Intensive Care Unit Arrhythmias

13 Pages·2007·0.35 MB·English

Intensive Care Unit Arrhythmias
S.M. Hollenberg
Introduction
Arrhythmias are common in the intensive care unit (ICU) and represent a major
source of morbidity and increased length of stay. Arrhythmias are most likely to
occurinpatientswithstructuralheartdisease.Theincitingfactorforanarrhythmia
in a given patient may be a transient imbalance, often related to hypoxia, infection,
cardiac ischemia, catecholamine excess (endogenous or exogenous), or an electro-
lyte abnormality. Management includes correction of these imbalances as well as
medical therapy directed at the arrhythmia itself.
The physiologic impact of arrhythmias depends on ventricular response rate
and duration. Bradyarrhythmias may decrease cardiac output due to heart rate
alone in patients with relatively fixed stroke volumes, and loss of an atrial kick
may cause a dramatic increase in pulmonary pressures in patients with diastolic
dysfunction. Similarly, tachyarrhythmias can decrease diastolic filling and reduce
cardiac output, resulting in hypotension, in addition to producing myocardial
ischemia.Clearly,theimpactofagivenarrhythmiainagivensituationdependson
thepatient’scardiacphysiologyandfunction.Similarly,urgencyandtypeoftreat-
ment is determined by the physiologic impact of the arrhythmia as well as by
underlying cardiac status.
Thepurposeofthischapteristoprovideanupdateregardingcurrentconceptsof
diagnosisandacutemanagementofarrhythmiasintheICU.Asystematicapproach
to diagnosis and evaluation will be presented, followed by consideration of specific
arrhythmias.
Diagnosis of Arrhythmias
Basic Principles
The first principle in managing arrhythmias is to treat the patient, not the electro-
cardiogram (EKG). Accordingly, one must first decide whether the problem is an
arrhythmiaoranartifactandwhetherthecardiacrhythmissufficienttoaccountfor
the patient’s problem.
The next step is to establish the urgency of treatment. Clinical assessment
includes evaluationofpulse,bloodpressure,peripheralperfusion,andthepresence
ofmyocardialischemiaand/orcongestiveheartfailure.Ifthepatientisunconscious
orhemodynamicallyunstableinthepresenceofatachyarrhythmiaotherthansinus
tachycardia, prompt cardioversion is indicated. If the patient is stable, there is time
to establish the rhythm diagnosis and decide upon the most appropriate course of
432 S.M.Hollenberg
treatment. Bradyarrhythmias produce less diagnostic challenge and treatment
options are relatively straightforward.
The goals of antiarrhythmic therapy depend on the type of rhythm disturbance.
The initial goal for the treatment of tachyarrhythmias in the critical care unit is to
slow the ventricular response (or to increase it in the case of a bradyarrhythmia).
The next goal is to restore sinus rhythm, if possible. If sinus rhythm cannot be
restored, prevention of complications becomes an issue.
Evaluation of Bradycardias
Acomprehensivedescriptionofthediagnosisofarrhythmiasisbeyondthescopeof
this chapter. A 12-lead EKG with a long rhythm strip and a previously obtained 12-
lead EKG for comparison are ideal; If a previous EKG is not available, a systematic
approach using a current 12 lead EKG is essential.
For evaluation of bradycardias, the first step is to locate the P wave. P-waves are
often best seen in leads II and V . Normal p-waves are upright in leads II, III, and
1
aVF, and may be biphasic in leads II and V . Ectopic atrial and junctional rhythms
1
often present with negative P-waves in leads II, III, and aVF. The next step is to
establish the relationship between the P-wave and the QRS complex. If there are
moreP-wavesthanQRScomplexes,thenAVblockispresent.IftherearemoreQRS
complexesthanP-waves,therhythmislikelyanacceleratedjunctionalorventricular
rhythm. If the relationship of the P-wave and QRS is 1:1, then measurement of the
PR interval can yield useful diagnostic clues.
Management of Bradycardias
Sinus Node Dysfunction
Bradycardias associated with sinus node dysfunction include sinus bradycardia,
sinus pause, sinoatrial block, and sinus arrest. These disturbances often result from
increasedvagaltone[1].Ifbradycardiaistransientandnotassociatedwithhemody-
namic compromise, no therapy is necessary. If bradycardia is sustained or compro-
misesend-organperfusion,therapywithantimuscarinicagents,suchasatropine,or
beta agonists, such as ephedrine, may be initiated. Transcutaneous or transvenous
pacing may be necessary in some cases.
