2. INTRODUCTION
Invasive cardiac electrophysiology (EP) is a collection of clinical
techniques for the investigation and treatment of cardiac rhythm
disorders.
Electrophysiology (EP) study can accomplish the following goals.
• Make a completely accurate diagnosis of an arrhythmia
• Establish the etiology for syncope/palpitations
• Evaluate prognosis and stratify risk of sudden cardiac death in
patients at risk
• Guide antiarrhythmic drug therapy
• Evaluate the requirement, feasibility or outcome of non
pharmacologic therapy (e.g. Pacemaker, radiofrequency ablation,
antiarrhythmic surgery, or implantable cardiac defibrillator).
3. INDICATIONS
The indications for invasive EP studies can be broken down to two
categories: diagnostic and risk stratification.
Diagnostic indications can be divided into :
Bradyarrhydhmias
Tachyarrhydhmias
Syncope of unknown etiology
4. DIAGNOSTIC INDICATIONS
Syncope when an individual is suspected of having sick sinus
syndrome, based on inappropriate sinus bradycardia. The detection
of a prolonged corrected sinus node recovery time may predict future
recurrence of syncope
Syncope in patients with bifascicular block (left or right bundle
branch block and hemifascicular block). The induction of infra-Hisian
block in patients with bifascicular block can predict future adverse
cardiovascular events.
To determine the site of block in patients with abnormal
atrioventricular conduction
5. DIAGNOSTIC INDICATIONS
Patients with wide complex tachyarrhythmias in whom a diagnosis
cannot be established by noninvasive means or who are suspected of
harboring a life-threatening arrhythmia should undergo EP studies.
6. DIAGNOSTIC INDICATIONS
Syncope in patients with ischemic heart disease or other structural
heart disease.
Syncope immediately following palpitations
Syncope in patients who are employed in high-risk occupations (eg,
airline pilots, school bus drivers, police officers) after failure of all
noninvasive diagnostic tools to arrive at a cause.
Unexplained syncope
In survivors of sudden cardiac death (SCD) with no established cause
(idiopathic VF), an EP study is considered a step in the diagnostic
cascade recommended to try to establish a diagnosis
7. RISK STRATIFICATION
In the primary prevention of SCD, patients with an ischemic
cardiomyopathy due to a prior myocardial infarction and who have
left ventricular ejection fraction (LVEF) <40 percent should undergo
ambulatory cardiac rhythm monitoring. EP studies are indicated if
they are found to have nonsustained VT. The induction of sustained
VT or VF constitutes a class I indication for the implantation of an ICD
8. RISK STRATIFICATION
Atrioventricular (AV) conduction abnormalities below the level of the
AV node may progress to complete AV block with catastrophic
consequences.
The site of block in patients with Mobitz type II second degree AV
block is infranodal (intra- or infra-Hisian), and this constitutes an
indication for pacing even if the patient is asymptomatic.
An EP study is indicated if the site of block cannot be determined
reliably in an asymptomatic individual with second degree AV block. If
the site is infranodal, pacing is indicated
9. RISK STRATIFICATION
Asymptomatic young (8 to 21 years) patients with
electrocardiographic manifestations of preexcitation may be at high
risk of SCD due to atrial fibrillation progressing to VF. These patients
are advised to undergo exercise stress testing. The clear and sudden
loss of preexcitation with exercise stress testing predicts a favorable
prognosis.
If clear loss of preexcitation is not seen or the data are
uninterpretable, invasive risk stratification via transesophageal pacing
or EP studies is recommended.
10. RISK STRATIFICATION
The role of EP studies in the Brugada syndrome is controversial.
Patients with the Brugada syndrome who have had a history of
syncope or have survived SCD are more likely to be inducible.
However, the role of EP studies in predicting future events is
controversial. The implantation of an ICD may be considered in a
patient with Brugada syndrome who is induced into VF.
