lecture 13- atrial and junctional arrythmias

premature atrial contractions (PACs)

• common cause of irregular rhythms originating from an ectopic atrial focus

• occur when excitable cells in the atrium fires before the SA node

• EARLY P wave present (often looks different from sinus)

• QRS remains normal (ventricular contraction is unchanged)

• usually benign

patterns of PACs

• may occur sporadically

• in pairs (couplets) or threes (triplet)

• every other beat= atrial bigeminy

• every third beat = atrial trigeminy

• ≥ 3 consecutive PACs→ atrial tachycardia - can be inifocal or multifocal

clinical relevance of PACs

• can cause sx that impact daily life

• may progress to sustained atrial arrhythmias (a fib, a flutter)

• increased PACs os associated with higher risk of:

  • atrial fibrillation→ clotting→ stroke

• if frequent PACs are suspected:

  • consider ambulatory monitoring to quantify freq

• risk increases with comorbidities:

  • structural heart disease

  • HTN

  • DM

• frequent sx PACs are also associated with:

  • stroke

  • heart failure

lifestyle contributors to address (PACs)

• reduce caffeine

• maintain

• hydration

• manage stress

• encourage good sleep hygiene

unifocal atrial tachycardia

• NO LONGER SINUS

• can occur in either atrium

• consistent abnormal P wave morphology

• ectopic focus overdrives and suppresses the sinus node

• can occurs in:

  • structurally normal hearts

  • structurally abnormal hearts

  • other medical conditions that cause stress

• non-sustained runs may appear regularly irregular

• sustained typically produces regular rhythm

causes of unifocal atrial tachycardia

• enhanced automaticity

  • increased excitability of atrial tissue

• triggered activity

  • often related to catecholamine surges (stress, illness, stimulants)

• microreentry

  • small localized reentry circuit causing repeated atrial firing

multifocal atrial tachycardia (MAT)

• caused by multi0pe atrial pacemaker foci firing at different rates

• slightly irregular rhythm with varying P wave morphologies

• each has different intrinsic rate, producing beat-beat varibaility

  • >100bpm

• most commonly seen in pts with COPD or congestive heart failure

wandering atrial pacemaker

• MAT that is <100 bpm

• looks more regular

atrial fibrilation

• irregularly irregular

• chaotic atrial activity with no dominant pacemaker

• results in absent organized P waves and an irregular ventricular response

• AV node acts as gatekeeper→ limit conduction

  • atria fire faster and faster→ AV node gets overwhelmed→ AV node slows itself down after each pulse to protect ventricles

  • each impulse makes AV node take longer to recover before it can conduct next signal

• “decremental conduction” : prevents dangerously rapid ventricular rates

• easier to see when slowed down

atrial flutter

• caused by reentry loop

  • commonly R atrium

• “saw tooth” flutter appearance (best seen in inferior leads)

• ventricular rate depends on AV conduction ratio

  • 2:1

  • 3:1

  • 4:1

• rhythm may appear regular or irregular

• P and T waves me burried

premature junctional contraction (PJC)

• narrow QRS that may occur without visible P wave or with retrograde P wave

• best occurs earlier than next expected sinus

• often followed by compensatory pause

• QRS morphology resembles normal sinus beat

• comes from AV nose

junctional escape

• rate~40-60bpm

• impulse originates from AV junction

• QRS is narrow or mildly prolonged

• P wave is nOT consistent with QRS

  • may be absent, inverted, or abnormal

• very SHORT P-R interval

when do junctional escape rhythms occur

• sinus impulses fail or are too slow

• AV junction takes over as a backup pacemaker

accelerated junctional rhythm (AJR)

• occurs when AV junction becomes dominant pacemaker, firign faster than sinus node

• enhanced automaticity of the VA junction alogn with suppressed or slower SA node activity

• narrow complex rhythm: QRS <120ms

• ventricualr rate ~60-200bpm

• retrograde P waves may be present and can appear before, during, or after QRS

  • usually inverted in inferior leads (II, III, aVF)

  • upright in aVR + V1

atrial tachycardia vs AJC

atrial tachy

• ectopic focus in atria

• usually 100-250bpm

• P waves present but ABNORMAL shape

• P waves are before QRS most of the time

• PR interval in variable

• atria fire first

AJC

• AV junction/AV node origin

• usually 60-100bpm

• P waves often absent, inverted, or after QRS

• P waves can be buried in QRS, before, or after QRS

• PR interval is short, IF VISIBLE

• ventricles activate first or simultaneously as atria

supraventricular tahcycardia (SVT)

• any fast heart rhythm that starts ABOVE ventricles

• HR is usually rapid and regualr

  • >150bpm

• exact source may not always be clear on 12lead EKG

• examples:

  • sinus tachy

  • a fib

  • AV nodal reetrant tachy (AVNRT)

examples of supraventricular arrhythmias

irregular rhythm

• wandering atrial pacemaker

• multifocal atrial tachy

• atrial fib

regular rhythm

• atrial flutter (or irregular)

• paroxymal atrial tachy

• AV nodal reentrant tachy

• AV reciprocating tachy

EKG characteristics of SVT

• narrow QRS

  • <120ms

• broad term for rapid rhythms originating above ventricles

• may appear wide if aberrant conduction or bundle branch block is present

• wide QRS can complicate rhythm interp and mimic verricualr arrythmias

dx supraventricular tachy- step 1: look for P waves

• P waves may be hidden, absent, or buried in T wave

• if visible:

