Brady Arrhythmias

7/26/2019 Brady Arrhythmias

1/11

THE BRADYARRHYTHMIAS:DISORDERS OF SINUS NODE FUNCTIONAND AV CONDUCTION DISTURBANCES

ANATOMY OF THE CONDUCTING SYSTEMSinoatrial (SA) node

o lies at thejunction of the riht !triu" !n# $u%erior &en! c!&!'

o approximately 1.5 cm long and 2 to 3 mm wideo supplied by the sinus node artery, which arises rom either the right coronary artery (!"#)or the let

circumlex coronary artery ($"#). %nce the impulse exits the sinus node and perinodal tissue, it tra&erses the atrium until it reaches the

atrio&entricular (A') node.Atrio&entricular (A') node

o he blood supply is deri&ed rom the posterior descending coronary artery ("#)

o lies at the base o the interatrial septum *ust abo&e the tricuspid annulus and anterior to the

coronary sinuso it+s electrophysiologic properties result in slow conduction, which is responsible or the normal

delay in A' conduction, i.e., the - inter&al. he bundle o is

o emerges rom the A' node

o enters the ibrous s/eleton o the heart, and courses anteriorly across the membranousinter&entricular septum.

o 0t has a dual blood supply rom the A' nodal artery and a branch o the anterior descending

coronary artery.o he branching (distal)portion o the bundle o is gi&es rise to a broad sheet o ibers that course

o&er the let side o the inter&entricular septum to orm the (eft )un#(e )r!nchand a narrow cableli/e structure on the right side that orms the riht )un#(e )r!nch

o he arboriation o both the right and let bundle branches gi&es rise to the distal isur/in*e

system, which ultimately extends throughout the endocardium o the right and let &entricles. he SA node, atrium, and A' node are signiicantly inluenced by autonomic tone.

arasympathetic ects

o depress automaticity o the SA node

o depress conduction

o prolong reractoriness in the tissue surrounding the SA node

o inhomogeneously decrease atrial reractoriness and slow atrial conduction

o prolong A' nodal conduction and reractoriness.

Sympathetic inluences exert the opposite eect.

E*ECTRO+HYSIO*OGIC +RINCI+*ES 0n the resting state, the interior o most cardiac cells, with the exception o the SA and A' nodes, is

approximately , -. to , /. "V, negati&e with respect to a reerence extracellular electrode.he resting membrane potential is determined primarily by the concentration gradient o potassium across

the cell membrane.Acti&ation o cardiac cells results rom mo&ement o ions across the cell membrane, causing a transient

depolariation /nown as the action potential

he action potential o the isur/in*e system has i&e phaseso hase "

rapid depolariing phase

mainly determined by an inlux o sodium into myocardial cells ollowed by a secondary

(slower) inlux o calcium, which produces a slow inward current.o hases 1 4 3

repolariation phases o the action potential

primarily related to outward lux o potassium.

o hase $


2/11

resting membrane potential

-ecent studies ha&e demonstrated heterogeneity o action potentials in the epicardium, midmyocardium,

and endocardium as well as between right and let &entricles. hese dierences are due to dierent ioncurrents in dierent layers.

he bradyarrhythmias result rom abnormalities either o

o impulse ormation, i.e., automaticity

o conduction.Auto"!ticit0

o normally obser&ed in the

sinus node

specialied ibers o the isur/in*e system

some specialied atrial ibers

o the property o a cardiac cell that causes it to depolarie spontaneously during phase $ o the

action potential, leading to the generation o an impulse.o o exhibit automaticity, the resting membrane potential must decrease spontaneously until

threshold potential is reached and an allornone regenerati&e response occurs.o he ionic currents producing spontaneous diastolic depolariation appear to in&ol&e the inward

currents o sodium andor calcium and a decreasing outward potassium current. Con#uction

o impulse propagation through cardiac tissues

o depends on the magnitude o inward current, which is directly related to the rate o rise and

amplitude o phase " o the action potential.o he more positi&e the threshold potential and the slower the rate o depolariation toward

threshold, the lower is the rate o rise and amplitude o phase " o the action potential and theslower is the conduction &elocity.

