PANCE/PANRE is giving me palpitations!

An Electrocardiography Review

Kirsten J. Bonnin, M.M.S., PA-C

Friday, March 8th, 2019

8:00-9:00 am

Learning Objectives

• Review basic electrophysiology• Recognize common cardiac dysrhythmias• Recognize common conductive disorders• Review axis, chamber enlargement & hypertrophy• Recognize common ECG changes associated with myocardial ischemia

& infarction• Review drug & electrolyte effects

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Basic Electrophysiology

• Sinoatrial (SA) node: heart’s primary pacemaker• High in posterior right atrium• Intrinsic rate 60-100 bpm

• Atrioventricular (AV) node: pathway for impulses to reach the ventricles• Low right atrium• Intrinsic rate 40-60 bpm

• Bundle of His• Right & left bundle branches

• On either side of the interventricular septum• Purkinje fibers: terminal branches of the right and left bundles, spread out

through myocardium• Intrinsic rate 20-40 bpm

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Normal Sinus Rhythm Characteristics

• P wave: atrial depolarization• Right precedes left (SA node in RA), often biphasic in V1• <0.10 s (100 ms; 2.5 small boxes), amplitude <0.25 mv (2.5 small boxes)

• PR interval• 0.12 to 0.20 s (120-200 ms; 3 to 5 small boxes)

• QRS complex: ventricular depolarization• Narrow, < 0.12 s (120 ms)

• R wave progression across precordium (across V1-V6)• ST segment: isoelectric• T wave: ventricular repolarization

• Upright, slightly asymmetrical

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Patient #1

• 26-year-old recent PA graduate comes to the clinic for evaluation of palpitations described as a “racing heart” with some “weird beats.” Denies angina or syncope. Has been stressed, drinking multiple energy drinks back-to-back while studying for PANCE. No tobacco use, no family history of premature heart disease.

• DDx?• Physical examination

• Occasionally irregular HR• Otherwise normal

Premature Atrial Complexes (PACs)

• Early ectopic beats, originate outside the SA node

• Followed by a non-compensatory pause

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Premature Ventricular Complexes (PVCs)

• Wide QRS complex (> 0.12 s; 120 ms)• Absent P waves• Followed by a compensatory pause

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Supraventricular tachycardia

• Atrial tachycardia• Rate 150 to 250 bpm

• Multifocal atrial tachycardia (MAT)• Changing P wave morphology• 120 to 150 bpm• Rhythm is irregular

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Patient #2

• A 64-year-old patient comes to the office for routine evaluation. History of mitral stenosis due to rheumatic heart disease as a child, which has been mostly asymptomatic. When asked, having some palpitations particularly with sudden exertion, excitement, and sexual activity.

• Physical examination• Murmur: Loud S1 with opening snap, mid-

diastolic rumble; no lifts/heaves• Best heard at apex in left lateral decubitus

position• Otherwise normal

• What are some expected ECG findings?

Left Atrial Enlargement (LAE)

• Increased left atrial pressure and left atrial dilation Wide (enlarged), notched or biphasic P waves

• Width > 0.10 s (100 ms) suggests LAE• Also called “P mitrale”

Leads II and V1

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The first part of the P wave is

due to right atrial depolarization

The second part of the P wave is due to left atrial depolarization

Atrial flutter

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Atrial fibrillation

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Patient #3

• A 75-year-old patient comes to the office for routine evaluation. History of HTN x 40 years, moderate aortic stenosis due to atherosclerosis, which has been asymptomatic.

• Physical examination• Murmur: harsh systolic ejection murmur

crescendo-decrescendo, radiates to neck• Otherwise normal

• What are some expected ECG findings?

Left Ventricular Hypertrophy (LVH)

• At least one of the following criteria is met:

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Left Ventricular Hypertrophy (LVH)Causes: HTN, valvular diseaseDeepest S wave in V1 or V2 PlusTallest R wave in V5 or V6 is > 35mm

R wave in Lead IPlusS wave in Lead III is > 25mm

R wave in aVL > 11mm

R wave Progression

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Left Axis Deviation (LAD)

• Look at Leads I and aVF

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Axis Deviation

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AxisMean QRS Deflection

Lead I Lead aVF

Normal Axis Positive Positive

RAD Negative Positive

LAD Positive Negative

Indeterminate(Extreme)

Negative Negative

Strong Axis Deviation

• Compare Lead I and aVLIf R in aVL > R in Lead I = Strong LAD

• Associated with LAHB

• Compare Lead III and aVFIf R in III > R in aVF = Strong RAD

• Associated with LPHB

18R in Lead II > R in aVF (Normal)

Is Lead II negative??