Patients with a combination of bradycardia with paroxysmal atrial tachycardias
duetopreexistingconductionsystemdiseasecanbechallengingtomanagepharma-
cologically. In these cases, insertion of a temporary pacemaker may allow the
administration of rate-lowering agents.
Heart Block
The most common cause of acquired chronic atrioventricular (AV) heart block is
fibrosis of the conducting system. Although pre-existing conduction system disease
isariskfactorforthedevelopmentofcompleteheartblock,nosinglelaboratoryor
clinical variable identifies patients at risk for progression to high degree AV block
[2]. In first-degree AV block there is prolongation of conduction time of the atrial
impulses to the ventricles, with a PR interval greater than 200 msec. In second-
degree AV block, conducted atrial beats are interspersed with non-conducted beats.
Intensive CareUnit Arrhythmias 433
Second-degree AV block is divided into Mobitz type I (Wenckebach) and Mobitz
TypeIIblock.In Mobitz I block, the PRinterval lengthens progressively untilthe P
wavefailstoconduct.InmostcasestheblockoccursattheAVnode.MobitzIblock
can occur in healthy individuals, the elderly and in patients with underlying heart
disease.In Mobitz type II AV blockthe PR intervalremains constantuntila Pwave
fails to conduct. Mobitz II block occurs below the AV node, and thus is more dan-
gerous since it is much more likely to progress to complete heart block. In third-
degree AV block none of the atrial impulses are conducted to the ventricles. The
escape rhythm, whether junctional or ventricular, is generally regular.
Asymptomatic bradyarrhythmias do not carry a poor prognosis and in general
no therapy is necessary [3]. If organ perfusion is compromised, or hemodynamic
instabilityoccurs,oneortwodosesofatropine(1.0mgi.v.)maybetried,butpacing
mayberequired.Pacingmayalsobeusefulinpatientswithbradycardia-tachycardia
(“sick sinus”) syndrome, in whom treatment for tachycardia results in symptomatic
bradycardia.
Conduction abnormalities, either transient or permanent, can complicate acute
myocardial infarctions. Conduction abnormalities associated with an acute inferior
myocardial infarction usually result from AV nodal ischemia, are transient, and
carry a low mortality rate. Conduction abnormalities in association with an acute
anterior myocardial infarction, however, represent extensive necrosis of the infra-
nodalconductionsystemandthemyocardium,andareassociatedwithhighin-hos-
pital mortality [4]. The ACC/AHA/NASPE recommended guidelines for temporary
pacing in patients with an acute myocardial infarction are shown in Table 1.
Table1.Recommendationsfortemporarytransvenouspacingafteranacutemyocardialinfarction.Adapted
from[49]
Class I
1. Asystole
2. Symptomatic bradycardia
3. Bilateralbundle branch block (alternating BBB or RBBBwith alternating LAFB/LPFB, any age)
4. New or indeterminate-age bifascicular block (RBBB with LAFB or LPFB, or LBBB) with first-degree
AV block
5. Mobitztype II second-degreeAVblock
Class IIa
1. RBBB and LAFBor LPFB (new or indeterminate).
2. RBBB with first-degreeAV block
3. LBBB, new or indeterminate.
4. Incessant VT, for atrialor ventricular overdrivepacing.
5. Recurrent sinus pauses (greater than 3 seconds) not responsive to atropine.
Class IIb
1. Bifascicular blockof indeterminateage.
2. New or age-indeterminate isolated RBBB.
Class III
1. First degree heart block.
2. TypeI second-degree AV block with normalhemodynamics.
3. Acceleratedidioventricular rhythm.
4. BBBor fascicular block known to exist before AMI
RBBB:rightbundlebranchblock;LBBB:leftbundlebranchblock;LAFB:leftanteriorfascicularblock;LPFV:
left posterior fascicular block; AMI: acute myocardial infarction.
434 S.M.Hollenberg
Evaluation of Tachyarrhythmias
The first step in the evaluation of the critically ill patient with a tachyarrhythmia is
to assess hemodynamic stability. If hemodynamics are compromised due to the
arrhythmia, cardioversion should be performed unless pharmacologic treatment is
immediately successful. However, before proceeding with cardioversion, one should
consider whether the arrhythmia is in fact the basis for the deterioration in hemo-
dynamics.
