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Tahiaritmii

Dr. Radu Vătăşescu


Pacing and Clinical Electrophysiology Lab., Cardiology Department
Clinic Emergency Hospital Bucharest
Semnificaţie – manifestări clinice
• Simptome:
– datorate ¯DC
• cerebral: vertij-lipotimii ® sincopa (É sd. Adams-Stokes)
• cardiace: angina pectorala
• renale: respiraţie acidotică ® comă
• musculare: astenie fizică / fatigabilitate
– datorate stazei
• pulmonare
• periferice
• Semne
– de DC¯
– de stază

NB!: manifestările clinice depind de mecanismul


tahidicardiei şi de substratul pe care apar
NB!: simptomele se pot datora şi 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 lente-
cale 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

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Tahicardia atriala multifocala

v automatism anormal
v tahiaritmie neregulata cu QRS inguste
v P de morfologie variabila (cp. 3 morfologii) 100-140/min
v PR variabil (RP lung/PR scurt)
v PP complet neregulat
v apare in boli cardiace organice: BPOC cu CPC si IC severa
v Poate evolua spre FA; clinic se aseamana cu FA
v Tratament: beta-blocante, verapamil, amiodaron
v Trat hipoxemiei, diselectrolitemiilor (magneziu, potasiu)
q 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
Context clinic sugestiv: regularizarea frecventei
– Miocardita, RAA cu cardita
cardiace la pt cu FA cronica tratat cu digitala
– IMA inferior
– Chirurgia valvei mitrale
• Tratament: in functie de cauza
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Tahicardia reintranta in NAV (TRNAV)

RS
PR=N
AVNRT

ESA
PR ↑

q Conducere anterograda = pe “calea lenta” in AD posteroseptal


q Conducere retrograda = pe “calea rapida” in AD anteroseptal
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V1
D1

V2

D2
V3

D3

aVR
V4

aVL

V5

aVF
V6

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Tratamentul Table 14 Therapy of AVNRT
EHRA 2016

TRNAV
Recommendation Reference
................................................................................
Acute therapy
66 – 69
Valsalva manoeuvre, preferably in the supine
position, is recommended.
70 – 73
IV adenosine is recommended.

• acut: Synchronized direct-current cardioversion is 239

recommended for haemodynamically


– SEE daca exista deteriorare h-d unstable patients in whom adenosine fails to
terminate the tachycardia.a

– Adenozina 6-12 mg IV
70,71,74 –
IV verapamil or diltiazem may be considered
76,79
in the absence of hypotension or suspicion of
VT or pre-excited AF.
– Verapamil 5-10 mg IV IV beta blockers (metoprolol or esmolol) 74,77,78

may be considered.
– Metoprolol 5 mg iv IV amiodarone may be considered. 240

• Cronic, profilactic:
241,242
Single oral dose of diltiazem and propranolol
may be considered.
Chronic Therapy
– paleativ Catheter ablation for slow pathway 243 – 247

• Beta blocante modification is recommended in


symptomatic patients or in patients with an
• Calciu blocante ICD.
248 – 251
Diltiazem or verapamil may be considered.

– Curativ Beta blockers may be considered. 242,250

225
DE ELECTIE: ablatia caii lente
No therapy for minimally symptomatic
patients with infrequent, short-lived episodes
of tachycardia. 15
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AHV

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A H V A V
H

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A
A
H
A H
A H V A
V
V

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A
A
H

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H
A H V A V

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A H V A

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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-excitație + tahiaritmii prin reintrare = SINDROM WPW

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Situatii clinice posibile in prezenta
caii accesorii atrio - ventriculare
• Sd de preexcitație = conducerea anterogradă pe calea
accesorie in RS
– Constantă - unda delta permanenta (uneori variabilă - efect de
acordeon)
asimptomatica
– Conducere intermitenta (unda delta intermitent)

– Aparent absentă - posibila pentru perioade indelungate ??


(fuziune)

• Tahiaritmii dependente/asociate = SINDROM WPW:


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

– Reintrare atrioventriculara antidromica simptomatica


– FA ,,preexcitată”

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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 (orientativă in dg¹TRNAV)

• 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
q tahiaritmie regulata cu QRS largi prin

prezenta undei delta

q raspuns ventricular rapid > 180-200/min

q mecanism:

q Conducere anterograda pe calea accesorie


q Conducere retrograda prin NAV

q dg diferential cu TV monomorfa sustinuta

q Risc crescut de moarte subita cardiaca in

caz de aparitia FA ® FV

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TSV in sdr. WPW cu conducere antidromica

vTahiaritmie 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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IV beta blockers, diltiazem, verapamil in
Guideline
orthodromic AVRTfor may
the be
Management
considered. of Adult Patients With Su
Table 16 Therapy of AVRT due to manifest or cular beta
Tachycardia report major complication
314 – 319 rates after
IV digoxin, blockers, diltiazem,
concealed accessory pathways
EHRA 2016 quency
verapamil
potentially
and,catheter ablation of are
possibly, amiodarone
respectively. 2
harmful in Although
3.0% and 2.8% for AVNRT a
these rates are higher than mo
patients with
Recommendation Reference
................................................................................ pre-excited
encedAF. electrophysiologists have in daily practice, in
Acute therapy Chronicmeta-analysis
therapy AVRT still carried a mortality rate of 0.1% a
320 – 322
Vagal manoeuvres (Valsalva and carotid 66 – 69 Catheter ablationablation,
frequency of the accessory
whereas there was no procedural-rel
sinus massage), preferably in the supine pathway is recommended in patients with
tality for AFL or AVNRT.244 In the recently publish
position, are recommended as the symptomatic AVRT and/or pre-excited
first-line approach to achieve SVT AF.a American Catheter Ablation Registry there was one dea
termination. However, reversion rates mortality)
Catheter ablationfollowing ablation
of concealed of a right
accessory accessory pathway
244 – 247

range from 45.9 to 54.3%. pathways may be considered in


Adenosine is recommended for 71,72,178 Chronic patients
symptomatic pharmacological therapy
with frequent
conversion to sinus rhythm but should be episodes of Ic
Class AVRT
antiarrhythmic drugs which act mainly on access
used with caution because it may 275 – 277,279,323,324
Oral flecainide or propafenone,
way, in combination with beta blockers, may be used in
precipitate AF with a rapid ventricular preferably
with in combination with
pre-excitation anda beta
symptomatic antidromic AVRT
rate and even ventricular fibrillation. blocker, may be considered in patients
64 not candidates for ablation, and in whom structural or
Synchronized DC shock is recommended with AVRT and/or pre-excited AF, and
in haemodynamically unstable patients heart
without disease
structural or has been heart
ischaemic excluded. Small trials have rep
with AVRT if vagal manoeuvres or safety and efficacy of this drug therapy in the context of W
disease.
323,324
adenosine are ineffective or not feasiblea drome,
Oral beta but no randomized
blockers, diltiazem, or trials in this setting have
248 – 251

83,310,311
IV ibutilide, procainamide, propafenone or verapamil may Amiodarone
formed. be considered should
for chronic
be used only in symptomati
flecainide in antidromic AVRT may be management
who didofnotAVRT if no pre-excitation
respond to other antiarrhythmic drugs, and
considered. sign on resting ECG are present. 325,326
catheter ablation is not an option.
IV beta blockers, diltiazem, verapamil in 77,312,313
Oral amiodarone may be considered only 325,326
orthodromic AVRT may be considered. among patient in whom other AADs are
IV digoxin, beta blockers, diltiazem, 314 – 319 Concealed
ineffective andandother accessory
or contraindicated, path
verapamil and, possibly, amiodarone are Concealed
catheter ablation is accessory
not an option.pathways
potentially harmful in patients with Concealed accessory pathways are defined as connections
a
pre-excited AF. the atria
Recommendation and ventricles
supported that are capable
by strong observational evidenceof retrograde
and authors’ co
Chronic therapy consensus but no specific RCT.
only. The true prevalence is unknown because they are not
Catheter ablation of the accessory 320 – 322 R.V. - Tahiaritmii 2017 37
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A H V

