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Tahiaritmii

Dr. Radu V!t!"escu Pacing and Clinical Electrophysiology Lab., Cardiology Department Clinic Emergency Hospital Bucharest

Semnifica!ie manifest"ri clinice


! Simptome:
! ! ! !

! datorate !DC

! datorate stazei

cerebral: vertij-lipotimii " sincopa (# sd. Adams-Stokes) cardiace: angina pectorala renale: respira!ie acidotic" " com" musculare: astenie fizic" / fatigabilitate

! Semne

! pulmonare ! periferice

! de DC! ! de staz"

NB!: manifest"rile clinice depind de mecanismul tahidicardiei #i de substratul pe care apar NB!: simptomele se pot datora #i bradiaritmiilor induse de tahiaritmii
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EGM intracavitare: EPS

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RVOT HRA HBE

CS

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Mecanismele TSV sustinute


" ! Reintrare: " ! in NSA " ! la nivelul caii lentecale rapida: TRNAV " ! la nivelul atriului = FiA, Fl A " ! pe cale accesorie: TRAV " ! Automatice: " ! Aritmii atriale automatice " ! Aritmii jonctionale automatice: " ! TJNP pura " ! TJNP cu bloc
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Tahicardia sinusala

! Unda P prezenta; morfologie constanta; frecventa > 100 / min ! Conditii fiziologice: efort, emotii, cafea, fumat ! Iatrogen: betamimetice, xantine (amfetamine, cocaina, etc) ! Conditii patologice:
! Boala ischemica ! Pericardite ! Miocardite ! Colaps, hipoTA ! soc ! Boli acute febrile, boli pulmonare cronice, hipertiroidia, IR, AVC, etc

! Se trateaza cauza
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Aritmia sinusala respiratorie

! Variatie fazica a frecventei sinusale cu mai mult de 120 msec ! Unda P de morfologie constanta, normala ! P-P se scurteaza in inspir profund, ! tonus vagal ! Varianta de normal la tineri = hipertonie vagala ! Dispare la efort sau la cresterea tonusului simpatic ! Poate fi produsa de supradozaj digitalic ! Dispare cu varsta, la diabetici (TS fixa)

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Extrasistolia atriala
! ! ! ! ! ! ! ! ! Automatism anormal P precoce de morfologie diferita de a P sinusal De obicei PR lung
! PR scurt in WPW sau in ESA din NAV

Uneori P extrasistolic blocat si pauza necompensatorie (decaleaza ritmul cardiac) QRS inguste (majoritatea cazurilor) Uneori interpolate, fara decalarea RS Daca sunt f. frecvente = risc FA Cauze: fumat, alcool, cofeina, stress, miocardite, ischemie atriala, hipoxie cronica, etc. Tratament:
! Cand sunt simptomatice ! Cand sunt frecvente, chiar asimptomatice, prin risc de FA, FlA ! beta blocante, Ca-blocante, eventual digitala, rareori AA Ic R.V. - Tahiaritmii feb 2012

Tahicardia atriala multifocala

!! automatism anormal !! tahiaritmie neregulata cu QRS inguste !! P de morfologie variabila (cp. 3 morfologii) 100-140/min !! PR variabil (RP lung/PR scurt) !! PP complet neregulat !! apare in boli cardiace organice: BPOC cu CPC si IC severa !! Poate evolua spre FA; clinic se aseamana cu FA !! Tratament: beta-blocante, verapamil, amiodaron !! Trat hipoxemiei, diselectrolitemiilor (magneziu, potasiu)
"! raspunde

greu la tratament
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Tahicardia jonctionala neparoxistica


! Automatism anormal ! Tahiaritmie regulata cu QRS inguste, 70-130/min ! Mecanism: automatism crescut in NAV-His ! Debut - intrerupere progresive ! P variabil: absent; negativ DII, DIII, aVF, inainte sau dupa QRS) ! Etiologie:
! Supradozaj digitalic ! congenitala ! Miocardita, RAA cu cardita ! IMA inferior ! Chirurgia valvei mitrale Context clinic sugestiv: regularizarea frecventei cardiace la pt cu FA cronica tratat cu digitala

! Tratament: in functie de cauza


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Tahicardia prin reintrare in NAV (TRNAV): mecanism

"! Conducere "! Conducere

anterograda = pe calea lenta in AD posteroseptal retrograda = pe calea rapida in AD R.V. anteroseptal - Tahiaritmii feb 2012

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V1 D1 V2 D2 D3 aVR aVL V5 aVF V6 V3

V4

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Tratamentul TRNAV
! acut:
! SEE daca exista deteriorare hemodinamica ! Adenozina 6-12 mg IV ! Verapamil 5-10 mg IV ! Metoprolol 5 mg iv

! Cronic, profilactic:
! paleativ
! Beta blocante ! Calciu blocante ! ??? Digoxin ! Alte AA (f.rar)

! Curativ DE ELECTIE: studiu electrofiziologic si ablatie prin RF a caii lente


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AHV

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A A A H V A A H H V V

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A H V

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H A H V A V

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A H

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Sdr. de preexcitatie
! Cale accesorie de conducere intre atrii si ventriculi:
! Intre AD si VD ! Intre AS si VS ! Cai multiple

Formata din tesut miocardic embrionar:


! Nu este intotdeauna manifesta = nu conduce intotdeauna ! Conducere f. rapida ! Conducere atrio-ventriculara sau ventriculo-atriala

! !

