Arrhythmias

Arrhythmias 101
101
Fundamentals and what you should
know for the big, bad BOARDS!
 The Basics
• SA Node and AV node cells are slow
conductors activated by calcium, thus
blocked by calcium channel blockers such
as verapamil

• Atrium, Bundle of His, and ventricle cells

are fast conducting and activated by
sodium, thus blocked by sodium channel
blockers (class 1 anti-arrhythmics) such as
quinidine, lidocaine and propafenone.
 4 Mechanisms of Arrhythmia
• reentry (most common)
• automaticity
• parasystole
• triggered activity
 Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

1. 2 distinct pathways that come together at beginning and

end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
 Reentry Mechanism
Premature Beat Impulse
Cardiac
Repolarizing Tissue Conduction
(long refractory period) Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The fast conducting pathway is blocked because of its
long refractory period so the beat can only go down the
slow conducting pathway
 Reentry Mechanism

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast
pathway
 Reentry Mechanism

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
 Reentry Circuits

AV Nodal Reentry
•SVT
Ventricular Re-entry
Atrial Reentry • ventricular tachycardia
• atrial tachycardia SA Node
• atrial fibrillation
• atrial flutter

Atrio-Ventricular
Reentry
• WPW
• SVT
 Reentry Requires…
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
Large reentry circuits, like a-flutter, involve the
atrium.
Reentry in WPW involves atrium, AV node, ventricle
and accessory pathways.
 Automaticity
• Heart cells other than those of the SA node
depolarize faster than SA node cells, and take
control as the cardiac pacemaker.
• Factors that enhance automaticity include:
 SANS,  PANS,  CO2,  O2,  H+,  stretch,
hypokalemia and hypocalcaemia.
Examples: Ectopic atrial tachycardia or multifocal
tachycardia in patients with chronic lung disease
OR ventricular ectopy after MI
 Parasystole…
• is a benign type of automaticity problem
that affects only a small region of atrial or
ventricular cells.
• 3% of PVCs
 Triggered activity…
• is like a domino effect where the arrhythmia is due
to the preceding beat.
• Delayed after-depolarizations arise during the
resting phase of the last beat and may be the cause
of digitalis-induced arrhythmias.
• Early after-depolarizations arise during the plateau
phase or the repolarization phase of the last beat
and may be the cause of torsades de pointes (ex.
Quinidine induced)
 Diagnosis…
Diagnosis…
What tools to use and when to use it…
 Event Monitors
• Holter monitoring: Document symptomatic and
asymptomatic arrhythmias over 24-48 hours. Can
also evaluate treatment effectiveness in a-fib,
pacemaker effectiveness and identify silent MIs.
• Trans-telephonic event recording: patient either
wears monitor for several days or attaches it
during symptomatic events and an ECG is
recorded and transmitted for evaluation via
telephone. Only 20% are positive, but still
helpful.
 Exercise testing
• Symptoms only appear or worsen with exercise.
• Also used to evaluate medication effectiveness
(esp. flecanide & propafenone)
You can assess SA node function with exercise testing.
Mobitz 1 (Wenkebach) is blockage at the AV node, so
catecholamines from exercise actually help!
Mobitz 2 is blockage at bundle of His, so it worsens as
catecholamines from exercise increase AV node conduction,
thus prognosis is worse.
*PVCs occur in 10% without and 60% of patients with
CAD. *PVCs DO NOT predict severity of CAD
(neither for nor against)!
 Signal Averaged ECG
• Used only in people post MI to evaluate risk for v-
fib or v-tach.
• Damage around the infarct is variable, so this
measures late potentials (low-signal, delayed
action potentials) as they pass through damaged
areas.
• Positive predictive value is 25%-50% but
negative predictive value is 90%-95%, thus if test
is negative, patient is at low risk.
 Electrophysiologic Testing…
• Catheters are placed in RA, AV node, Bundle of
HIS, right ventricle, and coronary sinus (to monitor
LA and LV).
• Used to evaluate cardiogenic syncope of unknown
origin, symptomatic SVT, symptomatic WPW, and
sustained v-tach.
*Ablative therapy is beneficial in AV node reentry,
WPW, atrial tachycardia, a-flutter, and some v-
tach. Complication is 1%
Bradyarrhythmias
Bradyarrhythmias
The slow pokes (HR<60)…
 Sick Sinus Syndrome

• Conduction problem with no junctional escape

during sinus pause
• Diagnose with ECG or Holter. If inconclusive,
need electrophysiologic testing.
• If asymptomatic, leave alone. If symptomatic,
needs pacemaker.
 First Degree AV Block

• Delay at the AV node results in prolonged PR

interval
• PR interval>0.2 sec.
• Leave it alone
Second Degree AV Block Type 1
(Wenckebach)

• Increasing delay at AV node until a p wave is not

conducted.
• Often comes post inferior MI with AV node ischemia
• Gradual prolongation of the PR interval before a skipped
QRS. QRS are normal!
• No pacing as long as no bradycardia.
Second Degree AV Block Type 2

• Diseased bundle of HIS with BBB.