11. RISK STRATIFICATION
For purposes of risk stratification for SCD, programmed electrical
stimulation can be considered (a class IIa indication) in patients with
cardiac sarcoidosis and an LVEF >35 percent despite optimal medical
therapy and immunosuppression
For purposes of risk stratification for SCD, programmed electrical
stimulation is occasionally used in asymptomatic patients with
arrhythmogenic right ventricular cardiomyopathy
12. RISK STRATIFICATION
In the risk stratification of adults with tetralogy of Fallot with risk
factors for SCD, such as left ventricular systolic and diastolic
dysfunction, QRS ≥180 milliseconds, extensive right ventricular
scarring, and nonsustained VT. It should not be used as a screening
test on patients with tetralogy of Fallot who do not have high risk
factors or in patients with repaired tetralogy of Fallot.
Adult patients with congenital heart disease of moderate to severe
complexity who display high-risk features such as syncope and
ventricular arrhythmias should undergo invasive EP studies to
determine if they are at risk of SCD and may benefit from an ICD
(class IIa indication)
14. PREPROCEDURAL EVALUATION
In all patients undergoing invasive EP study, the preprocedure
evaluation includes a thorough history and physical examination and
review of the available electrocardiograms (ECGs), both at baseline
and, if available, during the tachycardia.
Event monitoring for up to four weeks in an effort to document the
tachycardia. Event monitoring for longer periods is typically more
useful than short-term (24 to 48 hours) Holter monitoring in
documenting the tachycardia.
15. PREPROCEDURAL EVALUATION
Transthoracic echocardiography to assess for structural heart
disease.
Cardiac magnetic resonance imaging may also be considered for
special situations (eg, suspicion of arrhythmogenic right ventricular
cardiomyopathy, hypertrophic cardiomyopathy, etc).
Exercise testing, if there is a history of exercise-induced arrhythmia
Cardiac catheterization and coronary angiography, if indicated by the
patient's clinical presentation and symptoms suggesting coronary
heart disease. If the clinical presentation is prehospital cardiac arrest
or ventricular tachycardia causing hemodynamic collapse, coronary
angiography and an assessment of ventricular function (eg,
echocardiography, ventriculography) should usually be obtained prior
to invasive EP studies with programmed cardiac stimulation.
16. PREPARATION AND MONITORING
Patients should be fasting after midnight on the day of the procedure,
except for oral medications with sips of water.
Patients should hold their normal cardiovascular medications,
particularly medications which affect atrioventricular (AV) node
conduction (ie, beta blockers, dihydropyridine calcium channel
blockers, and digoxin) and antiarrhythmic medications.
Standard cardiorespiratory monitoring should include blood pressure
(noninvasively or via arterial monitoring), pulse, oxygen saturation,
and cardiac telemetry.
17. PREPARATION AND MONITORING
Defibrillation pads should be placed on the patient prior to beginning
the procedure.
Intravenous access is required for administration of sedation and for
management of any rhythm-related complications (ie, ventricular
fibrillation, sinus bradycardia, etc).
Supplemental oxygen, a suction device, and intubation equipment
should be immediately available for management of respiratory
complications (though supplemental oxygen should be removed prior
to delivery of any electrical shocks).
18. VASCULAR ACCESS
In nearly all EP studies, venous vascular access is required, often from
multiple sites. The Seldinger technique is employed to place multiple
venous accesses. The femoral approach is most common, but the
subclavian, internal jugular, or brachial approach may be used, most
often for placement of a catheter in the coronary sinus.
19. EP EQUIPMENT
Programmable stimulator
Multichannel lead switching box (junction box)
Electrode catheters
Ablation system –Generator, Irrigation Pump, Remote Panel, Cables,
Tubing
3D Navigational Mapping System
20. ELECTRODE CATHETER
PLACEMENT
Multipolar electrode catheters are positioned in the heart. Typical
positions include
The right atrium (high right atrium [HRA])
Anterior tricuspid valve annulus to record the bundle of His
The right ventricle (right ventricular apex [RVA])
A catheter may be placed in the coronary sinus to record left atrial
activation, particularly in studies of patients with supraventricular
tachycardia (SVT).
21. ELECTRODE CATHETER
PLACEMENT
When mapping and ablation are performed, electrodes may be placed
in the left heart. Left heart access may be obtained via either a
transseptal or retrograde aortic approach.
