifocal atrial tachycardia | ≥3 different P-wave morphologies |

Wide Complex Tachycardia (QRS > 0.12 sec):

• VT vs SVT with aberrancy — This is a critical differentiation
• Clues for VT:

1. AV dissociation (P-waves independent of QRS) 2. Fusion beats 3. Capture beats 4. Concordance (all precordial leads positive or all negative) 5. Extreme axis deviation (-90° to -180°) 6. RS > 100 ms in any precordial lead 7. Positive or negative concordance across precordial leads

• Clues for SVT with aberrancy:

1. P-waves related to QRS (1:1 relationship) 2. Typical RBBB or LBBB pattern 3. Previous EKG with similar aberrancy

Atrial Fibrillation — The 4 Most Common Cardiovascular Causes:

Hypertension

Coronary artery disease (CAD)

Mitral valve disease (especially mitral stenosis)

Heart failure (HF)

AVNRT (AV Nodal Reentrant Tachycardia):

• Most common PSVT (regular, narrow-complex, 150-250 bpm)
• Usually triggered by a PAC
• P-waves: Usually buried in QRS (most common), pseudo-R' in V1, or retrograde P-waves in II/III
• Vagal maneuvers (carotid massage) can help diagnose and terminate
• Can occur in healthy hearts with no structural disease

Are normal P-waves present?

Are the QRS complexes narrow or wide?

What is the relationship between P-waves and QRS complexes?

Is the rhythm regular or irregular?

Key Distinctions:

• Narrow QRS (≤0.12 sec) → origin at or above AV node
• Wide QRS (>0.12 sec) → origin below AV node (ventricular) or bundle branch block
• Normal P-QRS correlation → rhythm originates in atria (SA node or atrial focus)
• AV dissociation → atria and ventricles are independent

Sinus Rhythms: | Rhythm | Rate | P-Wave | Regularity |

--------	------	--------	------------
Normal sinus	50-100 bpm	Normal, one per QRS	Regular

Sinus tachycardia	>100 bpm	Normal	Regular
Sinus bradycardia	<50 bpm	Normal	Regular

Sinus arrhythmia	50-100 bpm	Normal	Slightly irregular (varies with respiration)
Sinus arrest/exit block	Variable	Missing pauses	Irregular with pauses

Atrial Arrhythmias: | Rhythm | Rate | P-Wave | QRS | Regularity |

--------	------	--------	-----	------------
Atrial fibrillation	Variable	Absent (fibrillatory baseline)	Narrow	Irregularly irregular

Atrial flutter	250-350/min (atrial)	Saw-tooth pattern	Narrow	Usually regular (2:1, 3:1, 4:1 block)
Atrial tachycardia	150-250/min (atrial)	Abnormal shape, one per QRS	Narrow	Regular

AVNRT (PSVT)	150-250/min	Buried/pseudo-R'/retrograde	Narrow	Regular
WPW/AVRT	Variable	Short PR, delta wave	Narrow or wide	Regular

| PAC | — | Abnormal P contour | Narrow | Premature, resets rhythm |

AVNRT (AV Nodal Reentry Tachycardia):

• Sudden onset, often triggered by PAC
• Regular, narrow-complex tachycardia (150-250 bpm)
• P-waves buried in QRS (most common), pseudo-R' in V1, or retrograde P-waves in II/III
• Carotid massage can help diagnose and terminate
• Can occur in healthy hearts

Junctional Rhythms:

Feature	Junctional Escape	Junctional Premature

Timing | Late (after pause) | Early (before next expected beat) |

P-wave	No P-wave or retrograde	No P-wave or retrograde
Rate	40-60 bpm	—

| Clinical significance | Benign escape mechanism | Benign |

Premature Beats:

Beat	Origin	P-Wave	QRS	Reset

PAC | Atrial | Abnormal P contour | Narrow | Usually resets |

Junctional premature	Near AV node	Absent/retrograde	Narrow	Usually resets
PVC	Ventricular	None (dissociated)	Wide (>0.12 sec)	Compensatory pause

Ventricular Arrhythmias:

Rhythm	Rate	QRS	Pattern

Ventricular tachycardia (VT) | 100-250 bpm | Wide (>0.12 sec) | Regular |

Torsades de pointes	150-250 bpm	Wide, twisting around baseline	Irregular
Ventricular fibrillation	—	Chaotic, no organized QRS	Chaotic

PVC	—	Wide, bizarre	Premature with compensatory pause
Ventricular escape	20-45 bpm	Wide	Late (rescue beats)

| Accelerated idioventricular rhythm | 45-100 bpm | Wide | Regular |

Heart Block:

Type	PR-Interval	Dropped Beats	Conduction

First-degree AV block | >0.20 sec | None | All conducted, just slow |

Second-degree Mobitz I (Wenckebach)	Progressive ↑	Yes	P:QRS ratio increases until dropped
Second-degree Mobitz II	Fixed (normal or prolonged)	Yes	Suddenly dropped without PR lengthening