V
A

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V A A V

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RF

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(Figure 11). and
Advances
AFL on thethe
scured inonce
baseselectrophysiologic
and separation
oftraditional AFLthe
ECG patterns.
scured on once
therate
Atrial mapping
bases of ECG
above
between haveAtrial
patterns.
or separation
traditional below
atrial tachycardia ob-ratestructures
other
between above
atrial
lated terior
or below
of RA,
the posterior
totachycardia
anisotropic extending
otherRAstructures
lated
conduction may
to also from
at anisotropic
the of the
play
crista thpo
acon
ro
termi

Flutter-ul atrial
240 bpm and the presence or 240 bpm
absence and
of anthe presence
isoelectric or absence
baseline of an isoelectric
superior turning baseline
point for the superior
activation turning
is point
variable, for
dep
scured the once and traditional
AFL on the basesseparation
and AFL between
on
of ECG patterns.
between
the
atrial
bases atrial
of
Atrial rate ECG
deflections,
above tachycardia
patterns.
or below
thatabsence
Atrial
were the
rate above lateddotoof anisotropic
or
other structures
diagnostic clues,
below the posterior RAconducti
other
thesuperior
presence
structures of
may also p
or absence
the
between240atrial
bpm deflections,
and the presencethat
240 were
bpm
or the
and
absence diagnostic
theof presence clues,
or
an isoelectric dobaseline thean
of presence
isoelectric
superior or absence
baseline
turning of transverse
point for the conduction
turning
activation acroso
is point
variab
and AFL on the bases
not discriminateof ECG
focal patterns.
not
(centrifugal Atrial
discriminate
activation)
between atrial fromrate
focalMRT above
(centrifugal
deflections,
between atrial deflections, that were the diagnostic clues, do mechan-
that or below
activation)
were from
terior
the RA MRT other
mechan- structures
terior RA of
the presence or absence of transverse conductioi
diagnosticwall and crista
clues, do terminalis.
the If wall
complete
presence the and
or post
crista
block
absenc
isms, since activation in slow conduction tracts associated with theterior
superior turning
isms, since
240 bpm and thenotpresenceactivation
discriminate orin slow conduction
focalabsence
(centrifugalof
not tracts
discriminate associated
an isoelectric
focal
activation) with
(centrifugal
from MRT mechan- the superior
baseline terior
activation) from MRTturning
superior
RA point
mechan-
wall isturning
the
and crista atrial roof,
terminalis. point
RA between
wall forpoin
and
If complete the
th
cris
areas isms,
of diseased myocardium, areas
since activation inisms, mayof
since
slow121 diseased
not be
activation
conduction myocardium,
recorded in
in slow
tracts the may
conduction
associated not
venabe
with tracts recorded
cava (SVC)
theassociated in
and the vena
tricuspid
with pointthe
superior turning cava
ring, but(SVC)
superior
is the in and
other
turning
atrial roof, the
cases
betw t
po
between atrial deflections,
ECG.121 that
areas of diseased myocardium,
were
ECG. the
areas of diseased diagnostic
may not myocardium,
be recorded may
clues, do
ing point
in thenot be vena may
recordedthe
be at
cava (SVC)
presence
different
in the ing or
point
levels of
vena cava
and the tricuspid
absence
may
the be at of
diffe
postero-lat
(SVC)
ring, but and
in othe
t
th
not discriminate ECG.
focal 121
(centrifugalECG. activation)
121
from MRT mechan- ing pointterior may beRA wall and
ing point
at different levelsmaycrista be at
of the terd
post
• Tahiaritmie regulata cu QRS inguste
isms, since activation in slow conduction tracts associated with the superior turning point is
• areas of diseased myocardium, may not be recorded in the
Produsa prin macroreintrare vena cava (SVC) and the tricu
121
ECG. ing point may be at differen
• Absenta undelor P, unde “F” 250-350 / min, fara Typical (CCW) flutter Typical (CCW) flutter
Typical (CCW) flutter Typical (CCW) flutter
linie izoelectrică:
– FlA “tipic” (antiorar): negative in DII, DIII, aVF

– FlA “tipic inversat” (orar): pozitive in DII, DIII, aVF


Typical (CCW) flutter
• FlA atipic: >350 / min, morfologie variabila și/sau
discordantă
– FA cu unde mari (,,fibrilo-flutter”)
Reverse (CW) typical flutter Reverse (CW) typical flutter

x2
– TA (m.a. tahic. de VP) Reverse (CW) typical flutter
Reverse (CW) typical flutter

x2
• 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 hipertiroidia
– Boala ischemica cardiomiopatii
– Alcoolism pericardite
– Valvulopatii Mi, Tri TEP, etc
– Postchirurgie cardiaca ptr CC

• Aritmie recurenta
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Fl.A: situatii speciale

Efectul adenozinei sau CSC

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FlA cu conducere 1:1
q sub efectul chinidinei
q produce “sincopa chinidinica”
efect anticolinergic pe NAV
scade viteza de depolarizare atriala R.V. - Tahiaritmii 2017 47
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Tratament
• acut
– cardioversie (SEE de energie joasa)
– antiaritmice de clasa I i-v
– CCB i-v
– βB i-v
– manevre vagale
– overdrive pacing (sonda esofagiana sau endocavitara
temporara)
• cronic
– profilaxie NB!: risc emboligen
• Controlul ritmului •TEE daca debutul este ≥48h si/sau
– curativ? incert
•anticoagulare
R.V. - Tahiaritmii 2017 50
Table 12 Therapy of atrial flutter/ macro-reentrant tachycardia

Recommendation EHRA 2016 Reference


...............................................................................................................................................................................
Acute therapy
Synchronised DC cardioversion is recommended for haemodynamically unstable patients with AFL/MRTa 131,132

133,134
IV anticoagulation may be considered in case emergency cardioversion is necessary. Anticoagulation should be continued for 4
weeks after sinus rhythm is established.
135 – 137
Intravenous beta blockers, diltiazem, or verapamil are recommended for acute rate control in patients with AFL who are
hemodynamically stable.
138 – 142
IV ibutilide or dofetilide, under close monitoring due to proarrhythmic risk, are recommended to cardiovert AFL.
143,144
Amiodarone may be considered to control ventricular rate in the acute setting.
145 – 148
Atrial overdrive pacing (via oesophagus or endocardial) may be considered for conversion of AFL/MRT.
149
Oral dofetilide may be considered to cardiovert AFL in non-urgent situations but only in hospitalized patients since there is a
proarrhythmic risk.
150,151
Class Ic antiarrhythmic drugs should not be used in the absence of AV blocking agents because of the risk of slowing atrial rate,
and leading to 1:1 AV conduction.
Chronic therapy
152,153
One-time or repeated cardioversion associated with AAD are recommended as a long-term alternative for patients with
infrequent AFL recurrences or refusing ablation.
153,154
In patients with recurrent or poorly tolerated typical AFL, CTI ablation is recommended for preventing recurrences with a low
incidence of complications.
155,156
In patients with depressed LV systolic function, ablation may be considered to revert dysfunction due to tachycardiomyopathy,
and prevent recurrences.
157,158
Atypical AFL/MRT appearing early (3 –6 months) after AF ablation may be initially treated by cardioversion and AAD, as it may
not recur in the long term.
159 – 164
In patients with recurrent atypical or multiple ECG AFL patterns, catheter ablation may be considered after documentation of
mechanism.
165 – 167
Given the high incidence of AF after CTI ablation for typical AFL, correction of ‘AF risk factors’ may be considered after ablation.
133,134,168 –
Oral anticoagulation may be considered for patients with episodes of atrial flutter.
170

