3-Stimulator should have:
-A constant current source
-Minimal current leakage (10 uA)
-Ability to pace at a wide range of CLs (10 to 2000 ms) from at least 2 simultaneous sites
-Ability to introduce multiple (minimum of 3) extrastimuli with a programming accuracy of 1 ms
-Ability to synchronize the stimulator to appropriate electrograms during intrinsic or paced rhythms
-A-V sequential pacing (when you don't have VA conduction so that you don't have intermittent conduction and capture
of the ventricle by the sinus rhythm which will disturb your recordings. Then you will program DDD on both channels 1
and 2 for the drive pacing train S1 and only S2, S3 and S4 for the ventricle when doing extrastimuli)
-Synchronized burst pacing
-Ability to introduce multiple sequential drive cycle lengths
-Deliver variable currents (0.1-10 mA) and the ability to change pulse widths (0.1-1 msec)
The current delivery to the catheter tip must remain constant despite any changes in resistance For consistency and
safety, stimulation has generally been carried out at twice the diastolic threshold. Observation suggests that the use
of higher currents of 10 mA with multiple extrastimuli can result in a high incidence of VF that has no clinical significance.
Custom designed unit manufactured by Bloom-Fisher, Inc (Denver, CO) fulfills all the standard requirements and can be
modified for a wide range of research purposes.
Biphasic waveform defibrillator have have enhanced efficacy compared to monophasic waveforms. (Physio Control
Medtronic Biphasic devices).
The success and/or complications of cardioversion / defibrillation depends on the rhythm requiring cardioversion, the
duration of that rhythm before attempted cardioversion, the amount of energy used, and the underlying cardiac disease.
VT or VF > 300 J monophasic or 200 J biphasic
Burning at the site of the R2 pad is common and is assuaged by the use of steroid creams
ST elevation and / or depression can be seen in 60% of cases post cardioversion and usually resolves within 15 min.
This is not accompanied by an elevation of CK and CKMB usually.
3 x 7 FR Right Groin
3 QUADS: RV - RA - His
2-3 nurse technitians (appropriate CPR training, monitoring hemodynamics and rhythms, delivering antiarrhythmic
medications and conscious sedation, collecting and measuring data online during the study).
Radiation technologist to assure proper functioning of equipment
Anesthesiologist and cardiac surgeon on call
CRNA for implants and for atrial fibrillation ablation
Image intensifier equipped for fluoroscopy - Pulsed Fluoroscopy (decrease radiation exposure)
Dacron (Bard, Billerica, MA - 2, 5, or 10 mm interelectrode distance) or Polyurethane. Dacron is preferred because of
greater durability and physical properties
Stiff enough to maintain their shapes and soften at body temperature for forming loops and bends in the vascular
Cool Tip Ablation Catheter
These include up to 24 poles that can be deflected to map large and/or specific areas of the atrium (CS, tricuspid
annulus...) which include the multipolar deflectable bidirectional catheters.
Catheters shaped in the form of a "halo" to record around the tricuspid ring.
Basket Catheters. A 64 pole retractable catheter with 8
splines useful for simultaneous multisite data acquisition for
an entire chamber.
Biosense Webster standard ablation catheter with a magnetic
sensor in the shaft near the tip. Together with a reflector
sensor it can be used to precisely map the position of the
catheter in 3D (x, y, and z - roll, yaw, and pitch).
Dacron catheters are the only ones that may be
sterilized and reused indefinitely.
1-Junction Box - pairs of numbered multiple switches matched to each recording and stimulation channel, permitting
the ready selection of any pair of electrodes for stimulation or recording. Capability to record uni or nipolar signals from
the same electrodes simultaneously on multiple amplifiers.
2-Signal Processor - filters and amplifiers, visualization screen, recording apparatus, often combined in a single unit
(Prucka now Marquette, Bard or EP Medical). They come with automatic gain control, variable filter settings, bank
switching, common calibration signals...). For any system 8 or 14 amplifiers should be available to process a minimum of
3 or 4 surface ECGs simultaneously with multiple intracardiac electrograms (to be able to determine the frontal plane
axis, morphology, and the P wave polarity). Amplifiers can vary from 3 to 128 depending on the intentions of the EPS.
The amplifiers used for recording intracardiac electrograms must have the ability to have gain modification as well as to
alter both high- and low- band pass filters to permit appropriate attenuation of the incoming signals.
