LU6 Enhancement Lectures PGH IM Residents 2011.

Generation of action potential

ECG Graph paper

Unipolar precordial leads

Normal ECG

Guide in Reading ECG

• Standardization & technique• Rhythm• Rate: atrial & ventricular• P wave morphology & duration• P-R interval• QRS complex morphology & duration• ST segment• T-wave• U wave• Q-T interval• Hypertrophy and enlargement• arrhythmias

Standardization

Heart rate 60 - 100 beats/minbradycardia < 60 tachycardia > 100

PR interval 0.12 – 0.20 secQRS < 0.12 secQRS axis - 30º to + 110ºQTc < 0.47 sec males

< 0.48 sec females


• Standardization & technique• Rhythm• Rate: atrial & ventricular• Axis• P wave morphology & duration• P-R interval• QRS complex morphology & duration• ST segment• T-wave• U wave• Q-T interval• Hypertrophy and enlargement• arrhythmias

Rhythm

SA node – sinus

AV node – junctional

Ventricular rhythm

Rhythm

Are there p waves? sinus, atrial fibrillation

Do they look similar? MFAT, wandering pacemaker

Are they regular? AF

Does a QRS complex follow each p wave? SVT, junctional rhythm, ventricular rhythm



Heart rate assessment by “rule of 300”

Determination of Heart Rate

Measurement of Rate

• Formula 1: 300

# big squares between R-R

• Formula 2: 1500

# small squares between R-R

Determination of Heart Rate• Is the atrial rate same as ventricular

rate?– PVC’s, PAC’s, 3rd degree AV block

• Is there normal-looking QRS complex after each p wave?

• What if there are no p waves?– Six second strip heart rate

RATE

1. Sinus Bradycardia

2. Sinus Tachycardia

3. AV junctional rhythm- Inherent rate of 40-60/min- No p waves- Normal looking QRS complex

4. Ventricular rhythm- Inherent rate of 20-40/min- No p waves- Bizaare-looking QRS complex



Hexaxial System

Determination of Axis

QRS axis

Vectorial Analysis

Determination of Axis

Axis = 90 x QRS in AVF

QRS in [ I] + QRS in [AVF]

Special cases:

• negative QRS deflection in I– Add 90 to result



P wave morphology and duration

• No p waves– Atrial fibrillation

• Multiple p waves– Multifocal atrial tachycardia– Wandering pacemaker

• Notched p wave– Left atrial enlargement

• Peaked p wave– Right atrial enlargement



P-R Interval

P-R interval

• Prolongation– Hypokalemia– 1st degree AV block

• Shortening– Wolff-Parkinson White



QRS morphology and duration

• Normal looking– Supraventricular origin

• Bizarre looking– Ventricular in origin– Paced rhythm



ST segment

• Elevation– Infarction

• >1mm in limb leads• >2 mm in chest leads

• depression– Ischemia

• >1 mm in all leads from the J point



T and U waves

• T wave – Hypokalemia– 1st degree AV block

• Shortening– Wolff-Parkinson White



Determination of QT interval

Corrected QT interval = QT (actual)

R-R

QT interval

• prolongation– hypocalcemia

• shortening– hypercalcemia

Chamber Enlargement

Atrial Enlargement (due to chronic lung disease or pulmonay embolus

Atrial Enlargement (commonly seen in mitral valve disease)

II V1

B

V1

Ventricular Enlargement

Ventricular Enlargement

Right Ventricular Hypertrophy

R in V1 + S in V5-V6 >11 mm

R in V1 >7mm

R:S in V1 >1

RAD > +90 degrees

Ischemic Heart Disease

Anatomy of Myocardial Infarction

Infarction area

ECG leads Coronary Artery

Branch

Extensive anterior

A, AVL, V1 – V6 Left, LM LAD, LCX

Anteroseptal V1 – V4 Left LAD Anterolateral I, AVL, V3 – V6 Left LCX

Inferior II, III, AVF Right 80% Left 20%

PDA

True posterior V1 – V2 (reciprocal)

Variable left/right

LCX PL

Anterior V3 – V4 Left LAD

*LAD = left anterior descending aretery; LCX = left circumflex arteryLM = left main artery; PDA = posterior descending artery; PL = posterolateral branches

Evolution of Infarct

1. ST segment elevation2. Progressive decrease in ST segment elevation3. Q wave formation4. T wave flattening/inversion5. Q wave with upright T wave

Significant Q wave

RULES on Q waves

• Not significant in aVR• Ignored in V1 unless with abnormalities in

other precordial leads• Ignored in III unless with abnormalities in

II, AVFmore reliable if with St-T segment changes

• Not significant if located in V1-V3 in LBBB• Significant in V1-V2 in the presence of

RBBB• Pathologic if >= 0.04 sec and >25% of R

wave amplitude

RHYTHM DISORDERS

ATRIAL Arrhythmias

1. Atrial fibrillation

2. Atrial flutter

3. Wandering Pacemaker

4. Multifocal Atrial tachycardia

ATRIAL FIBRILLATION

- Most common sustained arrhythmia associated with increased CV mortality and morbidity

- Prevalence increasing with age, doubling with each successive decade, 70% in ages 65-85