In cazul conducerii pe cale accesorie complexul QRS este rezultatul fuziunii intre depolarizarea prin NAV si cea pe CA ECG:
! Interval PR scurt < 0.12 sec ! Aparitia undei delta ! QRS larg > 0.12 sec ! Unda T negativa

Pre-excita!ie + tahiaritmii prin reintrare = SINDROM WPW


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Situatii clinice posibile in prezenta caii accesorii atrio - ventriculare


! Sd de preexcita!ie = conducerea anterograd pe calea accesorie in RS
! Constant - unda delta permanenta (uneori variabil - efect de acordeon) ! Conducere intermitenta (unda delta intermitent) ! Aparent absent - posibila pentru perioade indelungate ?? (fuziune)

asimptomatica

Tahiaritmii dependente/asociate = SINDROM WPW:


! Reintrare atrioventriculara ortodromica
NB!: (uneori prin CA ,,oculte - conducere doar retrograd V-A)

! Reintrare atrioventriculara antidromica ! FA ,,preexcitat

simptomatica

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Unda delta intermitenta

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Preexcitatie permanenta

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Efectul de acordeon: unda delta de durata variabila

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Tahicardia reintranta atrioventriculara (TRAV) ortodromica


! Tahiaritmie regulata cu QRS inguste ! Frecventa 180-200 / min (orientativ in dg$TRNAV) ! A doua cauza de TSV sustinuta ! Mecanism:
! Conducerea anterograda prin NAV ! Conducere retrograda VA ascunsa
! Complexe QRS sunt inguste ! Pre-excitatia nu este evidenta

! Nu (???) se asociaza cu risc de moarte subita cardiaca

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TRAV cu conducere antidromica


"! tahiaritmie regulata cu QRS largi prin prezenta undei delta "! raspuns ventricular rapid > 180-200/min "! mecanism: "! Conducere anterograda pe calea accesorie
"! Conducere retrograda prin NAV

"! dg diferential cu TV monomorfa sustinuta "! Risc crescut de moarte subita cardiaca in caz de aparitia FA " FV
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TSV in sdr. WPW cu conducere antidromica

!!Tahiaritmie

regulata cu QRS largi; P ne-evidentiabil; dg dif TV monomorfa


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Sdr. WPW cu fibrilatie atriala

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Evaluarea riscului vital in WPW


! Neinvaziv ????:
! Preexcitatia intermitenta = risc redus (??) ! Disparitia preexcitatiei cu procainamida = risc redus (?) ! Test de effort (????) ! Intervalul RR in FA
! Cu cat RR este mai scurt risc vital mare (<250 ms)

! Invaziv = EPS:
! Determinarea perioadei refractare a caii accesorii

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Tratamentul in sdr. WPW


! Sdr de preexcitatie fara tahiaritmii (unda delta in RS): supraveghere ? ! Sdr WPW (preexcitatia cu tahiaritmii) acut (conversie la RS):
! SEE daca exista deteriorare hemodinamica (!!FA cu pre-ex.) ! Tahiaritmia ortodromica, QRS inguste:
! Adenozina IV

! Tahiaritmia antidromica, QRS largi:


! Antiaritmice de clasa Ia, Ic, III

! Profilactic, cronic:
! Antiaritmice de clasa Ia, Ic, III ! ABLATIE prin RF a caii / cailor accesorii

! CONTRAINDICATE:
! Digoxina ! Blocantele de calciu
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A H

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RF

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Flutter-ul atrial
! ! ! Tahiaritmie regulata cu QRS inguste Produsa prin macroreintrare Absenta undelor P, unde F 250-350 / min, fara linie izoelectric:
! FlA tipic (antiorar): negative in DII, DIII, aVF ! FlA tipic inversat (orar): pozitive in DII, DIII, aVF

FlA atipic: >350 / min, morfologie variabila "i/sau discordant


! FA cu unde mari (,,fibrilo-flutter) ! TA (m.a. tahic. de VP)

! ! !

