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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
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Figure7-3 Approachtobradyarrhythmias.ABG,arterialbloodgas;ACLS,advancedcardiaclife support;↓BP,hypotension;
CAD, coronary artery disease; CCB, calcium channel blocker; CHF, congestive heart failure; CP, chest pain; CVD,
cerebrovasculardisease;DOE,dyspneaonexertion;dz,disease;EPS,electrophysiologicstudy;HD,hemodynamic;HPI,history
of present illness; ↓HR, bradycardia; Hx, history; ↑K, hyperkalemia; LH, lightheadedness; ↑Mg, hypermagnesemia; OSA,
obstructivesleepapnea;PPM,permanentpacemaker;↓SaO2,hypoxia;SND,sinusnodedysfunction;SOB,shortnessofbreath;
TSH,thyroid-stimulatinghormone;VS,vitalsigns;VT,ventriculartachycardia.(ReprintedwithpermissionfromFanslerD,Chen
J. Bradyarrhythmias and permanent pacemakers. In: Cuculich PS, Kates AM, eds. The Washington Manual Cardiology
SubspecialtyConsult.3rded.Lippincott,Williams&Wilkins;2014.)
DiagnosticTesting
LABORATORIES
Thelaboratorytestingshouldincludeserumelectrolytesandthyroidfunctiontestsinmostpatients.
Digoxinlevelsandserialtroponinsshouldbedrawnwhenclinicallyappropriate.
ELECTROCARDIOGRAPHY
A12-leadECGisthecornerstonefordiagnosisinanyworkupwherearrhythmiaissuspected.
Rhythm strips from leads that provide best view of atrial activity (II, III, aVF, or V1) should be
examinedclosely.
EmphasisshouldbeplacedonidentifyingevidenceofSAnodedysfunction(Pwaveintervals)orAV
conductionabnormalities(PRinterval).
SPECIALCONSIDERATIONS
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Episodes of bradycardia are often transient and episodic; therefore, a baseline ECG may not be
sufficienttocapturebradycardia.Someformofcontinuousmonitoringcanberequired.
Ininpatientsetting,continuouscentraltelemetrymonitoringcanbeused.
Iffurtherworkupisdoneasanoutpatient,short-termHoltermonitoringcanbeusediftheepisodes
occursomewhatfrequently.Ifinfrequent,aneventrecorderorILRshouldbeconsidered.
Vital to correlate symptoms with rhythm disturbances discovered via continuous monitoring.
Importanceofaccuratesymptomdiariesinambulatorysettingshouldbeemphasizedtopatients.
To evaluate sinus node response to exertion (chronotropic competence), walking the patient under
supervisioniseasyandinexpensive.FormalexerciseECGcanbeordered,ifnecessary.
EPScanbeusedtoassesssinusnodefunctionandAVconductionbutisrarelynecessaryifrhythmis
alreadydiagnosedbynoninvasivemodalities.
DIFFERENTIALDIAGNOSIS
Sinusnodedysfunction,orsicksinussyndrome(SSS),representsmostcommonreasonforpacemaker
implantationintheUS.ManifestationsofSSSincludethefollowing(Figure7-4):
Sinusbradycardia—regularrhythmwithQRScomplexesprecededby“-sinus”Pwaves(uprightin
II, III, aVF)ata rateof<60bpm. Youngpatientsandathletesoften haverestingsinusbradycardia
thatiswelltolerated.Nocturnalheartratesarelowerinallpatients,butelderlytendtohavehigher
restingheartratesandsinusbradycardiaislesscommonnormalvariant.
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Figure 7-4 Examples of sinus node dysfunction.A, Sinus bradycardia. The sinus rate is approximately 45 bpm. B,
Sinoatrialnodeexitblock.NotethatthePPintervalinwhichthepauseoccursisexactlytwicethatofthenonpausedPP
interval. C, Blocked premature atrial complexes. This rhythm is often confused for sinus node dysfunction or
atrioventricular block. Note the premature, nonconducted P waves inscribedin the T wave that resets the sinus node
leadingtotheobservedpauses.D,Tachy–bradysyndrome.Notetheterminationoftheirregulartachyarrhythmiafollowed
by a prolonged 4.5-second pause prior to the first sinus beat.(Reprinted with permission from Fansler D, Chen J.
Bradyarrhythmiasandpermanentpacemakers.In:CuculichPS,KatesAM,eds.TheWashingtonManualCardiology
SubspecialtyConsult.3rded.Lippincott,Williams&Wilkins;2014.)
