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Approach Considerations

Acute ventricular fibrillation (VF) is treated according to Advanced Cardiac LifeSupport (ACLS) protocols. (See the current ACLS guidelines. [72 7!" ) #nterest ini$proving rates of public cardiopul$onar% resuscitation (C&') trainingith a

special e$phasis on use of earl% defibrillation ith auto$atic e*ternaldefibrillators (A+,s) b% public service personnel (eg police fire airline)isidespread.[7-"hese $easures can help to achieve the greatest public healthbenefits in the fight against sudden death.

&revention of VF is directed at the underl%ing cause (see +tiolog%)./edication therap% or surgical treat$ent (eg operable coronar% arter%disease [CA,") $a% be appropriate in so$e cases hile radiofre0uenc%ablation is effective in a variet% of disorders.

#$plantable cardioverter1defibrillators (#C,s) hich effectivel% provide earl%defibrillation are used for patients at high ris for recurrent VF. Studiesindicate that patients ith VF arrest ho receive #C,s have better long1ter$survival rates than do patients receiving onl% $edication.[73 74 77 75"

,efibrillation

+*ternal electrical defibrillation re$ains the $ost successful treat$ent for VF.A shoc is delivered to the heart to unifor$l% and si$ultaneousl% depolari6e acritical $ass of the e*citable $%ocardiu$. he obectives are to interfere ithall reentrant arrh%th$ia and to allo an% intrinsic cardiac pace$aers toassu$e the role of pri$ar% pace$aer.

Successful defibrillation largel% depends on 2 e% factors8 the duration of VFand the $etabolic condition of the $%ocardiu$. VF avefor$ usuall% beginsith a relativel% high a$plitude and fre0uenc%9 it then degenerates to as$aller and s$aller a$plitude until after appro*i$atel% :3 $inutes as%stoleis reached possibl% because of depletion of the heart;s energ% reserves.

Conse0uentl% earl% defibrillation is vital9 e$ergenc% $edical servicespersonnel can perfor$ defibrillation at the scene long before the patient could

be seen at the e$ergenc% depart$ent (+,). #n addition the place$ent ofA+,s in public places such as airports and casinos allos pro$pt use ofthese devices b% trained la%persons.

,efibrillation success rates decrease 31:

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Factors that affect the energ% re0uired for successful defibrillation include thefolloing8

i$e fro$ onset of VF to defibrillation

&addle si6e

&addle1to1$%ocardiu$ distance8 his is effected for e*a$ple b%

obesit% or $echanical ventilation

>se of conduction fluid (eg disposable pads electrode paste?ell%)

Contact pressure

Stra% conductive patha%s (eg electrode ell% bridges on sin)

&revious shocs hich decrease defibrillation threshold

he goal is to use the $ini$u$ a$ount of energ% re0uired to overco$e thethreshold of defibrillation. +*cessive energ% can cause $%ocardial inur% andarrh%th$ias.

Larger paddles result in loer i$pedance hich allos the use of loer1energ% shocs. Appro*i$ate opti$al si6es are 51:2.3 c$ for an adult 51:< c$for a child and -.313 c$ for an infant. &osition one paddle belo the outer halfof the right clavicle and one over the cardiac ape* (V-1V3).

@efore an% defibrillation re$ove all patches and oint$ents fro$ the chest allbecause the% create a ris of fire or e*plosion. he patient $ust be dr% andnot in contact ith $etallic obects. 'escuers $ust re$e$ber to ensure thesafet% of ever%one around the patient before each shoc is applied.

#f defibrillation reestablishes coordinated $%ocardial contraction a period oflo cardiac output (ie postcountershoc $%ocardial depression) $a% ensue.'ecover% of cardiac output $a% tae $inutes to hours.

,efibrillation causes seru$ creatine phosphoinase levels to increase inproportion to the a$ount of electric energ% delivered. #f custo$ar% voltage isused to defibrillate a patient the proportion of $%ocardial fraction (C1/@)should re$ain ithin reference ranges unless an infarction has caused$%ocardial inur%.

Although the precordial thu$p is less appropriate for VF than for V it actuall%is appropriate in neither. >se it onl% for itnessed $onitored arrests in hichno defibrillator is i$$ediatel% available.

ACLS Algorith$

CPR

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For an adult ho is unresponsive pulseless and not breathing (or has onl%agonal respirations) activate the e$ergenc% response s%ste$ dial B:: or thee$ergenc% nu$ber and retrieve an A+,. #nitiate C&' b% giving !< chestco$pressions then open the aira% and deliver 2 breaths. Continue C&' inthis co$pression1to1ventilation ratio (!

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Antiarrh%th$ic agents can be given before or after the shoc. A$iodarone isgiven as !

