Bradiaritmii !

i tahiaritmii
cu risc vital
Dr. Radu V!t!"escu
Pacing and Clinical Electrophysiology Lab., Cardiology Department
Clinic Emergency Hospital Bucharest
Bradiaritmiile
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Clasificare
Clasificare:
tulbur"ri ale ini#ierii $i/sau conducerii
impulsului electric la nivelul NSA
tulbur"ri ale sistemului de conducere
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Etiologie
Func#ionale (reversibile)
dezechilibru al SN vegetativ
intoxica#ii
diselectrolitemii
Organice
ischemie-necroz"
inflama#ie
fibroz"
boli infiltrative
boli degenerative
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Principii $i metode de tratament
orice bradiaritmie intens simtomatic"
necesit" cardiostimulare
Cardiostimularea
temporara
externa
mecanic"
electric"
intern"
permanenta
endocardic"
epicardic"
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Metode de investigare
Noninvazive
IHR (Frecven#a Cardiac" Intrinsec")
ECG diagramele ,,ladder
monitorizarea Holter
compresia de sinus carotidian
testul de inclinare
Invazive
studiul electrofiziologic (EPS)
dispozitive de monitorizare implantabile
(implantable loop recorder)
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Disfunc#iile sinusale
Bradicardia sinusal"
Opririle sinusale
Blocurile sino-atriale (BSA)
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Tratament

nl"turarea cauzei
atropin" sau preparate orale de
belladon"
implantarea de stimulator cardiac
permanent (de tip AAI sau DDD, n
func#ie de coexisten#a sau nu a
afect"rii NAV).
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Tulbur"ri ale sistemului de
conducere
BAV
Tulbur"ri de conducere intraventriculare
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BAV grad II
Mobitz I (sau cu perioade Luciani-Wenkebach):
n ! progresiv" dar decremen#ial" a intervalului PR, pn" cnd o b"taie atrial"
este blocat"
primul PR postbloc are acea$i valoare ca a ciclului de baz"
apare " progresiv" a RR.
QRS ngust # aproape ntotdeauna localizat supra- sau intranodal
QRS largi # EPS (frecvent blocul este infranodal)
Mobitz II:
PR este constant, intermitent este blocate un impuls la nivel AV
PP care include pauza este multiplu al PP de baz"
de obicei asociat cu BR sau bloc bifascicular (situa#ie n care aproape ntotdeauna
blocul este localizat intra- sau infrahisian)
foarte rar asociat cu QRS nguste (de obicei tot intra- sau infrahisian)
NB!: n prezen#a unor QRS nguste trebuie suspectat un BAV II Mobitz I cu
varia#ii minime ale PR
EPS confirm" de obicei sediul intra- sau infrahisian. Diferen#ierea este de tipul I
este important" ntru-ct tipul II frecvent progreseaz" n BAV complet.
BAV de gradul II tip 2/1:
Localizarea blocului poate fi sugerat" de tipul complexelor QRS (nguste sau largi)
$i probe de provocare (tipul I r"spunde de obicei la atropin" iv) dar cel mai corect
se face pe hisiogram".
BAV de grad nalt:
blocarea mai multor impulsuri consecutive (3/1, 4/1)
similar cu tipul Mobitz II ca localizare, dar poate fi simptomatic $i are poten#ial de
progresie mult mai rapid" c"tre BAV complet
excep#ional intranodal (asociat cu QRS nguste)
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BAV grad III
Clinic: bradicardie extrem", zgomotul de tun, sistola n
ecou

ECG:
nu exist" nici o rela#ie ntre undele P $i intervalele QRS,
care se succed regulat cu frecven#a generat" de focarul
de nlocuire (atriile $i ventriculii sunt disociate =
transmiterea impulsului de la A la V este complet blocat")
uneori la nivel atrial poate fi exista o aritmie (FlA sau FA)
morfologia QRS:
tipul A: complexe nguste, ritm mai stabil de 40-60 bpm,
sediul blocului intranodal
tipul B: complexe largi, ritm instabil de 20-40 bpm, risc de
oprire cardiac", sediul blocului intra- sau infrahisian

