Arrhythmias 101Arrhythmias 101Arrhythmias 101Arrhythmias 101

Fundamentals and what you Fundamentals and what you should know for the big, bad should know for the big, bad

BOARDS!BOARDS!

The Basics

• SA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamil

• Atrium, Bundle of His, and ventricle cells are fast conducting and activated by sodium, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as quinidine, lidocaine and propafenone.

4 Mechanisms of Arrhythmia

• reentry (most common)• automaticity• parasystole • triggered activity

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Reentry Requires…

Electrical Impulse

Cardiac Conduction

Tissue

1. 2 distinct pathways that come together at beginning and end to form a loop.

2. A unidirectional block in one of those pathways.

3. Slow conduction in the unblocked pathway.

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Premature Beat Impulse

Cardiac Conduction

Tissue

1. An arrhythmia is triggered by a premature beat

2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway

Repolarizing Tissue (long refractory period)

Reentry Mechanism

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 retrogradely (backwards) up the fast pathway

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Cardiac Conduction

Tissue

Reentry Mechanism

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 PathSlow Recovery

Slow Conduction PathFast Recovery

Cardiac Conduction

Tissue

Reentry Mechanism

Atrial Reentry• atrial tachycardia• atrial fibrillation• atrial flutter

Atrio-Ventricular Reentry• WPW• SVT

Ventricular Re-entry• ventricular tachycardia

AV Nodal Reentry•SVT

Reentry Circuits

SA Node

Reentry Requires…1. 2 distinct pathways that come together at

beginning and end to form a loop. 2. A unidirectional block in one of those

pathways. 3. Slow conduction in the unblocked pathway. Large reentry circuits, like a-flutter, involve the

atrium. Reentry in WPW involves atrium, AV node,

ventricle and accessory pathways.

Automaticity

• Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker.

• Factors that enhance automaticity include: SANS, PANS, CO2, O2, H+, stretch,

hypokalemia and hypocalcaemia.

Examples: Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung disease OR ventricular ectopy after MI

Parasystole…

• is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells.

• 3% of PVCs

Triggered activity…• is like a domino effect where the

arrhythmia is due to the preceding beat. • Delayed after-depolarizations arise during

the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias.

• Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)

Diagnosis…Diagnosis…Diagnosis…Diagnosis…

What tools to use and when to What tools to use and when to use it…use it…

Event Monitors• Holter monitoring: Document

symptomatic and asymptomatic arrhythmias over 24-48 hours. Can also evaluate treatment effectiveness in a-fib, pacemaker effectiveness and identify silent MIs.

• Trans-telephonic event recording: patient either wears monitor for several days or attaches it during symptomatic events and an ECG is recorded and transmitted for evaluation via telephone. Only 20% are positive, but still helpful.

Exercise testing• Symptoms only appear or worsen with

exercise. • Also used to evaluate medication

effectiveness (esp. flecanide & propafenone)

You can assess SA node function with exercise testing.

Mobitz 1 (Wenkebach) is blockage at the AV node, so catecholamines from exercise actually help!

Mobitz 2 is blockage at bundle of His, so it worsens as catecholamines from exercise increase AV node conduction, thus prognosis is worse.

*PVCs occur in 10% without and 60% of patients with CAD. *PVCs DO NOT predict severity of CAD (neither for nor against)!

Signal Averaged ECG

• Used only in people post MI to evaluate risk for v-fib or v-tach.

• Damage around the infarct is variable, so this measures late potentials (low-signal, delayed action potentials) as they pass through damaged areas.

• Positive predictive value is 25%-50% but negative predictive value is 90%-95%, thus if test is negative, patient is at low risk.

Electrophysiologic Testing…

• Catheters are placed in RA, AV node, Bundle of HIS, right ventricle, and coronary sinus (to monitor LA and LV).

• Used to evaluate cardiogenic syncope of unknown origin, symptomatic SVT, symptomatic WPW, and sustained v-tach.

*Ablative therapy is beneficial in AV node reentry, WPW, atrial tachycardia, a-flutter, and some v-tach. Complication is 1%

BradyarrhythmiasBradyarrhythmiasBradyarrhythmiasBradyarrhythmias

The slow pokes (HR<60)…The slow pokes (HR<60)…

Sick Sinus Syndrome

• Conduction problem with no junctional escape during sinus pause

• Diagnose with ECG or Holter. If inconclusive, need electrophysiologic testing.

• If asymptomatic, leave alone. If symptomatic, needs pacemaker.

First Degree AV Block

• Delay at the AV node results in prolonged PR interval

• PR interval>0.2 sec.• Leave it alone

Second Degree AV Block Type 1 (Wenckebach)

• Increasing delay at AV node until a p wave is not conducted.

