Transcript Fever in the ICU

Cardiac Arrhythmias in the SICU
Charles Hobson, MD MHA
Surgical Critical Care
NFSG VA Medical Center
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.
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
Mechanisms of Arrhythmias
Automaticity
or
Ectopic Foci
Reentry / Conduction Block
Decreased Automaticity
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Sinus Bradycardia
Increased/Abnormal Automaticity
Sinus tachycardia
Ectopic atrial tachycardia
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Junctional tachycardia
Ectopic Foci and Beats
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.
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
Rhythm usually begins
with PAC
Note REGULAR rhythm
in the tachycardia
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
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.
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
PVC's are Dangerous When:
•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
sinus beats
V-tach
Unconverted V-tach to V-fib
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
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
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
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
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

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
Atrio-Ventricular Nodal Re-entry
• supraventricular tachycardia
Atrial Re-entry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Ventricular Re-entry
• ventricular tachycardia
•ventricular fibrillation
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
Atrial Flutter
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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
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
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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
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
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
Disorganized electrical activity
Deflections continuously change in shape,
magnitude and direction
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)
st
1
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
nd
2
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
nd
2
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
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 it’s presence worsens the prognosis
• May cause syncopal symptoms, angina, or CFH
•Treatment: usually requires pacemaker
Right Bundle Branch Block (RBBB)
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 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.
Left Bundle Branch Block (LBBB)
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.
Antiarrhythmia Agents
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
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
Thanks, and questions?