The next step in evaluation is to determine whether the arrhythmia is supraven-
tricularorventricularinorigin.First,oneexaminesQRSwidth.AnarrowQRScom-
plex( ‹ 0.12seconds)indicatesasupraventriculartachycardia(SVT).Oneshouldtry
not to rely solely on a rhythm strip from one monitor lead for diagnosis, as there
can be variability in QRS width depending on which lead is examined. A 12-lead
EKG is more useful, and may also identify Q waves indicative of prior myocardial
infarctionorotherabnormalities.ComparisonwithapreviousEKGcanbeusefulas
well, to identify pre-existing bundle branch block, for example.
Carotid sinus massage and other maneuvers that increase vagal tone, slows AV
conduction time and increases refractoriness, and this can aid in the diagnosis
through demonstration of P waves or interruption of a re-entrant supraventricular
tachycardia.Intravenousadenosine(6mgbolus,withaseconddoseof12mg1to2
minutes later if there is no response) can also be used for this purpose. The effects
are more pronounced when given through a central venous line, in which case the
dosage is usually halved. Responses to vagal maneuvers or adenosine are listed in
Table 2. Side effects include bronchospasm, proarrhythmia (a 2.7% incidence of
inductionofatrialfibrillationhas beenreported)[5],andalso ventriculartachycar-
dia (VT) and fibrillation [6], as well as bradycardia including asystole; these effects
are usually transient because the half-life of adenosine is only 6 to 10 seconds.
VT can be diagnosed using some clinical and EKG clues. VT is approximately
four times more common than SVT with aberrancy [7]. VT is much more common
in patients who have a history of myocardial infarction or heart failure. Circulatory
collapse is more common with VT than SVT, but patients with VT may maintain a
normalblood pressure. A careful review of medications is important toexcludeiat-
rogenic causes of VT.
A QRS width of more than 0.14 seconds with right bundle branch block (RBBB)
or 0.16 seconds during left bundle branch (LBBB) block favors VT [8]. Comparison
ofQRSmorphologyduringthetachycardiawiththemorphologyofventricularpre-
mature beats in sinus rhythm can be helpful. Marked left axis deviation (–60° to
–120°) may indicate a ventricular origin of the arrhythmia. Other diagnostic clues
suggestiveofVTarefusionandcapturebeats,buttheseareseeninonly20–30%of
Table 2. Differentiation of tachycardias by responsetovagalmaneuvers
Arrhythmia Response to vagal maneuvers/adenosine
Sinus tachycardia Gradual slowing with resumption of the tachycardia
AVNRT Abrupt termination or only very transient slowing
Atrialfibrillation/flutter Increased AV block briefly with slowed ventricular response rate
Multifocal atrialtachycardia Increased AV block brieflywith slowed ventricular response rate
Ventricular tachycardia Usuallyno response
AV: atrioventricular; AVNRT: AV nodalre-entrant tachycardia.
Intensive CareUnit Arrhythmias 435
casesofVT[9].Fusionbeats,ahybridofthesupraventricularandventricularcom-
plexes,occurwhentwoimpulses,onesupraventricularandoneventricular,simulta-
neously activate the same territory of ventricular myocardium. The implication is
that the wide complexes are ventricular. Capture beats are occasional beats con-
ducted with a narrow complex, and such beats rule out fixed bundle branch block.
AV dissociation is diagnostic of VT, but is present in less than 50% of cases of VT
and is difficult to identify at faster heart rates.
ItisbettertoerronthesideofoverdiagnosisofVT.Inastudyanalyzingadverse
events incurred by patients with VT misdiagnosed as SVT and given calcium chan-
nelblockers[10],manyofthepatientsdecompensatedpromptlyandsomerequired
resuscitation, despite the fact that all study patients were hemodynamically stable
when first seen in VT.
It is also noteworthy that ST segment depression during SVT lacks specificity in
predicting ischemia. In one series of 100 patients with SVT, associated ST segment
deviation was only 51% specific (with a positive predictive value of only 6%) for
significant angiographic coronary artery disease or scintigraphic evidence of ische-
mia [11].
