Cardiac Rhythm & Conduction (M/A)

MA14 Cardiac Rhythm and Conduction

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BradyCardias, Conduction Abnormalities, Premature Beats

Sinus Node Dysfunction

-low resting HR

-low mean HR

-decr HR variability - not Sn to autonomic input

-decr peak HR = chronotropic incompetence

-prolonged sinus pauses

-sinus arrest

-sinus nd exit block w jctl rhythm

-May call it tachy-brady syndromes or Sick Sinus Syndrome

Etiology

-rarely is it congenital

-usually post atrial surgery- Mustard, Senning, Fontan, ASD closure

-via injury to SA nd or via intra-atrial conduction abNly w intra-atrial block causing bradies

-likely bc of fibrosis/hypertrophy

-often see a steady loss of sinus fx postoperatively

-Pt also gets tachy's bc the frequent pauses in sinus rhythm contirbute to abNl triggered activity which along with the abNl atrial activation and repel --> more likely to get tachys...

-damage to local neural inputs likely also contribute to loss of HR variability and altered chornotropic response

-Other causes for transient bradycardia and long sinus pauses:

-neurocardiogenic syncope

-apnea of premie

-breathholding spells

-sleep apnea

-usually episodic, but can --> Sx, though unlikely life threatening if otherwise well

Mgt

-Tx by Sx (syncope, exercise intolerance, cardiac dysfx worsened by AV dyssynchrony)--> pace

-prophylactic pacing has not been shown to reduce risk of sudden death

Px

-pacing improves Sx, but not sudden death

AV Block

= sinus/atrial impulse conduction to ventricles is delayed/stopped

-check site of block - atrial, AV nodal, infra nodal

-check degree of block (1st-3rd)

-check ratio of atrial:ventricular impulses (2:1 block, 1:1block, etc)

-ECG good to check type

-1st Degree = PR Interval Prolonged

-but PR Interval = 3 subintervals:

-PA Interval (Sinus nd to low septal atrium)

- AH Interval (low septal atrium to His bundle depol)

- HV Interval (His bundle depol to ventric depol)

-so 1st Degree AVB can be bc of any of these

-usually occurs fr the AV nd (AH Interval prolongation)

-usually fr incr vagal tn, PR prolonging meds, nonsinus atrial rhythm (latter not actually a

pathologic change in PR interval, but just reflects diff location of atrial impulse onset...)

-2nd Degree =

-Type I (Wenckebach periodicity) = progressive PR prolongation then dropped beat, and then the subsequent PR is shortened

-usually fr AH Interval prolongation = AV nd delay

-Type II = PR Interval stays same, then sudden blocked P wave

-usually from the HV Interval prolongation = infra nodal

-May suddenly change to 3rd degree AVB with an inadequate escape rhythm!

-multiple atrial impulses may be blocked for each one beat conducted, with regular or irregular pattern. If it is regular, then check the ratio (2:1, 3:1, etc).

-High Grade AV Block (3:1 or more) during sinus rhythm is usually

from infranodal block (Type II) +/- AV block as well

-DDx High grade 2nd Degree AVB from a 3rd Degree AVB:

-2nd degree will show variation in RR interval

-3rd degree will regular RR interval

-3rd Degree = no atrial impulses are conducted to ventricles

-Congenital AVB- somewhat variable HR in response to physiologic conditions, but surgical block shows a more fixed HR

-Irregular variation in RR interval--> c/s 2nd Degree AVB instead (w intermittent AV conduction)

-Don't confuse 3rd AVB with AV Dissociation:

=AV Dissociation is fr sinus or atrial bradycardia.

-The AV Dissociation rhythm QRS's are faster, and are an escape rhythm..

-Unlike with 3rd AVB, with aV Dissociation, when there is a P wave that comes at the right time, it should conduct approprately to the ventricles, causing th RR Interval to shorten.

-If the AVB occurs within the AV nd, then the escape rhythm has a Nl QRS (=junctional escape), with an intracardiac recording showing a his bundle potential before each ventricular electrogram (bc it goes AV nd, His Bundle, Ventricle). If the AVB occurs below teh His bundle, then the intracardiac recording would show appropriately related atrial and His depolarizations, but these are completely dissociated from the ventricular depolarizations, and the escape rhythm will often have a long QRS...

Etiology

-1st & 2nd AVB can be Nl in neonates, teens/young adults, especially if athletic

-can be a 2y finding in infection, CHD, postop pt...

