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CardiacPacingandICDsEllenbogenandWood

Chapter 1- Indications for Permanent and Temporary Pacing

I. Anatomy
A. SA node- junction of RA and SVC; fed by SA nodal artery and proximal
branch of RCA or left circumflex; lots of P cells (initiate impulses-
automaticity); normal impulse generator
B. AV node- fed by large AV nodal artery, RCA, and septal branches of
LAD, P cells too (not as many as SA); delays impulse (.04 seconds) to
allow complete atrial emptying, subsidiary ppm, acts as filter limiting
ventricular rates
C. His Bundle- purkinje fibers emerge from AV node to form this; fed by AV
nodal artery, branches of LAD; conduct impulses from AV node to
bundle branches
D. Bundle branches- starts in muscular septum and branches out in ventricles,
fed by LAD, RCA; activates ventricles
II. Indications for Permanent Pacing
A. Class I- conditions for which there is evidence and /or general agreement
that ppm placements is beneficial, useful, effective
B. Class II- conflicting evidence and/or divergence of opinion about the
usefulness/efficacy
i. IIa weight of evidence in favor of
ii. IIb usefulness/efficacy less well established
C. Class III- evidence or general agreement that ppm is not useful/effective
or might cause harm
III. Acquired AV Block
A. Acquired AV block with syncope (Stokes-Adams attacks) was first
indication for pacing
B. In the presence of symptoms documented to be DT AV block, pacing is
indicated regardless of the site of the block
C. AV Block- see cause of acquired high-grade AVB pg 11 Ellenbogen
i. Class I. Third degree and advanced second degree AV block
at any anatomic level (Neuromuscular disease- Kearnes-
Sayre syndrome, Erbs dystrophy)
ii. Class IIa
1. Asymptomatic third-degree AVB with rate >=40bpm
2. Asymptomatic type II second degree AVB with a narrow
QRS (if QRS is wide=class I)
3. Asymptomatic type I
4. First or second degree with symptoms similar to ppm
syndrome
iii. Class Iib pg 7-8 Ellenbogen
IV. Chronic Bifasicular or Trifasicular Block
Class I
1. Intermittent 3
rd
degree AVB
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2. Type II 2
nd
degree AVB
3. Alternating BBB
V. Sinus Node Dysfunction
A. Disorder includes brady, sinus arrest, SA block, SVT (atrial or junctional),
alternating periods of brady/asystole
B. Quite common, incidence increases with age; important to correlate
symptoms with bradyarrhythmia; more patients are implanted for this
reason than any other indication
C. Common meds that cause SA dysfunction or AVB- digitalis,
antihypertensive agents, beta adrenergic blockers, calcium channel
blockers, antiarrhythmic drugs, psychotropic meds
D. Class I- (see pages 17-18 ellenbogen)
i. SA node dysfunction with documented symptomatic brady or
sinus pauses
ii. Symptomatic chronotropic incompetence
VI. Neurocardiogenic Syncope/ Hypersensitive Carotid Sinus Syndrome- neurally
mediated syncope- form of abnormal autonomic control of the circulation
(syncope accounts for 6% of hospitalizations)
A. Three types
i. Cardioinhibitory- ventricular asystole of at least 3 seconds
due to sinus arrest or CHB- this one will be benefited most
by ppms
ii. Pure vasodepressor response
iii. Mixed
B. Pacemaker therapy considered in pts only when symp severe, recurrent
and cannot be controlled by more conservative measures (avoidance of
stimuli, beta blockers, midodrine hydrochloride- ProAmatine and or
fludrocortisone acetate- Florinef)
C. Class I- Recurrent syncope caused by CSS see pg 22 ellenbogen
V. Causes of Torsades- see pg 26 ellenbogen
VI Permanent PPM mode selection
A. largely based on the desire to maintain AV synchrony
VII. Disorders of AV conduction
A. Most commonly caused by inferoposterior infarct, supplied by LCX
B. Risk of progression from 1
st
degree to high grade AVB is 10-30%


Chapter 2- Basic Concepts of Pacing

I. Basic EP
A. Excitability- the property of biologic tissue to respond to a stimulus with a
response that is out of proportion to the strength of the stimulus
i. Cardiac myocytes- there is a separation of charge across the cell
membrane that results in a resting transmembrane electrical
potential; the concentration of NA+outside the cell exceeds the
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concentration inside; the inside of the cell has a 35- fold greater
concentration of K+versus outside
ii. See pg 48 ellenbogen for resting action potential
II. Stimulation Threshold- the delivery of a polarizing electrical impulse from an
electrode in contact with the myocardium with the generation of an electrical
field of sufficient intensity to induce a propagating wave of cardiac action
potentials.; definition: the minimum stimulus intensity and duration necessary
to reliably initiate a propagated depolarizing wavefront from an electrode.
A. Strength Duration Relation- a small change in pulse duration is associated
with a significant change in the threshold amplitude at short pulse
durations; however, only a small change at longer pulse durations
i. Rheobase- the least stimulus voltage that will electrically stimulate
the myocardium at any pulse duration (usually determined at
2.0ms)
ii. Chronaxie- as the threshold pulse duration at a stimulus amplitude
that is twice rheobase voltage (pg50)
iii. Energy-
E=V^2/Rt
E=the stimulus energy
V=stimulus voltage
R=total pacing impedance
t=pulse duration
****Since the energy of a pacing stimulus increases by the square of the voltage,
doubling the stimulus voltage results in fourfold increase in the stimulus energy.

-The chronaxie pulse duration approximates the point of minimum threshold
energy on the strength-duration curve; with pulse durations greater than
chronaxie, there is relatively little reduction in the threshold voltage; the wider
pulse duration results in the wasting of stimulation energy without providing a
substantial increase in safety margin; at pulse durations less than the chronaxie
there is a steep increase in threshold voltage and stimulation energy.
-Tripling a threshold pulse duration that is greater than 0.3ms may not provide
adequate safely margin
-Stimulus thresholds that are measured by decrementing stimulus voltage until
LOC are usually 0.1 to 0.2V lower than when the stimulus intensity is gradually
increased from subthreshold until capture is achieved.

