Basic interpretation of EP tracing

baseline intervals and refractory

periods
Right Atrial Electrogram

local sharp, large atrial electrogram and a smaller, far-field

ventricular electrogram. The catheter is usually positioned
in the RA appendage
His Bundle Electrogram
rapid biphasic spike, 15 to 25 milliseconds in duration, interposed between local
atrial and ventricular electrograms
it is important to verify that the spike actually represents activation of the most
proximal HB and not the distal HB or RB
Anatomically, the proximal portion of the HB originates in the atrial side of the
tricuspid annulus; thus, the most proximal HB deflection is the one associated with
the largest atrial electrogram
HIS potential can be recorded in the
noncoronary sinus of Valsalva (just above the aortic valve) or in the
LVOT along the interventricular septum (just below the aortic valve)
Validation of the HB recording
● HV interval should be 35 milliseconds or longer (in the absence of preexcitation).
In contrast, the RB potential invariably occurs within 30 milliseconds before ventricular
activation.
● Atrial pacing With a true His potential, the AH interval should increase with incremental pacing rates.
● HB pacing,The ability to pace the HB and obtain HB capture
QRS identical to that during normal sinus rhythm [NSR] and
stimulus-to-QRS interval identical to the HV interval during NSR
provides the strongest evidence validating the His potential.
● PITFALLS
inconsistent in accomplishing HB capture, especially at low current output.
Higher output can result in nonselective HB capture.
The use of closely spaced electrodes and the reversal of current polarity (i.e., anodal
stimulation) can facilitate HB capture.
● recording of pressure simultaneously with a luminal electrode catheter (which should reveal atrial
pressure wave when the catheter is at the proximal His electrogram position)
CS EGM The CS lies 2 cm superior to the
annulus as it crosses from the RA to
the LA

More distally, the CS frequently

overrides the LV.

most proximal CS electrodes (located

at the CS os) are closer to the atrium
and typically show a local sharp,
large atrial electrogram and a
smaller, far-field ventricular
electrogram.

The more distal CS electrodes, lying

closer to the LV than the LA, record
progressively smaller, less sharp, far-
field atrial electrograms and larger,
sharper, near-field ventricular
electrograms
BASELINE INTERVALS
accuracy of measurements made at a

screen speed of 100 mm/s is ±5 ms,

at a speed of 400 mm/s is ±1 millisecond.

large intervals (e.g SNRT ), a speed of 50 to 100 mm/s is adequate.

For refractory periods, a speed of 150 to 200 mm/s is adequate,

but for detailed mapping, a speed of 200 to 400 mm/s is required.

P Wave–Atrial Interval
The PA interval is measured from the

first evidence of sinus node depolarization, whether on the intracardiac or surface ECG,
to the atrial deflection recorded in the HB lead.

The PA interval reflects

conduction time from the sinus node to the AVN.

PA interval is 20 to 60 milliseconds.

prolonged PA interval

diseased atrial conduction

short PA interval

suggests an ectopic source of atrial activation.

Interatrial Conduction
Activation of the LA is mediated by three possible
routes.

Superiorly, activation proceeds through the

Bachman bundle;

this can be seen in 50% to 70% of patients and can

be demonstrated by CS os activation followed by
distal CS and then mid-CS activation

Activation also propagates through the mid-atrial

septum at the fossa ovalis and

at the region of the central fibrous trigone at the

apex of the triangle of Koch

Interatrial conduction is measured by the interval

between the atrial electrogram in the high RA lead
and that in the CS lead.

Normal retrograde atrial activation proceeds over

the AVN. The earliest atrial activation is recorded in
the AV junction (HB recording),
Atrial–His Bundle Interval

The AH interval is measured from the

first rapid deflection of the atrial deflection

in the HB recording to the

first evidence of HB depolarization in the

HB recording

AH interval is an approximation of the

AVN conduction time

because it represents conduction time

from the low RA at the interatrial septum
through the AVN to the HB.

