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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3597_Библиотеки_им_академика_М_И_Перельмана
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The Electrophysiology Laboratory and Electrophysiologic Procedures
1 sec
I
aV
F
V
1
V
6
RA
A A
AA (basic sinus cycle length) = 990 msec
A
HBE
V
H
A–H = 120 msec
H–V = 55 msec
Figure 6-20 Measurement of basic sinus cycle length and A–H and H–V
intervals. HBE, His bundle electrogram; RA , right atrium.
Table 6 -3
Pacing Interval Conversion Chart*
Pacing Interval (msec) Heart Rate (bpm)
200 300
222 270
231 260
240 250
250 240
261 230
273 220
286 210
300 200
311 193
316 190
333 180
353 170
375 160
400 150
429 140
462 130
500 120
545 110
550 109
600 100
667 90
750 80
857 70
1000 60
1200 50
1500 40
2000 30
*Pulse-to- pulse inter val (milliseconds) to b eats per minute (bpm).
at least 100 mm/sec in routine cases and at speeds of 100 to 200 mm/
sec in detailed mapping procedures. All measurements of rate and
conduction times are made in milliseconds. The pacing interval can
be converted to HR by the following formula (Table 6 -3): HR (beats
per minute [bpm]) = 60,000/interval (msec).
The A–H interval represents conduction time from the low RA at
the interatrial septum through the AV node to the His bundle and
approximates AV nodal conduction time. The measurement is made
V
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The Electrophysiology Laboratory and Electrophysiologic Procedures 303
from the earliest reproducible rapid deflection of the atrial electrogram on the His bundle recording to the onset of the His deflection
on that electrogram (see Fig. 6-20). Normal values for adults are
reported to range from 50 to 140 msec. The A–H interval is influenced
strongly by the patient’s autonomic tone and may vary by 50 msec
during a study in a given patient. The A–H interval normally increases
in response to increases in atrial pacing rates. It may also be altered
by drugs that affect AV conduction, and the measurement may be
influenced artificially by such factors as gain setting and position of
the atrial catheter.
The H–V interval represents conduction time from the proximal
His bundle to the ventricular myocardium. The measurement is made
from the earliest deflection of the His spike on the His bundle recording to the earliest onset of ventricular activation, recorded from any
intracardiac electrogram or surface ECG. Normal values range from
35 to 55 msec. In contrast to the A–H interval, the H–V interval normally remains relatively constant and is not significantly affected by
variations in autonomic tone or atrial pacing rates.
Sequence of Activation
Determination of the sequence of antegrade and retrograde atrial activation during spontaneous rhythms, atrial pacing, ventricular pacing,
and induced rhythms is essential in differentiating VT from SVT and
in defining the reentrant circuit in SVT. The atrial activation normally
begins in the high RA and spreads to the low RA and His bundle, with
LA activation recorded from the coronar y sinus catheter occurring
significantly later. When ventriculoatrial conduction is present during
ventricular pacing, the earliest retrograde atrial activity is recorded in
the His bundle electrogram, followed by the RA and coronar y sinus
recordings. Abnormal or eccentric sequences of retrograde atrial activation occur in the presence of AV accessory pathways (Fig. 6-21). This
is discussed in more detail in subsequent sections dealing with SVT
and catheter ablation.
1
HRA
HBEP
HBED
PCS
DCS
RVA
V
V
V
V
V
A B C
Figure 6-21 Pattern of retrograde atrial activation. Electrograms from the
high right atrium (HRA), proximal His bundle (HBEP), distal His bundle (HBED),
proximal coronary sinus (PCS), distal coronary sinus (DCS), and right ven tricular apex (RVA) are shown. A, Normal pattern of retrograde atrial activation through the atrioventricular (AV) node. B, Sequence of retrograde atrial
activation with a right-sided accessor y pathway showing earliest activation
in the HRA. C, Sequence of retrograde atrial activation with a left-sided
accessory pathway showing earliest activation in the DCS.
