Management of Patients
with Arrhythmias. Cardiac pacing, electrical cardioversion:
indications and technique.
Brief overview of the ECG diagnosis of arrhythmias
See also ACC/AHA/ESC Guidelines for the
Management of Patients with Atrial Fibrillation
1. P
wave = depolarization of the atria.
QRS = depolarization of the ventricle.
T wave = repolarization of the ventricle.
2. Cardiac
muscle cells depolarize with a positive wave of depolarization, then repolarize
to a negative charge intracellularly.
3. Skin
"leads" or electrodes have a positive and negative end.
4. A
positive wave form (QRS mainly above the baseline) results from the wave of
depolarization moving towards the positive end of the lead. A negative waveform
(QRS mainly below the baseline) is when a wave of depolarization is moving away
from the positive electrode (towards the negative end of the lead).
5. ECG
paper has
10 mm = 1.0 mVolt
6. Horizontal
axis is time.
.04 seconds for
.2 seconds for 1 large box = 5 small boxes = 5 x .04 seconds.
Figure 1:
Positive QRS in
Negative QRS in Lead aVR.
R wave = 7-
QRS wave = .06 seconds long in Lead I.
7. Lead
nomenclature.
|
Limb Leads |
Chest Leads |
Rhythm Strip |
|
I, II, III |
V1 - V6 |
Located on
the bottom of the ECG printout. Selected to give the best relationship of the
P wave to the QRS. |
8.
9.
Figure 2: A normal ECG and rhythm strip.
10.
ECG interpretation: look at five
areas, in order, on each ECG.
|
Rate |
|
Rhythm (Intervals) |
|
Axis |
|
Hypertrophy |
|
Infarct |
Rate
Rate is cycles or beats per minute.
Normal rate for the SA node 60-100.
|
<60 bradycardia |
>100 tachycardia |
SA node is the
usual pacemaker, other potential pacemakers (if SA node fails) are atrial
pacemakers with inherent rates of 60-80, AV node (rate 40-60), or ventricular
pacer (rate 20-40). In certain pathologic conditions ectopic (out of place)
pacemakers can go much faster at rates 150-250 cycles/minute. There are three methods of calculating
rate:
1. Most
Common Method:
(Most rates can be calculated this way). Find an R wave on a heavy line (large
box) count off "300, 150, 100, 75, 60, 50" for each large box you
land on until you reach the next R wave. Estimate the rate if the second R wave
doesn't fall on a heavy black line.
|
Rate calculation |
|
Memorize the number sequence: |
|
300, 150, 100, 75, 60, 50 |
Figure 4: Common
Method.
2. Mathematical
method:
Use this method if there is a regular bradycardia, i.e. - rate < 50. If the
distance between the two R waves is too long to use the common method, use the
approach: 300/[# large boxes between two R waves].
Figure 5: Count number of large boxes between first and second R
waves=7.5. 300/7.5 large boxes = rate 40.
3.
Six-second method:
Count off 30 large boxes = 6 seconds (remember 1 large box = 0.2 seconds, so 30
large boxes = 6 seconds). Then, count the number of R-R intervals in six
seconds and multiply by 10. This is the number of beats per minute. This is
most useful if you have an irregular rhythm (like atrial fibrillation) when you
want to know an average rate.
Figure 6: Count 30 large boxes, starting from the first R wave. There
are 8 R-R intervals within 30 boxes. Multiply 8 x 10 = Rate 80.
Rhythm (to include intervals)
We will focus on the basic
"core" of rhythms and measured "intervals" (PR, QRS, QT).
Rhythms are often the most challenging aspect of ECG's. You will see most
rhythms several times over the next few years of your training, and you will
eventually recognize them at a glance.
Now for some basics -
"arrhythmia" means abnormal rhythm.
The normal conduction pathway is: SA
node --> AV node --> Bundle of HIS --> Bundle Branches.
Arrhythmia can be understood by
realizing the existence of ectopic (out of place) foci (pacemakers) and
understanding the normal conduction pathway of the heart. Very simply put, if
the beat originates in the atria or AV node (supraventricular) the QRS
is usually narrow (normal), because it comes from above along the normal
pathway.