The AH interval can vary according to the

site of atrial pacing.
Atrial–His Bundle Interval
The AH interval (50 to 120 milliseconds)

Autonomic blockade with atropine (0.04 mg/kg) and propranolol (0.02 mg/kg) can be used to
evaluate AVN function in the absence of autonomic influences

Short AH intervals

increased sympathetic tone,

reduced vagal tone,

and preferential LA input into the AVN,

preexcitation (atrio-His BTs).

Long AH intervals

Drugs eg digoxin, beta-blockers, calcium channel blockers, and antiarrhythmic drugs),

enhanced vagal tone,

and intrinsic disease of the AVN.

His Potential
Disturbances of HB conduction can manifest as

fractionation,

prolongation (longer than 30 milliseconds), or

splitting of the His potential.

 His Bundle–Ventricular Interval
The HV interval is measured from the

onset of the His potential to the

onset of the earliest registered surface or intracardiac ventricular activation

not significantly affected by the autonomic tone

range of HV intervals- 35 to 55 milliseconds

prolonged HV interval

consistent with diseased distal conduction in all fascicles or in the HB itself.

short HV interval suggests

ventricular preexcitation via a BT.

A falsely shortened HV interval in accelerated idioventricular rhythm that is isorhythmic with sinus rhythm,

or when an RB potential rather than a His potential is inadvertently recorded.

Pacing Techniques.
Pacing Output
Pacing threshold is defined as the

lowest current required for consistent capture

determined in late diastole with a stimulus of a given duration

Influenced by drugs and PCL

Pacing output at twice (2×) diastolic threshold is generally used

pulse duration

of 1 or 2 milliseconds is generally used.

Pacing rate (per min) = 60,000 (milliseconds/min)

CL (in milliseconds
PACING MANEUVERS

Overdrive Pacing (“Straight Pacing”)

Pacing stimuli are delivered at a constant pacing rate (constant PCL)

The pacing rate is faster than the rate of the baseline rhythm
 A A
A A
Burst Pacing
Pacing stimuli are delivered at a constant rate for a relatively short duration

but at successively faster rates with each burst

generally used for induction or termination of tachycardias.

Stepwise Rate-Incremental Pacing
After pacing at a given rate for a predetermined number of stimuli or seconds, the
rate is increased (with intervening pauses) in a series of steps until predetermined
endpoints are reached. It is important to maintain the pacing at any given rate for
at least 15 seconds (period of accommodation) before increasing the pacing rate
Ramp Pacing
Ramp pacing implies a smooth change in the
interval between successive stimuli, with
gradual decrease of the PCL every several
paced complexes (without intervening pauses).

Ramps are often used as an alternative to the

stepwise method for assessment of
conduction.

The pacing rate is slowly increased at 2 to 4

beats/min every several paced beats until
block occurs.
Extrastimulus Technique
S1-S1 drive stimuli.

The eight drive beats are each termed S1 stimulus.

The S1-S1 drive stimuli are sometimes called trains.

These S1drive stimuli can be followed by first, second, third, and nth premature extrastimuli,
which are designated as S2 , S3, S4, and SN

For multiple extrastimuli. In the simple sequential method,

the S1-S2 coupling interval is decreased until it fails to capture,at which time the coupling
interval is increased until it captures (usually within 10 to 20 milliseconds).

In the tandem method, the S1-S2 coupling interval is decreased until S2 the S1 fails to
capture, and thenS1 -S2 coupling interval is increased by 40 to 50 milliseconds and held
there. S3 is then introduced and the S2 S3 fails to capture.
▪Decremental conduction: Progressively shorter coupling results in slower conduction velocity.

• Decremental conduction is seen with tissues dependent on “slow” inward calcium current for
depolarization (e.g., AVN).

•Purkinje fibers are dependent on “fast” sodium channels resulting in nearly no decrement.

•Myocardium (atrial and ventricular) has minimal decremental properties.

▪Latency is the delay between the extrastimulus and the EGM generated by the tissue.

• Latency is observed when the short-coupled extrastimulus impinges on the refractory period
of the adjacent myocardium.
Effective refractory period.

The ERP is the longest premature coupling interval (S1 -S2)

at a designated stimulus amplitude (usually 2× diastolic threshold)

that results in failure of propagation of the premature impulse through a tissue

(i.e., fails to capture).