A
A
A
A
A
A
V
A
V
A
A
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A
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The Electrophysiology Laboratory and Electrophysiologic Procedures
Programmed Electrical Stimulation
Programmed electrical stimulation involves observing the EP effects
of incremental pacing and the introduction of programmed extrastimuli coupled to normal sinus rhythm or paced rhythms. The major
purposes of programmed electrical stimulation are to characterize the
EP properties of cardiac tissue and to induce and analyze the mechanism of arrhythmias. The most commonly used types of pacing during
the EPS are burst pacing, incremental pacing, and programmed stimulation. Fixed burst pacing involves the delivery of a series of impulses
at a constant rate. A decremental burst consists of a series of impulses
at progressively increasing rates. Programmed stimulation involves the
coupling of premature extrastimuli to a short train (six to eight beats)
of pacing or to sinus rhythm. The number of extrastimuli may vary
from one to four. The pacing train is referred to as S
as S
, and second extrastimulus as S3. Coupling intervals are decreased
2
, first extrastimulus
1
progressively and systematically by 10-msec decrements until an
arrhythmia is induced or the first extrastimulus loses capture (the
effective refractory period [ERP] of the tissue is reached).
Assessment of Sinus
Node Function
Many studies begin with an evaluation of AV node function and assessment of atrial and AV nodal refractoriness. Assessment of sinus node
function is not routinely performed anymore due to the lack of sensitivity of the results; however, in studies performed to assess bradycardia
or syncope, a sinus node recovery time measurement can be considered. Measurement of sinus node recovery time is performed by
pacing the RA, most commonly near the region of the sinus node, at
a slightly faster rate than the intrinsic sinus rate for approximately
30 sec, then abruptly terminating pacing. Sinus node recovery time is
the time from the last paced atrial complex on the RA recording to the
return of the first sinus complex (Fig. 6-22). Generally, the slower the
intrinsic sinus rate, the longer the sinus node recovery time. The absolute sinus node recovery time may be corrected for HR by subtracting
the basic sinus cycle length (corrected sinus node recovery time).
I
aV
F
V
1
V
6
HRA
HBE
RV
Figure 6-22 Demonstration of a normal sinus node recovery time in a
patient undergoing electrophysiologic study (EPS) for the evaluation of
syncope of unknown cause. After a train of atrial pacing at a cycle length
of 450 (approximately 133 bpm), 1050 msec elapsed before the return of
sinus node activity. The absolute sinus node recovery time is 1050 msec.
HBE, His bundle electrogram; HRA, high right atrium; RV, right ventricle;
SNRT, sinus node recovery time.
A A A A A A A A
V
V
A
A
H
H
V V V V V V V V V
SNRT
1050 msec
V
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The Electrophysiology Laboratory and Electrophysiologic Procedures 305
Normal values for absolute sinus node recovery time are up to 1.5 sec
and for corrected sinus node recovery time up to 550 msec. Secondary
pauses are other indicators of sinus node dysfunction (SND).
Assessment of Atrioventricular
Nodal and His-Purkinje
System Function
AV nodal function is assessed by determining the point at which 1 : 1
AV conduction ceases and AV nodal Wenckebach (WB) begins. The
normal response to incremental atrial pacing at progressively faster
rates is to develop a longer AH interval and, ultimately, block in the
AV node (Fig. 6-23). Most normal individuals develop WB AV block at
paced atrial cycle lengths of 500 to 350 msec (HRs of 120 to 170 bpm).
AV nodal block does not usually occur during exercise when similar
HRs are achieved, because catecholamines enhance conduction
through the AV node. The point at which WB AV block occurs in
response to atrial pacing may be influenced by drugs that affect AV
nodal conduction and by autonomic tone. WB AV block occurs at
longer cycle lengths (slower pacing rates) in patients with enhanced
vagal tone and at shorter cycle lengths (faster pacing rates) in patients
with enhanced sympathetic tone. In contrast to the A–H interval, the
H–V interval remains relatively constant during decremental atrial
pacing, and block below His (intra-Hisian block) is considered pathologic at pacing cycle lengths >
400 msec (rates <150 bpm).
Determination of
Refractory Periods
The refractoriness of cardiac tissue is defined by the response of the
tissue to the introduction of premature stimuli. For most routine EPSs,
the ERP is defined as the longest coupling interval between the basic
drive and the premature stimulus that fails to propagate through the
1 sec
I
aV
F
V
1
V
6
Figure 6-23 Type-I second-degree atrioventricular (AV) block (Wenckebach
[WB]) in the AV node induced by atrial pacing at a cycle length of 410 msec.