EPS localizeaz" cu precizie blocul: V este precedat de
H n tipul suprahisian $i este disociat de H n cel
infrahisian.
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Stimularea cardiac"
Camera
stimulat!
Camera
detectat!
Modul de
r!spuns
Func"ii
speciale
Func"ii
antitahicardice
V V I R P
A A T
D D D
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BAV
Clas l
1. BAV lll sau ll avansat la orice nivel anatomic asociat cu oricare din urmtoarele:
a. Bradicardie simptomatic ($ lCC)
b. Aritmii sau alte patologii al cror tratament induce bradicardie simptomatic
c. Asimtomatici dar cu asistol < 3 sec sau orice AV de ,,scpare'' < 40 bpm n stare de veghe
d. Dup abla|ia NAV
e. BAV postoperator anticipat ireversibil
f. boli neuromusculare cu BAV (myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy
and peroneal muscular atrophy) cu sau fr simptome.
2. BAV ll indiferent de tip si sediu dac este asociat cu bradicardie simptomatic.

Clas lla
1. BAV lll asimptomatic la orice nivel anatomic cu AV medie in stare de veghe < 40 bpm (m.a.
asociat cu cardiomegalie/lVS)
2. BAV ll tip 2 asimptomatic cu QRSingust (n prezen|a QRS larg devine clas l)
3. BAV ll tip 1 asimptomatic intra- sau infra-Hisian (descoperit la EPS efectuat pt alte indica|ii)
4. BAV l sau ll cu simptome de dissinergie A-V

Clas llb
1. BAV l cu PR<0.30 sec la pacien|i cu %VS si simptome de lCC la care " intervalului AV poate
ameliora hemodinamica ("p AS)
2. boli neuromusculare cu BAV l

Clas lll
1. BAV l asimptomatic
2. BAV ll tip 1 asimptomatic supra-Hisian
3. BAV reversibil si/sau improbabil a fi recurent (intoxica|ii medicamentoase, b. Lyme, OSA
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Bloc bi/trifascilular
Clas" I
1. BAV III intermitent
2. BAV II tip 2
3. BR alternativ
4. Descoperirea la EPS a unui interval HV % 100 ms sau a unui bloc
infra-Hisian nefiziologic la testarea dinamic" (pacing) la pacient
simptomatic

Clas" IIa
1. Sincop" f"r" leg"tur" clar" cu BAV dar la care alte cauze au fost
excluse (m.a. TV)
2. Boli neuromusculare
3. Descoperirea la EPS a unui interval HV % 100 ms sau a unui bloc
infra-Hisian nefiziologic la testarea dinamic" (pacing) la pacient
asimptomatic

Clas" IIb

Class III
1. Bloc fascicular f"r" BAV sau simptome
2. Bloc fascicular cu BAV I dar asimptomatic
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Tulbur"ri de conducere post IM recent
Clas" I
1. BAV III persistent precedat sau nu de tulbur"ri de
conducere intraventriculare
2. BAV II tip 2 persistent asociat cu BR cu sau f"r" PR
lung
3. BAV II tip 2 tranzitoriu asociat cu BR cu debut recent