ropagation is more rapid parallel to iber orientation than trans&erse to it, a property termed anisotropic

conduction Refr!ctorine$$

o is a property o cardiac cells that deines the period o reco&ery that cells re6uire ater being

discharged beore they canbe reexcited by a stimulus absolute refractory period

o

deinedby that portion o the action potential during which no stimulus, regardless o its strength,can e&o/e another response.effective refractoryperiod

o that part o the action potential during which a stimulus can e&o/e only a local, nonpropagated

response.relativerefractory period

o extends rom the end o the eecti&e reractory period to the time that the tissue is ully reco&ered.

o 7uring this time, a stimulus o greater than threshold strength is re6uired to e&o/e a response,

which is propagated more slowly than normal.0n the normalisur/in*e system or &entricular myocytes, excitability is reco&ered ollowing completion o

the action potential, and e&o/ed responses ha&e characteristics similar to the spontaneous normal response.0n theA' node, reco&ery o excitability occurs well ater completion o theaction potential.

SINUS NODE DYSFUNCTION he SA node is normally the dominant cardiac pacema/er because its intrinsic discharge rate is the highest

o all potential cardiac pacema/ers 0ts responsi&eness to alterations in autonomic ner&ous system tone is responsible or the normal acceleration

o heart rate during exercise and the slowing that occurs during rest and sleep.0ncreases in sinus rate normally result rom an increase in parasympathetic tone acting &ia muscarinic

receptors andor an increase in sympathetic tone acting &ia 8adrenergic receptors.Slowing o the heart rate is normally due to opposite alterations.

0n adults, the normal sinus rate under basal conditions is 1. to 2.. )e!t$3"in'


3/11

o Sinus bradycardiais said to exist when the sinus rate is 9 !" beatsmin

o Sinus tachycardiawhen it is : 1"" beatsmin

o there is wide &ariation among indi&iduals, and rates 9 !" beatsmin do not necessarily indicate

pathologic states.o ;or example, trained athletes oten exhibit resting rates 9 5" beatsmin due to increases in &agal

tone.


4/11

o reers to a combination o symptoms (diiness, conusion, atigue, syncope, and congesti&e heart

ailure) caused by SA node dysunction and maniested by mar/ed sinus bradycardia, sinoatrialbloc/, or sinus arrest.

o =ecause these symptoms are nonspeciic, and because >? maniestations o sinus node

dysunction are oten intermittent, it may be diicult to pro&e that such symptoms are actuallycaused by SA node dysunction.

Atrial tachyarrhythmias such as atrial ibrillation, atrial lutter, or atrial tachycardia may be accompanied by SAnode dysunction.bradycardia-tachycardia syndrome

o reers to paroxysmal atrial arrhythmia that upon termination is ollowed by prolonged sinus pauses

or in which there are alternating periods o tachyarrhythmia and bradyarrhythmia.o Syncope or presyncope may result rom ailure o the sinus node to reco&er unction ollowing

suppression o automaticity by atrial tachyarrhythmia.

DIAGNOSISFirst-degree sinoatrial exit block

o denotes a prolonged conduction time rom the SA node to the surrounding atrial tissue.

o 0t cannot be recognied on a standard (surace)>? but re6uires in&asi&e intracardiac recordings,

which can detect this condition indirectly, by measuring the sinus response to atrial premature

beats, or directly, by recording SA node electrograms Second-degree sinoatrial exitblock

o denotes the intermittent ailure o conduction o sinus impulses to the surrounding atrial tissue it is

maniested as the intermittent absence o wa&esThird-degree6 or complete, sinoatrial block

o characteried by a lac/ o atrial acti&ity or by the presence o an ectopic subsidiary atrial

pacema/er.o %n the standard >? it cannot be distinguished rom sinus arrest, but direct intracardiac

recordingso SA node acti&ity permit this distinction.he bradycardiatachycardiasyndrome is maniested on the standard >? as tachyarrhythmias

o Bost oten these are !tri!( f(utter or fi)ri((!tion, althoughany tachycardia during which the atria

are acti&ated may cause o&erdri&esuppression o the sinus node, resulting in clinical appearanceo this syndrome.

he most important step in the diagnosis o sic/ sinus syndrome is to correlate symptoms with >?e&idence o SA node dysunction.