Relative refractory period.
.The RRP is defined as the longest premature coupling interval (S1-S2) that
results in prolonged conduction of the premature impulse

(an increase in stimulus to distal response time)

compared with the conduction of the stimulus delivered during the basic drive
train.

RRP is generally slightly longer than the ERP by an amount called the latency
period.
Atrioventricular Node Response to Atrial Pacing
AVN Wenckebach CL is the longest PCL at which Wenckebach block in the AVN is
observed.

Normally, Wenckebach CL is 500 to 350 milliseconds, but it is sensitive to the

autonomic tone

Prolongation of the HV interval or infranodal block at a PCL longer than 400

milliseconds is abnormal and indicates infranodal conduction abnormalities.
AERP
atrial premature beat
is coupled at a slightly
shorter interval of 260
ms and in this case
the premature
extrastimulus does not
capture atrial tissue,
so the atrial effective
refractory period
would be calculated to
be 260 ms. However,
since atrial
refractoriness was
reached before AV
node refractoriness,
the clinician cannot
assess the
electrophysiologic
properties of the AV
node
AVnERP
In order to evaluate AV node refractoriness the electrophysiologist takes
advantage of a property of atrial and ventricular tissue:

with earlier coupling intervals, refractory periods decrease.

By using first and second extra- stimuli (S2 and S3), the first
extrastimulus can be used as a “conditioning” impulse to shorten the
refractory period of atrial tissue.

In this way more closely coupled atrial activation can be used to measure
the refractory period of “downstream” tissue such as the AV node.
Ventricular
overdrive pacing

At slower rates the

atrial response to
ventricular stimuli
will remain 1 : 1
but with more rapid
ventricular pacing
VA conduction
block will occur
Ventricular premature stimulation
When the ventricular stimulus is delivered slightly earlier an atrial signal is not
observed, because one of the tissues connecting the ventricles to the atria (His
bundle, AV node) is now refractory. This interval is the ventriculoatrial refractory
period.

When the ventricular stimulus is delivered even earlier and the stimulus does not
produce ventricular depolarization (a QRS complex), then the ventricular effective
refractory period has been reached.
Normal Response to Atrial Premature Stimulation

Sinus Node Response to Atrial Extrastimulation

Four zones of response of the sinus node to AES have been identified:

zone of collision,

the zone of reset,

the zone of interpolation,

and the zone of reentry

Normal Response to Rate-Incremental Atrial Pacing
Sinus Node Response to Atrial Pacing
Sinus node recovery time is the interval between the end of a period of pacing-
induced overdrive suppression of sinus node activity and the return of sinus node
function, manifested on the surface ECG by a post-pacing sinus P wave.
Zone [Link] of collision
A late-coupled AES with very long A1-A2 intervals

(with A2 falling in the last 20% to 30% of the sinus CL)

collides with the impulse already emerging from the sinus node, resulting in fusion
of atrial activation (fusion between the AES [A2 ] with the spontaneous sinus
impulse [A1 ]) or paced-only atrial activation sequence;

it fails to affect the timing of the next sinus beat, thus producing a fully
compensatory pause.
Zone of collision 2* (A1-A1)= A1-A2 + A1-A3
 Zone [Link] of reset
An earlier coupled AES results in penetration of the sinus node with resetting so that
the resulting pause is less than compensatory

(i.e., A1-A3 is <2 × [A1-A1]),

This zone is typically of long duration (40% to 50% of the sinus CL

Hence, A2 should equal the spontaneous sinus CL (A1 -A3 -A1) plus the time it takes
the AES (A2 ) to enter and exit the sinus node.

The difference between A2-A3 and A1 -A1 therefore has been taken as an estimate of
total sinoatrial conduction time.
Zone [Link] of reset

A1 -A3 is <2 × [A1-A1])

Zone [Link] of interpolation
A very early coupled AES encounters a refractory sinus node (following the last sinus
discharge) and fails to enter or reset the sinus node.

The next sinus discharge is on time because the atrium is already fully recovered
following that early AES.