Clas" IIa

Clas" IIb

Class III
1. BAV III sau BAV II f"r" BR
2. HBAS recent instalat sau prezent de la internare
3. BAV I persistent
Tahiaritmiile
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Semnifica#ie manifest"ri clinice
Simptome:
datorate "DC
cerebral: vertij-lipotimii & sincopa (' sd. Adams-Stokes)
cardiace: angina pectorala
renale: respira#ie acidotic" & com"
musculare: astenie fizic" / fatigabilitate
datorate stazei
pulmonare
periferice
Semne
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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Sdr. de preexcitatie
Cale accesorie de conducere intre atrii si ventriculi:
lntre AD si VD
lntre 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
ln cazul conducerii pe cale accesorie complexul QRS este
rezultatul fuziunii intre depolarizarea prin NAV si cea pe CA
ECG:
lnterval PR scurt < 0.12 sec
Aparitia undei delta
QRS larg > 0.12 sec
Unda T negativa
Pre-excita!ie + tahiaritmii prin reintrare = SlNDROM 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)
Tahiaritmii dependente/asociate = SlNDROM WPW:
Reintrare atrioventriculara ortodromica
NB!: (uneori prin CA ,,oculte - conducere doar retrograd V-A)
Reintrare atrioventriculara antidromica
FA ,,preexcitat
asimptomatica
simptomatica
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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 (????)
lntervalul RR in FA
Cu cat RR este mai scurt risc vital mare (<250 ms)
lnvaziv = 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 lV
Tahiaritmia antidromica, QRS largi:
Antiaritmice de clasa la, lc, lll
Profilactic, cronic:
Antiaritmice de clasa la, lc, lll
ABLATlE prin RF a caii / cailor accesorii
CONTRAlNDlCATE:
Digoxina
Blocantele de calciu
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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 Dll, Dlll, aVF
FlA tipic inversat (orar): pozitive in Dll, Dlll, 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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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 l i-v
CCB i-v
B i-v
manevre vagale
overdrive pacing (sonda esofagiana sau endocavitara
temporara)
cronic
profilaxie
Controlul ritmului
curativ?
NB!: risc emboligen
TEE daca debutul este #48h si/sau
incert
anticoagulare
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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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Consecintele FA. Implicatii terapeutice
1. Pierderea sistolei atriale = " DC
" SAo, CMHO
" CMDil, CMR, CHT
2. Scaderea duratei diastolei = " DC
" SMi, SAo, CMHO
" Boala coronariana
3. Riscul tromboembolic
CONVERSIA LA RS
REDUCEREA AV
PROFILAXIA EMBOLIILOR
SISTEMICE
Cardioversia
Candida$i:
instabilitate h-d #$ SEE
1-ul episod
episoade rare non-paroxistice
apari$ia/agravarea unor simptome datorit! apari$iei FiA (ex ICC)
de evitat:
asimptomatici (m.a. vrstnicii >80 ani)
risc de sngerare #$ anticoagularea pericardioversie riscant!
Predictori de insucces
FiA continuu # 1 an
AS foarte dilatat (% transvers >50 mm)
vrstnici >80 ani
Comorbidit!$i (DVS, HVS, HTA, valvulopatii, tireotoxicoz!, pericardite)
Recuren$e de FiA in ciuda tratamentului corect cu AAD
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Probleme speciale
cardioversie
Controlul AV (bB, CCB)
% confortul pacientului
poate facilita conversia spontan"
!! cardiopatia de fond
Timing vs anticoagulare
Risc embolic (!! CHA
2
DS
2
-VASc)
mic <24 h
acceptabil <48 h
ecocardiografia transesofagiana
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Controlul frecventei cardiace
- in FA permanenta sau in caz de contraindicatii de conversie -
1. Acut:
Digoxin lV: de prima
linie in lC
Beta-blocante:
Metoprolol: 5-15 mg lV
Propranolol (1-5 mg)
Esmolol
Blocante de calciu:
Diltiazem 20-25 mg lV
Verapamil 5-15 mg lV
2. Cronic:
" Se prefera (B sau Ca
blocante in afara lC
" (B +/- digoxin in lC; de evitat
Ca-blocante
" Bronhospasm: Ca-blocante
" Greu de controlat AV la efort
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Risc AVC in FA: CHA
2
DS
2
-VASc
(range, 2.03.0), unless contraindicated. Such a practice appears to
