BRADIARITMIE
Pacemaker
Sistema di conduzione
Fascio di
Bachmann
Nodo SA
Fascio di His
Branca Sinistra
Via internodale
superiore
Via internodale
media
Fibre di
Purkinje
Via internodale
posteriore
Nodo AV
Branca Destra
Disfunzione sinusale
Anomalie della formazione o della propagazione
dell’impulso sinusale
Pause
sinusali
Idiopatica (degenerativa)
Cardiopatie (ischemica,
ipertensiva, reumatica,
cardiomiopatie, malattie infiltrative,
collagenopatie)
Iatrogena (CCH, ablazione)
Trapianto cardiaco ortotropico
Neuromiopatie
Sindrome
tachi-bradi
ESTRINSECA
INTRINSECA
Bradicardia
sinusale
Insufficienza
cronotropa
Farmaci
Influenza autonomica
Disionie (K, Ca)
Ipotermia
Ipotiroidismo
Diagnosi
•  ECG
•  Basale
•  Monitoraggio ambulatoriale
•  Test da Sforzo
•  Modulazione autonomica
•  SEF
Sintomo o
non
sintomo?
Bradicardia sinusale
•  Persistente
•  Inspiegata
•  Inappropriata (ore diurne)
Pause sinusali
•  Arresto sinusale
•  Blocco SA
800 ms
1600 ms
CHAPTER 16
Sick Sinus Syndrome
Sindrome tachicardia-bradicardia
•  BS alternata a tachiaritmie atriali
Figure 16.8 Sinus arrest after termination of atrial fibrillation. After a single sinus beat atrial fibrillation recurs.
•  Pause automatiche
Figure 16.9 Bradycardia–tachycardia syndrome. Atrial tachycardia arises during sinus bradycardia.
response without AV nodal blocking drugs, suggesting coexistent impaired AV nodal
function.
Clinical features
Sinus arrest without an adequate escape rhythm may cause syncope or near-syncope,
depending on its duration. Tachycardias often produce palpitation, and subsequent
sinus node depression may lead to syncope or near-syncope as palpitation ceases.
Some patients will experience symptoms several times each day, whereas in others
symptoms will be infrequent.
Systemic embolism is common in the bradycardia–tachycardia syndrome.
Chronotropic incompetence
Impaired sinus node function may result in an inadequate increase in heart rate dur-
Incompetenza Cronotropa
•  Holter
•  Test da Sforzo
Modulazione autonomica
Denervazione farmacologica per valutare la frequenza sinusale
intrinseca (ipervagotonia?)
Atropina
Propranololo
0.04 mg/Kg
0.02 mg/Kg
SNRT is the longest pause from the last paced beat to the
first sinus return beat at any pacing CL.
Ratio of Sinus Node Recovery Time to Sinus Cycle
Length. The ratio of
Studio Elettrofisiologico
(SNRT sinus CL) × 100%
tempo
recupero
del nodo del seno
isTRNS
lower(SNRT),
than 160%
in di
normal
subjects.
Total Recovery Time. On cessation of atrial pacing,
the pattern of subsequent beats returning to the basic sinus
I
II
III
V1
HRA
S1
Sinus CL ! 720 ms
S1
S1
S1
SNRT ! 1625 ms
Secondary pause ! 920 ms
400 ms
FIGURE 5–5 Sinus node recovery time (SNRT). Surface ECG leads and
high right atrial (HRA) recordings arev.n.
shown
at the end of a burst of atrial
< 1500 msec
pacing, suppressing sinus node automaticity.
interval
corretto per cicloThe
di base
< 550 msecat which the
first sinus complex returns (SNRT) is abnormally long at 1625 milliseconds.
With a baseline sinus cycle (CL) equals 720 milliseconds, the corrected
Disturbi di conduzione AV
Ritardo o impossibilità degli impulsi sinusali di raggiungere
in ventricoli
BAV II
Idiopatico (degenerativa)
Cardiopatie (ischemica,
ipertensiva, reumatica,
cardiomiopatie, malattie infiltrative,
collagenopatie)
Iatrogeno (CCH, ablazione)
Congenito
Neuromiopatie
BAV III
ESTRINSECO
INTRINSECO
BAV I
(BTF)
Farmaci
Influenza autonomica
Diagnosi
•  ECG
•  Basale
•  Monitoraggio ambulatoriale
•  Test da Sforzo
•  Modulazione autonomica
•  SEF
NAV
o
non NAV?
NAV o non-NAV?
500
PRI
I
r
a
e
PA AH HV
II
HRA
A
H
V
Hisprox
Hisdist
CSprox
AH = NAV
HV = sotto il NAV
RVA
200 ms
BDx
fascio di His
BSx
FIGURE 2–19 Intracardiac intervals. Shaded areas
represent the
2 branche
CSdist
BDx
pulmonary artery (PA) (blue), atrial–His
bundle (AH)
(pink), and His
3 fascicoli
FASx
bundle–ventricular (HV) (yellow) intervals. It is important that the HV
FPSx
interval be measured from the onset of the His potential in the recording
showing the most proximal (rather than the most prominent) His
2
Electrophysiological Testing
s
ur
41
1000
e
nud
d-e
d
or
y
ee
r
r.
yk
ee
.
k
e
h
trhn
mne
d
eed
d
uh
dx
e.
he
xe
o.
e
3)
ee
degree
AVN
whereas
exercise
and atropinetoimprove
than 300
milliseconds;
Fig. 6-1).
sinus
rate block,
and allowing
HPS refractoriness
recover. (Fig. 6-2).
most
common
site
of
delay
(87%
when
the
QRS
complex
is
Atrium.
First-degree AV block caused by intra- or interAVN
conduction
because
of
sympathetic
stimulation
and/or
However, exercise
and atropine
worsen infranodal
block delay
His-Purkinje
System.
Intra-Hisian
conduction
atrial conduction delay is not uncommon. Left atrial enlargeparasympatholysis.
In90%
contrast,
carotid
sinus
massage
may
narrow,
and
more
than
when
the
interval
is more
because
of the
increased
rate
of
impulses
conducted
to the
or HPS disease
can
cause
first-degree
AVPR
block.
First-degree
I
10,15second-degree infranodal block by slowing the
improve
than
300 HPS.
milliseconds;
Fig. of
6-1).
II
AV block
in
the
presence
BBB
is
caused
by
infranodal
allowing HPS refractoriness to recover.
6 sinus rate and
PR 80 ms
His-Purkinje
System.
conduction
delay
Figureof
15.2
First-degree
Exercise
Testing
However,
exercise
and atropine
worsen
infranodal
block
IIIAV block and sinus tachycardia (lead I). PR interval = 0.24 s.
conduction
delay
in
45%
ofIntra-Hisian
cases.
A combination
delay
AH 196 ms
or
HPS disease
cause
AV
block.
because
ofcan
the
increased
rate
of impulses
conducted
toconsidered
the
within
the
AVN
and
in first-degree
the
HPS
must
also
beFirst-degree
Vagolysis
and
increased
sympathetic
drive
that occur
with
IV1
10,15
HPS.
AV
in theenhance
presence
of BBB is
caused
infranodal
HV 51 ms
exercise
AVN conduction.
Thus,
patientsby
with
firstII
(Fig.block
6-2).
6
V6
PR
80 ms
degree
AV block
can have
shorter
exerconduction
delay
in 45%
of cases.
Aintervals
combination
of
Exercise
Testing
III
Atrium.
First-degree
AV
block PR
caused
byduring
intraor delay
interHRA
cise,
and patients
with
type
1 second-degree
AVbe
block
can
AH 196 ms
within
the
AVN
and
in
HPS
must also
considered
V1
atrial conduction
delay
isthe
not
uncommon.
atrial
Vagolysis
increased
sympathetic
withenlargeHis
develop and
higher
AV conduction
ratiosdrive
(e.g., 3that
:Left
2 atoccur
rest
becomprox
(Fig. 6-2).
HV 51 ms
exercise
AVN conduction. Thus, patients with firsting 6 : 5enhance
during exercise).
H
H
V6
A
A
degree
AV
block
can
have
shorter
PR
intervals
during
exerAtrium.