Figure 6a: QRS is narrow (normal).
If the beat is ventricular in
origin, the QRS is wide and bizarre because it doesn't come down
the normal pathway.
Figure 6b: QRS is wide.
Aberrancy is an exception to this
rule - here it does actually follow the normal pathway (atria - AV node -
ventricle) but for some reason the pathway is refractory to the beat and you
get a wide QRS.
A reasonable way to group arrhythmias
is in four general groups. Let us briefly review these four groups, then we
will develop some common sense principles for evaluating rhythm (to include
intervals).
Group 1
Irregular rhythms.
(main clue is QRS is not
spaced evenly apart anywhere, total irregularity of the beat).
A) Sinus arrhythmia.
P waves and P-R intervals are
all identical because they originate from the sinus node. Sinus rate may vary
normally a bit (increase with inspiration, decrease with expiration), but if
the rate varies a lot, this term is used.
Figure 7: Sinus arrhythmia: P waves are identical.
B) Wandering atrial pacemaker.
Pacemaker discharges from different
atrial locations - the clue here is the P waves are of varying shape and
differing PR intervals. PR interval is measured from the beginning of the the
Pwave to the beginning of the QRS - if the atrial pacemaker location varies it
will take different lengths of time to get to the ventricle - resulting in
different PR intervals. If the rate of the wandering atrial pacemaker is
>100 it is descriptively called multifocal atrial tachycardia.
Figure 8: Multifocal atrial tachycardia.
C) Atrial fibrillation.
You will frequently see this arrhythmia.
There are no P waves, only irregular or wavy baseline. The QRSs are irregularly
spaced, therefore it is included under irregular rhythms.
Figure 9: Atrial fibrillation.
Group 2
Escape (late) beats
and premature (early) beats.
The bottom line for Group 2
arrhythmias is that the rhythm is fairly regular - then you will notice an
early or late beat; try to figure out whether that beat is a premature atrial
contraction, premature ventricular contraction, etc.
A) Escape beats.
The usual pacemaker fails, so
a slower pacemaker fires at its inherent rate.
Atrial
escape
Different appearing and late P
wave.
Figure 10: Atrial Escape Rhythm. Note differing appearance of the P
waves for Sinus Rhythm vs. Atrial Escape Rhythm.
Junctional
escape
No P wave, normal QRS if not
aberrant.
Figure 11: Note all beats are junctional escape.
Ventricular
escape
No P, wide, bizarre QRS.
Figure 12: Ventricular escape.
B) Premature Beats.
An ectopic pacemaker fires
early before the next scheduled beat.
Premature
atrial contraction
"PAC", early and
differently shaped P wave, narrow QRS.
Figure 13: Premature Atrial Contraction noted by arrow.
Premature
junctional
No P, normal QRS if not
aberrant.
Figure 14: Note the two early, narrow beats at the arrow. These are
probably PJCs.
Premature
ventricular contraction
No P, wide bizarre QRS. PVCs
that occur three (3) or more in a row (ventricular tachycardia), multifocal
PVCs (different shapes), or PVCs that land on a previous T wave (R on T
phenomenon) can be dangerous ion a patient with underlying heart disease.
Figure 15: Note: Every fourth beat is a PVC (beginning with the second
beat).
Group 3 Rapid
ectopic (out of place) rhythms.
Ectopic rate nomenclature:
|
[150-250] |
Paroxysmal tachycardia |
|
[250-350] |
Flutter |
|
[350+] |
Fibrillation |
So, the descriptives paroxysmal
tachycardia, flutter, and fibrillation refer to the "rates" of the
arrhythmia, e.g. - it could be atrial fibrillation (wavy baseline refers to the
atria going >350 bpm.), or ventricular fibrillation (with the ventricle not
contracting in a coordinated fashion resulting in only an erratic line that
isn't possible to count).
Figure 16: Paroxysmal supraventricular tachycardia: note accelerated
rate and narrow QRS complexes.
Figure 17: Ventricular tachycardia: note fast rate and wide bizarre
QRS.
Figure 18: Ventricular fibrillation: erratic and wavy baseline.
Group 4
Atrioventricular heart blocks.