His Bundle deflection - 30 or 40 Hz filters (High Pass)
Intracardiac electrogram - 400 or 500 Hz (Low Pass)
The capability of simultaneously acquiring open (0.05-0.5 to 500 Hz) and variably closed filters is imperative in order to
use both unipolar and bipolar recordings. This is critical for selecting an ablation site that requires demonstration that
the ablation tip electrode is also the source of the target signal to be ablated.
Below: Note that the clearest recording of the His bundle electrogram occurs with a filtering signal of < 40 and > 500 Hz
Modified Seldinger technique
Premedication with topical lidocaine 2% or sensorcaine and diazepam (valium, has not been found to have EP side
effects) or its congener the short acting midazolam (Versed)
Major contraindication for femoral vein approach: recurrent ileofemoral thrombophlebitis
Relative contraindications: inability to palpate the femoral artery pulse and severe PAD.
Seldinger Technique Femoral Vein: Locate the femoral artery by placing fingertip between the groin crease inferiorly
and the line of the inguinal ligament superiorly (extends between the symphysis pubis and the anterior superior lilac
spine). The femoral vein lies parallel and within 2 cm medial. Some references advise to make a local stab wound with
an 11 blade before sticking with the needle and with a small straight hemostat or curved clamp to make a plane into the
subcutaneous tissue. A 2.75-inch, 18 Gauge, thin walled Cournand needle or an 18 Gauge Cook needle is
advanced in the stab wound until the vein or the pelvic bone is encountered. The bone is painful and additional
lidocaine may be infiltered in the periosteum. Then attach a syring half filled with flush solution to the hub of the needle
and withdraw both needle and syringe slowly with the left heand steadying the needle and the right hand withdrawing
gently on the syringe.
Once the vein is entered insert a short, flexible tip, fixed core (straight or floppy J), Teflon coated stainless
steel guidewire. Often depressing the needle hub (making it more parallel to the vein) and using gentle traction result
in a better intraluminal position of the needle tip and facilitates passage of the wire.Then pass th sheath over the wire
with a twisting motion into the femoral vein with 1 cm of wire protruding out of the sheath. The second stick should be ~
1 cm cephalad or caudal to the first one.
Heparinization should be used in all studies lasting > 1 hour.
During venous studies a bolus of 2500 U of Heparin is administered followed by 1000 U/hr.
During arterial sticks a bolus of 5000-7000 U of Heparin is administered followed by 1000-2000 U/hr.
ACT is checked q15-30 min. ACT > 250 for right sided studies. 300-350 for AF ablations and left sided studies.
At the groin crease artery and vein lie very closely together. Directing the needle a little bit laterally may result in
puncture of the femoral artery. Withdraw the needle and put pressure for 5 min.
If you can't thread the wire. Point more medially at a lower angle.
Upper Extremity Approach
Easier to get to the CS. Apply a tourniquet. Identify ample sized veins that run medially for use. Do not use lateral
coursing veins because they tend to join the cephalic vein and enter the axillary vein at a right angle that makes it
harder to negotiate with a catheter. Later veins can be used successfully in 50-75% of cases. If you cannot identify a
superficial good vein to use then aim for the median basilic vein which is generally superficial to the brachial artery
pulsation, or the brachial vein that lies deep within the vascular sheeth alongside the artery. Arm approach is
preferrable to subclavian or axillary approach (inadvertent pneumothorax or carotid artery puncture)/.
First passed catheter should go right away to the RV apex for pacing because manipulation in the A-V junction can
precipitate traumatic RBBB and thus complete heart block.
Most common site for stimulation and recording is the high posterolateral wall at the
junction of the SVC in the region of the SN or RAA. The SVC-atrial junction is the site
depolarized earliest in 50% of the people and in the other 50% it's the midposterolateral RA
(2-3 cm inferior to the SVC junction)
Best approached from the CS if only for diagnostic recording or pacing purposes. Easier
from the upper extremity, routinely done from the leg using a steerable catheter.
The os of the CS lies posteriorly and its canulation may be confirmed by advancement of
the catheter to the left heart border, where it will curve toward the left shoulder in
LAO, and posteriorly in RAO which can be seen as posterior to the AV sulcus
visualized routinely as a translucent area. It can also be confirmed by recording of
simultaneous A and V electrograms with the atrial electrogram in the later part of the P
wave and withdrawal of very desaturated blood (30%).