B. Strength-Duration Curves for Constant-Voltage and Constant-Current
Stimulation
i. Constant-voltage stimulation usually results in a flat curve at
pulse durations greater than 1.5 milliseconds, whereas
constant-current stimulation curve may be slowly
downsloping beyond this duration. (see. Pg 54).
ii. Small changes in pulse duration less than 0.5ms may result in
significantly greater reduction in stimulation safety margin
for constant-current than for constant-voltage generators.
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Because of this diff. In the shape of the strength duration
curves, the chronaxie pulse duration of a constant-current
strength duration relation is significantly greater than that
observed with constant-voltage stimulation. Therefore a
constant- voltage generator can be set to deliver a narrower
pulse duration than a constant-current generator and yet
provide the same safety margin.

C. Time-Dependent Changes in Stimulation Threshold.
i. See pg. 55 chart; acute rise in threshold that begins within
the first 24 hours. Threshold usually continues to rise over
the next several days, usually peaking at approximately one
week. The typical stimulation threshold then gradually
declines over the next several weeks. By 6 weeks, the
myocardial stimulation threshold has usually stabilized at a
value that is significantly greater than that measured at
implantation, but less than acute peak.
ii. Active fixation electrodes may produce, immed. Following
implant, an increased stimulation threshold that gradually
decreases over the next 20 to 30 minutes. This is likely RT
acute injury at the myocardial-electrode interface and is
generally not observed with atraumatic passive fixation leads
(current of injury).
iii. In general, the more stable and the less traumatic the
interaction of the electrode and lead with the myocardium,
the lower the rise in threshold over time.
iv. Programming the stimulus intensity greater than 2.8v results
in a marked increase in current drain from the battery.
v. Patients subject to major shifts in potassium concentration or
acid-base balance, such as those with renal failure, may have
transient increases in pacing threshold.
vi. The smaller the surface area of the electrode, the lower the
pacing threshold.
D. Effects of Pacing Rate on Myocardial Stimulation
i. At pacing rates exceeding 250 bpm, pacing stimuli might be
delivered during the relative refractory period, resulting in an
increase in threshold, which may have implications for ATP.
E. Pharmacologic and Metabolic Effects on Stimulation Threshold
i. Stimulation threshold generally increases during sleep and
falls during waking hours. Decreases during exercise DT
autonomic tone and circulation catecholamines.
ii. Increases following eating, hyperglycemia, hyperkalemia,
hypoxemia, hypercarbia, and metabolic acidosis and
alkalosis.
iii. Increases dramatically during acute viral illnesses, esp. in
children.
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iv. Isoproterenol may restore exit block in some patients. Beta-
blockers increase threshold. Corticosteroids can decrease
stim threshold.
v. Raise stim threshold: type I antiarrhythmic drugs quinidine,
procainamide, flecainide, and encainide.
vi. Amiodarone (Type III) is questionable if raises stim. thresh.
III. Impedance- the sum of all factors that oppose the flow of current in an electric
circuit. Not necessarily the same as resistance.
Ohms Law: V=IR current=I, resistance=R
i. the leading edge voltage of a constant-voltage ppm is fixed, and
the lower the resistance, the greater the current flow. In contrast,
the greater the resistance, the lower the current flow.
ii. Powered by lithium iodine batteries with a fixed amount of charge;
pacing impedance is an important determinant of battery longevity.
iii. Total pacing impedance is determined by factors that are RT the
lead conductor (resistance), the resistance to current flow form the
electrode to the myocardium (electrode resistance), and the
accumulation of charges of opposite polarity in the myocardium at
the electrode-tissue interface (polarization).
iv. The resistance to current flow by the lead conductor results in a
voltage drop across the lead with a portion of the pacing pulse
converted into heat =inefficient use of electrical energy and does
not contribute to myocardial stimulation. The ideal pacing lead
would have a very low conductor resistance.
v. In contrast, the ideal pacing lead would also have a relatively high
electrode resistance to minimize current flow and maximize battery
life. The electrode resistance is largely a function of the electrode
radius, with higher resistance provided by a smaller electrode.
vi. An electrode with a small radius minimizes current flow in an
efficient manner.
vii. Electrodes with a small radius also provide increased current
density and lower stimulation thresholds
viii. A lead with 500 ohms of resistance vs. a lead with 1000 ohms,
would decrease current drain by 50% with each pacing pulse.
ix. But cant get too small because risk microdislodgement.
x. Polarization impedance- is an effect of electrical stimulation and is
RT the movement of charged ions in the myocardium toward the
cathode. Caused by the negatively charged cathode inducing the
accumulation of two layers of oppositely charged ions in the
myocardium.
xi. Because polarization impedes the movement of charge in the
myocardium, it is inefficient and results in an increased voltage
requirement for stimulation. Thus polarization impedance reduces
the effectiveness of a pacing stimulus to stimulate the myocardium
and wastes current.
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xii. Polarization is directly RT the duration of the pulse and can be
minimized by the use of relatively short pulse durations. It is
inversely RT surface area.
xiii. To maximize electrode resistance but minimize polarization, the
surface area of the electrode can be made large but the geometric
radium small by the use of a porous coating on the electrode.
xiv. Electrodes constructed with activated carbon, or coated with
platinum black or iridium oxide are effective in minimizing the
wasteful effects of polarization and in diminishing afterpotentials
which can interfere with sensing.
xv. Pacing impedance is characterized by a fall over the first 1 to 2
weeks following implantation. The chronic pacing impedance then
