Bradi Si Tahi Cu Risc Vital

Bradyarrhythmias
Classification
Classification:
Disturbances of the initiation and/or
conduction of the electrical impulse
in the SAN
Disturbances of the conductions
system
R.V. - Life threatening Brady & Tachy 2013
Etiology
Functional (reversible)
Impairment of the autonomous NS

Intoxication
Dyselectrolytemia
Organic
Ischaemia-necrosis
Inflamation
Fibrosis
Infiltrative diseases
Degenerative diseases
Significance clinical aspects

Symptoms:
Due to cardiac output
cerebral: dizziness-fainting syncope ( Adams-Stokes Sd.)

cardiac: angina
renal: Kussmaul breathing coma
muscular: fatigue
Due to congestion
pulmonary
peripheral
Signs
Of cardiac output
Of congestion
NB!: clinical picture depends on the mechanism of

the bradycardia and substrate
NB!: symptoms can be due to tachyarrhythmia
induced by bradyarrhythmia
Treatment principles and methods

Any intensely symptomatic
bradyarrhythmia requires cardiac pacing
Cardiac pacing
temporary
external
mechanical
electrical
internal
permanent
endocardial
epicardial
during syncope (symptom-arrhythmia correlation) is warran

(see below).
When an intermittent bradyarrhythmia is suspected but
proven, the suspicion should be corroborated by an ECG docum
tation of bradyarrhythmia or, alternatively, by laboratory testing
The most useful tests and their diagnostic yield are listed in Tab
Diagnosis
Noninvasive
ECG monitoring. Short-term monitoring (Holter, telemetry and

ternal loop recorder) is useful, soon after the index episod
patients who have very frequent symptoms (at least once
week). Since most patients with syncope have infrequent sy
toms, recurring over months or years, ILRs are often neces
to establish a diagnosis (Table 7). The diagnostic yield of ILR
function of the duration of the monitoring. The actuarial diagno
IHR (Intrinsic Heart Rate)

ECG ,,ladder diagrams
Holter monitoring / external LR / home telemetry
Table 6 Diagnosing bradyarrhythmic syncope after
Carotid sinus compressionthe initial evaluation: most useful tests
Prolonged electrocardiogram
Provocative (laboratory) test
Tilt-test
monitoring strategy
strategy
Holter
Carotid sinus massage
ECG exercise test
External loop recorder
Tilt table test
Invasive
Remote at-home telemetry

Implantable loop recorder
Electrophysiological study
Exercise test
ECG electrocardiogram
Electrophysiologic study (EPS)
Implantable monitoring devices (implantable
loop recorder)
EPS
SAN function
SAN automaticity: SNRT
Impulse conduction from the SAN: SACT
Conduction system status

Hissian electrogram at rest: HBE
Dynamical behavior: Wenckebach point
retrograde conduction (V-A)
ILR
05:41:41
05:42:09
05:42:23
11:24:04
11:24:14
11:24:24
Patients considered
for antibradycardia
PM therapy
Intermittent bradycardia
Persistent Bradycardia
Sinus node
disease
AV block
Sinus rhythm
Atrial fibrillation
ECGdocumented
Intrinsic
Paroxysmal AV block
Sino-atrial block and sinus
arrest (including brady-tachy
form of SSS)
Atrial fibrillation with slow
ventricular conduction
Suspected
(ECG-undocumented)
Extrinsic
(functional)
Vagal induced sinus

arrest or AV block
Idiopathic AV block
(adenosine-mediated)
BBB
Reflex
syncope
Unexplained
syncope
Carotid sinus
Tilt-induced
SAN dysfunction
Sinus bradycardia
Sinus arrests
Sino-atrial conduction block (SAB)
Treatment
Elimination of the cause
Atropine or other oral belladone
compounds
Permanent cardiac pacemaker
implantation (AAI or DDD if there is
coexisting AVN disease).
Conduction system disturbances

AV block
Intraventricular conduction disturbances
First degree AV block

Delay in AV conduction
ECG: PR interval > 0.20
NB!: PR interval needs to be adjusted by HR (PR
varies with 0,003-0,004 for every 10 bpm
variation of the cardiac rhythm;
Location:
supranodal/intranodal
exceptionally infranodal
Additional criteria:
A PR interval 0,30 sec = always functional

