Arrhythmias

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 Path Slow Recovery

Slow Conduction Path Fast Recovery
Reentry Requires… Electrical Impulse
Cardiac Conduction Tissue
2 distinct pathways that come together at beginning and end to form a loop. A unidirectional block in one of those pathways. Slow conduction in the unblocked pathway.

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 Path Slow Recovery
Slow Conduction Path Fast 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 Path Slow Recovery
Slow Conduction Path Fast Recovery
Cardiac Conduction Tissue
Reentry Mechanism


Reentry … 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)

What tools to use and when to 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. Loop event monitors.

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)!

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%

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 impulseQRS 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 impulseQRS is widened (at least 3 boxes)V1 and V2 have rSR’Pacemaker if syncope occurs.

Bifascicular Block

RBBB plus LABB OR RBBB plus LPBBQRS is widened (at least 3 boxes)V5 and V6 have RR’ (rabbit ears)V1 and V2 have rSR’Pacemaker if syncope occurs


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


SVT

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 Flutter is aminor form of AF.

Atrial Fibrillation

Rapid AF

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-blockersContinuation after CABG may prevent a-fibGood for hyperthyroid or post-MI patients with a-fibCarvedilol decreases mortality in patients with CHFEsmolol 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 BlockersNondihydropyridines (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 conductionAdenosine is too short acting to be of any use in a-fibLast 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, mexilitine, 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

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

Torsades de Pointes

“Twisting of the points” is usually caused by medication (quinidine, disopyramide, sotalol, TCA), hypokalemia or bradycardia especially after MIHas prolonged QT intervalAcute: Remove offending medication. Shorten the QT interval with magnesium, lidocaine, or temporary overdrive pacingChronic: 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.

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. Digoxin induced arrhythmias. 4.Refractory VT.

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.