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- Limb leads
- - → + gives a positive deflection
- + → - gives a negative deflection
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ECG leads
anatomical representation, coronary artery responsible
- Anteroseptal leads: V1, V2 → LAD
- Anteroapical leads: V3, V4 → LAD (distal)
- Anterolateral leads: I, aVL, V5, V6 → CFX
- Inferior leads: II, III, avF → RCA
- Posterior: V1, V2 (tall R wave, not Q wave) → RCA
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- P wave: atrial depolarization; atrial repolarization is masked by QRS complex
- PR interval: conduction delay through AV node (nl < 200 msec)
- QRS complex: ventricular depolarization (nl <120 msec)
- QT interval: mechanical contraction of the ventricle
- T wave: ventricular repolarization; T wave inversion may indicate recent MI
- ST segment: isoelectric, ventricles depolarized
- U wave: caused by hypokalemia, bradycardia
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Sequence of ECG Interpretation
- 1. Calibration
- 2. Rhythm
- -Sinus if:
- -each P wave is followed by QRS; each QRS is preceded by P wave
- -P wave is upright in leads I, II, and III
- -PR interval is >0.12 sec (3 small boxes)
- -If not, determine type of arrhythmia
- 3. Heart rate
- - Large box: 300-150-100-75-60-50
- - (HR = 300/# of large boxes)
- - nl, tachycardia, bradycardia
- 4. Intervals
- - PR = 0.12-0.2 sec (3-5 small boxes)
- - QRS ≤ 0.10 sec (≤~3 small boxes)
- - QT ≤ half the R-R interval, if heart rate is normal
- 5. Mean QRS axis
- -Nl if QRS is primarily upright in leads I and II (between +90° to -30°)
- -abnl: determine axis by isoelectric/perpendicular method
- 6. P wave abnormalities
- -P waves in leads II and V1 for left and right atrial enlargement
- 7. QRS wave abnormalities
- - Left and right ventricular hypertrophy
- - Bundle branch block
- - pathologic Q waves; what's the anatomica distribution
- 8. ST segment or T wave abnormalities
- - ST elevations:
- - ST segment elevation MI
- - pericarditis
- - ST depression or T wave inversions:
- - Myocardial ischemia or non-ST elevation MI
- -Usual accompany ventricular hypertrophy or bundle branch blocks
- -Metabolic or chemical abnormalities
- 9. Compare pt's previous ECG
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Mean QRS axis
Normal: -30° to +90°
- Left axis deviation: more negative than -30°
- -Inferior wall MI
- -Left anterior fascicular block
- -Left ventricular hypertrophy (sometimes)
- Right axis deviation: more positive than +90°
- -Right ventricular hypertrophy
- -Acute right heart strain (e.g. massive pulmonary embolism)
- -Left posterior fascicular block
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- Right ventricular hypertrophy
- -R > S in lead V1
- -Right axis deviation
*The large R wave of V 1 gets progressively smaller from V 2 to V 3 to V 4 etc.
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- Left ventricular hypertrophy
- -S in V1 + R in V5 or V6 > 35mm
- OR
- -R in aVL > 11mm
- OR
- -R in lead I > 15mm
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Atrial hypertrophy
Diphasic P wave (both positive and negative)
- Right atrial hypertrophy:
- -initial component of diphasic P wave (in lead V1) is larger
- *Right atria has the SA node; it gets depolarized first
- Left atrial hypertrophy:
- -terminal portion of a diphasic P wave in V1 is large and wide
- *Mitral stenosis can cause left atrial enlargment
- *systemic hypertension is the most common cause
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Bundle branch block
- RBBB:
- -Widened QRS
- -RSR' in V1 ("Rabbit ears")
- -Prominent S in V6
- LBBB:
- -Widened QRS
- -Broad, notched R in V6
- -Absent R and prominent S in V1
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Digoxin therapy
- ST "scooped" depression
- Mild PR prolongation
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Hyperkalemia, Severe hyperkalemia, Hypokalemia
- Hyperkalemia: Peaked T waves
- Severe hyperkalemia: Flattened P; Widened QRS
- Hypokalemia:ST depression, flattened T; Prominent U wave
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Hypercalcemia, Hypocalcemia
- Hypercalcemia: Shortened QT interval
- Hypocalcemia: Prolonged QT interval
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- Torsades de pointes
- -Ventricular tachycardia, characteriezed by shifting sinusoidal waveforms on ECG
- -Can progress to V fibrillation
- *Anything that prolongs QT interval can predispose to torsades de pointes
- Tx: magnesium sulfate
- **Congenital long QT syndromes are most often due to defects in cardiac sodium or potassium channels
- --Can present with severe congenital sensorineural deafness (Jervell and Lange-Nielsen syndrome)
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- Atrial fibrillation
