Arrhythmias

Heme-Cardiovascular Block
Notes on a Difficult Concept  Combined from Lecture and Lilly

2 basic mechanisms of arrhythmias:

 Automaticity Slowed conduction
o Ectopic focus takes over
 Re-entry
o “Circus rhythm”
o Most common mechanism for the
arrhythmias we encounter!

Evaluating Cardiac Rhythm:

1. What are the atria doing?
 (P waves)
2. What are the ventricles doing?
 (QRS complexes)
3. Relationship between P and QRS?
 (Is there a P in front of every QRS?)

Supraventricular Arrhythmias:
 Simple deviations from normal sinus rhythm:
o Sinus arrhythmia
o Sinus tachycardia
o Sinus bradycardia
 More complex abnormal rhythms:
o Ectopic atrial tachycardia (PAT*)
 *Previously known as paroxysmal atrial tachycardia?
o Wandering atrial pacemaker (WAP)
o Multifocal atrial tachycardia (MAT)
o Atrial flutter
o Atrial fibrillation (AFIB)
 Re-entrant supraventricular rhythms:
o AV nodal re-entrant tachycardia (AVNRT)
o AV re-entrant tachycardia (AVRT)

Boring:
Sinus Arrhythmia
  Largely benign speeding and slowing of impulses that originate at the
SA node
 Often seen in healthy young people
Sinus Bradycardia
 Impulses originate in SA node, but too slow!
 BPM < 50
Sinus Tachycardia
 Impulses originate in SA node, but too fast!
 BPM > 100

Ectopic Atrial Tachycardia (PAT)

 Will have P-waves that are regularly associated with QRS complexes
 P-waves may look different than a normal P-wave, but do not look
different from each other
o PAT has an ectopic focus, but it is not wandering

Wandering Atrial Pacemaker (WAP)

 Impulses originate in varying atrial locations
o This results in different P-wave morphologies (at least 3)
o But they are each associated with a QRS complex!
 There will be a normal rate with WAP, it is not a tachycardia

Multifocal Atrial Tachycardia (MAT)

 Like PAT or WAP there are P-waves associated with each QRS
complex
 However, they have multiple (at least 3) morphologies
 The rate of impulses is also very fast (>100) in MAT
 EKG appearance:
o The strange and varied morphologies of P waves can often look
like AFIB, however there should be an isoelectric baseline
appearing in the EKG of MAT, unlike in AFIB, which is
consistently chaotic and undulating
 Is associated with very sick patients and hypoxia
o Occurs most often in the setting of severe pulmonary disease
and hypoxemia
 Treatment
o Must target the underlying causative disorder to cure!
o However, the ventricular rate can be temporarily stabilized
  Calcium channel blocker (verapamil) is often effective for
this measure
Atrial Flutter
 A type of circus rhythm
 Classically occurs at exactly 300/minute, but under some
circumstances may be slower
o Does not occur at higher rates in adults
 The AV node cannot conduct 300 impulses a minute
o Acts as a “brake” that slows down the transmission of impulses
and prevents excessively fast ventricular contractions from the
flutter
o Classical pattern is for the AV node to block/fail to transmit
every other beat
 Results in a HR of 150bpm
o The transmission rate through the AV node can be variable,
however
 Depends on the health of the AV node – still might not be
able to transmit at 150bpm
 Also depends on treatment – atrial flutter is often treated
with drugs that slow conduction through the AV node
 EKG appearance:
o Often described as a “picket fence” or “saw-tooth pattern”
Atrial Fibrillation (AFIB)
 A type of circus rhythm
 Most common abnormal rhythm seen, especially in older patients
 Can occur at even faster rates than atrial flutter
 Again, the AV node cannot conduct impulses that fast
o The actual HR depends on the rate of AV node conduction
 EKG appearance:
o Unorganized and chaotic undulating baseline
o Helpful for distinguishing from MAT, which has a flat and
isoelectric appearing baseline
AVNRT
 A premature atrial beat uses the “alpha” pathway to conduct through
the AV node
o The “beta” pathway is still recovering (refractory)
 By the time the impulse is transmitted to the ventricles, it can also be
transmitted retrograde, up the “beta” pathway
o The “beta” pathway has had enough time to recover
  More common than AVRT
 EKG appearance:
o Fast rhythm
o Narrow complexes
o Upside down (retrograde) P-waves, that occur after QRS
complexes