Sinusarrest andsinuspauses—failureofsinus nodetodepolarize;manifestsasperiods ofatrial
asystole(noPwaves).Maybeaccompaniedbyventricularasystoleorescapebeatsfromjunctional
tissue or ventricular myocardium. Pauses of 2–3 seconds can be found in healthy, asymptomatic
people,especiallyduringsleep.Pauses>3seconds,particularlyduringdaytimehours,raiseconcern
forsinusnodedysfunction.
Sinusexitblock—appropriatefiringofsinusnode,butwaveofdepolarizationfailstotraversepast
perinodal tissue. Indistinguishable from sinus arrestonsurfaceECGs exceptthat the RR interval
willbeamultipleofRRprecedingthebradycardia.
Tachy–bradysyndrome—when tachyarrhythmias alternate withbradyarrhythmias. Canbe seen in
conjunctionwithanumberoftypesofSVTbutismostcommonlynotedinpatientswithparoxysmal
AF.
Chronotropic incompetence—inability to increase the heart rate appropriately in response to
metabolicneed.Usuallydeterminedbyexercisingpatients.
AVconductiondisturbances
AV conduction can be diverted (fascicular or bundle branch blocks); delayed (first-degree AV
block); occasionally interrupted (second-degree AV block); frequently, but not always,
interrupted(advanced or high-degree AV block); or completelyabsent (third-degree AVblock).
Assignment of the bradyarrhythmia under investigation to one of these categories determines
prognosisandguidestherapy.
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First-degreeAVblock—conductiondelaythatresultsinPRinterval>200msonsurfaceECG.
Second-degree AV block—periodic interruptions (i.e., “dropped beats”) in AV conduction.
DistinctionbetweenMobitzIandII isimportant becauseentities possessdiffering naturalratesof
progressiontocompleteheartblock.
MobitztypeIblock(Wenckebach)—progressivedelayinAVconductionwithsuccessiveatrial
impulses until an impulse fails to conduct. On ECG, classic Wenckebach block manifests as
follows:
□ ProgressiveprolongationofPRintervalofeachsuccessivebeatbeforedroppedbeat.
□ ShorteningofeachsubsequentRRintervalbeforedroppedbeat.
□ AregularlyirregulargroupingofQRScomplexes(groupbeating).
□ TypeIblockusuallywithintheAVnodeandportendsmorebenignhistorywithprogressionto
completeheartblockunlikely.
□ MobitztypeIIblockcarrieslessfavorablelong-termprognosisandischaracterizedbyabrupt
AVconductionblockwithoutevidenceofprogressiveconductiondelay.
□ OnECG,PRintervalsremainunchangedprecedingnonconductedPwave.
□ Presence of type II block, particularly if bundle branch block is present, often antedates
progressiontocompleteheartblock.
Presence of 2:1 AV block makes differentiation between Mobitz type I and II mechanisms
difficult.Diagnosticcluestothesiteofblockincludethefollowing:
□ Concomitant first-degree AV block, periodic AV Wenckebach, or improved conduction (1:1)
with enhanced sinus rates or sympathetic input suggests more proximal interruption of
conduction(i.e.,MobitztypeImechanism).
□ Concomitant bundle branch block, fascicular block, or worsened conduction (3:1, 4:1, etc.)
with enhanced sympathetic input localizes site of block more distally (Mobitz type II
mechanism).
Third-degree (complete) AV block—all atrial impulses fail to conduct to ventricles. Complete
dissociation between the atria and ventricles (“A > V” rates). Should be distinguished from
dissociationwithcompetitionatAVnode(“V>A”rates).
Advanced or high-degree AV block—more than one consecutive atrial depolarization fails to
conduct to the ventricles (i.e., 3:1 blockor greater). On ECG,consecutive Pwaves seenwithout
associatedQRScomplexes.However,therewillbedemonstrableP:QRSconductionsomewhereon
therecordtoavoida“third-degree”designation(Figure7-5).
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Figure7-5 Examplesofatrioventricularblock(AVB).A,First-degreeAVB.Therearenodroppedbeats,andthePRinterval
is>200ms.B,3:2second-degreeAVB—MobitzI.Notethe“groupbeating”andtheprolongingPRintervalpriortothedropped
beat.ThethirdPwaveinthesequenceissubtlyinscribedintheTwaveoftheprecedingbeat.C,Second-degreeAVB—Mobitz
II.Notetheabruptatrioventricularconductionblockwithoutevidenceofprogressiveconductiondelay.D,2:1AVB.Thispattern
makesit difficulttodistinguishbetween MobitzI versusII typemechanisms ofblock. Notethe narrowQRS complex,which
supports a more proximalorigin of block(typeI mechanism).A wider QRS(concomitant bundle branchor fascicular block)
wouldsuggestatypeIImechanism.E,Completeheart block.Notetheindependentregularityofboththeatrialandventricular
rhythms (junctional escape) with no clear association witheach other throughoutthe rhythm strip.(Reprintedwith permission
from Fansler D,Chen J. Bradyarrhythmias and permanent pacemakers. In: CuculichPS,Kates AM, eds. The Washington
ManualCardiologySubspecialtyConsult.3rded.Lippincott,Williams&Wilkins;2014.)