translate to better outcomes in AF patients in routine care.
10,51
As shown in Table 7, there is a clear relationship between
CHADS
2
score and stroke rate.
50
The original validation of this
scheme classied a CHADS
2
score of 0 as low risk, 12 as mod-
erate risk, and .2 as high risk.
The Stroke in AF Working Group performed a comparison of
12 published risk-stratication schemes to predict stroke in
patients with non-valvular AF, and concluded that there were sub-
stantial, clinically relevant differences among published schemes
designed to stratify stroke risk in patients with AF. Most had
very modest predictive value for stroke (c-statisticsas a
measure of the predictive valueof 0.6); also, the proportion
of patients assigned to individual risk categories varied widely
across the schemes. The CHADS
2
score categorized most subjects
as moderate risk and had a c-statistic of 0.58 to predict stroke in
the whole cohort.
In the present guidelines, we have tried to de-emphasize the use
of the low, moderate, and high risk categorizations, given the
poor predictive value of such articial categories, and recognize
that risk is a continuum. Thus, we encourage a risk factor-based
approach for more detailed stroke risk assessment, recommending
the use of antithrombotic therapy on the basis of the presence (or
absence) of stroke risk factors.
Support for this approach comes from various published ana-
lyses, where even patients at moderate risk (currently dened
as CHADS
2
score 1, i.e. one risk factor) still derive signicant
benet from OAC over aspirin use, often with low rates of
major haemorrhage. Importantly, prescription of an antiplatelet
agent was not associated with a lower risk of adverse events.
Also, the CHADS
2
score does not include many stroke risk
factors, and other stroke risk modiers need to be considered
in a comprehensive stroke risk assessment (Table 8).
Major risk factors (previously referred to as high risk
factors) are prior stroke or TIA, or thrombo-embolism, and
older age (75 years). The presence of some types of valvular
heart disease (mitral stenosis or prosthetic heart valves) would
also categorize such valvular AF patients as high risk.
Clinically relevant non-major risk factors (previously
referred to as moderate risk factors) are heart failure [especially
moderate to severe systolic LV dysfunction, dened arbitrarily as
left ventricular ejection fraction (LVEF) 40%], hypertension, or
diabetes. Other clinically relevant non-major risk factors (pre-
viously referred to as less validated risk factors) include female
sex, age 6574 years, and vascular disease (specically, myocardial
infarction, complex aortic plaque and PAD). Note that risk factors
are cumulative, and the simultaneous presence of two or more
clinically relevant non-major risk factors would justify a stroke
risk that is high enough to require anticoagulation.
This risk factor-based approach for patients with non-valvular
AF can also be expressed as an acronym, CHA
2
DS
2
-VASc [con-
gestive heart failure, hypertension, age 75 (doubled), diabetes,
stroke (doubled), vascular disease, age 6574, and sex category
(female)].
52
This scheme is based on a point system in which 2
points are assigned for a history of stroke or TIA, or age 75;
and 1 point each is assigned for age 6574 years, a history of
hypertension, diabetes, recent cardiac failure, vascular disease
(myocardial infarction, complex aortic plaque, and PAD, including
prior revascularization, amputation due to PAD, or angiographic
evidence of PAD, etc.), and female sex (Table 8). Thus, this
acronym extends the CHADS
2
scheme by considering additional
stroke risk factors that may inuence a decision whether or not
to anticoagulate (see Section 4.1.1).
Table 8 CHA
2
DS
2
VASc score and stroke rate
(a) Risk factors for stroke and thrombo-embolism
in non-valvular AF
Major risk factors Clinically relevant non-major
risk factors
Previous stroke, TIA,
or systemic embolism
Age > 75 years
Heart failure or moderate to
severe LV systolic dysfunction
(e.g. LV EF < 40%)
Hypertension - Diabetes mellitus