• Often comes post inferior MI with AV node ischemia

• Gradual prolongation of the PR interval before a skipped QRS. QRS are normal!

• No pacing as long as no bradycardia.

Second Degree AV Block Type 2

• Diseased bundle of HIS with BBB. • Sudden loss of a QRS wave because p

wave was not transmitted beyond AV node. QRS are abnormal!

• May be precursor to complete heart block and needs pacing.

Third Degree AV Block

• Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles.

• Must treat with pacemaker.

LBBB

Left Bundle Branch Block

• Left ventricle gets a delayed impulse• QRS is widened (at least 3 boxes)

• V5 and V6 have RR’ (rabbit ears)

• Be careful not to miss any hiding q waves!

• Pacemaker if syncope occurs

Right Bundle Branch Block

Right Bundle Branch Block

• Right ventricle gets a delayed impulse• QRS is widened (at least 3 boxes)

• V1 and V2 have rSR’

• Pacemaker if syncope occurs.

Bifascicular Block

• RBBB plus LABB OR RBBB plus LPBB

• QRS is widened (at least 3 boxes)

• V5 and V6 have RR’ (rabbit ears)

• V1 and V2 have rSR’

• Pacemaker if syncope occurs

TachyarrhythmiasTachyarrhythmiasTachyarrhythmiasTachyarrhythmias

The speed demons…(HR >100)The speed demons…(HR >100)

Tachyarrhythmias

• Supraventricular tachycardia• Atrial fibrillation• Atrial flutter• Ventricular tachycardia

» Monomorphic» Polymorphic (Torsades de pointe)

• Ventricular fibrillation

Supraventricular Tachycardia

SVT• Reentrant arrhythmia at AV node that is

spontaneous in onset • May have neck fullness, hypotension

and/or polyuria due to ANP• Narrow QRS with tachycardia• First line is vagal maneuvers • Second line is adenosine or verapamil• For chronic SVT, class 1A or 1C or

amiodarone or sotalol work well• Ablation will cure it too, but we usually

do this only in young patients

Multifocal Atrial Tachycardia

MAT• Automatic atrial rhythm from

various different foci • Seen in hypoxia, COPD, atrial

stretch and local metabolic imbalance.

• Three or more types of p waves and a rate > 100

• Digoxin worsens it, so treat with oxygen and slow channel blocker like verapamil or diltiazem.

Wolf Parkinson White

WPW

• Ventricles receive partial signal normally and partially through accessory pathway

• Symptomatic tachycardia, short PR interval (<0.12), a delta wave and prolonged QRS (>0.12)

• Electrophysiologic testing helps to identify the reentry pathway and location of the accessory pathway

WPW Because WPW has both normal conduction

through the AV node and accessory pathway conduction that bypasses the AV node, a-fib can happen via the accessory pathway

Inhibition of the AV node will end up in worsening the a-fib because none of the signals are slowed down by the AV node before hitting the ventricle.

* Do not use any meds that will slow AV node conduction, ie digoxin, beta-blockers, adenosine or calcium channel blockers.

* The best choice is procainamide as it slows the accessory pathway. *If patient becomes hypotensive, cardiovert immediately!

Atrial Flutter

Atrial Flutter• Atrial activity of 240-320 with sawtooth

pattern. Usually a 2:1 conduction pattern; if it is 3:1 or higher, there is AV node damage

• Treatment is to slow AV node conduction with amiodarone, propafenone or sotalol

• DC cardiovert if <48 hours or unstable• You can also ablate the reentry

pathway within the atrium between the tricuspid and the IVC.

Atrial Fibrillation

A-Fib

• Can be due to HTN, cardiomyopathy, valvular heart desease, sick sinus, WPW, thyrotoxicosis or ETOH

• Therapy is either rate control via slowing AV node conduction with stroke prophylaxis or rhythm control

Rate control Beta-blockers

Continuation after CABG may prevent a-fib Good for hyperthyroid or post-MI patients with

a-fibCarvedilol decreases mortality in patients with

CHFEsmolol is good for acute management

Digoxin actually increases vagal tone, thus indirectly slowing AV node conduction. But it is used essentially only in patients with LV dysfunction because it’s inotropic.

Rate control

Calcium Channel Blockers Nondihydropyridines (verapamil or

dilitiazem) block AV node conduction but also have negative inotropy, so don’t use in CHF.