Best done using a 6 or 7 Fr tripolar or quadripolar catheter from the femoral vein. If activation of the triangle of Kocjh is
analyzed it's better to use tightly spaced octapolar or decapolar catheters. Passed into the RV first then withdrawn
across the tricuspid valve with a slight clockwise torque which helps to keep the electrodes in contact with the septum.
by withdrawing the catheter from the RV you will see: a large ventricular potential -> a narrow spike representing the
RBB potential may appear just before (30 ms) the ventricular electrogram -> A -> A=V which is where you should see
the His (biphasic or triphasic deflection).
The initial portion of the His bundle originates in the membranous atrial septum, and recordings that do
not display a prominent A may be recording more distal His or BB potentials and may miss important
intra-His bundle disease.
Standard bard Josephson multipurpose Quadripolar catheter: allows recording of 3 simultaneous bipolar pairs,
which can help evaluate intra-His conduction.
AH: 90 -120 ms HV: 35 - 55 ms
If unsuccessful locating the His pass again in the RV with a slightly different rotation to explore other portions of the
tricuspid ring. The orientation of the tricuspid ring may not be normal (perpendicular tothe frontal plane) in certain
patients, especially those with congenital heart disease. If after several attempts the His cannot be located the catheter
should be withdrawn and reshaped or exchanged for a catheter with a deflectable tip. Occasionally continuous torque
on the catheter shaft is required to obtain a stable recording. This can be accomplished by making a loop in the
catheter shaft remaining outside and placing wet towels on it to hold it in place.
The femoral vein should be avoided in the presence of a known or suspected femoral vein or IVC
thrombosis or interruption, active LE thrombophlebitis or postphlebitic syndrome, infection in the groin,
bilateral lower extremity amputation, severe PVD or extreme obesity.
The natural course of a catheter passed from the UE generally does not permit the recording of a His bundle
electrogram, because the catheter does not lie across the superior margin of the tricuspid annulus.
1st technique to obtain a His from the UE: use a deflectable catheter with a torque control knob that allows the
distal tip to be altered from a straight to a J shaped configuration once it has passed to the heart. The tip is then
hooked across the tricuspid annulus to obtain a His bundle recording.
2nd technique to obtain a His from the UE: with a standard electrode catheter, rather than passing it with the tip
leading, a wide loop is formed in the RA with a figure of 6 with the catheter tip pointing towards the lateral right atrial
wall. The catheter is then gently withdrawn so that the loop opens in the RV with the tip resting in a position to record
the his bundle electrogram.
1% in diagnostic studies and 2.5% in ablation studies
Arrhythmias (the risk of VF can be minimized by stimulating the ventricle at twice the threshold using PW < 2 msec).
Strokes, systemic emboli and protamine reactions in Left Heart Catheterizations
Tamponade 0.08% (0.05% in ablation procedures)
The most common asides from extarcardiac noise is repolarization artifact (T wave) seen below
HBE 15-25 ms
> 90% of A-V conduction defects can be defined within the HBE.
Rapid biphasic or triphasic spike. 15-25 ms.
Make sure it's the most proximal His away from the distal His or the RBB potential.
RBB potential invariably occurs < 30 ms before ventricular activation.
If HV < 30 ms suspect RBB potential or pre-excitation
HV 35-55 ms
The most proximal His is associated with a large atrial electrogram (on the atrial side of the tricuspid annulus)
Occasionally a His spike can be recorded more posteriorly in the triangle of Koch. Abnormal sites of HBE may be noted in
congenital heart disease (ASD septum primum).
A-H demonstrates decremental pacing properties.
HBE can also be recorded on the NCC of the AV or under the AV (at level of Central Fibrous Body CFB.
LBB and RBB are activated simultaneously. LBB potential on the left side can be used to distinguish a true His from a RBB
potential on the right side.
His pacing can also differentiate it from a RBB potential by generating an identical to sinus QRS. It has to be done at low
outputs 1.5-4 mA to avoid non selective HB pacing especially if using a catheter with a 1 cm interelectrode distance.
A-H 45-140 ms
In the HB recording. Earliest A deflection to the onset of the HBE. Use same gain.
