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


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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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

Automaticity or
Ectopic Foci
Reentry / Conduction Block

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Sinus tachycardia
Ectopic atrial tachycardia
Junctional tachycardia

Atrial Escape Beats
QRS is slightly different but still narrow , indicating that conduction through the ventricle is relatively normal 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.

• 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
Rhythm usually begins with PAC
Note REGULAR rhythm in the tachycardia

•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

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.

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

•They are frequent (> 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

• 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

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

The Reentry Mechanism of Ectopic Beats & Rhythms
Premature Beat Impulse
Repolarizing Tissue
(long refractory period)
Cardiac
Conduction
Tissue
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

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

The Reentry Mechanism of Ectopic Beats & Rhythms
Fast Conduction Path
Slow Recovery
Cardiac
Conduction
Tissue
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 ‘reenters’ the pathway and continues in a ‘circular’ movement.
This creates the re-entry circuit

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

Reentry Circuits as Ectopic Foci and Arrhythmia Generators
Atrial Re-entry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular Nodal Re-entry
• supraventricular tachycardia
Ventricular Re-entry
• ventricular tachycardia
•ventricular fibrillation
Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular 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 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, and morphology 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

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 infusion – have paddles ready
•Rapid pacing or low voltage DC cardioversion is effective
•Anticoagulation as per atrial fibrillation

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 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 </= 7 days (most last <24h)
Persistent: AF that last >/=7 days
Permanent: paroxysmal or persistent AF with failure to cardiovert or not attempted

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 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
Disorganized electrical activity
Deflections continuously change in shape, magnitude and direction


– 1 st degree AV block
– Type 1 2 nd degree AV block
– Type 2 2 nd degree AV block
– 3 rd degree AV block


st
EKG Characteristics:
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
Prolongation of the PR interval, which is constant
All P waves are conducted
Usually benign

nd
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

nd
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

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

1.
Depolarization spreads from the left ventricle to the right ventricle.
2.
This creates a second Rwave (R’) in V1 , and a slurred S-wave in V5 - V6 .
3.
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.

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 is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.

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 )

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

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

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

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
May need to reduce the dose of digoxin and class 1 antiarrhythmics

Class III agents: Amiodarone, sotalol, ibutilide
Sotalol
Uses
Wide spectrum: supraventricular and ventricular tachycardia
Side effects
Proarrhythmia, fatigue, insomnia

Class III agents: Amiodarone, sotalol, ibutilide
Ibutilide
Uses conversion of atrial fibrillation and flutter with rapid IV infusion
Side effects
Torsades de pointes

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 β blocker is on board
Caution when hypotension, decreased CO or sick sinus
Some gastrointestinal problems

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

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 selective muscarinic antagonist
Cardiac effects blocks vagal activity to speed AV conduction and increase HR
Uses treat vagal bradycardia

ACC/AHA/ESC Practice Guidelines:
 Supraventricular Arrhythmias – JACC 2003;42:1993-531.
 Atrial Fibrillation – JACC 2006;48:854-906
 Ventricular Arrhythmias – JACC 2006;48:1064-1108