-High Grade AVB

-CHD - espec AV canal defects, and defects of looping (L-TGA, LA isomerism)

-due to fibrous disruption bn atrium and AV nd, or bc absent penetrating AV nd bundles

-Holt-Oram Syndrome- deformed upper extrem + CHD + AV conduction xx; bc of TBX5 mutation

-Nkx2.5 mutation (auto dom) --> AV nd conduction xx assoc w CHD

-Infection- myocarditis, Lyme, RMSF, Yersinia ent, Chaga, Dipheria, Typhoid, Valvar Endocarditis

-Rheum- RA, Reiters, Guillan Barre

-Neuro- myotonic dystrophy, Emery-Dreyfus dyst,

-Kearns-Sayre synd-progressive external ophthalmoplegia, retinal pigmentation, sev cardiac conduction xx early in life, bc of a mtDNA deletion

-Infiltrative- TB, Lymphoma, Amyloidosis, Sarcoidosis

-Trauma- postop, blunt chest trauma, radiation

-Transient postop AV block- bc of edema/hemorrhage, resolved by POD7, but still may have ongoing recurrence of AVB; if it continued beyond POD8, it is usually permanent and due to fibrous infiltration of conduction tissue

-Seen post ASD, VSD, TOF, TAPVC to CS, MC replaement, HOCM LVOT resection, single ventricle w subAo outflow chamber, Konno procedure to relieve subAo/Ao stenosis

-Especially at risk with displaced AV nd/His bundle in the endocardial cushion defects and congen corrected TGA

-Fx'l- resting tone, head trauma/cerebral edema, neuro mediated reflex, Carotid Sinus HyperSn.

-Rx- TCA's, Digoxin, Clonidine, Antiarrhythmic Rx

-Congenital AV Block- fr maternal Ab- Anti-Ro & Anti-La --> cross react w fetal tissue...

-DDx -if pt has a congen Long QT, they may get a fxl 2:1 AV block bc the QT is still in refractory pd at the time the next P wave comes, so it is blocked at every other beat

Mgt

-If Sx--> Atropine infusion is effective and immediate

--+/- adrenergic agonists and CPR if indicated

-Temporary pacing via transcutaneous or transvenous pacing

-transcut. usually temporary till you can get transvenous pacing

-ensure you regularly recheck pacer location w CXR and pacer thresholds

-Active fixation (screw in) temp pacing leads avail by fluoro, vs balloon tipped (floating) leads can be done at bedside initially via an IJ or subclavian vn

-2002 Guidelines for Permanent Pacing in peds

-Kearns Sayre syndrome & Postop persistent AVB are 2 situations that have enough risk to def warrant permanent pacing, and possibly for a CAVB with a wide QRS escape rhythm

Px

-Congenital AVB is nearly always irreversible

-Acquired AVB assoc w myocarditis, Lyme, postop is usually transient

-better Px if permanent AVB but Nl cardiac structure/fx

-Often first detect congenital AVB as a fetus, and can dvp hydrops fetalis and survival d/o the escape rate. Intrauterine pacing attempts have not yet been successful

-often do NOT need permanent pacer for acute Rh fever, Lyme dz, though often due need temp pacing

Bundle Branch Block & Fascicular Block

-QRS duration is short because of fast conduction thru the ventricular conduction system

-IF there is a block or delay, then --> long QRS (usually >80-100msec)

-Right BBB --> large superior terminal deflection in V1

-Left BBB--> large superior terminal deflection in V6

-Incomplete RBBB = rSR' pattern in V1 without QRS prolongation (actually this may just be bc of variation in RV free wall thickness, and not a conduction xx)

Etiology

-Proximal part of the conduction network is the part that transitions from the distal part of the AV node to the penetrating bundle, and is enclosed in the fibrous annular tissue

-Penetrating bundle crosses the AV ring and goes beneath the central fibrous body bn the membranous RV septum and the muscular septum. It then crosses the muscular septum.

-Beneath the R coronary leaflet and Noncoronary leaflet, the penetrating bundle divides, with RBB continuing inferiorly to the RV apex, and then turns ant'ly to be continuous w the moderator band to the outflow tract. The LBB quickly divides into several sheetlike fascicles that fan across the LV subendocardial surface and then interconnect distally.

-The proximal LBB supplies the muscular septum, which depols from L to R (thus initial QRS deflectn)

-The RV depolarizes only after subendocardial fibers arise from the RBB at the apex, and both R and L ventricles depol from the subendocardial to epicardial surfaces...

