SINUS PAUSE

• Temporary cessation of sinus node activity

• Synonymous with sinus “arrest” – pertains to prolonged
sinus pause
• Difference from sinus exit block: sinus pause/arrest is not
a multiple of the normal P-P interval
 2nd degree SA Block, Type 1

• Wenckebach pattern: progressive lengthening of sinoatrial

conduction time until the impulse is blocked at the level of atrial
tissue
• Progressive shortening of P-P intervals, followed by a pause in
sinus rhythm that is < the sum of any 2 preceding P-P intervals
 2nd degree SA Block, Type 2

• Classic sinus exit block

• Failure of impulse transmission
• No visible P-QRS-T complex for ≥1 cycle, the P-P interval of
the pause is an exact multiple of the normal P-P interval
ATRIOVENTRICULAR BLOCK
 1st Degree AV Block

• P wave: always followed by a QRS complex, but

with a slight delay
• PR interval: Fixed, prolonged (>0.20 secs)
• QRS Complex: usually narrow
 2nd Degree AV Block: MOBITZ type 1 (Wenckebach)

• Rhythm: Irregular
• PR interval: Progressivelylengthening
• (+) P wave not followed by a QRS complex “dropped beat”
• After the pause, an ECG complex with shorter PR interval (compared to that preceding
the pause)
• QRS Complex: usually narrow
 2nd Degree AV Block: MOBITZ type 2

• PR interval: Constant in length

• (+) P wave not followed by a QRS “dropped
beat” (no warning)
 2nd Degree AVBlock
TYPE 1 TYPE 2
Due to conduction defects in the AVnode Due to conduction defects in the distal or infra-
His conduction system
Prolonging PR interval No changes in the PR and RR interval
Shortening RR interval

(+) Dropped beat (+) Dropped beat

Responds to pharmacologic treatment Does not respond well to drugs.

Rarely requires pacing Requires pacing
 3rd Degree AV Block / Complete AV block

• PP interval and RR interval: constant

• P and QRS waves: occur regularly but are independent of
each other
• Escape rhythm is either junctional (narrow QRS) or
ventricular (wide QRS)
High Grade AV Block / Advanced Heart Block

• Ratio of P waves to successfully conducted QRS

complexes is at least 3:1 or higher
• PR interval: Constant
 SINUS BRADYCARDIA

• Normal upright P wave in lead II preceding every QRS

complex
• Ventricular rate of < 60 bpm
 JUNCTIONAL RHYTHM

• Pacemaker: AV junction with ventricular rate of 40-60 bpm

• Rhythm (R-R interval): Regular
• P wave: appear before, after or buried w/in QRS complex
• QRS complex: Narrow (≤ 0.12 s)
 IDIOVENTRICULAR RHYTHM

• Pacemaker: His-Purkinje System (HPS) with ventricular

rate of 20-40 bpm
• Rhythm (R-R interval): Regular
• P wave: absent
• QRS complex: Wide (> 0.12 s)
 SINUS TACHYCARDIA

• Normal upright P wave in lead II preceding every QRS

complex
• Atrial rate of > 100 bpm
• Ventricular rate of > 100 bpm
 SINUS ARRHYTHMIA

• Rate: normal (within 60-100 bpm)

• Rhythm: variation in P-P or R-R interval ≥ 120 msecs
• P wave, PR interval, QRS complex: Normal
SUPRAVENTRICULAR TACHYCARDIA

• Various morphologies of P waves (may be buried in

the QRS complex in AV nodal reentry, or following the
QRS in concealed bypass tract)
• Narrow QRS complex
Tachycardias Originating from Atria
 ATRIAL FLUTTER
macroreentrant atrial tachycardia

• Rhythm: Regular (but may be variable)

• P-WAVE: Sawtooth flutter waves w/ atrial rate 240-300 bpm
• QRS: usually normal (narrow complex)
• Organized reentry creates organized but rapid atrial activity
 ATRIAL FIBRILLATION

• Rate: atrial ≥ 350 bpm producing fibrillatory waves

• Rhythm: Irregularly irregular
• P-WAVE: no discernable P-wave
• QRS: usually normal (narrow complex)
 ATRIAL FIBRILLATION

• Most common sustained cardiac arrhythmia in adults

• Most common correctable cause is HYPERTHYROIDISM
• Rapid, erratic electrical discharge from multiple atrial foci
 FOCAL ATRIAL TACHYCARDIA