Each paced atrial depolarization is followed by a progressively longer A–H
interval until the fourth atrial depolarization is blocked in the AV node (no
His depolarization is seen af ter the atrial electrogram). The A–H interval
after the blocked atrial depolarization is shor ter (130 msec) compared with
the A–H inter val preceding the block beat (280 msec). The H–V interval
remains constant despite the progressive increase in A –H interval during
the WB sequence.
A
130 60
A A A A
410
A
H
410 410
V
A
V
180
A
H
60 280 60 130 60
410
V
A
H
V
A
H
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Table 6 -4
The Electrophysiology Laboratory and Electrophysiologic Procedures
Normal Intervals and Refractory Periods
Parameter Normal Duration (msec)
A–H 50 -150
H–V 30-55
His 10-25
Atrial ERP 150 -360
AV nodal ERP 230-430
HPS ERP 330-450
Ventricular ERP 170-290
AV, Atrioventricular; ERP, effective refractor y period; HPS, His-Purkinje system.
tissue. Normal values for AV nodal, atrial, and ventricular refractory
periods have been established (Table 6-4). The ERP of cardiac tissue
may be affected by the current strength used, pacing rate, medications, and autonomic tone in the AV node.
Atrioventricular Nodal
Function Curves
AV nodal function curves can be constructed by plotting the coupling
interval of the premature stimulus (A
axis versus the A–H interval (AV nodal conduction time) of the premature stimulus (A
interval) on the vertical axis. In individuals
2H2
without dual AV nodal pathways, a progressive and gradual increase
occurs in the A–H interval before premature stimulus blocking in the
AV node, and the function curve is continuous (Fig. 6-24). A sudden
large increase (at least 50 msec) in the A–H interval (often referred to
as a jump) in response to a small decrement (10 msec) in the coupling
interval of the premature beat is evidence of functional dual AV nodal
pathways (Fig. 6-25). This represents a shift from conduction over the
fast AV nodal pathway to conduction over the slow AV nodal pathway
(with a longer A–H interval), and the AV nodal function curve is discontinuous (see Fig. 6 -24, B). During programmed stimulation in
patients with dual AV pathways, SVT is often initiated when the jump
to the slow pathway occurs. Multiple extrastimuli may be used in
patients with suspected or known SVT in an attempt to induce a clinically significant tachycardia. Drugs that modify refractoriness and
conductive velocity in the AV node, such as isoproterenol or atropine,
may be given in attempts to induce a clinically significant SVT.
interval) on the horizontal
1A2
Ventricular Stimulation
The safety and efficacy of programmed electrical stimulation in the
diagnosis and treatment of patients with ventricular arrhythmias have
been well established. The reported sensitivity and specificity of ventricular stimulation vary depending on the stimulation protocol used,
presenting arrhythmia, and underlying cardiac disease. The sensitivity
and specificity of programmed ventricular stimulation have been
defined best in patients with coronary artery disease whose arrhythmia is spontaneous sustained monomorphic VT. In these individuals,
the yield (and sensitivity) of the EPS increases with the addition of up
to three extrastimuli; the addition of more extrastimuli provides little
or no added benefit. In most patients, the clinical VT is initiated reproducibly by programmed electrical stimulation. The clinical significance of arrhythmias induced by programmed electrical stimulation
must be interpreted with regard to the specific arrhythmia for which
a patient is being evaluated. With more aggressive stimulation
400
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The Electrophysiology Laboratory and Electrophysiologic Procedures 307
300
200
(msec)
2
H
2
A
100
200 300 400 500 600
(msec)
A
400
300
200
(msec)
2
H
2
A
100
B
Figure 6-24
patient without functional dual AV nodal pathways. In this graph, the conduc tion intervals (A1A2) are displayed on the x axis and the resulting A– H interval
(A2H2) is displayed on the y axis. With progressively shorter coupling intervals, premature atrial beats are followed by progressively longer A–H intervals (A2H2), which represents progressive conduction delay in the AV node.
