Category: EKG- Summing it up

EKG Finding	Differentials
RAD (Right Axis Deviation)	Normal Variation: vertical heart with an axis of 90º Right Ventricular Hypertrophy (RVH) Right heart strain (e.g. PE) Left Posterior Fascicular Block Pre-excitation Syndrome (Wolff-Parkinson-White) Lateral Wall Myocardial Infarction
LAD (Left Axis Deviation)	Normal Variation Left ventricular hypertrophy Left bundle branch block Left anterior fascicular block Pre-excitation syndromes (Wolff-Parkinson-White) Inferior wall myocardial infarction
Early R-wave progression	Posterior MI RVH RBBB WPW
Poor R-wave progression	Anterior MI LVH RVH Cor-pulmonale
Important differentials for Q waves	MI LVH RVH Cor-pulmonale (Q waves in inferior and anterior leads) Cardiomyopathy
Important ST-T changes	Non-specific ST-T changes: < 1 mm ST elevation/ depression; flat T- waves or < 1 mm inversion of T- waves MI/ Angina Pericarditis Early repolarization Juvenile T waves LVH: ST depression and T- inversion, typically in I, aVL, V5, V6. Can be seen in other leads as well RVH: ST depression and T- inversion, typically in V1-3 Bundle Branch blocks Persistent ST- elevation (Usually present for over 3 weeks): Consider ventricular aneurysm
Peaked T-waves	Hyperkalemia MI Intracranial bleed LVH/ RVH LBBB
Deep T-waves	MI Intracranial bleed LVH/ RVH Takusubo cardiomyopathy Apical Hypertrophic cardiomyopathy Digoxin ST elevation in aVR with ST depression in multiple leads: suspect 3 vessel disease or left main disease
Short QTc	Hypercalcemia, Hyperkalemia, Congenital
Long QTc	Drugs Antiarrhythmics: IA, IC, III Antipsychotics, tricyclics Methadone Antibiotics: Floroquinolones, Macrolides Fluconazole Most antiemetics Hypocalcemia (T- waves usually normal) Hypomagnesemia Hypokalemia Congenital
Important differentials for U-waves	Hypokalemia Hypothermia Bradyarrhythmias Drugs (e.g., digoxin, class IA, and class III anti-arrhythmics)
Electrical alternans	Pericardial effusion Tachyarrhythmias Severe CHF/ CAD/ HTN
Inverted P-QRS-T in I and aVL and upright in aVR	Dextrocardia (shows reverse R wave progression) LA/RA lead reversal (Shows normal R- progression)
In WPW pattern, be cautious diagnosing the following on EKG	Ventricular hypertrophy MI and ischemia (since WPW can cause Q-waves and ST-T changes) Axis deviation Any other conduction abnormalities

T-waves

Condition	EKG Changes
Normal	Upright in all leads other than aVR and V1 with the amplitude normally being less than 5 mm in limb leads and 10 mm in precordial leads
Hyperkalemia MI	Tall T-waves
Kids and young adults	T-wave inversions in V1-3 are normal in kids(Juvenile T-wave pattern). May persist into adulthood (Persistent Juvenile T-wave pattern)
LBBB/ LVH/ Paced rhythm/RBBB/ RVH	Discordant T-waves
PE	S1Q3T3 pattern. T-wave inversions in inferior leads and V1-V3.
Hypertrophic cardiomyopathy	Deep inverted T-waves in all precordial leads
Raised Intracranial pressure	Deep inverted T-waves
Wellens Syndrome	Biphasic (positive and then negative deflection- Type A) or inverted (deep symmetric inversion of T-waves- Type B) in V2 and V3. Suggests a LAD lesion.
Hypokalemia	T-waves may be biphasic (negative and then positive) and will progressively disappear while U waves become more pronounced. With U waves, the QU interval becomes prolonged.
Double peaking T-waves	Either because of U-waves or because of P-waves getting superimposed on T-waves.
Ischemia/ Infarction	Ischemia: T-wave flattening/ inversion. In Infarction, “hyper acute T waves” (very tall T-waves) may be seen with reciprocal changes.

U-waves

Condition	EKG Changes
Normal	usually a small deflection after the T-waves, in the same direction as the T-wave. Usually seen at lower heart rates.
Bradycardia Hypokalemia/ Hypomagnesemia/ Hypocalcemia Hypothermia Raised Intracranial Pressure LVH Drugs like Class Ia, III anti-arrhythmics, Digoxin	Prominent U-waves (>1 mm or 25% of the height of the T wave.)
Severe Heart Disease (ischemia/ valvular/ congenital/ cardiomyopathy,etc.)	Inverted U-waves.