First-degree
AV
block
caused
by
intraor
interExercise testing can be a useful tool to help confirm the
His
•  Nodale
HRA
cise,
and
patients
with
type
1 second-degree
AV block
canenlarge-dist
atrial conduction
delay
is not
atrial
level
of block
in secondoruncommon.
third-degree
AV Left
block
associated
HisCS
develop
AVorconduction
ratios
(e.g., 3Patients
: 2 at restwith
becomproxproxAV block (lead V1). The P wave is superimposed on the terminal portion of the preceding
•  Raramente,
sottonodale
Figure
15.3 First-degree
with ahigher
narrow
wide QRS(QRS)
complex.
pre-
BAV I
CS s.
ing
6 : 5 during
H
H
T wave.
PR interval = 0.38 mid
sumed
type 1 exercise).
block or congenital complete heart block
and
A
A
CSdist
Exercise
testing
can
be
a
useful
tool
to
help
confirm
the
His
dist
a normal QRS complex usually have an increased ventricuRVA
level
block
in secondthird-degree
AV
blockpatients
associated
lar of
rate
with
exercise.orOn
the
other
hand,
with
CS
PR
80
ms
prox
300 ms
a narrow
or wide
QRS
complex.
with
preIII with
acquired
complete
heart
block
and a Patients
wide QRS
complex
CSmid
I
sumed
type
1
block
or
congenital
complete
heart
block
and
ms in ventricular rate.
FIGURE 6–1 First-degree atrioventricular block caused by intranodal
usually show minimal or AH
no 196
increase
CS
dist
V1
II
a normal
QRS
complex
usually
have
an
increased
ventricuconduction
delay, as indicated by the prolonged atrial–His bundle (AH) and normal
Additionally, patients with 2 : 1 AV block in whom the site
RVA
PR
80
ms
HV
51
ms
PA
and
His
bundle–ventricular (HV) intervals.
larof rate
with
exercise.
On
the
other
hand,
patients
with
conduction block is uncertain can benefit from exercise
III
300 ms
V6
acquired
complete
heart
block
and
a
wide
QRS
complex
testing by observing whether
the
AV conduction ratio
AH
196
ms
FIGURE
6–1
First-degree
atrioventricular
block
caused
by intranodal
HRA
usually
show
or no increase
in (e.g.,
ventricular
rate.
Figure
15.4 Wenckebach AV block.
V1
increases
in aminimal
Wenckebach-like
manner
to 3 : 2 or
4 : 3)
conduction
delay,
as
indicated
by
the
prolonged
atrial–His
bundle
(AH) and normal
Additionally,
: 1280
block
in whom
the site
ms
HV
51
ms
decreasespatients
(e.g., towith
3 : 1 2PR
or
4AV
: 1).
In the
latter case,
the PA and His bundle–ventricular (HV) intervals.
Hisprox oforconduction
block
is uncertain
canHPS
benefit
from exercise
I
V6
increase in the
sinus
rate finds the
refractory,
causing
Second-degree atrioventricular
block
testing
by
observing
whether
the
AV
conduction
ratio
H
II block there is intermittent failure of conduction of atrial impulses
HRA
the
isHalways In
abnorsecond-degree AV
A higher degrees of block. This response
A
III some P waves are not followed by QRS complexes.
a Wenckebach-like
manner (e.g.,
to 3 :which
2 orto4the
:will
3) ventricles. Thus,
Hisdist increases
mal and in
it indicates
intra- or infra-Hisian
block,
Hisprox
orrequire
decreases
(e.g.,
to
3
:
1
or
4
:
1).
In
the
latter
case,
the
Second-degree V1
block is subdivided into Mobitz type I (also termed Wenckebach)
permanent cardiac pacing.
I
CSprox increase in
causing
and Mobitz type II block.
H the sinus rate finds the HPS refractory,
H
II
Ahigher degrees ofTesting
A is always abnorElectrophysiological
block. This response
CSmid the
His
III
dist
and it indicates intrainfra-Hisian
block,
willfor
PR 285 ms
CSdist mal
Electrophysiological
(EP)ortesting
is usually
notwhich
required
Mobitz type IV1
(Wenckebach)
atrioventricular block
V6
require
permanent
cardiac
pacing.
CSRVA
the diagnosis or treatment of AV block, because theInabove
prox
this form of second-degree block, delay in AV conduction increases with each
noninvasive measures
thesuccessive
other atrialHRA
CSmid
Electrophysiological
Testing are usually adequate. On300
impulse until an atrial impulse fails to be conducted to the venms
hand, EP testing can be of value in symptomatic patients
CSdist
tricles,
i.e.
there
is progressive increase in PR
PRinterval
285 ms until a P wave is not folHisprox
Electrophysiological
(EP) testing
is usuallyare
not suspected
required for
in First-degree
whom AV conduction
abnormalities
butby a QRS
FIGURE
6–1
atrioventricular
block
caused
by
intranodal
lowed
complex.
After
the
non-conducted
P wave, AV conduction recovers
V6
RVA the diagnosis or treatment of AV block, because the above
cannotas indicated
be documented
or thoseatrial–His
with equivocal
andECG
the
sequence
starts
again
(Figures 15.4,
15.5
).
Typically, the increments in PR
conduction
delay,
by
the
prolonged
bundle
(AH)
and
normal
HRA
A H
noninvasive
measures are usually adequate. On 300
the ms
other
findings.
His
interval
progressively
shorten
during
the
sequence,
resulting in progressive
mid
PA and Hishand,
bundle–ventricular
(HV)
EP testing can be
of intervals.
value in symptomatic patients
AH 120 ms
decrease
in
the
interval
between
QRS
complexes.
His
FIGURE 6–1in whom
First-degree
atrioventricular
block are
caused
by intranodal
prox
AV conduction
abnormalities
suspected
but
HV 125 ms
His
conductioncannot
delay, asbe
indicated
by the prolonged
bundle (AH)
and normalwide
documented
or those atrial–His
with equivocal
ECG
A H
ELECTROCARDIOGRAPHIC
FEATURES
PA and Hisfindings.
bundle–ventricular
(HV) intervals.
Hismid
I
II
124
RV
AH 120 ms
300 ms
without
discernibleoforthe
measurable
the 2 block. Con
more likely to occur with block
in the
HPS.
ment
may
actually increaseblock
for the
PR interval
last increments
absent inintype
whereas
presence
BBB conducted
suggests
(butbeat
does
not
prove)
sequences
(as
in
Holter
recordings),
a
true
type
2
block
can
PR
intervals
is
the
actual
diagnosis;
sinus
slowing
with
AV RP interval (im
Site oftheBlock.
Theofdegree
of PR interval
prolongation
in the cycle (Fig. 6-6); (2) very little incre- 26 lowing a long
HPS
involvement.
short the
baseline
PRblock.
interval
be safely
excludedrules
because
narrow
QRS type
1 and
type 2
block
essentially
out type
2 block.
and QRS
durationFurthermore,
can help predict
site of
A
When
a narrow
mental
conduction
no discernible
change
in
the the isHB.
identical
to that followin
and
small
interval
increments
preceding
the delay
block and
blocks
almost
coexist
within
Sustained
normal
QRSPR
duration
usually
indicates
AVN involvement,
QRS type
2-likenever
pattern
occurs
with intermittent
type 1
24,26,27
duration
of
the
PR
intervals
for
a
few
beats
just
before
terately
preceding
the noncon
suggest
involvement.
advanced
AV block isa true
far more
in
whereasHPS
the presence
of BBB suggests (but does not prove)
sequences second-degree
(as in Holter recordings),
type common
2 block can
mination
of a sequence
issafely
seen excluded
most often
during
long
cannot
diagnosed
if the fi
HPS involvement. Furthermore,
short baseline
PR interval(thisbe
because
narrow
QRS type
1 andbe
type
2
Wenckebach
cycles
and in blocks
association
increased
absent
or if the PR interva
and small PR interval increments
preceding
the block
almost of
never
coexist vagal
within the isHB.
Sustained
suggest HPS involvement.24,26,27
advancedbysecond-degree
is far more
tone, and is usually accompanied
slowing of AV
theblock
sinus
thancommon
all theinother PR inter
BAV II
rate; see Fig. 6-5); (3) the PR interval can actually shorten
regardless of the number of
FIGURE
6–5 Atypical Wenckebach
and then lengthen in the middle of a Wenckebach
sequence;
block. The P-P intervals re
340periodicity
200 beat can280
(type 1 second-degree
and (4) a junctional escape
end the pause
following
encompassing the noncond
+ 60
+80
atrioventricular block). Note the very small 24
a nonconducted P wave, resulting in an apparentincrements
shortening
P-P
interval.