-May have a congenital or acquired BBB; +/- asspc w CHD_ Ebsteins and RBBB

-RBBB is usually postop

-Systemic dz can --> BBB too- Kaearns-Sayre, myotonic dystrophy

-Often seen post OHT

-Physiologic response to fast HR (and sometimes to slow HR too)

Mgt

-no Tx needed unless possible higher grade AV block too

-If higher grade AV block, then = class I pacing indication

-Kearns Sayre syndrome also = class I pacing indication to prevent sudden death fr complete AVB

-If residual postop bifascicular block, it is usually transient so just follow it till resolution bc it does incr risk for late AV block, =class II pacing indication

-If pt p/w syncope/arrest with a RBBB, then c/s the Sx might not be bc of block but bc of VT/VF

-RBBB in pt w syncope/arrest without a clear heart dz as etiology, may indicate Arrhythmogenic RV Cardiomyopathy, or Brugada syndrome. = ICD indication

-A pt w DCM and assoc BBB may get a VT including bundle branch re-entry tacky = ICD indication

Px

-d/o the cause

-if residual BBB after postop AVB, myocarditis, CM --> risk for late complete AVB

-checking the HV interval may help assess the pt's risk

Extrasystoles

Supraventricular Extrasystoles

-usually atrial (PACs), but may be jctl

-may conduct w Nl or abNl QRS, or may block at AV nd which would --> a pause on rhythm strip

-the PAC will reset the sinus node, but not with the full compensatory pause (the interval isn't the usual PP interval, it is shorter). However, if the sinus nd had just discharged, it's entrance block may prevent the PAC's impulse from resetting the sinus node, so that there is a full compensatory pause following the PAC)

-Frequent blocked PACs may mimic bradycardia

-Aberrantly conducted extrasystoles may be hard to DDx from PVCs, especially if they are jctl extrasystole

-Neonatal PACs common, then stop after a few weeks old, and atrial bigemony is a rare

Ventricular Extrasystoles

-Aberrant and premie QRS that is not preceded by an atrial depol

-QRS might be only somewhat prolonged bc the QRS is age dependent

-Then (usually) see a compensatory pause (bc the P wave that came was not conducted bc ventricle was in refractory pd, thus see a pause till the next P wave comes)

-If the PVC is conducted retrograde over the AT nd, it may reset the sinus nd and thus be followed by a less than full compensatory pause, like an atrial extrasystole... (bc the next P wave comes early)

-Bigemony/Trigemony = PVCs occurring every 2 or 3 beats

-The PVC can be interpolated (occurring at the right time so that it doesn't effect the underlying rhythm), or be only slightly premature so that it fuses with the Nl QRS- there you'll see a fusion beat that looks like a cross bn Nl and wide, and has a short PR interval

-DDx Fusion Complex from late PVC vs those fr intermittent pre-excitation

-Couplet = pair of PVCs, and 3 or more = Nonsustained VT

-Parasystole = when the couplet interval vary in their relationship to the sinus impulses, but are related to each other by a fixed interval

-PVCs - usually a marker for signif cardiac xx, but at certain ages it may be Nl variation

-Can occur in otherwise healthy neonates, but then it usually stops soon thereafter until teen years

-In teens, PVCs can be more common - usually in LBBB QRS morphology w inf axis = originate at RvOT

-mainly at slow HR, often suppress w exercise, and only sometimes occur in 2-4 beats,

-Usually benign if pt is otherwise well

-if DCM/HCM etc, then nonsustained VT--> incr risk of sudden death

AV Nodal Re-Entry, AV Tachycardias, and Pre-excitation Syndromes

AV Re-entrant Tachycardias

-aka SVT and paroxysmal atrial tachycardia

-#1 tachys in peds

-check abrupt onset/termination

-check fixed cycle length

-check Nl QRS complex

-check absence of clearly discernible P waves (usually), or flutter waves

-AVRT and AVNRT are the main types in kids (JET & Primary Atrial Tachycardias are 2 other types of SVT, see below)

- = reciprocating tachycardias- use 2 diff antegrade/retrograde limbs of a reentry circuit

ECG

-tachycardia w Nl QRS duration

-P waves usually follow QRS in 1:1, w regular rate

-AVNRT might have variations in AV and VA conduction and 1:1. AVB sometimes seen, and rarely has intermittent retrograde block or VA dissociation.