The normal AV nodal conduction curve is smooth and continuous. B, A typical AV nodal function cur ve in a patient with functional dual AV nodal path ways. Premature atrial impulses with longer coupling intervals conduct down
the fast pathway and have short A– H inter vals. With progressively earlier
pre mature atrial impulses, the refractor y period of the fast pathway is
reached, and conduction shifts to the slow pathway. The jump from the
fast pathway to the slow pathway is manifested by a sudden lengthening
of the A2H2 inter val and discontinuity in the AV nodal function curve.
(A, From Forgoros RN: Electrophysiologic testing, Cambridge, MA, 1991,
Blackwell Scientific.)
A, Normal atrioventricular (AV) nodal function curve in a
A
1A2
200 300 400 500 600
(msec)
A
1A2
protocols, polymorphic VT or VF that may represent a nonclinical (or
false-positive) response may be initiated. Even in normal individuals,
at close coupling intervals of the extrastimuli (usually <180 msec), VF
or polymorphic VT may be induced. In contrast, sustained monomorphic VT is considered a specific response to programmed electrical
stimulation and generally occurs only in patients with previous spontaneous VT or a pathologic substrate known to predispose to VT.
Although ventricular stimulation protocols var y slightly among
different laboratories, the minimal complete protocol usually involves
the introduction of three extrastimuli coupled to ventricular pacing at
two cycle lengths from two RV sites, typically RV apex and RV outflow
tract (Box 6-4). LV stimulation may be performed in some individuals
who have documented sustained monomorphic VT but whose arrhythmia is noninducible from the RV. The yield is relatively low from LV
stimulation, and LV stimulation may increase the morbidity of the
procedure. In individuals with exercise-induced VT or catecholaminedependent VT, isoproterenol may be infused and programmed stimulation repeated.
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aV
V
V
HRA
HBE
RV
A
aV
V
The Electrophysiology Laboratory and Electrophysiologic Procedures
1 sec
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H
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170
1 sec
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HRA
HBE
RV
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A
1
600
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600
600
A
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1V1
H
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1
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A
340600600
A
V
A
1
1
H
1
V1V
2A1
2
300
V
2
H
2
2
B
Figure 6-25
a patient with functional dual AV nodal pathways. Premature atrial stimuli
are coupled to a train of atrial pacing at a cycle leng th of 600 msec. A, At
a coupling interval of 350 msec, the premature atrial stimulus has an A–H
interval of 170 msec. B, At a coupling inter val of 340 msec, the A–H inter val
of the premature impulse suddenly increases to 300 msec, representing a
shift to the slow pathway. HBE, His bundle electrogram; HRA, high right
atrium; RV, right ventricle.
Box 6 -4 Ventricular Stimulation Protocol
Standard Protocol
Single extrastimulus coupled to ventricular pacing at cycle lengths of 600
and 400 msec from RV apex and RV outflow tract
Double extrastimuli coupled to ventricular pacing at cycle lengths of 600
and 400 msec from RV apex and RV outflow tract
Rapid ventricular pacing (400 msec to loss of 1 : 1 ventricular capture)
Triple ex trastimuli coupled to ventricular pacing at cycle lengths of 600 and
400 msec from RV apex and RV outflow tract
Additional Maneuvers That May Be Performed
Extrastimuli may be coupled to sinus rhythm or other paced cycle lengths
A fourth extrastimulus may be coupled to ventricular pacing at cycle
lengths of 600 and 400 msec from both RV sites
Stimulation may be per formed at additional RV sites or from the LV
Isoproterenol may be infused and the stimulation protocol repeated
IV procainamide may be infused and the stimulation protocol rep eated
A 130-msec jump in atrioventricular (AV) nodal conduction in
IV, Intravenous; RV, right ventricular.
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The Electrophysiology Laboratory and Electrophysiologic Procedures 309
I
aV
F
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1
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6
S
SSS
HBE
S
RV
500
S
V
A A
V
V
V
V
V
V
V
V
V
V
A
A
V
V V
V
V
V
A A
V
V
V V
A
Figure 6-26 Induction of sustained ventricular tachycardia (VT) with triple
extrastimuli coupled to a train of ventricular pacing at 500 msec. During
induced V T, atrial activity is dissociated from ventricular activity. This may
be obser ved on the His channel (HBE) by the atrial electrogram (A) marching
randomly through the tachycardia. HBE, His bundle electrogram; RV, right
ventricle; S1, train; S2, first ex trastimulus; S3, second extrastimulus;
S4, third extrastimulus.