ambulatory >? (olter) monitoring

o remains a mainstay ine&aluating sinus node unction, most episodes o syncope are paroxysmal

and unpredictable.o Single and e&en multiple 2$h olter monitorrecordings may ail to include a symptomatic episode.

o >autionmust be ta/en in interpreting the olter monitor results

carotid sinus pressure

o can be particularly useul in patients in whom paroxysmal diiness or syncope is compatible with

the hypersensiti&e carotid sinus syndrome.o 0n such patients, the response can be dramatic, and sinus pauses in excess o 5 s may occur.

o Although pausesin excess o 3 s are considered abnormal, in elderly, asymptomatic patients such

pauses are common and do not re6uire therapy.o his isa ma*or limitation o the use o carotid sinus pressure as a diagnostic test in the elderly.

hysiologic or pharmacologicmaneu&ers that are &agomimetic

o 'alsal&a maneu&er orphenylephrineinduced hypertension

o &agolytic (atropine)

o sympathomimetic(isoproterenol or hypotension by nitroprusside)

o sympatholytic( 8adrenergic bloc/ing agents)


5/11

hese studies are designed to test the response o the sinus node to autonomic

stimulation and inhibition and thereby characterie the status o autonomic regulation othe sinus node.

Abnormalities o the autonomic control o sinus unction are particularly common in

patients in whom asymptomatic sinus bradycardia is documented.Intrin$ic He!rt R!te

his is a maniestation o the primary acti&ity o the SA node, and its determination re6uires chemicalautonomic bloc/ade o the heart with a combination o atropine and a beta bloc/er. Nor"!( &!(ue$ of intrin$ic he!rt r!te 8in )e!t$ %er "inute9 !re c!(cu(!te# )0 the for"u(! 22-'2 , 8.'; 4

!e9'he use o autonomic bloc/ade can separate patients with asymptomatic sinus bradycardia into a group with

%ri"!r0 $inu$ no#e #0$function(slow intrinsic heart rate)and a group with !utono"ic i")!(!nce(normalintrinsic heart rate).Autonomic bloc/ade is particularly useul when combined with in&asi&e assessment o sinus node unction.

Autonomic bloc/ade may depress conduction in patients with intrinsic disease o the conduction system and

should be carried out only in a setting where arrhythmias can be monitored and treated rapidly.

EVA*UATIONhe in&asi&e electrophysiologic in&estigation o SA node dysunction should be underta/en in patients who

ha&e had symptoms compatible with SA node dysunction and in whom no documentation o the arrhythmiaresponsible or these symptoms has been obtained by prolonged monitoring.Asymptomatic patients with sinus bradycardia need not be tested, since no therapy is indicated.

symptomatic patients


6/11

he specialied cardiac conducting system normally ensures synchronous conduction o each sinus impulse

rom the atria to the &entricles Abnormalities o conduction o the sinus impulse to the &entricles may portend the de&elopment o heart

bloc/, which can ultimately lead to syncope or cardiac arrest.0n order to e&aluate the clinical signiicance o conduction abnormalities, the physician must assess

o the site o conduction disturbance

o the ris/ o progression to complete bloc/o the probability that a subsidiary escape rhythm arising distal to the site o bloc/ will be

electrophysiologically and hemodynamically stable his latter point is perhaps the most important, since the rate and stability o the escape

pacema/er determine what symptoms result rom heart bloc/.he escape pacema/er ollowing A' nodal bloc/ is usually in the is bundle, which generally has a stable

rate o =. to 1. )e!t$3"inand is associated with a D-S complex o normal duration (in the absence o apreexisting intra&entricular conduction deect).his contrasts with escape rhythms arising in the distal is ur/in*e system, which ha&e lower intrinsic rates

8> to = )e!t$3"in96maniest wide D-S complexes with prolonged duration, and are unstable. hus, the most important issue is to assess the ris/ o inra or intrais bloc/ (which always mandates a

pacema/er)or A' nodal bloc/ in which the re6uency o the escape pacema/er is not suicient to meethemodynamic re6uirements

Although prolonged D-S complexes are in&ariable when the distal isur/in*e pacema/ers orm the escapemechanism, wide D-S complexes can also coexist with A' nodal bloc/ and a is bundle rhythm. hereore,D-S morphology alone may not be ade6uate to identiy the site o bloc/.