rises to a stable value that is, on average 15% higher than at
implant. See pg 64 for chart
IV. Biventricular Pacing- review impedance
IV. Sensing
A. Intracardiac Electrograms- produced by the movement of electrical current
thru myocardium.
i. During depolarization, the outside of the cell becomes electrically
neutral with respect to the inside. Therefore, as a wavefront of
depolarization travels toward an endocardial electrode that records
from resting myocardium, the electrode becomes positively
charged relative to the depolarized region. This is manifested in the
intracardiac electrogram as a positive deflection. As the wavefront
of depolarization passes under the recording electrode, the outside
of the cell suddenly becomes negatively charged relative to resting
myocardium, and a brisk negative deflection is inscribed in the
EGM. The peak negative deflection in the EGM is known as the
intrinsic deflection, is considered the moment of myocardial
activation underlying the recording electrode.
ii. B/c of greater mass, the normal vent EGM is usually of far greater
amplitude than the normal atrial EGM. See pg 70 for deflection
iii. By using Fourier transformation one can express the frequency
spectrum of an electrical signal as a series of sine waves of varying
frequency and amplitude. Maximum density of frequencies for R
waves is usually found between 10 and 30 Hz. Removing
frequencies below 10Hz markedly attenuates the T wave amplitude
without significantly influencing the R wave. The T wave is
usually a slower, broader signal that is composed of lower
frequencies, generally less than 5 Hz.
iv. Similarly , the FFRW in the atrial EGM is composed
predominantly of low-frequency signals. Therefore by high-pass
filtering of the intracardiac EGM, many of the low frequency
components can be removed.
v. In contrast, the frequency spectrum of myopotentials ranges
approx 10 to 200 Hz, with overlap of P and R waves. Despite the
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high frequency filtering, inappropriate sensing of myopotentials
remains a potential prob with unipolar config.
vi. For the EGM to be sensed by the sense amplifier of an implantable
ppm, the signal must be of sufficient amplitude, measured in peak-
to-peak voltage. In addition, the intrinsic deflection must have a
sufficient slope. The peak slope (dV/dt) of the EGM (slew rate) is
of critical importance to sensing. The sense amplifier of most ppm
has a center frequency (the freq for which the amplifier is most
sensitive) in the range of 30 to 40 Hz, so frequencies greater than
this are attenuated and less likely to be sensed. In general, the
higher the slew rate, the higher the frequency content.
vii. Thus slow, broad signals with a low slew rate may not be sensed,
even if peak-to-peak amplitude is large.
B. Unipolar and Bipolar Sensing
i. Bipolar lead- electrodes are within the heart with an interelectrode
distance that is usually less than 3cm. A unipolar lead has
interelectrode distance of 30 to 50 cm.
ii. Because the bipolar config represents the signal at the cathode
minus the signal at the anode, the net EGM may be considerably
different.(see pg 72 for further explanation)
iii. Normal PVARP begins after a sensed or paced vent event
C. Time related Changes in EGM
i. The injury of current usually returns to the isoelectric line over a
period ranging form several minutes to several hours.
ii. The amplitude of the EGM typically declines abruptly within
several days following implantation, with a gradual increase
toward the acute value by 6 to 8 weeks. Chronic R wave amplitude
about 85% of implant value and slew rate about 50-60% of implant
value.
iii. Active fixation leads follow a different pathimmediately
following lead placement, there is a markedly attenuated amplitude
and slew rate. Over the next 20-30 minutes, the EGM amplitude
increases- likely due to current of injury.
D. Sensing Impedance
i. The electrode resistance is inversely RT electrode surface area.
Polarization impedance is also inversely RT to electrode surface
area. Thus electrodes with large surface area minimize source
impedance and contribute to improved sensing.
E. Automatic Capture Features
i. The Autocapture feature of STJ M ppm allows the ppm to
automatically adjust the amplitude of the stimulation pulse by
detecting capture in the vent. These ppms require a bipolar vent
pacing lead that must have low polarization properties for the distal
electrode. The presence or absence of vent capture is determined
by sensing ER from the ring electrode. See pg 79 for further
explanation.
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ii. The MDT Vent Capture Mgmt features a strength duration
threshold at a programmed interval see pg 81-82 for further details.
V Lead Design- leads have 5 major components- the electrode, the conductor,
insulation, connector pin, the fixation mechanism.
A. Electrodes
a. The smaller the radius of the electrode, the greater the current
density.
b. The resistance at the electrode-myocardial interface is higher
with smaller electrodes, providing efficient use of a constant-
voltage pulse and improving battery longevity.
c. Sensing impedance and polarization are decreased with
electrodes of larger surface area.
d. The ideal pacing lead would have an electrode with a small
radius (to increase current density) and a large surface area (to
reduce polarization). The solution to these conflicting
considerations for optimal stimulation and sensing
characteristics has been addressed by the development of
electrodes that have a small radius but a complex surface
structure that provides a large surface area.
B. Electrode Shape
a. Electrodes with a smooth, hemispherical shape produce a
uniform current density. In contrast, electrodes with more
complex shapes typically produce an irregular pattern of
current density, with hot spots at the edges and points of the
electrode (good).
C. Surface Structure
a. The use of electrodes with a textured surface has resulted in a
dramatic increase in the surface area of the electrode without in
increase in radius. The textured surface of modern leads
minimizes polarization and improves sensing and stimulation
efficiency (Elgiloy, platinum, or iridium oxide).
b. The performance of carbon electrodes has been improved by
roughening of the surface, a process known as activation; this
structure can lead to the ingrowth of tissue into the electrode.
c. The importance of low polarization has greatly increased the