(occur in three (3) degrees,
like skin burns; third degree is the worst).
1st degree
PR interval > 0.2 seconds
(1 large box), each P is followed by a QRS. PR interval is measured from the
beginning of the P wave to the beginning of the QRS.
Figure 19: The PR interval is approximately 0.28 seconds.
2nd degree block - type 1
Also called
"Wenkebach". PR interval gets progressively longer each beat until
finally a QRS is "dropped" (missing).
Figure 20: Note the increasing PR interval before the QRS is dropped,
then the cycle is repeated.
2nd degree block - type 2
Also called "Mobitz
II". Look out! A more serious conduction problem than Type 1. PR intervals
are constant and a QRS is "dropped" intermittently.
Figure 21: Note the dropped QRS after the second and sixth P wave in
lead II (the rhythm strip).
3rd degree block
The atrial rate is independent
of the ventricular rate (P wave and QRS march out separately. The clue here is
no relationship at all of the P-R intervals). The P-R interval is constantly changing,
the QRS is usually wide and bizarre because it is ventricular origin.
Figure 22: Note the P waves and QRS waves are independent of each
other.
Intervals
An interval is a portion of the
baseline and at least one wave. We measure an interval on the horizontal axis
in seconds. The PR, QRS, and QT are the intervals which should be routinely
scanned on each ECG. For measuring intervals, look at the widest form in any
lead.
Figure 23: Intervals.
1. PR
interval (beginning of P wave to the beginning of the next QRS). Normally, <
.2 seconds or one large box. If it is > .2 seconds, it is a first degree
block. (Note: this concept was introduced under blocks).
Figure 24: Note the prolonged PR interval (.28 seconds), especially at
the second beat.
2.
QRS interval (beginning of Q to the
end of the S wave) should be < .12 seconds (< 3 small boxes). If QRS
is > .12, check for bundle branch block.
A QRS >
.12 and RR (2 peaks or R waves in QRS) occurring in the right chest leads
(V1-V2) indicates a right bundle branch block.
Figure 25: RBBB.
If QRS is
> .12 and RR occurs in the left chest leads (V5-V6), this indicates a left
bundle branch block.
Figure 26: LBBB.
3. QT
interval (beginning of QRS to end of T wave) should be less than half of the preceding
RR interval - this varies with the rate. For normal rates, QT < .4 seconds
(2 large boxes). "QT prolongation" (too long) can lead to a
refractory form of ventricular tachycardia called torsades de pointes.
Figure 27: The QT interval is greater than half the preceding RR
interval. Look at lead I.
|
Rhythm Guidelines |
|
1.
Check the bottom of the rhythm strip for regularity, i.e. - is it completely
regular, mostly regular with a few extra beats, or totally irregular? |
|
2. Check
for a P wave before each QRS, QRS after each P. |
|
3. Check RR
interval (for AV blocks) and QRS interval (for bundle branch blocks). Check for prolonged QT. |
|
4. Continue
to recognize "patterns" such as atrial fibrillation, PVCs, PACs,
escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV
blocks and bundle branch blocks. |
Fasicular
Blocks
Fasicular blocks are blocks of part
of the left bundle, either the posterior or anterior division:
Figure 28: Divisions of the bundles.
Anterior
fasicular block - the most common.
You will see left axis deviation (-30
to -90) and a small Q wave in lead I and an S in lead III (Q1S3). The QRS will
be slightly prolonged (0.1 - 0.12 sec).
Figure 29: Anterior fasicular block.
Posterior
fasicular block - less common.
You will see right axis deviation, an
S in lead I and an Q in lead III (S1Q3). The QRS will be slightly prolonged
(0.1 - 0.12 sec).
Figure 30: Posterior fasicular block.
Bifasicular
block.
This means two (2) of the three (3)
fascicles (in diagram) are blocked. The most important example is a right
bundle branch block and a left anterior fascicular block. Watch out for this.
Only one fascicle is left for conduction, and if that fasicle is intermittently
blocked, the dangerous Mobitz 2 is set up!
Figure 31: Right bundle branch block and left anterior fascicular
block.