133,134
Stroke prevention is recommended with the same indications as in AF amongst patients with typical FL and associated episodes
of AF.a R.V. - Tahiaritmii 2017 51
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RA
LA
T 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)
• Tratament:
– Neinfluentata de manevrele vagale
– Nu poate fi initiata prin stimulare atriala • de obicei rezistenta la tratament

– In general nu poate fi oprita prin “overdrive • Stop digitala; fenitoina


pacing” • b-blocante, potasiu, Ca-blocante
• Uneori asociat cu: • in BPOC = O2
– TahiCMP (10%)
– Disf(x) NSA
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P -/0 in aVL si + in V1
Da Nu

Focar AS Focar AD

ÅP in V1≥80 ms focare ÅP in D1≥50 µV Da P – in aVR Nu

nonPV Inel tricuspidian


Tahicardii
cristale Sept i-a

PVs stangi PVs drepte P– P+ P – sau ± P + in V5,6


D2,3 aVF D2,3 aVF in 3 deriv durata P in
V2-6 SVT < RS

P in D2 ≥ 100 µV infero-lateral supero-lateral


anular septal

superior

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isthmus in the R
Recommendation
EHRA 2016 Reference
................................................................................ sponsible for mo
Acute therapy opposite activat
Synchronised DC cardioversion is 65 wise perimitral
recommended for hemodynamically unstable the anterior LA
patientsa LA (or coronar
103,105
Adenosine may be used in terminating a complementary
non-reentrant AT or diagnosing the which return cyc
tachycardia mechanism.
70,76,106
Ablation of macr
IV beta blockers or verapamil or diltiazem
deployed at the
may be used for pharmacologic cardioversion
or rate control. ging, particularly
IV flecainide or propafenone may be used for 107,108 entrant circuits,
pharmacologic cardioversion in the absence are localized in
of structural or ischaemic heart disease. slow conduction
80,109
IV amiodarone may be used for ted signal which
pharmacologic cardioversion or rate control. and are the targ
110
IV ibutilide may be used for pharmacologic lowing entrainm
cardioversion of micro-reentrant AT.
distance from th
Chronic therapy
111,112
get closer to th
Catheter ablation is recommended, especially
Catheter abl
for incessant AT.b
113,114 rate,111,120 and
Beta blockers or verapamil or diltiazem may
be considered. in a randomized
107,108,115
Flecainide or propafenone in the absence of
structural or ischaemic heart disease may be Macro-ree
considered. R.V. - Tahiaritmii 2017 58
R.V. - Tahiaritmii 2017 59
R.V. - Tahiaritmii 2017 60
R.V. - Tahiaritmii 2017 61
R.V. - Tahiaritmii 2017 62
R.V. - Tahiaritmii 2017 63
R.V. - Tahiaritmii 2017 64
R.V. - Tahiaritmii 2017 65
R.V. - Tahiaritmii 2017 66
R.V. - Tahiaritmii 2017 67
R.V. - Tahiaritmii 2017 68
Fibrilatia atriala • QRS complet neregulate
• Frecventa ventriculara
• Absenta undelor P variabila:
• Unde “f” 450-600 / min; pot lipsi – F. rapida > 150/min
– Rapida > 100 / min
– FA cu “unde mici”
– Medie 60 – 100 / min
– FA cu “unde mari” – Joasa < 60 / min
R.V. - Tahiaritmii 2017 69
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


R.V. - Tahiaritmii 2017 70
Etiologia FA

• Valvulopatii RAA • Boala de nod sinusal

• Boala coronariana • Prolapsul valvular mitral

• Cardiomiopatii • Cardiopatia hipertensiva

• Hipertiroidie • Pneumopatii cronice

• asociata cu WPW • Etilism acut

FA IDIOPATICA: pana la 30% din cazuri !


R.V. - Tahiaritmii 2017 71
of spontaneous conversion is low and anticoagulation must

Clasificare
considered (see Section 4.1).
(3) Persistent AF is present when an AF episode either la
FA depistata prima oaralonger than 7 days or requires termination by cardioversi
either with drugs or by direct current cardioversion (DCC
(4) Long-standing persistent AF has lasted for ≥1 year wh
it is decided to adopt a rhythm control strategy.
(5) Permanent AF is said to exist when the presence of
PAROXISTICA PERSISTENTA
arrhythmia is accepted by the patient (and physician). Hen

(autolimitata) (ne-autolimitata)
rhythm control interventions are, by definition, not pursu
in patients with permanent AF. Should a rhythm cont

PERMANENTA
First diagnosed episode of atrial fibrillation

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 2017 72
R.V. - Tahiaritmii 2017 73
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

R.V. - Tahiaritmii 2017 74


Permanentă Paroxistică

Substrat Trigger

Page 9 of 6

strip (recorded at 25 mm/s) by six. The


,,Perpetuatori’’
ications is not different between short
d forms of the arrhythmia.12 It is there- ‘Upstream’ therapy of concomitant conditions
t paroxysmal AF in order to prevent Anticoagulation
Persistentă
(e.g. stroke). However, short ‘atrial high- Rate control
ed by pacemakers, defibrillators, or other
Antiarrhythmic drugs
first documented

ot be associated with thrombo-embolic


Ablation
r duration exceeds several hours (see
Cardioversion

y as an ischaemic stroke or TIA, and it is AF


most patients experience asymptomatic, silent paroxysmal persistent long-standing permanent
persistent
hythmia episodes before AF is first diag-
currence is 10% in the first year after the R.V. - Tahiaritmii 2017 75
Paroxistică Persistentă Permanentă

Durata

R.V. - Tahiaritmii 2017 76


Consecintele FA. Implicatii terapeutice

1. Pierderea sistolei atriale = ¯ DC


v SAo, CMHO CONVERSIA LA RS
v CMDil, CMR, CHT

2. Scaderea duratei diastolei = ¯ DC


v SMi, SAo, CMHO
REDUCEREA AV
v Boala coronariana

3. Riscul tromboembolic PROFILAXIA EMBOLIILOR


SISTEMICE
R.V. - Tahiaritmii 2017 77
sk factors.OAC
a
Vascular disease Age 65–74 1
pproach
Risc AVC in FA: CHA2DS2-VASc
tients
(b) comes
Risk factor-based

at maximum
(Note: ‘moderate
from variousapproachpublished

score isrisk’
expressed asana-
scoring system, with the acronym CHA2DS2-VASc
9 since(currently
a point based