QRS morphology
Narrow QRS - almost always supranodal or intranodal ( AH

or exceptionally PA)
With BBB an EPS is necessary, sometimes sensitized by
procainamide, because in of patients the location of the
block is infranodal ( or x2 of H and/or HV)
Second degree AV block
Mobitz I (with Luciani-Wenkebach periods):
Mobitz II:
Progressive but decremential in PR interval, until one atrial beat is blocked

The first post-block PR interval is equal to the PR of the normal cycle
progressive of RR interval is present.
Narrow QRS almost always supranodal or intranodal
Wide QRS EPS (frequently the block is infranodal)
Constant PR interval, intermittently an impulse is blocked in the AVN

PP that includes the block is a multiple of the basic PP
Usually associated with BBB or bifascicular block (situation in which the block is
almost always intrahissian or infrahissian)
Very rarely associated with narrow QRS (usually also intrahissian or infrahissian)
NB!: in the presence of narrow QRS AV block 2nd degree type Mobitz I with
minimal PR variability is to be suspected
EPS usually confirms the intrahissian or infrahissian location. Differentiating from

type I is important, as type Ii frequently progresses to complete AV block.
Second degree AV block type 2/1:
High degree AV block:
Location of the block can be suggested by the type of the QRS (narrow or large)
and by challenge tests (type I usually responds to i.v. atropine) but most correctly
by a hissiogram.
Block of more than one consecutive impulses (3/1, 4/1)
Similar to type Mobitz II regarding location, can be symptomatic and potentially
progresses to complete AV block much faster
Exceptionally intranodal (associated with narrow QRS)
Third degree AV block

Clinical: extreme bradycardia, cannon heart sounds,
echo systole
ECG:
No relationship between P-waves and QRS complexes,

that succeed regularly, being generated by a replacing
pacemaker (atria and ventricles are dissociated =
transmission of the impulse from the atria to the
ventricles is completely blocked)
Sometimes within the atria an arrhythmia can occur (Afib
or AFlu)
QRS morphology:
A type: narrow complexes, more stable 40-60 bpm rhythm,

the site of the block is intranodal
B type: wide complexes, unstable 20-40 bpm rhythm, risk of
cardiac arrest, site of the block is intrahissian of infrahissian
EPS can precisely indicate the site of the block: V is

preceded by H in the suprahissian type and is
dissociated by H in the infrahisian type.
Cardiac pacing
Chamber
(s) paced
Chamber Type of
(s) sensed response
Special
functions
Antitachycardia
functions
RVA vs. septal stimulation
nms
ieis
0
e
yw
ler
mm-
at
a
a
e
oat
is
is
ac
gs
d
ay
severity of symptoms and the risk of progression to complete AV block.

Indication for pacing in intermittent documented
bradycardia
Indication for pacing in patients with persistent

bradycardia
Recommendations
Recommendations
1) Sinus node disease.
Pacing is indicated when
symptoms can clearly be
attributed to bradycardia.
Pacing may be indicated when
symptoms are likely to be due
to bradycardia, even if the
evidence is not conclusive.
Pacing is not indicated in
patients with SB which is
asymptomatic or due to
reversible causes.
4) Acquired AV block.
Pacing is indicated in patients
with third- or second-degree
type 2 AV block irrespective of
symptoms.
Class
Level
Ref.
1, 69
IIb
III
Class a
Level b
Ref. C
1) Sinus node disease

(including brady-tachy
form).
affected by sinus node disease
who have the documentation
of symptomatic bradycardia
due to sinus arrest or sinusatrial block.
1, 69
2) Intermittent/
paroxysmal AV block
(including AF with slow
ventricular conduction).
with intermittent/paroxysmal
intrinsic third- or seconddegree AV block.
IIa
5, 18, 19
3) Reflex asystolic
syncope.
Pacing should be considered
in patients 40 years with
in patients with second-degree
type 1 AV block which causes
symptoms or is found to be
located at intra- or infra-His
levels at EPS.
IIa
Pacing is not indicated in
patients with AV block which
is due to reversible causes.
III
syncopes and documented

symptomatic pause/s due to
sinus arrest or AV block or the
combination of the two.
brad
spec
DDD
brad
Forc
singl
caus
in p
patie
sync
gram
to re
dia o
In
(wit
men
com
paci
used
rapid
rate
has e
Ch
4) Asymptomatic pauses
(sinus arrest or AV
block).
in patients with history of
syncope and documentation
of asymptomatic pauses >6 s
due to sinus arrest, sinus-atrial
block or AV block.
IIa
5) Pacing is not indicated