J-point

Condition	EKG Changes
Normal	The point where QRS complex joins the ST segment. Often slightly above the baseline.
Early Repolarization Pericarditis Myocardial ischemia/ Infarction	J-point elevation
Hypothermia	J-waves/ Osborne waves: long slow positive deflection just before the J-point.

ST-segment

Condition	EKG Changes
Normal	flat, isoelectric line between J-point and the start of T-wave
1. Acute MI 2. Printzmetal’s angina 3. Takotsubo cardiomyopathy	ST- elevation: Classically, STEMI has been associated with a “convex upwards” morphology- but the morphology may be convex/ concave/ oblique! Reciprocal changes are typically seen with MI and Printzmetal’s angina but usually absent with Takotsubo. Changes in Printzmetal’s angina are usually transient.
Pericarditis	ST-elevation- usually concave upwards. Reciprocal ST depression and PR elevation in leads aVR and V1.
Early Repolarization	ST-elevation- J-point notching is sometimes seen with early repolarization
LBBB/ Paced rhythm/ LVH	ST- elevation/ depression: main vector of QRS and ST-T segments are usually discordant.
Ventricular aneurysm	Persistent ST segment elevation after an MI, along with Q-waves.
Raised Intracranial Pressure (Intracranial bleed)	ST-elevation/ depression with deep inverted T-wave inversions
Brugada syndrome	Brugada Sign: ST elevation with a coved morphology and a partial RBBB pattern in V1-V2.
J-point elevation	can simulate ST elevation
Sodium Channel Blocking Drugs	QRS prolongation, tall R wave in aVR, QTc prolongation. can also cause ST elevation
LAD lesion	De Winter pattern: Upsloping ST-depression at J point in precordial leads that is >1mm + reciprocal ST elevation in aVR + tall and symmetrical T waves in precordial leads (De Winter T-waves)
Myocardial Ischemia	Horizontal/ downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia Diffuse ST depression with ST elevation in aVR is seen with LAD lesions as well as 3 vessel disease.
Tachycardia (sinus/ supraventricular)	widespread ST depression
Digoxin effect	Downsloping ST depression creating a “reverse check mark” appearance.
Hypokalemia	Downsloping ST depression with T-wave flattening or inversion and prominent U waves with increased QU interval.
RVH, RBBB	ST depression and T-wave inversion in V1-V3.

QT interval

Condition	EKG changes
Normal	Varies with heart rate and so corrected QTc is used- A common way to correct it is using Bazett formula (QTC = QT / √ RR). QTC is usually 0.35-0.44 seconds in men and 0.35-0.46 seconds in women.
Drugs: Class IA, IC, and III antiarrhythmics, Antipsychotics, Antiemetics, Tricyclic antidepressants, azaleas like fluconazole, antibiotics such as floroquinolones and macrocodes, etc. Hypokalemia/ Hypomagnesemia/ Hypocalcemia Myocardial Ischemia Hypothermia Raised ICT Congenital long QT syndromes	Long QTC
Congenital Short QT syndromes Digoxin Hypercalcemia	Short QTC

Q-wave

Condition	EKG changes
Normal	Small septal Q waves may be seen in I, AVL, V5, V6. Deep Q waves may be seen in III and aVR
Pathological Q waves may be seen in MI, cardiomyopathies, lead placement errors, etc.	Pathological Q-waves: Leads V2 to V3: Any Q wave ≥20 milliseconds or a QS complex. Other Leads (I, II, aVL, aVF, V4 to V6): Q wave ≥30 milliseconds and ≥0.1 mV deep in two contiguous leads or a QS complex.
LBBB	no Q-waves in LBBB

R-wave changes

Condition	EKG Changes
Anteroseptal MI LVH/ RVH Cardiomyopathy lead misplacement	Poor R wave Progression
Posterior MI RBBB RVH/ Right heart strain Cardiomyopathy Dextrocardia Lead misplacement	R>S in V1
Tricyclic Antidepressant poisoning; other Na channel blocking drugs	R in aVR > 3 mm
Dextrocardia Ventricular tachycardia LA/ RA lead reversal	Dominant R-wave in aVR