II
the duration
of the PR
FIGURE 6–5 in Atypical
Wenckebach
I•  Tipico (raro):
6 of the PR interval.24,26,27
A
true Mobitz type II bloc
intervals
for(type
a few1beats
just before
periodicity
second-degree
termination
of a sequence.
Thethe
firstcomplex
conducted
QRS
AVN block
can
completely
or parAH
AH
A H progressivo
AH
A be reversed
AH
A H
1.  Prolungamento
PRAusually
atrioventricular
block). Note
very
small P is relatively
H
His
after
the
pause,
however,
is
associated
withwithout associ
II
slowing
and
tially by altering autonomic tone (e.g., withwave
atropine).
increments in the duration of the PR
2.  Riduzione progressiva
prolungamento
PR 1000 fail,
intervals for a few
just before
of Wenckebach block
However, del
occasionally,
these del
measures
especially
in beats forms
ms
termination
of
a
sequence.
The first conducted
P
AH
A
A
A
A
A
A
A
variation
should
be exclude
the
presence
of
structural
damage
(congenital
heart
disease
H
H
H
H
H
H
3.  Riduzione progressiva dell’intervallo RR
His
wave after the pause, however, is associated with
type II AV block can be ob
or inferior wall MI) to the AVN. In such cases, progression
1000
ms
increased vagal tone during
to
complete
AV
block
can
occur,
although
such
an
event
is
•  Nodale
block without discernible o
more likely to occur with block in the HPS.
•
Talora,
sottonodale
(QRS
o
se
provocato
da
esercizio)
PR intervals is the actual di
Site
of
Block.
The
degree
of
PR
interval
prolongation
V1
FIGURE 6–6 Atypical Wenckebach
(type A
1 second-degree
block essentially rules out
and QRS duration can help predict the site periodicity
of block.
atrioventricular [AV] block)QRS
causedtype
by
normal QRS duration usually indicates AVN involvement,
2-like pattern oc
heightened
vagal
tone.
Note
the
greatest
V6
V1
FIGURE
6–6
Atypical
Wenckebach
whereas the presence of BBB suggests (but does
not prove)
PR piùofbreve
increment
occurs
the PRsequences
interval
the (as
last in Holter reco
(type 1insecond-degree
HPS involvement. Furthermore, short baselineperiodicity
PR
interval
be
safely
excluded
because
conducted
beat in
theblock)
cycle and
not inby
the second
atrioventricular
[AV]
caused
HRA
PR
interval
thetone.
pause.Note
Also
the slowing
in the never coex
and small PR interval increments preceding
the after
block
blocks
almost
heightened
vagal
the
greatest
V6
24,26,27
sinus
rate
coinciding
with
significant
increase
the
suggest HPS involvement.
second-degree
AV
increment occurs in the PRadvanced
interval of thein
last
tipo 1
I
HRA
His
AH
A H
A
H
A
AH
A H
1000 ms
His
AH
A H
A
H
A
AH
I
A H
PR
interval beat
and in
then
block,
suggesting
that
conducted
theAV
cycle
and not
in the second
increased
vagal
tone
is
responsible
for
both
slowing
PR interval after the pause. Also the slowing in the
sinus rate coinciding with significant increase in the
PR interval and then AV block, suggesting that
220
190
increased vagal tone is responsible for both slowing
1000 ms
II
His
AH
AH
AH
AH
AH
A
AH
A H
1000 ms
FIGUR
perio
atriov
incre
interv
termi
wave
BAV II
tipo 2
•  Sottonodale
•  Hissiano (qrs)
•  Sotto-hissiano (QRS)
138
I
FIGURE 6
(Mobi* t
Sinus rhy
complex
waves is
(224 mill
conduct
a His pot
II
V1
V6
A
His
H
A
H
A
H
A
H
A
A
H
500 ms
0 msec during
at least
three
beats
the blocked
P
kebach
periodicity
with
minor
PRbefore
prolongation
of 20
in
50% Pofwave
patients.
Another
pattern
observed
was
re aonly
blocked
in 29%
of patients.
A third
pattern,
kebach
with
minor PR prolongation
of 20
patientsperiodicity
and termed
pseudo–Mobitz
type II AV block,
re
a blocked
P wave
in 29% of
patients.
A third pattern,
early
constant
P-R intervals
before
the blocked
P wave,
patients
and
termed
pseudo–Mobitz
type
II
AV
block,
shortening on the subsequent conducted beat (see
Fig.
early
constant
P-R
intervals
before
the
blocked
P
wave,
2:1 II second-degree AV block, with constant
Mobitz type
shortening
onbeats
the subsequent
conducted
beat followed
(see Fig.
at least three
before the blocked
P wave,
Mobitz
typeafter
II second-degree
block,
with in
constant
R interval
the blocked P AV
wave,
was seen
4% of
•
Nodale
at
least
three
beats
before
the
blocked
P
wave,
followed
g. 14-4). A mixed, type I Wenckebach and pseudo–
RAV
interval
the blocked
P wave,
was seen
4% of
• was
qrsseen
block after
in 6% of
all patients.
Ofinpatients
g.
A
mixed,
type
I IIWenckebach
s of14-4).
pseudo–Mobitz
type
block,
44%(>and
also
demon•  P
condotta
con
PR
lungo
300pseudo–
msec)
AV
block
was
seen
in
6%
of
all
patients.
Of
patients
Wenckebach
conduction
patterns at some time.12
•  Atropina
migliora
s of pseudo–Mobitz type II block, 44% also demon•  MSC
peggiorapatterns at some time.12
Wenckebach
conduction
BAV II
often
by noting
the in
company
that
block be
is indetermined
the His-Purkinje
system
80% and
keeps.
: 1 AVAblock
associated
a wid
of casesWhen
(Fig. 214-7).
longisP-R
interval with
(>0.30
sec
block
is in the
system
in 80%
t
beats during
2 : His-Purkinje
1 AV block with
a narrow
QRSand
com
of
cases
(Fig.
14-7).aAnormal
long P-R
nodal
site,
whereas
P-Rinterval
interval(>0.30
favorssec
in
beats
during
2
:
1
AV
block
with
a
narrow
QRS
com
In general, the response of the block, particular
nodal
site, whereas
a normal
P-Rtointerval
favors
pharmacologic
agents
may help
determine
thein
general, AV
theconduction
response ofinthe
block,with
particular
allyInimproves
patients
AV n
pharmacologic
agents
may
help
to
determine
the
atropine is expected to worsen conduction in patie
ally
AV conduction
in patients
withofAV
izedimproves
to the His-Purkinje
system,
because
itsne
atropine
is expected
worsen conduction
in patie
sinus rates
without to
improving
His-Purkinje
cond
ized
to
the
His-Purkinje
system,
because
of
itsbe
Carotid sinus stimulation is expected to worsen
sinus
rateswhereas
withoutitimproving
cond
AV node,
either has His-Purkinje
no effect or impr
Carotid sinus stimulation is expected to worsen b
AV node, whereas it either has no effect or impr
1
1540
1550
2
1
3
2
1540
1550
V
31
V1 A
775
HRA
V
AA
775
HRA
H
HBE A290 V
H
HBE
290
T
A
785
AA
785
A
A
785
V
AA
785
H
270
A
V
H
270
A
765
AA
765
A
A
785
V
AA
785
H
270
A
V
H
270
A
AA
A
500 msec
500 msec
pontaneousT 2 : 1 (high-grade) atrioventricular (AV) block localized to the AV node. Surface leads I (1), II (
ntracardiac electrograms recorded from the high right atrium (HRA), His bundle (HBE), and right ventricular
pontaneous
2 : 1 followed
(high-grade)
atrioventricular
localized
to the AV On
node.
I (1), ele
II (
tions (A) are not
by either
a His bundle(AV)
or ablock
ventricular
depolarization.
theSurface
basis ofleads
a surface
ntracardiac
from the
right
(HRA),
bundle
and right
ventricular
V block withelectrograms
a narrow QRSrecorded
is compatible
withhigh
a block
atatrium
either the
AV His
node
or an (HBE),
infra-Hisian
bundle
site. The
14
of the A-H interval (i.e., AV nodal conduction time).