-Usually though it is 1:1, unlike primary atrial tachys (a-fib, flutter), JET, and VT each of which have varied AV relationship

-Any tachy can be 1:1 d/o antegrade/retrograde conduction, but only AVNRT/AVRT will stop if you interrupt the relationship bn A and V

-Abrupt onset- bc they're initiated by a specific trigger- a PAC or Jctl escape beat after a sinus pause

-less commonly triggered by a sinus acceleration (infants w AVRT, pts w PJRT)

-DDx PJRT is incessant, with only brief periods of sinus for a few beats at a time

-PJRT & atypical AVNRT has long RP interval, inverted P waves in inf leads

-DDx atypical AVNRT- usually more paroxysmal

-Might have a wide QRS if:

-transient, rate related BBB, espec if pt got an antiarrhythmic med to slow intraventric conduction

-pt has preexcitation syndrome, when the tachy uses the accessory pathway for antegrade Q, causing a pre-excited or antidromic tachycardia

-pt w an underlying conduction xx will also have wide QRS complex w tachycardia

Etiology

-AVNRT = involved peri AV nd tissue

-AVRT = involves accessory AV connection

-the accessory connection links atria and ventricular tissue at some site along the AV vlv ring, except where the mitral and aortic vlvs are in fibrous continuity

-the connection can be in subendocardial, endocardial, or epicardial location

-AVRT Types: divide by direction of conduction in the accessory pathway

-Orthodromic Reciprocating Tachycardia

-the AP is the retrograde limb of the tachy, and AVNd the angetgrade limb

-Nl QRS, unless there's a rate related BBB

-Antidromic Reciprocating Tachycardia

-less common

-the AP is the antegrade limb of the tachy, and the AVNd or 2nd AP is the retrograde limb

-the tachy is maximally pre-excited w a prolonged QRS so might not be able to DDx fr VT on ECG

-Wolf Parkinson White Syndrome

-the AP is the antegrade limb of the tachy (= pre-excitation), and the AVNd the retrograde limb

-PJRT- Permanent form of Junctional Reciprocating Tachycardia

-the incessant form of AVRT

-Antegrade via AV Nd, Retrograde through slowly conducting AP that inserts into atrial septum

-Reentry tachy using Mahaim Fibers

-uses Mahaim fibers

-a variant of antidromic recip tachy where the AP (here called teh atriofascicular connection) starts at RA free wall and insterts into RV His-Purkinje system --> prolonged QRS w RBBB pattern during the tachy

-AVNRT

-Antegrade & Retrograde conduction occurs over 2 fxly and anatomically discrete parts of atrial inputs, w diff conduction properties

-the Slow connection = posterior and inf inputs into the AV nd - slow condctn, short refract pd

-the Fast connection = ant and supinputs into the AV nd - --> fast conduction but block at a longer coupling intervals bc of its longer refractory pd.

-this allows for unidirectional block (usually in the fast limb), w conduction propagating over the slow limb with enough delay to allow for the recovery of the fast limb and thus re-entry via the fast limb

-2 AVNRT Types:

-Common Typical AVNRT - fast pathway is the retrograde limb, slow is antegrade

-the rapid retrograde conduction to atrium --> local atrial activation just after the onset of the ventricular activation, so the P wave is usually obscured in the QRS = short VA interval (<70msec) on intracardiac or transesoph recording

-Less Common Atypical AVNRT - slow pathway is the retrograde limb (long VA interval on intracardaic recording), and antegrade conduction goes over the fast pathway (--> short PR interval)

-this looks similar to PJRT on ECG.

Mgt

-if unstable, DC cardioversion

-if possible, transiently blocking AV nd helps Dx and Tx

-vagals

-adenosine

-if it failed to stop w adenosine, then AV nd not likely involved, or the dose not given well

-but must ddx failure to stop, w stopped briefly and then restarted

-if repeated reinitation occurs, then c/s transesoph pacing to terminate the process, or use IV procainamide, esmolol, verapamil if >1yo, or amiodarone to suppress the acute reinitiation until you can start maintenance Tx

-after stopping teh tachy, get an ECG in sinus to check for ventricular pre-excitation, other conduction xx, and clues to underlying hrt dz

-c/s thyroid fx check, electrolytes, BCx check

-if there isn't preexcitation, can start a betablocker, or verapamil if >1yo

-digoxin not as effective

-if +preexcitation, than do NOT use digox or verapamil (c/i xx)

-most other antiarrhythmic Rx also can Tx it- Class IC- flecainide and propafenone are very effective for both AVNRT & AVRT, while class IA Rx quinidine and disopryamide is mainly good for AVRT

-if still not effective, c/s sotalol, amio, or combos...