ETIO*OGY>hronic slowing o A' nodal conduction may be seen in highly trained athletes who ha&e hyper&agotonia at

restdiseases and drugs that inluence A' nodal conduction

o myocardial inarction (particularly inerior)

o coronary spasm (usually o the right coronary artery)

o digitalis intoxication

o excesses o beta andor calcium bloc/ers

o acute inections

&iral myocarditis

acute rheumatic e&er

inectious mononucleosis

o miscellaneous disorders

Eyme disease

Sarcoidosis

Amyloidosis


7/11

ypertension and aortic andor mitral stenosis are speciic disorders that either accelerate the degeneration

o the conducting system or ha&e a direct eect by calciication and ibrosis in&ol&ing the conducting system. First-degree A block

o more properly termedprolonged A conduction

o classically characteried by a - inter&al : ".2" s

o 0n the presence o a D-S complex o normal duration, a - inter&al : ".2$ s almost in&ariably is

due to a delay within the A' node.Second-degree heart block

o intermittent A' bloc/

o present when some atrial impulses ail to conduct to the &entricles.

o Mo)it5 t0%e I $econ#,#eree AV )(oc?

A' Cenc/ebach bloc/

characteried by progressi&e - inter&al prolongation prior to bloc/ o an atrial impulse

he pause that ollows is less than ully compensatory (i.e., is less than two normal sinus

inter&als), and the - inter&al o the irst conducted impulse is shorter than the lastconducted atrial impulse prior to the bloc/ed wa&e.

Fsually the dierence between the longest and shortest - inter&als exceeds 1"" ms.

his type o bloc/ is almost always localied to the A' node and associated with a normal

D-S duration, although bundle branch bloc/ may be present.

seen most oten as a transient abnormality with inerior wall inarction or with drug

intoxication, particularly digitalis, beta bloc/ers, and occasionally calcium channelantagonists.

his type o bloc/ can also be obser&ed in normal indi&iduals with heightened &agal tone.

can progress to complete heart bloc/ this is unco""on, except in the setting o

acute inerior wall myocardial inarction.

&en when it does, howe&er, the heart bloc/ is usually well tolerated because

the escape pacema/er usually arises in the proximal is bundle and pro&ides astable rhythm.

the presence o Bobit type 0 seconddegree A' bloc/ rarely mandates aggressi&e

therapy. herapeutic decisions depend on the &entricular response and the symptoms o the

patient

0 the &entricular rate is ade6uate and the patient is asymptomatic, obser&ationis suicient.o Mo)it5 t0%e II $econ#,#eree AV )(oc?

conduction ails suddenly and unexpectedly without a preceding change in - inter&als

0t is generally due to disease o the isur/in*e system and is most oten associated

with a prolonged D-S duration Chen it occurs with a normal D-S duration, an intrais site o bloc/ should be expected

0t is important to recognie this type o bloc/ because it has a high incidence o

progression to complete heart bloc/ with an unstable, slow, lower escape pacema/er. pacema/er implantation is necessary in this condition

may occur in the setting o anteroseptal inarction or in the primary or secondary

sclerodegenerati&e or calciic disorders o the ibrous s/eleton o the heart -egardless o the site o origin o the escape rhythm, i it is slow and the patient is

symptomatic, a cardiac pacema/er is mandatory.

Third-degree A block

o present when no atrial impulse propagates to the &entricles

o 0 the D-S complex o the escape rhythm is o normal duration, occurs at a rate o $" to 55

beatsmin, and increases with atropine or exercise, A' nodal bloc/ is probable.o >ongenital complete A' bloc/ is usually localied to the A' node. 0 the bloc/ is within the is

bundle, the escape pacema/er is usually less responsi&e to these perturbations. 0 the escaperhythm o the D-S is wide and associated with rates G $" beatsmin, bloc/ is usually localied in,


8/11

or distal to, the is bundle and mandates a pacema/er, since the escape rhythm in this setting isunreliable

o Some patients with inrais bundle bloc/ are capable o retrograde conduction. 0n such patients, a

Hpacema/er syndromeI (see below) may de&elop i a simple &entricular pacema/er is used.o 7ualchamber pacema/ers eliminate this potential problem.