• P-WAVE: discrete with morphology different from that of sinus P-

wave
• PR interval: variable
• QRS: normal
• Rhythm: Regular
• Rate: Fast (>100bpm)
 FOCAL ATRIAL TACHYCARDIA

• Single focus (distict from the SA node) in the atria

that is exhibiting automaticity and discharging at a
faster rate than the SA node, effectively overriding
it.
MULTIFOCAL ATRIAL TACHYCARDIA

• P-WAVE: > 3 different forms

• QRS: normal
• PR Interval: variable
• Rhythm: irregular
• Rate: Fast (>100bpm)
MULTIFOCAL ATRIAL TACHYCARDIA

• Similar to atrial tachycardia but with multiple

discharging foci
• Seen in patients with pulmonary disease
Atrioventricular Nodal Reentrant
Tachycardia
 AVNRT
• MC paroxysmal sustained tachycardia in healthy young adults;
more common in women
• Reentry circuit involves fast and slow pathways within the AV
node
• Regularly tachycardia with retrograde conducted P-waves visible at
the end of the QRS complex or buried in QRS
• Pseudo-S wave in leads II, III, aVF
• Pseudo-r’ wave in lead I
• Narrow QRS tachycardia with short RP-interval (<70 msec)
Atrioventricular Reentry
Tachycardia
 AVRT
• Paroxysmal sustained tachycardia similar to AVNRT
• Reentry circuit involving AV node and accessory pathway
connecting atria and ventricles (acts as a “shortcut” that
bypasses the AV node)
• Regular narrow-QRS tachycardia with a short RP-interval
• RP interval > 70 msec
• During sinus rhythm (when patient is not having an episode of
tachycardia), the Wolff-Parkinson-White or WPW pattern may be
observed in the resting 12-lead ECG.
 VENTRICULAR TACHYCARDIA

• Non-sustained: terminates spontaneously within 30 s

• Sustained: persists ≥ 30 s or is terminated by an
active intervention due to hemodynamic instability
 I. MONOMORPHIC VT

• P-WAVE: Not usually visible(dissociation)

• QRS: Broad, all beats within 1 lead have the same
appearance
 MONOMORPHIC VENTRICULAR
TACHYCARDIA: Ventricular Flutter

• Rapid monomorphic ventricular tachycardia with a

sinusoidal appearance
• T wave indiscernible from the QRS complexes
 II. POLYMORPHIC VT

• Beat to beat variations in appearance

(continually changing QRS morphology)
 POLYMORPHIC VENTRICULAR
TACHYCARDIA: Torsades dePointes

• characterized by QRS complexes of changing amplitude

that appear to twist around the isoelectric line and occur
at rates of 200-250/min
• May have prominent U wave or it may merge with the T
wave
Pulseless VT: no effective cardiac output
(-) pulse, (-) BP = DEFIBRILLATION

Unstable VT: (+) pulse, (+) hypotension =

ELECTRICAL CARDIOVERSION

Stable VT: (+) pulse, (+) normal BP = MEDICAL

or PHARMACOLOGIC CARDIOVERSION
Ventricular Fibrillation

• P-WAVE: none
• QRS: no discrete QRS complex
• Rate: > 300 bpm
• NO effective cardiac output
 PREMATURE ATRIAL COMPLEX

• P wave: (+) Premature, flattened or notched

• QRS: Irregular rhythm; Narrow (<0.12s)
 PREMATURE VENTRICULAR COMPLEX

• QRS: Broad (> 0.12 sec); Abnormal Morphology, no

preceding P wave
• T wave: opposite in direction to the major deflection of
QRS
Premature Ventricular Complex
 Premature VentricularComplex
BIGEMINY

• PVC’s alternate with sinusbeats

 Premature VentricularComplex
TRIGEMINY

• PVC’s occur after every 2 sinus beats

 Premature VentricularComplex
QUADRIGEMINY

• PVC’s occur after every 3 sinus beats

 Premature VentricularComplex
COUPLETS

• 2 successive PVC’s
 POOR R WAVE PROGRESSION

In leads V1-V3 (R wave < 3 mm or 0.3 mV) and normal R

wave in V4-V6
 LOW VOLTAGE COMPLEXES
• Chest leads are more significant
• QRS complexes <5 mm in limb leads or <10 mm in
chest leads
 ATRIAL MECHANISMS
WOLFF-PARKINSON-WHITE