defined
age may contribute 0, 1, or 2 points)
Sex category (i.e. female sex)
Maximum score
1
9
1, i.e.Riskonefactor risk factor) still derive significant Score (c) Adjusted stroke rate according to CHA2DS2-VASc score
OAC (or aspirin)
overCongestive
aspirinheart use,failure/LV
oftendysfunction
with low rates of 1
Nothing (or aspirin) CHA2DS2-VASc Patients (n = 7329) Adjusted stroke
Importantly,
Hypertension prescription of an antiplatelet 1 score rate (%/year)b
iatedAgewith >75 a lower risk of adverse events. 2
0 1 0%
score does
Diabetes not include many stroke risk 1
mellitus
e prevention in AF. AF ¼ atrial fibrillation; OAC ¼ oral anticoagulant; 1 422 1.3%
roke risk
on modifiers’
Stroke/TIA/thrombo-embolism
be found page 13. need to be considered 2
trokeVascular
risk disease
assessment
a (Table 8 ). 1 2 1230 2.2%
ors Age (previously
65–74 referred to as ‘high’ risk 1 3 1730 3.2%
troke Sexor
Table 10 TIA,(i.e.
category or
Clinical
femalethrombo-embolism,
characteristics comprising
sex) and the 1 4 1718 4.0%
s). HAS-BLED
The presence
Maximum score of
bleeding some
risk types
score of valvular 9 5 1159 6.7%
stenosis or prosthetic
(c) Adjusted stroke rate according heart valves) would
to CHA2DS2-VASc score
Letter Clinical characteristica Points awarded 6 679 9.8%
valvular’
CHA2DS AF patients
-VASc as ‘high
Patients risk’.
(n = 7329) Adjusted stroke
HscoreHypertension
2
1
ant non-major’ risk factors (previously rate (%/year)b 7 294 9.6%
Abnormal renal and liver
rate’ risk A factors)
0 function (1are pointheart
each) failure
1 [especially
1 or 2 0%
8 82 6.7%
systolic SLV1 Stroke dysfunction, defined 422 arbitrarily 1as 1.3% 9 14 15.2%
on fraction (LVEF) ≤40%],1230
B 2 Bleeding hypertension, or 1 2.2%
cally relevant
L 3 Labilenon-major’
INRs risk
1730 factors (pre- 1 3.2%
See text for definitions.
s ‘less validated
E 4 Elderly (e.g. riskagefactors’)
>65 years)
1718 include female 1 4.0% a
Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates
and vascular
D 5 Drugs disease
or alcohol(specifically,
(1 point each) myocardial
1159 1 or 2 6.7% of stroke in contemporary cohorts may vary from these estimates.
b
Based on Lip et al. 53
ortic plaque 6
and PAD). Note 679
that risk factors
Maximum 9 points
9.8% AF ¼ atrial fibrillation; EF ¼ ejection fraction (as documented by
he simultaneous presence of two or more echocardiography, radionuclide ventriculography, cardiac catheterization, cardiac
a
7 294 9.6%
Hypertension’ is defined as systolic blood pressure .160 mmHg. ‘Abnormal magnetic resonance imaging, etc.); LV ¼ left ventricular;
n-major’ risk factors would justify a stroke
8
kidney function’ is defined as the presence82 of chronic dialysis or renal
6.7%
TIA ¼ transient ischaemic attack.
gh transplantation
to requireoranticoagulation.
serum creatinine ≥200 mmol/L. ‘Abnormal liver function’ is
R.V. - Tahiaritmii 2017 78
9 14 15.2%
R.V. - Tahiaritmii 2017 79
1 for M, 2 for W* ≥2 for M, ≥3 for W

New! 1. NOAC is recommended in preference to a VKA (I).


2. Patients on VKA may be considered for NOAC if TTR is not
well controlled or if patient preference (IIb).
R.V. - Tahiaritmii 2017 80
Conversia la RS
INDICATII CONTRAINDICATII
• FA paroxistica cu Dh-d • AS, AD cu diametru > 50 mm
• FA recenta < 6 luni – 1 an • Durata > 6 luni – 1 an
• AS cu diametru< 45-50 mm • Antecedente AVC embolic
• FE VS > 40% • Tromboza AS/AAS fara
– Fara tromboza AS/AAS anticoagulare
– Fara tratament digitalic /
verapamil • Boala de nod sinusal
– Dupa anticoagulare corecta

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


R.V. - Tahiaritmii 2017 81
Similar to flecainide, propafenone should be avoided in patients than AF.

Conversia la RS: chimica sau electrica


• Tratament anticoagulant cu 3-4 sapt
Table 12 inainte
Drugs and doses for pharmacological conversion of (recent-o

• internare la UTIC: Drug Dose Follow-up dose R


Amiodarone 5 mg/kg i.v. over 1 h 50 mg/h P
– SEE: 260-360 J x 3 (max) A
Flecainide 2 mg/kg i.v. over N/A N
SAU 10 min, d
or in
– Antiaritmice: 200–300 mg p.o. d
v
Ibutilide 1 mg i.v. over 1 mg i.v. over 10 min after C
10 min waiting for 10 min p
W
Propafenone 2 mg/kg i.v. over N
10 min, d
or t
450–600 mg p.o. v
c
Vernakalant 3 mg/kg i.v. over Second infusion of 2 mg/kg i.v. S
Ia: CHINIDINA: max 2g / 24 ore 10 min over 10 min after15 min rest

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


a
Vernakalant has recently been recommended for approval by the European Medicines Agency for rapid car
• Dupa conversie: anticoagulare orala 4 saptamani
non-surgical patients; ≤3 days for surgical patients).68,69 A direct comparison with amiodarone in the AVR
Active-controlled, multi-center, superiority study of Vernakalant injection versus amiodarone in subjects with
amiodarone for the rapid conversion of AF to sinus rhythm (51.7% vs. 5.7% at 90 min after the start of treatm
• Fara dovezi clare de eficienta: sotalol, disopiramida, procainamida, digoxin, beta-
over 10 min), followed by 15 min of observation and a further i.v. infusion (2 mg/kg over 10 min), if necess
pressure ,100 mm Hg, severe aortic stenosis, heart failure (class NYHA III and IV), ACS within the previo
blocante, Ca-blocante should be adequately hydrated. ECG and haemodynamic monitoring should be used, and the infusion can b
R.V.
patients with stable coronary artery disease, hypertensive heart- disease,
Tahiaritmii heart failure. The clinical82
or mild 2017 pos
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
AA de clasa Ic preferabil asociate cu bB
FLECAINIDA: 100-200 mg/zi

• 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
R.V. - Tahiaritmii 2017 83
Terapia ablativă

PVI
PVp PVp PVp

R.V. - Tahiaritmii 2017 84


Selection of further rhythm control therapy after therapy failure to improve symptoms of AF

Failure of Failure of Failure of


dronedarone amiodarone catheter ablation
flecainide
propafenone
or sotalol

Patient choice Patient choice Patient choice

Amiodarone another Catheter ablation Hybrid therapy Repeat ablation another


(IA) AAD (IIa) (IA/IIaB) a (IIaC)c (IA/IIaB)a AAD (IIa)

Patient choice informed by AF Heart Team

AF surgery (IIaC)b Rate control (IB) Hybrid therapy (IIaC)c

R.V. - Tahiaritmii 2017 85


Controlul frecventei cardiace
- in FA permanenta sau in caz de contraindicatii de conversie -

1. Acut: 2. Cronic:
– Digoxin IV: de prima v Se prefera bB sau Ca
linie in IC blocante in afara IC
– Beta-blocante: v bB +/- digoxin in IC; de evitat
• Metoprolol: 5-15 mg IV
Ca-blocante
• Propranolol (1-5 mg)
v Bronhospasm: Ca-blocante
• Esmolol