Intracardiac recordings and programmed electrical stimulation (PES)
are performed via the electrode catheters.
Typically, for evaluation of ventricular arrhythmias requiring LV
mapping, a retrograde aortic approach is employed,
while the transseptal approach is preferred for left-sided SVTs.
Either approach may be used for patients with a suspected left-sided
accessory pathway.
22. ELECTRODE CATHETER
PLACEMENT
When catheters are placed into left-sided cardiac chambers, systemic
anticoagulation is required to prevent thromboembolic complications.
Typically intravenous heparin is initiated at the time of the procedure
and continued until the catheters are removed from the left-sided
cardiac chambers.
23.
24. ELECTROCARDIOGRAPHIC AND
ELECTROPHYSIOLOGIC RECORDINGS
Baseline recordings obtained during a typical invasive EP study include several
surface electrocardiograms (ECGs) to time events from the body's surface and
several intracardiac electrograms, all of which are recorded simultaneously. The
intracardiac electrograms are generally displayed in the order of normal cardiac
activation
25. ELECTROCARDIOGRAPHIC AND
ELECTROPHYSIOLOGIC RECORDINGS
The first intracardiac tracing is a recording from the high right atrium
(HRA) close to the sinus node. Pacing at this position allows
evaluation of sinoatrial node function and atrioventricular (AV)
conduction; the addition of premature atrial stimulation or burst atrial
pacing may result in the induction of supraventricular
tachyarrhythmias.
Sinus node function is determined by measuring the sinus node
recovery time (SNRT), a reflection of the node's automaticity, and the
sinoatrial conduction time (SACT), a reflection of peri-sinus node
conduction properties.
26. ELECTROCARDIOGRAPHIC AND
ELECTROPHYSIOLOGIC RECORDINGS
The next intracardiac tracing is the His bundle recording (HBE),
obtained from a catheter positioned at the bundle of His (in the area
of the tricuspid annulus).
One to three recordings may be obtained from the coronary sinus
(CS) in patients with supraventricular tachyarrhythmias or
preexcitation. Since the coronary sinus runs in the mitral annulus,
these recordings reflect left atrial activation.
27. ELECTROCARDIOGRAPHIC AND
ELECTROPHYSIOLOGIC RECORDINGS
The next is a recording from a right ventricular apex (RVA) electrode
catheter.
Depending upon the particular study, other required recordings may
include right bundle branch recording, left ventricular recording,
transseptal left-atrial recording, and atrial and ventricular mapping
catheter tracings for EP mapping and ablation.
28.
29. AH INTERVAL
The AH interval is measured on the His bundle electrogram and
represents the interval from the earliest rapid deflection of the atrial
recording (activation of the lowest part of the right atrium) to the
earliest onset of the His bundle deflection. This interval approximates
AV nodal conduction.
More precisely, however, it is the sum of conduction through the low
right atrial inputs into the atrioventricular node, the atrioventricular
node proper, and the proximal His bundle.
The AH interval has a wide range in normal subjects (50 to 120
milliseconds) and is markedly influenced by the autonomic nervous
system
30. AH INTERVAL
Short AH intervals
Increased sympathetic tone
Enhanced AV nodal conduction,
which may be due in some
patients to steroid use or
pregnancy
Preferential left-atrial input into
the atrioventricular node
Long AH interval
Impaired or delayed AV node
conduction from drugs such as
digoxin, beta blockers, calcium
channel blockers, and
antiarrhythmic drugs, particularly
amiodarone
Increase parasympathetic (vagal)
tone
Intrinsic disease of the
atrioventricular node
31. HIS BUNDLE ELECTROGRAM
DURATION
The His bundle electrogram duration reflects conduction through the
short length of compact His bundle that penetrates the fibrous
septum.
This interval is normally short (15 to 25 milliseconds), with
fractionation and prolongation or even splitting of the His bundle
potential, seen with disturbances of His bundle conduction
32. HV INTERVAL
The HV interval is measured from the earliest onset of the His bundle
deflection to the earliest registered surface or intracardiac ventricular
activation anywhere. This measurement reflects conduction time
through the distal His-Purkinje system.