Netratat: conducere AV 2/1 (~ 150 / min) Posibila conducerea variabila: succesiv 2/1, 4/1, 3/1 Manevrele vagale scad AV in trepte prin cresterea progresiva a gradului de bloc

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Caracterele FlA
! Mai rar decat FiA ! FlA paroxistic poate surveni pe cord normal (? FlA atipice) ! FlA cronic = cord patologic (?) ! Cauzele = aceleasi ca pentru FiA (demascarea substratului?)
! Miocardita, inclusiv RAA ! Boala ischemica ! Alcoolism ! Valvulopatii Mi, Tri ! Postchirurgie cardiaca ptr CC hipertiroidia cardiomiopatii pericardite TEP, etc

! Aritmie recurenta
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Fl.A: situatii speciale

Efectul adenozinei sau CSC

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FlA cu conducere 1:1


"! sub efectul chinidinei "! produce sincopa chinidinica " ! efect anticolinergic pe NAV
" ! scade viteza de depolarizare atriala
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Tratament
! acut
! cardioversie (SEE de energie joasa) ! antiaritmice de clasa I i-v ! CCB i-v ! B i-v ! manevre vagale ! overdrive pacing (sonda esofagiana sau endocavitara temporara) ! profilaxie ! curativ? NB!: risc emboligen !TEE daca debutul este !48h si/sau incert !anticoagulare
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! cronic

! Controlul ritmului

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RA T

LA M

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Tahicardiile atriale focale


! ! ! ! ! ! Automatism anormal/microreintrare Tahiaritmie regulata cu QRS inguste frecventa 150 - 200/min P de morfologie nesinusala PR normal sau prelungit (BAV de gr) Dg dif ECG: flutter atrial atipic (uneori exista P blocate)
! Neinfluentata de manevrele vagale ! Nu poate fi initiata prin stimulare atriala ! In general nu poate fi oprita prin overdrive pacing

! Tratament: ! de obicei rezistenta la tratament ! Stop digitala; fenitoina ! %-blocante, potasiu, Ca-blocante ! in BPOC = O2

! Uneori asociat cu:


! TahiCMP (10%) ! Disf(x) NSA

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P -/0 in aVL si + in V1
Da

Nu

Focar AS

Focar AD

&P in V1!80 ms focare nonPV

&P in D1!50 V

Da

P in aVR

Nu

Tahicardii cristale PVs drepte


P D2,3 aVF P+ D2,3 aVF

Inel tricuspidian Sept i-a


P sau in 3 deriv V2-6 P + in V5,6 durata P in SVT < RS

PVs stangi

P in D2 ! 100 V superior

infero-lateral supero-lateral

anular

septal

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Fibrilatia atriala !
! Absenta undelor P ! Unde f 450-600 / min; pot lipsi
! FA cu unde mici ! FA cu unde mari

QRS complet neregulate ! Frecventa ventriculara variabila:


! ! ! ! F. rapida > 150/min Rapida > 100 / min Medie 60 100 / min Joasa < 60 / min
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Epidemiologia FA
! Cea mai frecventa aritmie sustinuta:
! 0.4% din populatia totala ! Incidenta creste cu varsta
! 50-59 ani = 0.5-0.9% ! > 65 ani = 6% ! 80-85 ani = 10%

! 25% din pacientii cu IC


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Etiologia FA
! Valvulopatii RAA ! Boala coronariana ! Cardiomiopatii ! Hipertiroidie ! asociata cu WPW ! Boala de nod sinusal ! Prolapsul valvular mitral ! Cardiopatia hipertensiva ! Pneumopatii cronice ! Etilism acut

FA IDIOPATICA: pana la 30% din cazuri !


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FA depistata prima

PAROXISTICA (autolimitata)

48 h time point is clinically importantafter this the likelihood of spontaneous conversion is low and anticoagulation must be considered (see Section 4.1). (3) Persistent AF is present when an AF episode either lasts longer than 7 days or requires termination by cardioversion, oara either with drugs or by direct current cardioversion (DCC). (4) Long-standing persistent AF has lasted for 1 year when it is decided to adopt a rhythm control strategy. (5) Permanent AF is said to exist when the presence of the arrhythmia is accepted by the patient (and physician). Hence, rhythm control interventions are, by denition, not pursued in patients with permanent AF. Should a rhythm control

Clasificare

PERSISTENTA (ne-autolimitata)

PERMANENTA
First diagnosed episode of atrial brillation Paroxysmal (usually <48 h) Persistent

(>7 days or requires CV)

Long-standing Persistent (>1 year) Permanent (accepted)


ESC Practice Guidelines. EHJ 2010

R.V. - Tahiaritmii feb 2012 Figure 2 Different types of AF. AF atrial brillation; CV

cardioversion. The arrhythmia tends to progress from paroxysmal

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Fiziopatologie
! Mecanisme:
! Focare ectopice: initiere ! Reintrare dezordonata:
! MASA CRITICA ATRIALA ! Perioade refractare scurte

! Sistemul nervos vegetativ:


! ' vag: dupa masa, somn ! ' simpatic: stress, efort, isuprel

! Functia mecanica atriala dispare ! AV mediata de:


! conducerea ascunsa in NAV ! Functia NAV: PRE = 0.3 sec ! Anularea fronturilor de unda in A

! AF begets AF: cardiomiopatie atriala

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Permanent!