Patient #4

• A 68-year-old patient with a longstanding history of COPD comes to the office for routine evaluation.

• What are some expected ECG findings?

Citation: Pulmonary Hypertension, Crawford MH. CURRENT Diagnosis & Treatment: Cardiology, 5e; 2017. Available at: https://accessmedicine.mhmedical.com/ViewLarge.aspx?figid=152996840&gbosContainerID=0&gbosid=0&groupID=0 Accessed: March 04, 2019Copyright © 2019 McGraw-Hill Education. All rights reserved

Electrocardiogram in a patient with pulmonary arterial hypertension and right ventricular hypertrophy.

Right Ventricular Hypertrophy (RVH)

• At least one of the following criteria is met:

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Right Ventricular Hypertrophy (RVH)Causes: Pulmonary HTN, Pulmonic stenosisRight axis deviation

R wave > S wave in V1

S wave > R wave in V6

R wave Progression

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Right Axis Deviation (RAD)

• Look at Leads I and aVF

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Right Atrial Enlargement (RAE)

• Increased right atrial pressure and right atrial dilation Tall, rounded or peaked P waves

• Amplitude > 2.5 mm suggests RAE• Also called “P pulmonale”

Leads II and V1

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Intraventricular Conduction Delay: RBBB

• Right Bundle Branch Block (RBBB)• QRS > 0.12 s (120 ms)

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Right Bundle Branch Block (RBBB)

RR’ (M-shaped) in V1

Wide S wave in Lead I and V6

ST-T waves oriented opposite direction to terminal QRS forces

Ischemia or Infarction

• New LBBB• ST elevation• Q wave

Challenger Learning Series27

Intraventricular Conduction Delay: LBBB

• Left Bundle Branch Block (LBBB)• QRS > 0.12 s (120 s)

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Left Bundle Branch Block (LBBB)

Tall, prolonged R waves (may be notched or flattened tops)

Wide R wave in Lead I and V6

Ischemia, Injury, Infarct

Ischemia Injury Infarct

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Subendocardial ST depression > 1mm

in 2 or more leads Inverted or Tall

peaked T wave Reversible i.e. positive stress test

Transmural ST elevation > 1 mm

in 2 or more leads Release of enzymes Necrosis Irreversible

Cell damage, but not cell death

Usual ECG evolution of a Q-wave MI

A. Normal ECG B. Hyperacute T wave changes

with ST elevationC. Marked ST elevation with

hyperacute T wave changesD. Pathologic Q waves, less ST

elevation, terminal T wave inversion

E. Pathologic Q waves, T wave inversion

F. Pathologic Q waves, upright T waves

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Evolution of an MI

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Reversible Irreversible

Ischemia Injury Infarct

Key Cardiac Regions on an ECG

LateralInferior

AnteriorLateral

Lateral

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Reciprocal ChangesLocation of Infarct(ST elevation MI)

Reciprocal changes* seen(ST depression)

Anterior (V1-V6) Inferior leads (II, III, aVF)

Anteroseptal (V1-V2) Inferior (II, III, aVF) or lateral leads (I, aVL, V5, V6

Lateral (I, aVL, V5-V6) Inferior (II, III, aVF) In some cases leads V1-V2**

Inferior (II, III, aVF) Lead I and aVLIn some cases leads V1-V3**

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*Reciprocal changes are the same ST segment shifts as seen from a different angle or direction.

**May be reciprocal, but more likely represents posterior MI.

Posterior wall MI may be missed on typical ECG! High degree of suspicion if ST depression in V1-V3

Pathologic Q waves

• Deep (>1 mm) and wide (0.04 s; 40 ms) in two contiguous leads• Indicative of prior MI

• Develop in hours to days• May persist for life

• Location dependent on location of MI• Not always present

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Pericarditis

• Inflammation of pericardium• Diffuse, ST segment elevation (many leads)

• Usually flat or concave

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Pericarditis with Pericardial Effusion

• Low voltage• May still see ST segment/T wave changes consistent with pericarditis• If large effusion:

• Electrical alternans – changing amplitude of QRS complex

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Junctional rhythms

• Absent or inverted P waves • Before/after QRS or buried in it

• Premature Junctional complex• Single early electrical impulse from AV junction

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Junctional rhythm Rate

Junctional escape rhythm 40 to 60 bpm

Accelerated junctional rhythm 60 to 100 bpm

Junctional tachycardia 100 to 180 bpm

AV Blocks

1st-Degree AV heart block

• Prolonged PR interval• Fixed

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2nd-Degree AV heart block, Type I

• Progressive lengthening of PR intervals until a QRS complex is dropped• Cycle repeats