May vary 20-50 ms based on patient's autonomic state.
HV 35-55 ms
Earliest H deflection on the His catheter to the earliest onset of V on multiple-surface ECG leads or the V on the His catheter.
Not affected by variations in autonomic tone.
Usually the earliest ventricular activation is on lead V1 or V2 in case of a narrow QRS.
Ventricular activation can occur before the onset of the QRS on the surface leads. This is particularly true when infarctions of
the septum and/or IVCD are present. Even if V1 is used, the H-V interval can be falsely long.
Onset of P wave on surface leads to onset of A on the His recording.
Could be unsuitable to measure intra-atrial conduction (onset of endocardial activation can precede the P, a more distal
position of the His catheter can yield a longer P-A, in sinus tachycardia the P waves in the inferior leads are more upright and
onset of atrial activation is most often recorded in the HRA, during slow rates the earliest onset of atrial activation can be
recorded at the midlateral atrial sites.
Activation of the LA is by 3 routes:
-Superiorly through Bachman's bundle
-Through the mid-atrial septum at the F.O
-Inferiorly through the central fibrous trigone at the apex of the
Triangle of Koch.
Marchlinski => 0.5 mV
Josephson => 0.1 mV
Normal LV: rapid deflection and distinct components
Scar: split, fractionated, late
Normal LV activation:
Inferior border of middle septum =>
Superior-basal free wall =>
Basal infero-posterior wall
Isolated constant current source that delivers a rectangular impulse at a current strength that is twice the diastolic
threshold. Threshold is determined in late diastole.
Always in sync (alteration of the coupling interval of the first beat of a drive can affect subsequent A-V conduction).
Site: HRA near the sinus node
CL: slightly lower than sinus rate, shortening by 20 ms decrements to a minimum of 250 ms and/or CL at which WB.
Ramp pacing to stepwise decremental pacing have identical results. Stepwise decremental also allows measurement of
SNRT. Ramp pacing shortens the time of the study.
Drive trains should be maintained for 15-30 sec to ensure stability of conduction intervals and overcome 2 factors:
-Accomodation (Lehman et al): if the coupling interval of the first beat of the drive is not sync'd one can observe increasing,
decreasing or stable A-H pattern for several cycles (shifting from one drive train to another without a pause). This will result
in a longer A-H for the first beat of the second drive train and oscillations of A-H interval or even WB.
-Autonomic influence: rapid pacing can produce variations in A-V nodal conduction. A stable interval is usually achieved
after 15-30 seconds.
A-H lengthens as CL decreases until A-V nodal block appears. Infranodal conduction (HV) remains unaffected.
Atypical WB block frequently occurs: A-H does not gradually prolong, it might remain the same before block or it may show
its greatest increment only the last conducted beat before block. The incidence of Atypical WB is highest during long WB
cycles (> 6:5).
False WB: secondary to loss of capture or to atrial echo beats before the A stim rendering the atrium refractory and
resulting in loss of capture for one beat and the appearance of pseudo-block.
With further shortening of CLs higher degrees of AV block may appear (2:1, 3:1)
Majority of AVNWB: 500-350 ms.
Differences in CLs at which WB appears are related in differences of basal autonomic tone.
AVNWB: Progressive A-H
prolongation terminating in
block of the P wave inthe his
node (A no H)
Pseudo-WB due to loss of
capture (Stim no A echo on
the CS catheter).
Infra-His Block: can be normal at short A pacing CLs. If pacing is begun in NSR, the 1st or 2nd complex may act as a long-short
sequence. The long preceding cycle will prolong the HB refractoriness and the next impulse will block. HB also may show
accomodation following the initiation of a drive of AP similar to the AV node. Block in the HB occurs initially followed by decreasing
HV intervals before resumption of 1:1 conduction at a fixed H-V interval.
Prolongation of HV interval or infra-his block at gradually reduced AP CLs < 400 ms is abnormal
Functional 2:1 infranodal block.
This response occured because
the ERP of the HPS was 350 ms,
longer than the paced CL of 290
Occurs in 40-90% depending on the population studied. VA conduction can occur in the presence of CHB if the AV block occurs at
the level of the HPS. However most studies have demonstrated that at paced rates, antegrade conduction is better than
retrograde (750 patients Josephson data: antegrade conduction better than retrograde in 62% of patients, worse in 18% and
same in 20%). Patients with prolonged P-R intervals are much less likely to have retrograde conduction. Antegrade block in the
AVN is almost always associated with failure to retrogradely conduct. Antegrade block in the HPS may be associated with some
degree of VA conduction in 40% of patients.