  • is there one P for every QRS

  • is it before, after, or inside QRS

startegies to find P waves

• look for pauses or breaks in rhythm

• examine before, after, and within QRS/T wave

• compare with prior EKG if available

dx supraventricular tachy- step 2: evaluate onset and termination

• look at how rhythm starts and stops

  • did it start suddenly or gradually

  • gradual increase/decrease=more consistent with sinus tachy

  • check for triggering beat: PAC → often triggers SVT

  • PVC less commonly involved

atrial fibrilation

• most common sustained arrythmia

• from rapid firing irritable focus within pulmonary veins or LA (90%)

• enlarged atrium allows for reentry circuits to develop

• atria are “quivering” with no coordinated conduction, therefore no coordinated atrial contraction

  • ventricles rely on passive filling

characteristics of A fib

• electrical activity is chaotic and uncoordinated

• atrial tissue becomes highly excitable

• AV node acts as filter, preventing all impulses form reaching ventricles

• atrial rate can reach 400-700bpm

• typical uncontrolled ventricular rate= 110-180bpm

• lack of clear P wave with flat or fibrillating baseline

  • fibrilatoiry waves can vary from fine to coarse that can be confused with P wave

• irregularly irregular QRS

• can have rapid ventricular rate (RVR) if uncontrolled

typical vs atypical atrial flutter

typical

• singel circuit around tricuspid valve

• usually counter clockwise

• EKG:

  • negative flutter waves in II, III, aVF

  • positive in V1

atypical

• multiple or altered reentrant circuits

• no consistent EKG pattern

• often harder to treat

paroxysmal atrial tachy EKG features

• P waves:

  • usually present but abnormal in shape

  • morphology differa from sinus

• at faster rates:

  • P waves may be hidden in QRS or T wave

• rhythm typically is regular

paroxysmal atrial tachy- rate related changes

• as atrial rate increases:

  • PR interval may lengthen

  • due to increasing AV nodal refractoriness

• with very rapid rates:

  • P waves may become difficult ot impossible to ID

• as rate slows:

  • P waves become visible again

atrioventricular nodal reentrant tachy (AVNRT)

• common form of PSVT

• oftenhealty pts with structurally normal hearts; women >men

• cause dby reentry circuit within AV node

• occcurs due to two pathways within AV node:

  • fast pathway → fast conduction,s slow recovery

  • slpw pathway → slow conduction, fast recovery

AVNRT: typical dual AV node physiology

• normal= as signal from AV node travel down, fast pathway reaches ventricles firts→ shuts down slow pathway signal

• in AVRT= both pathways are capable of

  • anterograde conduction (atria → vent)

  • retrograde conduction (ventricles → atria)

how AVRT starts (reentry)

step 1- fast pathway is blocked

• a premature beat occurs

• fast pathway is still recovering and cannot conduct so it is blocked

step 2- signal goes down slow pathway

• slow pathway is readym so the impulse travels down it

step 3- fast pathway recovers

• by the time the impulse reaches the bottom, the fast pathway has recovered

step 4- signal travels backward up the fast pathway

• impulse goes back up to the atria through the fast pathway

step 5- circuit repeats

• impulse keeps going:

  • down slow pathway and back up the fast pathway

creates a rapid reentry loop=AVNRT

typical AVNRT characteristics

• rate usually 150-220bpm

• regular rhythm- R-R intervals regular

• QRS is typically narrow

• initiated by PAC; P waves usually hidden in QRS; can also be retro

• ST segment may be depressed

• abrupt onset after a PAC with prolonged PR interval

atrioventricular reentrant tachycardia (AVRT)

• type of SVT

• caused by extra electrical pathway outside the AV node

  • most commonly involves Bundle of kent (WPW)

  • extra pathway lets electrical signals bypass AV node

• two types

  • wolff parkinson white pre excitation

  • concealed accessory

wolf parkinson white (WPW)

• type of AVRT SVT

• happens when the accessory pathway conducts signals:

  • atria→ ventricles (anterograde conduction)- wrong way and bypasses AV node

• part of ventricles activate earlier than normal

• EKG findings:

  • short PR interval

  • delta wave

  • wide QRS due to early ventricular contraction

  • appearance of delta wave varies base don pathway location

• biggest danger= atrial fibrillation with rapid conduction

  • lack of AV node “speed bump”→ extremely fast ventricular rate → potential ventricular fibrillation and cardia arrest

concealed accessory pathway

• type of AVRT SVT

• some pathways only conduct retrograde (ventricles→ atria)

• bc there is no preexcitation, no delta wave seen in normal sinus

• hidden until tachycardia occurs

• recurrent narrow complex SVT and normal baseline EKG without delta wave- suspect concealed accessory

orthodromic tachy in WPW

• common in 90% of cases

• signal goes down AV. node→ UP the accessory pathway→ produce a narrow QRS (looks liek normal fast HR)

• impulse travels:

  • anterograde through the AV node and His- purkinje system

  • produces narrow QRS

  • returns retrograde through accessory pathway to atria

  • shows ventricular rate of 150-220, narrow QRS, inverted P wave (if can be seen)

antidromic AVRT

• impulse travels:

  • anterograde through the accessory pathway (bypassing AV node)

  • produces wide QRS that can mimic ventricular tachy

  • then returns retrograde through His bundle and AV node

  • EKG shows ventricular rate 150-20, wide QRS, inverted P wave