Third-degree (complete)	Variable (dissociated)	Complete	No P-QRS correlation
2:1 AV block	Variable	Every other P	Can't classify as I or II without longer tracing

| High-grade AV block | — | ≥2 consecutive dropped | Advanced block |

Atrial Fibrillation:

• Most common and clinically significant sustained arrhythmia
• Key: Irregularly irregular QRS + no discrete P-waves
• Cardiovascular causes: Hypertension, CAD, mitral valve disease, heart failure (PALS-HF mnemonic)
• Lifestyle risk factors: Obesity, excessive alcohol
• Risk of thromboembolism (CHADS₂-VASc score) → anticoagulation

Atrial Flutter:

• Reentrant circuit around tricuspid annulus
• Classic saw-tooth pattern in II, III, aVF
• Counterclockwise (most common): negative flutter waves in II, III, aVF
• Ventricular rate varies with conduction ratio (2:1, 3:1, 4:1)

#### 8. Pre-excitation Syndromes

Wolff-Parkinson-White (WPW):

• Accessory pathway (bundle of Kent) bypassing AV node
• Short PR interval (<0.12 sec) + delta wave (slurred upstroke of QRS) + wide QRS
• Associated tachyarrhythmias: AVRT (most common), atrial fibrillation
• Atrial fibrillation in WPW can degenerate to VF (accessory pathway conducts at very high rates)
• Treatment: Catheter ablation

Lown-Ganong-Levine (LGL):

• Short PR interval WITHOUT delta waves
• Diagnosis requires documented tachyarrhythmia

#### 9. Electrolyte & Drug Effects

Hyperkalemia (Progressive Changes):

K+ Level	EKG Changes

Mild (5.5-6.5) | Tall, peaked T-waves (widespread, all leads) |

Moderate (6.5-7.5)	PR prolongation → P-wave flattening/disappearance
Severe (7.5-8.5)	Wide QRS, extreme right axis deviation

| Critical (>8.5) | Sine wave → VF/asystole |

• Hyperkalemia clue: Rightward axis (negative QRS in I, positive in aVF)

Hypokalemia:

K+ Level	EKG Changes

Mild (3.0-3.5) | ST depression, flattened T-waves |

Moderate (2.5-3.0)	U-wave appearance, prolonged QU interval
Severe (<2.5)	ST elevation (rare), arrhythmias

• U-wave becomes prominent as T-wave flattens

Calcium Abnormalities:

Abnormality	QT Interval	Risk

Hypocalcemia | ↑ Prolonged QT | Torsades de pointes | | Hypercalcemia | ↓ Shortened QT | — |

Digitalis (Digoxin):

• Therapeutic: ST-segment depression with gradual downslope ("digitalis effect"), T-wave flattening/inversion
• Toxic: PAT (paroxysmal atrial tachycardia) with block is most characteristic; also PVCs, junctional tachy, AV block
• Slows conduction through AV node
• Can suppress sinus node

#### 10. Pericarditis & Other Conditions

Acute Pericarditis:

• Diffuse (widespread) ST-segment elevation, concave upward
• PR-interval depression (early sign)
• Later T-wave flattening/inversion
• No reciprocal changes (unlike STEMI)
• Differentiate from STEMI: Pericarditis is diffuse (not in a single territory), concave upward

Pericardial Effusion:

• Low voltage in all leads (QRS <0.5 mV limb, <1.0 mV precordial)
• Electrical alternans (alternating QRS amplitude) — highly specific

Pulmonary Embolism:

• S1Q3T3 pattern (S in I, Q in III, T inversion in III)
• RVH pattern, right axis deviation
• Right bundle branch block (may be transient)
• Sinus tachycardia

Chronic Obstructive Pulmonary Disease (COPD):

• Low voltage
• Right axis deviation
• Poor R-wave progression in precordial leads

Hypothermia:

• Bradycardia
• Prolongation of all intervals
• Osborn waves (J waves) — prominent deflection at J point, best seen in II, V5-V6
• Muscle tremor artifact (may simulate atrial flutter/flutter)

Brugada Pattern:

Feature	Description

V1-V3 | ST elevation

(coved type) |

V1	RBBB pattern with slow descent of R'
V1-V2	T-wave inversion

| Clinical | Risk of sudden cardiac death (Brugada syndrome) |

Central Nervous System (CNS) Events:

• Subarachnoid bleed, CVA, head trauma
• Diffuse T-wave inversions plus QT prolongation
• Prominent U-waves

#### 11. Systematic 9-Step EKG Interpretation

Heart rate: Calculate (300 method or 6-second method)

Rhythm: Regular? P-waves present? P-QRS relationship?

Axis: Check I and aVF → normal, LAD, or RAD

Intervals: PR, QRS, QT

Conduction blocks: LBBB, RBBB, fascicular, AV block

Hypertrophy/Enlargement: LVH, RVH, atrial enlargement

ST-T Changes: Ischemia, injury, electrolyte, digoxin, pericarditis

Q-waves: Significant? Pathological?

Comparison with prior EKG: New changes?