Paroxistic!

Substrat

Trigger

Page 9 of 61

rst documented

the 10 s strip (recorded at 25 mm/s) by six. The ed complications is not different between short d sustained forms of the arrhythmia.12 It is thereto detect paroxysmal AF in order to prevent Persistent ! highplications (e.g. stroke). However, short atrial g. detected by pacemakers, debrillators, or other es, may not be associated with thrombo-embolic nless their duration exceeds several hours (see

,,Perpetuatori
Upstream therapy of concomitant conditions Anticoagulation Rate control Antiarrhythmic drugs Ablation Cardioversion AF silent paroxysmal persistent long-standing permanent persistent

est initially as an ischaemic stroke or TIA, and it is sume that most patients experience asymptomatic, nating, arrhythmia episodes before AF is rst diagof AF recurrence is 10% in the rst year after the and 5% per annum thereafter. Co-morbidities

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Figure 1 Natural time course of AF. AF atrial brillation.

Paroxistic!

Persistent!

Permanent!

Durata

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Consecintele FA. Implicatii terapeutice


1.! Pierderea sistolei atriale = ! DC
!! SAo, CMHO !! CMDil, CMR, CHT

CONVERSIA LA RS

2.! Scaderea duratei diastolei = ! DC


!! SMi, SAo, CMHO !! Boala coronariana

REDUCEREA AV

3.! Riscul tromboembolic

PROFILAXIA EMBOLIILOR SISTEMICE


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Conversia la RS
INDICATII
! FA paroxistica cu (h-d ! FA recenta < 6 luni 1 an

CONTRAINDICATII
! AS, AD cu diametru > 50 mm ! Durata > 6 luni 1 an

! AS cu diametru< 45-50 mm ! Antecedente AVC embolic ! FE VS > 40%


! Fara tromboza AS/AAS ! Fara tratament digitalic / verapamil ! Dupa anticoagulare corecta

! Tromboza AS/AAS fara anticoagulare ! Boala de nod sinusal

! 50% din FA paroxistice = conversie spontana in 24-48 ore de la debut


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efcacy for conversion of persistent AF and for atrial utter. Similar to ecainide, propafenone should be avoided in patients

is, however, more e than AF.

Conversia la RS: chimica sau electrica


! !
Table 12 Drugs and doses for pharmacological conversion of (recent-onset) AF Tratament anticoagulant cu 3-4 sapt inainte

internare la UTIC: ! SEE: 260-360 J x 3 (max) SAU ! Antiaritmice:

Drug Amiodarone Flecainide

Dose 5 mg/kg i.v. over 1 h 2 mg/kg i.v. over 10 min, or 200300 mg p.o. 1 mg i.v. over 10 min 2 mg/kg i.v. over 10 min, or 450600 mg p.o. 3 mg/kg i.v. over 10 min

Follow-up dose 50 mg/h N/A

Risks

Phlebitis, hypot AF conversion

Not suitable fo disease; may pr interval; and m due to convers ventricles.

Ibutilide

1 mg i.v. over 10 min after waiting for 10 min

Can cause pro pointes; watch Will slow the v

Propafenone

Not suitable fo disease; may pr the ventricular ventricular rate conduction to Second infusion of 2 mg/kg i.v. over 10 min after15 min rest

Ia: CHINIDINA: max 2g / 24 ore

Vernakalant

So far only eva

! ! !

Rate de conversie variabile 50-80%; studii comparative putine


a

Dupa conversie: anticoagulare orala 4 saptamani blocante, Ca-blocante

Fara dovezi clare de eficienta: sotalol, disopiramida, procainamida, digoxin, beta-

Vernakalant has recently been recommended for approval by the European Medicines Agency for rapid cardioversion of r non-surgical patients; 3 days for surgical patients).68,69 A direct comparison with amiodarone in the AVRO trial (Phase Active-controlled, multi-center, superiority study of Vernakalant injection versus amiodarone in subjects with Recent Onset amiodarone for the rapid conversion of AF to sinus rhythm (51.7% vs. 5.7% at 90 min after the start of treatment; P , 0.00 over 10 min), followed by 15 min of observation and a further i.v. infusion (2 mg/kg over 10 min), if necessary. Vernakala pressure , 100 mm Hg, severe aortic stenosis, heart failure (class NYHA III and IV), ACS within the previous 30 days, or should be adequately hydrated. ECG and haemodynamic monitoring should be used, and the infusion can be followed by R.V.heart - Tahiaritmii feb 2012 patients with stable coronary artery disease, hypertensive disease, or mild heart failure. The clinical positioning of this used for acute termination of recent-onset AF in patients with lone AF or AF associated with hypertension, coronary artery failure.