5. Re-enters and keeps 4. Depolarizes atrium in

going in a “circus rhythm” retrograde direction

1. APB conducts in
the anterograde
direction

3. “Re-enters” the beta

2. It successfully pathway, conducting in the
depolarizes the ventricle retrograde direction

AVRT
 Also called pre-excitation syndrome or Wolf-Parkinson-White
Syndrome (WPW)
 Occurs in patients with a congenital anomaly where there is an extra-
fast conduction pathway between the atrium and ventricle
o Called “accessory pathway” or “bypass tract”
o Conducts really fast
 SO this can have different appearances depending on whether a
premature atrial beat randomly decides to go down the normal AV
node path, or the accessory pathway
 Normal conduction without tachycardia:
o You can have an impulse randomly decide to go down either
the accessory pathway or regular AV node
 o If it goes down the accessory pathway:
 Suuuper fast conduction
 Causes the ventricles to depolarize pretty much
immediately
 Lose the PR interval, which gives the appearance of a
slightly widened QRS complex
 The early ventricular depolarization is called a “delta
wave”
 “Delta wave” considered the “footprint” of WPW
 If you get a circus rhythm from an atrial premature beat entering the
accessory pathway (and going up the regular pathway) it looks a lot
like VT
 Called the “antidromic” AVRT
 If you get a circus rhythm from an atrial premature beat entering the
normal AV node pathway (and going back up the accessory pathway)
it looks a lot like AVNRT on EKG
o There is normal conduction down AV node, but then fast
retrograde conduction up the accessory pathway with
retrograde depolarization of the atria
o There aren’t any delta waves on this so-called “orthodromic”
AVRT
 Because the accessory pathway is not being used for
conduction to ventricles, the regular AV node is!

Lilly Clinical Arrhythmias Chapter Outline:

 Arrhythmias – are they fast or are they slow?
o Bradyarrhythmias
 o Tachyarrhythmias
 Bradyarrhythmias – where is the origin?
o Sinoatrial node
o Escape rhythms
o Atrioventricular conduction system
 Tachyarrhythmias – where is the origin?
o Supraventricular
o Ventricular

 Bradyarrhythmias – sinoatrial node

o Sinus bradycardia
o Sick sinus syndrome
 Bradyarrhythmias – escape rhythms
o Junctional
o Ventricular
 Bradyarrhythmias – atrioventricular conduction system
o First degree
o Mobitz I
o Mobitz II
o Third degree
 Supraventricular tachyarrhythmias
o Sinus tachycardia
o Atrial premature beats (APBs or PABs)
o Atrial flutter
o Atrial fibrillation
o Paroxysmal atrial tachycardias (PATs or ectopic/focal atrial
tachycardia)
o Multifocal atrial tachycardias (MATs)
o AVNRT
o AVRT
 Ventricular tachyarrhythmias
o Ventricular premature beats (VPBs or PVBs)
o Ventricular tachycardia
 Torsades de Pointes
o Ventricular fibrillation
Bradyarrhythmias
 Sinus Bradycardia
o Straightforward, <60bpm
 o Originates in SA node
 Sick Sinus Syndrome (SSS)
o Caused by an intrinsic dysfunction of the SA node
o Results in periods of bradycardia
o Symptoms:
 Dizziness
 Confusion
 Syncope
o Treatment
 IV anticholinergic drugs
 IV beta-adrenergic agents
 Both transiently accelerate HR
 If problem is chronic and not corrected by removal of
“aggravating factors”
 Requires placement of a pacemaker
o Common in elderly patients
 Can be seen combined with AF
 AF produces tachycardia which overdrive suppresses the
SA node
 Once the fibrillation stops, there is a period of profound
sinus bradycardia
 Treatment includes anti-arrhythmic drugs to suppress
tachyarrhythmias plus pacemaker placement to prevent
bradycardia
 Escape Rhythms
o Junctional Escape Rhythm
 No P waves are present
 Has a normal, narrow QRS complex
 May see retrograde P waves
 Will be inverted (negative) on leads II, III, and aVF
 Because the atria are being activated from the
inferior direction!
 Approximately 40-60 bpm
o Ventricular Escape Rhythm
 No P waves are present
 Has a widened QRS complex
 Can have appearances similar to the BBBs, depending on
the origin of the escape rhythm
 Approximately 30-40 bpm
 o Treatment
 Similar to that for SSS
 First-Degree AV Block
o Prolongation of PR interval
 >5 small boxes (>0.2 seconds)
o Often benign and asymptomatic, but it can be associated with
disease in the AV node or iatrogenic causes
 Second-Degree AV Block
o Has intermittent failure of AV conduction
o Results in some P waves that are not followed by a QRS
o Mobitz I
 Wenckebach block
 Progressive increase of PR interval
 Eventually results in a dropped QRS complex, for a single
beat
 Results from impaired AV node conduction
 Treatment
 Not necessary in many cases
 Often benign or transient
o Can be transient with an acute MI
 If symptomatic:
o IV atropine
o IV isoproterenol
 Improve AV conduction
o May require pacemaker placement if the block
is symptomatic, does not resolve, or persists
when aggravating factors are corrected
o Mobitz II
 Non-Wenckebach block
 No gradual lengthening of PR interval, QRS complexes
are dropped without warning
 High-grade AV block:
 When two or more sequential P waves are not
followed by QRS complexes
 Often from more distal impairments of conduction, i.e.
Bundle of His or Purkinje fibers
 Can result in a widened QRS, but often normal width
 Treatment
  Pacemakers are typically placed, even in
asymptomatic patients
 Because may progress to complete heart block
without warning
o Third-Degree AV Block
 Most common cause(s):
 Adults:
o Acute MI
o Degeneration of conduction pathways with
age
 Children:
o ?
 There is no connection between P waves and QRS
complexes
 A type of AV dissociation
 P waves may be said to be “marching through”
 Escape rhythm for QRS complexes can be
junctional or ventricular
 Symptoms
 Light-headedness
 Syncope
 Treatment
 Pacemaker placement is almost always necessary