A His deflection can be seen in 85% of cases during VP when using a narrow bipolar pair at relatively low gain settings. V pacing
at the base of the heart opposite the AV junction (parahisian pacing) makes it more easy to see the retrograde H (V activates
much earlier relative to the His because the impulse must propagate from the base to the apex before it engages the RBB and
subsequently conduct to the HB). Retrograde His is hard to see with ipsilateral BBB.
V-H > H-V
Gradual prolongation of V-A conduction as VP CL is decreased. Although WB usually signifies retrograde delay in the AVN, it is
only when a retrograde His is present that retrograde WB and higher degrees of block can be documented to be localized to the
AVN. Retrograde H will be seen before the local V on the HBE unless RBBB is present or pacing from base of RV.
VA Echos: occasionally seen (25-30%) following retrograde VAWB and look like a normal beat with normal QRS morphology and
a relatively short A-H interval. Due to reentry secondary to a longitudinally dissociated AVN and require a critical degree of V-A
conduction delay for their appearance. Patients with dual AVN physiology manifesting this type of retrograde WB and reentry are
generally not prone to develop clinical SVTs due to AVN reentry.
1:1 VA Conduction
VAWB at PCL 500 ms.
SH is constant. VA prolongs
2:1 VA Block. The site of block
is onthe AVN because the
retrograde H is recorded.
terminated by an echo beat -
conduction (S-A) is noted in
response to decreasing
When retrograde His is not recorded during V-A pacing, the site of block can be determined from the effects of the V-Paced beat
on spontaneous or induced atrial depolarizations. The site of block is localized by analyzing the level of concealed retrograde
If the A-H interval of the spontaneous or induced atrial depolarization is independent of the time relationship of VP beats, then, by
inference, the site of retrograde block is infranodal in the HPS. On the other hand, variations in the A-H interval that depend on
the coupling interval of the atrial complex to the VP beat or failure of the atrial impulse to depolarize the HB suggest retrograde
penetration and block in the AVN.
Another method of evaluating the site of retrograde block in the absence of a recorded retrograde His potential is to note the
effects of drugs which only affect A-V Nodal conduction on VA conduction. Improvement of conduction following
administration of atropine or isoproterenol suggests that the site of block is in the AV node.
Diagnosis of site of V-A Block
by Inference: during VPacing
A-V dissociation is present.
Despite the presence of a visible
retrograde His antegrade AVN
conduction depends on the
relationship of the sinus beats
(A) to the ventricular complexes
demonstrating the site of block
at the level of the AVN.
-RRP: longest coupling interval that results in prolonged conduction of S2 relative to the basic drive. It marks the end of the full
recovery period, the zone during which conduction of the premature and basic drive impulses is identical.
-ERP: longest coupling interval between the basic drive and the premature impulse that fails to conduct through that tissue. It
therefore must be measured proximal to that tissue.
-FRP: minimum interval between two consecutively conducted impulses through a tissue. Because the FRP is a measure of output
from that tissue it is described by measuring points distal to that tissue. It follows that determination of the ERP of a tissue requires
that the FRP of more proximal tissue be less than the ERP of the distal tissue (i.e. the ERP of the HPS can be determined only if it
exceeds the FRP of the AVN).
The Extrastimulus is delivered after a train of 8-10 paced complexes to allow time for reasonable (>95%) stabilization of
refractoriness (accomplished after 3-4 paced beats). ERP is inversely related to the current used and will decrease when higher
stim strengths are used (standard is twice the diastolic threshold). Using higher strengths (10 mA) is useful to determine the effects
of antiarrhythmics on ventricular excitability and refractoriness. Fibrillation (non clinically significant) is more common when mutliple
stimuli are delivered at higher strengths.
-ERP A: longest S1-S2 that fails to result in atrial depolarization.
-ERP AVN: longest A1-A2 measured in the HBE that fails to propagate to the His bundle.
-ERP HPS: longest H1-H2 that fails to result in ventricular depolarization.