IMAGING
PresenceorabsenceofstructuralheartdiseaseshouldbeinitiallyevaluatedbyTTE.
Furtherimagingshouldbeobtainedbasedonsuspectedetiology.
TREATMENT
PharmacologicTherapy
Bradyarrhythmias leading to significant symptoms and hemodynamic instability should be managed
emergentlyasoutlinedinACLSguidelines(seeAppendixC).
Atropine,ananticholinergicagentgivenindosesof0.5–2.0mgIV,iscornerstonepharmacologicagent
foremergentbradycardiatreatment.
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Dysfunction localizedmore proximallyinconductionsystem (i.e., symptomaticsinusbradycardia,
first-degreeAVblock,MobitzIsecond-degreeAVblock)tendstoberesponsivetoatropine.
Distaldiseaseisnotresponsiveandcanbeworsenedbyatropine.
Reversible causes of bradyarrhythmias should be identified, and any agents (digoxin, calcium
channel blockers, β-adrenergic blockers) that caused or exacerbated the underlying dysrhythmia
shouldbewithheld.
NonpharmacologicTherapies
For bradyarrhythmias thathave irreversible etiologies or that are secondary to medically necessary
pharmacologictherapy,pacemakertherapyshouldbeconsidered.
Temporarypacingindicatedforsymptomaticsecond-orthird-degreeheartblockcausedbytransient
drugintoxicationorelectrolyteimbalanceandcompleteheartblockorMobitzIIsecond-degreeAV
blockinthesettingofanacuteMI.
Sinusbradycardia,AFwithaslowventricularresponse,orMobitzIsecond-degreeAVblockshould
betreatedwithtemporarypacingonlyifsignificantsymptomsorhemodynamicinstabilityispresent.
TemporarypacingisachievedpreferablyviainsertionofaTVP.Transthoracicexternalpacingcan
be used,althoughthelackofreliabilityofcapture andpatientdiscomfortmakethis a second-line
modality.
Oncehemodynamicstabilityhasbeenestablished,attentionturnstotheindicationsforPPMplacement.
Insymptomaticpatients,keydeterminantsincludepotentialreversibilityofcausativefactorsand
temporalcorrelationofsymptomstothearrhythmia.
In asymptomatic patients, key determinant based on whether discovered conduction abnormality
hasnaturalhistoryofprogressiontohigherdegreesofheartblockthatportendspoorprognosis.
Permanentpacing
Permanent pacing involves placement of anchored, intracardiac pacing leads for the purpose of
maintaining heartratesufficient toavoid symptoms andhemodynamic instability. Currentdevices,
through maintenanceofAVsynchrony andrate-adaptive programming, morecloselymimic normal
physiologicheartratebehavior.
ClassIandIIaindicationsforpermanentpacingarelistedinFigure7-3.
Pacemakers are designed to provide anelectrical stimulus tothe heartwhenever theratedrops
below a preprogrammed lower rate limit. Therefore, the ECG appearance of a PPM varies
dependingontheheartrateandstateofAVconduction.
Pacing spikes produced by modern pacemakers are low amplitude, sharp, and immediately
preceding thegeneratedPwave orQRScomplexindicatingcapture ofthechamber.Figure 7-6
illustratessomecommonECGappearancesofnormallyandabnormallyfunctioningpacemakers.
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Figure 7-6 Pacemaker rhythms.A, Normal dual-chamber device (DDD) pacing. First two complexes are
atrioventricular(AV)sequentialpacing,followedbysinuswithatrialsensingandventricularpacing.B,Normalsingle-
chamber(VVI)pacing.Theunderlyingrhythmisatrial fibrillation(nodistinctPwaves),withventricularpacing at60
bpm.C,Pacemakermalfunction.The underlyingrhythmissinus(P)at80bpmwith 2:1heart blockandfirst-degree
AVblock(longPR).Ventricularpacingspikesareseen(V)aftereachPwave,demonstratingappropriatesensingand
tracking ofthe P waves; however,there is failure to capture. D,Pacemaker-mediated tachycardia. A,pacedatrial
events;P,sensedatrialevents; R,sensedventricular events;V,pacedventricular events.(Reprintedwithpermission
from Fansler D, Chen J. Bradyarrhythmias and permanent pacemakers. In: Cuculich PS, Kates AM, eds. The
WashingtonManualCardiologySubspecialtyConsult.3rded.Lippincott,Williams&Wilkins;2014.)