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Chec for co$plications (eg aspiration pneu$onia C&'1related inuries) andestablish the need for e$ergent interventions (eg thro$bol%tics antidotesdeconta$ination).

Careful postresuscitative care is essential to survival because studies have

shon a 3

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>nfortunatel% $ost cases of VF are not a$enable to radiofre0uenc% ablationith such patients re0uiring #C, place$ent.

#n patients ith Golff1&arinson1Ghite (G&G) s%ndro$e VF $a% be due topree*cited atrial tach%cardias9 patients ith G&G and VF should undergo

catheter ablation of the accessor% patha%.

#$plantable Cardioverter1,efibrillators

Survivors of VF that does not have a clear and readil% reversible cause shouldbe i$planted ith an #C,. ransvenous #C,s can be placed ith $ini$al$orbidit% and $ortalit%. Several $ulticenter trials have de$onstrated theproph%lactic value of #C, therap% in patients at high ris for VF.

A $ultiorgani6ational tas force that includes the A$erican College of

Cardiolog% and the A$erican Deart Association has developed guidelines forthe use of #C,s.[53" hese guidelines are updated annuall%.[54"

#n several studies that co$pared #C, place$ent ith antiarrh%th$ic therap% inpatients ith V?VF and?or prior cardiac arrest #C, place$ent as shon tobe associated ith a significantl% decreased $ortalit% rate.[57 73 55" Doever #C,place$ent $a% also be appropriate in conunction ith antiarrh%th$ic therap%./atsue et al de$onstrated the benefit of #C, place$ent and $edication inpatients ith vasospastic angina ho had been resuscitated fro$ lethalventricular arrh%th$ia.[5B"

he use of #C,s as pri$ar% prevention for VF has also been de$onstrated inpatients ith LV d%sfunction. Jeer #C,s have pacing capabilities and haveaddressed brad%arrh%th$ias that either cause or co$plicate V or VF. #C,sare indicated for the secondar% prevention of VF and for the pri$ar%prevention of VF in patients ith an LV eection fraction of less than !3=hether due to ische$ic or non1ische$ic cardio$%opath%.[53 B

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@% itself CA@ prevents recurrent VF onl% if the eection fraction is nor$aland ische$ia as the cause of the arrest.

Surgical treat$ent of ventricular arrh%th$ias in patients ith nonische$icheart disease includes e*cision of V foci after endocardial $apping and

e*cision of LV aneur%s$s. his is practiced ver% infre0uentl% due to significant$orbidit% and li$ited efficac%.

Aortic valve replace$ent is associated ith i$proved outco$e in patients ithhe$od%na$icall% significant valvular stenosis and ell1preserved ventricularfunction. /itral valve replace$ent is indicated for patients ith $itral valveprolapse ho have $alignant tach%arrh%th$ias such as V and VFassociated ith significant valvular regurgitation and LV d%sfunction.

Hrthotopic heart transplantation is indicated in patients ith refractor% heart

failure and?or ventricular arrh%th$ias in ho$ significant i$prove$ent inactuarial survival is e*pected. iven a li$ited donor suppl% this for$ oftreat$ent is e*pected to be beneficial for ver% fe people ho survive VF.

Screening for D%pertrophic Cardio$%opath%

o prevent VF screen for h%pertrophic cardio$%opath% in %oung patients hoare at high suspicion for h%pertrophic cardio$%opath% particularl% those hoare prospective candidates for co$petitive1level athletics.[22" Features in thehistor% that indicate increased ris include the folloing8

S%ncope

Abnor$al blood pressure response (ie h%potension) to e*ercise

Jonsustained or sustained V

&aro*%s$al supraventricular tach%cardia (&SV)

&aro*%s$al atrial fibrillation

Fa$il% histor% of sudden cardiac death fro$ suspected or diagnosed

h%pertrophic cardio$%opath%Ghen h%pertrophic cardio$%opath% is identified in a %oung patient treat$entshould be initiated as 0uicl% as possible.

Consultations

A cardiologist $ust be involved in the care of patients ho have had a V?VFcardiac arrest or ho have s%$pto$s of ische$ic heart disease valvulardisorders or presentations ith co$ple* arrh%th$ias. Cardiac

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electroph%siologists should also be involved in the care of these patientshich generall% involves #C, place$ent.

Hther consultants include an interventional cardiologist and a cardiacsurgeon. Such consultations are $ade on a case1b%1case basis. &atients

should be cared for at centers here intensive cardiac $onitoring andappropriate invasive and noninvasive studies can be perfor$ed. #n general acardiovascular service including interventional cardiolog% electroph%siolog%and cardiac surger% is needed.