ability of ppms to sense evoked response.
D. Chemical Composition
a. Metals such as zinc, copper, mercury, nickel, lead and silver
are assoc with toxic reactions in the myocardium and are
unsuitable in the use chronically implanted leads.
b. These metals also result in increased chronic stimulation
thresholds.
c. Stainless steel alloys are variably assoc with potential for
corrosion.
d. Titanium and tantalum have been shown to acquire a surface
coating of oxides, which may impede charge transfer.
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e. However, titanium that is coated with microscopic particles of
platinum or vitreous carbon has been found to have excellent
long-term performance as a pacing electrode.
f. Elgiloy is acceptable when used as a cathode, but corrosive
when used as an anode.
g. The materials presently in use for the electrodes of permanent
pacing leads include platinum-iridium, Elgiloy, platinum
coated with platinized titanium, vitreous or pyrolytic carbon
coating a titanium or graphite core, platinum, or iridium oxide.
The platinized-platinum and iridium-oxide have been
associated with a reduced degree of polarization. Carbon
corrodes the least.
E. Steroid-Eluting Electrodes
a. Incorporates a silicone core that is impregnated with a small
quantity of dexamethasone. The core is surrounded by a porous
titanium electrode that is coated with platinum.
b. It should be emphasized that the corticosteroid eluted from the
lead does not affect acute stim thresholds. Rather, the steroid
controls chronic evolution of pacing thresh.
D. Fixation Mechanism
a. Passive fixation leads, in general, are more difficult to
extract than active fixation.
F. Active Fixation Leads
a. inactive helix leads are assoc with lower acute thresholds.
b.Active fixation leads have significantly reduced the risk of atrial
lead dislodgement, but the chronic pacing thresholds are somewhat
higher.
c.Risk of myocardial perf is higher
F. Condutors
i. The most common site for lead fracture is at the fulcrum of a freely
moving conductor with a stationary point (subclavian vein and first
rib).
ii. Leads also may fail at the site of mechanical injury, such as with
tight fixation sutures.
iii. Stainless steel has the potential of corrosion and therefore was
abandoned for the use of conducting coils of early multifilar leads.
It was replaced by Elgiloy or MP35N, an alloy of nickel.
iv. More recently, conductors made of DBS (drawn-brazed-strand),
six nickel alloy wires that are drawn together with heated silver,
has been introduced.
v. DBS is no longer used with polyurethane because of the potential
for internal oxidation of the poly by the silver chloride from the
DBS conductor.
G. Insulation
i. Platinum-cured silicone rubber, which is characterized by
improved mechanical strength. The coefficient of friction has been
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greatly reduced by the development of a lubricious fast pass
coating. Improved leads are smaller external diameter and are far
easier to manipulate when in contact with another lead.
ii. See chart pg 93 on pacemaker lead insulation.
iii. The 55D polymer is now the predominant form of poly used for
leads(greater tensile and tear strength but stiffer than P80A).
iv. surface cracks are likely RT environmental stresses rather than to
biologic degradation. The surface cracks likely develop in the
manufacturing process as the heated poly cools more rapidly than
the inner core, leading to opposite stresses within insulation.
H. Epimyocardial Leads
i. Used in clinical situations involving abnormalities of the tricuspid
valve, congenital heart disease, or when ppm leads are implanted
during intrathoracic surgical procedures.
ii. The use of three turns has been shown to reduce exit block as
compared with a two-turn screw.
I. Connectors
i. Industry wide standard of IS-1, sealing rings on a 3.2mm lead
connector see pg 96-97 for lead connectors
J . Specialized Coatings to Prevent Tissue Ingrowth
i. The first consideration is to make the lead isodiametric so that
there are no ridges or areas of increased diameter along the lead
that would increase the risk of removal.
ii. ePTFE- prevents the ingrowth of tissue into the coil electrodes
while having no significant effect on the conduction of electrical
energy.
V. Pulse Generators
A. Power Source- modern ppms use lithium as the anodal element and iodine
as the cathodal element
i. A major advantage of the LiI battery is the solid nature of the
material- allowing the cell to be hermetically sealed and relatively
persistent to corrosion
ii. LiI cell generates approx 2.8v at BOL. A voltage multiplier may be
used to allow output pulses of greater than that generated by the
battery.
iii. The net result is that by programming the ppm to a voltage that is
double the battery voltage, the charge taken from the battery is
equal to twice that delivered to the lead and the total amount of
charge drained from the battery increases fourfold.
iv. The longevity of the battery is determined by the chemical
elements of the battery, the size, the amount of internal discharge,
and the voltage decay charact.
v. To maximize battery life, the ideal electrochemical cell would have
no internal discharge.
vi. LiI has a self discharge of about 1% a year.
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vii. For a battery to be suitable for a ppm, the decay charc should be
predictable. The ideal battery should have a predictable fall in
voltage near the end of life, yet provide sufficient service life after
the initial voltage decay to allow time for the ERI to be detected.
viii. The voltage produced by a LiI cell is inversely RT the internal
battery impedance. The internal impedance of the battery increases
with the thickness of the LiI electrolyte layer, from less than 1k
ohm at the beginning of life to over 15k ohm at the extreme EOL.
The voltage generated by the cell declines almost linearly rom the
initial value of 2.8v to 2.4v at approx 90% of the useable battery
life. Following this, the voltage declines exponentially to 1.8v at
the EOL. The magnet related pacing rate of a ppm is RT to the cell
voltage.
ix. In order, output pulse and impedance are major factors of current
drain.
x. The cost of doubling the output voltage (2.8 to 5.6- uses two
capacitors in parallel) is a fourfold increase in current drain from
