CHAPTER and posterior fascicles (Edwards, 1991). Under


The cardiac conductive
system and its electrical connection structures have been provided strongly by
anatomical and electrophysiological studies (Saremi
et al., 2009).

   The conductive system of the heart is
composed of the sinoatrial node (SAN), Bachmann’s bundle,  the atrioventicular node (AVN), the HIS
bundle, the right bundle and left bundle branches, the anterior fascicles
and the Purkinje fibers (Ho  et al, 2002; Sanchez-Quintana 
Ho , 2003; Malouf et al., 2004)

   The SA node is the primary pacemaker of the heart,
situated in the upper right atrium, generating electrical pulses automatically.
These pulses spread as waves of electrical excitation all over the atria,
atrial contraction occurs due to fast propagation to the left atrium achieved
by the Bachmann’s bundle (Tusscher& Panfilov, 2008).

   The region of the AV node is the only
electrical connection between the atria and ventricles through it the excitation
passes from atria to ventricles. Physiological delay in the passage of the
electrical wave from the atria to the ventricles occurs due to the slow
propagation in the AV node, ensuring that the ventricles contract after the
atria (Tusscher& Panfilov, 2008).

His bundle runs through the right fibrous trigone and before it divides into
the left and the right bundle branches; it runs through the junction between
the membranous and musclular septum (Anderson & Brown, 1996).

   Along the
moderator bands the right bundle branch proceeds to reach the anterior
papillary muscle (Saremi et al., 2009). While the left bundle branch
forms a broad sheet of conductive fibers which divides through the
interventricular septum (left side) to anterior and posterior fascicles (Edwards,

physiological condition , the electrical impulses generated from the sinus node
is transmitted to the AV node and then rapidly conducted through the
His-purkinje conducive system to the right ventricle and to the left ventricle
simultaneously resulting in ‘synchronous’ electrical activity and contraction
of the heart (van Geldorp et al., 2011).

   Electrical activation normally starts at the
endocardium of the apex and progresses towards the epicardium of the base
resulting in a coordinated and efficient mechanical contraction that is
essential for ideal ventricular execution. (Ikonnikov and Yelle, 2009).

  ‘Synchronous activation’, ‘electrical
synchrony’, ‘euchrony’ those terms are used to describe normal physiological
and electrical activity (van Geldorp et al., 2011).

   During normal electrical activation,
synchrony is observed between both ventricles (interventricular synchrony) and
within each ventricle (intraventricular synchrony) ,atrium & ventricle
(atrio-ventricular synchrony), (Baronait?-D?donien?a et al., 2014)

arrhythmias can occur due to any abnormality in any part of the conductive
pathway (Tusscher& Panfilov, 2008).  Left bundle branch block LBBB is an example
of abnormal conductive pattern involving the His-purkinje system which leads to
indirect delay in electrical and mechanical activation of the left ventricle (Imanishi
et al., 2006; Fantoni et al., 2005; Niu et al., 2006).

 An artificial pacemaker is a device that
generate stimulus from a pulse generator through a lead wire to the heart causing
myocardial depolarization resulting in myocardium contraction. ‘Mechanical
capture’ is the term that describe myocardial contraction following electrical
depolarization.  (Wang et al., 2008)

were developed for patients with symptomatic marked bradycardia or asystole due
to high degree AVN or SAN dysfunction who usually suffered from cardiac syncope
or heart failure (Corcoran and Davis, 2012).

   Through the
venous system one or two pacing lead wires are implanted to right ventricle and/or right
atrium.The leads are connected to a subcutaneously implanted pulse generator
(Christoffels and Moorman, 2009)

    Pacemakers might pace a single chamber
(atrium or ventricle)  or might pace both
“dual chamber”, activating the atria and ventricles in sequential manner with
preservation of AV synchrony. (Lamas & Ellenbogen, 2004).











NASPE/BPEG Generic pacemaker code

1987 , the classification of pacemaker function developed as the NASPE/BPEG (
North American Society of Pacing and Electrophysiology/British Pacing and
Electrophysiology Group).After that this classification modified to contain
rate modulated and multisite pacing (Wang
et al., 2008) (Table A).