Trifascicular
II
326
SECTION 2 Clinical Concepts
block should be used only to refer to alternating RBBB and LBBB,
m disease
by causing
sinus
RBBB with
a prolonged
H-V node
interval (regardless of the presence or
III
absence
of
left
anterior
or
posterior
drug, however, may be difficult tofascicular block), and LBBB with
prolonged
addition,
sinus anode
mayH-V
be interval.
greaterInthan
its the term can Vbe1 used in a patient
I system with
with second- or third-degree AV block in the His-Purkinje
ple, atropine
may
improve
AV
node
(a) permanent block in all three fascicles, (b) permanent block in two
sn-excessive
SAwith
node
acceleration,
AV in the third,II(c) permanent
1175
fascicles
intermittent
conduction
HRA
m
block
oneall.
fascicle
intermittent
two fascicles,
ally or
notin at
Thewith
response
to block in the other
AH 100
A
A
III
V1
or (d) intermittent
block
in allconthree fascicles. Thus, according to its
ar.
Isoproterenol
may
improve
HV
70
gh
V1
H
•  Sottonodale
HAV node
as well as occasionally in
HBE
AH
AH
A
A
he
H
H
A HBE
•  QRS
Control
4021
His
BAV II
2:1
block
(CHB) rests on demonstration
in
•  P condotta con PR normale
on atrial and
ventricular activation.
I
2,
•  Atropina peggiora
RV
Atropine 1 mg
H
A
H
AH
IV
transient AV dissociation caused by
V1
or ventricular
rhythms
with similar
•  II MSC
migliora
Figure 14-7 Intracardiac tracing of 2 : 1 second-degree atriovensociation). If sufficiently long monide
tricular (AV) block located in the His-Purkinje system. Sinus rhythm
III
to
mittent
conduction of appropriately
770 is present. Surface leads I, II, III, and V1
with left bundle branch block
V
ts
HRA
1
rary atrial pacing can be performed
are displayed with AH
intracardiac
electrograms recorded from the high
60RR 1175
de
A
V
A His
V bundle (HBE), and
erdrive
the
competing
junctional
or
right atrium,
H ventricular apex (RV). The A-H
H
HV 80AH 100 right
AV
1175
intervals
other atrial complex fails to activate the
HRAAV conduction. In the
ating intact
HV 70
HBE are constant, but every
to
AH 100
A ventricle even though each atrial depolarization is followed by a His
A
F),
n- CHB can be inferred when
HV the
70
H
B bundle
H
deflection. This finding shows that the site of AV block is within
in
ather
thanHBE
the typical, irregular venthe His-Purkinje system. (From Josephson ME: Clinical cardiac electroA may be the cause of heart
xin toxicity
physiology: techniques and interpretations, ed 3, Philadelphia, 2002,
on
Atropine
1.5 mg IV
rn.drug toxicity should be ruled out
Lippincott–Williams & Wilkins,
pp 92-109.)
Atropine 1 mg IV
al
by AV conduction disease is present.
V1
AA 550
AH 75
V
1
ar R-R intervals may occasionally be
ar
patients with His-Purkinje system disease by causing sinus node
AH 75
HV 75
A The effect of anyHgiven
RR 1100
(AA 550) slowing.
i- (i.e., no evidence of atrial
drug, however,
may be difficult to
m
activity
H
A
A
H
ly
AH 75
770
HBE because its effect on the sinus node may be greater than its
predict
waves)
and
HRAnot heart block or digied
AH
HV 60
75
(2:1)
effect on the AV node. For example, atropine may improve AV node
A
V
A
V
or
H
H
HV 80
conduction, but if atropine 1100
causes excessive SA node acceleration, AV
ay
by the AV junction,
he be generated
HBE
RV
C conduction
may improve marginally or not at all. The response to
he
distal
conduction
system. Rarely, the
B
infusion
less clear. Isoproterenol
improve
connFigure
14-8of isoproterenol
His-Purkinjeis atrioventricular
blockmay
after
atropine-
d
b
o
w
w
o
b
R
a
a
w
(
f
b
o
BAV II
alto grado (≥ 3:1)
•  Sottonodale
•  Hissiano (qrs)
•  Sotto-hissiano (QRS)
ormalities
with
ythm
ith
I
II
BAV III
III
Sede? Vedi ritmo di scappamento
aVR
•  Nodo AV (qrs, FC normale)
•  Fascicoli (QRS, FC molto bassa)
•  His (qrs, FC bassa)
•  Ventricolo (QRS, FC estremamente
aVL
aVF
ree AV block is seen on the
sociated P waves and QRS
n pacemaker rate, with connship as the P waves march
icular cycle in the presence
m (Fig. 6-14). Every possible
ed, with the P waves occurerval, but the atrial impulse
cles. The atrial rate is always
26,27
bassa)
Site of Block
Atrioventricular Node. Most cases of congenital third-
degree AV block are localized to the AVN (see Fig. 6-14), as
is transient AV block associated with acute inferior wall MI,
beta blockers, calcium channel blockers, and digitalis toxicity. Complete AVN block is characterized by a junctional
escape rhythm with a narrow QRS complex and a rate of 40
to 60 beats/min, which tends to increase with exercise or
atropine. However, in 20% to 50% of patients with chronic
AV block, a wide QRS escape rhythm may occur. Rhythms
Blocco “trifascicolare”
Disturbo di conduzione AV distale (dei 3 fascicoli)
•  Blocco bifascolare + HV lungo
PR = AH + HV
Blocco His?
BDx
FASx
FPSx
Blocco trifascicolare
Blocco trifascicolare
Sindromi sincopali riflesse neuromediate
Disturbi della regolazione di FC e/o pressione arteriosa
dovuti a riflessi neurovegetativi
Riduzione PA
> 50 mmHg
input
Pausa
> 3 secondi
PM?
Risposta
Ø  cardioinibitoria
Ø  vasodepressiva
Ø  mista
sinus node exit block,35 but it can result from atrioventricular (AV)
block as well. A vasodepressor response to CSM is defined as a drop
in systolic blood pressure of 50 mm Hg or more during massage;
this may be difficult to demonstrate in patients who have a significant cardioinhibitory component. In contrast to the induced cardioinhibitory component of carotid sinus hypersensitivity, the
vasodepressor response may have a slower, more insidious onset and
a more prolonged resolution.
Sindrome del
seno carotideo
Sincope/pre-sincope
+ ipersensibilità del
seno carotideo
Correlazione con
sintomo
Complications
Carotid sinus massage is safe if done carefully. CSM is contraindicated
in patients with a history of cerebrovascular disease or carotid bruits,
because it can cause cerebrovascular accident (CVA, stroke). In a
review of 3100 episodes of CSM performed on 1600 patients, the seven
complications (0.14%) were neurologic and transient.37 In another
review of CSM on 4000 patients, complications were observed in 11
patients (0.28%);38 all were neurologic. After 1 month, nine patients
V1
I
II
III
AVR
5s
140/76
Arterial 100
pressure
(mm Hg) 0
CSM On
76/42
CSM Off
Arterial 100
pressure
(mm Hg) 0
(risposta mista)
Arterial 100
pressure
(mm Hg) 0
1s
Figure 15-1 Combined cardioinhibitory and vasodepressor response to carotid sinus massage (CSM). Note slow return of blood pressure despite
resolution of asystole. (From Almquist A, Gornick C, Benson W, et al: Carotid sinus hypersensitivity: evaluation of the vasodepressor component.
Circulation 71:927, 1985. Copyright 1985 American Heart Association.)
epts
Sincope vaso-
MAP (mm Hg)
Sincope/pre-sincope
+ riflesso vasovagale
Riflesso secondario a
ted because
many
patients may
trigger
definiti
40
ex AV block. In general, patients
uential pacing, even when a sigor CSS is present. VVI pacing
intact ventriculoatrial (VA) conaker syndrome. Lack of VA conoes not ensure against its future
mend dual-chamber pacemakers
nus rhythm.
of rate-responsive pacing in CSS.
ore may have bradycardic comoror chronotropic incompetence,
herefore, rate-responsive pacing
dies have
prospectively
(risposta
mista)examined
pabilities, which has the theoretiher-rate AV sequential pacing to
nent during CSS attacks.42
120
100
80
60
40
20
120
HR (beats/min)
gic symptoms persisted in two
vagale
tions include
asystole and ven-
100
80
60
40
20
300
Supine
Head-up
tilt
SYNCOPE
400
500
600 700 800
Time (seconds)
900 1000 1100
Figure 15-2 Hypotension and bradycardia induced during a positive
drug-free passive tilt-table test. HR, Heart rate; MAP, mean arterial
pressure.
Chi beneficia di un PM?