ItisusefultodivideSVTsintoregularandirregularrhythms,asthisnarrowsthe
differentialdiagnosisandtherapeuticoptions.RegularnarrowcomplexSVTinclude
sinus tachycardia, atrioventricular node reentrant tachycardia (AVNRT), AV re-
entrant tachycardia (AVRT), ectopic atrial tachycardia, and atrial flutter with fixed
conduction.
Management of Regular Narrow Complex Tachycardias
Sinus Tachycardia
Sinustachycardiaoftenoccursasaresponsetoasympatheticstimulus,suchashyp-
oxia, vasopressors, inotropes, pain, hypovolemia, or hyperthyroidism. Treatment
focusesonidentifyingandtrying to correctthe underlyingcause.If ischemiaisthe
causeandtreatmentiswarranted,beta-blockersarethefirsttreatmentoption.How-
ever,itisworthconsideringthatthesinustachycardiamaybeanappropriatehemo-
dynamic response to hypotension, hypovolemia, or low cardiac output; if this is the
case, overzealous use of beta-blockers can reduce cardiac output, with potentially
disastrous consequences.
AVNodalReentrantTachycardia
AVNRT typically occurs with sudden onset at a heart rate of 140–180 beats per
minute.Itismoreprevalentinfemalesandisnotusuallyassociatedwithstructural
heartdisease.AVNRTinvolvesdualAVnodalpathwaysandre-entry.TypicalAVNRT
is initiated by a premature atrial contraction that conducts antegrade down a slow
AVpathwaywithashortrefractoryperiodandthenretrogradeupafastAVpathway
with a long refractory period (which had been refractory to antegrade conduction
when the premature beat occurred but has now recovered) (Fig. 1).
The key to treatment is to block AV conduction. Acute treatment may include
Vagal maneuvers and intravenous adenosine may terminate the re-entrant cycle, or
other AV nodal blockers, such as non-dihydropyridine calcium-channel blockers,
beta-blockers, and digoxin may be used [12]. Preventive therapy usually entails
medications that suppress the initiating premature atrial contractions, with beta-
436 S.M.Hollenberg
Fig.1.aAtrioventricular(AV)nodedemonstratingdualpathways:aslowpathwaywithashortrefractory
periodandafastpathwaywithalongrefractoryperiod.bAprematureimpulseconductsdowntheslow
pathway while the fast pathway is still refractory to conduction. c As the impulse conducts down slow
pathway,thefastpathwayrecovers.dTheimpulsegoesupfastpathwayandalsoconductstotheventri-
cle. e The impulse cycles around theAV node, completingthere-entrant circuit.
blockers as the first choice. Catheter ablation of one of the pathways is another
option for recurrences refractory to medications.
AV Re-entrant Tachycardia (Wolff-Parkinson White Syndrome)
AVRT using an accessory bypass tract occurs in 0.1 to 0.3% of the general popula-
tion. The accessory pathway bypasses the AV node and can activate the ventricles
prematurelyinsinusrhythm,producingthecharacteristicdeltawave.Thediagnosis
of Wolff-Parkinson White syndrome (WPW) is reserved for patients with both pre-
excitationandtachyarrhythmias.InAVRT,conductioncangodownthebypasstract
andbackuptheAVnode,producingawideQRScomplex(antidromic)ordownthe
Intensive CareUnit Arrhythmias 437
AVnodeandbackupthebypasstract,producinganarrowQRScomplex(orthodro-
mic). AVRT should be suspected in any patient whose heart rate exceeds 200 bpm.
Atrial fibrillation (AF) is a potentially life-threatening arrhythmia in patients with
WPW syndrome, as it can generate a rapid ventricular response with subsequent
degeneration into ventricular fibrillation. This is important, as one third of patients
with WPW syndrome have AF [13].
Adenosineshouldbeusedwithcautioninanyyoungpatientsuspectedofhaving
WPWasitmayprecipitateAFwitharapidventricularresponseratedownanante-
grade accessory pathway. Procainamide, ibutilide, and flecainide are preferred
agents, since they slow conduction through the bypass tract. The long-term treat-
ment of choice for symptomatic patients is radiofrequency catheter ablation of the
accessory pathway.
Management of Irregular Narrow Complex Tachycardias
Irregular narrow complex SVTincludes atrialfibrillation,multifocal atrialtachycar-
dia,atrialflutterwithvariableblock,andsinustachycardiawithfrequentpremature
atrial complexes.