Female sex - Age 6574 years
Vascular disease
a
(b) Risk factor-based approach expressed as a point based
scoring system, with the acronym CHA
2
DS
2
-VASc
(Note: maximum score is 9 since age may contribute 0, 1, or 2 points)
Risk factor Score
Congestive heart failure/LV dysfunction 1
Hypertension 1
Age >75 2
Diabetes mellitus 1
Stroke/TIA/thrombo-embolism 2
Vascular disease
a
1
Age 6574 1
Sex category (i.e. female sex) 1
Maximum score 9
(c) Adjusted stroke rate according to CHA
2
DS
2
-VASc score
CHA
2
DS
2
-VASc
score
Patients (n = 7329) Adjusted stroke
rate (%/year)
b
0 1 0%
1 422 1.3%
2 1230 2.2%
3 1730 3.2%
4 1718 4.0%
5 1159 6.7%
6 679 9.8%
7 294 9.6%
8 82 6.7%
9 14 15.2%
See text for denitions.
a
Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates
of stroke in contemporary cohorts may vary from these estimates.
b
Based on Lip et al.
53
AF atrial brillation; EF ejection fraction (as documented by
echocardiography, radionuclide ventriculography, cardiac catheterization, cardiac
magnetic resonance imaging, etc.); LV left ventricular;
TIA transient ischaemic attack.
ESC Guidelines Page 14 of 61
(range, 2.03.0), unless contraindicated. Such a practice appears to
translate to better outcomes in AF patients in routine care.
10,51
As shown in Table 7, there is a clear relationship between
CHADS
2
score and stroke rate.
50
The original validation of this
scheme classied a CHADS
2
score of 0 as low risk, 12 as mod-
erate risk, and .2 as high risk.
The Stroke in AF Working Group performed a comparison of
12 published risk-stratication schemes to predict stroke in
patients with non-valvular AF, and concluded that there were sub-
stantial, clinically relevant differences among published schemes
designed to stratify stroke risk in patients with AF. Most had
very modest predictive value for stroke (c-statisticsas a
measure of the predictive valueof 0.6); also, the proportion
of patients assigned to individual risk categories varied widely
across the schemes. The CHADS
2
score categorized most subjects
as moderate risk and had a c-statistic of 0.58 to predict stroke in
the whole cohort.
In the present guidelines, we have tried to de-emphasize the use
of the low, moderate, and high risk categorizations, given the
poor predictive value of such articial categories, and recognize
that risk is a continuum. Thus, we encourage a risk factor-based
approach for more detailed stroke risk assessment, recommending
the use of antithrombotic therapy on the basis of the presence (or
absence) of stroke risk factors.
Support for this approach comes from various published ana-
lyses, where even patients at moderate risk (currently dened
as CHADS
2
score 1, i.e. one risk factor) still derive signicant
benet from OAC over aspirin use, often with low rates of
major haemorrhage. Importantly, prescription of an antiplatelet
agent was not associated with a lower risk of adverse events.
Also, the CHADS
2
score does not include many stroke risk
factors, and other stroke risk modiers need to be considered
in a comprehensive stroke risk assessment (Table 8).
Major risk factors (previously referred to as high risk
factors) are prior stroke or TIA, or thrombo-embolism, and
older age (75 years). The presence of some types of valvular
heart disease (mitral stenosis or prosthetic heart valves) would
also categorize such valvular AF patients as high risk.
Clinically relevant non-major risk factors (previously
referred to as moderate risk factors) are heart failure [especially
moderate to severe systolic LV dysfunction, dened arbitrarily as
left ventricular ejection fraction (LVEF) 40%], hypertension, or
diabetes. Other clinically relevant non-major risk factors (pre-
viously referred to as less validated risk factors) include female
sex, age 6574 years, and vascular disease (specically, myocardial
infarction, complex aortic plaque and PAD). Note that risk factors
are cumulative, and the simultaneous presence of two or more
clinically relevant non-major risk factors would justify a stroke
risk that is high enough to require anticoagulation.
This risk factor-based approach for patients with non-valvular