Px

...

Pre-Excitation Syndromes

-A group of xx where the atrial impulses are conducted partly or completely prematurely to the ventricles via a mech other than the Nl AV nd. Can have Nl or wide QRS

-Wolff Parkinson White Syndrome

-#1 preexcitation syndrome

-usually Nl heart, but WPW pts have incr incidence of CHD- Ebsteins, HCM, rhabdo

-0.1-0.3% of gen pop has it,

-usually sporadic but 3% pts have affected 1st degree relative

-Early depol via an AP w simultaneous depol over the AV nd --> shorter PR interval, QRS prolongation, and early slurring of the QRS (delta wave)

-the AP may serve as one limb of a reentry circuit during tachycardia

-may be associated with Orthodromic Reciprocating Tachys (less often w Antidromic)

-also incr risk of a-flutter a fib, AVNRT

-some pts will lose fx at the accessory fiber... WPW resolves

Nodoventricular, Nodofascicular, Fasciculoventricular, and Atriofascicular Connections

= Mahaim Fibers

= connections bn AV Nd/His bundle and the interventric septum

-usually no CHD, but sometimes Ebsteins associations...

-ECG usually Nl, but may show subtle suggestion of delta waves, then as atrial impulse rate increases, the delay over the AV nd allows preferential conduction over the AP --> PR prolongation and appearance of prolonged QRS w LBBB and LAD pattern (seen best if u pace fr RA wall near the TV)

-usually the antegrade limb is teh atriofascicular connection

...

Atrial Flutter & Intra-Atrial Re-Entry Tachycardia

-common to transition bn A-fib, a-flutter, and IART

-A-flutter = regular, rapid atrial tachy with visible saw-toothed flutter waves (best seen in II, III, F)

-AV block usually present. --> The RR interval is regular, and with an interval that is an integer multiple of the atrial cycle length...

-sometimes RR interval may be varying (so you give wrong Dx of a-fib)

-2 types:

-Type I = Typical = Common a-flutter = saw tooth flutter w inverted W waves at inf frontal lds

-if no structural hrt dz, it correlates w a very reproducible re-entry circuit

-Type II = Atypical = Uncommon a-flutter = less dramatic saw tooth look, w upright P waves in frontal lds. Some have used atypical a-flutter interchangeably w IART

-IART - unclear distinction fr a-flutter

-a-flutter rate is usually 240-360, w continuous atrial activation by ECG

-IART- usually slower, and w a clear isoelectric segment separating discrete P waves, and P waves are of various morphs depending on the pattern of atrial activation

-with the slower atrial rate of IART and w the robust AV nd conduction in CHD pts--> more likely to have 1:1 AV conduction, so more likely to look like sinus tachy (depending on P morph)

-IART term is only used in pts who've had prev CV surg

-IART & a-flutter have similar EP substrates ... diff bn the 2 is semantics...

-you can't clearly tell the etiology by P wave morph alone, must use intracardiac mapping, so it is most appropriate to refer to all paroxysmal atrial tachy in CHD pts as IART.

-both IART & a-flutter have regular PP intervals, but hard to see if there's variable AV conduction

-must DDx a-flutter/IART fr chaotic atrial tachycarida, both of which --> irreg irregular or intermittently varying atrial activation. Giving adenosine or getting direct atrial recording (via transesoph/epicardial/transvenous atrial leads) can help ddx the two.

-Other inter-atrial re-entry tachy:

-L sided a-flutter - seen if h/o MV surgery

-Sinus Node re-entry tachy

--> atrial rates <200, w P waves look like sinus P waves

-initiated and stopped w atrial pacing, or w adenosine/vagals

-often regarded as artifact of programmed atrial stim, but can be seen in pts w +Sx tachy

-need EP lab to check if it is a micro-reentry circuit near SA nd or a macro reentry w exit site near the SA nd

-more likely to terminate w vagals/adenosine than IART of the same morph

Etiology

-a stable macrore-entry circuit in the atria, with a fixed, stable activation pattern

-TV annulus, PVns, IVC-SVC jct w the heart are boundaries of conduction delay/block needed for a-flutter/IART to occur. Scars and other changes fr atrial dilation/hypertrophy/fibrosis/ablation can all contribute too