Atrial Flutter and Fibrillation
Atrial flutter is a macro-re-entrant arrhythmia identified by flutter waves often best
seeninthe inferiorleads,at250to350bpm.Patientsoftenpresentwithtwo-to-one
AVconductionwithaventricularrateof150bpm,althoughtheAVconductionratio
can change abruptly. Acute treatment consists of AV-nodal-blocking drugs for rate
control.Ifthepatientbecomesclinicallyunstable,lowenergyDC-synchronizedcar-
dioversion(50–100 joules)hasasuccessrate of95 to 100%[14].Intravenous ibuti-
lideconvertedabout75%ofpatientstosinusrhythminclinicaltrials,butprolongs
theQTinterval,andcanprovokesustainedpolymorphicVTin1–2%ofcases.Ibu-
tilideshouldnotbeusedinpatientswithaprolongedQT interval(greaterthan420
c
msec) [15, 16]. If a temporary or permanent pacemaker with an atrial lead is in
place, atrial overdrive (burst) pacing can sometimes restore sinus rhythm via over-
drive suppression.
Atrial fibrillation is the most common narrow complex tachyarrhythmia in the
ICU [17]. The prevalence of atrial fibrillation in the general population increases
exponentially withage[18].ThemostimportantriskfactorsfordevelopmentofAF
in the general population are structural heart disease (70% in Framingham study
over22yearfollow-up),hypertension(50%)[19],valvularheartdisease(34%)[20],
and left ventricular hypertrophy.
The three goals of therapy for atrial fibrillation are to control the rate, to restore
and maintain normal sinus rhythm, and to prevent complications. Pharmacologic
agents for acute rate control include beta-blockers, non-dihydropyridine calcium
channel blockers, and digoxin.
Beta-blockers provide more effective rate control than calcium channel blockers
at rest and during exercise [21]. The intravenous medication most often used is
metoprolol given at 2.5–5 mg i.v. over 1–2 minutes every 5–10 minutes for a total
of15mgasbloodpressuretolerates.Esmolol,0.5mg/kgbolus,then0.05mg/kg/min
infusion,isanalternativewithamorerapidonsetandoffset,whichcanbeusefulin
unstable patients.
438 S.M.Hollenberg
Non-dihydropyridine calcium channel blockers (diltiazem and verapamil) are
alsoeffectiveAVnodalblockers.Verapamilmayhavemorenegativeinotropicprop-
ertiesthandiltiazemandthusmayinducehypotensioninpatientswithleftventric-
ular dysfunction and borderline blood pressure [22]. Diltiazem is available in i.v.
formandiscommonlyusedasacontinuousinfusionatarateof5–15mgperhour.
Digoxincontrolsventricularresponsethroughacentrallymediatedvagalmecha-
nism andbydirectactiononthe AVnode.Itcontrolsrestingheartratesinpatients
who do not have increased catecholamine levels, but is less effective in the ICU.
Intravenous digoxin begins to slow the heart rate in 30 minutes [23].
Hemodynamically unstable patients with atrial fibrillation require emergent car-
dioversionwithoutwaitingforprioranticoagulation,andthosewithacuteheartfail-
ure orischemia shouldbe considered forurgent cardioversion.Electricalcardiover-
sionmaybemoreeffectivewhenthedefibrillatorpadsareplacedinananterior/pos-
terior orientation to direct the current through the atria.
Forotherpatients,cardioversioncarriesastrokerisk,evenifthedurationofatrial
fibrillationislessthanoneweek[24].Duetodelaybetweenresumptionoforganized
atrial electrical activity and of organized mechanical contraction, there can be delay
betweencardioversionandemboliceventsrangingfrom6hoursto7days[25].Anti-
coagulation with i.v. heparin should be considered if atrial fibrillation persists for
greater than 48 hours. The stroke risk in non-anticoagulated patients taken as a
whole is about 2% per year (0.05% per day), but individual factors modulate that
risk.Theriskfactorsforstrokeareheartfailure,hypertension,age 8 75years,diabe-
tes, prior history of transient ischemic attack or stroke, and female gender [26].