in reversible causes of
bradycardia.
III
ge 10 of 49
ESC Guid
Sinus node disease
Persistent
Chronotropic
incompetence
No chronotropic
incompetence
1 choice:
DDDR + AVM
2 choice:
AAIR
1 choice:
DDD + AVM
2 choice:
AAI
AV block
Intermittent
Persistent
Intermittent
SND
No SND
AF
1 choice:
DDDR + AVM
2 choice:
DDDR, no AVM
1 choice:
DDDR
2 choice:
DDD
1 choice:
DDD
2 choice:
VDD
VVIR
3 choice:
AAIR
3 choice:
VVIR
3 choice:
VVIR
DDD + AVM
(VVI if AF)
Consider CRT if low EF/HF
igure 3 Optimal pacing mode in sinus node disease and AV block. AF atrial fibrillation; AV atrioventricular; AVM AV delay manageme
. to prevent unnecessary right ventricular pacing by means of manual optimization R.V.

of AV-interval
or programming
of AV
hysteresis;
SND si
Life threatening
Brady
& Tachy
2013
massage or EPS) and who were treated accord-
in those with HV interval of 70100 ms and 24% in those with HV

nch
(LBBB)
onin successive
ECGs or RBBB
ncopalblock
recurrence
was observed
7%; in coninterval .100 ms. The development of intra- or infra-His block at inIndication for cardiac pacing in patients with BBB
d in 33% of 52fascicular
untreated patients
(duringon
ILR onecremental
atrial pacing
is highly predictive of impending AV block, but is
anterior
block
ECG and
asso001). Mortality was 6% during 19 months of
rarely observed and has low sensitivity. For example, in the study by
fascicular
blockwithonthose
another
Patients
with
n-arrhythmic;
compared
who had ECG.
Gronda
et al. on 131
patients,27 HV prolongation of .10 ms was
rence in mortality rate between patients diagobserved in 6% and induction of second degree
AV block in 5% of
Recommendations
Class a
Level b
Ref. C
nwho
ofreceived
alternating
BBB
are
rare.
There
is
general
appropriate treatment.
cases. Complete AV block developed in 40% of these patients during
sbased
not associated
an increased incidence
of
a mean
follow-up
of 42 months. In five studies evaluating
the diagnostic
on with
anecdotal
casesthat
these
patients
1) BBB,
unexplained
nts with preserved cardiac function, a high incivalue of pharmacological stress testing for a total of 333 patients,27 31
syncope
and abnormal
oward
AV
Therefore
a high-degree
PM isAVusually
(about one
third block.
sudden) was
observed in
block was induced in 50 (15%) of the patients. During
EPS.
as the alternating BBB is detected, even in the
of syncope.w70 w73
with syncope, BBB and positive
BBB and unexplained syncope
of evidence is modest, there is a strong consensus

alternating BBB will benefit from cardiac pacing.
of 70 ms, or second- or
third-degree His-Purkinje
block demonstrated during
incremental atrial pacing
or with pharmacological
challenge.
EF <35%
>35%
ck, unexplained
syncope EF
and
non-diagnostic
ommendation 3)
5,w64 Consider
Consider
showed
half of patientsAppropriate
with Therapy
ICD/CRT-Dthat only about
CSM/EPS
e and BBB had a documentation of AV block
2) Alternating BBB.
of observation. In a recent(if negative)
randomized, singleAppropriate Therapy
with alternating BBB with or
Consider ILR
patients with bifascicular
block assigned to
without symptoms.
m pacing were compared with 49 patients with
3) BBB, unexplained
(if(DDI
negative)30 bpm). At 2
ssigned to inactive pacing
Clinical follow-up
syncope non diagnostic
re-syncope recurred in 45% of patients in the
investigations.
utic algorithm for patients presenting with unexplained syncope and bundle branch block (BBB). CRT-D cardiac resynchro5%
of
patients
in
the
treatment
group
(hazards
may be
defibrillator; CSM carotid sinus massage; EF ejection fraction; EPS electrophysiological study; ICDPacing
implantable
car- considered
r; ILR implantable loop recorder.
in selected patients with
05). Overall, a bradycardia was documented in
unexplained syncope and BBB.
symptomatic AVB, 2 brady-tachy, 1 sinus bradymanent AF with slow ventricular response),
4) Asymptomatic BBB.
Pacing is not indicated for BBB
overall incidence of 7.4% per year. Albeit the
in asymptomatic patients.
ardiac pacing was able to achieve a significant rems, only one out of five patients actually had a
25, 31
IIb
32
III
26, 33, 34
Lifethreatening
Brady
& Tachy
BBB bundle branchR.V.
block;- EPS
electrophysiological
study.
2013
Indication for cardiac pacing in patients with

