Cardiac Arrhythmias in the SICU

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Cardiac Arrhythmias in the SICU

• Charles Hobson, MD MHA
• Surgical Critical Care
• NFSG VA Medical Center

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Objectives

• Review the etiology and recognition of common
  arrhythmias seen in the SICU.
• Review management of cardiac arrhythmias, with a
  focus on the relevant recent literature.

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Normal Sinus Rhythm
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Implies normal sequence of conduction,
originating in the sinus node and proceeding to
the ventricles via the AV node and His-Purkinje
system. EKG Characteristics Regular
narrow-complex rhythm Rate 60-100 bpm Each
QRS complex is proceeded by a P wave P wave is
upright in lead II downgoing in lead aVR
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Mechanisms of Arrhythmias

• Automaticity or
• Ectopic Foci
• Reentry / Conduction Block

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Decreased Automaticity
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Sinus Bradycardia
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Increased/Abnormal Automaticity
Sinus tachycardia
Ectopic atrial tachycardia
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Junctional tachycardia
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Ectopic Foci and Beats
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
Atrial Escape Beats
normal ("sinus") beats
sinus node doesn't fire leading to a period of
asystole (sick sinus syndrome)
p-wave has different shape indicating it did not
originate in the sinus node, but somewhere in the
atria.
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Ectopic Foci and Beats
Paroxysmal Supraventricular Tachycardia (PSVT)

• A single ectopic focus fires near the AV node,
  which then conducts normally to the ventricles
  (usually initiated by a PAC)
• The rhythm is always REGULAR
• Prolonged runs of PSVT may result in atrial
  fibrillation or atrial flutter
• May be terminated by carotid massage
• Treatment carotid massage, adenosine, Ca
  channel blockers, ablation
• Adenosine preferred in hypotension, previous IV
  B-blocker

Note REGULAR rhythm in the tachycardia
Rhythm usually begins with PAC
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Ectopic Foci and Beats
Multifocal Atrial Tachycardia (MAT)

• Multiple ectopic foci fire in the atria, all of
  which are conducted normally to the ventricles
• The rhythm is always IRREGULAR
• P-waves of different morphologies (shapes) may
  be seen
• Commonly seen in pulmonary disease, acute
  cardiorespiratory problems, and CHF
• Treatment
• Ca channel blockers, beta blockers, but
  antiarrhythmic drugs are often ineffective
• potassium, magnesium (McCord et al, Chest 1998),

Note IRREGULAR rhythm in the tachycardia
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Ectopic Foci and Beats
Junctional Escape Beats
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
there is no p wave, indicating that it did not
originate anywhere in the atria, but since the
QRS complex is still thin and normal looking, we
can conclude that the beat originated somewhere
near the AV junction.
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Ectopic Foci and Beats
Ventricular Escape Beats PVCs
QRS is wide and much different looking than the
normal beats. This indicates that the beat
originated somewhere in the ventricles.

• no p wave, indicating that the beat did not
  originate anywhere in the atria

• a "retrograde p-wave may sometimes be seen on
  the right hand side of beats that originate in
  the ventricles, indicating that depolarization
  has spread back up through the atria from the
  ventricles

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PVC's are Dangerous When

• They are frequent (gt 30 of complexes) or are
  increasing in frequency
• The come close to or on top of a preceding
  T-wave (R on T)
• Three or more PVC's in a row (run of V-tach)
• Any PVC in the setting of an acute MI
• PVC's come from different foci ("multifocal" or
  "multiformed")
• These may result in ventricular tachycardia or
  fibrillation.

R on T phenomenon
time
Unconverted V-tach to V-fib
sinus beats
V-tach
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Causes of Ectopic Foci and Beats

• hypoxic myocardium - chronic pulmonary
  disease, pulmonary embolus
• ischemic myocardium - acute MI, expanding MI,
  angina
• sympathetic stimulation - nervousness,
  exercise, CHF, hyperthyroidism
• drugs electrolyte imbalances -
  antiarrhythmic drugs, hypokalemia,
  imbalances of calcium and magnesium
• bradycardia - a slow HR predisposes one to
  arrhythmias
• enlargement of the atria or ventricles
  producing stretch in pacemaker cells

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The Reentry Mechanism of Ectopic Beats Rhythms
Electrical Impulse
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery

• Tissues with these type of circuits may exist
• in the SA node, AV node, or any type of heart
  tissue
• in a macroscopic structure such as an
  accessory pathway in WPW

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The Reentry Mechanism of Ectopic Beats Rhythms
Premature Beat Impulse
Cardiac Conduction Tissue
Repolarizing Tissue (long refractory period)
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery
1. An arrhythmia is triggered by a premature
beat 2. The beat cannot gain entry into the
fast conducting pathway because of its long
refractory period and therefore travels down the
slow conducting pathway only
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The Reentry Mechanism of Ectopic Beats Rhythms
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path 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 retrograde (backwards) up the
fast pathway
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The Reentry Mechanism of Ectopic Beats Rhythms
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path 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
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Reentrant Rhythms