– Blocante de calciu: v Greu de controlat AV la efort


• Diltiazem 20-25 mg IV
• Verapamil 5-15 mg IV

R.V. - Tahiaritmii 2017 86


TAHIARITMIILE

VENTRICULARE

Tahiaritmii cu QRS larg

R.V. - Tahiaritmii 2017 87


Aritmii V: def. și mec.
• Reintrare >90% (miocite restante în cicatrice,
fibroză)
• activitate declanșată – PDP și PDT
• automatism anormal - RIVA în IMA

de Bakker JMT et al. JECG 2007

de Bakker JMT et al. Circulation 1993


Attin M et al. Heart Rhythm 2008 88
R.V. - Tahiaritmii 2017
R.V. - Tahiaritmii 2017 89
Extrasistolele ventriculare

• QRS larg > 120 msec, precoce

• de obicei neprecedat de unda P, eventual unda P retrograda

• Daca nu depolarizeaza retrograd NSA: pauza compensatorie (P’P” = 2 PP)

• Uneori interpolate

• Incidenta creste cu varsta

• Cauze: stress, alcool, ischemie, miocardite, diselectrolitemii, medicamente

(AA, digoxina, etc)

R.V. - Tahiaritmii 2017 90


Clasificare si semnificatie clinica
• Clasa 0
• Clasa 1: monomorfe ocazionale < 1/’ sau 30/h
• Clasa 2: monomorfe frecvente > 1/’ sau 30/h
• Clasa 3a: polimorfe
• Clasa 3b: sistematizate (bi-/trigeminate)
• Clasa 4a: repetitive - cuplete
• Clasa 4b: repetitive 3 sau mai multe (TVNS)
• Clasa 5: R/T
Lown B et all, JAMA 1967
R.V. - Tahiaritmii 2017 91
Clasificare si semnificatie
clinica
DUPA FRECVENTA DUPA MORFOLOGIE
• Clasa 0 • Clasa A: monomorfe, monofocale
• Clasa 1: rare < 1 / h • Clasa B: polimorfe, polifocale
• Clasa C: repetitive
• Clasa 2: putin frecvente
– Cuplete
(1-9 / ora) – Salve (3-5 ESV)
• Clasa 3: intermediare • Clasa D: TV-NS (6 ESV ® 30
(10-29 / ora) sec)
• Clasa 4: frecvente (> • Clasa E: TV-S
30 / ora)
Myerburg et al. Am J Cardiol 1984;54:1355-8.
R.V. - Tahiaritmii 2017 92
Clasificare si semnificatie clinica

Potential maligne
Benigne Maligne
FE>35% FE<35%
ESV, TVNS,
Tip aritmie cuplete
ESV, cuplete, TVNS TVNS, TVS, FV

Moderat
Cardiopatie Lipsa Moderata
severa
Severa

Semnific. Sincopa,
Nu Nu Sincopa, MSC
hemodin. MSC

Risc MSC Minim Moderat Mare Major

Holter,
Evaluare ECG, Holter Holter
PVT, VRS
Holter, SEF

Morganroth et al. JACC 1986.


R.V. - Tahiaritmii 2017 93
Evaluarea riscului
• simptome (≅corelate cu alterarea h-d)
• ECG 12 derivații: RS (substrat) și ESV (localizare anatomică !)
• cardiopatia subiacenta
• cord N
• canalopatii
• BCI
• CMP (D,H,A)
• miocardite
• CpCo
• prezența și severitatea DVS/DVD/DbiV
• încarcătura aritmică (çè risc tahiCMP)
• răspunsul la efort (ECG de efort)
• util la cei cu cord aparent N
• controversat la cei cu CP structurale

R.V. - Tahiaritmii 2017 94


Tratamentul ESV
• ESV, cuplete, TVNS asimptomatice: b-blocante (FE > 40%)

– NU flecainida, encainida, propafenona pe cord ischemic și/sau


DVS

• ESV frecvente in IMA: amiodarona sau betablocant IV (-/+xilina)

• Cuplete sau TVNS pe cord patologic in afara ischemiei acute:

– Amiodarona

– Ablatie prin RF a focarelor endocardice:


• PALEATIVA (?)

• curativă

R.V. - Tahiaritmii 2017 95


Studiul CAST-I:
cresterea mortalitatii sub AA clasa I la pacienti cu IM in
antecedente

R.V. - Tahiaritmii 2017 96


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 (TVNS/TV)
• Disociatie atrioventriculara
– Activare atriala indepedenta sau conducere VA retrograda

• RISCURI:
– Degradare hemodinamica
– Degenerare in FV
R.V. - Tahiaritmii 2017 97
TV monomorfa:
diagnostic

• tahiaritmie regulata > 120/’


• QRS larg > 120 msec
• Disociatie AV
• Batai de fuziune
• Capturi ventriculare
•Criterii morfologice

R.V. - Tahiaritmii 2017 98


Criterii morfologice
pe baza derivatiilor V1,2 si V6
Semnul “urechii de iepure”

• Tip BRD TSV TV


– V1,2 rsR’ R(r’)
• R monofazic
• qR
• RsR’ cu R>R’

qR
– V6 rS
• rS

R/S > 1 R/S < 1

Wellens 1978
R.V. - Tahiaritmii 2017 99
R.V. - Tahiaritmii 2017 100
Criterii morfologice
pe baza derivatiilor V1,2 si V6
TSV TV
• Tip BRS
– V1,2 > 0.03
• R inițial larg >30 ms
• deflexiunea
descendenta S
– lentă > 0.06
– Incizură
Fără q q
– Încep. QRS ® nadir
S ≥ 60 ms

– V6
• Q sau QS

Kindwall, 1988 R.V. - Tahiaritmii 2017 101


R.V. - Tahiaritmii 2017 102
Absenta unui complex RS in DT

Da Nu

TV Interval R – S > 100msec ?

Da Nu

TV Disociatie A-V ?

Da
Nu

TV
Criterii de VT in V1,2 si V6 ?

Da
Nu

TV
TSV cu aberanta
R.V. - Tahiaritmii 2017 103
Criteriile Vereckei V4

Vi & Vt
Unda R in AvR
.

Vi > Vt => SVT


V2

Vi=0.3 Vt= 0.65


V3
Vi < Vt => VT

** *
*
Vereckei et al, Eur Heart J, ;28:589-600,
R.V.March 2007 2017 104
- Tahiaritmii
Disociatie AV ?

Da Nu

TV Unda R initiala in AvR ?

Da Nu

Morfologie QRS
TV “unlike BBB or FB” ?

Da
Nu

TV
Vi < Vt

Da Nu

TV TSV cu aberanta
R.V. - Tahiaritmii 2017 105
Dg ¹ TV vs. TSV cu QRS largi
• 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


NB!:
• 80% din tahicardiile cu QRS larg = TV (>90% la cei cu afectare structurală
cardiaca)
• !! trat unei TV cu medicatie pentru TSV o poate destabiliza
• orice tahicardie cu QRS larg si degradare h-d = SEE

• 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 (m.a. >160 msec)
R.V. - Tahiaritmii 2017 106
TV polimorfa

R.V. - Tahiaritmii 2017 107


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.
R.V. - Tahiaritmii 2017 108
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
– CPHT cu HVS hipoxia din BPOC
– Iatrogen: medicamente, diselectrolitemii, cateterism cardiac
– Sdr. de QT lung cu TdP SEE asincron
• Precedata sau nu de TV
R.V. - Tahiaritmii 2017 109
Tahicardia ventriculara
neparoxistica (RIVA) =
AUTOMATISM CRESCUT

R.V. - Tahiaritmii 2017 110


Tratament TV
• TV fara decompensare hemodinamica: AA
– Xilina, procainamida, amiodaron, bB in anumite situatii
– TV digitalice: fenitoina, xilina +/- AC anti-digitalici

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


– SEE sincron (> 50 J) pt cele monomorfe
– SEE asincron (>150J) pt cele polimorfe/FV
– IOT, MCE
– Bicarbonat iv daca CPR > 60 sec
– amiodaronă, Lidocaina iv (FV recur/rezistentă la SEE)

• Alternative:
– “Overdrive pacing” – TV monomorfe
– “thump version” (?!)