AF can also be expressed as an acronym, CHA
2
DS
2
-VASc [con-
gestive heart failure, hypertension, age 75 (doubled), diabetes,
stroke (doubled), vascular disease, age 6574, and sex category
(female)].
52
This scheme is based on a point system in which 2
points are assigned for a history of stroke or TIA, or age 75;
and 1 point each is assigned for age 6574 years, a history of
hypertension, diabetes, recent cardiac failure, vascular disease
(myocardial infarction, complex aortic plaque, and PAD, including
prior revascularization, amputation due to PAD, or angiographic
evidence of PAD, etc.), and female sex (Table 8). Thus, this
acronym extends the CHADS
2
scheme by considering additional
stroke risk factors that may inuence a decision whether or not
to anticoagulate (see Section 4.1.1).
Table 8 CHA
2
DS
2
VASc score and stroke rate
(a) Risk factors for stroke and thrombo-embolism
in non-valvular AF
Major risk factors Clinically relevant non-major
risk factors
Previous stroke, TIA,
or systemic embolism
Age > 75 years
Heart failure or moderate to
severe LV systolic dysfunction
(e.g. LV EF < 40%)
Hypertension - Diabetes mellitus
Female sex - Age 6574 years
Vascular disease
a
(b) Risk factor-based approach expressed as a point based
scoring system, with the acronym CHA
2
DS
2
-VASc
(Note: maximum score is 9 since age may contribute 0, 1, or 2 points)
Risk factor Score
Congestive heart failure/LV dysfunction 1
Hypertension 1
Age >75 2
Diabetes mellitus 1
Stroke/TIA/thrombo-embolism 2
Vascular disease
a
1
Age 6574 1
Sex category (i.e. female sex) 1
Maximum score 9
(c) Adjusted stroke rate according to CHA
2
DS
2
-VASc score
CHA
2
DS
2
-VASc
score
Patients (n = 7329) Adjusted stroke
rate (%/year)
b
0 1 0%
1 422 1.3%
2 1230 2.2%
3 1730 3.2%
4 1718 4.0%
5 1159 6.7%
6 679 9.8%
7 294 9.6%
8 82 6.7%
9 14 15.2%
See text for denitions.
a
Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates
of stroke in contemporary cohorts may vary from these estimates.
b
Based on Lip et al.
53
AF atrial brillation; EF ejection fraction (as documented by
echocardiography, radionuclide ventriculography, cardiac catheterization, cardiac
magnetic resonance imaging, etc.); LV left ventricular;
TIA transient ischaemic attack.
ESC Guidelines Page 14 of 61
a CHA
2
DS
2
-VASc score of 1) may consider aspirin rather than
OAC therapy.
4.1.4. Risk of bleeding
An assessment of bleeding risk should be part of the patient assess-
ment before starting anticoagulation. Despite anticoagulation of
more elderly patients with AF, rates of intracerebral haemorrhage
are considerably lower than in the past, typically between 0.1 and
0.6% in contemporary reports. This may reect lower anticoagula-
tion intensity, more careful dose regulation, or better control of
hypertension. Intracranial bleeding increases with INR values
.3.54.0, and there is no increment in bleeding risk with INR
values between 2.0 and 3.0 compared with lower INR levels.
Various bleeding risk scores have been validated for bleeding
risk in anticoagulated patients, but all have different modalities in
evaluating bleeding risks and categorization into low-, moderate-,
and high-risk strata, usually for major bleeding risk. It is reasonable
to assume that the major bleeding risk with aspirin is similar to that
with VKA, especially in elderly individuals.
56
The fear of falls may be
overstated, as a patient may need to fall 300 times per year for
the risk of intracranial haemorrhage to outweigh the benet of
OAC in stroke prevention.
Using a real-world cohort of 3978 European subjects with AF
from the EuroHeart Survey, a new simple bleeding risk score,
HAS-BLED (hypertension, abnormal renal/liver function, stroke,
bleeding history or predisposition, labile INR, elderly (.65),
drugs/alcohol concomitantly), has been derived (Table 10).
60
It
would seem reasonable to use the HAS-BLED score to assess
bleeding risk in AF patients, whereby a score of 3 indicates
high risk, and some caution and regular review of the patient is
needed following the initiation of antithrombotic therapy,
whether with VKA or aspirin.