Profilaxia recurentei: chimica


! ! RS la > 50% din pts convertiti la 1 an Aceleasi medicamente ca si cele folosite ptr conversie:
! Ic: PROPAFENONA: 450-600 mg/zi
FLECAINIDA: 100-200 mg/zi

AA de clasa Ic preferabil asociate cu %B

! III: AMIODARONA: incarcare (1g/10 kgcorp) intretinere 200-400 mg/zi


DOFETILIDA: 500 mg x 2 PO

! ! !

Recurenta asimptomatica a FA = frecventa Beneficiul tratamentului = ! nr. de episoade si a duratei totale a FA Amiodarona: RS la 1 an = 66%: TOXICITATE PROBLEMELE TRATAMENTULUI PE TERMEN LUNG

! ! !

Efecte proaritmice Pe cord patologic, in primele zile de tratament La doze mari de medicamente sau crescute rapid TRATAMENT IN SPITAL CU DOZE MICI CRESCUTE LENT
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Controlul frecventei cardiace


- in FA permanenta sau in caz de contraindicatii de conversie -

1.! Acut:
! Digoxin IV: de prima linie in IC ! Beta-blocante:
! Metoprolol: 5-15 mg IV ! Propranolol (1-5 mg) ! Esmolol

2.! Cronic:
!! Se prefera %B sau Ca blocante in afara IC !! %B +/- digoxin in IC; de evitat Ca-blocante !! Bronhospasm: Ca-blocante !! Greu de controlat AV la efort

! Blocante de calciu:
! Diltiazem 20-25 mg IV ! Verapamil 5-15 mg IV

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Riscul de AVC in FA: CHADS2


"!

Elemente scorului CHADS2:


" ! Insuficienta

cardiaca congestiva: 1 pt 1 pt

" ! Hipertensiune: " ! Varsta: " ! Diabet: " ! AVC

1 pt 1 pt

sau AIT: 2 pt
Rockson SG, Albers GW. JACC 2004;43:929.

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m OAC overCongestive aspirinheart use, often with low rates of 1 failure/LV dysfunction CHA2DS2-VASc Patients (n = 7329) Adjusted stroke Nothing (or aspirin) morrhage. Importantly, prescription of an antiplatelet score Hypertension 1 rate (%/year)b e use not with n the associated Age >75 a lower risk of adverse events. 2 0 1 0% CHADS does not include many stroke risk 1 gnize 2 score Diabetes mellitus ion for stroke prevention in AF. AF atrial brillation; OAC oral anticoagulant; 1 422 1.3% ased othercan stroke risk modiers need to be considered 2 Stroke/TIA/thrombo-embolism be found on page 13. HADS 2 nding 2 1230 2.2% ehensive stroke risk disease assessment (Table 8). a 1 Vascular e (or risk factors Age (previously referred to as high risk 1 3 1730 3.2% 6574 r than eanaprior stroke TIA, or thrombo-embolism, and the Table 10 Clinical characteristics comprising Sexor category (i.e. female sex) 1 4 1718 4.0% HAS-BLED bleeding risk score 75 years). The presence of some types of valvular ned Maximum score 9 5 1159 6.7% se (mitral stenosis or prosthetic heart valves) would cant (c) Adjusted stroke rate according to CHA2DS2-VASc score Letter Clinical characteristica Points awarded 6 679 9.8% s of rize such valvular AF patients as high risk. CHA DS -VASc Patients ( n = 7329) Adjusted stroke 2 2 assessH Hypertension 1 telet score rate (%/year)b ly non-major risk factors (previously 7 294 9.6% ion relevant of Abnormal renal and liver ents. A factors) 1 or 2 0% as moderate risk are heart [especially rrhage 0 function (1 1 8 82 6.7% point each) failure risk 0.1 and o severe systolic SLV dysfunction, dened as 1.3% 1 Stroke 422 arbitrarily 1 ered 9 14 15.2% oagulaular ejection fraction (LVEF) 40%], hypertension, or B 2 Bleeding 1 2.2% 1230 trol of ther risk risk clinically relevant L 3 Labilenon-major INRs 1 3.2% 1730 factors (prevalues See text for denitions. and a rred to as less validated risk factors) include female E Elderly (e.g. age >65 years) 1 4 1718 4.0% Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates h INR vular of stroke in contemporary cohorts may vary from these estimates. 74 disease (specically, ls. years, and vascular D 5 Drugs or alcohol (1 point each) myocardial 1 or 2 6.7% 1159 b ould Based on Lip et al. 53 eeding aortic plaque and PAD). Note that risk omplex factors Maximum 9 points 6 679 9.8% AF atrial brillation; EF ejection fraction (as documented by ties in ive, and the simultaneous presence of two or more echocardiography, radionuclide ventriculography, cardiac catheterization, cardiac ously 7 294 9.6% erate-, a Hypertension is dened as systolic blood pressure . 160 mmHg. Abnormal magnetic resonance imaging, etc.); LV left ventricular; levant non-major risk factors would justify a stroke cially onable kidney function is dened as the presence 8 82 of chronic dialysis or renal 6.7% TIA transient ischaemic attack. high enough to require anticoagulation. transplantation or serum creatinine 200 m mol/L. Abnormal liver function is ly as to that R.V. - Tahiaritmii feb 2012 15.2% of dened as 9 chronic hepatic disease (e.g.14 cirrhosis) or biochemical evidence n, or factor-based approach for patients with non-valvular may be signicant hepatic derangement (e.g. bilirubin . 2 x upper limit of normal, in
pre-