the battery. A threefold increase (8.4v- three capacitors in parallel)
results in a nine-fold increase in current drain.
xi. The lower the impedance, the greater the current delivered and the
greater the drop in voltage from leading edge to trailing edge
during the pulse. Even, though the term constant voltage is used to
describe the stimulus waveform of ppms, in the reality the output
voltage of the pulse is not constant beginning from end.
xii. The constant current pulse is typically flat, with little or no change
in current from leading edge to trailing edge. However as the
polarization impedance rises during the pulse, the resulting voltage
must also rise proportionally to maintain the current at a constant
level. At extremely high lead impedances, the voltage required to
maintain a constant-current pulse may exceed the capabilities of
the battery.
xiii. The output waveform of the pulse generator is followed by a low-
amplitude, long-duration wave of opposite polarity known as the
afterpotential. The afterpotential is caused by the polarization at
the electrode-tissue interface and is dependent on the stimulus
amplitude and duration.
xiv. To reduce the afterpotential, the output circuit of some
manufacturers incorporates a fast recharge pulse, during which the
electrode polarity is reversed for a short period following the
output pulse.
B. Power Source
i. To minimize attenuation of the signal the sensing amplifier must
have an input impedance greatly in excess of the sensing
impedance. The greater the input the impedance, the less the EGM
is attenuated by the amplifier. The input impedances of the sense
amplifiers used in ppm systems are greater than 25,000 ohms.
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ii. The bandpass filters of different manufacturers vary significantly
with regard to center freq (from approx 20 to 40Hz), so
intracardiac egms measured with a PSA of one manufacturer may
provide different values compared to the next.
iii. Signals with amplitude greater than the sensitivity threshold level
are sensed as intracardiac events, whereas signals of lower
amplitude are discarded as noise.
iv. Ppms also contain noise reversion circuits that change the pulse
generator to an asynch pacing mode when the sensing threshold is
exceeded at a rate faster than the noise reversion rate.
v. The Zener diode protects the integrated circuit from high external
voltages such as may occur during defib shocks or electrocautery.
When the input voltage carried by the pacing leads exceeds the
Zener voltage, the excess energy is shunted back to the
myocardium thru the leads.
vi. During the ventricular blanking period, the ventricular sensing
amplifier is turned off immediately following the atrial pacing
pulse.
C. Timing Circuits
i. The pulse generator contains a rate-limiting circuit that prevents
the pacing rate from exceeding an upper limit in the case of a
random component failure. This runaway protection rate is
typically in the range of 180 to 220ppm.
D. Microprocessors
i. ROM (typically 1 to 2 kilobytes of 8 to 32 bits) is used to guide
sensing and output circuits. RAM is used to store diagnostic
information regarding pacing rate, intrinsic heart rates, and sensor
output.
E. Rate-Adaptive Sensors
i. The ideal sensor demonstrates sensitivity and specificity.
F. Activity Sensors and Accelerometers
i. A piezoelectric ceramic crystal functioning as a strain gauge is
bonded to the inside of the pulse generator case or to the circuit
board. As the crystal flexes and deforms in response to mechanical
vibration or pressure, an electric current is generated. The
magnitude of the electric current for the crystal is RT the freq and
amplitude of vibrations. The output of the sensor is processed
electronically and used to modulate changes in pacing rate.
ii. The piezoelectric accelerometer is mounted to the hybrid circuitry-
standard method for detection of body vibrations.
iii. In contrast, piezoresistive accelerometers measure changes in
electrical resistance that occur with mechanical deformation of the
sensor and require a somewhat greater current to drain to power
the sensor.
iv. Exercise workload is more proportional in the anterior-posterior
axis than in the vertical axis.
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v. Accelerometers have been shown to produce a RR that is closer to
the expected behavior of the SA node during exercise.
vi. Because the frequency range of the accelerometer signal associated
with exercise is known to have a maximal amplitude less than 4
Hz, the signal can be filtered to remove external noise, which
typically is between 10 and 50 Hz
vii. B/c accelerometers have a constant coupling mass of the sensor
that is independent of the body, these devices offer a more
predictable range of responses during exercise that do activity
sensors.
G. MV Sensors
i. Resp rate, tidal volume, and minute ventilation (the product of
these 2 parameters) increase in proportion to changes in carbon
dioxide production (VCO2). At exercise workloads less than
anaerobic threshold, the MV is closely assoc with oxygen
consumption (VO2).
ii. MV is estimated by freq measurements of transthoracic impedance
between an intracardiac lead and the ppm using the tripolar system.
A low energy pulse of 1mA @15ms is delivered from the ring
electrode. The resultant voltage between the tip and the pulse
generator is measured and an impedance is calculated. The
impedance pulses are subthreshold and are delivered every 50ms.
iii. The impedance is mostly RT the volume and resistivity of blood in
the right heart chambers and systemic venous system.
iv. The impedance signal fluctuates in response to both respiration and
cardiac motion (right ventricular ejec). The signal may also change
in response to arm movement.
v. To minimize the cardiac-related component of the impedance
signal, low-pass filtering of frequencies greater than 48 to 60 hz is
performed.
H. QT Interval
i. QT interval has been demonstrated to shorten with exercise or
sympathetic tone and to lengthen at rest.
ii. Measured from the onset of a pacing stimulus
iii. Although it varies widely among individuals, it is quite consistent
in an individual at rest.
iv. Can be markedly influenced by meds or electrolyte concentrations
v. Disadvantages of the QT sensor involve the requirement for a low-
polarization electrode
vi. Advantages are its responsiveness to emotional factors and the lack
of a specialized lead