-FRP A: shortest A1-A2 in response to any S1-S2
-FRP AVN: shortest H1-H2 in response to any A1-A2
-FRP HPS: shortest V1-V2 in response to any H1-H2
-RRP A: longest S1-S2 at which S2-A2 > S1-A1 (latency)
-RRP AVN: longest A1-A2 at which A2-H2 > A1-H1
-RRP HPS: longest H1-H2 at which H2-V2 > H1-V1 or results in aberrant complex
-ERP V: longest S1-S2 that fails to evoke a V response
-ERP HPS: longest S1-S2 or V1-V2 at which S2 or V2 blocks below the HB. This measurement can be made only if H2 is recorded
before the occurence of retrograde block.
-ERP AVN: longest S1-H2 or H1-H2 at which H2 fails to propagate to the A.
-FRP V: shortest V1-V2 measured on the surface.
-FRP HPS: shortest S1-H2 or H1-H2 in response to any V1-V2
-FRP AVN: shortest A1-A2 n response to any H1-H2
-RRP V: longest S1-S2 at which S2-V2 > S1-V1. V is measured from surface ECG or local ventricular EGM.
Shortening of S1-S2 results in
lengthening of A2-H2
FRP AVN: shortest H1-H2 in response
to any A1-A2
RRP A: longest S1-S2 at which
S2-A2 > S1-A1 (latency)
ERP AVN: longest A1-A2 measured at
the HBE that fails to propagate, no H2
ERP A: longest S1-S2 that fails to
result in atrial depolarization
|Measures of atrial and ventricular RP are taken at the site of stimulation.
And measures of AVNRP and HPS RP are taken from the HBE.
At long coupling intervals there is
no retrograde delay.
With S1-S2 < 420 you start seeing
retrograde delay, with gradual
prolongation of S2-H2 .
At 270 ms V-ERP is reached.
-RP HPS shorten as paced CL decreases.
-The RP of the RBB, which is longer than the LBB
during SR, tends to shorten more than the LBB
explaining the prevalence of RBBB aberration
at long CLs and LBBB aberration at short CLs.
-The AVN behaves in an opposite fashion, AVN
ERP decreases with decreasing CLs. This is
due to a fatigue phenomenon that most likely
results because AVN refractoriness (unlike HP
refractoriness), is time dependent and exceeds its
-The FRP of the AVN is variable but tends to
decrease with decreasing CLs. Because the
FRP is significantly determined by the AV nodal
conduction time of the basic drive beat (A1-H1).
The longer the A1-H1 the shorter the calculated
FRP at any A2-H2 interval:
FRP = H1-H2 = [(A1-A2 + A2-H2) - (A1-H1)]
-Ventricular refractoriness seems to be more
closely associated with the basic drive cycle
length. It demonstrates a cumulative effect of
preceding cycle lengths.
-HPS refractoriness demonstrates a marked
effect of the immediately preceding CL.
A change from long to short drive CL
shortens the ERP of the HPS and ventricular
muscle. A shift from a short to a long CL
markedly prolongs the HPS ERP but alters the
ventricular ERP little if at all.
Dispersion of refractoriness
Dispersion of RP has been suggested to be an indicator of arrhythmogenic substrate in animal studies.
Ischemic tissue has longer RP than normal tissue.
Types of Response to Atrial ES
Type I: Block occurs in the A or the AVN.
Type II: delay is noted initially in the AVN, but at shorter coupling intervals progressive delay in the HPS appears. Block usually
occurs in the AVN first but it may occur in the A and occasionally in the HPS (modified type II).
Type III: least common, initial slowing occurs at the AVN first but at critical coupling intervals sudden and marked prolongation of
conduction occurs in the HPS which is invariably the first site of block in this type.
Although it has been stated before that any prolongation of HP conduction is abnormal it is not. The only requirement for such
prolongation to occur is that the FRP of the AVN (shortest H1-H2 at any A1-A2) be < than the RRP HPS (longest H1-H2 at which
H2-V2 > H1-V1). 15-60% of normal patients can show some prolongation in HV in response to atrial ES. Infranodal block is
more likely to occur at longer basic drive CLs because HP refractoriness frequently exceeds the FRP of the AVN at slower rates.
Atropine shortens the FRP of the AVN and allows the impulse to reach the HPS during its RRP and ERP, as a result a
type I pattern could be changed to a type II or III with infranodal block.