•  Bradiaritmie secondarie a disfunzione sinusale o blocco
atrioventricolare, intrinseche o estrinseche
Ø  Sintomatiche
Ø  *Asintomatiche, ma potenzialmente fatali se non trattate
Ø  Non reversibili
Pazienti
sintomatici*
Bradicardia
Persistente
Bradicardia
Intermittente
ECG
documentato
ECG non
documentato
Pazienti
sintomatici*
Bradicardia
Persistente
Bradicardia
Intermittente
Disfunzione sinusale
Sintomatica
IB
Sintomatica*
IIb C
Asintomatica
III C
ECG
documentato
ECG non
documentato
BAV acquisito
Sintomatico
Asintomatico
*correlazione non definita
BAV II tipo 2
BAV III
IC
BAV II tipo 2
BAV III
IC
mortalità
Reversibile
III C
BAV II tipo 1
IIa C
BAV II tipo 1*
IIa C
*sottonodale
European Heart Journal (2013) 34, 2281–2329
Pazienti
sintomatici*
Disfunzione sinusale
BAV acquisito
Sintomatica
Sintomatico
Pause
sinusali
IB
Bradicardia
Persistente
Bradicardia
Intermittente
BAV II, III
IC
ECG
documentato
ECG non
documentato
Sincope riflessa
cardioinibitoria
> 40 anni
ricorrente
senza
prodromi
IIa B
Sincope
pause
asintomatiche
> 6 sec
IIa C
Reversibile
III C
European Heart Journal (2013) 34, 2281–2329
Pazienti
sintomatici*
Bradicardia
Persistente
Bradicardia
Intermittente
HV ≥ 70 ms
BHP II o III
IB
BB alternante
IC
FE < 35%
(ICD/CRT-D)
IIb B
ECG non
documentato
Sincope riflessa
cardioinibitoria
Blocco di branca
Sincope
ECG
documentato
Asintomatico
BB alternante
IC
altro
III
MSC
Tilt test
pausa
> 6 sec
IB
> 40 anni
refrattaria
senza
prodromi
IIb B
Indagini
negative
III
European Heart Journal (2013) 34, 2281–2329
Cos’è un pacemaker?
Dispositivo elettronico che genera energia elettrica
sufficiente a depolarizzare il miocardio, dando il via alla
contrazione meccanica
•  Generatore
•  Elettrocatere
(catetere + elettrodi)
•  Miocardio
Generatore
27
Pacing and Defibrillation
P1: OTE/PGN
part-Ia
P2: OTE/PGN
BLBK303-Barold-fig
QC: OTE/PGN
March 9, 2010
T1: OTE
9:42
Trim: 276mm×219mm
Printer Name: Yet to Come
compares the interval to the rates and int
grammed by the clinician. For example, if
∼10 cc
17
events occur with a separation of 1,500 ms
∼20 g
heart rate is 40 bpm (HR=60/measured b
interval; 60/1.5=40 bpm). In order to und
logic behind sensing algorithms and pacing
grams, the terminology needs to be introduced
Cassa titanio
includes the most commonly used terms an
(sigillata)
tions. These terms will be freely used in fur
sions of the logic behind pacing and defibrillat
and therapies without further explanation. Th
also provide the reader with the vocabulary r
Blocco di
interpreting and understanding current lite
connessione
ERIon the topic.
publications
(elective replacement
indicator)
The decision
process and
behavior of
Batteria Li-I
EOL
pacing algorithm are usually described usin
(end of life)
diagram (Fig. 27.14). An understanding o
Circuiti e componenti gram will provide the basis for the anal
behavior of pacing systems and will comm
associate
various parameters that the clinician and d
ufacturer must be concerned with. The con
Fig. 27.10 Cutaway view of an implantable pulse generator (IPG
ate implantation; and they must include an electhat provides good mechanical and electrical
Elettrocateteri
he difference in voltage
mplitude, which is
ts per second and should
Fig. 1.9 Diagram of a pacing pulse, constant voltage, with leading
edge and trailing edge voltage and an afterpotential with opposite
polarity. As described in the text, afterpotentials may result in sensing
abnormalities.
Trasmettono gli impulsi elettrici (dal generatore al
miocardio e viceversa)
Isolante
9 Diagram of a pacing pulse, constant voltage, with leading
nd trailing edge voltage and an afterpotential with opposite
. As described in the text, afterpotentials may result in sensing
alities. Elettrodo
Conduttore
Elettrodo
Connettore IS-1
brillation and Resynchronization
31
yurethane that have had the
e 80A (P80A) and Pellathane
oduction of polyurethane as
t became clear that clinical
fic leads were higher than
igation revealed that the failmarily in leads insulated with
croscopic cracks developed in
ally occurring as the heated
manufacture; with additional
se cracks propagated deeper
ulting in failure of the lead
A
Unipolare vs Bipolare
o undergo oxidative stress in
containing cobalt and silver
radation of the lead from the
ad failure. Some current leads
ethane coating, incorporating
ty of silicone with the ease of
while maintaining a satisfaceter. Silicone rubber is well
to abrasion wear, cold flow
n, and wear from lead-to-lead
Current silicone leads have
hat improve lubricity and
Preliminary studies have sugating of silicone and polyproved wear.39 Despite lead
y testing, and premarketing,
nadequate to predict the longds, so that clinicians implantrming follow-up in patients
ust vigilantly monitor lead
se of internet-enabled remote
generator based algorithms
generation in the event of
nd connectors are standardational guidelines (IS-1 standleads have a 3.2-mm diameter
pin.40 These standards were
ago because some leads and
incompatible, requiring the
adaptors. The use of the IS-1
B
Fig. 1.15 Lead connectors and configurations. (A) Connector types
in defibrillator leads. The top panel shows the proximal end of a
defibrillation lead with a three connectors. Top and bottom pins are
DF-1 connectors used for high voltage shock delivery for
defibrillation, while the middle pin is an IS-1 connector used for
pacing and sensing. Bottom images shows a DF-4 connector, in
which all four conductors (two for defibrillation and two for pace/
sense) are mounted on a single pin. (B) Unipolar vs. bipolar leads
pacing leads. In a unipolar configuration, the pacemaker case serves
as the anode, or (+), and the electrode lead tip as the cathode, or
(−). In a bipolar configuration, the anode is located on the ring, often
referred to as the “ring electrode,” proximal to the tip, or cathode.
The distance between tip and ring electrode varies among
manufacturers and models.
two high-voltage and two low-voltage connections so
that a single connector (with single screw) can provide
pace-sense and dual coil defibrillation support, signifi-
Fissazione attiva vs passiva
Pacemaker senza fili
Terminologia
DDD/VVIR/XYZ
Uscita
Frequenza base
Sensibilità
Isteresi
Frequenza massima
Intervallo AV
Cosa fa?
DDD/VVIR/XYZ
!