Post-operativeatrialfibrillationiscommon,especiallyaftercardiacsurgery,when
the incidence is 25 to 40% of patients, with peak onset on day two [27, 28]. There
are numerous risk factors for postoperative atrial fibrillation, with advanced age
being the most important. Rate control should be initiated, but atrial fibrillation
often runs a self-correcting course in this setting, with resumption of sinus rhythm
in more than 90% of patients by 6–8 weeks after surgery, and so cardioversion is
notalwaysnecessary[29].Immediatecardioversionshouldbeperformedinpatients
with recent onset atrial fibrillation accompanied by symptoms or signs of hemody-
namic instability resulting in angina, myocardial ischemia, shock, or pulmonary
edema without waiting for prior anticoagulation.
Antiarrhythmic agents may be chosen to reduce the risk of recurrence of atrial
fibrillation. The choice of an antiarrhythmic agent depends on the clinical setting.
Propafenone may be used in patients without structural heart disease, although
otheragentsmaybemoreeffective.Sotalolcanbe usedforadrenergicallymediated
atrialfibrillation.Amiodaroneisrecommendedasthefirstlinedruginpatientswith
structural heart disease, with dofetilide as an alternative. Class IC antiarrhythmic
agents (flecainide, encainide, moricizine) should be avoided in patients with coro-
nary heart disease dueto theincreased mortality shown in theCardiac Arrhythmia
Suppression Trial (CAST) [30, 31].
Multifocal Atrial Tachycardia
Multifocal atrial tachycardia is an irregular atrial tachycardia diagnosed by identifi-
cation of three or more P wave morphologies and PR intervals. Multifocal atrial
tachycardia is most often associated with hypoxia in the setting of pulmonary dis-
ease, but may occasionally be due to use of theophylline, metabolic derangements,
andend-stagecardiomyopathy.Treatmentconsistsofcorrectinghypoxiabytreating
Intensive CareUnit Arrhythmias 439
underlying pulmonary disease and/or correcting electrolyte abnormalities [32]. AV
nodal blockers are sometimes useful to control the ventricular response in the
interim.
Ventricular Tachycardia
VTcanbemonomorphicorpolymorphic,sustainedornon-sustained.SustainedVT
is defined as persisting for longer than 30 seconds; non-sustained VT has at least 3
or more ventricular beats but lasts less than 30 seconds. Differentiation of VT into
monomorphic and polymorphic varieties is useful because they occur in different
settings and respond differently to treatment. Polymorphic VT, in turn, can be
divided into that with a long QT interval (torsades de pointes) and that without QT
prolongation,whichisanischemicrhythm.Threeormoredistinctepisodesofven-
tricular tachycardia or fibrillation within a 24 hour period is termed ventricular
storm.
Non-sustained VTis fairly common following a myocardialinfarction. Prognosis
is dependent upon the timing of onset of VT in relation to the incident myocardial
infarction. Non-sustained VT occurring during the first 48 hours of myocardial
infarction is most likely related to myocardial reperfusion and has no prognostic
significance.However,non-sustainedVToccurringmorethan1weekaftermyocar-
dial infarction doubles the risk of sudden cardiac death in patients with preserved
left ventricular (LV) function [33]. Evaluation for recurrence of ischemia is appro-
priate, as is assessment of LV performance. The risk of sudden cardiac death is
increasedmorethanfive-foldinpatientswithLVdysfunction(ejectionfractionless
than 40%) [34].
Monomorphic Ventricular Tachycardia
SustainedmonomorphicVTisare-entrantrhythmthatusuallyoccurs froma fixed
substrate rather than acute ischemia; it most commonly occurs more than 48 hours
after a myocardial infarction, or in the setting of cardiomyopathy. Initial manage-
ment of sustained monomorphic VT with a history of structural heart disease
dependsonitsrate,duration,andthepatient’shemodynamicstatus.UnstableVTis
anindicationforpromptdefibrillation.Hemodynamicallystablepatientswitharisk
of imminent circulatory collapse may be treated with an antiarrhythmic such as i.v.