• Sudden loss of a QRS wave because p wave was
not transmitted beyond AV node. QRS are
abnormal!
• May be precursor to complete heart block and
needs pacing.
 Third Degree AV Block

• Complete heart block where atria and ventricles

beat independently AND atria beat faster than
ventricles.
• Must treat with pacemaker.
LBBB
 Left Bundle Branch Block

• Left ventricle gets a delayed impulse

• QRS is widened (at least 3 boxes)
• V5 and V6 have RR’ (rabbit ears)
• Be careful not to miss any hiding q waves!
• Pacemaker if syncope occurs
Right Bundle Branch Block
 Right Bundle Branch Block

• Right ventricle gets a delayed impulse

• QRS is widened (at least 3 boxes)
• V1 and V2 have rSR’
• Pacemaker if syncope occurs.
 Bifascicular Block

• RBBB plus LABB OR RBBB plus LPBB

• QRS is widened (at least 3 boxes)
• V5 and V6 have RR’ (rabbit ears)
• V1 and V2 have rSR’
• Pacemaker if syncope occurs
 Tachyarrhythmias
Tachyarrhythmias
The speed demons…(HR >100)
 Tachyarrhythmias
• Supraventricular tachycardia
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia
» Monomorphic
» Polymorphic (Torsades de pointe)
• Ventricular fibrillation
Supraventricular Tachycardia
 SVT
• Reentrant arrhythmia at AV node that is
spontaneous in onset
• May have neck fullness, hypotension and/or
polyuria due to ANP
• Narrow QRS with tachycardia
• First line is vagal maneuvers
• Second line is adenosine or verapamil
• For chronic SVT, class 1A or 1C or amiodarone
or sotalol work well
• Ablation will cure it too, but we usually do this
only in young patients
Multifocal Atrial Tachycardia
 MAT
• Automatic atrial rhythm from various
different foci
• Seen in hypoxia, COPD, atrial stretch and
local metabolic imbalance.
• Three or more types of p waves and a rate
> 100
• Digoxin worsens it, so treat with oxygen
and slow channel blocker like verapamil or
diltiazem.
Wolf Parkinson White
 WPW
• Ventricles receive partial signal normally and
partially through accessory pathway
• Symptomatic tachycardia, short PR interval
(<0.12), a delta wave and prolonged QRS (>0.12)
• Electrophysiologic testing helps to identify the
reentry pathway and location of the accessory
pathway
 WPW
 Because WPW has both normal conduction through the
AV node and accessory pathway conduction that bypasses
the AV node, a-fib can happen via the accessory pathway
 Inhibition of the AV node will end up in worsening the a-
fib because none of the signals are slowed down by the
AV node before hitting the ventricle.
* Do not use any meds that will slow AV node conduction,
ie digoxin, beta-blockers, adenosine or calcium channel
blockers.
* The best choice is procainamide as it slows the accessory
pathway. *If patient becomes hypotensive, cardiovert
immediately!
Atrial Flutter
 Atrial Flutter
• Atrial activity of 240-320 with sawtooth pattern.
Usually a 2:1 conduction pattern; if it is 3:1 or
higher, there is AV node damage
• Treatment is to slow AV node conduction with
amiodarone, propafenone or sotalol
• DC cardiovert if <48 hours or unstable
• You can also ablate the reentry pathway within
the atrium between the tricuspid and the IVC.
Atrial Fibrillation
 A-Fib
• Can be due to HTN, cardiomyopathy,
valvular heart desease, sick sinus, WPW,
thyrotoxicosis or ETOH
• Therapy is either rate control via slowing
AV node conduction with stroke
prophylaxis or rhythm control
 Rate control
 Beta-blockers
 Continuation after CABG may prevent a-fib
 Good for hyperthyroid or post-MI patients with a-fib
Carvedilol decreases mortality in patients with CHF
Esmolol is good for acute management
Digoxin actually increases vagal tone, thus indirectly
slowing AV node conduction. But it is used
essentially only in patients with LV dysfunction
because it’s inotropic.
 Rate control
 Calcium Channel Blockers
 Nondihydropyridines (verapamil or dilitiazem) block
AV node conduction but also have negative inotropy,
so don’t use in CHF.
 Dihydropyridines (nifedipine, amlodipine, felodipine)
have no effect on AV node conduction
 Adenosine is too short acting to be of any use in
a-fib
 Last choice is AV node ablation and permanent
pacing
 Rhythm control
 Rhythm control does not decrease
thromboembolic risk and may be proarrhythmic
 Class 1A (quinidine, procainamide, disopyramide) slows
conduction through HIS can cause torsades de pointes during
conversion. They also enhance AV node conduction, so they
should be used only after rate is controlled
 Class 1B (lidocaine, meilitine, tocainide) are useless for a-fib
 Class 1C (propafenone, and flecainide) slow conduction
through HIS are good first choice.
• Amiodarone is good if patient is post-MI or has
systolic dysfunction.
 Cardioversion for A-Fib
• Cardiovert if symptomatic
• Patients with a-fib for more than 2 days
should be receive 3 weeks of
anticoagulation before electrical
cardioversion.
• Give coumadin for 4 weeks after
cardioversion
 Anticoagulation Rules for A-
Fib
 Everybody who has rheumatic heart disease
should be anticoagulated
 If <65 yo and with h/o DM, HTN, CHF, CVA,
prosthetic valves, thyrotoxicosis, LV dysfunction
or LA enlargement, then give coumadin
 If no risk factors, do nothing.
 65-75 yo with any of above risk factors, give
coumadin; if no additional risk factors, give coumadin
or aspirin
 >75 yo give coumadin but keep INR 2-2.5 due to
increased risk of bleed
Ventricular Tachycardia
 Ventricular Tachycardia