undocumented reflex syncope
Recommendations
Class a
Level b
Ref. C
1) Carotid sinus
syncope.
with dominant cardioinhibitory
carotid sinus syndrome and
recurrent unpredictable
syncope.
3540
2) Tilt-induced
cardioinhibitory
syncope.
Pacing may be indicated in
patients with tilt-induced
cardioinhibitory response
with recurrent frequent
unpredictable syncope and
age >40 years after alternative
therapy has failed.
IIb
20, 21, 24
III
22, 23
3) Tilt-induced
non-cardioinhibitory
syncope.
Cardiac pacing is not
indicated in the absence of a
documented cardioinhibitory
Class of recommendation.
Level of evidence.
c
Reference(s) supporting recommendation(s).
b
2.4.3 Unexplained syncope (and fall)

The cause of syncope may remain unexplained at the end o
plete work-up performed in accordance with the recommen
C
Recommendations
Class afor diagnosis
Level b andRef.
of the 2009 ESC Guidelines
managem
syncope.w25
4) Carotid sinus
syncope.
In patients with carotid sinus
B
4143
Unexplained syncope and Ipositive adenosine
triphosph
syndrome, dual-chamber
pacing (Recommendation
is the preferred mode 1)
The role of the adenosine triphosphate test is controversia
of pacing.
studies showed no correlation between AV block induced
5) Tilt-induced
enosine triphosphate and ECG findings (documented
cardioinhibitory
during spontaneous syncope.w76 w78 Thus, the low pr
syncope.
value
of the test does not support its use as a solitary di
In patients
with
I
C
test for selecting
cardioinhibitory
vasovagal patients for cardiac pacing. Adenosine
phate
may, however,
syncope,
dual-chamber
pacing have a role to play in assessing patie
is the preferred
moderecurrent
of
unexplained,
syncope, presenting without or w
pacing.short prodrome and absence of cardiac and ECG abnor
suspected
to have an idiopathic paroxysmal AV block.4 In
6) Lower
rate and rate
multi-centre
hysteresis
should be trial performed on 80 highly selected elderly
with unexplained
programmed
in order to syncope, who had a positive response to in
C
achieveous
back-up
pacingof a bolus of IIa
injection
20 mg of adenosine
triphospha
function
which preserves
chamber
cardiac pacing significantly reduced 2-year syncopa
native heart
rhythm
and AV
rence from 69%
in the control group to 23% in the active
conduction.
For the above considerationswhether the efficacy of pac
due to adenosine triphosphate response or to other fact
a
patient selection)remains to be determined. Because of
Class of recommendation.
b
Level of evidence.
certainty
the mechanism
of &efficacy
pacing, th
R.V. - over
Life threatening
Brady
Tachy of
2013
Choice of pacing mode
Tachyarrhythmias
Significance clinical aspects

Symptoms:
Due to cardiac output
cerebral: dizziness-fainting syncope ( Adams-Stokes Sd.)

cardiac: angina
renal: Kussmaul breathing coma
muscular: fatigue
Due to congestion
pulmonary
peripheral
Signs
Of cardiac output
Of congestion
NB!: clinical picture depends on the mechanism of

the tachycardia and on their substrate
NB!: symptoms can be due to bradyarrhythmia
induced by tachyarrhythmia
Preexcitation syndrome
Accessory pathway between atria and ventricules:

Between RA and RV
Between LA and LV
Multiple pathways
Consists of embryonic myocardial tissue:

Not always symptomatic = does not always conduct
Extremely rapid conduction
Atrio-ventricular or ventriculo-atrial conduction
In case of conduction on an accessory pathway the QRS

complex is the fusion result of depolarization through the AVN
and the AP
ECG:
Short PR interval < 0.12 sec
Delta wave
Wide QRS > 0.12 sec