• Tratamentul cauzelor corectabile sau producatoare:


• Ischemia acuta
• Hipo K, hipo Mg
• BS excesiva
R.V. - Tahiaritmii 2017 111
Oprirea TV prin “overdrive pacing”

R.V. - Tahiaritmii 2017 112


Tratamentul profilactic al TV
• TVNS asimptomatica pe cord normal sau

patologic: b-blocante (FE > 40%) sau

amiodaron

– NU flecainida, encainida, propafenona (CAST)

• TVS:

– DEFIBRILATOR IMPLANTABIL

– Amiodarona.
TVNS cu deteriorare
– Ablatie prin RF a focarelor endocardice hemodinamica

– Chirurgia AA
R.V. - Tahiaritmii 2017 113
Defibrilatorul implantabil - ICD
Funcții anti-tahi è sonda VD± VS&,# Bradicardii è sonda VD ± AD* ±
? Diagnostic VS&,#
? Detecție ? Detecţia bradicardiei*
? Discriminare* ? Pacing antibradicardic
? Terapie ? TRC#
? Defibrilare/Cardioversie
? Pacing antitahicardic&

Indicatii:
Proflilaxie secundară Profilaxie primară
Orice CP structurală/electrică cu un BCI FEVS<35-40%
eveniment (MSC resuscitată, TV CMD FEVS <30-35% și NYHA ≥II
sustinută, FV) la care nu se decelează CMH
o cauză reversibilă CAVD
LQT
Brugada
SQT
R.V. - Tahiaritmii 2017 114
ICD reduc mortalitatea cu ~ 40%
atât in prevenţia primară cât şi în cea secundară
40
Control
54%
73% 51% ICD
30
39%
36%
20% 38% 0 31%
0
20
41% 0 23%

10

Prevenţie secundară Prevenţie primară

R.V. - Tahiaritmii 2017 115


Al-Khatib SM et al, Am Heart J 2005

R.V. - Tahiaritmii 2017 116


R.V. - Tahiaritmii 2017 117
R.V. - Tahiaritmii 2017 118
kinje network. Catheter ablation is curative in most affected patients

Catheter ablation
.5 Interventional therapy and procedural complications
arrhythmic aresubstrate cardioverter
rare. in patients with a history of myocardial infarc-
5.1 Catheter ablation tion198 or in patients presenting with epicardial VT.199
Polymorphic VT is defined as a continually changing Psychosocial QRS morph- m
4.5.2 Anti-arrhythmic surgery
ology often associated with acute myocardial ischaemia, acquired im
defibrillator
Catheter ablation for the treatment of sustained
or inheritable channelopathies or ventricular hypertrophy. In
monomorphic ventricular tachycardia Surgical ablation of ventricular tachycardia
some of these patients who are refractory to drug treatment,
Recommendatio
Purkinje-fibre triggered polymorphic VT may be amenable to cath-
eter ablation.200,201Classa Levelb Ref.c Assessment of psyc
Recommendations Classa Levelb Recommendations Ref.c
treatment of distres
Urgent catheter ablation is Surgical ablation guided Non-invasive
by imaging of cardiac structure, best doneinbypatients magnetic with rec
recommended in patients with resonance imaging, can be used to plan and guide
preoperative and intraoperative ablation
shocks.
I B 183
scar-related heart disease presenting electrophysiological mapping
procedures for VT.198 Mapping and ablation may beDiscussion performed of qualit
with incessant VT or electrical storm. Page 25 of 87 at an experienced centre is
performed
during ongoing VT (activation mapping). 212– A three-dimensional
recommended befo
recommended in patients with VT I B
Catheter ablation is recommended in electro-anatomical mapping system 215 aid in localization
may and of
during disease
abnor-
refractory to anti-arrhythmic drug
patients with ischaemic heart disease 184– after failuremal ventricular tissue and permits catheter ablation in sinus rhythm patients.
I B therapy of catheter
and recurrent ICD shocks
Correction of electrolyte imbalances is due to 186 by experienced
ablation (substrate ablation) without induction of VT that may prove
sustained
recommended
ESC VT. in patients with
Guidelines I C 179
electrophysiologists. Page 29 of 87
haemodynamically unstable. A non-contact mappingICD a
¼ implantable
system may car
recurrent VT or VF.
Catheter ablation should be considered Class of recommenda
Surgical ablation at be the utilized
time of cardiac in patients with haemodynamically unstablebLevel VT.ofSeveral
evidence.
after
Oral atreatment
first episode with ofbeta-blockers
sustained VT in 184–role
surgery in the relief
(bypass or of symptoms
valve surgery) and
may the
be reduction of arrhythmic c
Therapy with sodium channel blockers IIa B 130 techniques, including point-by-point 216, ablation at the exit site of the
Reference(s) supporti
patients
should be with ischaemic
considered
(class heart the
during
IC) is not recommended disease
to 186, episodes
considered in inpatients
this group withof patients.
clinically IIb C
257, For symptomatic (PVCs or 217
and an ICD.
hospital prevent sudden death in patients with
stay and continued thereafter III
IIa B
B131 documented VT or re-entry
VFbut after circuit
failure of (scar
not life-threatening dechanneling),
arrhythmias deployment of linear lesion
2818 CAD or who survived myocardial 259 , short and slow NSVT), amiodarone is the drug of choice since it
in all ACS infarction.
patients without catheter ablation. sets or ablation of local abnormal ventricular activity to scar hom-
suppresses arrhythmias without worsening prognosis.293,294
ESC Guidelines