QRS Complex

Condition	EKG changes
Normal Supraventricular origin without ventricular conduction defect	QRS < 100 ms
Ventricular origin of QRS including ventricular pacing Hyperkalemia Hypothermia Bundle Branch Block Sodium Channel Blockers WPW	QRS > 100 ms
WPW	Delta Wave
Pericardial effusion Infiltrative cardiomyopathies (amyloidosis, sarcoidosis, etc.) Lung diseases (COPD) Hypothyroidism Obesity	Amplitude < 5mm in all limb leads or Amplitude < 10 mm in all precordial leads (Low voltage)
Pericardial effusion/ tamponade PE CHF Severe tachycardia Ventricular tachycardia COPD Altering conduction pathways (intermittent change in velocity/ blockage)	Changing morphology of QRS complexes (Electrical Alternans)
LVH Biventricular Hypertrophy	high amplitude QRS
Arrhythmogenic right ventricular dysplasia	Epsilon wave

PR-Segment

Condition	EKG changes
Normal	flat and isoelectric
Pericarditis	depressed in all leads except aVR and V1 where it is elevated
Atrial infarct/ ischemia (Liu’s Major criteria)	Elevation of the P-Ta segment of over 0.5 mm in V5 and V6, with reciprocal depression of the same segment in V1 and V2. Elevation of the P-Ta segment exceeding 0.5 mm in lead I, with reciprocal depression of the same segment in leads II or III P-Ta segment Depression greater than 1.5 mm in the precordial leads and 1.2 mm in leads I, II, and III, particularly in the context of any atrial arrhythmia.

PR Interval

Condition	EKG Changes
Normal	PR interval = 0.12 to 0.2 seconds (3-5 small squares)
First degree AV block	PR interval > 0.2 seconds
Second Degree Type 1	Progressively prolonging PR segment before a dropped QRS
Preexcitation Syndromes: Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL) Junctional Rhythm	PR interval < 0.12 seconds

Condition	EKG Findings
Normal P-waves	– Upright in II, Biphasic in V1, and inverted in aVR with an axis of 0° to 75° and a duration < 120 msec (3 small squares) – II: < 2.5 mm tall and < 3 mm wide – V1: Positive component is < 1.5 mm tall and Negative component is < 1 mm wide and < 1mm deep.
Right Atrial Abnormality	– II: > 2.5 mm tall – V1: > Positive deflection is > 1.5 mm tall
Left Atrial Abnormality	– II: > 3mm wide ± notched p-wave – V1: > 1 mm wide or > 1 mm deep negative deflection
Ectopic beats not from SA node	– P-wave morphology changes based on origin. – PR interval is usually normal since the AV nodal delay is present.
Junctional beats, AVNRT	– P-waves are inverted – P-waves may be immediately before (so short PR), embedded within, or shortly after the QRS.
– Multifocal Atrial Tachycardia (HR≥100) – Wandering Atrial Pacemaker (HR < 100)	– ≥ 3 morphologies of P-waves
Atrial Flutter	– P-waves are replaced by F-waves, typically with a rate of around 300 beats per minute
Atrial Fibrillation	– No P-waves. Coarse Atrial fibrillation may show waves that are irregular with many different morphologies and a very high rate.
Tachycardia, PACs, severe first degree heart block	– P-waves may be embedded in T-waves and not be immediately obvious.
Supra-ventricular tachycardia	– P-waves may be embedded in QRS and not be immediately obvious.
– Sinus Arrest, 3rd degree Sinoatrial exit block – Atrial Flutter (has F-waves) – Atrial Fibrillation	– Absent P-waves

Lead	Region Viewed	Anatomical Structures	Usual feeding vessel
I, aVL	High- Lateral	High lateral wall of the left ventricle	Left Circumflex Artery (LCx)
II, III, aVF	Inferior	Inferior wall of the left ventricle	Right Coronary Artery (RCA)
aVR	Right Upper Side	Right atrium, part of the interventricular septum	Not specific; reflects global activity
V1	Septal	Interventricular septum	Left Anterior Descending Artery (LAD)
V1	Right Ventricle	best but sub-optimal view of Right Ventricle (RV)	RV is supplied by the RCA
V2	Septal/Anterior	Interventricular septum and anterior wall of the left ventricle	Left Anterior Descending Artery (LAD)
V3, V4	Anterior	Anterior wall of the left ventricle	Left Anterior Descending Artery (LAD)
V5, V6	Lateral	Lateral wall of the left ventricle	Left Circumflex Artery (LCx)
V7, V8, V9	Posterior	Posterior wall of the left ventricle	Posterior Descending Artery (PDA)- usually a branch of RCA
V1R, V2R, V3R, V4R, V5R, V6R	Right Ventricle	Right Ventricular Free Wall	Right Coronary Artery (RCA)