- Multiplier effect on risk- 3-5x stroke- 3x CHF- 1.5-3x death

- Associated with heart disease but ~30% are without underlying heart disease

ATRIAL FIBRILLATION

- Rapid and irregular atrial fibrillatory waves at a rate of 350 to 600/minute

- CRITERIA- Absent P waves- F waves vary in amplitude, morphology and

intervals- R-R intervals are irregularly irregular- Ventricular rate usually ranges from 90-170- QRS complexes are narrow unless AV

conduction is abnormal - Hypothesized to be due to multiple wavelets in

the atrium competing for the conduction to the AV node

ATRIAL FIBRILLATION

ATRIAL FLUTTER

- Atrial rate of 220 to 350/minute- CRITERIA

- Absent p waves- Biphasic saw-toothed flutter waves, fairly

regular- F waves vary in amplitude, morphology and

intervals- R-R intervals are irregularly irregular- Ventricular rate usually ranges from 90-170- QRS complexes are narrow unless AV

conduction is abnormal - Hypothesized to be due to multiple wavelets in

the atrium competing for the conduction to the AV node

ATRIAL FLUTTER

Escape Rhythm/Beat

1. Atrial - Sinus arrest causing escape rhythm- With p’ waves

2. Junctional- No P waves- 40-60/min inherent rate- Produces a series of lone QRS complexes

3. Ventricular

- may occur in complete AV block

Escape Rhythm/Beat

Sinoatrial block

- Complete failure of a P wave to appear- A cycle appears which is twice the

anticipated P-P interval- Transient doubling of P-P interval

- SA exit block- No visible P-QRST complex for more than 1 cycle

- Normal P wave morphology, before and after the pause

- Pause is preceded and followed by a normal P-P cycle

- P-P interval is a mutliple of the normal P-P interval

SA block

SINUS ARREST vs SINUS PAUSE

Wandering Pacemaker

- Impulses originate from different foci in the atrium and even AV node

- Sinus node may still be dominant- >= 3 P wave morphologies, with varying

P-R intervals, resulting in varying R-R intervals

- Heart rate <100- May be seen in

- Increased vagal tone- Digitalis effect- Organic heart disease

Wandering Pacemaker

Multifocal Atrial Tachycardia

- Irregular atrial rate > 100- P wave shows >= 3 different morphologic

patterns and varying PR intervals- Varying P-P and P-R intervals result in

avrying R-R intervals

Multifocal Atrial Tachycardia

HEART BLOCKS

1. 1st degree

2. 2nd degree- Type 1 Wenkeboch- Type 2 Mobitz II

3. Complete AV block

4. Bundle Branch Block- Right bundle branch block- Left bundle branch block

5. Hemiblocks- Left anterior hemiblock- Left posterior hemiblock

• 1st degree– PR interval > 0.20s

• 2nd degree (type1 and 2)– Type 1 – PR interval becomes longer until depolarization is

not conducted anymore– Type 2 – AV conduction is blocked

• 3rd degree– AV dissociation– Variable PR and RP intervals– QRS rate is usually constant and lies within the range of 15-

70 beats /min

Trifascicular Conduction System

Right Bundle Branch Block

• Lead V1 late intrinsicoid, M-shaped QRS (RSR pattern)

• Lead V6 early intrinsicoid, wide S wave• Lead I wide S wave


• Associated with– RHD– Cor pulmonale/RVH– Myocarditis– IHD– Degenerative disease of the conduction system– Pulmonary embolus– ASD


Left Bundle Branch Block

• Lead V1 QS or rS• Lead V6 late intrinsicoid, no Q waves,

monophasic R• Lead I monophasis R, no Q wave


• Associated with – CAD– HHD– Dilated cardiomyopathy

-- unusual for LBBB to exist in the absence of organic disease


Left Anterior Hemiblock

• LAD (usually -30 to -60 degrees)• Small Q in leads I and aVL, small R in II, III and aVF• Usually normal QRS duration• Late intrinsicoid deflection in aVL• Increased QRS voltage in limb leads


• Usually benign in the absence of apparent organic heart disease and not associated with block in the other fascicles

• Can also occur in– CAD– Chagas disease– Infiltrative and inflammatory diseases– CHDs– Sclerodegenerative disorder


Left Posterior Hemiblock

• RAD (usually + 120 degrees)• Small R in leads I and aVL, small Q in II, III and aVF• Usually normal QRS duration• Late intrinsicoid deflection in aVF• Increased QRS voltage in limb leads• No evidence of RVH


• Can occur in– Cardiomyopathies– Myocarditis– Hyperkalemia– Acute cor pulmonale– chronic degeneerative and fibrotic processes of the

conducting system– Aretriosclerotic cardiovascular disease


Bifascicular Block

• Complete LBBB• RBBB with either LAHB or LPHB• Duration of QRS complex is prolonged to 0.12s

Bifascicular Block

Trifascicular Block

• Bifascicular block associated with 1st degree AV block

Trifascicular Block

Premature Complexes

1. Premature Atrial Complex

2. Junctional Premature Beats

3. Ventricular Premature Beats

Premature Complexes - PACs

- Premature atrial activation arising from a site other than the sinus node

- P wave occuring relatively early in the cardiac cyle

- with a different morphology from the sinus P wave

- PR interval different from that during the sinus rhythm


- Not life-threatening by themselves- But may also start a VT- May be asymptomatic or cause a

sensationof “skipping” or palpitations- May be associated with normal conduction

or aberrant conduction


Premature Complexes – Junctional Premature Beats

- Arise from the AV node or in the His bundle

- A premature normal QRS complex is closely accompanied by an “upside down” P wave

Premature Complexes – Ventricular Premature Beats

- Duration of more than 0.12s- Bizarre morphology T wave in the

opposite direction from the QRS vector- A fully compensatory pause- Ventricular bigeminy, trigeminy,

quadrigeminy, couplet

Premature Complexes – Ventricular Premature Beats

- May be present in - Normal individuals- MVP- Hypertension and LVH- Chronic HD- Acute MI- cardiomyopathy

Miscellaneous• Poor R wave progression

– < 3mm R wave in V3

• Low QRS– < 5mm QRS amplitude in limb leads– <10mm QRS amplitude in chest leads

LU6 Enhancement Lectures PGH IM Residents 2011.

Documents

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