Negative T wave
Pre-excitation + re-entry tachyarrhythmias= WPW SYNDROME
Clinically possible situations in the

presence of AV accessory
pathways
Preexcitation sd. = antegrade conduction through the AP
during SR
Constant permanent delta wave (sometimes variable
concertina effect)
asymptomatic
Intermitent conduction (intermitent delta wave)

Apparently absent eventually for prolonged periods ?? (fusion)
Dependent/associated tachyarrhythmia = WPW SYNDROME:

Ortodromic A-V re-entry
NB!: (sometimes through concealed AP only retrograde V-A conduction)
Antidromic A-V re-entry

Pre-excited AFib
symptomatic
Intermitent delta wave
Permanent pre-excitation
Concertina effect:
delta wave of variable duration
AV re-entrant
tachycardia with
antidromic conduction
q Regular tachyarrhythmia with wide QRS
through presence of the delta wave
q fast ventricular response > 180-200/min
q mechanism:
q Antegrade conduction through the AP
q Retrograde conduction through the AVN
q Differential diagnosis with sustained

monomorphic VT
q Increased risk of sudden death -> in case
of Afib -> VFib
SVT in WPW sdr. with antidromic conduction
Regular tachyarrhythmia with wide QRS; no P-waves; dif. dg. with monomoprhic V
WPW sdr. with AFib
Risk of death evaluation in

WPW syndrome
Non-invasive ????:
Intermitent pre-excitation = low risk(??)
Dissapearance of pre-excitation upon procainamide
administration = low risk(?)
Stress-testing (????)
RR interval during AFib
The shorter the RR interval, the higher the risk of death (<250
ms)
Invasive = EPS:
Determining the refractory period
of the AP
Treatment of WPW sd.

Pre-excitation syndrome with no tachyarrhythmia (delta wave during SR):
follow-up?
Acute WPW syndrome (pre-excitation with tachyarrhythmia) ->
conversion to SR:
EES if hemodynamically unstable (!!Pre-excited AFib)
Ortodromic tachyarrhythmia, narrow QRS:
i.v. Adenosine
Antidromic tachyarrhythmia, wide QRS:

Class Ia, Ic, III antiarrhythmic drugs
Chronic, profilaxis:
Class Ia, Ic, III antiarrhythmic drugs
RF ablation of the AP/APs
CONTRAINIDICATION:
Atrial flutter
Regular tachyarrhythmia with narrow QRS
Through macro-reentry
No P-waves, flutter F waves with 250-350 / min, NO isoelectric line:
Typical AFlu (counter-clockwise): negative in DII, DIII, aVF
Inversed typical AFlu (clockwise): positive in DII, DIII, aVF
Atypical AFlu: >350 / min, variable and/or discordant morphology

AFib with large waves (,,fibrilo-flutter)
Atrial tachycardia (especially PV tachycardias)
Untreated: 2/1 AV conduction (~ 150 / min)
Possibly variable conduction: successive 2/1, 4/1, 3/1
Vagal maneuvers decrease HR stepwise through progressive increase of block degree
1:1 conduction of AFlu

q under quinidine
q induces quinidine syncope
anticholinergic effect on AVN
decreases the atrial depolarizationR.V.
velocity
- Life threatening Brady & Tachy 2013
Treatment
acute
cardioversion (low energy EES)

Class I i-v antiarrhythmic drugs
i-v CCB
i-v B
vagal maneuvers
overdrive pacing (temporary esophageal or endocavitary
lead)
chronic
profilaxis
NB!: risk of embolysm
cure?
TEE if onset 48h and/or

uncertaind
Rhythm control
anticoagulation
Atrial fibrillation
Absence of P waves
f waves 450-600/min; can be

absent
small waves Afib
large waves AFib
Completely irregular QRS

Variable HR:
Very rapid > 150/min

Rapid > 100 / min
Medium 60 100 / min
Low < 60 / min
Consequences of Afib. Influence on

therapy
1. Loss of atrial systole = Cardiac output
v Ao stenosis, OHCM
CONVERSION TO SR
v DilCM, RCM, CHT
2. Decrease in dyastole duration = Cardiac output

v Mi stenosis, Ao stenosis, OHCM
HR DECREASE
v Coronary artery disease
3. Thromboembolic risk
PROFILAXIS OF
SYSTEMIC EMBOLISM
Cardioversion
Candidates:
Hemodynamically unstable EES