"Fasicular Blocks" may seem
a bit complicated - simply remember that axis deviation is the clue.
In your differential, consider posterior fasicular blocks with right axis
deviation and consider anterior fasicular blocks with left axis deviation.
Fascicular blocks cause axis deviations, like infarcts and hypertrophy. If you
see a left or right axis deviation, first look for infarct or hypertrophy. If
neither are present, the remaining diagnosis of fasicular block is usually
correct. Review differential diagnosis of right and left axis deviation.
SYSTEMATIC
INTERPRETATION GUIDELINES for Electrocardiograms
RATE
Rate calculation
Common method: 300-150-100-75-60-50
Mathematical method: 300/# large boxes between R waves
Six-second method: # R-R intervals x10
RHYTHM
Rhythm Guidelines:
1. Check the bottom rhythm strip for regularity, i.e. - regular, regularly
irregular, and irregularly irregular.
2. Check for a P wave before each QRS, QRS after each P.
3. Check PR interval (for AV blocks) and QRS (for bundle branch blocks). Check
for prolonged QT.
4. Recognize "patterns" such as atrial fibrillation, PVC's, PAC's,
escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks
and bundle branch blocks.
AXIS
|
|
Lead I |
Lead aVF |
|
1. Normal axis (0 to
+90 degrees) |
Positive |
Positive |
|
2. Left axis deviation (-30 to -90) Also check lead II. To be true
left axis deviation, it should also be down in lead II. |
Positive |
Negative |
|
3. Right axis
deviation (+90 to +180) |
Negative |
Positive |
|
4. Indeterminate axis
(-90 to -180) |
Negative |
Negative |
Left axis deviation differential: LVH, left anterior fasicular block,
inferior wall MI.
Right axis deviation differential: RVH, left posterior fascicular block,
lateral wall MI.
HYPERTROPHY
1. LVH -- left ventricular hypertrophy = S wave in V1 or V2 + R wave in V5 or
V6 > 35mm or aVL R wave > 12mm.
2. RVH -- right ventricular hypertrophy = R wave > S wave in V1 and gets
progressively smaller to left V1-V6 (normally, R wave increases from V1-V6).
3. Atrial hypertrophy (leads II and V1)
Right atrial hypertrophy -- Peaked P wave in lead II >
Left atrial hypertrophy -- Notched wide (> 3mm) P wave in II. V1 has increase in the terminal negative
direction.
INFARCT
|
Ischemia |
Represented by symmetrical T wave inversion (upside down). Look in
leads I, II, V2-V6. |
|
Injury |
Acute damage -- look for elevated ST segments. |
|
Infarct |
"Pathologic" Q waves. To be significant, a Q wave must be at
least one small square wide or one-third the entire QRS height. |
Certain leads
represent certain areas of the left ventricle:
|
V1-V2 |
anteroseptal wall |
II, III, aVF |
inferior wall |
|
V3-V4 |
anterior wall |
I, aVL |
lateral wall |
|
V5-V6 |
anterolateral wall |
V1-V2 |
posterior wall
(reciprocal) |
Supraventricular Tachycardia
A
28-year-old woman suddenly has rapid palpitations accompanied by
chest pain and dizziness while playing her cello. She is brought to
an emergency department. She has a faint regular pulse of 190 beats
per minute. Her blood pressure is 82/54 mm Hg. Cardiovascular
examination reveals no signs of heart failure. An electrocardiogram
shows a regular tachycardia with a narrow QRS complex and no
apparent P waves. How should her case be managed?
The Clinical Problem
The term "supraventricular
tachycardia"
refers to paroxysmal tachyarrhythmias, which require atrial or
atrioventricular nodal tissue, or both, for their initiation and
maintenance. The incidence of supraventricular tachycardia
is about 35 cases per 100,000 persons per year, and the prevalence
is about 2.25 per 1000 (excluding atrial fibrillation, atrial
flutter, and multifocal atrial tachycardia, which are not
covered in this review).1 Supraventricular tachycardias
are often recurrent, occasionally persistent, and a frequent cause
of visits to emergency rooms and primary care physicians.