Pacemaker generator is commonly placed subcutaneously in pectoral region on the side of the
nondominantarm. Theelectroniclead(s)is/areplacedinthecardiacchamber(s)viacentralveins.
Complications of placement include pneumothorax, device infection, bleeding, and, rarely,
cardiacperforationwithtamponade.
Beforeimplantation,patientmustbefreeofanyactiveinfections,andanticoagulationissuesmust
becarefullyconsidered.Hematomasinthepacemakerpocketdevelopmostcommonlyinpatients
whoarereceivingIVheparinorSClow-molecular-weightheparin.
Followingimplant,posteroanteriorandlateral CXRare obtainedtoconfirmappropriate lead
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placement. Pacemakeris interrogatedatappropriateintervals—typically, beforedischarge,2–6
weeksfollowingimplantation,andevery6–12monthsthereafter.
Pacingmodes—classifiedbysequenceofthreetofiveletters.Mostpacemakersarereferredtoby
thethree-lettercodealone.
PositionIdenotesthechamberthatispaced:Aforatria,Vforventricle,orDfordual(A+V).
PositionIIreferstothechamberthatissensed:Aforatria,Vforventricle,Dfordual(A+V),
orOfornone.
Position IIIdenotes the type ofresponse thepacemakerwillhaveto a sensedsignal:Ifor
inhibition,Tfortriggering,Dfordual(I+T),orOfornone.
Position IV is used to signify the presence of rate-adaptive pacing (R) in response to
increasedmetabolicneed.
ThemostcommonpacingsystemsusedtodayincludeVVI,DDD,orAAI.
AAI systems used only for sinus node dysfunction in the absence of any AV conduction
abnormalities.
PresenceofAV nodalor His–Purkinje disease makesa dual-chamber device (i.e., DDD)more
appropriate.
PatientsinpermanentAFwarrantasingleventricularleadwithVVIprogramming.
Modern-daypacemakersalsohavethecapabilityofmodeswitching.
Useful in patients with DDD pacers who have concurrent paroxysmal atrial tachyarrhythmias.
Whenanatrialarrhythmiafasterthanaprogrammedmodeswitch ratedevelops,thedevicewill
changetoa mode (i.e., VVI) thatdoes not trackatrial signals. Itwill return to DDDwhen the
tachyarrhythmiaresolves.
Anothercommonmodeswitchsettingisusedinpatientswithlow-gradeorintermittenthigh-grade
AVconductiondiseasetominimizeventricularpacing.ThedevicewillattempttostayinAAIand
switch to DDD only when conduction through the AV node fails. This allows for preferential
conductiontotheventriclesthroughthenativeconductionsystemasmuchaspossibleandreduces
thechanceforpacemaker-mediatedcardiomyopathy.
Althoughinfrequent,pacemakermalfunctionispotentiallylife-threatening,particularlyforpatients
whoarepacemaker dependent.Theworkupofsuspectedmalfunctionshould beginwitha 12-lead
ECG.
If nopacingactivity isseen,place amagnet overthepacemakertoassessforoutput failureand
ability to capture. Application of the magnet switches the pacemaker to an asynchronous
pacingmode.Forexample,VVImodebecomesVOO(ventricularasynchronouspacing)andDDD
modebecomesDOO(asynchronousAVpacing).
If malfunction is obvious or if the ECG is unrevealing and malfunctionis still suspected, then
formal interrogation of the device should be performed. Patients are given a card on
implantationthatwillidentifythemakeandmodelofthedevicetofacilitatethisevaluation.
Two view CXR should also be obtained to assess for evidence of overt lead abnormalities
(dislodgement,fracture,migration,etc.).
General categories of pacemaker malfunction include failure to pace (output failure), failure to
capture,failuretosense(undersensing),andpacemaker-mediateddysrhythmias.
Syncope
GENERALPRINCIPLES
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Syncopeisacommonclinicalproblem.Primarygoalofevaluationistodeterminewhetherthepatientis
atincreasedriskofSCD.
Definition
Sudden,self-limitedlossofconsciousnessandposturaltonecausedbytransientglobalcerebral
hypoperfusion,followedbyspontaneous,complete,andpromptrecovery.
Classification
Fourmajorcategoriesbasedonetiology
28
Neurocardiogenic(mostcommon):vasovagal,carotidsinushypersensitivity,andsituational.