I
aV
F
V
1
V
6
RV
V V V V V V V VA
HBE
310
S
S
V
1
1S1S1S1S1S1S1S1S1S1S1
VVVVV
270
A
A VVA
V
V
A
V
A
270
A A
A
V
V
V
V
V
V
V
A
Figure 6 -27 Termination of monomorphic ventricular tachycardia (VT) with
ventricular burst pacing at a rate faster than that of tachycardia. On the
right ventricle (RV) channel, cycle length of monomorphic VT is measured
at 310 msec. Ventricular burst pacing (indicated by arrows and S1) at a
cycle leng th of 270 msec terminates the tachycardia. HBE, His bundle
electrogram.
To perform the stimulation protocol, the operator systematically
decreases the coupling interval between the last beat of the pacing
train and the extrastimuli until the tissue reaches refractoriness
(the first extrastimulus fails to capture) or an arrhythmia is induced
(Fig. 6-26). If the patient is hemodynamically stable, a 12-lead ECG of
the induced VT is recorded before attempts to terminate the tachycardia. The morphology of the VT is noted, and the cycle length is
obtained. The most common method of terminating the VT is ventricular burst pacing at a cycle length less than that of the tachycardia.
The cycle length of the burst pacing is decreased gradually until the
tachycardia either terminates (Fig. 6-27) or accelerates and results in
hemodynamic compromise, at which point cardioversion or defibrillation is performed on the patient. An initial 200-J biphasic shock is
routinely used for sustained VT.
The most specific endpoint of the ventricular stimulation protocol
is the induction of a sustained monomorphic VT that is identical to a
patient’s clinical VT. Sustained VT is commonly defined as VT lasting
at least 30 sec or requiring termination because of hemodynamic collapse before 30 sec. Noninducibility by ventricular stimulation refers
to the failure to induce sustained VT after the use of at least three
extrastimuli at two pacing rates from two RV pacing sites. The arrhythmia may be noninducible on the initial EPS or may be rendered noninducible by antiarrhythmic drug therapy. Partial drug efficacy refers
to significant lengthening (>
100 msec) of the cycle length of the
induced tachycardia or rendering a previously intolerable tachycardia
hemodynamically stable.
Complications
Complications associated with diagnostic EPSs are low and mortality is extremely rare. Complications are usually associated with
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catheterization and catheter manipulation rather than stimulation and
induction of arrhythmias. Reported complications include hemorrhage, venous thromboembolism (<1%), phlebitis (<1%), cardiac per-
foration and tamponade, and refractory VF. Hemothorax and
pneumothorax, recognized complications, can occur when the subclavian or internal jugular venous approaches are used. Arterial catheterization increases associated morbidity, including vascular
complications, stroke, systemic embolism, and protamine reactions.
Most reported deaths have resulted from incessant VF and have
occurred in patients with severe LV dysfunction, active myocardial
ischemia, hypertrophic obstructive cardiomyopathy, or because of the
proarrhythmic effect of drugs administered during the evaluation.
Defibrillation through an intracardiac electrode is effective in situations in which transthoracic defibrillation fails and death might otherwise result. Pneumothorax, cardiac perforation/tamponade, and
pocket and systemic infection are risks associated with implanting
pacemakers and defibrillators.
chronic pacemaker and defibrillator leads. A special mention of the
complications during and after catheter ablation of AF is necessary.
In a worldwide survey of more than 8000 patients who underwent this
procedure, Cappato et al report an overall 4% incidence of major
complications, such as pericardial effusion and tamponade, cerebrovascular events, pulmonary vein stenosis, and devastating consequences of a fistula developing between the LA and the esophagus.
Pulmonary vein stenosis and atrio-esophageal fistula can occur
several weeks after the procedure.