-A-flutter- usually uses a predictible zone of slow conduction as the tachy goes counterclockwise fr atrial free wall thru the isthmus of myocardium bn IVC and TV annulus twd the septum (so goes up by the atrial septum and down by atrial free wall along the crista terminalis)

-IART can use the same isthmus as part of its circuit, but may have additional conduction anomalies bc of postop scars that add to the pattern; may have multiple re-entrant circuits

-In kids >1yo, usually pt has underlying structural heart dz and mostly in postop pts. In infants, it is usually a-flutter occurring w/o other heart dz, but often is assoc w an AV AP +/- pre-excitation

Mgt

-Goals:

-Control Sx

-Sx are mainly bc of the ventricular rate- can cause HD xx, exertional Sx, ventric dysfx

-Thrombi can --> stroke/PE

-Stop tachycardia

-Re-establish NSR

-Prevent recurrence

-DC cardioversion is best Tx in acute setting w HD xx, but not if pt is stable

-Like a-fib, IART & a-flutter respond to DC cardioversion but can also be stopped w pacing (transvenous/transesoph)

-pacing can transiently convert atrial tachy to a-fib which often spontaneously stops

-If pt has a pacemaker, you can use it to pace them out of the rhythm

-Can give Rx to stop it acutely - Ibutlide better than procainamide but has incr risk of arrhythmia

-Sometimes, adenosine given for Dx can stop it

-If longstanding (24-48hrs), then there is signif risk of acute CVA, so check a TEE for thrombi if >24hrs or an unknown duration, or wait 3-4 weeks to cardiovert after giving anticoagulation (but must ensure they can tolerate the wait).

-CCBs and beta blockers are more reliable to control the ventric rate than digoxin

-For acute ctrl of the ventricular rate, CCB is preferred

-Diltiazem IV bolus or continuous infusion, while you wait to check the TEE etc

-Avoid Digox and Verapamil in pts w a-fib + WPW bc it may enhance the antegrade AP conduction

-Long Term Tx:

-Class I and Class III drugs

-Class IA w anticholinergic effects that potentiate antegrade conduction at AV nd during flutter/fibrillation should be given with another Rx that offsets this effect- diltiazam, digox, betablocker

-Class IC drugs- propafenone and flecainide- might be a bit better but may incr risk for serious proarrhythmias in pts w a-flutter/fib, and they may potentiate more AV nd conduction w faster ventric rate bc of the relative amt they slow the atrial rate vs the AV nd rate...

-Class III drugs- just as good to reduce Sx/recurrence, ? bc they slow atrial conduction more than slowing atrial rate--> more likely to have slower ventric rate

-No Rx is uniformly effective to stay in NSR

-Nonmedical Tx often needed:

-Antitachycardia pacing

-may also be needed to prevent bradycardia fr the Rx

-If need pacer for SA nd dysfx fr IART/A-fib, then use an AAIR (atrial pacer w rate response), or use a DDDR (dual chamber pacer) w both rate response and mode switching

-Catheter Ablation

-has better success w IART than others, but still can be tough

-Surgical Revision

-often needed for Fontan pts, may need conversion to a lateral tunnal or extracardiac connection w intraoperative cryoablation at the most likely sources

Px

-Infants w a-flutter and no other hrt dz- usually self limited w/o much recurrence after cardioversion

-IART d/o underlying dz

-Hardest pts to treat are postop CHD pts w bradycardia and atrial tachy, bc the IART has much M&M and so must be treated aggressively.

-Symptomatic brady--> pacer needed

-Tachycardia needing an antiarrhythmic Rx other than digoxin--> pacer needed (class II rec)

-pacer might not prevent the adverse events during Rx Tx of a-flutter/fib

-M&M incr fr CVA, espec in pts w ch rheumatic hrt dz --> need chronic anticoagulation if ch/freq a-flutter. Anticoag also being used more commonly for a-flutter + CHD

Atrial Fibrillation

-DDx fr a-flutter by marked irregularity of RR interval and by inconsistent pattern of atrial depolarization

-Irregularly Irregular ventric response bc of irreg intervals of atrial impulse to AV nd

-Might be hard to ddx flutter and fib fr a short rhythm strip. Must compare atrial cycle lengths by measuring a group of 4-5 atrial cycles instead of a single cycle. If the P wave morph, axis, cycle length differ, then it is more likely a-fib even if you think you see a saw toothed pattern

-Atrial recordings also help DDx a-flutter and a-fib

Etiology

-?why in kids

-usually due to a disorganized re-entrant process involving multiple wavelets that go thru atria w diff degrees of organization/repetitiveness --> sometimes it can look more like a-flutter or chaotic atrial tachy

-the reason there is no fixed, consistent re-entrant circuit (w fixed timing/morph) is that the substrate for re-entry d/o fx'l, and not anatomical, conduction abNlies...