The first litter in the code refers to the paced
cardiac chamber , which may be the atrium (A), ventricle (V) , both the atrium
and the ventricle(D or dual), or none(O).


The second litter in the code represents the sensed cardiac
chamber, which may include the atrium (A), ventricle (V), both atrium and
ventricle (D or dual), or none (O).


The third litter in the code represents the function that the
pacemaker performs: triggered (T), inhibited (I), triggered and inhibited (dual
or D), or none (O).


    Triggered means pacing in the chamber paced
after the sensing of intrinsic activity in the chamber sensed (Wang et al.,
2008) or in another words, the pacing device will emit a pulse only in
response to a sensed event (Hayes &  Furman ,2004).

forth litter in the code represents the rate modulation. Rate modulation is the
ability of the pacemaker increases the patient’s heart rate in response to
patient activity and exercise (Wang et
al., 2008). Its aim to imitate the normal physiological heart rate in
response to activity and exercise (Corcoran
and Davis, 2012).

  Rate adaptive pacing may be programmed as
needed to manage symptomatic chronotropic incompetence (Gillis et al., 2012).

   Improvement in exercise performance with
rate adaptive pacing versus non-rate adaptive pacing modes has been proved by
exercise studies (Lau, 2009).

  Many sensors (vibration, respiration and
pressure) are used to detect patient activity and exercise (Wang et al., 2008). The most physiological imitation sensor is the
respiration sensor, as it responds to changes in the respiratory rate (Corcoran and Davis, 2012).


   The fifth litter in the code is the site of
multisite pacing (Wang et al., 2008), atrial multisite pacing is a
method to prevent atrial fibrillation(AF) & ventricular multisite pacing is
a treatment for pacing a patient with dilated cardiomyopathy (Hayes
Furman ,2004).

A: NASPE/BPEG Generic Pacemaker Code (Wang et al., 2008)

I Chamber Paced

II Chamber Sensed

III Response to sensing

IV Rate modulation

V Multi-sites pacing


















Dual (T+I)




(B): different pacing modes (Wang et al., 2008)




Clinical uses


Needs only single atrial lead
Preserve AV & VV synchrony

Avoided if AV block present due
to no ventricular pacing

SND without AVN disease


Needs only single ventricular

AV synchrony is not preserved

AV block in patients with  chronic AF


AV synchrony is maintained for
patients with SND disease

Needs 2 leads
More complex

Bradycardia caused by SND or AVN


AV synchrony is maintained for
patients with AVN disease
One special designed  lead can be used

AV synchrony not preserved if the
patients develop sinus bradycardia

Bradycardia caused by AVN disease
with intact sinus node


AV synchrony is preserved during
atrial pacing

AV synchrony is not preserved
during atrial sensing

For patients with sinus
bradycardia sensing of atrial arrhythmia.
Occasionally used as a
stand-alone pacing mode but more frequently as a mode switching pacing mode.



In the VVI mode, the
ventricle is the sensing and pacing chamber so, Pacing occurs if there is no
intrinsic ventricular activity. Inhibition of the ventricular pacing occurs
after sensing ventricular activity.Atrial events are not sensed in that mode.

The best candidates for
VVI or VVIR pacing are chronic AF patients (wang
et al., 2008).



Atrial and ventricular
sensing and pacing are present in that dual chamber DDD mode (Wang et al., 2008)

events inhibits atrial and ventricular stimulus delivery (Streckenbach, 2008). Atrial pacing occurs when there is no
intrinsic atrial activity ( e.g sinus arrest or sinus bradycardia) (Wang et al., 2008).