Hypertension - Diabetes mellitus emes Age > 75 years ntithrombotic therapy on the basis of the presence (or Female sex - Age 6574 years had Vascular diseasea OAC stroke risk factors. as a (b) comes Risk factor-based approach expressed as a point based rtion or this approach from various published anascoring system, with the acronym CHA2DS2-VASc idely e even patients at maximum moderate risk (currently dened (Note: score is 9 since age may contribute 0, 1, or 2 points) jects score 1, i.e. one risk factor) still derive signicant Score Risk factor OAC (or aspirin) ke in

Vascular diseasea Age 6574 Sex category (i.e. female sex) Maximum score

1 1 1

Risc AVC in FA: CHA2DS2-VASc


9 (c) Adjusted stroke rate according to CHA2DS2-VASc score

Recomandarile de tratament anti-trombotic in functie de profilul de risc in FiA (ACCP/VII)


Nivel de risc
Risc scazut

Indicatorii riscului
varsta " 65 ani fara FR aditionali

Tratament
Aspirina 325 mg/zi

Intermediar

Varsta 65-75 ani DZ B coronara

ACO (INR: 2,0-3,0) sau ASA

Inalt

Varsta > 75 ani Istoric de AVC, AIT sau ES HTA, DZ Disfunctie VS sau ICC

ACO (INR: 2,0-3,0)

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Terapia ablativ"

PVI PVp PVp PVp

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TAHIARITMIILE VENTRICULARE
Tahiaritmii cu QRS larg

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Extrasistolele ventriculare

! QRS larg > 120 msec, precoce ! neprecedat de unda P, eventual unda P retrograda ! Daca nu depolarizeaza retrograd NSA: pauza compensatorie (PP = 2 PP) ! Uneori interpolate ! Cuplaj fix = reintrare ! Incidenta creste cu varsta ! Cauze: stress, alcool, ischemie, miocardite, diselectrolitemii, medicamente (AA, digoxina, etc)
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Clasificare si semnificatie clinica


DUPA FRECVENTA ! Clasa 0 ! Clasa 1: rare < 1 / ora ! Clasa 2: putin frecvente (1-9 / ora) ! Clasa 3: intermediare (10-29 / ora) ! Clasa 4: frecvente (> 30 / ora)
Myerburg et al. Am J Cardiol 1984;54:1355-8.
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DUPA MORFOLOGIE ! Clasa A: monomorfe, monofocale ! Clasa B: polimorfe, polifocale ! Clasa C: repetitive
! Cuplete ! Salve (3-5 ESV)

! Clasa D: TV-NS (6 ESV " 30 sec) ! Clasa E: TV-S

Clasificare si semnificatie clinica


Benigne Tip aritmie Cardiopatie Semnific. hemodin. Risc MSC Evaluare
ESV, TVNS, cuplete Lipsa Nu Minim ECG, Holter

Potential maligne FE>35% FE<35%

Maligne
TVNS, TVS, FV Severa Sincopa, MSC Major Holter, SEF

ESV, cuplete, TVNS Moderata Nu Moderat Holter Moderat severa Sincopa, MSC Mare Holter, PVT, VRS

Morganroth et al. JACC 1986.


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Tratamentul ESV
! ESV, cuplete, TVNS asimptomatice: %-blocante (FE > 40%) ! NU flecainida, encainida, sotalol mai ales pe cord ischemic dupa studiul CAST ! ESV frecvente in IMA: xilina, amiodarona sau betablocant IV ! Cuplete sau TVNS pe cord patologic in afara ischemiei acute: ! Amiodaron. ! Ablatie prin RF a focarelor endocardice:
! PALEATIVA (?) ! curativ
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cresterea mortalitatii sub AA clasa I la pacienti cu IM in antecedente

Studiul CAST-I:

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TV: definitie si caractere ECG