• Key feature: slurred upstroke in the QRS complex

• Widened QRS complex
• Shortened PR interval
Ventricular Paced Rhythm
 Ventricular Paced Rhythm
• Pacing stimulus is initiated by a lead in the RV 
ventricular depolarization
• RV and LV depolarization not simultaneous  QRS
complex is widened
• Good capture: pacemaker spike (blip) is followed by QRS
• Poor capture: some pacemaker spikes are not followed by
QRS
Ventricular Paced Rhythm
with Loss of Capture
 Atrial Paced Rhythm

• Pacing stimulus is initiated by a lead in the RA  atrial

depolarization
• Pacemaker spike (blip) is followed by P wave and narrow
QRS
• This setting cannot be used for patients with AV blocks
Atrioventricular Sequential
Paced Rhythm
 Etiologies of Prolonged QT

• Hypocalcemia
• Congenital
• Drugs
 HYPERCALCEMIA

• Shortened QTinterval

• T wave flattening,
inversion or notching
 HYPOKALEMIA

• Broad flat T waves, T wave inversion

• ST depression
• Increased U wave prominence
• QT prolongation
 HYPOKALEMIA

• Broad flat T waves, T wave inversion

• ST depression
• Increased U wave prominence
• QT prolongation
Chronic Renal Failure

• PeakedT waves (from hyperkalemia)

• QT prolongation(from hypocalcemia)
• LVH (from hypertension)
 Posterior LV Wall Involvement
• Posterior LV wall infarction
• Usually associated with
lateral or inferior involvement
• Indirectly recognized by
reciprocal or “mirror-image”
ST depressions in V1 to V3
Reciprocal Changes
• ST-depression in leads opposite those
demonstrating ST-elevation
 Stages of Pericarditis
STAGES DESCRIPTION TIMELINE
1 Widespread ST elevation and PR depression with First 2 weeks
reciprocal changes in aVR
2 Normalization of ST changes: generalized T wave 1 to 3 weeks
flattening
3 Flattened T waves become inverted 3 to several
weeks
4 ECG returns to normal Several weeks
onward
 Pericarditis vs. MI
PERICARDITIS MYOCARDIAL INFARCTION

ST Diffuse ST-segment elevations Localized to leads representing

elevation which are concave upward ischemic LV segments; ST elevations
are convex upward
 Pericarditis vs. MI
PERICARDITIS MYOCARDIAL INFARCTION
T-waves Not inverted until after ST- May begin to invert even before
segment becomes isoelectric ST-segment becomes isoelectric
Q-waves Absent Present
Residual ST- Unusual Common
segment
changes
PR depression Present Absent
STEMI
Arrhythmogenic Right Ventricular
Cardiomyopathy

Epsilon wave in V1 Prolonged S-wave upstroke in

V2 with localized QRS widening
ARVC
 Brugada Pattern
TYPES DESCRIPTION
1 Widespread ST elevation
and PR depression with
reciprocal changes in aVR
2 Normalization of ST
changes: generalized T
wave flattening
3 Flattened T waves
become inverted
Electrical Alternans
 Dextrocardia

• Predominantly negative P-wave, QRS complex, and T-wave in lead I

• Predominantly positive P-wave, QRS complex, and T-wave in lead aVR
• Low voltage in leads V3-V6
Pulmonary Embolism
• McGinn-White sign: S1-Q3-T3 pattern
(deep S-wave in lead I, Q-wave in lead
III, and inverted T-wave in lead III)
• Sinus tachycardia: most commonly
cited abnormality
• T wave inversion in V1-V4: another
commonly cited abnormality
• RBBB (may be complete or incomplete)
• Low amplitude deflections
TEST YOURSELF!
Ventricular Fibrillation

Atrial Fibrillation
Premature Ventricular Complex (Bigeminy)

Supraventricular Tachycardia
 Ventricular Tachycardia

Premature Ventricular Complex

 Atrial Flutter

Pacemaker - Failure to Capture

 Sinus Exit Block

Junctional Tachycardia
Wolff-Parkinson- White Syndrome

Asystole
Premature Atrial Complex

Sinus Tachycardia
Idioventricular Rhythm

Normal Sinus Rhythm

 Wandering Atrial Pacemaker

Second Degree Heart Block Type I

 Accelerated Junctional Rhythm

Pacemaker – Single Chamber - Atrial

 Sinus Arrhythmia

Third Degree Heart Block

Pacemaker AV Sequential

Sinus Bradycardia
 Junctional Escape Rhythm

Second Degree Heart Block Type II

 Pacemaker – Failure to Pace

Pacemaker – Single Chamber - Ventricular

References