Chapter 3- Hemodynamics of Cardiac Pacing
I. AV Synchrony
A. Advantages of AV Synchrony
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a. AV synchrony generally provides similar or slightly greater systolic
and mean blood pressure than vent pacing
B. Cardiac Output
a. Properly timed atrial contraction provides a significant increase in vent
end-diastolic volume and is responsible for the so-called atrial kick
b. There has been a general perception that patients with abnormal
cardiac function benefit most from maintenance of AV synchrony- not
freq DT cardiac output
C. Effects of AV Interval
a. An excessively long AV delay may inadequately fill the ventricle by
causing early mitral valve closure and truncating diastolic filling time
b. Diastolic AV valvular regurgitation may occur with re-opening of the
valve before ventricular systole.
c. An excessively short AV delay may limit active filling of the ventricle
and promote systolic AV valvular regurgitation as ventricular
contraction begins while the AV valves are still open.
d. At rest, 125-200ms is generally the optimal range if the right atrium
and ventricle are paced.
e. Doppler echo is commonly used to optimize the AV interval by
assessing the pattern of early and late diastolic mitral valve flow and
the aortic flow velocity integral. While AV interval can be optimized
at rest, assessing the adequacy of this parameter upright and during
exercise presents greater technical difficulty.
f. With exercise there is a relatively linear decrease in PR interval. The
total reduction in spontaneous PR interval in normal individuals
appears to be about 20-50ms or approx 4ms for each 10-beat
increment in HR.
g. Because some atrial activation has already occurred at the time a
sensed event marks the initiation of the ppm AV interval, the SAV
interval should be about 20-50ms less than a PAV interval.
D. Pacemaker Syndrome
a. Most often results from VVI pacing, but can result in any mode that
cause AV dyssynchrony, even AAI pacing with long PR interval.
b. Syncope, a very uncommon result, is RT profound hypotension- and in
some, a decrease in cardiac output.
c. Additional symptoms of decreased CO include, malaise, easy
fatigability, a sense of weakness, lightheadedness, and dizziness.
d. Symptoms RT higher atrial and venous pressures include dyspnea,
orthopnea, paroxysmal nocturnal dyspnea, fullness and/or pulsations in
the neck and chest, as well as palpitations, chest pain, nausea, and/or
peripheral edema.
e. You sometimes can visualize continuous or fluctuating pulsations in
the neck, neck vein distension, with prominent cannon A waves,
pulmonary rales and rarely peripheral edema.
f. PPM syndrome is most severe when intact retrograde VA is present.
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g. This symptoms result from reduced stroke volume and cardiac output
from the loss of atrial kick, and elevated venous pressures resulting
from atrial contraction against closed AV valves.
h. For patients with PPM syndrome, to help can upgrade to DDD system,
reduce LR to encourage intrinsic conduction, use of hystersis , or
withdrawal of meds that impair SA node function, ensure atrial
capture, avoidance of atrial non-pacing modes (VDD) or atrial non-
tracking modes (DDIor DVI).
II. Hemodynamics of Pacing in HOCM
Hypertrophic obstructive cardiomyopathy represents a special situation for which
pacing may have a role in some patients. These patients have obstruction to LV outflow
caused by hypertrophy of the interventricular septum typically in the subaortic valve area,
combined with systolic anterior motion of the mitral valve. Studies show that by
producing dyssynchrony of LV contraction, dual-chamber pacing reduces the degree of
outflow obstruction and symptoms in many patients.