Orthostatichypotension:hypovolemia,medication-induced(iatrogenic),andautonomicdysfunction.
Cardiovascular
Arrhythmogenic:sinusnodedysfunction,AVblock,pacemakermalfunction,VT/VF,SVT(rare).
Mechanical:HCM,valvularstenosis,aorticdissection,myxomas,pulmonaryembolism,pulmonary
HTN,acuteMI,subclaviansteal,etc.
Miscellaneous(nottruesyncope):seizures,stroke/TIA,hypoglycemia,hypoxia,psychogenic,etc.
Atherosclerotic cerebral artery disease is a rare cause of true syncope; the exception is severe
obstructivefour-vesselcerebrovasculardisease(expectfocalneurologicfindingspriortosyncope).
Epidemiology
Commoningeneralpopulation:6%ofmedicaladmissionsand3%ofemergencyroomvisits.
29
Incidenceissimilaramongmenandwomen;oneofthelargestepidemiologicstudiesrevealedan11%
incidenceduringanaveragefollow-upof17years,withsharpriseafterage70years.
29
Pathophysiology
Two components of neurocardiogenic syncope are described as cardioinhibitory, in which
bradycardiaorasystoleresultsfromincreasedvagaloutflowtotheheart,andvasodepression, where
peripheralvasodilationresultsfromsympatheticwithdrawaltoperipheralarteries.Mostpatientshave
acombinationofbothcomponentsasmechanism.
Specific stimuli (e.g., micturition,defecation, coughing, swallowing) may evoke a neurocardiogenic
mechanism,leadingtosituationalsyncope.
RiskFactors
Cardiovascular disease, history of stroke or TIA, and HTN have been shown to predispose
patientstosyncope.
30
Low body mass index (BMI), increased alcohol intake, and diabetes are also associated with
syncope.
30
DIAGNOSIS
ClinicalPresentation
HISTORY
Meticuloushistoryandphysicalexaminationarevitaltoaccuratediagnosisofetiologyofsyncope.In
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40%ofepisodes,themechanismofsyncoperemainsunexplained.
31,32
Special attention should be focused on symptoms that precede and follow syncopal episode,
eyewitnessaccountsduringtheevent,timecourseoflossandresumptionofconsciousness(abruptvs.
gradual),andpatient’smedicalhistory.
Characteristicprodromeofnausea,diaphoresis,visualchanges,orflushingsuggestsneurocardiogenic
syncope.
Identification of emotional or situational trigger and post-episode fatigue are also clues to
neurocardiogenic/situationalcauseofsyncope.
Alternatively, unusual sensory prodrome, incontinence, or a decreased level of consciousness that
graduallyclearssuggestsaseizureasalikelydiagnosis.
Withtransientventriculararrhythmias,abruptlossofconsciousnesswithrapidrecoverymayoccur.
Syncopewithexertionconcerningforstructuralheartdisease,pulmonaryHTN,and/orCAD.
PHYSICALEXAMINATION
Cardiovascularandneurologicexaminationsareprimaryfocusofinitialevaluation.
Orthostatic vital signs aid in the diagnosis of orthostatic hypotension. Patients should have blood
pressurecheckedinbotharms.
Cardiacexaminationfindingsmaydetectvalvularheartdisease,LVdysfunction,pulmonaryHTN,etc.
Neurologicfindingsareoftenabsentbut,ifpresent,maypointtoaneurologicetiology.
Carotid sinus massage for 5–10 secondswith reproduction of symptoms andconsequent ventricular
pause>3secondsisconsideredpositiveforcarotidsinushypersensitivity.Takeproperprecautionsof
telemetrymonitoring,availabilityofbradycardiatreatments,andavoidanceofthemaneuverinpatients
withknownorsuspectedcarotiddisease.
DiagnosticTesting
Presence of known structural heart disease, abnormal ECG, age >65 years, focal neurologic
findings, and severe orthostatic hypotension suggest more ominous etiology of a syncopal event.
Thesepatientsshouldbeadmittedforfurtherworkuptoavoiddelayandadverseoutcomes.
Afterhistoryandphysicalexamination,ECGisthemostimportantdiagnostictoolintheevaluationof
syncope. It will be abnormal in50% of cases butalonewill yield a diagnosis inonly5% of these
patients.
If no history of heart disease or baseline ECG abnormalities, tilt table testing has been used to
evaluate hemodynamic response during transition from supine to an upright state to precipitate a
neurocardiogenicresponse.Inanunselectedpopulation,thepredictivevalueofthistestislow.
RefertoFigure7-7forthediagnosticapproachtosyncope.
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