Introduction to Electrocardiography III

John C. Evans, MD Fellow Division of Cardiovascular Medicine Oregon Health and Science University 9/25/07

Disclaimer
Some of these slides were made using images found on the web. In particular ABC of Electrocardiography by Morris and Brady from the British Medical Journal. Please use the web to track down the images and use the respective pages. Dont rat Dr. Luft out to the publishers. If you are a publisher, dont sue me; its Dr. Luft.

Lecture Topics:
Lecture 1
Introductory Approach to ECG Interpretation

Lecture 2
Introduction to Rhythm Analysis

Lecture 3
Introduction to clinical ECG changes/Ischemia

ECGinterpretation
identification standardization rate rhythm axis intervals voltage/chambers/hypertrophy geography/ischemia/infarction

Bradycardia
Sinus bradycardia Sinus arrest with subsidiary pacemaker
Ectopic atrial Junctional Ventricular

Block
Second degree Type I (Wenckebach) Second degree Type II Complete Heart Block

Bradycardia Algorithm
Regular? AV dissociation?
If AV dissociated
And A>V: heart block And V>A: ventricular pacemaker

How irregular?
Irregularly Irregular
Atrial Fibrillation

Wandering Pacemaker

If notLook for the P waves

Sinus

Grouped
Second Degree Block

Ectopic Atrial focus

Junctional Ventricular

Tachycardia
Wide Complex
Ventricular Tach SVT w/ aberrancy -preexisting -rate-related -AVRT

Narrow Complex
Regular Sinus Tach Atrial Flutter AV Reentry Tach AVN Reentry Tach Atrial Tach Junctional Tach Irregular Atrial Fib Multifocal AT Variable Conduction

Anatomy

Anatomy

Lead location of ST changes can allow wall segment localization of Infarct/ischemia

Lead Localization

R wave progression
Normally
No q anteriorly R:S should increase until V5 R:S should be 1:2 by V3 and 1:1 by V4 Septal q laterally

Lead localization can correlate with coronary anatomy

Left Anterior Descending Artery: Anterior and lateral leads V1-V4 Right Coronary Artery: Inferior leads: II, III, aVf Left Circumflex: Lateral leads V4-V6, I, aVL (notorious for being ECG silent)

Plaque Rupture

STEMI Evolution
Hyper acute T waves - minutes ST elevation (Injury/Acute MI) hours Deep Q waves with ST elevation (Recent MI) - days Q waves with T wave inversion (Age indeterminant) - weeks Q wave with normalization of T wave (Old) - months

ST Elevation

The ST segment elevation may fuse with the QRS and T wave - yielding a Tombstone complex.

Reciprocal ST Depression

ST depression often develops at in leads opposite the sight of infarction. Known as reciprocal depression. Can be helpful to confirm STEMI. May represent mirror image phenomenon.

Acute Anterior LAD artery distribution

ST elevations

Reciprocal depressions

Acute Inferior Infarct Right Coronary Artery Distribution

Reciprocal depression

ST elevation

Old Inferior Infarct (Q waves)

Q waves are considered significant or pathological if they are > 30msec wide and/or > 1/4 of the R wave amplitude. Q waves in III and aVR can be normal (even if significant). Look for an anatomic pattern!

Acute Lateral MI Left Circumflex or Diagonal artery

ST elevations

Reciprocal depressions

Old Lateral Infarct

Lateral Infarct

Inferior/Posterior Infarct

Posterior Infarct vs. LAD Ischemia

ST Depressions V1-V3 Represent ST Elevations behind V1-V3

Flip or Use a Mirror!

Difficult to Diagnose STEMI RV Infarction (with IMI)

Right sided leads with ST elevation Inferior STEMI

Complications of STEMI
Complications can include: pericarditis, CHF, VSD, papillary muscle rupture (acute MR), aneurysm formation, thrombus, and LV rupture.

LV rupture

LV aneurysm

ST Segment Elevation
Causes of ST segment elevation
Acute myocardial infarction Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm Coronary vasospasm/Printzmetal's angina Pericarditis Brugada syndrome Subarachnoid haemorrhage

Pericarditis

Pericarditis
ST Segment Elevation

PR Depression

Early Repolarization

Early Repolarization

Vasospasm

Baseline

Spasm

Spasm Resolving

Reversible ST segment Elevation Associated With Vasospasm

ST Elevation in LBBB
Up to 5mm of discordant ST elevation may be normal.

Infarction in LBBB
Note >5mm discordant elevation in V2-V4. Note > 1mm concordant ST elevation in V5 and V6. This may represent acute infarction.

T waves
Different T wave morphologies can represent ischemia. T wave abnormalities can also reflect normal variation, youth, electrolyte abnormalities, drugs, CNS abnormalities, lead misplacement, etc. T waves should generally be <10mm tall and be approximately >1/8 the height of the R wave. T wave inversion in III, aVR and V1 may be normal. T wave inversion V1-V3 seen in juvenile pattern.

T Waves (biphasic)
Biphasic T waves are frequently associated with ischemia and acute coronary syndrome. Usually seen in V1-V3. Correlate with LAD disease. Sometimes referred to as Wellens waves.

T waves
Tall T waves (> 10mm) may represent ischemia.

Also seen with hyperkalemia and young patients.

T waves

T waves (non-specific)

T waves

T waves (Deep, Symmetrical)

ST Depression
ST segment depression may also represent ischemia. Like T wave inversions and ST elevations, it is not specific to ischemia.

ST Depression
Note deep, downsloping ST depressions. High probability of ischemia (espically if new or associated with chest pain).

ST Depression (Digoxin Toxicity)

ST Depression (LVH)

Hyperkalemia
Elevated K+ can result in deadly rhythms. The typical progression of EKG change with rising potassium is roughly: Peak T waves (tall) K+>6 QRS widening and P flattening K+>7 Sinusodial tachycardia K+>8

1. 2. 3.

Hyperkalemia (Peaked T Waves)

Hyperkalemia (Sinusodal VT)

Hyperkalemia (Sinusodial)

Hyperkalemia needs immediate treatment.

Cardiac membrane stabilization with calcium. Insulin, glucose, beta2 agonists, K-exalate, or hemodialysis to bring down potassium.

Other electrolyte abnormalities

Hypokalemia
U waves ST depression QTU

Hypo/hypercalcemia Hypo/hypermagnesemia

Back to axis
Left axis deviation
LAFB LVH IMI AMI

Right axis deviation

RVH LMI WPW Lead misplacement LPFB

So much more
Blocks
Block above and below the AV node Complete heart block with a-fib

Syndromes
Lown-Ganong-Levine Brugada ARVD Short QT

Findings of systemic disease

Infiltrative Hypothermia

So remember.

ECGinterpretation
identification standardization rate rhythm axis intervals voltage/chambers/hypertrophy geography/ischemia/infarction

Thank you
Dr. Luft for his slides Ryan Palmer for all his help The facilitators of the small groups You (questions AND feedback are greatly appreciated)