Chapter 4 Techniques of Pacemaker Implantation and Removal
I. Implant Procedure
A. Site
a. Persistent Left Superior Vena Cava (0.3-0.5%)- drainage into the CS,
which complicates lead positioning. Suspicion of this anomaly may be
raised by finding greater distension and a double A wave in the left
jugular vein compared with that of the right vein, a left
paramediastinal venous crescent on the chest radiograph, and an
enlarged CS on the echo.
b. With PLVC, right sided implants are easier
B. Ventricular Lead Position
a. Under fluro, the RV apical lead is one in which the leads tip is well to
the left of the spine and in pointing anteriorly and slightly caudal.
b. In the AP projection it may not be possible to distinguish whether a
lead is in a posterior coronary vein, the LV, or the RV apex.
c. In the right anterior oblique position, you can observe the position of
the lead with respect to the tricuspid valve which allows you to
visualize how far the lead is in the RV.
d. Failure to record a large current of injury after fixing active-fixation
leads suggests and unstable position.
e. All lead positions should be confirmed by both left anterior oblique
and right anterior oblique views in the lab.
f. It is common for capture thresholds to decrease significantly 15 to 30
mins after active fixation.
C. Atrial Lead Implantation
a. Right atrial appendage preferred site
b. Studies suggest that dislodgement is not more common with atrial
leads, but reliance on the appendage location may mandate the
acceptance of less than ideal pacing characteristics that become
unacceptable over time.
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c. There is no evidence that the atrial stimulation site influences
hemodynamics per se although atrial septal pacing near bachmans
bundle may be of some importance when atrial tachycardia algorithms
are applied
d. The j shaped active fixation can be positioned almost anywhere in the
atrium but may increase dislodgement risk because of the undue
tension at the site of attachment to the endocardium.
D. Single lead VDD Pacing
a. Proximal atrial sensing electrode as well as a tip electrode to sense and
pace the ventricle
b. Good for AVB patients who have normal sinus mechanism.
c. Functionally VVI(R)
E. Complications of Implantation
a. PASE study, 6.1% of 407 patients had a complication- lead
dislodgement, pneumothorax, perforations
b. Harcombe and coworkers found that the rate of late complications
(later than 6 weeks after the procedure) is higher for elective
replacement than initial system implantation.
c. Air embolus can occur when a central vein is accessed by a sheath.
May be signaled by a hiss as air is sucked into the sheath by negative
intrathoracic pressure and may occur suddenly when a heavily sedated
pt, deeply inspires and control over the sheaths orifice is uncontrolled.
d. Symptoms of air embolus include respiratory distress, chest pain,
hypotension, and arterial oxygen desaturation (is significant blockage
of pulmonary artery), however is air amount is small, usually well
tolerated
e. Perforation may occur internally (into another cardiac chamber) or
externally (into the pericardial space) by the pacing lead
f. Old age, female gender, steroid therapy, recent RV infarct, stiff leads
or stylets may be considered risk factors
g. Silent venous thrombosis is not uncommon, 11-12% of patients suffer
asymptomatically with this.
F. Infection
a. Diabetes and postoperative hematoma are predisposing factors.
b. Usually staph aureus or staph epidermidis, more than 1/3 to occur
with new systems
c. Most will warrant an explant with antibiotic therapy
G. Complications of BiV Pacing
a. Unable to place LV lead, 9%
b. Unique complications such as extensive coronary sinus dissection, 4-
7% and coronary venous dissection 2%
H. Lead Extraction
a. A lead that has been in place for 3 months or less should be easily
removed wheras one in place longer than a year may well present
difficulties to fibrosis
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b. Non-isodiametric leads and those with anchoring appendages (tines or
fins) present additional problems
c. Lead extraction/explantation can be done percutaneously or
transthoracically
d. The Accufix J - there was a small metal wired placed within the lead
only to maintain a J shape is subject to fracture under the stress and
strain of clinical use
e. Lead extraction using modern tools has an associated risk of death of
0.6% and a 2.5% risk of potentially life-threatening complications.
f. With modern tools, there is about a 90% success rate of lead
extraction- laser