• Impulse is initiated from the ventricle itself

• Wide QRS, Rate is 140-250
• If unstable DC cardiovert
• If not, IV Amiodarone and/or DCCV
• Consider procainamide
• Nonsustained ventricular tachycardia needs no treatment
 Torsades de Pointes

• “Twisting of the points” is usually caused by medication

(quinidine, disopyramide, sotalol, TCA), hypokalemia or
bradycardia especially after MI
• Has prolonged QT interval
• Acute: Remove offending medication. Shorten the QT
interval with magnesium, lidocaine, isoproterenol, or
temporary overdrive pacing
• Chronic: may need pacemaker/ICD, amiodarone, beta-
blockers
 Ventricular Fibrillation

• Most common in acute MI, also drug overdose,

anesthesia, hypothermia & electric shock can
precipitate
• Absence of ventricular complexes
• Usually terminal event
• Use Amiodarone if refractory to DCCV.
 Treatment
Treatment
Here comes the fun part!
 Classification of Anti-arrhythmics
Cla ss Actio n Exa mp le s Sid e Effe cts
1A Fa st so d ium chan ne l bloc ke r va ries Q uinidine , Cla ss: na use a , vo miting
d e p o la riza tio n a nd a ction p o te ntial p ro ca ina mid e, Q uinidine : h e mo lytic
d ura tio n d isop yra mid e a ne mia, thro mbo cyto pe nia ,
tinnitus
Proc ai na mid e : lup us
1B Lido ca ine, Lido ca ine: d izz ines s,
Mex ile tine co nfusio n, se izure s, co ma
Mex ile tine : tre mo r, a ta xia,
ras h

1C Fle ca inide, Fle ca inide: p ro-a rrhythmia ,

Prop af en o ne na use a , diz zy ne ss
2 b et a-b locke rs ↓SA node & ↓A V node Propranolol, C lass: C H F, bronchospasm ,
conduct ion m e toprolol bradycardia, hypote nsion
3 Prolong acti on potenti
alby blocking A m iodarone, A m iodarone: he patiti s,
K+ channe ls sotalol pul m onary fi brosis, htyroid
disorde rs, pe riphe ral
neuropathy
Sotalol: bronchospasm
4 calciu
m channe lblocke rs ↓A V node Ve rapam il, C lass: A V block,
conduction dilit
iaze m hypote nsion, bradycardia,
constipati on
 Where did you say you
worked?

Loc at ion of A ctivity Anti-arrh ythmic

AV N o de Aden osine, Ca lcium chann el b locke rs, B-
blocker s, D igoxi n
AV N o de , A ccesso ry Pa thway, Bundle of Propaf eno ne, Amioda ro ne, Soto lol
HIS, ve ntricle
Atria l, Ven tricular, Acce sso ry Pa thwa y, Q uinidine , Pro ca ina mide , Lido ca ine,
Bund le of HIS Disopy ram ide, F le can ide, Ibu tilide,
Bret ylium, Dofet ilide
When in doubt…Amiodarone

Amiodarone
IV

SVT VT Atrial Fib or flutter

 Amiodarone.
Modes of action.
• Mainly class III action on the outgoing K +
channels.
• Class Ib action on the Na+ channels.
• Non competitive alpha antagonism (class
III)
 Magnesium indications.
• 1. Torsades de point from any reason.
• 2. Arrhythmias in a patient with known
hypomagnesaemia.
• 3. Consider its use in acute ischaemia to prevent
early ventricular arrhythmias.
• 4. Digoxin induced arrhythmias.
 Who gets a pacemaker?
Syncope, presyncope or exercise intolerance that
can be attributed to bradycardia
 Symptomatic 2nd or 3rd degree AV block
 Congenital 3rd degree AV block with wide QRS
 Advanced AV block after cardiac surgery
 Recurrent type 2 2nd degree AV block after MI
 3rd degree AV block with wide QRS or BBB.
QUESTIONS
QUESTIONS