Tachyarrhythmias
 There are 3 main mechanisms for tachyarrhythmias
o Enhanced automaticity
o Re-entry
o Triggered activity

Tachyarrhythmias
Supraventricular Arrhythmias
 SVTs can be broken down into two large classes:
o Regular rhythm (constant PP interval)
o Irregular rhythm
 Those with a regular rhythm are:
o Sinus tachycardia
o PATs (ectopic or focal atrial tachycardia)
o Reentrant SVTs (AVNRT, AVRT, etc.)
 o Atrial flutter
 Those with an irregular rhythm are:
o MATs
o Atrial fibrillation
 Sinus Tachycardia
o Pretty straightforward, just a fast SA node discharge
o >100bpm
o Often caused by:
 Increased sympathetic tone
 Decreased vagal tone
 Physiologic response to exercise
o May come from some pathologic conditions as well
 Treatment should focus at the underlying cause
 Atrial Premature Beats (APBs or PABs)
o Very common in healthy and diseased hearts
o Usually asymptomatic
 Can occasionally cause palpitations
o P waves will occasionally appear earlier than normal
 Do not arise in the SA node
 Gives the P wave an abnormal shape
 If the P wave fires while the AV node is still refractory,
there will be no QRS complex = blocked APB
 If the P wave fires after the AV node has recovered, but
one or part of the bundle branches is still refractory, there
will be an abnormally wide QRS complex = APB with
aberrant conduction
o Treatment
 Only required if symptomatic
 Beta-blockers are preferred first line
 Atrial Flutter
o Rapid, regular atrial activity
o >180bpm
o Often, not all impulses will be conducted through the AV node
 Ex: Atrial rate is 300 bpm and ventricular rate is 150 bpm
 AV node is “blocking” every other beat = 2:1 block
 Vagal maneuvers decrease AV node conduction
 Thus, it increases the degree of the block (i.e. slows
the ventricular rate)
o Commonly caused by reentry over a large, fixed circuit
 Most common is atrial tissue along the tricuspid valve
annulus
o P waves have saw-tooth (or picket fence) appearance
o Pre-existing heart disease = more likely to have atrial flutter
o Symptoms
 If the ventricular rate < 100bpm
 Usually asymptomatic
 If the ventricular rate > 100bpm
 Palpitations
 Dyspnea
 Weakness
o Anti-arrhythmics that decrease speed of atrial flutter may
paradoxically increase the ventricular rate
 Gives the AV node enough time to recover, potentially to
transmit the flutter in a 1:1 fashion
 Potentially a more dangerous rhythm!
o Treatment
 Recent onset with symptoms may use electrical
cardioversion to restore sinus rhythm
 Can be terminated by rapid atrial stimulation using a
pacemaker, most useful for patients who have pacing
wires already present
 Pharmacologic choices:
 Increase AV block
o This slows the ventricular rate
o Beta-blockers
o Calcium channel blockers
 Verapamil or diltiazem
o Digoxin
 After the ventricular rate has been slowed,
antiarrhythmic drugs can be used to restore sinus
rhythm
o May slow conduction
o Or may prolong refractory period of atrial
myocardium
 Once sinus rhythm is restored, anti-arrhythmics may
be used chronically to prevent recurrences
  Catheter ablation may be preferred to pharmacologic
therapy to prevent recurrence in some patients
 Atrial Fibrillation
o Chaotic rhythm
o No discernable P waves
o >300-350 bpm
o Will typically have an irregularly irregular rhythm of ventricular
discharge (depending on which impulses are randomly
transmitted through the AV node)
o Patients may shift between fibrillation and flutter
o Mechanism:
 Multiple wandering reentrant circuits within the atria
 Enlarged atrium increases potential for this to occur!
o Symptoms:
 If ventricular rate is < 100 bpm
 Often asymptomatic
 If ventricular rate is > 100 bpm
 Hypotension
 Pulmonary congestion
 Increased risk of thrombus formation and stroke
o Treatment:
 3 main goals:
 Ventricular rate control
 Assess need for anticoagulation – to prevent
thromboembolism
 Consider restoration of sinus rhythm
 Pharmacologic treatment:
 Similar to atrial flutter
 Control ventricular rate:
o Beta-blockers
o [Certain] calcium channel blockers
 Diltiazem or Verapamil
o Digitalis
 Less useful for fibrillation than flutter
 Anticoagulation is usually warranted if AFIB has been
present for >48hrs
 If symptoms persist, despite control of ventricular rhythm,
may need to convert to sinus rhythm
 Chemical cardioversion with antiarrhythmic drugs
  Electrical cardioversion
 Various non-pharmacologic methods for management
have been devised
 AVNRT
o Atrioventricular nodal reentrant tachycardia = AVNRT
o Description of technical conditions that trigger:
 APB occurs
 Transient unidirectional block in the fast pathway
 Relatively slow conduction through the slow, but
recovered, pathway
 Leads to a circus rhythm!
o EKG
 Regular tachycardia
 P waves may not be apparent, as the retrograde P
depolarization may be hidden in the QRS complex
 However, sometimes they may be seen after the
QRS complex
 In this case, will have a negative deflection in leads
II, III, and aVF
o Because of the caudal-to-cranial direction of
atrial activation!
 Normal width of QRS complexes
o Very uncommon for the opposite pathway to occur
 Anterograde conduction down the fast pathway
 Retrograde conduction up the slow pathway
 Results in a distinctly visible P wave following QRS
complex on EKG
o Symptoms:
 Often asymptomatic, especially in healthy young people
 Palpitations
 Light-headedness
 Dyspnea
 In patients with underlying heart disease or the elderly
can lead to severe symptoms, such as:
 Syncope
 Angina
 Pulmonary edema
o Treatment:
 Goal:
  Termination of reentry
 Method:
 Impair the conduction in the AV node
 Increases in vagal tone (transiently) can block AV
conduction enough to stop the tachycardia
 Valsalva maneuver
 Carotid sinus massage
 Pharmacologic options:
 IV adenosine
 IV calcium channel blockers
o Verapamil or diltiazem
 Beta-blockers
 AVRT
o Very similar to AVNRTs
o Key difference – one limb of the reentry loop is an “accessory
pathway” (“bypass tract”), rather than one of the pathways in
the AV node itself
o Ventricular Pre-excitation Syndrome = Wolff-Parkinson-
White (WPW) Syndrome
 Has an accessory pathway that can conduct impulses in
an anterograde direction
 Bypass tract is faster than AV node
 EKG has distinctive appearance during sinus rhythm:
 Shortened PR intervals
 “Slurred” upstroke of QRS = delta wave
 Widened QRS complex
 Tachycardias in WPW can be orthodromic or antidromic
 Othodromic
 Impulse travels anterograde down the AV node
 Travels retrograde up the accessory tract
 Has no delta wave
 Has normal width of QRS
 Can see retrograde P waves following QRS
complex
 Antidromic
 Rarer than orthodromic pattern
 Impulse travels anterograde down the accessory
pathway
 Travels retrograde up the AV node
  Has wide QRS complex
 May be difficult to distinguish from VT on EKG
o Treatment:
 Pharmacologic:
 Many drugs that normally slow AV node conduction
can increase the speed of the accessory
pathway