Congestive heart failure,

Hypertension. Age > 75 years
Diabetes.
Stroke/TIA/thrombo-embolism
(doubled)
*Other clinically relevant
non-major risk factors:
age 6574, female sex,
vascular disease
e
A
ro rr
lly
k
ma
se
CHADS
2
score >2

OAC
OAC (or aspirin)
Nothing (or aspirin)
Age >75 years
>2 other risk factors*
1 other risk factor*
Yes
Yes
Yes
Yes
No
No
No
No
Consider other risk factors*
Figure 4 Clinical owchart for the use of oral anticoagulation for stroke prevention in AF. AF atrial brillation; OAC oral anticoagulant;
TIA transient ischaemic attack. A full description of the CHADS
2
can be found on page 13.
Table 10 Clinical characteristics comprising the
HAS-BLED bleeding risk score
Letter Clinical characteristic
a
Points awarded
H Hypertension 1
A
Abnormal renal and liver
function (1 point each)
1 or 2
S Stroke 1
B Bleeding 1
L Labile INRs 1
E Elderly (e.g. age >65 years) 1
D Drugs or alcohol (1 point each) 1 or 2
Maximum 9 points
a
Hypertension is dened as systolic blood pressure .160 mmHg. Abnormal
kidney function is dened as the presence of chronic dialysis or renal
transplantation or serum creatinine 200 mmol/L. Abnormal liver function is
dened as chronic hepatic disease (e.g. cirrhosis) or biochemical evidence of
signicant hepatic derangement (e.g. bilirubin .2 x upper limit of normal, in
association with aspartate aminotransferase/alanine aminotransferase/alkaline
phosphatase .3 x upper limit normal, etc.). Bleeding refers to previous bleeding
history and/or predisposition to bleeding, e.g. bleeding diathesis, anaemia, etc.
Labile INRs refers to unstable/high INRs or poor time in therapeutic range (e.g.
,60%). Drugs/alcohol use refers to concomitant use of drugs, such as antiplatelet
agents, non-steroidal anti-inammatory drugs, or alcohol abuse, etc.
INR international normalized ratio. Adapted from Pisters et al.
60
ESC Guidelines Page 17 of 61
R.V. - Bradi si Tahi cu risc vital 2012
TAHIARITMIILE
VENTRICULARE
Tahiaritmii cu QRS larg
R.V. - Bradi si Tahi cu risc vital 2012
TV: definitie si caractere ECG
Tahiaritmie regulata cu QRS > 120 msec:
ASPECT MONOMORF sau POLlMORF
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
RlSCURl:
Degradare hemodinamica
Degenerare in FV
R.V. - Bradi si Tahi cu risc vital 2012
Mecanismele TV
RElNTRARE:
Postinfarct
AUTOMATlSM ANORMAL:
lMA: TV neparoxistica (RlVA)
POSTDEPOLARlZARl PRECOCE Sl TARDlVE
TV digitalice
Sdr. de QT lung congenital
chinidina
R.V. - Bradi si Tahi cu risc vital 2012
TV monomorfa: diagnostic
tahiaritmie regulata >
120/
QRS larg > 120 msec
Disociatie AV
Batai de fuziune
Capturi ventriculare
Criterii morfologice
R.V. - Bradi si Tahi cu risc vital 2012
Criterii morfologice
pe baza derivatiilor V1,2 si V6
BRD like
V1,2
R monofazic
qR
RsR' cu R>R'
V6
rS
BRS like
V1,2
R ini!ial larg >40 ms
deflexiunea descendenta S
lent
lncizur
ncep. QRS & nadir S < 60 ms
V6
Q sau QS
R.V. - Bradi si Tahi cu risc vital 2012
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. - Bradi si Tahi cu risc vital 2012
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
R.V. - Bradi si Tahi cu risc vital 2012
Tratament TV
TV fara decompensare hemodinamica: AA
Xilina, procainamida, amiodaron, (B in anumite situatii
TV digitalice: fenitoina, xilina +/- AC anti-digitalici
TV cu hipoTA, lVS, angina, hipoperfuzie cerebrala:
SEE: sincron > 50 J
Alternative:
Overdrive pacing
thump version
Tratamentul cauzelor corectabile sau producatoare:
lschemia acuta
Hipo K, hipo Mg
BS excesiva
R.V. - Bradi si Tahi cu risc vital 2012
Oprirea TV prin overdrive pacing
R.V. - Bradi si Tahi cu risc vital 2012
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: PALEATlVA (?)
Chirurgia AA
DEFlBRlLATOR lMPLANTABlL
R.V. - Bradi si Tahi cu risc vital 2012
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 CPR, IOT
Bicarbonat EV daca CPR > 60 sec Lidocaina,
bretiliu, amiodaron EV
Corectarea cauzei
Profilactic: DI sau amiodaron
R.V. - Bradi si Tahi cu risc vital 2012
Tratamentul aritmiilor V maligne:
defibrilatorul implantabil
lndicatii:
Proflilaxie secundar
Orice CP structural/electric cu un
eveniment (MSC resuscitat, TV
sustinut, FV) la care nu se deceleaz
o cauz reversibil
Profilaxie primar
BCl FEVS<35-40%
CMD FEVS <30-35% "i NYHA <III
CMH
CAVD
LQT
Brugada
SQT
Avantaje tehnice:
Pacing anti-tahi si anti-bradi
Conversie defibrilare cu energie "
Stocarea ECG
" mortalitatea fata de amiodaron in AV
maligne simptomatice