• AV nodal reentrant tachycardia (AVNRT)
• Supraventricular tachycardia
• AV reentrant tachycardia (AVRT)
• Wolf Parkinson White syndrome
• Atrial flutter
• Ventricular tachycardia
• Atrial fibrillation
• Ventricular fibrillation

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Reentry Circuits as Ectopic Foci and Arrhythmia
Generators

• Atrio-Ventricular Nodal Re-entry
• supraventricular tachycardia

• Ventricular Re-entry
• ventricular tachycardia
• ventricular fibrillation

• Atrial Re-entry
• atrial tachycardia
• atrial fibrillation
• atrial flutter

• Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia

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AV Nodal Reentrant Tachycardia
Rate 100-270 Normal QRS Aberrancy possible

• Acute Rx
• Vagal maneuvers
• Adenosine 6-12 mg IV push beware of
  pro-arrhythmia
• Ca channel blockers

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Atrial Flutter
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Atrial flutter is caused by a reentrant circuit
in the wall of the atrium EKG Characteristics Ty
pical sawtooth flutter waves at a rate of
300 bpm Flutter waves have constant amplitude,
duration, and morphology through the cardiac
cycle There is usually either a 21 or 41
block at the AV node, resulting in
ventricular rates of either 150 or 75 bpm
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Dx and Rx of Flutter
Unmasking of flutter waves with adenosine.

• Acute Rx
• ventricular rate control can be difficult
• AV nodal blockers prevent 11 conduction
• Ibutilide 1-2mg rapid IV infusion have paddles
  ready
• Rapid pacing or low voltage DC cardioversion is
  effective
• Anticoagulation as per atrial fibrillation

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Ventricular Tachycardia
Rate 100-20 Wide QRS Monomorphic vs Polymorphic

• Beware
• Accelerated idioventricular rhythm. Rate below
  150, stable hemodynamics, benign prognosis.
• SVT with aberrancy. Look at the 12 lead not
  just a rhythm strip
• Monomorphic vs. Polymorphic (long QT,
  bradycardia, ischemia)
• Rx
• Unstable DC cardioversion
• Stable monomorphic Procainamide, Amiodarone
• Stable polymorphic - treat underlying etiology

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Atrial Fibrillation
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Atrial fibrillation is caused by numerous waves
of depolarization spreading throughout the atria,
leading to an absence of coordinated atrial
contraction. Classified as Recurrent when AF
occurs on 2 or more occasions Paroxysmal
episodes that generally last lt/ 7 days (most
last lt24h) Persistent AF that last gt/7
days Permanent paroxysmal or persistent AF with
failure to cardiovert or not attempted
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Dx and Rx of Atrial Fibrillation
Absent P waves Irregularly irregular ventricular
response

• Acute Rx
• rate control not rhythm control AFFIRM trial
  (NEJM 2002)
• B-blockers, Ca channel blockers, digoxin,
  amiodarone
• Ibutilide 1-2mg rapid IV infusion have paddles
  ready
• Oral propafenone or flecainide beware
  pro-arrhythmia
• Low voltage DC cardioversion
• Anticoagulation as per atrial fibrillation
• On the horizon vernakalant, an atrial-selective
  Na and K channel blocker for conversion of
  short-duration atrial fibrillation

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Ventricular Fibrillation
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Ventricular fibrillation is caused by numerous
waves of depolarization spreading throughout the
ventricles simultaneously, leading to
disorganized ventricular contraction and
immediate loss of cardiac function.
EKG Characteristics Absent P waves Disorganize
d electrical activity Deflections continuously
change in shape, magnitude and direction
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Rhythms Produced by Conduction Block

• AV Block (relatively common)
• 1st degree AV block
• Type 1 2nd degree AV block
• Type 2 2nd degree AV block
• 3rd degree AV block
• SA Block (relatively rare)

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1st Degree AV Block
The Alan E. Lindsay ECG Learning Center
http//medstat.med.utah.edu/kw/ecg/
EKG Characteristics Prolongation of the PR
interval, which is constant All P waves are
conducted Usually benign
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2nd Degree AV Block
Mobitz 1 (Wenckebach)
EKG Characteristics Progressive prolongation of
the PR interval until a P wave is not
conducted. As the PR interval prolongs, the RR
interval actually shortens Usually benign unless
associated with underlying pathology, i.e. MI
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2nd Degree AV Block
Mobitz 2

• EKG Characteristics Constant PR interval with
  intermittent failure to conduct
• Rhythm is dangerous as the block is lower in the
  conduction system
• May cause syncope or may deteriorate into
  complete heart block
• Causes anterioseptal MI, fibrotic disease of
  the conduction system
• Treatment may require pacemaker in the case of
  fibrotic conduction system

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3rd Degree (Complete) AV Block

• EKG Characteristics No relationship between P
  waves and QRS complexes
• Constant PP intervals and RR intervals
• May be caused by inferior MI and its presence
  worsens the prognosis
• May cause syncopal symptoms, angina, or CFH
• Treatment usually requires pacemaker

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Right Bundle Branch Block (RBBB)

• Depolarization spreads from the left ventricle to
  the right ventricle.
• This creates a second R-wave (R) in V1, and a
  slurred S-wave in V5 - V6.
• The T wave should be deflected opposite the
  terminal deflection of the QRS complex. This is
  known as appropriate T wave discordance with
  bundle branch block. A concordant T wave may
  suggest ischemia or myocardial infarction.