o This can precipitate faster ventricular rates
and hemodynamic collapse
o Digitalis, beta-blockers, certain calcium
channel blockers
 Sodium channel blockers and some other anti-
arrhythmics can slow the conduction speed of both
the AV node and accessory pathway
o Preferred pharmacologic patients
 If patients are not hemodynamically stable, immediate
cardioversion is required
 If patients are hemodynamically stable, chemical
cardioversion with procainamide or ibutilide can terminate
arrhythmias in WPW
 Radiofrequency ablation of the accessory pathway may
be the preferred route of treatment in modern patients
 Focal Atrial Tachycardia or Ectopic Atrial Tachycardia or PAT
o Can be caused by:
 Automaticity of an ectopic site in the atria
 Reentry
o Looks like a sinus tachycardia, but the P wave differs from
NSR
o Can by caused by:
 Digitalis toxicity
 Elevated sympathetic tone
o Treatment:
 Correction of contributing factors
 Vagal maneuvers will not effect
 Beta-blockers, calcium channel blockers, and some anti-
arrhythmics can be effective
 Multifocal Atrial Tachycardia (MAT)
o Irregular rhythm with at least 3 different P wave
morphologies
 o Distinguished from AFIB by the flat/isoelectric baseline
between P waves (AFIB has the chaotic, undulating baseline)
o Treatment:
 Underlying cause must be treated
 Temporary stabilization of ventricular rate can be
achieved with verapamil
Tachyarrhythmias
Ventricular Tachyarrhythmias
 Often more dangerous than supraventricular rhythm disorders
 Ventricular Premature Beats (VPBs, PVBs)
o Ectopic ventricular focus fires an action potential
o Will have a widened QRS complex
 QRS complex will not be related to a preceding P wave
o Can occur in repeating patterns
 Every alternate beat is a VPB = bigeminy
 Two normal beats precede each VPB = trigeminy
 Consecutive VPB = couplets, triplets
o Common in healthy and diseased hearts
o Often benign, but can use beta-blockers for symptomatic
control if necessary
o If patients have heart disease that places them at risk for life-
threating arrhythmias related to VPBs, then an implantable
cardioverter-defibrillator is recommended
 Ventricular Tachycardia
o Series of 3 or more consecutive VPBs
o Categories:
 Sustained VT:
 Persists for > 30 seconds
 Produces severe symptoms, i.e. syncope
 Requires termination by cardioversion
 Non-sustained VT
 Self-terminates
o EKG
 Has wide QRS complexes
 Rate is > 100-200 bpm
 If each QRS appears the same and rate is regular =
monomorphic VT
 If the QRS complexes change and rate varies =
polymorphic VT
  Usually degenerates to VFIB
 The wide complexes can look like specific situations with
various SVTs, and it can be difficult to tell VT apart
 Concordance of the QRS complexes in the
precordial leads can support VT
 Patient’s clinical status should also be considered –
VT more likely to be in worse shape, SVT more
likely to be well tolerated
o Symptoms:
 Syncope
 Pulmonary edema
 Progression to cardiac arrest
 However, if VT is sustained at a relatively slow rate, it
may only cause palpitations
 Torsades de Pointes
o Specific type of polymorphic VT
o There are varying amplitudes of the QRS complexes
 Appear to be “twisting” around the baseline
 May also be described as a waxing and waning pattern
 Ventricular Fibrillation
o What nobody wants to see
o Rapid stimulation of ventricles
 No coordination of contractions
 Results in cessation of CO, and death
o EKG lacks discrete QRS waveforms and has a chaotic,
irregular appearance