Unlike the AV node, the His-Purkinje system is far less influenced by
the autonomic nervous system, and the range in normal subjects is
narrow (35 to 55 milliseconds)
33. HV INTERVAL
A prolonged HV interval is
consistent with diseased distal
conduction in all fascicles.
In patients with symptoms
suggesting a bradyarrhythmia, a
prolonged HV interval (>55
milliseconds) warrants pacemaker
therapy.
In asymptomatic patients with an HV
interval >100 milliseconds, a
pacemaker is also indicated.
A validated short HV interval
suggests one of two situations:
Ventricular preexcitation via an AV
bypass tract
Ventricular origin for the beats, such
as ventricular premature beats
(VPBs) or an accelerated
idioventricular rhythm that is
isorhythmic with the sinus rhythm
A spurious explanation for a short
HV interval is the inadvertent
recording of a right bundle branch
potential rather than a His potential.
34.
35. VA CONDUCTION
The assessment of ventriculoatrial (VA) conduction is also important
in the EP study, particularly for patients with a supraventricular
tachycardia (SVT). This is performed by ventricular extrastimulus and
incremental ventricular pacing. Absence of VA conduction makes
certain SVTs less likely (ie, atrioventricular reciprocating tachycardia
and atrioventricular nodal reentrant tachycardia) and suggests an
atrial tachycardia (AT), since AT is independent of retrograde VA
conduction.
36. SINOATRIAL CONDUCTION TIME
Sinus nodal (SN) function is assessed by sinoatrial conduction time
and sinus nodal recovery time.
Measuring Sino-atrial conduction time (SACT) involves placement of a
catheter near the sinus node from which progressively premature
atrial extra stimuli are introduced after every eighth to tenth beat of
either a stable sinus rhythm (Strauss method) , or atrial pacing for 8
beats is done at a rate just lower than the sinus rate (Narula method).
The difference of time of the recovery beat post pacing versus that of
the sinus cycle length gives us 2 times the SACT value. Interval of
upto 250 msec is considered normal.
37. SINOATRIAL CONDUCTION TIME
Due to the limitations of indirect methods in assessing the SACT,
techniques for direct recording of the sinus electrogram (EGM) have
been developed. Endocardial recordings demonstrate diastolic phase
4 activity followed by a slow upstroke culminating in a rapid atrial
EGM. The directly measured SACT was defined as the interval between
the local EGM and the rapid atrial deflection.
Normal SACT times generally range from 40 to 150 milliseconds,
depending upon the laboratory. Studies have shown a good
correlation between indirect and direct methods of measuring SACT.
However, SACT is a relatively insensitive test for SA node dysfunction.
38. SINUS NODE RECOVERY TIME
The sinus node recovery time (SNRT) is performed by placing a
catheter near the SA node and pacing (overdrive suppression) for at
least 30 seconds at a fixed cycle length starting slightly faster than
the intrinsic sinus rate. This is repeated at progressively shorter cycle
lengths.
Pacing rates up to 200 beats per minute may be employed for
improved sensitivity. It is important to wait at least one minute
between pacing sequences to allow full recovery of the SN.
39. SINUS NODE RECOVERY TIME
The maximum SNRT is the longest pause from the last pacing
stimulus to the first spontaneously occurring sinus beat at any paced
cycle length. As the sinus cycle length (SCL) affects the SNRT, it is
often normalized or corrected:
The SNRT is normalized by dividing this value by the SCL.
The corrected sinus node recovery time (CSNRT) is determined by
subtracting the SCL from the SNRT.
A total recovery time (TRT) can also be calculated, which is the time
required to return to the basal sinus rate.
40. SINUS NODE RECOVERY TIME
Normal values have generally been estimated as follows:
SNRT/SCL <150 percent
CSNRT <550 milliseconds
TRT less than five seconds
There are several limitations to the use of overdrive suppression in
determining SN function, which include changes in autonomic tone
due to the effects of pacing, changes in P-wave morphology or atrial
activation suggesting a pacemaker shift, sinoatrial entrance block,
and secondary pauses.
41.