Posizione
I
II
III
IV
V
Categoria
Camera stimolata
Camera sentita
Risposta al
sensing
Modulazione in
Frequenza
Stimolazione
multisito
O = nessuna
O = nessuna
O = nessuna
O = nessuna
O = nessuna
A = atrio
A = atrio
T = stimolo
R = modulazione
in frequenza
A = atrio
V = ventricolo
V = ventricolo
I = inibizione
V = ventricolo
D = doppia (A&V)
D = doppia (A&V)
D = doppia (T&I)
D = doppia (A&V)
Revised NASPE/BPEG Generic (NBG) Code
NASPE > HRS; BPEG > HRUK
PACE 25:260-264, 2000
23
Stimolazione
Spike
all’ECG
Impulso
Ampiezza
5V
Uscita
Durata
0.4 ms
21
VOO
Lower Rate Interval
LRI
QRS
stimolato
LRI
QRS
spontaneo
LRI
QRS
spontaneo
LRI
stimolo nel
periodo
refrattario
ventricolare
Impulso
unipolare
Frequenza base
QRS
stimolato
Frequenza base
LRI in bpm
PM monocamerale programmato in VOO 60 bpm, uscita 2 V x 0.4 ms
68
Rilevazione (sensing)
Sensibilità
adeguata
Sensibilità
Sensibilità alta
(sente troppo)
ECG
Elettrogramma
ventricolare
Livello di
sensibilità
5 mV
Sensibilità bassa
(non sente)
Voltaggio*
12 mV
*differenza di segnale tra 2 elettrodi
Sensibilità
adeguata
42
VVI
LRI
QRS
stimolato
LRI*
Impulso
unipolare
QRS spontanei
sentiti
QRS spontaneo
che inibisce il PM
e resetta il timer
PM monocamerale programmato in VVI 60 bpm, uscita 2 V x 0.4 ms, sensibilità 5 mV
Isteresi
LRI
Isteresi
LRI*
Impulso
unipolare
FC
(bpm)
FC spontanea
FB
FdI
QRS
stimolato
LRI
QRS
spontaneo
LRI*
Impulso
unipolare
FC
(bpm)
FC spontanea
FB
FdI
QRS
stimolato
QRS
spontaneo
PM monocamerale programmato in VVI 60 bpm, isteresi 40 bpm, uscita 2 V x 0.4 msec, sensibilità 5 mV
VVIR
FC di
stimolazione
RISPOSTA CURVILINEA
URI
Sensori
Non fisiologici
Upper Rate
Interval
Vibrazione
Accelerazione
Velocità di
risposta
LRI
Riposo
Frequenza massima
URI in bpm
Fisiologici
Ventilazione minuto
Esercizio
Frequenza massima
PM monocamerale programmato in VVIR 60/120 bpm, isteresi 40 bpm, uscita 2 V x 0.4 msec, sensibilità 5 mV
DDD
PAV
Intervallo AV
SAV
Intervallo AV
sentito (SAV)
stimolato (PAV)
PM bicamerale programmato in DDD 60/120 bpm, intervallo AV 120/150 msec, uscita 2 V x 0.4 msec, sensibilità 5 mV
PREPARAZIONE DEL PAZIENTE
Indicazione
Rischi
Limitazioni alla guida
Venografia
Antibiotici
Analgesia
Sedazione
Cefazolina
Vancomicina
(allergici/MRSA)
Sala di
elettrofisiologia
Fluoroscopia
Monitor parametri vitali
Ossigeno
Kit pericardiocentesi
Carrello emergenza
Fig. 5.1 Pacemaker and implantable cardioverter-defibrillator implantation suite. Cardiac resynchronization therapy systems are impla
different area that is larger and has additional cine-angiographic capabilities.
EQUIPMENT
Apart from the fluoroscopy equipment and vital
observation monitors—for example, automated
Materiale
A.
B.
C.
D.
E.
F.
G.
H.
I.
Forbici
Divaricatori
Copriamplificatore
Ciotole
Garze
Suture
Cavi per test
Pinze
Porta-aghi
le
d
P
ge
50
b
P
Figure 2 Pacing trolley laid out with instruments and
equipment before permanent pacemaker implantation.
These include: (A) a selection of scissors, (B) self
A
(i
ep
si
so
w
le
p
p
o
m
su
to
re
145
Sterilità
Disinfezione
clorexidina 10%
regione pettorale sx
Procedure
Campo sterile
7 Antiseptic solution can be colored with a red
ow) to help ensure that the appropriate area of
ainted
Fig. 7.19 The axilla, neck, and supraclavicular region
should be included in the area being cleaned
Fig. 7.25 Positioning the window over the site of incision
Fig. 7
7
148
Tasca
Implantation Technique
148
Anestesia locale
Lidocaina 1%
Bupivacaina 0.25%
maggiore durata
Sede
sottoclaveare
prepettorale
25 Positioning the window over the site of incision
Fig. 7.28 Skin incision
Fig. 7.29 A retractor may be used to help dissection
(identify the cephalic vein if necessary) and make a pocket
Fig. 7.27 1% lignocaine is infiltrated into the operation site
than one lead is to be inserted. Leads are inserted
via an infraclavicular subclavian vein puncture,
anchored with sutures and then connected to the
generator which is then placed in a subcutaneous Fig. 7.28 Skin incision
Fig. 7.30 The fingers are used effectively for blunt Fig. 7.31 Making the pacemaker pocket
pocket fashioned
by blunt dissection over pectodissection
ralis major.
Fig. 7.2
(identif
7 Implantation Technique
156
Accesso
venoso
Percutaneo
Ascellare
Fig. 7.61 Vessel dilator and sheath being inserted into
the cephalic vein over the guidewire
Succlavia
IJV
EJV
RIV
150
IJV
EJV
LS-CV
RS-CV
AxV
LIV
SVC
BV
CV
MBV
MCV
Fig. 7.34 In
Electrode Positioning
Chirurgico
Cefalica
Axillary Vein Approach
Fig. 7.63 Venous anatomy of the upper limb/upper mediProcedure
astinum relevant to pacing. MCV median cephalic vein,
MBV median basilic vein, BV basilic vein, CV cephalic
vein, AxV axillary vein, RS-CV right subclavian vein, RIV
right innominate vein, LIV left innominate vein, LS-CV
left subclavian vein, EJV external jugular vein, IJV internal jugular vein, SVC superior vena cava
The axillary vein is an alternative conduit for the
placement of pacing and defibrillation leads for
several reasons. Unlike the cephalic vein, the
axillary vein is almost always large enough to
accommodate multiple pacing leads. When compared to the subclavian vein, the axillary vein
affords a less acute course. This potentially
decreases mechanical stress on the implanted
leads or catheters and results in a lower incidence
of mechanical lead failure. Additionally, subclavian access is associated with the risk of inadvertently accessing the noncompressible subclavian
artery and the potential for increased mechanical
stress on the lead from crossing the subclavius
muscle and the clavipectoral fascia. Finally, use
the axillary system. The axillary vein begins at
the lower margin of the teres major muscle as a
continuation of the brachial vein. It continues its
course proximally until it terminates at the lateral
margin of the first rib to become the subclavian
vein. Along its course, it receives tributaries from
the cephalic and basilic veins (Fig. 7.63). The
vein is accompanied, along its course, by the
axillary artery, which lies slightly superior and
posterior to the vein. Overlying the vein are the
Fig. 7.54
Self-retaining
retractor
canfolbe used to help
pectoralis
minor
and clavipectoral
fascia,
identify
cephalic
veinmajor.
lowed
more and
superanchor
ficiallythe
by the
pectoralis
A clinician can thus accurately and reliably cannulate the target vessel while minimizing the
Fig. 7.62 Lead being inserted into the cephalic vein
155
Fig. 7.35 G
Fig. 7.65
Fig. 7.64 Fluoroscopic-guided axillary vein puncture.
The arrow shows the tip of the needle just lateral to the
medial border of the first rib
Fig. 7.57 A “vein-picker” (yellow) is used to help insertion of a guidewire into the cephalic vein and beyond
an essential component of pacemaker and ICD
insertion, ultrasonography is rarely, if ever, used
Fig. Vessel
7.43 Vessel
blue)guidewire
and guidewire
Fig.Vessel
7.40 dilator
Vessel dilator
and being
sheathadvanced
being advanced
Fig. 7.43
dilator dilator
(blue) (and
being being
Fig. 7.40
and sheath
over over
removed
from
sheath
(
white
)
the
guidewire
and
through
the
clavipectoral
fascia
under
the guidewire and through the clavipectoral fascia under removed from sheath (white)
the clavicle
the subclavian
the clavicle
into theinto
subclavian
vein vein
Fig. 7.35 Guidewire inside needle within subclavian vein
Introduttore
Pelabile
Attenzione a
inspirazione!
Fig. 7.33 Puncture of the subclavian vein. Top:
Landmarks: The subclavian vein passes between the junction of the medial and middle thirds of the clavicle and
the suprasternal notch/sternoclavicular joint. Bottom: The
needle is kept parallel to the frontal plane and close to the
deep surface of the clavicle/sternum in order to avoid
puncture of the pleura and subclavian artery
(Fig. 7.36). If a second lead is being inserted, a
second SCV puncture is made and a second
guidewire inserted as just described (Figs. 7.37
and 7.38). Some operators screen the wire to
Fig. 7.36
removed
guidewire
within
the Fig.
Fig.The
7.44ventricular
The ventricular
is inserted
the introFig. Needle
7.41 pressure
Firm
pressure
is necessary
to advance
the 7.44
lead is lead
inserted
into theinto
introFig.
7.41
Firm
isand
necessary
toleft
advance
the
subclavian
vein
ducer sheath
introducer
into
the
subclavian
vein
ducer sheath
introducer into the subclavian vein
below the diaphragm in order to ensure that the
guidewire has not been inadvertently placed into
the subclavian artery – before advancing the
introducer sheath. This may be particularly helpful in patients with low systemic pressures.