AMI
ICD ¼ implantable cardioverter defibrillator; VT ¼ ventricular tachycardia. 5.3.4 Catheterogenization,
contraindications.
260
can be used.202 – 205 Epicardial mapping and ablation are
CAD ¼ coronary artery disease; VA ¼ ventricular arrhythmia.
more
Post-MI
ablation
5.1.3.2 Use of anti-arrhythmic
VT often
drugs in acute coronary
required ininfarction,
patientsoften with dilated cardiomyopathy
Controlled defibrilla
a
Class of recommendation.
Radiofrequency a catheter
Reprogramming
Class of recommendation. ablation
a previously at a
implanted VF ¼ ventricular
VT occurs fibrillation;
in 1– 2% of ¼ ventricular
patients late after tachycardia.
myocardial
b a syndromes—general considerations
Level of ICD
Levelshould
evidence.
b be considered to avoid IIa C 272 Class of recommendation. 206 207
c c
of evidence.
specializedunnecessary
ablationICD centre
shocks.
Reference(s) supporting
followed by
recommendations. b
after an interval
Electrical (DCM)
of
cardioversionseveral oryears. or ARVC
Recurrent
defibrillation can undergoing
VTintervention
is the be treated effect-VT ablation. Potential
of choice qualitycomplica-
of life in rec
Reference(s) supporting recommendations. Level ofively
evidence.
with catheter ablation, which dramatically
1,271 reduces VT recur- 223,224
the implantation of an ICD should be c
to acutely terminate
tions VAs in ACS
ofseries patients.
epicardial Early
puncture and (possibly i.v.)
ablation are damage in to
controls.
the coron- N
ICD implantation or temporary use of a 261–administration
Reference(s)
rence supporting recommendations.
in smallof patient
beta-blockers cantreated
help in specialized
prevent recurrent centres.
arrhyth-
considered WCDin patients with
may be considered recurrent
,40 days after IIa C (5– 41%) are left
commo
The role of anti-arrhythmic drugs in the prevention of SCD in post- 267 mias.
myocardial infarction in selected patients Whether257,269,271
primary ary vasculature
ablation
Anti-arrhythmic of well-tolerated or inadvertent
drug treatmentsustained puncture of surrounding
withmonomorph-
amiodarone organs,
VT, VF or electrical
myocardial storms
infarction despite
patients with preserved ejection 170,
fraction is
5.1.1 Patients with
(incomplete scar-related
revascularization, d
heart disease
IIb C
273
ic VT in be
should patients with
phrenic
considered anonly
LVEFnerve
if.40%
episodes without
palsy
of VTaor
backup ICDfrequent
or significant
VF are is bene-bleeding resulting nounced in patients
in pericardial
complete revascularization
limited. MostLVEF
pre-existing of the data and
dysfunction,come optimal
from the CAST study,129
occurrence which ficialcan
and deserves
no longerfurther study. Untilby
be controlled then, ICD implantation
successive should be
electrical cardiover-
atheter
medicalablation
treatment.
showed has
of arrhythmias
that evolved
sodium
.48 h after theinto
channel onset an important
of
blockers (class IA and treatment In the option
IC agents) era of transvascular
considered in survivors 1,271 catheter ablation for the treatment of
tamponade. of Intravenous
a myocardiallidocaine
infarctionmaysuffering from sus-
shocks (e.g. more th
sion or defibrillation. be considered
ACS, polymorphic VT or VF). VA, theVT requirement for surgical ablation has become
r Transvenous
patients increase
with mortality
scar-related after myocardial
heart disease infarction. Class II drugs
presenting with tained
for or VT or VF
recurrent Patients
in the
sustained absence
VT or VF with
ofnotacuteVT related
ischaemia,
responding toeventoafter suc- a rarity.
post-myocardial
beta-blockers scarquently
tend togohave unrecog
a
ICD catheter
implantation
(beta-blockers) overdrive
havefor the primary
an established role in reducing mortality in cessful catheter ablation. 261 – 265
274,Anatomically on guided LV aneurysmectomy was first described While immediate
with VT m
or amiodarone or in the case of contraindications to amiodarone.
F. stimulation
Data from two ofbe
should
prevention
post-myocardial prospective
SCDconsidered
is generally
infarction ifrandomized
not
patients is IIIreducedmulticentre
VTwith ALVEF and this
trials better outcome following
In patients with recurrent VT or VF triggered by premature ven-
catheter ablation than patients
indicated ,40 days after myocardial 275 .50 years ago. Large aneurysms may be accompanied by 208 VAs, vice firing, multi-
treating p
utcome
frequentlyin patients
recurrent
protective with
despite
role may alsoischaemic
use ofin patients
persist heart IIadisease
with preserved Cdemonstrated
LVEF, tricular complexdue (PVC)to non-ischaemic
arising from partially injured cardiomyopathy.
Purkinje fibres, Five prospective
infarction. 6. Therapies for patients with
decreases the likelihood ofand map-guided resection of the and aneurysm not only improves The levels of distres
but their effect on SCD is unproven. Finally, the class III agent amio- 261 – 265
atanti-arrhythmic
catheter ablation drugsfor andVT catheter
darone has not been shown to reduce SCD in post-myocardial
subsequent catheter ablation
left ventricular
is very effective
centre studies
dysfunction
should be considered
have evaluated the- role
R.V. of catheter
Tahiaritmii 2017 ablation in the119
(see section 6.3.2).
nd may be the consequence or cause of LV dysfunction. PVCsblocker treatment alone [HR 0.27 (95% CI 0.14, 0.52), P , 0.001] lack of RCTs comparing catheter ablatio

org/ by guest on August 16, 2016


and
Treatment of patients with left ventricular dysfunction

PVC and structural


uns of NSVT in subjects with structural heart disease contribute andtosotalol [HR 0.43 (95% CI 0.22, 0.85), P ¼ 0.02]. However, drug substrate-based approach. In addition, there
Table C. Cardiac
n increased mortality risk, and .10 PVCsa per hour or runs of
resynchronization
discontinuation therapy
was more frequent in patients and
taking premature
sotalol or a com-ventricular respect complex
to the ideal procedural endpoint. W
defibrillator
NSVT are an acceptable marker of increased risk. in the primary
344 prevention of sudden
bination of amiodarone and a beta-blocker. The rates of study drug
If patients clinical VTs should be attempted, non-inducib

heart disease/LVD
death in patients
re symptomatic due to PVCs or NSVTs, or if PVCs or NSVTs con- in sinus rhythm with mild (New York
discontinuation at 1 year were 18.2% for amiodarone, 23.5% for so- lation may be the preferred procedural endp
a b
Heart Association class II) heart failure Recommendations Patients may Class
present Level Ref.c storms
with electrical
ribute to reduced LVEF (‘tachycardia-induced cardiomyopathy’), talol and 5.3% for beta-blocker alone.
In the SCD-HeFT trial, patients with LV dysfunction ESC
In patients with
and Guidelines acutely terminate this potentially life-threatin
frequent symptomatic
NYHA
miodarone or catheter ablation should be considered.
A high PVC burden (.24%) in patients with LV dysfunction and classa II or III bHF received PVC or
conventional HF therapy, conventional NSVT: shown to decrease the rate of recurrent ele
Recommendations Class Levelc Ref.d when compared
ather short coupling interval of the PVCs (,300 ms) suggest therapy plus amiodarone or conventional therapy and a single-
– Amiodarone should be considered. IIa with medical
B treatment
64 onl
33% in the control group to 12% in the ablation arm. Furthermo
VC-induced cardiomyopathy. CRT-D 342 is recommended
In such to reduce
patients, catheter
64
chamber ICD. Compared with conventional –HFCatheter
ablation therapy,ablation
the add- related to post-myocardial scar tend to have
should be ICD shocks decreased from
the rate of appropriate 341–31% to 9% fo
an suppress PVCs and restoreall-cause mortality
LV function. 341 in patients with a
ition of amiodarone did not 148,
increase mortality.considered. lowing catheter IIaablationBthan patients with VT
lowing catheter ablation. 343
QRS duration ≥130 ms, with an LVEF 322, cardiomyopathy. Five prospective studies hav
≤30% and with LBBB despite at least 323, The Ventricular
Catheter ablation should be Tachycardia
considered Ablation in Coronary Heart Disea
I A catheter ablation in the treatment 341–of sustaine
3 months of optimal pharmacological 325, in patients with LV dysfunction
(VTACH) study prospectively randomized IIa Bpatients with previo
6.3.2 Catheter ablation ticenter Thermocool study reported 343 an acute
therapy who are expected to survive 327, associated with PVCs. infarction, reduced ejection fraction (≤50%) a