The Atrium as a 1st site of block occurs when the patient is agitated (increased sympathetic tone) or at slow pacing CLs.
AVN is 1st site of block in ~ 57% of patients, A in 33% and HPS in 10%.
Types of response to Ventricular ES
In patients with A-V dissociation simultaneous A and V pacing is used (DDD) during the basic drive to prevent supraventricular
capture from altering refractoriness by producing sudden changes in CL and also preventing hemodynamic changes which could
also affect ERPs.
SNRT 1500 ms
cSN 525 ms
SNRT / BCL > 160%
SACT 50-125 ms
Narula method (slightly faster than baseline CL) vs Strauss method (PAC)
Return time = SACT + BCL + SACT
IHR = 118.1 - (0.57 x age)
Propranolol 0.2 mg/kg + Atropine 0.04 mg/kg
AH 50-120 ms
HV 35-55 ms
HH 25 ms
Abnormal Block in HPS (H no V) at H1-H2 > 400 ms
Normal AVNWB pacing CL < 450 ms
RBBB 1% in 50's, 10% in 80's - RHC has a 5% chance of causing RBBB
LBBB 0.5% in 50's, 5-6% in 80's
Bifascicular Block and MI = indication for PPM
AVN RRP: when AH starts prolonging
AVN ERP: when AH stops conducting (A no H)
AVN FRP: shortest H1-H2
FRP of the fast pathway as the minimum H–H interval before the jump up and the FRP of the slow pathway as the minimum H–H
interval after the jump up obtained by extra stimuli from the HRA.
-HRA entr: AHA = AVNRT, AHHA=PJRT
-Early PAC: engage FP and terminates Tach = AVNRT, Bring His/QRS early without termination = PJRT
-HRPAC: no effect = PJRT, preexcites following n+1 His by engaging SP = AVNRT
SUPERNORMALITY of conduction: is manifested with better than expected but not more rapid than normal
conduction. It is only described in abnormally functioning cardiac tissue and has been demonstrated in the HPS but not in the AVN,
the His bundle or the atrial or ventricular myocardiums. The first example was one of complete heart block with conduction during the
In man, the most common manifestation of "supernormal" conduction is an unexpected normalization of BB
conduction at an RR interval shorter than that responsible for the BBB aberration.
The paradox of unexpected improved AV conduction can be explained by a number of alternate mechanisms (gap phenomenon,
peeling, or dual AV nodal conduction). Premature beats evoked early during the repolarization phase of the action potential often
reached the more distant electrode earlier than did later responses evoked at membrane potentials closer to maximum resting
1-More rapid than normal conduction of premature impulse in a Purkinje fiber
<=> enhanced conduction due to "supernormal excitability" associated with late repolarization
2-More rapid Purkinje fiber conduction with hyperkalemia <=> Increased excitability associated with slight potassium induced
3-Wedensky facilitation: Conduction across a site of bidirectionnal block in a Purkinje strand following an appropriately timed
impulse that blocked distally. Enhanced excitability at the site of block due to summation of a sub-threshold response
4-Gap phenomenon: a proximal delay on a premature impulse allow stime for recovery of excitability of a distal site of block
5-Peeling Back of a refractory barrier due to premature engagement and early recovery of excitability. Conduction of a previously
blocked atrial impulse following an appropriately timed retrogradely concealed ventricular impulse.
PEELING BACK of a Refractory Barrier by premature beats: An ectopic ventricular response resulting
in the conduction of a previously blocked PAC (apparent supernormal conduction). The PVC conducts retrogradely to the Purkinje
system and His bundle with block retrogradely to the atrium in the AVN (retrograde concealed penetration by the PVC). Retrograde
activity caused preexcitation of the site within the AVN where block of the PAC had previously occurred. The early recovery of the
AVN resulting from its preexcitation by the retrograde activity from the PVC allowed the previously blocked PAC to traverse this
region and be conducted to the ventricles. Numerous examples of "peeling back" of refractory barrier by junctional, atrial, and
infranodal premature beats have also been shown.
Example of peeling back of refractoriness by a PVC that
retrogradely penetrated the HPS and not the AVN and allowed
preexcitation of the AVN where the PAC previously blocked was
now able to traverse to the ventricles.
Example of supernormal conduction in a sick HPS (Long HV)
where a PAC is paradoxically conducted.