-a-fib may originate fr PVn ostia

-a-fib can --> atrial remodeling --> incr risk for arrhythmia over time

-Older kids/teens w WPW have incr risk of a-fib, can --> sudden death if a-fib conducted rapidly at AP

-ablation eliminates this risk, and decr overall risk of a-fib

-sometimes a-fib may be the presenting Sx of hyperthyroidism, myocarditis, or digox toxicity

-Genetics has a role in some familial forms...

Mgt

-same principles as Tx for IART/aflutter

-Rx to slow AV nd conduction may work better than w IART, but the risk of thromboembolic risk is higher for afib than IART

-If pt is awaiting cardioversion for more than a 'brief period", then start anticoagulation and a rate controller. You must be able to temporarily pace since there might be signif bradycardia prior to the emergence of a stable spontaneous escape rhythm. Unlike w IART, you can't pace them out of it usually, so don't try...

-Rx choice is like w IART, w goal to decrase both the frequency and duration of episodes

-c/s no Rx if just brief, self limited a-fib w/o a rapid ventric response

-In past, would ablate AV nd and then put in a ventricular pacer, but that--> lose AV synchrony and are pacer dependent (now only use if Rx failed multiple attempts)

-Some may respond to ablation - focal a-fib fr rapid firing fr PVn site, though can be hard to isolate the target. Pulm vn stenosis is a risk of ablation.

Px

-d/o underlying CV dz

-ASD, postop lesions, AV vlv regurg, DCM, HCM, ch rh MV dz, Emery Drefus MD pts often recur

-once established, Tx other than Maze is unlikely to help

-a-fib fr hyperthyroid stops when pt is euthyroid

-otherwise well teens w a-fib have recurrences only rare through their 20s at least, but ? later on

-Pts at highest risk are those w/o palpitations bc it goes unrecognized for a while and fx drops

Ectopic Atrial Tachycardias

-Localized automatic foci within atrium (not re-entrant)

-usually chronic & often incessant

-may have severe cardiac dysfx bc of it (though the tachy might falsely be attributed as a Sx of the dysfx instead of a cause)

-Pts rarely get palpitations bc of its insidious nature

-Atrial rates only moderately incr fr Nl, w an exaggerated response to exercise

-Little short term beat to beat variability, though HR can vary considerably over time

-Usually incessant, but may stop (e.g. w sleep), whereupon you would see a subtle P wave change

-Has a warm up/cool down (acceleration and slowing) at start/stop

-1st or 2nd AV block during an apparent sinus tachy is a good clue!!!

Etiology

-? cause in an otherwise well pt

-some pts classified as a mircro-reentrant foci fr a tachycardia foci bc of an abNl automaticity, w the latter having a warm-up pd and does not start/stop w extrastimulus testing, and it resets during an extrastimulus to the atria during the tachycardia, but none of this definitively excludes a micro-reentrant tachy.

-Usually at RAA or near PVn connection to LA, ? why

Mgt

-does not respond to pace termination, DC cardioversion, vagals, or adenosine --> c/s EAT

-is sensitive to adrenergic stimulation

-Thus must avoid adrenergic stim, even if there is overt CHF. Instead use beta-blockers

-Rx

-Class IA

-Class IC

-Beta blockers

-Class III

-Amiodarone

-if Rx refractory, can ablate the focus

Px

-d/o #/size of foci, tendency to regress over time

-ventric dysfx usually improves p tx

-ablation attractive bc usually fails Rx Tx, but bc there is potential for spontaneous regression it is good to first try Rx

Chaotic Atrial Tachycardia

-multifocal - 3 or more P wave morphs, w an isoelectric baseline (unlike a-flutter/fib)

-use Multifocal Atrial Tachy term to describe adults w h/o pulm dz; use Chatoic Atrial Tachy to describe young kids/infants w otherwise Nl hearts

-Rates vary much, PP interval is irregular though P waves are discrete. Can be hard to ddx fr a-fib and a-fib periods are assoc w it!

-? if it is bc of competing automatic foci, multiple re-entrant circuits or something else

-often assoc w bronchiolitis/RSV

-some have a severe or fatal bradycardia (?!)