AV DISSOCIATIONA' dissociation exists whene&er the atria and &entricles are under the control o two separate pacema/ers

and, while present in complete A' bloc/, can occur in the absence o a primary conduction disturbance.A' dissociation unrelated to heart bloc/ may occur under two circumstances@

o it may de&elop with an A' *unctional rhythm in response to se&ere sinus bradycardia

Chen the sinus rate and the escape rate are similar and the wa&es occur *ust beore,

in, or ollowing the D-S complex, isorhythmic A' dissociation is said to be present. reatment usually consists o

remo&al o the oending cause o sinus =radycardia

accelerating the sinus node by &agolytic agents

insertion o a pacema/er i the escape rhythm is slow and results in symptoms

o A' dissociation can be caused by an enhanced lower (*unctional or &entricular) pacema/er that

competes with normal sinus rhythm and re6uently exceeds it.

his has been called interference A dissociationbecause the rapid lower pacema/erresults in bombardment o the A' node in a retrograde ashion, rendering it reractory tothe normal sinus impulses.

hus ailure o antegrade conduction is a physiologic response in this circumstance.

0ntererence dissociation commonly occurs during

&entricular tachycardia

accelerated *unctional or &entricular rhythms seen with digitalis intoxication,

myocardial ischemia andor inarction

local irritation ollowing cardiac surgery.

he accelerated rhythm should be treated with

antiarrhythmic drugs

remo&al o an oending drug

correction o the metabolic abnormality or ischemia

INTRACARDIAC E*ECTROCARDIOGRA+HIC RECORDINGS IN DIAGNOSIS AND MANAGEMENT0ntracardiac >? recordings can be useul in at least the ollowing our groups o patients

o Patients with syncope and bundle branch or bifascicularblock without documentation of AV block

o Patients with 2:1 AV conduction

o Patients with Wenckebach block in the presence of bundle branch block.

o Asymptomatic patients with third-degree AV block

.TREATMENT

+h!r"!co(oic Ther!%0harmacologic therapy is usually reser&ed or acute situations

o Atropine (".5 to 2." mg intra&enously) and isoproterenol (1 to $ Jgmin intra&enously)are useul in

increasing heart rate and decreasing symptoms in patients with sinus bradycardia or A' bloc/localied to the A' node hey ha&e an insigniicant eect on lower pacema/ers.

0n patients with neurocardiac syncope, beta bloc/ers and disopyramide ha&e been suggested as methods to

depress let &entricular unction and decrease mechanoreceptorrelated relexes.Bineralocorticoids, midodrine, ephedrine, and theophylline ha&e also been reported to be o beneit to

occasional patients.Fnortunately, no controlled study has shown that any o these pharmacologic modalities wor/s in a

predictable ashion in all patients.


9/11

-ecently, serotoninreupta/e inhibitors ha&e been shown to beneit some patients. ;urther wor/ on

delineating dierent mechanisms in dierent patient groups may allow us to apply pharmacologic agentsmore appropriately. Eongterm therapy o bradyarrhythmias is best accomplished by pacema/ers.

+!ce"!?er$xternal energy sources can be used to stimulate the heart when disorders in impulse ormation andor

transmission lead to symptomatic bradyarrhythmias.acer stimuli can be applied to the atria andor &entricles

T!"#$%A%& #A'()*

o his is usually instituted to pro&ide immediate stabiliation prior to permanent pacema/er

placement or to pro&ide pacema/er support when a bradycardia is precipitated by what ispresumed to be a transient e&ent such as ischemia or drug toxicity.

o emporary pacing is usually achie&ed by the trans&enous insertion o an electrode catheter with

the catheter positioned in the right &entricular apex and attached to an external generator.o his procedure is associated with a small ris/ o cardiac peroration, inection at the insertion site,

and thromboembolism the ris/ o the latter two complications increases mar/edly i the pacing wireis let in place or: $K h.

o he de&elopment o an entirely external transthoracic cardiac pacing system may preclude the

need or trans&enous pacing in selected patients.