Common
symptoms of supraventricular
tachycardia
include palpitations, anxiety, light-headedness, chest pain,
pounding in the neck and chest, and dyspnea. Syncope is uncommon,
but some patients have serious psychological distress. Polyuria can
occur in prolonged episodes, mainly owing to the release of atrial
natriuretic factor.2
Most types of tachycardia
have a reentry mechanism (Figure 1), and
they are classified according to the location of the reentry circuit
(Figure 2).
Approximately 60 percent of cases are due to an atrioventricular
nodal reentry circuit, and about 30 percent are due to an
atrioventricular reentry circuit mediated by an accessory pathway —
a short muscle bundle that directly connects the atria and
ventricles.3 Atrial tachycardia
comprises about 10 percent of cases and often has a focal origin.4 However,
paroxysmal or persistent atrial tachycardia occurring long after
cardiac surgery that involved a large atrial incision is usually caused
by an intraatrial reentry.5
Sinus-node reentrant tachycardia, inappropriate sinus tachycardia, ectopic junctional tachycardia, and nonparoxysmal junctional tachycardia are rare.3
Figure 1. Mechanism of Reentry.
An impulse (Panel
A, arrows), initiated normally in the sinus node, passes through two pathways —
for example, the atrioventricular nodal connection and an accessory pathway. A
premature atrial impulse (Panel B) occurs and reaches the accessory pathway
when it is still refractory but conduction can occur in the atrioventricular
node. The impulse takes sufficient time to circulate through the
atrioventricular node and across the ventricle to allow the accessory pathway
to recover its excitability and conduct the impulse back to the atrium (Panel
C). The wave front reenters the atrioventricular node, continually encounters
excitable tissue, and is perpetuated as a reentry circuit.
Figure 2. Main Mechanisms and Typical
Electrocardiographic Recordings of Supraventricular
Tachycardia.
In patients with atrioventricular
(AV) nodal reentrant tachycardia
(Panels A and B), the atrioventricular node is functionally divided into two
pathways that form the reentrant circuit. In the majority of patients, during
this type of tachycardia,
antegrade conduction to the ventricle occurs over the slow pathway and
retrograde conduction over the fast pathway. The activation of atria and
ventricles is synchronous so that the retrograde P wave is buried in the QRS
complex, or it may be visible soon after the QRS complex (as pseudo r' in V1 or
pseudo s in the inferior leads). Orthodromic AV reentrant tachycardia (Panels A and B) is the
most frequent arrhythmia in patients who have an accessory pathway, with
antegrade conduction through the AV node, activation of the ventricles, and
retrograde conduction through the accessory pathway. Typically, there is a
short RP interval, but a long RP interval may be associated with
slow-conducting accessory pathways. With the use of adenosine or vagal
maneuvers (Panel C), tachycardia
often terminates with a retrograde P wave. In the approximately 70 percent of
patients with this type of tachycardia
who have an obvious accessory pathway, preexcitation may be seen in the ensuing
beats; however, it is absent in the approximately 30 percent of patients with a
concealed accessory pathway. In antidromic AV reentrant tachycardia (Panels A and B), the activation wave front travels in
the opposite direction. On electrocardiography, it is impossible to distinguish
antidromic AV reentrant tachycardia
from ventricular tachycardia.
Atrial tachycardias (Panels A
and B) typically have a focal origin (star), and different mechanisms might be
involved (reentry within several millimeters, automaticity, and triggered
activity). RP intervals are typically long (longer than PR intervals), but this
depends on the rate of tachycardia
and properties of AV conduction. The PR interval can be prolonged by the use of
vagal maneuvers and adenosine (Panel C), which may also produce a transient AV
block. A substantial proportion of focal atrial tachycardias are terminated with the use of adenosine. Atrial
flutter with 2:1 AV conduction (Panels A and B) may resemble atrial tachycardia or another type of supraventricular tachycardia and can be revealed when
vagal maneuvers or adenosine is used (Panel C).
Supraventricular tachycardias
are not usually associated with structural heart disease, although
there are exceptions (e.g., the presence of accessory pathways
associated with hypertrophic cardiomyopathy or Ebstein's anomaly and
atrial tachycardias
in patients with congenital or acquired heart disease). Reentry arrhythmias
are usually induced by premature atrial or ventricular ectopic
beats, and precipitating factors — such as excessive intake of
caffeine, alcohol, or recreational drugs and hyperthyroidism — can
increase the risk of recurrence.