Dihydropyridines (nifedipine, amlodipine, felodipine) have no effect on AV node conduction

Adenosine is too short acting to be of any use in a-fib

Last choice is AV node ablation and permanent pacing

Rhythm control

Rhythm control does not decrease thromboembolic risk and may be proarrhythmic

Class 1A (quinidine, procainamide, disopyramide) slows conduction through HIS can cause torsades de pointes during conversion. They also enhance AV node conduction, so they should be used only after rate is controlled

Class 1B (lidocaine, meilitine, tocainide) are useless for a-fib

Class 1C (propafenone, and flecainide) slow conduction through HIS are good first choice.

• Amiodarone is good if patient is post-MI or has systolic dysfunction.

Cardioversion for A-Fib

• Cardiovert if symptomatic• Patients with a-fib for more than 2

days should be receive 3 weeks of anticoagulation before electrical cardioversion.

• Give coumadin for 4 weeks after cardioversion

Anticoagulation Rules for A-Fib

Everybody who has rheumatic heart disease should be anticoagulated

If <65 yo and with h/o DM, HTN, CHF, CVA, prosthetic valves, thyrotoxicosis, LV dysfunction or LA enlargement, then give coumadin

If no risk factors, do nothing. 65-75 yo with any of above risk factors,

give coumadin; if no additional risk factors, give coumadin or aspirin

>75 yo give coumadin but keep INR 2-2.5 due to increased risk of bleed

Ventricular Tachycardia

• Impulse is initiated from the ventricle itself

• Wide QRS, Rate is 140-250• If unstable DC cardiovert• If not, IV Amiodarone and/or DCCV• Consider procainamide• Nonsustained ventricular tachycardia needs

no treatment

Ventricular Tachycardia

Torsades de Pointes

• “Twisting of the points” is usually caused by medication (quinidine, disopyramide, sotalol, TCA), hypokalemia or bradycardia especially after MI

• Has prolonged QT interval• Acute: Remove offending medication. Shorten

the QT interval with magnesium, lidocaine, isoproterenol, or temporary overdrive pacing

• Chronic: may need pacemaker/ICD, amiodarone, beta-blockers

Ventricular Fibrillation

• Most common in acute MI, also drug overdose, anesthesia, hypothermia & electric shock can precipitate

• Absence of ventricular complexes

• Usually terminal event• Use Amiodarone if refractory to DCCV.

TreatmentTreatmentTreatmentTreatment

Here comes the fun part!Here comes the fun part!

Classification of Anti-arrhythmics

Class Action Examples Side Effects1A Fast sodium channel blocker varies

depolarization and action potentialduration

Quinidine,procainamide,disopyramide

Class: nausea, vomitingQuinidine: hemolyticanemia, thrombocytopenia,tinnitusProcainamide: lupus

1B Lidocaine,Mexiletine

Lidocaine: dizziness,confusion, seizures, comaMexiletine: tremor, ataxia,rash

1C Flecainide,Propafenone

Flecainide: pro-arrhythmia,nausea, dizzyness

2 beta-blockers ↓SA nod e & ↓A V nodeconduction

Propranolo ,lmetoprolol

Class: CHF, bronchospasm,bradycardia, hypotension

3 Prolon g actio n potential b y blocking+K channels

Amiodaron ,esotalol

Amiodaron :e hepatiti ,spulmonar y fibrosi ,s thyroiddisorders, peripheralneuropathySotalol: bronchospasm

4 calciu mchannel blockers ↓A V nodeconduction

Verapamil,dilitiazem

Class: A V block,hypotension, bradycardi ,aconstipation

Where did you say you worked?

Location of Activity Anti-arrhythmicAV Node Adenosine, Calcium channel blockers, B-

blockers, DigoxinAV Node, Accessory Pathway, Bundle ofHIS, ventricle

Propafenone, Amiodarone, Sotolol

Atrial, Ventricular, Accessory Pathway,Bundle of HIS

Quinidine, Procainamide, Lidocaine,Disopyramide, Flecanide, Ibutilide,Bretylium, Dofetilide

When in doubt…Amiodarone

SVT VT Atrial Fib or flutter

AmiodaroneIV

Amiodarone.Modes of action.

• Mainly class III action on the outgoing K+ channels.

• Class Ib action on the Na+ channels.

• Non competitive alpha antagonism (class III)

Magnesium indications.

• 1. Torsades de point from any reason.• 2. Arrhythmias in a patient with known

hypomagnesaemia.• 3. Consider its use in acute ischaemia

to prevent early ventricular arrhythmias.

• 4. Digoxin induced arrhythmias.

Who gets a pacemaker? Syncope, presyncope or exercise

intolerance that can be attributed to bradycardia

Symptomatic 2nd or 3rd degree AV block Congenital 3rd degree AV block with wide

QRS Advanced AV block after cardiac surgery Recurrent type 2 2nd degree AV block

after MI 3rd degree AV block with wide QRS or

BBB.

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