Atrial Fibrillation w/ rapid ventricular response (RVR, >100 bpm) or slow ventricular response
(<100 bpm) => parasystolic event.
 Irregular
 No P waves
 Risk for strokes and PE => requires anticoagulation
 No “A” waves in JVP
Wandering Atrial Pacemaker (W.A.T)
 Irregular
 HR <100 bpm
 P-waves look different
Multifocal Atrial Tachycardia (M.A.T)
 Irregular
 HR >100
 P-waves look different
 Does not require anticoagulation => in order to precisely differentiate may use
methods to slow AV conduction.
Escape Rhythms: occurs when there is a sufficient pause to allow a slower pacemaker to
depolarize.
Atrial Escape Rhythm
 Regular
 After pause, HR slightly slower than 60-80 and previous rhythm
 After pause, P-waves look different
 Narrow QRS <0.12 s
Junctional Escape Rhythm
 Regular
 After pause, HR between 40-60 bpm
 No P-waves
 Narrow QRS
*Retrograde P wave: may be present and can appear before, during or after the QRS complex.
Retrograde P waves are usually inverted in the inferior leads. The electrical impulse travels
forward, or in an antegrade direction, to produce a NORMAL QRS complex. Retrograde P waves
that are very close to the QRS, or within it, are presumed to occur from a junctional rhythm, as
the impulse leaves the ectopic pacemaker and travels forward and backward at the same time.
*Accelerated Junctional Rhythm => regular, after pause = HR 60-80, no P-waves, narrowed
QRS.
Ventricular Escape Rhythm
 Regular
 After pause, HR between 20-40 bpm
 No P-waves
 Wide QRS
*Ventricles are not affected by parasympathetic NS, unlike SA and AV node.
Premature Atrial Contraction: focus in the atrium (not the sinoatrial node) generates an action
potential before the next scheduled SA node action potential.
 After PAC, HR may be different after resetting of SA node.
 Abnormally shaped P wave (occurred outside of SA node) that appears before time
according to previously regular P-P interval. Before PAC, P-P interval is regular; during
PAC, P-P interval is irregular; after PAC, P-P interval is regular. Compensatory pause
following contraction => the extra atrial action potential causes the SA node to become
refractory to generate its next scheduled beat, and thus it must “skip a beat” and will
resume exactly 2 P-P intervals after the last normal sinus beat.
 QRS complex changes depending on the prematurity of the atrial beat =>
o if AV node is not on refractory period => narrow QRS
o if AV node is partially on refractory period => wide QRS
o if AV node is on refractory period => no QRS
*Atrial Bigeminy: pattern of heart beats that occurs in couplets. A regular (or sinus) beat is
followed by a “premature” atrial beat.
 P wave typically has a different morphology and axis to the sinus P waves.
 Last P wave is the premature one.
 Last QRS is the widest one.
 Resetting of SA node occurs.
Bigeminy — every other beat is a PAC.
Trigeminy — every third beat is a PAC.
Quadrigeminy — every fourth beat is a PAC.
Couplet – two consecutive PACs.
Triplet — three consecutive PACs.
Premature Junctional Complex (PJC)
 Narrow QRS complex, either (1) without a preceding P wave or (2) preceded by an
abnormal P wave with a PR interval of < 120 ms (these “retrograde” P wave are usually
inverted in leads II, III and aVF).
 Occurs sooner than would be expected for the next sinus impulse.
 Followed by a compensatory pause.
Bigeminy — every other beat is a PJC.
Trigeminy — every third beat is a PJC.
Premature Ventricular Complex (PVC)
 Broad QRS complex (≥ 120 ms) with abnormal morphology (mostly negative deflection
as the direction of vector of foci in ventricle propagate in opposite direction).
 P waves are not affected. P-P interval are regular.
 Premature — i.e. occurs earlier than would be expected for the next sinus impulse.
 Discordant ST segment and T wave changes.
 Usually followed by a full compensatory pause. With a full compensatory pause, the
next normal beat arrives after an interval that is equal to double the preceding R-R
interval (see diagram below).
 Retrograde capture of the atria may or may not occur => concealed retrograde
conduction, depolarization of AV node by ventricular extrasystole.
Classification
 Unifocal — Arising from a single ectopic focus; each PVC is identical.
 Multifocal — Arising from two or more ectopic foci; multiple QRS morphologies.
Patterns
 Bigeminy — every other beat is a PVC.
 Trigeminy — every third beat is a PVC.
 Quadrigeminy — every fourth beat is a PVC.
 Couplet — two consecutive PVCs.
 Triplet — three consecutive PVCs.
 >3 consecutive PVC = Ventricular Tachycardia.
*Multifocal PVCs
*Ventricular Bigeminy
Tachyarrhythmias
Paroxysmal Atrial Tachycardia (PAT, aka Paroxysmal supraventricular tachycardia, PSVT)
Etiology: multiple causes including digoxin toxicity, atrial scarring, catecholamine excess,
congenital abnormalities; may be idiopathic.
 Atrial rate 200 +/- 50 bpm.
 P wave morphology is abnormal when compared with sinus P wave due to ectopic
origin.
 There is usually an abnormal P-wave axis (i.e. inverted in the inferior leads II, III and
aVF).
 At least three consecutive identical ectopic p waves.
 QRS complexes usually normal morphology unless pre-existing bundle branch block,
accessory pathway, or rate related aberrant conduction.
 Isoelectric baseline (unlike atrial flutter).