- Chaotic, erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes
- Atrial stasis → clotting → stroke
- Tx: rate control, anticoagulation, possible cardioversion
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- Atrial flutter:
- Rapid succession of identical, back-to-back atrial depolarization waves
- "Sawtooth" appearance
- Tx:
- -pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmiccs
- -Rate control: β-blockers or calcium channel blockers
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- Ventricular fibrillation:
- Completely erratic rhythm with no identifiable waves
- Fatal arrhythmia without immediate CPR and defibrillation
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AV block
- 1st degree: PR interval is prolonged (>200 msec). Asymptomatic
- 2nd degree (Mobitz type I): Progressive lengthening of PR interval until a beat is dropped. Usually asymptomatic
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- First degree AV block
- Asymptomatic
- prolonged PR interval
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- 2nd degree
- Mobitz type I
- Wenckebach
- Progressive lengthening of PR interval, until beat is dropped
- Asymptomatic (usually)
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- 2nd degree
- Mobitz type II
- Abrupt, nonconductant P waves result in pathologic condition
- Often found as 2:1 block; 2 or more P waves to 1 QRS complex
- May progress to 3rd degree block
- Tx: pacemaker
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- 3rd degree (complete)
- Atreia and ventricles beat independently
- atrial rate is faster than ventricular rate
- Tx: pacemaker
- **Lyme disease can result in 3rd degree heart block
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Common bradyarrhythmias
location
- SA node:
- -sinus bradycardia
- -sick sinus syndrome
- AV node:
- -Conduction bocks
- -Junctional escape rhythm
- Ventricles:
- -Ventricular escape rhythm
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- Sick sinus syndrome
- Presentation: dizziness, confusion, syncope; elderly patients
- Tx: IV anticholinergic (atropine) or β-adrenergic agents (isoproterenol)
- *pts susceptible to SVTs: combination is bradycardia-tachycardia syndrome
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- Junctional escape rhythm
- Arises from the AV node or proximal bundle of His
- 40-60bpm
- normal, narrow QRS complex
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- Ventricular escape rhythm
- Slower rates (30-40bpm)
- widened QRS complex
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Common Tachyarrhythmias
Location
- SA node:
- -Sinus tachycardia
- Atria:
- -Atrial premature beats
- -Atrial flutter
- -Atrial fibrillation
- -Paradoxysmal supraventricular tachycardias
- -Focal atrial tachycardia
- -Multifocal atrial tachycardias
- AV node:
- -Paroxysmal reentrant tachycardias (AV or AV nodal)
- Ventricles:
- -Ventricular premature beats
- -Ventricular tachycardia
- -Torsades de pointes
- Ventricular fibrillation
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Supraventricular tachyarrhythmias
Regular vs irregular rhythm
- Regular rhythm:
- -Sinus tachycardia
- -Reentrant SVTs (AVNRT, AVRT)
- -Focal atrial tachycardia
- -Atrial flutter
- Irregular rhythm:
- -Multifocal atrial tachycardia
- -Atrial fibrillation
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SVT with regular rhythm
- Sinus Tach:
- -100-180
- -normal p waves
- -atrial may slow in response to carotid massage
- Reentrant SVTs:
- 140-250 bpm
- -P wave: hidden or retrograde
- -May abruptly terminate with carotid sinus massage
- Focal atrial tachycardia:
- 130-250
- P waves differ from normal
- AV block may increase; doesn't usually revert with carotid sinus massage
- Atrial flutter:
- -180-350
- -Saw toothed p waves
- -AV block may increase with carotid sinus massage
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- Atrial premature beats:
- Atrial focus outside the SA node
- Common in normal and diseasesd hearts
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- Atrial flutter
- Rate: 180-350bpm
- P wave: "saw-toothed"
- Carotid massage: AV block may increase
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Wolfff-parkinson-white syndrome
- ECG: characteristic delta wave indicates pre-excitation of the ventricles
- Shortened PR interval
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Multifocal atrial tachycardia
- Irregular rhythm
- Each QRS is preceded by a P wave
- P waves vary in morphology
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Ventricular tachycardias
- Monomorphic VTs:
- -structural abnormality that supports a reentry circuit
- Polymorphic VTs:
- -multiple ectopic foci or continually changing reentry circuit
- Torsades de pointes:
- -most common cause of polymorphic VT
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