! Tahiaritmie regulata cu QRS > 120 msec:
! ASPECT MONOMORF sau POLIMORF

! C.p. 3 depolarizari ventriculare succesive cu frecventa >120/ min ! Durata variabila: 3 QRS " > 30 sec (ore) ! Disociatie atrioventriculara
! Activare atriala indepedenta sau conducere VA retrograda

! RISCURI:
! Degradare hemodinamica ! Degenerare in FV
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Mecanismele TV
! REINTRARE:
! Postinfarct

! AUTOMATISM ANORMAL:
! IMA: TV neparoxistica (RIVA)

! POSTDEPOLARIZARI PRECOCE SI TARDIVE


! TV digitalice ! Sdr. de QT lung congenital ! chinidina
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TV monomorfa sustinuta de obicei REINTRARE

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TV monomorfa: diagnostic
! tahiaritmie regulata > 120/ ! QRS larg > 120 msec ! Disociatie AV ! Batai de fuziune ! Capturi ventriculare
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Criterii morfologice
pe baza derivatiilor V1,2 si V6

! BRD like
! V1,2
! R monofazic ! qR ! RsR cu R>R

! BRS like
! V1,2
! R ini!ial larg >40 ms ! deflexiunea descendenta S
! lent ! Incizur ! ncep. QRS " nadir S 60 ms

! V6
! rS

! V6
! Q sau QS

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Tahicardia ventriculara neparoxistica (RIVA) = AUTOMATISM CRESCUT

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TV polimorfa: torsada varfurilor PDP


! TV rapida, degenereaza in FV ! produsa prin PDP ! cu QT lung sau cu QT normal ! Cauze: ! sdr. de QT lung ! hipo K, hipo Mg ! AA Ia si III ! Tratament: ! MgSO4 IV ! Overdrive pacing ! isuprel lent ! xilina, fenitoina ! QT lung: AICD, beta-blocante, flecainida, stelectomie.
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Dg $ TV vs. TSV cu QRS largi


! Tahiaritmii cu QRS largi:
! ! TV TSV cu QRS largi
! ! ! TSV + BR pre-existent TSV cu aberanta de conducere TSV + TRAV prin mecanism antidromic (WPW)

! !

Dg. dif. posibil pe ECG standard la > 90% din cazuri Criterii ECG de diferentiere TV TSV cu QRS largi:
1.! Batai de fuziune; capturi V 2.! Disociatia AV 3.! Conducere retrograda VA (P retrograde) 4.! QRS > 140 msec (160 msec = TV cert) 5.! Morfologie unica a QRS in precordiale = TV
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Tratament TV
! TV fara decompensare hemodinamica: AA
! Xilina, procainamida, amiodaron, %B in anumite situatii ! TV digitalice: fenitoina, xilina +/- AC anti-digitalici

! TV cu hipoTA, IVS, angina, hipoperfuzie cerebrala:


! SEE: sincron > 50 J

! Alternative:
! Overdrive pacing ! thump version

! Tratamentul cauzelor corectabile sau producatoare:


! Ischemia acuta ! Hipo K, hipo Mg ! BS excesiva
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Oprirea TV prin overdrive pacing

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Tratamentul profilactic al TV
! TVNS asimptomatica pe cord normal sau patologic: %blocante (FE > 40%) sau amiodaron
! NU flecainida, encainida, sotalol dupa CAST

! TVNS cu deteriorare hemodinamica sau TVS:


! Amiodaron. ! Ablatie prin RF a focarelor endocardice: PALEATIVA ! Chirurgia AA ! DEFIBRILATOR IMPLANTABIL
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Fibrilatia ventriculara
! Unde fibrilatorii de amplitudine diferita, in absenta complexelor QRS ! Asistola mecanica urmata de asistola electrica ! Colaps, stop respirator si deces in 3-5 minute de la instalare in absenta CPR ! Cauze:
! Ischemia acuta din IMA aritmii V spontane severe ! Cardiomiopatii (CMHO !) FA din WPW ! CHT cu HVS hipoxia din BPOC ! Iatrogen: medicamente, diselectrolitemii, cateterism cardiac ! Sdr. de QT lung cu TdP SEE nesincron

! Precedata sau nu de TV ! Tratament:


! SEE 200-300 J
R.V. - Tahiaritmii feb 2012 CPR, IOT

Tratamentul aritmiilor V maligne: defibrilatorul implantabil


! Indicatii:
! Proflilaxie secundar
! Orice CP structural/electric cu un eveniment (MSC resuscitat, TV sustinut, FV) la care nu se deceleaz o cauz reversibil

! Profilaxie primar
! BCI FEVS<35-40% ! CMD FEVS <30-35% "i NYHA III ! CMH ! CAVD ! LQT ! Brugada ! SQT
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Avantaje tehnice:
! Pacing anti-tahi si anti-bradi ! Conversie defibrilare cu energie ! ! Stocarea ECG

! mortalitatea fata de amiodaron in AV maligne simptomatice

ICD reduc mortalitatea cu ~ 40%


att in preven#ia primar$ ct %i n cea secundar$
40 30 20 10 0 73% 39% 20% 38% 0 0 31% 41% 0 51% 54%
Control ICD

36% 23%

Preven!ie secundar"

Preven!ie primar"

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Al-Khatib SM et al, Am Heart J 2005

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RMVT Gallavardin

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Caracteristici
! 70% din VT idiopatice ! Origine
! 90-85% RV
! ! ! septul RVOT zona de admisie r$d$cina a.P.