The range of A1-A2 coupling intervals at which A2 -A3 is less than A1 -A1,

and A1 -A3 is less than 2 times (A1-A1), defines zone III, also known as the zone of
interpolation

(A1-A2) + (A2 -A3) = A1 -A1

and sinus node entrance block is said to exist.

Zone [Link] of interpolation

(A1-A2) + (A2 -A3) = A1 -A1

Atrioventricular Node Response to Atrial Pacing
The normal AVN response to rate-incremental atrial pacing is for the PR and AH
intervals to increase gradually as the PCL decreases until AVN Wenckebach block
appears (Fig. 4.21). With further decrease in the PCL, higher degrees of AV block
(2 : 1 or 3 : 1) can appear. Infranodal conduction (HV interval) generally remains
unaffected.

Prolongation of the HV interval or infranodal block at a PCL longer than 400

milliseconds is abnormal and indicates infranodal conduction abnormalities.
Atrioventricular Nodal Response to Atrial Extrastimulation

Progressively premature AES results in prolongation of PR and AH intervals, with inverse

relationship between the AES coupling interval (A1-A2) and the AH interval (A2-H2)

Plotting the A1 -A2 interval versus the H1 -H2 and V1 -V2 intervals illustrates the
functional input-output relationship between the basic drive beat and the AES and provides
an assessment of the FRP of the AV conduction system.

In contrast plotting the A2 -H2 interval (AVN conduction time of the AES) and the H2 -V2
interval (HPS conduction time of the AES) versus the A1 -A2 interval (the AES coupling
interval)

allows determination of the conduction times through the various components of the AV
conduction system.
Type I response.

This response is characterized by initial shortening of the H1-H2 and V1 -V2 intervals as the AES
coupling interval (A1 -A2) shortens,

whereas AVN conduction (A2 -H2 ) and HPS conduction (H2 -V2) remain stable .

With further shortening of the A1 -A2 interval,

the RRP of the AVN is encountered, resulting

in progressive prolongation of the A2-H2 interval) accompanied by

stable HPS conduction (H2 -V2) and a

progressive prolongation of both the H1 -H2 and V1 -V2 intervals,

until the AES is blocked within the AVN (AVN ERP) or until the atrial ERP is reached.

The minimum H1-H2 and V1 -V2 intervals attained define the FRP of the AVN and entire AV
conduction system

AVN conduction (A2 -H2) usually increases by 2 to 3× baseline values before block.
Type I response.
Type II response

A1 -A2 interval shortens conduction delay develops initially in the AVN (manifesting as

progressive prolongation of the A2-H2 interval)

in the HPS (manifesting as aberrant QRS conduction and

progressive prolongation of the H2 -V2 interval)

Therefore in contrast to type I response,

both A2 -H2 and

H2 -V2 intervals prolong in response to progressively shorter A1 -A2, resulting in

divergence in the H1 -H2 and V1-V2 curves

until the AES is blocked within the AVN (AVN ERP), in the HPS (HPS ERP), or until the atrial ERP is
reached
Type II response
Type III response

In type III response, conduction delay occurs initially in the AVN;

at a critical AES coupling interval, sudden and marked delay develops in the HPS.

At longer A1-A2 intervals, type II response is similar to type I response; however, as the A1 -
A2 interval shortens,

progressive prolongation in the A2 -H2 interval), then a

sudden delay of conduction in the HPS occurs (manifesting as

aberrant QRS conduction and a

sudden jump in the H2-V2 interval).

This results in a break in the V1-V2 curve,

The FRP of the HPS occurs just before the marked jump in H2-V2.

AVN conduction (A2 -H2) usually increases by less than 2× baseline values before block.
Type III response
Functional refractory period.
FRP as a response-to-response measurement (in contrast, the ERP is a
stimulusto-stimulus measurement).

Therefore the FRP is a measure of both refractoriness and conduction velocity of

a tissue
CL shorting can affect different structures differently.

For example, normally at relatively long cycle lengths, the RB ERP exceeds that of
the left bundle (LB), so that functional right bundle branch block (RBBB) is
common.

At short CLs, the LB ERP exceeds that of the RB so that left bundle branch block
(LBBB) is more common.