A 20 cm long vessel dilator/sheath combination is then placed over each guidewire in turn
Fig.Lead
7.45 isLead
is advanced
the sheath
Fig. Introducer
7.42 Introducer
fully inserted
overofone
the 7.45
advanced
throughthrough
the sheath
and intoand into
Fig. 7.42
fully inserted
over one
the of Fig.
theatrium
right atrium
guidewires
the right
guidewires
7
158
Elettrocatetere
Implantation Technique
7 Implantation Technique
160
Stiletto
LIV
LIV
RIV
RIV
Fluorsocopia
SVC into the lumen of
SVC Fig. 7.69 Steel stylet being introduced
Fig. 7.68 This curve on the distal end of the stylet will
help the operator to get the pacing lead across the tricus- the lead via the plastic “funnel”
pid valve and the lead’s tip into the RV apex. A bigger
PA
PA
curve can be made on the stylet to help in positioning the
RA
RA
tip of an active-fixation lead onto the interventricular sepTV
tum or RV outflow tract
TV
RV
RV
IVC
IVC
b
a
RIV
SVC
Fig. 7.70 LIV
Gray knob on the proximal end of theLIVstylet
which is inside this bipolar lead. Note
the plastic “funnel”
RIV
which helps to place the stylet into the lead’s lumen
SVC
PA
PA
RA
RA
TV
TV
RV
IVC
c
Fig. 7.75 Technique for placing a permanent ventricular
lead into the right ventricular apex. (a) The lead and its stylet are inserted via the axillary or subclavian vein, innominate vein, and SVC into the Right atrium. Notice the position
of the tip of the stylet (---) within the lead. (b) With the
IVC
RV
d
Once the lead tip has been shown to enter the RVOT, there
is no doubt that the lead is not in the coronary sinus or in the
low RA. (f) The lead/stylet can then be withdrawn slightly.
(g) The curved stylet may then be advanced to the tip of the
lead and the two advanced forward into the RV apex with
170
Lead Measurements at Implantation
Test
elettrocateteri
Cavi per test
169
Fig. 7.95 Disposable wire connections for lead parameter testing during implantation. The black/red connections in the left hand are inserted into the pacemaker
analyzer while the other black/red connections (arrow)
are attached to the distal and proximal electrodes on the
pacemaker lead
Fig. 7.95 Disposable wire connections for lead parameter testing during implantation. The black/red connections in the left hand are inserted into the pacemaker
analyzer while the other black/red connections (arrow)
are attached to the distal and proximal electrodes on the
pacemaker lead
172
Analizzatore (PSA)
Fig. 7.97 Close-up of the connecting wire and its terminals
Lead Measurements at Implantation
Fig. 7.96 Connection wire stretched across the operating
For satisfactory long-term pacing, low stimulation and sensing thresholds should be present at
implantation. High thresholds or poor R- or
P-wave amplitudes suggest that the cathode tip is
not abutting excitable myocardium. If this is the
case, the leads should be repositioned.
Thresholds rise after pacemaker implantation,
and usually peak 1–3 months after lead fixation.
Thresholds are measured using a commercially
available pacing systems analyzer (PSA) – ideally
matched to the generator to be implanted. This
should ensure that they both have similar sensing
and generating circuits. It is important that the unipolar7.96
or bipolar
electrodewire
constretched
figurationacross
shouldthe
beoperating
the
Fig.
Connection
drape
same as that being used in the implanted system.
Fig. 7.98 Close-up view of the analyzer’s lead being Fig. 7.99
attached to the distal (black) and more proximal (red) attached to
increasepacemaker
output by
electrodes of this bipolar lead
to capture.
With a pulse d
Fig. 7.100 Technician
threshold of <1 V
Fig.performing
7.97 Close-up
the connecting wire and its terminals
leadofsensing,
RV and <1.5 V in t
pacing and impedance
in the RV if the
checks
active fixation lead
Lead Measurements at Implantation high, e.g.,1.5 V in
but it should fall w
When testing b
For satisfactory long-term pacing, low stimula-ensure that the dis
tion and sensing thresholds should be present atelectrode are conne
implantation. High thresholds or poor R- orand anode (+ve),
P-wave amplitudes suggest that the cathode tip isreversed, the pacing
not abutting excitable myocardium. If this is thea longer duration
energy is delivered
case, the leads should be repositioned.
Thresholds rise after pacemaker implantation,threshold will be lo
ear, however, and 0
and usually peak 1–3 months after lead fixation.of efficient impulse
Thresholds are measured using a commercially When testing un
available pacing systems analyzer (PSA) – ideallythe lead should be
matched to the generator to be implanted. This(−ve) and the proxim
should ensure that they both have similar sensinga metal object such
wound. paced
In this situ
distal circuits.
tip negative
electrode
the lead
m
andthe
generating
It is important
that on
the unipoanode
should
be sim
7.97electrode
–7.99). The
technician
then begins
lar (Figs.
or bipolar
confi
guration should
be the the satisfactor
otherwise
falselyrec
hi
sensing
pacing
measurements
the PSA
should
same
as thatand
being
used in
the implantedusing
system.
Pacing the RV
(Fig.
7.100
). Forlead
unipolar
the negative
gram of >
A
sterile
bipolar
is usedleads
to connect
the
Fig. 7.103 Technician doing atrial lead tests using the complex with LBB
(black)
PSA
lead
is
connected
to
the
single
distal
shift
due t
uni/bipolar
electrodes on the pacing leads to thepacing the
pacemaker analyzer/programmer
RV outfl
7
174
Implantation Technique
Fig. 7.108 Suturing the
ventricular lead to the fascia
over pectoralis major
Fig. 7.112 Once the leads have been anchored, the connector pins are inserted into the ports on the header of the
pacemaker
Per finire
Fig. 7.120 The pacemaker is inserted into the pocket
ensuring that the header is placed inferiorly away from the
skin edges
Fig. 7.114 The atrial lead is inserted into its relevant port
and particular notice has to be taken to ensure that the
distal pin has passed beyond the second securing screw
Fig. 7.123 Braided, absorbable Vicryl suture is suitable
Fig.
The skin edges
for closure
of7.126
this subcutaneous
layerare now easy to approximate
Fig. 7.129 Subcuticular suture being inserted
Fissazione EC
Connessione con
Fig. 7.109 Suturing the
ventricular lead
generatore
Chiusura tasca
punti intradermici
punti sottocutanei
Fig. 7.121 The leads are placed behind the generator
punti cutanei
Lead Measurements at Implantation
Fig.The
7.127
Absorbable
3:0tissue
Dexonand
II on
a straight
Fig. 7.124
subcutaneous
fatty
pocket
are cutting
needle
is
ideal
for
the
subcuticular
layer
closed with interrupted absorbable sutures II
Fig. 7.113 Ventricular lead is inserted into its appropriate port
Fig. 7.120 The pacemaker is inserted into the pocket
ensuring that the header is placed inferiorly away from the
skin edges
secure fix inside the pacemaker (Fig. 7.117).
Some operators check the serial numbers on
each lead with the pacing technician to ensure
Fig. 7.110 Anchoring the atrial
lead
Fig. 7.122 The subcutaneous fatty tissue and pocket are
closed with interrupted absorbable sutures I
177
Fig. 7.130 A pleasing end result is obtained by placing
each subcuticular “bite” in close proximity to each other
Fig. 7.115 The screwdriver is used to secure the leads
inside the header
Fig. 7.123 Braided, absorbable Vicryl suture is suitable
for closure of this subcutaneous layer
that the atrial and ventricular leads are inserted
into the correct respective ports in the pacemaker header.
Fig. 7.128 A continuous subcuticular suture is used to
bringThe
thesubcutaneous
skin edges together
Fig. 7.125
fatty tissue is closed with
interrupted sutures III
Fig. 7.131 The suture is completed by applying tension
to both ends of the subcuticular suture and the ends are
then removed
Complicanze
Tasca
•
•
•
•
Ematoma
Erosione
Sindrome di Twiddler
Infezione
Elettrocatetere
•  Pneumotorace, emotorace,
embolismo gassoso
•  Perforazione miocardica
•  Dislocazione
•  Stimolazione
diaframmatica, pettorale,
intercostale
•  Trombosi venosa e
sindrome della cava
superiore
•  Rottura conduttore e/o
isolante
•  Infezione
Dislocazione
EC
Fig. 12.12 Histology in this case shows a perforation track
into the epicardial fat and an atrophic RV myocardium. It
was not clear whether this had been caused by the emergency TPM (removed) which had been placed during the
resuscitation of this elderly lady brought in unconscious in
complete heart block and a ventricular rate of 10 per min
Fig. 12.14 Some active fixation leads are firmly fixed to
the myocardium and forceful traction may result in myocardial avulsion and fatal, sudden hemopericardium unless
surgical drainage and repair is not urgently performed
unlikely to solve the problem and surgical intervention is likely to be required. If the guidewire
is still in situ, an attempt can be made to close
such a perforation with the Angioseal™ device
or similar percutaneous closure device. Early
recognition and immediate vascular repair is
Fig. 12.10 Transthoracic
echocardiogram (subcostal
paramount.
view) shows the helical coil tip (red arrow) of this activeVenous oozing from the insertion site of a
fixation lead protruding through the apex of the right ventemporary electrode is more likely to occur if the
tricle (RV). The green
arrow shows the lead within the RV
central venous pressure is raised, for example, in
cavity, and the yellow
arrows
the failure
anterior,
andis antipatients
with heart
or ifapical,
the patient
septal portions of the
RV. RV right
ventricular
free wall
coagulated.