! ECG
! TV 140-180/min ! BRS cu ax inferior ! tranzi'ia( (>precoce = >septal/stg)

! EPS - PDT
! induse de burst/catech ! oprite de A, V, )B

! 10-15% LVOT (cuspele coronariene stg>dr)

! mecanisme
! denerv$ri simpatice localizate ! alter$ri localizate ale recapt$rii NA# $catech sinaptice &i %rec ! 20-30Y, XX!XY, >anduran'$ ! asimtomatici / discret (dup$ efort)
! palpita'ii ! vertij discret ! sincopa excep'ional

! Evolu'ie
! benign$ la majoritatea ! MSC rar
! ! ! tachyCMP forma malign$ (short-coupled) ARVC/D

! risc$
! ! ! ! sincop$ AV f. rapid$ (>230bpm) frecvente (>20 000/zi) ESV cu cuplaj foarte scurt
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TV fascicular" Belhassen
! ! ! ! ! 20-40 ani r$spunde la V nu depinde de efort simtomatic$ (rar sincop$) evolu'ie
! benign$ ! rar MSC ! excep'ional tachyCMP

! ECG
! BRD cu ax sup. >> ax inferior

! EPS
! indus$ de ! programat$ ! entrainment ! isuprel NU induce (poate fi util asociat cu pacingul)

! Tratament:
! V ) B ! abla'ia

! Origine cel. Purkinje aN (conducere decremental$)


! VS midseptal/post.-sept. inferior (FPI) ! rar VS ant.-sup (FAS)

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LQT

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Genetica LQT

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SQT
! tip 1: ($-fx HERG/KCNH2, IKr ! tip 2: ($-fx KVLQT1/KCNQ1, IKs ! tip 3: ($-fx KCNJ2/Kir2.1, IK1; ECG caracteristic
! unde T ample &i marcat asimetrice
! ram ascendent cvasinormal ! ram descendent extrem de abrupt

! ,,overlaping syndromes: (%-fx can. Ca2+ de tip L


! subunitatea )1 (CACNA1C, sindromul de QT tip 4) ! subunitatea % (CACNB2b, sindromul de QT tip 5) ! fenotipul mixt: QTc% + (ECG sd. Brugada

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Sd. Brugada

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FV idiopatic" sd. de repolarizare precoce malign

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ARVC/D

! Au. dom. / recesiv ! boal$ desmozomal$ ! nlocuirea fibro-gr$soas$ a pere'ilor VD VS [#75%] (siv relativ conservat)
! clasic$ (39%): afectare VD izolat / predominant ! biventricular$ (56%): afectare ambii V ! dominant$ stg. (5%): afectare predominant$ VS

! prevalen'$ 1/1000 (posibil subdg. n anumite zone)


! N Italiei: 11% din MSC la tineri &i 22% din MSC la atleti
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Manifest"ri clinice
! vrsta medie 30y (10-50) ! simptome
! MSC
! * n timpul activit$'ilor de rutin$ ! 10% perioperator ! 3,5% sport

Aritmiile V ! %# cu severitatea bolii ! de obicei simptomatice


! ESV#TV sus'inute

! morfologie BRS
! ax inf#RVOT ! ax sup
! QS n toate precordialele (m.a.V3,4) # apex VD ! ax inf, QS <V4 # subtricuspidian

! ! ! ! ! !

sincopa 32% palpita'ii 67% dureri toracice atipice 27% dispnee 11% IC dr. tardiv 6% asimptomatici descop. ntpl$tor
! (ECG ! ESV/TVNS Holter/ECG de efort

Aritmii SV
! # 25% ! FA / TA (macroreinrari AD) / FL.A

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ECG

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ECG
40-50% au ECG normal initial, n 6 ani TO+I au (ECG
! QRS largit >110 ms (24-75%) ! BRD incomplet ! panta S prelungit$ > 55 ms ! unda , (30%) ! unde T inversate V1-3 ! $ dispersiei QT

( ECG evolutive
! $ pantei S cu >10 ms #69% ! $QRS cu >10 ms #66% ! extensia T ,,- n 1 deriv precord ! BR nou ap$rut (11%)

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Localizare

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Boulos M. et al. J Am Coll Cardiol 2001

Garcia FC. et al. Circulation 2009

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