 AV block may be present — this is generally a physiological response to the rapid atrial
rate, except in the case of digoxin toxicity where there is actually AV node suppression
due to the vagotonic effects of digoxin, resulting in a slow ventricular rate =>
o “PAT with block”:
Paroxysmal Junctional Tachycardia (Atrioventricular Nodal Reentrant Tachycardia, AVNRT –
similar but not the same)
Etiology: Digoxin toxicity (= the classic cause of AJR), Beta-agonists, i.e. isoprenaline,
adrenaline, Myocardial ischemia, Myocarditis, Cardiac surgery.
 Atrial rate 200 +/- 50 bpm.
 Retrograde P waves inverted in II, III and aVF; upright in V1 and aVR.
 No visible P-waves (hidden within the QRS complex) or P-waves immediately before
the QRS or P-waves immediately after the QRS complex.
 Short PR interval (< 120 ms) => junctional rather than atrial focus.
Paroxysmal Ventricular Tachycardia (V-Tach)
Etiology: CAD, aortic stenosis, cardiomyopathy, hypokalemia or hypomagnesemia, hypoxemia.
Duration:
 Sustained = Duration > 30 seconds or requiring intervention due to hemodynamic
compromise.
 Non-sustained = Three or more consecutive ventricular complexes terminating
spontaneously in < 30 seconds.
Features:
 Rapid heart rate (200 +/- 50 bpm).
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Broad QRS complexes (> 140 ms).
Absence of typical RBBB or LBBB morphology.
Extreme axis deviation (“northwest axis”, -90 to -180 degrees) — QRS is positive in aVR
and negative in I + aVF.
AV dissociation (P and QRS complexes at different rates).
o Capture beats — occur when the sinoatrial node transiently ‘captures’ the
ventricles, in the midst of AV dissociation, to
produce a QRS complex of normal duration (<120
ms).
o Fusion beats — occur when a sinus and ventricular
beat coincide to produce a hybrid complex of
intermediate morphology.
Positive or negative concordance throughout the chest
leads, i.e. leads V1-6 show entirely positive (R) or entirely
negative (QS) complexes, with no RS complexes seen.
Brugada’s sign – The distance from the onset of the QRS
complex to the nadir of the S-wave is > 100ms.
Josephson’s sign – Notching near the nadir of the S-wave.
RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favor
of VT. This is in contrast to RBBB, where the right rabbit ear is taller.
AV dissociation: P waves (arrowed) appear at a different rate to the QRS complexes.
Capture beat: the sinus node “captures” the ventricles producing a narrow-complex beat.
Fusion beats: the first of the narrower complexes is a fusion beat (the next two are capture
beats).
POSITIVE concordance in the precordial leads/ NEGATIVE concordance in the precordial leads
Brugada’s sign (red callipers) and Josephson’s sign (blue arrow).
Atrial or Junctional (Supraventricular) Tachycardia w/ Bundle Branch Block (BBB, aka
Aberrancy) vs. Ventricular Tachycardia.
*Typically, does pt. have CAD? Yes => V-Tach; QRS: <140 => PSVT vs. >140 => VT.
*SVT w/ BBB can be treated w/ Beta-blockers vs. VT cannot be treated w/ Beta-blockers!!!
Brugada Criteria
 Absence of an RS complex in all precordial leads (V1-6)? Yes => V-Tach.
Precordial R waves only/Precordial S waves only
Precordial RS waves => go to step 2
 R to S interval >100 ms in one precordial lead? Yes => V-Tach.
*<100 ms => go to step 3
 AV dissociation? Yes => V-Tach.
P waves can be spotted in between QRS complexes (circled) and superimposed upon the T
wave causing a peaked appearance (arrow)/No AV dissociation => go to step 4
 Morphology criteria for VT present both in V1-2 and V6? Yes => V-Tach or NO => SVT
w/ Aberrancy (BBB).
VT is frequently either in a right bundle branch block pattern (upright in V1) or a left bundle
branch block pattern (downward in V1).
If upward in lead V1 (RBBB pattern), then VT is present in the following situations:
 A monophasic R or biphasic qR complex in V1.
 If an RSR' pattern (“bunny-ear”) is present in V1, with the R peak being higher in
amplitude than the R’ peak, then VT is present.
 An rS complex in lead V6 favors VT.
If downward in lead V1 (LBBB pattern), then VT is present in the following situations:
 The presence of any Q or QS wave in lead V6 favors VT.
 A wide R wave in lead V1 or V2 of 40 ms or more favors VT.
 Slurred or notched downstroke of the S wave in V1 or V2 favors VT.
 Duration of onset of the QRS complex to peak of QS or S wave > 60 ms favors VT.
Polymorphic VT and Torsades de Pointes (TdP)
*Fatal rhythm
Etiologies: prolonged QT interval (> 440 ms) => induced by medications such as Levaquin,
Azithromycin, Amiodarone, Fluconazole, Zofran, Type 1A and Type III Antiarrhythmic drugs;
congenital; hypokalemia, hypomagnesemia, hypocalcemia.
Treatment: IV magnesium (initially), if not converted to NSR => asynchronized electrocardioversion.
*The QTc rule of thumb is this: If the QT interval is less than half the RR interval, then the
corrected QT (QTc) is not prolonged.
*"R-on-T phenomenon" is the superimposition of an ectopic beat on the T wave of a
preceding beat. Early observations suggested that R-on-T was likely to initiate sustained
ventricular tachyarrhythmias.
*TdP is initiated when a PVC occurs during the preceding T wave, known as ‘R on T’
phenomenon.
*HR => 250-350 bpm
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Sinus rhythm with inverted T waves, prominent U waves and a long Q-U interval due to
severe hypokalemia (K+ 1.7)
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A premature atrial complex (beat #9 of the rhythm strip) lands on the end of the T wave,
causing ‘R on T’ phenomenon and initiating a paroxysm of polymorphic VT.
Because of the preceding long QU interval, this can be diagnosed as TdP.