Chapter 6 Pacemaker Timing Cycles
A three-letter code describing the basic function of the various pacing system was first
proposed in 1974 by a combined task force from the American Heart Assoc and the
American College of Cardiology

- Elimination of crosstalk may be accomplished by extending the ventricular blanking
period, decreasing atrial output, or reducing the ventricular sensitivity

-in an atrial-based timing system, the AA interval is fixed whereas in a ventricular-based
system, the AEI is fixed

-in an atrial-based system, the alternation of the longer AVI with the shorter AR interval
results in ventricular rates that are both faster and slower than the programmed base rate.

-in ventricular based timing, the LR is never violated

-NCAP is used to minimize competition between the sensor and sinus rhythm. If atrial
depol occurs within the alert period, it inhibits atrial output and triggers ventricular
output.

Chapter 7 The Implantable Cardioverter Defibrillator
I. Indications-initially devices were only implanted in patients who had survived a
cardiac arrest or an episode of sustained VT see page 381 for indications of ICD
A. AVID study- compared ICD implantation with antiarrhythmic drug use
(primarily amiodarone) in patients with aborted cardiac arrest or poorly
tolerated VT. There was a significant reduction in mortality in the grps
randomized to ICD implantation. Benefit showed most in pts with a reduced
EF of <35%.
B. MADIT and MUSTT trials evaluated pts with CAD, left ventricular systolic
dysfunction, nonsustained VT, and inducible sustained monomorphic VT
C. In MADIT, patients were randomized to either receive an ICD or
conventional medical therapy, most commonly amiodarone.
D. In MUSTT pts were randomized to either no antiarrhythmic therapy or EP
guided drug therapy
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E. Both trials showed a 50% decreased mortality in those with ischemic
cardiomyopathy.
F. MADIT II was a prospective randomized study of 1232 pts with previous MI
and EF of 30% or less, spontaneous VT or EP testing was not required for
enrollment
G. SCDHeFT study evaluated more than 2500 subjects with CHF (II and III) and
EF <=35%, ischemic or nonischemic. ICD implantation, but not amiodarone,
was shown to reduce all-cause mortality.
H. One cohort that is particularly difficult to manage is those pts with structural
heart disease and a history of syncope.
I. Lead insulation can have an important impact on long-term stability and
function. Silicone is inert, biostable, and biocompatible, but has a high
coefficient friction. It is soft which can make it prone to damage and swell
over time. Poly is biocompatible, has a high tensile strength making small lead
diameters possible, and a low coefficient of friction but it is prone to
environmental stress and metal ion oxidation. Fluoropolymers (PTFE and
ETFE) are the most biocompatible, have high tensile strength allowing small
lead size, but are stiff, susceptible to damage from traction when the lead
migrates, and they are prone to insulation micro defects and have a difficult
manufacturing process.
J . Todays systems have an insulating body of silicone, and in some instances
supplemented by an outside poly layer (not used for insulation) to reduce
friction, abrasion, and scar formation. Metal ion oxidation is avoided as poly
is not in direct contact with the conductors
K. The first large study to evaluate directly the impact of dual chamber pacing
among ICD patients was DAVID.
L. Defibrillation testing
a. A single termination of fibrillation with a given energy level identifies
an energy that may terminate fibrillation in as few as 25% of repeated
attempts DT the probabilistic nature of defibrillation
b. By demonstrating that this same shock energy terminates VF three
times without failure, it may be concluded that the energy level is high
on the probability curve for success and in fact has at least a 75%
chance of terminating VF on further attempts.
c. Two methods predominated DFT- the single energy success and the
step-down protocol
d. Upper limit of vulnerability (ULV)- by delivering shocks of
decreasing energy synchronized to the T wave, a minimal energy level
is found that does not induce VF while lower energies induce VF. The
lowest energy value that does not induce VF is the ULV.
M. Undersensing was most commonly observed with the redetection of VF
following failed shocks. The most likely mechanism of this phenomenon is
stunning of local myocardium following shocks, resulting in diminution of the
EGM near the tip of the lead. With positioning of the RV shock coil farther from
the rate sensing electrode tip, post-shock undersensing is minimized (be careful bc
DFTs can rise with this) see page 395 for auto adjusting sensitivity.
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M. Implantable Cardioverter-Defibrillator Therapies
a. Approx 70% of new ICD systems are dual chamber devices.
b. BiVs are indicated for severe CHF (NYHA III-IV), left ventricular
systolic dysfunction and QRS prolongation, typically left bundle
branch block.
c. The success rates for spontaneous VT are higher than induced
episodes, at about 90%, whereas arrhythmia acceleration rates are low
(1% to 3%).
N. Defibrillation
a. is achieved when a critical mass of myocardium is depolarized by
establishing a critical voltage gradient throughout the ventricular
tissue.
b. The resulting waveform is an exponentially declining voltage, which is
prematurely terminated or truncated before full capacitor discharge.
Thus the maximal delivered energy for an ICD is always less than the
stored energy necessary to fully charge the capacitor.
c. In early ICD systems, monophasic waveforms were used that were
truncated at about 35% of the leading edge voltage; this is referred to
as a 65% tilt monophasic shock.
d. Adjusting pulse width is unlikely to have significant effects of
defibrillation efficacy.
e. For biphasic shocks, the polarity of the voltage pulse is reversed after
the termination of the initial positive phase and a second negative
phase is delivered.
f. Initially the polarity of shocks used the RV coil as the cathode,
however reverse polarity or anodal shocks result in significantly lower
DFTs
g. Besides biphasic waveforms, the most important advance for lowering
DFTs was the development of active pulse generators
h. With a dual coil shocking vector and an active can, mean DFTs
decreased by about 36%; this benefit was DT more to the lowering of
impedance with the active can than to an improvement in shocking
vector
i. In a right-sided implant, there is no significant change in thresholds
with the use of an active can compared with a dual-coil transvenous
lead. This is bc an active can increases defibrillation current
requirements DT a worsened shock vector, which is directed away
from the RV and toward the right shoulder. The reduction in
impedance with the active can offsets the increased current resulting in
no net effect on threshold.
j. Results from the LESS (low energy safety study) suggests that a safety
margin of approx 5j may be adequate in modern ICD systems that
employ biphasic waveforms, transvenous leads and active pectoral
pulse generators.
O. Future Directions
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a. Currently there are over 2 million people in the US with HF, including
about 400,000 new cases annually.
b. With first generation devices in the 1980s, the annual mortality of
patients with CHF was 20-40%, so devices with a 3 yr longevity were
often sufficient.
c. The annual mortality today is less than 7% in pts receiving
angiotensin-converting enzyme inhibitors, aldosterone antagonists and
beta blockers, even for those with NYHA III.
Chapter 9 Cardiac Resynchronization Therapy
I. Heart Failure Epidemic
a. There are 4-5 million people living with chronic heart failure and an
additional 400,000 newly diagnosed yearly.
b. The incidence of HF is 10 per 1000 for individuals who are older than
65 years of age.
c. The increasing incidence of HF is due primarily to the advancing age
of the population with CAD, which is the principal cause of HF,
associated with reduced vent func.(dilated cardiomyopathy)
d. In the Framingham study, total mortality was 24% and 55% within 4
years of developing symptomatic HF for women and men.
e. Recognizing the benefits of ACE inhibitors, diuretics, digoxin, and
beta-blockers has yielded substantial reductions in mortality DT
progressive pump failure. However these improvements in medical
therapy, symptomatic HF still confers a 20-25% risk of premature
death in the first 2.5 yrs after diagnosis.
f. Almost all HF pts will have at least one acute episode with symptoms
requiring hospitalization and treatment with IV meds. Hospital
discharges for HF totaled approx 1million in 2001 and have increased
more than 150% form 1979. Hospitalization for management of HF
imposes the highest cost by DRG
g. There are four levels of electromechancial abnormalities associated
with DCM: prolonged AV delay, interventricular delay,
intraventricular delay, and intramural delay.
i. Prolonged AV delay- the normal AV interval results in atrial
contraction just before the pre-ejection (isovolumic) period of
ventricular contraction that maximizes vent filling (LV end
diastolic pressure, or pre-load) and CO by the Starling
mechanism. The optimal timing relationship also results in
diastolic filling throughout the entire diastolic filling period,
prevents diastolic MR and maintains left atrial pressure at low
levels.
ii. Interventricular delay- more important that AV coupling for
maximum ventricular pumping function. This refers to
coordinated contraction of the RV and LV. Typically LBBB
occurs where RV begins contraction before LV. Chronic DCM
is often accompanied by delayed ventricular electrical
activation manifested by prolonged QRS duration, most
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commonly in the form of LBBB. Prevalence in HF is in the
range of 25-50%. Potent predictor of mortality in HF assoc.
with DCM. This delay causes abnormal septal deflections that
alter EF. Regions of late activation are subject to greater wall
stress and develop local myocyte hypertrophy and aggravated
MR.
iii. Intraventricular delay-exists within ventricle. With LBBB, the
septum begins contraction substantially earlier than the lateral
wall causing the lateral wall to stretch. This causes diminished
ejection at increased metabolic cost and acute decline in
systolic function.
iv. Intramural delay- delay difference between endocardial and
transmural activation
II. CRT
a. therapeutic strategy is that left ventricular preexcitation may correct
inter- and intraventricular conducation delays and permit optimization of left-
sided AV delay, thereby improving vent pumping function.
A. Mechanisms of CRT
a. When the programmed AV interval is too short, LV preexcitation
occurs too early relative to atrial systole. Note that diastolic filling
occurs throughout all of diastole. Atrial contraction now occurs
simultaneously with LV contraction resulting in increased left atrial
pressure and loss of atrial contribution to vent systole, reducing CO.
Abolishes premature mitral valve closure, eliminating diastolic MR.
b. Reverse LV remodeling- reduction in left vent volume, redistribution
of cardiac mass, reduced mitral orifice size and reduced mitral
regurgitation.

B. Implementation of CRT
a. Inability to cannulate the CS- 1-5%
b. As many as 20% of patients dont have a vein that reaches optimal LV
free wall.
c. Epicardial LV leads are usually placed using the OM branches of the
circumflex artery, approx 1 cm apical to the mitral annulus.
d. See page 444-447 for BiV pacing and differences in 12 lead EKG
e. See rest of chapter 9 to read about nonresponders
Chapter 10 ICD Followup and Troubleshooting
See pg 480 for drugs that elevate the DFT