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2nd-Degree AV heart block, Type II

• Fixed PR interval• Random QRS drops

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3rd-Degree AV heart block

• Atria & ventricles are beating independently of each other

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Mobitz I

Mobitz II

3◦ AVB 2:1 AVB

Fixed PRIVariable PRI

Irregular Rhythm

Regular Rhythm

AV Blocks

2nd / 3rd Degree AVB Differentiation

Atrioventricular Block other names… Definition Rhythm PRI State2nd degree type I Mobitz I / Wenkebach Progressive PRI prolongation; dropped QRS Irregular Variable2nd degree type II Mobitz II Fixed PRI, often prolonged; dropped QRS Irregular Fixed2:1 AVB* (could be Mobitz I / II) QRS associated with every other P-wave Regular Fixed3rd degree AVB Complete Heart Block Dissociation of P waves / QRS Regular Variable

Pre-excitation SyndromesWolff-Parkinson White (WPW) Syndrome

Lown-Ganong-Levine (LGL) Syndrome

PR Interval < 0.12 s < 0.12 s

QRS complex Wide Normal

Delta waves Present Absent

Accessory pathway Bundle of Kent James fibers

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Hyperkalemia

• Tall, peaked T waves **• Flattened P waves• 1st-Degree AV heart block• Widened QRS complexes• Merging of S and T waves forming a “sine-wave” pattern

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Hypokalemia

• Flattening of the T wave • Appearance of U waves **• ST segment depression

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Hypercalcemia

• Decreased automaticity with slowed conduction• Increased PR interval and QRS• Bundle branch blocks and AV block

• Shorter refractory period• Shorter ST segment and shorter QT interval

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Hypocalcemia

• Prolonged QT interval• May progress to ventricular tachycardia or Torsades de Pointes

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Ventricular Tachycardia

• 100 to 250 bpm• Wide, bizarre QRS complexes (>140 ms)

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Torsades de Pointes

• Polymorphic ventricular tachycardia

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Ventricular Fibrillation

• Ventricles quiver as opposed to effective contraction• No cardiac output

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Digoxin

• Increases myocardial contractility• Slows heart rate and AV conduction• Therapeutic drug levels

• “Digoxin effect” (expected ECG changes, no need to discontinue)• Shortened QT interval• Flattened T waves• Gradual downslope of ST segment

• Digoxin Toxicity• Toxic blood levels (> 2.0 ng/mL)

• Can see conduction blocks or tachy-dysrhythmias or both• Increased risk with renal disease, hypokalemia, aging

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Pulmonary Embolism

• S1 Q3 T3

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T

Biatrial Enlargement

• Increased amplitude and duration of P wave

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Where to find what you’re looking for…

• Axis• Lead I and aVF

• P waves• Lead II and v1

• Ischemia/Infarct• ST segments in contiguous leads• Q waves

• Atrial enlargement• P wave

• Ventricular hypertrophy• Precordial leads

• Intraventricular delay• QRS complexes (wide)

• LBBB – Lead I and v6• RBBB – Lead I and v6

• Dysrhythmias• PR interval• QRS complex (rhythm)

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Intraventricular Conduction Delay

• Bundle Branch Block• QRS > 0.12 s (120 ms)

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Left Bundle Branch Block (LBBB)

Right Bundle Branch Block (RBBB)

Tall, prolonged R waves (may be notched or flattened tops)

RR’ (M-shaped) in V1

Wide R wave in Lead I and V6 Wide S wave in Lead I and V6

ST-T waves oriented opposite direction to terminal QRS forces

Systematic approach!• Heart rate

• Bradycardia (<60 bpm) or tachycardia (>100 bpm)?• Rhythm

• Regular or Irregular?• P waves? P:QRS complex? PR interval constant?

• Axis• Left or right axis deviation?

• Intervals• Short or long PR interval? QRS duration? QT interval?

• P wave• Left or right atrial enlargement?

• QRS complex• Bundle branch block? Pre-excitation? Ventricular hypertrophy? Q waves suggestive of infarction?

• ST-T wave• Elevation or depression? T wave inversion?

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References

• Shade, Bruce. Fast and Easy ECGs: A Self-Paced Learning Program, 2nd Edition. McGraw Hill: Boston, 2013.

• UpToDate• ECG Interpretation Made Incredibly Easy, 4th Ed. Lippincott, Williams &

Wilkins: Philadelphia• Jones SA. ECG Success: Exercises in ECG Interpretation. FA Davis,

2008.• Dubin D. Rapid Interpretation of EKG’s, 6th Edition. COVER Publishing

Co, 2000.

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