#!%"A)!)T #A'()*

o his mode o pacing is instituted or persistent or intermittent symptomatic bradycardia not related

to a sellimiting precipitating actor or or documented inranodal second or thirddegree A' bloc/.o ermanent pacing leads are usually inserted trans&enously through the subcla&ian or cephalic &ein

with the leads positioned in the right atrial appendage or atrial pacing and the right &entricularapex or &entricular pacing.

o he leads are then attached to the pulse generator, which is inserted into a subcutaneous poc/et

below the cla&icle.o picardial lead placement is used when

trans&enous access cannot be obtained

the chest is already open, i.e., in the course o a cardiac operation

ade6uate endocardial lead placement cannot be achie&ed

o Bost pacema/er generators are powered by lithium batterieso he lie expectancy o the generator is related to

&oltage output re6uired or capture

re6uirement or incessant or intermittent pacing

number o cardiac chambers paced

o Eie expectancy o the simple &entricular demand pacema/er can exceed 1" years

#A'()* '$+!

o A code consisting o three to i&e letters has been de&eloped or describing pacema/er type and

unctiono he irst letter indicates the chamber(s) paced and is designated

or &entricular pacing

Aor atrial pacing,

+or dualchamber (both atrial and &entricular) pacingo he second letter indicates the chamber in which electrical acti&ity is sensed and is also indicated

byA, V, or D.o An additional designation, $, has been used when pacema/er discharge is not dependent on a

sensed electrical acti&ity.o he third letter reers to the response to a sensed electric signal.

o he letter $represents no response to an underlying electric signal, usually related to the absence

o associated sensing unctiono ( represents inhibition o pacing unction


10/11

o Trepresents triggering o pacing unction

o + indicates a dual response, i.e., spontaneous atrial and &entricular acti&ity inhibiting atrial and

&entricular pacing and atrial acti&ity triggering a &entricular response.o Additional ourth and ith letters o the pacing code ha&e been recommended to indicate whether

the pacema/er is programmable and has rate modulation (ourth)and whether specialantitachycardia unctions are a&ailable (i.e., antitachycardia pacing, , and deli&ery o high or low

energy shoc/s).o 0n the ourth category, " represents multiprogrammability and % represents rate response

(HphysiologicI) pacing.o (%

!&entricular demand pacema/er)

paces the &entricle, senses the &entricle, is inhibited by sensed spontaneous &entricular

acti&ity, and has rate modulationo +++%

capable o sensing and pacing both the atria and &entricles and has a dual response to

the sensed atrial and &entricular acti&ity as described abo&eo HhysiologicI pacema/ers use sensors (muscular acti&ity, respiratory rate, temperature, %2

saturation, D inter&al, etc.)as methods to allow the pacema/er to increase the heart rate inresponse to physiologic demands, i.e., exercise

o hese pacema/ers are essential when chronotropic incompetence is present and an increase inheart rate is re6uired to enhance physiologic perormance

o Studies ha&e shown that such HphysiologicI pacema/ers impro&e exercise tolerance and relie&e

symptoms to a greater degree than ixedrate pacema/erso Selection o the appropriate pacema/er and pacing mode depends on the clinical condition and the

type o bradyarrhythmia being treated.o The t


11/11

he pathophysiologic contributors to the pacema/er syndrome include

loss o atrial contribution to &entricular systole

&asodepressor relex initiated by cannon a wa&es, which are caused by atrial

contractions against a closed tricuspid &al&e and obser&ed in the *ugular&enous pulse

systemic and pulmonary &enous regurgitation due to atrial contraction against

a closed A' &al&e.o he symptoms associated with the pacema/er syndrome can be pre&ented by maintaining A'

synchrony by dualchamber pacing or, in the case o a &entricular demand pacema/er, byprogramming an escape rate 15 to 2" beatsmin below that o the paced rate (i.e., hysteresis).

o As a result o this programming, sinus acti&ity and thus atrial contraction will be less li/ely to occur

at the same time as &entricular pacing and &entricular contractiono pacemaker-mediated tachycardia

0n this instance, retrograde depolariation o the atria, resulting rom a premature

&entricular depolariation or a paced &entricular complex, is sensed and leads tosubse6uent triggering o &entricular pacing.

his, in turn, can result in repetition o the phenomenon o &entriculoatrial conduction with

the de&elopment o an endlessloop, pacema/ermediated tachycardia. 0t may be corrected by reprogramming the atrial reractory period.

Brady Arrhythmias

Documents

Transcript of Brady Arrhythmias