First episode
Rare, non-paroxysmal episodes
New-onset/aggravated symptoms due to AFib (ex CHT)
To avoid:
Asymptomatic (especially elderly > 80 ani)
Bleeding risk risky pericardioversion anticoagulation
Predictors of failed cardioversion
Continous AFib 1 an
Extremely dilated LA (transverse > 50 mm)
Elderly >80 ani
Comorbidity (LVD, LVH, HBP, valve disease, thyrotoxicosis, pericarditis)
AFib recurrences in spite of correct AAD therapy
Special problems with

cardioversion
HR control (bB, CCB)
patient s confort
May facilitate spontaneous
conversion
!! Underlying cardiopathy
Timing vs anticoagulation
Embolic risk (!! CHA2DS2-VASc)
low <24 h
acceptable <48 h
TEE
HR control
- in permanent AFib or in case of cardioversion contraindications -
1. Acute:
IV Digoxin: first-line in
CHF
Beta-blockers:
Metoprolole: 5-15 mg IV
Propranolole (1-5 mg)
Esmolole
CCBs:
2. Chronic:
v B or CCBs are preferred in
the absence of CHF
v B +/- digoxin in CHF; CCBs
are to be avoided
v Bronchial spasm: CCBs
v Hardly controllable effort HR
Diltiazem 20-25 mg IV
Verapamile 5-15 mg IV
Stroke risk in AFib: CHADS2

CHADS2
Score elements:
Congestive
Heart Failure: 1 pt
Hypertension:
Age:
1 pt
1 pt
Diabetes:
Stroke
1 pt
of transient ischaemic
attack: 2 pt
Rockson SG, Albers GW. JACC 2004;43:929.
Age 6574
1
Vascular disease
sk factors.OAC
(b) comes
Risk factor-based
approachpublished
expressed asanaa point based
Sex category (i.e. female sex)
1
pproach
from various
scoring system, with the acronym CHA2DS2-VASc
tients
at maximum
moderate
defined
Maximum score
9
(Note:
score isrisk
9 since(currently
age may contribute
0, 1, or 2 points)
1, i.e.
risk factor) still derive significant Score
Riskone
factor
(c) Adjusted stroke rate according to CHA2DS2-VASc score
OAC
(or aspirin)
overCongestive
aspirinheart
use,failure/LV
oftendysfunction
with low rates of 1
CHA2DS2-VASc
Patients (n = 7329)
Adjusted stroke
Nothing (or aspirin)
Importantly,
prescription
of
an
antiplatelet
score
Hypertension
1
rate (%/year)b
iatedAgewith
>75 a lower risk of adverse events. 2
0
1
0%
score
does
not include many stroke risk 1
Diabetes
mellitus
e prevention in AF. AF atrial fibrillation; OAC oral anticoagulant;
1
422
1.3%
roke
risk
need to be considered 2
Stroke/TIA/thrombo-embolism
be found
on modifiers
page 13.
2
1230
2.2%
trokeVascular
risk disease
assessment
(Table 8).
a
1
ors Age
(previously
referred to as high risk 1
3
1730
3.2%
6574
troke
TIA,(i.e.
or
thrombo-embolism,
and the
Table
10
Clinical
characteristics comprising
Sexor
category
female
sex)
1
4
1718
4.0%
bleeding
risk
score
s). HAS-BLED
The
presence
of
some
types
of
valvular
Maximum score
9
5
1159
6.7%
stenosis
or
prosthetic
heart
valves)
would
(c) Adjusted stroke rate according
to CHA2DS2-VASc score
Letter
Clinical characteristica
Points awarded
6
679
9.8%
valvular
AF
patients
as
high
risk.
CHA2DS
-VASc
Patients
(n
=
7329)
Adjusted stroke
2
HscoreHypertension
1
rate (%/year)b
ant non-major
risk factors (previously
7
294
9.6%
Abnormal renal and liver
A factors)
1 or 2 0%
rate risk
[especially
0 function (1are
1
8
82
6.7%
pointheart
each) failure
systolic SLV1 Stroke
dysfunction, defined
422 arbitrarily 1as 1.3%
9
14
15.2%
on fraction
(LVEF) 40%],1230
hypertension, or
B 2 Bleeding
1 2.2%
cally relevant
risk
L 3 Labilenon-major
INRs
1 3.2%
1730 factors (preSee text for definitions.
a
s less validated
riskagefactors)
include
female
E 4 Elderly (e.g.
>65 years)
1
1718
4.0%
Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates
of stroke in contemporary cohorts may vary from these estimates.
and vascular
disease
(specifically,
D 5 Drugs
or alcohol
(1 point
each) myocardial
1 or 2 6.7%
1159
b
Based on Lip et al. 53
ortic plaque
and
PAD).
Note
that
risk
factors
Maximum
9 points
6
679
9.8%
AF atrial fibrillation; EF ejection fraction (as documented by
he simultaneous presence of two or more
echocardiography, radionuclide ventriculography, cardiac catheterization, cardiac
7
294
9.6%
a
Hypertension is defined as systolic blood pressure .160 mmHg. Abnormal magnetic resonance imaging, etc.); LV left ventricular;
n-major risk factors would justify a stroke
kidney function
is defined as the presence
8
82 of chronic dialysis or renal
6.7%
TIA transient ischaemic attack.
gh transplantation
to requireoranticoagulation.
serum creatinine 200 mmol/L. Abnormal liver function is
a
Stroke risk in AFib: CHA2DS2-VASc
14
15.2%
VENTRICULAR
TACHYARRHYTHMIAS
Wide QRS tachyarrhythmias
VT: definition and ECG