The Electrophysiology Laboratory and Electrophysiologic Procedures
Mortality is a real concern in patients undergoing extraction of
Utility of Electrophysiologic Study
for Specific Diagnosis
Sinus Node Dysfunction
The clinical applications of EPS in SND are limited. Although abnormal sinus node recovery times and sinoatrial conduction times have
been reported to have a specificity of 90% to 100% in patients documented to have spontaneous SND, sensitivity is significantly less. In
contrast to most induced tachyarrhythmias on EPS, it is difficult to
correlate symptoms with an abnormal sinus node recovery time. In
symptomatic patients with sinus bradycardia, an abnormal sinus node
recovery time has been reported to predict which patients may benefit
from cardiac pacing. The finding of an abnormal sinus node recovery
time in an asymptomatic patient being studied for tachyarrhythmias
may influence a decision to use certain medications.
Disorders of Atrioventricular Conduction
Abnormalities of AV conduction are classified as first-degree, seconddegree, or third-degree AV blocks. Clues to the site of AV block can
be derived by observing serial changes in the P–R interval in sequences
of block that are <
of the escape rhythm, and presence or absence of underlying intraventricular conduction delays on ECG. Compared with prolonged conduction in the AV node, conduction disease within or below the His
bundle is associated with a high likelihood that complete AV block
will develop. Complete AV block that occurs within or below the His
bundle is associated with a slower and less stable escape rhythm than
what occurs with complete AV block situated within the AV node. EPS
can confirm the site of spontaneous AV block or conduction delay and
assess the response of the conduction system to various pacing rates
and the introduction of premature impulses. EPS may identify
2 : 1 (i.e., 3 : 2 or 4 : 3), rate and duration of the QRS
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The Electrophysiology Laboratory and Electrophysiologic Procedures 311
indications for permanent pacemaker implantation in individuals with
syncope of unknown cause. Long H–V intervals (>
80 to 100 msec) and
block below the His bundle at atrial pacing rates of <150 bpm indicate
disease in the His-Purkinje system and are associated with a relatively
high incidence of subsequent CHB.
Sustained Ventricular Arrhythmias
For more than two decades, EPS was used to determine the efficacy
of antiarrhythmic drug therapy in patients with sustained VT and
survivors of cardiac arrest. This practice was based on the supposition
that the (1) induced ventricular arrhythmia represents the patient’s
clinical arrhythmia and (2) inability to induce arrhythmia after drug
treatment in a patient whose arrhythmia was previously inducible
correlates with freedom from the clinical recurrence of the arrhythmia. The predictive accuracy of serial EPS is highest in patients with
previous MI and spontaneous sustained monomorphic VT. There may
be a significant number of false-negative results with EPS in patients
with nonischemic cardiac disease or polymorphic VT or VF as a presenting clinical arrhythmia. Another important limitation of the
technique is that even in patients whose arrhythmia is rendered noninducible by antiarrhythmic therapy, there is a significant clinical
recurrence rate of sustained ventricular arrhythmia and cardiac arrest,
reported to be as high as 50% during 4 years. Data indicate that survivors of cardiac arrest or sustained VT derive a significant survival
benefit from an ICD compared with antiarrhythmic drug therapy. Most
patients surviving a hemodynamically unstable ventricular arrhythmia
receive an ICD without a preceding EPS. In rare cases, bundle-branch
reentry tachycardia or AF with rapid ventricular response (in the
setting of WPW syndrome) may precipitate a patient’s cardiac arrest
or unstable ventricular arrhythmia. If these circumstances are suspected, EPS may be useful because these arrhythmias are potentially
curable by radiofrequency catheter ablation. In patients with hemodynamically stable monomorphic VT in whom ablative therapy is being
considered, EPS is indicated.
Syncope of Unknown Cause
Syncope is a common clinical disorder, the workup of which can be
expensive and nonproductive. The diagnostic use of EPS in patients
with recurrent syncope has been reported to range from 12% to 79%.
The reported abnormalities are listed in Box 6-5. The yield is highly
Box 6 -5 Reported Abnormalities in Patients with Syncope
on Electrophysiologic Study
Sinus Node Dysfunction
Prolonged sinus node recovery time
Prolonged sinoatrial conduction time
Secondary pauses
Abnormalities of Atrioventricular Conduction
Prolonged AV nodal refractory period
Prolonged AV nodal WB cycle length
Prolonged H –V interval
Block induced within or below the His bundle
Induced Tachyarrhythmias
Rapid SVT
Sustained V T
AV, Atrioventricular; SV T, supraventricular tachycardia; VT, ventricular ta chycardia;
WB, Wenckebach.
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