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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
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
Sinus Bradycardia
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Increased/Abnormal Automaticity
Sinus tachycardia
Junctional tachycardia
Ectopic atrial tachycardia
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normal ("sinus") beats
sinus node doesn't fire leading
to a period of asystole (sick
sinus syndrome)p-wave has different shapeindicating
it did not originate in the sinus node,
but somewhere in the atria.
QRS is slightly different but still narrow,
indicating that conduction through theventricle is relatively normal
Atrial Escape Beats
Ectopic Foci and Beats
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Paroxysmal Supraventricular Tachycardia (PSVT)A single ectopic focusfires 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 tachycardiaRhythm usually beginswith PAC
Ectopic Foci and Beats
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Multifocal Atrial Tachycardia (MAT)
Multiple ectopic focifire 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 seenCommonly 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 IRREGULARrhythm in the tachycardia
Ectopic Foci and Beats
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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 canconclude that the beat originated somewhere near
the AV junction.
Junctional
Escape BeatsQRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
Ectopic Foci and Beats
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a "retrogradep-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
QRS is wideand much different looking than thenormal beats. This indicates that the beat originated
somewhere in the ventricles.
VentricularEscape Beats
PVCs
no p wave, indicating that the beat did notoriginate anywhere in the atria
Ectopic Foci and Beats
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They arefrequent(> 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.
PVC's are Dangerous When:
sinus beats Unconverted V-tach to V-fibV-tach
R on T
phenomenon
time
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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 ventriclesproducing stretch in pacemaker
cells
Causes of Ectopic Foci and Beats
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Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
The Reentry Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
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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Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
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
Repolarizing Tissue
(long refractory period)
The Reentry Mechanism of Ectopic Beats & Rhythms
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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
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
The Reentry Mechanism of Ectopic Beats & Rhythms
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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
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
ConductionTissue
The Reentry Mechanism of Ectopic Beats & Rhythms
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Reentrant Rhythms
AV nodal reentrant tachycardia (AVNRT) Supraventricular tachycardia
AV reentrant tachycardia (AVRT)
Wolf
Parkinson
White syndromeAtrial flutter
Ventricular tachycardia
Atrial fibrillation
Ventricular fibrillation
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Atrial Re-entry
atrial tachycardia
atrial fibrillation
atrial flutter
Atrio-Ventricular Re-entry
Wolf Parkinson Whitesupraventricular tachycardia
Ventricular Re-entryventricular tachycardia
ventricular fibrillation
Atrio-Ventricular Nodal Re-entry
supraventricular tachycardia
Reentry Circuits as Ectopic Foci and Arrhythmia Generators
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AV Nodal Reentrant Tachycardia
Rate 100-270
Normal QRS
Aberrancy possible
Acute Rx:
Vagal maneuvers
Adenosine 6-12 mg IV pushbeware of pro-arrhythmia
Ca++ channel blockers
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Atrial Flutter
Atrial flutter is caused by a reentrant circuit in the wall of the atrium
EKG Characteristics: Typical: sawtooth flutter waves at a rate of ~ 300 bpm
Flutter waves have constant amplitude, duration, andmorphology through the cardiac cycle
There is usually either a 2:1 or 4:1 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 1:1 conduction
Ibutilide 1-2mg rapid IV infusionhave paddles ready
Rapid pacing or low voltage DC cardioversion is effectiveAnticoagulation as per atrial fibrillation
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Ventricular Tachycardia
Beware:Accelerated idioventricular rhythm. Rate below 150, stable
hemodynamics, benign prognosis.
SVT with aberrancy. Look at the 12 leadnot just a rhythm strip
Monomorphic vs. Polymorphic (long QT, bradycardia, ischemia)
Rx:
UnstableDC cardioversion
Stable monomorphicProcainamide, Amiodarone
Stable polymorphic - treat underlying etiology
Rate 100-20Wide QRS
Monomorphic vs
Polymorphic
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Atrial Fibrillation
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
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Dx and Rx of Atrial Fibrillation
Absent P waves
Irregularly irregular
ventricular response
Acute Rx:
rate control not rhythm controlAFFIRM trial (NEJM 2002):B-blockers, Ca++ channel blockers, digoxin, amiodarone
Ibutilide 1-2mg rapid IV infusionhave paddles ready
Oral propafenone or flecainidebeware 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 ventriclessimultaneously, leading to disorganized
ventricular contraction and immediate loss of cardiac function.
EKG Characteristics: Absent P waves
Disorganized electrical activity
Deflections continuously change in shape,
magnitude and direction
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Rhythms Produced by Conduction Block
AV Block (relatively common)
1stdegree AV block
Type 1 2nddegree AV block
Type 2 2nddegree AV block
3rddegree AV block
SA Block (relatively rare)
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1stDegree AV Block
EKG Characteristics: Prolongation of the PR interval, which is constant
All P waves are conducted
Usually benign
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
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2ndDegree 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 benignunless associated with underlying pathology, i.e. MI
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2ndDegree AV Block
EKG Characteristics: Constant PR interval with intermittent failure
to conduct
Rhythm is dangerousas the block is lower in the conduction system
May cause syncope or may deteriorate into complete heart blockCauses: anterioseptal MI, fibrotic disease of the conduction system
Treatment: may require pacemaker in the case of fibrotic conduction
system
Mobitz 2
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3rdDegree (Complete) AV Block
EKG Characteristics: No relationship between P waves and QRS
complexes
Constant PP intervals and RR intervals
May be caused by inferior MIand its presence worsens the prognosis
May cause syncopal symptoms, angina, or CFH
Treatment: usually requires pacemaker
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1. Depolarization spreads from the left
ventricle to the right ventricle.
2. This creates a second R-wave (R) in V1,
and a slurred S-wave in V5 - V6.
3. The T wave should be deflected oppositethe terminal deflection of the QRS complex.
This is known as appropriate T wave
discordancewith bundle branch block. A
concordant T wave may suggest ischemia
or myocardial infarction.
Right Bundle Branch Block (RBBB)
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1. Depolarization enters the right side of the right
ventricle first and simultaneously depolarizes the
septum from right to left.
2. This creates a QS or rS complex in lead V1 and a
monophasic or notched R wave in lead V6.
3. The T wave should be deflected opposite the
terminal deflection of the QRS complex. This isknown as appropriate T wave discordancewith
bundle branch block. A concordant T wave may
suggest ischemiaor myocardial infarction.
Left Bundle Branch Block (LBBB)
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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 effectsHypotension, 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
acute : 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 deathespecially 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
treating 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 fibrosisHepatic injury
Increase LDL cholesterol
Thyroid disease
Photosensitivity
May 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 blocker is on board
Caution when hypotension, decreased CO or sick sinus
Some gastrointestinal problems
Additi l t
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Additional agents
AdenosineAdministration
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
Magnesiumtreatment 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
Usestreatment of atrial fibrillation and flutter
AtropineMechanism
selective muscarinic antagonistCardiac 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 ArrhythmiasJACC 2003;42:1993-531.
Atrial FibrillationJACC 2006;48:854-906
Ventricular ArrhythmiasJACC 2006;48:1064-1108
Thanks, and questions?