/+,#CA#HJ

/edication Su$$ar%

#n acute ventricular fibrillation (VF) drugs (eg vasopressin epinephrinea$iodarone) are used after ! defibrillation atte$pts are perfor$ed to restore

nor$al rh%th$. A$iodarone can also be used on a long1ter$ basis in patientsho refuse an i$plantable cardioverter1defibrillator (#C,) or ho are notcandidates for an #C,. Doever a$iodarone has not been shon to be of valuefor pri$ar% prevention of VF in patients ith a depressed left ventricular (LV)eection fraction.

Antid%srh%th$ics #a

Class Summary

Class #a antiarrh%th$ics increase the refractor% periods of the atria andventricles. /%ocardial e*citabilit% is reduced b% an increase in the threshold for

e*citation and inhibition of ectopic pace$aer activit%.

Vie full drug infor$ationProcainamide (Procanbid, Pronestyl, Pronestyl [SR])

&rocaina$ide is a third1line drug of choice for VF. his drug is generall% notreco$$ended for VF patients but because of its long loading ti$e it can beused to prevent recurrences of VF or for treat$ent of sustained ventriculartach%cardia (V).

Antid%srh%th$ics #bClass Summary

Class #b antid%srh%th$ics suppress auto$aticit% of conduction tissue b%increasing the electrical sti$ulation threshold of the ventricle and Dis1&urines%ste$ and b% inhibiting spontaneous depolari6ation of the ventricles duringdiastole b% a direct action on the tissues. Class #b antid%srh%th$ics bloc theinitiation and conduction of nerve i$pulses b% decreasing the neuronal

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$e$brane;s per$eabilit% to sodiu$ ions resulting in inhibition of depolari6ationith resultant blocade of conduction.

Vie full drug infor$ationidocaine (!ylocaine, "er#ocaine, idoPen, Duo$%rac&)

Lidocaine is a local anesthetic and a class #b antiarrh%th$ic agent that increasesthe electrical sti$ulation threshold of the ventricle suppressing the auto$aticit%of conduction through the tissue. Class #b agents particularl% shorten the actionpotential. Lidocaine $a% be tried in patients ith V due to ische$ia.

Antid%srh%th$ics ###

Class Summary

Class ### antid%srh%th$ics prolong the action potential duration. So$e agents inthis class inhibit adrenergic sti$ulation (alpha1 and beta1blocing properties)9

affect sodiu$ potassiu$ and calciu$ channels9 and prolong the action potentialand refractor% period in $%ocardial tissue. hese effects result in decreasedatrioventricular (AV) conduction and sinus node function.

Vie full drug infor$ationAmiodarone (Pacerone, Cordarone, "e'terone)

A$iodarone is a class ### antiarrh%th$ic agent indicated for the $anage$ent oflife1threatening recurrent VF.

A$iodarone $a% be ad$inistered intravenousl% or orall%.'ecurrent VF that is not due to a reversible cause can be treated ithintravenous (#V) a$iodarone. #t decreases AV conduction and sinus nodefunction. #t also prolongs action potential and refractor% period in $%ocardiu$and inhibits adrenergic sti$ulation. A$iodarone can also be used orall% on along1ter$ basis in patients ho refuse #C,s are not candidates for #C,s or havefre0uent ventricular arrh%th$ias.

Antid%srh%th$ics V

Class Summary

Class V antid%srh%th$ics have a $echanis$ of action different fro$ those ofagents in classes #1#V9 in $an% cases their $echanis$ of action is unnon.

Vie full drug infor$ationagnesium sulfate

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/agnesiu$ acts as an anti1arrh%th$ic agent and di$inishes the fre0uenc% ofpre$ature ventricular contractions particularl% hen secondar% to acuteische$ia. Clinical trials have been inconclusive in de$onstrating its abilit% toi$prove $ortalit% rates in the setting of refractor% VF.

VasopressorsClass Summary

hese agents aug$ent the coronar% and cerebral blood flo that is presentduring the lo1flo state associated ith he$od%na$ic co$pro$ise fro$ VF.

Vie full drug infor$ation*ine*&rine (Adrenalin)

+pinephrine is considered to be the single $ost useful drug in cardiac arrestalthough it has never been shon to benefit long1ter$ survival or functional

recover%. +pinephrine sti$ulates alpha beta: and beta2 receptors resulting inrela*ation of s$ooth $uscle cardiac sti$ulation and dilation of $usclevasculature.

Vie full drug infor$ationVaso*ressin (AD+, Pitressin)

Vasopressin is a peptide hor$one that regulates the bod%;s retention of ater b%increasing ater absorption in the collecting duct of the idne% nephron. #t alsoincreases arterial blood pressure b% affecting peripheral vascular resistance.

Vasopressin has an off1label indication for VF that is causing pulseless arrest.his agent $a% i$prove vital organ blood flo cerebral o*%gen deliver% thepatient;s abilit% to be resuscitated and the patient;s neurologic recover%.

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