42. PES
The technique of PES is used to assess the atrioventricular (AV)
conducting system and to induce supraventricular and ventricular
arrhythmias. Premature beats can be introduced during a
tachyarrhythmia to probe the mechanism of the tachycardia.
43. VENTRICULAR PACING
Normally during ventricular pacing the impulse travels retrograde into
the atrium through the AV node.
VA dissociation is referred when while pacing the ventricle, no
impulse travels back to the atrium.
Ventricular pacing is then done at decreasing cycle length till VA
conduction is blocked.
Thereafter ventricular extra stimuli (single or multiple) are given at
decreasing interval till a VA block is obtained (Figure 5 b).
During ventricular pacing atrial activation pattern whether central (His
A is earliest) or eccentric (His A is later that A in either RA or LA
recording catheter) is seen.
44. VENTRICULAR PACING
Lengthening of VA interval with decrement in the stimulus interval
suggests decremental conduction. Central and decremental
conduction generally suggests conduction through the nodal tissue
(Figure 5a).
Eccentric and non-decremental conduction suggests presence of a
retrograde conducting accessory pathway (Figure 5c).
Multiple (3 to 5) ventricular extrastimuli may be needed to induce
ventricular arrhythmia sometimes.
45.
46.
47.
48. ATRIAL PACING
Atrial pacing from either the right atrium or the left atrium as
clinically indicated is done to see for antegrade conduction
characteristics through the AV node.
In presence of WPW syndrome, there can be eccentric activation with
increasing preexcitation which can be easily appreciated on a 12 lead
electrocardiogram during the study. Atrial extra-stimuli are then
given (single and if required multiple).
49. ATRIAL PACING
Atrial extra stimuli may show
an AH jump (wherein there is AH
prolongation of more than 50
msec with a decrement of 10
msec on atrial extra-stimuli
interval),
induce a tachycardia or
bring out preexcitation with or
without decremental antegrade
conduction with a preexcited
QRS complex.
50. TACHYCARDIA STUDY
Once tachycardia is induced relationship of the atrium and ventricular
signals are noted. 1:1 AV activation generally suggests AVNRT (Figure
7a), AVRT (Figure 7b) and atrial tachycardia but rarely ventricular
tachycardia (VT). A>V suggests atrial tachycardia and rarely AVNRT
but never an AVRT or VT. V>A suggests ventricular tachycardia
(Figure 7c). During SVT atrial activation patterns helps to diagnose
the nature of tachycardia (Figure 7a and b).
51.
52.
53.
54.
55.
56. PACING MANEUVERS DURING
TACHYCARDIA
Continuous pacing at a slightly faster than that of the tachycardia
(Figure 8a) or programmed single extra-stimuli when the His is
refractory (Figure 8b), can be used to differentiate the mechanism of
arrhythmia.
57.
58.
59. MAPPING FOR LOCALIZING SITE
OF ABLATION
In many cases, catheter ablation immediately follows the diagnostic
electrophysiologic study.
Mapping refers to careful movement of a mapping or ablation
catheter in the area of interest, probing for the site at which
radiofrequency ablation will be successful at curing the arrhythmia.
60. MAPPING FOR LOCALIZING SITE
OF ABLATION
Activation mapping: - Where the activation signal in the mapping
catheter shows earlier signals as compared to the surface P/QRS
(Figure 9a) suggests the area to be near the origin of the arrhythmia
and suggests an appropriate site for treatment.
Pace-mapping: - In a patient especially with ventricular tachycardia,
pacing at the same cycle length as the tachycardia from the mapping
catheter and comparing the 12 lead ECG obtained during pacing with
that of tachycardia is called pace-mapping. If there is a 12/12 match
it suggests the origin of the tachycardia to be nearby (Figure 9b) and
is especially helpful for treatment of idiopathic ventricular outflow
tachycardias.
61.
62.
63. COMPLICATIONS
reported complication rates of approximately 2 percent
Serious complications of these procedures are generally related to the
catheterization process itself, including
vascular injury,
tricuspid valve damage,
pulmonary embolism,
hemorrhage requiring transfusion therapy,
cardiac chamber perforation resulting in pericardial tamponade,
sepsis from catheterization site abscess,
myocardial infarction, stroke, and death