characteristics
Regulated tachyarrhythmia with QRS > 120 msec:
MONOMORPHIC or POLYMORPHIC ASPECT
C.p. 3 successive ventricular depolarizations with > 120/min

Variable duration: 3 QRS > 30 sec (hrs)
AV dissociation
Independent atrial activation or retrograde VA conduction
RISKS:
Unstable hemodynamics
Transition to VFib
VT mechanisms
RE-ENTRY:
PostMI
ABNORMAL AUTOMATICITY:
AMI: unparoxysmal VT (AIVR)
EARLY AND LATE POSTDEPOLARIZATIONS

Digitalis VT
Congenital long QT syndrome
Quinidine
Sustained monomorphic VT
usually RE-ENTRY
Monomorphic VT: diagnosis

Regular tachyarrhythmia >
120/
Wide QRS > 120 msec
AV dissociation
Fusion beats
Ventricular captured beats
Criterii morfologice
Morphology
leads V1,2 and V6

Rabbit ear sign
RBBB
V1,2
VT
SVT
rsR
R(r)
Monophazic R
qR
RsR cu R>R
V6
qR
rS
rS
R/S > 1
R/S < 1
Wellens 1978
Morphology
leads V1,2 si V6
LBBB type
V1,2
> 0.03
Wide initial r >30 ms

S wave deflection
slow
noch
bQRS nadir S 60
ms
TV
TSV
> 0.06
Fr q
V6
Q sau QS
Kindwall, 1988
wo RS in precordial leads
yes
no
R S > 100msec ?
VT
yes
No
VT
A-V dissociation?
Yes
VT
VT morphology V1,2 and V6 ?
yes
VT
No
No
SVT with aberancy
TV polimorfa
Polymorphic VT: torsade du pointes

EPD
Fast VT, transition to VFib
through EPD
with long QT or normal QT
Causes:
Long QT syndrome
hipo K, hipo Mg
Type Ia and III AAD
Treatment:
IV MgSO4
Overdrive pacing
Isuprel
Lidocaine, phenytoine
Long QT: AICD, bBlockers,
flecainide, stelectomy.
Dg VT vs. SVT with wide QRS
Wide QRS tachyarrhythmias:
VT
SVT with wide QRS
SVT + pre-existent BBB

SVT with aberrant conduction
SVT + AVRT through antidromic mechanism (WPW)
Dif. Dg. Possible on standard ECG in > 90% of cases
ECG criteria for differentiating VT from wide QRS SVT:

1. Fusion beats; ventricular captured beats
2. AV dissociation
3. VA retrograde conduction (retrograde P-waves)
4. QRS > 140 msec (160 msec = certainly VT)
5. Unique QRS morphology within precordial leads = VT
VT Treatment
VT with no hemodynamical instability: AADs
Lidocaine, Procainamide, Amiodarone, B in some cases
Digitalis VT: phenytoine, lidocaine +/- anti-digitalis antibodies
VT with low BP, LVD, angina, cerebral hipoperfusion:

EES: synchronous > 50 J
Alternative:
Overdrive pacing
thump version
Treatment of correctable or inducing causes:

Acute ischaemia
Hipo K, hipo Mg
Excessive sinus bradycardia
VT termination through overdrive

pacing
Prophilactic treatment of VT
Asymptomatic NSVT on normal/pathological myocardium:
Blockers (EF > 40%) or amiodarone
NO flecainide, encainide, sotalole after CAST
NSVT with hemodynamic deterioration or SVT:

Amiodarone
RF ablation of endocardial foci: palliative(?)
AA surgery
ICD
Ventricular
fibrillation
Fibrillation waves of different amplitude, in the absence of
QRS complexes
Mechanical asystole followed by electrical asystole
Shock, cardiac arrest and death in 3-5 minutes from onset
in the absence of CPR
Causes:
Acute ischaemia in AMI
spontaneous severe
ventricular arrhythmias
Cardiomyopathy (OHCM !)
AFib in WPW
CHT with LVH
COPD hypoxia
Iatrogenic: drug, dyselectrolytemia, cardiac catheterization
QT long syndrome with TdP
asynchronous EES
Preceded or not by VT:

Treatment:
Treatment of malignant
ventricular arrhythmias: ICD
Indications:
Secondary prophylaxis
Any structural/electrical
cardiomyopathy with one event
(resuscitated SCD, sustained VT,
VFib) in which no reversible cause is
observed
Primary prophylaxis
Technical advantages:
IHD with LVEF < 35-40%
Anti-tachy and anti-brady pacing
Dil. CM with LVEF < 30-35% and
Conversion-defibrillation with energy
NYHA III
HCM
ARVC
LQT Sd.
ECG storage
mortality compared to amiodarone in

malignant symptomatic ventricular
arrhythmias

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Bradyarrhythmias

R.V. - Life threatening Brady & Tachy 2013

Impairment of the autonomous NS

Significance clinical aspects

Due to cardiac output

cerebral: dizziness-fainting syncope ( Adams-Stokes Sd.)

NB!: clinical picture depends on the mechanism of

R.V. - Life threatening Brady & Tachy 2013

Treatment principles and methods

R.V. - Life threatening Brady & Tachy 2013

during syncope (symptom-arrhythmia correlation) is warran

ECG monitoring. Short-term monitoring (Holter, telemetry and

IHR (Intrinsic Heart Rate)

Remote at-home telemetry

R.V. - Life threatening Brady & Tachy 2013

Conduction system status

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

Vagal induced sinus

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

Conduction system disturbances

Intraventricular conduction disturbances

R.V. - Life threatening Brady & Tachy 2013

First degree AV block

A PR interval 0,30 sec = always functional

Narrow QRS - almost always supranodal or intranodal ( AH

R.V. - Life threatening Brady & Tachy 2013

Second degree AV block

Mobitz I (with Luciani-Wenkebach periods):

Progressive but decremential in PR interval, until one atrial beat is blocked

Constant PR interval, intermittently an impulse is blocked in the AVN

EPS usually confirms the intrahissian or infrahissian location. Differentiating from

Second degree AV block type 2/1:

High degree AV block:

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

Third degree AV block

No relationship between P-waves and QRS complexes,

A type: narrow complexes, more stable 40-60 bpm rhythm,

EPS can precisely indicate the site of the block: V is

R.V. - Life threatening Brady & Tachy 2013

R.V. - Life threatening Brady & Tachy 2013

RVA vs. septal stimulation

R.V. - Life threatening Brady & Tachy 2013

severity of symptoms and the risk of progression to complete AV block.

Indication for pacing in patients with persistent

1) Sinus node disease

syncopes and documented

5) Pacing is not indicated

R.V. - Life threatening Brady & Tachy 2013

Sinus node disease

Consider CRT if low EF/HF

. to prevent unnecessary right ventricular pacing by means of manual optimization R.V.

massage or EPS) and who were treated accord-

in those with HV interval of 70100 ms and 24% in those with HV

of evidence is modest, there is a strong consensus