amiodarone. Amiodarone can be given as a 150 mg i.v. bolus over 10 minutes fol-
lowed by an infusion of 360 mg (1 mg/min) over six hours, and then 540 mg (0.5
mg/min)overtheremaining18hours.Bradycardiaandhypotensioncanresultfrom
i.v.amiodarone,in whichcasethe rate oftheinfusionshouldbedecreased.Current
ACLS guidelines consider lidocaine and i.v. procainamide alternative choices,
although lidocaine is more effective in VT due to ischemia than that due to post-
infarctionscar.Lidocaineisadministeredbyi.v.bolusof0.5to0.75mg/kg,followed
by continuous infusion at 1 to 4 mg/min. Procainamide is administered at 20 mg/
mini.v.for aloadingdoseof 17mg/kg,thencontinuedas aninfusion at1 to4 mg/
min.TheinfusionshouldbestoppedifthepatientbecomeshypotensiveortheQRS
widens by 50% above baseline. The most serious side effects of procainamide are
hypotension and proarrhythmia (most commonly torsades de pointes), both of
which increase in frequency in patients with renal insufficiency because of
decreased excretion.
440 S.M.Hollenberg
RecurrentmonomorphicVTisanindicationfori.v.antiarrhythmicdrugtherapy,
with either amiodarone, lidocaine, or procainamide. Enthusiasm for the use of
chronic antiarrhythmic agents to prevent ventricular arrhythmias was considerably
dampened after CAST, which showed an increase in mortality in patients receiving
flecainideorencainideinpatientswithcoronaryarterydisease[30].Therehasbeen
concern that other antiarrhythmic agents could have the same proarrhythmic
effects. Available data suggest that amiodarone and sotalol are the most effective
antiarrhythmic drugs for preventing sustained VT.
Clinical trials comparing insertion of automated implantable cardioverter defi-
brillators(AICD)toantiarrhythmicdrugtherapyhavegenerallyshownabenefitfor
AICD placement, particularly in high-risk patients with decreased ejection fraction
orinduciblesustainedVT[35,36].TheMADIT-II(MulticenterAutomaticDefibrilla-
tor Implantation-II) trial demonstrated that prophylactic placement of an ICD in
patients with LV ejection fraction (LVEF) e 30% after myocardial infarction
improved survival [37]. The timing of ICD implantation however, is uncertain. In
the recent DINAMIT (Defibrillator in Acute Myocardial Infarction Trial) study,
placement of an ICD immediately after a myocardial infarction did not reduce all-
cause mortality [38]. and analysis of MADIT-II demonstrated that patients with a
remote myocardial infarction (at least 18 months previous) benefited greatly from
the ICD, whereas those with a more recent myocardial infarction (less than 18
months) did not [39]. Data from the SCD-Heft (Sudden Cardiac Death-Heart Fail-
ure)trialalsoshowedasurvivalbenefitinpatientswitheitheranischemicoranon-
ischemic cardiomyopathy and EF ‹ 35% after implantation of an ICD compared to
amiodarone [40]. Due to the outcomes of these trials, referral for ICD implantation
isrecommendedforsurvivorsofsuddencardiacdeathandpatientswithaprevious
myocardial infarction and LVEF of less than 35%.
Polymorphic Ventricular Tachycardia
PolymorphicVTwithanormalQTintervalisconsideredtobeanischemicrhythm
that typically degenerates into ventricular fibrillation (VF). It is almost never
asymptomatic and thus direct current synchronized cardioversion is the initial rec-
ommendedtreatment.PolymorphicVTwithanormalcorrectedQT(QTc)isamore
ominoussignthanmonomorphicVTinpatientswithmyocardialischemia.Medica-
tions that might predispose to ischemia, such as inotropes or vasopressors, should
be stopped or tapered, if possible, and beta-blockers started if blood pressure per-
mits. Intra-aortic balloon pumping may be useful as a supportive measure, but
revascularization is usually required. If withdrawal of vasopressors is contraindi-
catedonaclinicalbasis,intravenousinfusionoflidocaineoramiodaroneshouldbe
initiated.
Torsades de Pointes
Torsades de pointes (‘twisting of the points’) is a syndrome comprised of polymor-
phic VT and a prolonged QTc interval (by definition & 460 msec). This may be due
to various medications, including procainamide, disopyramide, sotalol, phenothia-
zines,quinidine,some antibiotics(erythromycin,pentamidine,ketoconazole),some
antihistamines(terfenadine,astemizole),andtricyclicantidepressants.Otheretiolo-
giesincludehypokalemia,hypocalcemia,subarachnoidhemorrhage,congenitalpro-
longation of the QTc interval, and insecticide poisoning [41]. A key to treatment is