Professional Documents
Culture Documents
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.
www.uptodate.com
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:
Mechanisms of Arrhythmias
Automaticity
Ectopic Foci Reentry / Conduction Block
or
Decreased Automaticity
www.uptodate.com
Sinus Bradycardia
Increased/Abnormal Automaticity
Sinus tachycardia
Junctional tachycardia
QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal
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.
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.
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
R on T phenomenon
time
sinus beats
V-tach
The Reentry Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery
The Reentry Mechanism of Ectopic Beats & Rhythms Premature Beat Impulse Cardiac Repolarizing Tissue Conduction (long refractory period) 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
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 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 reenters the pathway and continues in a circular movement. This creates the re-entry circuit
Reentrant Rhythms
supraventricular tachycardia
Atrial Re-entry
Ventricular Re-entry
Atrio-Ventricular Re-entry
Acute Rx: Vagal maneuvers Adenosine 6-12 mg IV push beware of pro-arrhythmia Ca++ channel blockers
Atrial Flutter
www.uptodate.com
EKG Characteristics:
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 infusion have paddles ready Rapid pacing or low voltage DC cardioversion is effective Anticoagulation as per atrial fibrillation
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
Atrial Fibrillation
www.uptodate.com
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
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
Ventricular Fibrillation
www.uptodate.com
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
st 1
Degree AV Block
EKG Characteristics:
Usually benign
nd 2
Degree AV Block
Mobitz 1
(Wenckebach)
EKG Characteristics:
As the PR interval prolongs, the RR interval actually shortens Usually benign unless associated with underlying pathology, i.e. MI
nd 2
Degree AV Block
Mobitz 2
EKG Characteristics:
Rhythm is dangerous as the block is lower in the conduction system May cause syncope or may deteriorate into complete heart block
EKG Characteristics:
May be caused by inferior MI and its presence worsens the prognosis May cause syncopal symptoms, angina, or CFH Treatment: usually requires pacemaker
Antiarrhythmia Agents
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)
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
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
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
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
Atropine
Mechanism selective muscarinic antagonist Cardiac effects blocks vagal activity to speed AV conduction and increase HR Uses treat vagal bradycardia
Selected References:
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