cardiac arrhythmias hobson

8/13/2019 Cardiac Arrhythmias Hobson

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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



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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



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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



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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



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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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Slow Recovery


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)



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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


Slow Recovery


Fast Recovery

Cardiac

Conduction

Tissue



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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


Slow Recovery


Fast Recovery

Cardiac

ConductionTissue



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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

www.uptodate.com


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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

www.uptodate.com

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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Sotalol

Uses

Wide spectrum: supraventricular and ventricular tachycardia

Side effects

Proarrhythmia, fatigue, insomnia


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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

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cardiac arrhythmias hobson

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