Sustained VT
6.3 Sustained ventricular tachycardia myocardial
at least 1 year with good functional 329
as abolishment of all inducible VTs, of 49% an
haemodynamically stable VT to catheter ablation or no addition
.3.1 Drug therapy status. Prevention of ventricular tachycardia recurrences in from VT of 53% over 1886 months of follow-up
therapy, NSVT
LV ¼ left ventricular; apart ¼from subsequent
non-sustained ICD.tachycardia;
ventricular The primary
PVC ¼ endpoi
patients with left ventricular dysfunction and sustained Multi Center Investigators Group study, acu
CRT-D may be considered to prevent premature ventricular complex.
was time to first recurrence of VT or VF. The rate of survival fr
Treatment of patients with left ventricular ventricular tachycardia elimination of all inducible VTs, was achieved
for HFdysfunction
a
hospitalization in patients with a Class of recommendation.
from recurrent VT over 24 months was higher in the ablation gro
and sustained recurrent monomorphic QRS duration ≥150 ventricular
ms, irrespective of 148,
b
Level of evidence. Freedom from recurrent VA was noted in 4
c compared
Reference(s) supportingwith the control arm [47% vs. 29%, HR 0.61 (95% CI 0.3
recommendations.
tachycardia QRS morphology, and an LVEF ≤35% 327– 8 + 5 months of follow-up. In the prospectiv
despite at least 3 months of optimal Recommendations
IIb A
329, Classa Levelb0.99), P c¼ 0.045]. The mean number of appropriate ICD shocks p
Ref. tion was acutely successful in 81% of patients
patient per year decreased from 3.4 + 9.2 to 0.6 + 2.1 in patien
pharmacological therapy who are Urgent catheter ablation in334 specialized PVCs and runs of NSVTcatheter current inVT
are common was achieved in 51% of patien
Recommendations expected to Class a
surviveLevel
b
at least 1Ref.
c
year with or experienced centres is recommended undergoing ablationpatients
(P ¼ 0.018). with LV dysfunction
Catheter ablation d
and may be the consequence Mapping
or cause and
of Ablation
LV in
dysfunction.Sinus Rhythm
PVCs andto Halt
in patients presenting with incessant VT I B not affect
183 mortality.
Optimization of HF medicationgood functional status. dia Trial (SMASH-VT) evaluated the role of c
or electrical storm resulting in ICD runs of NSVTOverall, in subjects with structural
theGuidelines
success rate ofheart
catheter disease contribute
ablation for VTto is dete
826according to current HF guidelines is ESC tients with previous myocardial infarction a
I C 8 shocks. an increased mortality
mined by the risk,
amount andof.10 PVCs perscar
infarct-related hour or runs
burden, of
represent
recommended in patients withCRT-D LV ¼ cardiac resynchronization therapy defibrillator; HF ¼ heart failure; Patients underwent ICD implantation 344 for
209VF,
dysfunction and sustained VT. LBBB ¼ left bundle branch block; LVEF ¼ left Amiodarone or catheter
ventricular ejection ablation
fraction; ms ¼ is NSVT are as anlow-voltage
acceptableareas marker of increased risk.
on electro-anatomic mappingIfsystems,
patients wh
64,156, stable VT or syncope with inducible VT during
milliseconds. recommended in patients with are symptomatic
dedicateddue to
unitsPVCs
for or
the NSVTs,
treatment or if
of PVCs
patients or NSVTs
undergoing con- cathet
I B 184–
Amiodarone treatment shouldaThese be recommendations refer specifically to recurrent ICD
CRT-D, since Amiodarone
shockson
studies due ortoeffect
the catheter
sustained ablation should 64, ology testing. The control 210 arm underwent IC
tribute to ablation
186 ofLVEF
reduced VT may positively impact outcome.
(‘tachycardia-induced cardiomyopathy’),
considered to prevent VT in patients IIa C 64 VT. be
of resynchronization in patients with NYHA class II only used CRT-D. considered after a first episode of IIa B 184– None of the patients received anti-arrhythmic
with or without an ICD. b
Class of recommendation. sustained VT in patients with anamiodarone
ICD. or catheter ablation
186 tion should
was be considered.
performed using a substrate-guided
ICD implantation is recommended in
c
Level of evidence. patients undergoing catheter ablation
A high ESCPVC burden
This
Guidelines
6.3.2.2
(.24%)normal
Bundle branch
inre-entrant
patients with LV
ventricular
tachycardia
dysfunction
potentials during and a rhy
sinus
d
Reference(s) supporting recommendations. I
rather C
short panel of
coupling interval of the PVCs (,300 ms) suggest
HF ¼ heart failure; LV ¼ left ventricular; ICD ¼ implantable cardioverter whenever they ICD satisfy eligibility
¼ implantable criteria defibrillator; VT ¼ ventricular tachycardia. for VT induction. During a mean follow-up o
cardioverter
experts 342
defibrillator; VT ¼ ventricular tachycardia. for ICD. aClass of recommendation. PVC-induced cardiomyopathy.was aInsignificant
such patients, catheter
reduction ablation
in the incidence
a
Class of recommendation. Two controlled trials randomized 3618 patientsLevel
withofmild HF to op-
evidence. b Prevention of ventricular tachycardia
341
recurrences in
nebLevel
treatment should be
of evidence. Amiodarone c
or catheterpharmaco-
ablation should can suppress patients
PVCs
64, andwith
restore LV function.
bundle branch re-entrant tachycardia
c timal pharmacological therapy plus an ICD orReference(s)
optimal supporting recommendations.
d to prevent VT
Reference(s) in patients
supporting IIa
recommendations. C 64 327,329 be considered after a first episode of IIa B 184–
ithout an ICD. logical treatment plus CRT-D. sustained VT in patients with an ICD. 186
The MADIT-CRT study329 enrolled 1820 patients Dependingwhoon themildly
were underlying substrate, catheter ablation for sus-
Recommendation Classa Levelb Ref.c
tained VT may result in acute
with a VT ¼6.3 termination and reduction of recur-
failure; LV ¼ left ventricular; ICDsymptomatic (NYHA class I or II) andICD
¼ implantable cardioverter who had an LVEF
¼ implantable ≤30%defibrillator;
cardioverter Sustained
ventricular tachycardia. ventricular
Catheter ablation tachycardia
as first-line therapy is
atients with LV dysfunctionQRS
VT ¼ ventricular tachycardia. with duration
or without ≥130 ms. The initial
HF presenting report
a
Class
with sus- of rent
showed VT
a episodes
34%
recommendation. in
reduction patients
in with structural heart disease.
commendation. b
Level of evidence.
6.3.1 Drug therapy
recommended in patients presenting
I C
345,
ained
dence.
VT should be treated theaccording
primary endpoint
to recentlyof all-cause
publisheddeath
c or HF events [25.3% vs. 17.2%
HF Reference(s) supporting recommendations.
with bundle branch re-entrant 346
uidelines,
s) supportingsimilar to patientsfor
recommendations. with LV vs.
ICD dysfunction
CRT-D; without
HR 0.66VT. 8
(95%InCI
add-
0.52, 0.84),6.3.2.1 Patients In
P ¼ 0.001]. with left ventricular dysfunction tachycardia.R.V. - Tahiaritmii 2017
a long- 120
ECG

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 121


Echocardiography

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 122


Rx

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 123


Substrate mapping

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VT on SHD Vatasescu Curs EP CNC Sinaia 2017 125
Spontaneous VT1 induction

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 126


Endocardial activation mapping

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 127


Endocardial mapping VT1

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 128


Rx

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 129


VT on SHD Vatasescu Curs EP CNC Sinaia 2017 130
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 131
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 132
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 133
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 134
VT2

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 135


VT on SHD Vatasescu Curs EP CNC Sinaia 2017 136
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 137
VT2 VT3 VT3 accelerated

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 138


VT on SHD Vatasescu Curs EP CNC Sinaia 2017 139
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 140
VT on SHD Vatasescu Curs EP CNC Sinaia 2017 141
Post ablation testing

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 142


1 week later

No arrhythmias, NYHA III

VT on SHD Vatasescu Curs EP CNC Sinaia 2017 143