Generally
the subclavian
route should
be avoided if the patient is anticoagulated with
Fig. 12.8 A smaller pneumothorax may be localized to
heparin or coumarin anticoagulants and the
the apex (green arrow)
cephalic vein used instead.
After permanent pacemaker implantation,
Fig. 12.13 Echocardiography should confirm hemopericontinued bleeding into the pacemaker pocket is
cardium (arrow) and be helpful in determining the success
usually as a result of a missed bleeding arteriole
of pericardiocentesis
or vein within the pocket. Hematoma formation
with the old “helifix” leads than the more modern usually occurs within the first few hours and if
“screw-in” electrodes.
large/tense or if associated with pain requires
drainage by opening the pocket under sterile conditions in theater without delay (Fig. 12.15).
Hemorrhage
Anticoagulant therapy should be stopped prior
to pacemaker implantation and the INR normalSerious bleeding only occurs if the subclavian ized with vitamin K or fresh frozen plasma if
artery is punctured. Swift removal of the needle necessary. Wherever possible, aspirin and clopiwill often solve the problem. However, if the dogrel should be stopped for 1 week before in an
operator is unaware of the inadvertent arterial attempt to minimize hematoma formation which
puncture and the introducer sheath is pushed may increase the incidence of later pocket
into the artery, simply removing the sheath is infection.
Perforazione
miocardica
Fig. 12.11 Frail elderly patients may have extremely
thin RV myocardium and RV perforation is not difficult,
especially when positioning the lead with the stiffening
stylet in position. RV lead is shown in situ with tip close
Early Complications
251
Pneumotorace
Emotorace
Hemothorax
Fig. 12.4 Underwater sealed chest drain (arrow) is
Hemothorax may occur
inserted
if the needle is inserted
through both walls of either
the subclavian artery
Fig. 12.6 Large pneumothorax (arrows) requires inseror vein (Fig. 12.16) and
especially
tion of
chest drain if the introducer sheath is also pushed into the subclavian
artery and then withdrawn. A widening mediastinal shadow, a new ipsilateral pleural effusion, or
total opacification of the ipsilateral thorax on the
chest X-ray might follow serious bleeding following subclavian artery puncture and suggests
hemothorax. A fall in hemoglobin and typical
signs on examination of the chest would support
this serious complication that demands urgent
surgical referral.
Fig. 12.16 Hemothorax is a serious complication –
254
Fig. 12.15 Small hematoma
as a result of venous oozing
within pacemaker pocket
Ematoma
Hemothorax
12 Complications of Pacemaker Implantation
Late Complications
261
Trombosi
venosa e
sindrome VCS
Fig. 12.34 Multiple leads placed in the subclavian vein
(arrow) may lead to fibrosis and/or thrombosis and signs
of venous obstruction
Lead Displacement
Atrial and ventricular pacing leads may dislodge
from their implantation positions between discharge and the first follow-up appointment. Loss
of atrial or ventricular pacing or sensing on the
ECG may be the first clue to a problem, although
a recurrence of dizziness/near syncope/syncope
may result from ventricular lead displacement if
the patient is pacemaker dependent. X-ray of theFig. 12.37 Venography of
chest in PA and lateral views should confirm thethe left axillary/left
subclavian vein identifies
diagnosis (see Figs. 12.21–12.23). Repositioning
subclavian/axillary vein
of the leads will be necessary to restore the
thrombosis (black arrow).
function.
Distended collateral veins
Twiddler’s syndrome can be a cause of earlyare evident
Fig. 12.35
subclavian vein thrombosis causes disonLeft
venography
lead displacement.
tended
veins) in the left pectoral region, left side of neck
(white
arrows
(arrow) and left arm as well as discomfort and swelling of
the left arm
268
12 Complications of Pacemaker Implantation
Fig. 12.48 Insulation breaks
on leads can result in local
muscle twitching, premature
battery depletion, and loss of
capture. Careful scrutiny of
the chest X-ray might suggest
the problem (arrow)
Rottura
conduttore e/o
isolante
Late Complications
Infection
Pacemaker pocket infection is a serious complication which invariably necessitates removal of the
whole system – generator and electrode(s), and
implantation of a new pacing system. It is usually
due to poor aseptic technique, poor skin preparation, and poor practical technique and prolonged
Fig. 12.49 Magnified view
of the site in question
confirms a section of lead
without its insulation (green
arrow). Loss of capture and
low lead impedance result
Fig. 12.51 Magnified view showing fractured lead insulation at site of “anchoring” silk suture
proced
of ear
tion in
Wi
comm
Patien
discom
may b
and 1
or pus
pocke
the wo
antibio
started
IV an
ods, w
may g
treat.
to ex
(Fig.
remov
quentl
If
course
of the
may d
diogra
12 Complications of Pacemaker
280
Sindrome di
Twiddler
Late Complications
Fig. 12.76 Defibrillator lead removed in a patient with
Twiddler syndrome. Constant rotation of the device within
281
the lead displaced into the left brachiocephalic vein. The
lead had to be extracted and a new lead inserted
wound releases bloody,
yellow pus
phylococcus aureus or Staphylococcus
is. It is best to remove the infected elecproceed to permanent pacing as soon as
if indicated – in order to avoid this
on which can lead to septicemia. When
rary pacemaker is required to be left in
2 days, for example in acute MI, the
Tasca
ite should
be washed daily with chloror povidone iodine solution and then
ith a sterile,
transparent dressing. When
Elettrocatetere
s obvious or confirmed, the electrode
removed after inserting a new electrode
erent route. Blood cultures should be
antibiotics administered intravenously.
on of a permanent pacemaker site
r in <1% of cases. Again the responnism is nearly always staphylococcus
0). Superficial infection of the wound
usually be promptly treated with antiocket infection, however, will require
generator extraction, wound drainage
onged systemic, anti-staphylococcal
(Figs. 12.31–12.33). Lead extraction
ot too difficult early after implantation,
screw-in leads have to be unscrewed
myocardium before applying traction to
). Removal late after implantation can
Infezione
Fig. 12.33 Large globules
of pus (arrow) can be sent
for culture and antibioticsensitivity testing. Leads and
generator have to be
removed
Fig. 12.31 Redness, pain, swelling, and tenderness of
the pacemaker pocket are the usual signs of serious
Staphylococcus aureus infection. Although antibiotics
diminish the signs of inflammation, chronic exudates/disfrom an old pacing system that could not be
charge from the wound forms
a crust
covering
the
removed
in entirety)
(Fig. 12.34
). Itwound
presents as
discomfort and swelling in the ipsilateral arm
and shoulder, often with distended veins in the
upper arm and in the subclavicular and pectoral
region and often an engorged external jugular
vein (Figs. 12.35 and 12.36). Venography of the
axillary/subclavian vein will confirm the diagnosis and the exact site of occlusion (Figs. 12.37
and 12.38).
Patients should be treated initially, at least, by
analgesia and anticoagulant therapy for
3–6 months. Usually the swelling, discomfort,
However, it should be avoided in patients with
bacteremia and in younger/fitter individuals who
will require a new pacing system, since persistent
bacteremia, tricuspid endocarditis, and infection
of the new system is likely to follow. Extraction
procedures are discussed in Chap. 19.
Subclavian Vein Thrombosis/
Thrombophlebitis
and signs of phlebitis will disappear as recanalization of the thrombosed subclavian vein occurs
within the first 4–6 weeks.
In the rare event of persistent, progressive
edema and pain in the arm, removal of the pacing
leads and generator will be necessary and a new
system will be required on the contralateral side.
Late Complications
Complications seen after hospital discharge are
listed in Table 12.2.