If there is no
intrinsic ventricular event, the ventricular paced events track the intrinsic
atrial activity that occurs with a specific programmed interval ( the AV
interval, AVI) (Wang et al., 2008)

If the atrial rate increases
the pacemaker will track it up to maximum programmed rate (upper tracking rate)
to prevent supraventricular tachycardias which will interfere with ideal
ventricular filling ( Streckenbach,

and permanent pacemaker:

The second most common
indication for permanent pacemaker after AVN dysfunction is SND. (Mond and whitlock 2011; Gillis et al.,

SND includes sinus bradycardia,
senatorial block , sinus arrest , chronotropic incompetence and
Tachycardia-bradycardia ( sick sinus syndrome ) (Gillis et al., 2011; Semelka et al., 2013)

Permanent pacemaker is
the ideal treatment in irreversible symptomatic SND (Gillis et al., 20012)

AV block and AF are the
two important points should be assessed in SND patients (Gillis, 2011; Semelka et al., 2013)

In SND patients the
incidence of occurrence of AV block after pacemaker implantation within 5 years
is 3 – 35% (Kristensen et al., 2001)

The developing
incidence of AF in SND patients is affected by pacing duration, pacing mode and
percentage of ventricular pacing (Gillis and morck, 2002; Gillis, 2011)

The incidence rate of
AF in SND patients at the diagnosis time is 40-70% (Gillis and morck, 2002; lamas 2002; Nielsen
et al., 2011). AF occurs in 68% of the SND patients on dual chamber pacing
during long term follow up (Gillis and
morck, 2002)

of pacemaker device and mode for SND patients according to ACCF/AHA/HRS 2012

Single chamber atrial pacing (AAI) or dual chamber pacing (DDD) is indicated in
patients with SND without impairment in AV conduction (Class I A). (Lamas et al., 2002; Kerr et al., 2004;
Hearley et al., 2006)

Rate adaptive pacing can be helpful in significant symptomatic chronotropic
incompetence patients (Class IIa C). (Padeleti
et al., Lamas et al., 2007)

Single chamber pacing is indicated when frequent pacing is not expected and
when the patient has significant comorbidities that affect survival expectance.
(Class IIb C). (Connolly et al., 2000;
Lamas et al., 2002; Kerr et al., 2004)

Dual chamber pacing or single chamber atrial pacing is not recommended in
permanent AF patients (Class III C). (Gillis,
2006; Epstein et al., 2008; Gillis et al., 2011; Nielsen et al., 2011)

block and permanent pacemaker:

(AV) block is classified into first, second, and third-dgree (complete) block (Mymin D et al., 1986), second degree
heart block divided into Mobitz type 1 (wenckebach) and Mobitz type 2. (Barold and Herweg, 2012)

As a role in
first degree heart block no need for any intervention (Corcoran and Davis, 20012), but if symptoms related to impairment
of ventricular filling especially with exercise, pacing may be helpful. (Barold et al., 2006; Carroz et al., 2010)

Mobitz type 1
occurs at the AV node level (Vardas et al.,
2007; Barold and Herweg, 2012), and pacing is not indicated except if the
patients developed bradycardia related symptoms (Barold and Vardas et al., 2007)

Mobitz type 2
occurs at the His purkinje system level
(Vardas et al., 2007; Barold and Herweg, 2012), and pacing indicated in
asymptomatic Mobitz type 2 because the condition commonly progress to
symptomatic complete heart block (Barold
and Herweg, 2012; Seiler 2014)

The most common
bradyarrythmia indicated for permanent pacemaker is complete heart block (Kearney et al., 2015)

Generally asymptomatic
BBB has a very low risk to progress to complete heart block and there are no
benefits from pacing (Corcoran and
Davis, 2012)

of pacemaker device and mode for AV block patients according to ACCF/AHA/HRS

Patients with AV block are indicated for dual chamber pacemaker (class I C) (Toff et al., 2005)

Developing of pacemaker syndrome in AV block patients is an indication for dual
chamber pacing (Class I B) (Dretzke et
al., 2004)

Single chamber pacing is indicated in AV block patients when the patient has
significant comorbidities that have effects on the clinical outcomes and who
has vascular access problems that limits implantation of an atrial lead (Class
I B) (Toff et al., 2005)

Patients with AV block and normal SAN function can take benefits from dual
chamber (VDD) pacing (Class IIa C) (Schaer
eet al., 2007)

Patients with AV block and permanent AF are not indicated for dual chamber
pacing (Class III C) (Epstein et al.,



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