-Pacing, DC cardioversion, and adenosine don't work --> so Tx like EAT

-Verapamil and Propranolol slow ventric response may be enough to reduce Sx

-Complete suppression possible w Class IA, IC, III Rx, espec propafenone & amio

-Often regressess in days-months, but 17% of young pts in one review had sudden death! (2 witnessed as severe bradycardia) - ? if bc of the Rx Tx or the underlying dz ==> close inpt monitoring needed

Junctional Ectopic Tachycardia

-uncommon, automatic tachycardia in peds

-seen in early postop pd after CPB in infant/toddler w CHD - can have HD xx

-also seen in non-postop pts in a congenital form of JET

-see tachy w Nl QRS duration at 180-240 bpm w AV dissociation and a slower atrial rate (Q>P)

-see RR interval shorten periodically as the P waves march through and sometimes an appropriately timed P wave marches through the AV nd

-may have regular ventric rate if there is 1:1 VA conduction or complete antegrade AV block

-the former, it looks like SVT but is refractory to arial pacing, DC cardioversion, or adenosine

-c/s complete AV block if you see RR interval doesn't vary despite AV dissociation, and if you see the HR slowing fails to yield to an appropriately timed atrial impulse. An ECG fr atrial wires can help Dx

-in Postop pts, may have wide QRS so hard to DDx fr VT - check intracardiac wires- His depol precedes each ventricular depol, so it is JET and not VT. Pacing in this setting might entrain the His bundle but not stop the tachy, unlike w a His bundle reentry tachy.

-Congenital JET- seen prenatally often, or by <1mo

-recessive inheritance, so check FHx

-HR to 370bpm seen --> CHF, acute HD xx

Etiology

-fr enhanced automaticity of tissue at/near AV nd

-?fr surgical trauma--> irritable focus, vs reperfusion xx vs anesthestic...

Mgt

-if HD xx --> must slow it down, ideally to NSR

-usually resists antiarhythmic Rx

-Amio most effetive for congenital JET --> ctrl in 80% (at least partially)

-may need to ablate it

-Postop JET is transient so usually only need temporary Tx

-stop inotropes, cool the pt

-R wave synchronized atrial pacing to get AV synchrony, but has risk of inducing atrial tachy bc of asynchronous atrial pacing

-flecainide and amio can be used

-digox, betablockers, CCP not effective

-class IA & IC response very variable

Px

-congenital JET- high risk of CHF & mortality...

-Postop JET - transient, w most stopped by 24-72hrs postop regardless of Tx

General Aspects of Ventricular Tachycardia

-DDx of wide complex tachy:

-VT, pre-excited SVT, any tachy w aberrant conduction bc of fixed, fxl, or rate related BBB

-pacemaker mediated tachy- w a wide complex w paced QRS morph

-Hallmark of VT: wide QRS and dissociation bn P waves and the QRS during tachy (w atrial rate slower than ventric rate)

-these features might not be present in infants/young kids bc QRS duration varies w age

-pts w CHD might have long QRS w NSR, so compare to prior ecg's

-Younger pts might have 1:1 VA relationship w VT bc of retrograde conduction at high rates (so now ther is no AV dissoc, despite it being VT)

-might be helpful to check atrial lead to eval AV relationship during the potential VT

-You can confirm it is VT if you see that there is VA dissoc w a slower atrial rate, or w variations in the retrograde conduction during the tachycardia (especially if it retrograde conduction slows w vagals/adenosine). 1:1 VA conduction does not exclude VT, unless you can confirm that block to the retro or anterograde conduction consistently stops the tachycardia.

-If there is VA dissociation, then seeing varied RR interval w a sinus capture beat might help Dx VT

-intermittent fusion complexes helps DDx VT fr SVT w variable conduction

-VT Sx vary widely and dont help DDx fr another arrhythmia...

-Termination with vagals, adenosine, atrial pacing, or verapamil doesnt confirm/give evidence that it is SVT bc they can also stop certain types of VT!

-Nonsustained VT = >3 & <30 consecutive ventricular beats

-Monomorphic vs Polymorphic

-Torsades de Pointes - assoc w long QT, occurs w congen/acquired long QT, w QRS undulate/twist around the isoelectric line as QRS morph changes shape/axis gradually

-Bidirectional VT - assoc w digox toxicity, Andersen-Tawil synd, or catecholaminergic polymorphic VT

-beat to beat alternation in QRS axis during the VT (DONT MISTAKE FOR VENTRIC BIGEMONY)