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Left Bundle Branch Block (LBBB)

• Depolarization enters the right side of the right
  ventricle first and simultaneously depolarizes
  the septum from right to left.
• This creates a QS or rS complex in lead V1 and a
  monophasic or notched R wave in lead V6.
• The T wave should be deflected opposite the
  terminal deflection of the QRS complex. This is
  known as appropriate T wave discordance with
  bundle branch block. A concordant T wave may
  suggest ischemia or myocardial infarction.

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Antiarrhythmia Agents
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Class 1A agents Procainamide,
quinidine    Uses Wide spectrum, but side
effects limit usage Quinidine maintain sinus
rhythms in atrial fibrillation and flutter and to
prevent recurrent tachycardia and fibrillation
     Procainamide acute treatment of
supraventricular and ventricular arrhythmias (no
longer in production)  Side effects Hypotension,
reduced cardiac output Proarrhythmia
(generation of a new arrhythmia) eg. Torsades
de Points (?QT interval)               Dizziness,
confusion, insomnia, seizure (high
dose)               Gastrointestinal effects
(common)               Lupus-like syndrome (esp.
procainamide)
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Class 1B agents Lidocaine, phenytoin Uses a
cute Ventricular tachycardia and fibrillation
(esp. during ischemia) Not used in atrial
arrhythmias or AV junctional arrhythmias      
Side effects                 Less proarrhythmic
than Class 1A (less QT effect)              
CNS effects dizziness, drowsiness
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Class 1C agents Flecainide, propafenone Uses
Wide spectrum Used for supraventricular
arrhythmias (fibrillation and
flutter)               Premature ventricular
contractions (caused problems)
Wolff-Parkenson-White syndrome Side
effects Proarrhythmia and sudden death
especially with chronic use (CAST study)
Increase ventricular response to
supraventricular arrhythmias CNS and
gastrointestinal effects like other local
anesthetics
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Class II agents Propranolol, esmolol Uses t
reating sinus and catecholamine dependent tachy
arrhythmias converting reentrant
arrhythmias in AV protecting the ventricles
from high atrial rates (slow AV
conduction) Side effects        bronchospasm  
            hypotension               beware in
partial AV block or ventricular failure
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Class III agents Amiodarone, sotalol,
ibutilide Amiodarone Uses Very wide spectrum
effective for most arrhythmias Side effects
many serious that increase with time Pulmonary
fibrosis Hepatic injury Increase LDL
cholesterol Thyroid disease Photosensitivity Ma
y need to reduce the dose of digoxin and class 1
antiarrhythmics
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Class III agents Amiodarone, sotalol,
ibutilide Sotalol Uses   Wide spectrum
supraventricular and ventricular
tachycardia                     Side
effects    Proarrhythmia, fatigue, insomnia
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Class III agents Amiodarone, sotalol,
ibutilide Ibutilide Uses conversion of atrial
fibrillation and flutter with rapid IV
infusion             Side effects Torsades de
pointes
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Class IV agents Verapamil and
diltiazem Uses control ventricular rate
during supraventricular tachycardia convert
supraventricular tachycardia (re-entry around
AV) Side effects Caution when partial AV block
is present. Can get asystole if ß blocker
is on board Caution when hypotension, decreased
CO or sick sinus Some gastrointestinal problems
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Additional agents Adenosine Administration
                    rapid i.v. bolus, very
short T1/2 (seconds) Cardiac effects Slows AV
conduction Uses convert re-entrant
supraventricular arrhythmias hypotension during
surgery, diagnosis of CAD Magnesium treatment
for tachycardia resulting from long QT
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Additional agents Digoxin (cardiac
glycosides) Mechanism enhances vagal activity,
inhibits Na/K ATPase ? refractory period, slows
AV conduction Uses treatment of atrial
fibrillation and flutter Atropine Mechanism sele
ctive muscarinic antagonist Cardiac
effects blocks vagal activity to speed AV
conduction and increase HR Uses treat vagal
bradycardia
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• Selected References
• ACC/AHA/ESC Practice Guidelines
• Supraventricular Arrhythmias JACC
  2003421993-531.
• Atrial Fibrillation JACC 200648854-906
• Ventricular Arrhythmias JACC 2006481064-1108
• Thanks, and questions?