Strategies and Evidence
General Evaluation of Patients
While considering the patient's
history, the clinician should assess the duration and frequency of
episodes, the mode of onset, and possible triggers (including the
intake of alcohol and caffeine or other drugs) as well as previous
cardiac or other disease. These features are useful in
distinguishing supraventricular tachycardia
from other tachyarrhythmias (Table 1).
Supraventricular
tachycardias
have a sudden onset and termination, in contrast to sinus tachycardias,
which accelerate and decelerate gradually; however, some patients do
not perceive the sudden onset of supraventricular tachycardia.
It may be misdiagnosed as panic disorder.6
Physical
examination during episodes may reveal the "frog sign" —
prominent jugular venous A waves due to atrial contraction against
the closed tricuspid valve.7 When sinus
rhythm is restored, physical examination is usually normal, but a
careful examination is warranted to rule out evidence of structural
heart disease.
The
usual presentation of supraventricular tachycardia
on electrocardiography (ECG) is as a narrow-QRS-complex tachycardia
(a QRS interval of less than 120 msec), but in some cases (less than
10 percent), wide-complex tachycardia is the
manifestation of supraventricular tachycardia.
After the restoration of sinus rhythm, the 12-lead ECG should be
examined for the presence of delta waves, which indicate an
accessory pathway (Figure 2C). However,
evidence of preexcitation may be minimal or absent if the accessory
pathway (e.g., a left lateral accessory pathway) is located far from
the sinus node or if, as occurs in approximately 30 percent of
patients, the accessory pathways are "concealed" (i.e., they support
exclusively retrograde conduction from the ventricle to the atrium
and do not cause preexcitation of the ventricle during sinus
rhythm). In ambulatory patients with frequent episodes (two or more
per month) of supraventricular tachycardia,
ECG recordings or event recorders (which record arrhythmias for
up to seven days) may be useful to document arrhythmias.
An
echocardiogram should be considered to rule out structural heart
disease, even though it is uncommon. Because electrolyte abnormalities
and hyperthyroidism may contribute to supraventricular tachycardia,
it is reasonable to check potassium and serum thyrotropin levels;
however, the tests for these values appear to have a low yield.
Electrophysiological
testing allows for identification of the mechanism of arrhythma, but
this procedure is generally performed only if catheter ablation is
considered. Table 2 summarizes
conditions for which this testing is generally recommended.
Treatment
Short-Term Therapy
Figure 3 shows an
algorithm for the management of acute supraventricular tachycardia.
In rare cases, episodes of arrhythmia are so poorly tolerated that
they require immediate electrical cardioversion. Most supraventricular
tachycardias
depend on the atrioventricular node for maintenance of the reentry
circuit and can be interrupted by vagal maneuvers or pharmacologic
agents that slow conduction through the atrioventricular node.
Figure 3. Algorithm for the Short-Term
Management of Supraventricular Tachycardia (SVT).
If the diagnosis of SVT with
aberration or SVT with preexcitation is not certain, tachycardia
with a wide QRS complex must be considered as an unknown mechanism and treated
as such. SVT with preexcitation can be the result of either antidromic
atrioventricular reentry or, uncommonly, another type of SVT (e.g., atrial tachycardia)
with an accessory pathway that is not critical for the maintenance of the
arrhythmia. BBB denotes bundle-branch block, VT ventricular tachycardia,
IV intravenous, and ECG electrocardiogram. Adapted from Blomstrom-Lundqvist et
al.8
Vagal Maneuvers
Massage of the carotid sinus
stimulates baroreceptors, which trigger a reflexive increase in the
activity of the vagal nerve and sympathetic withdrawal, slowing
conduction through the atrioventricular node. If the physical
examination does not reveal a carotid bruit and there is no history
suggesting carotid artery disease, pressure may be applied at the
level of the cricoid cartilage for about five seconds with a firm
circular movement. If the tachyarrhythmia persists, the procedure
may be repeated on the opposite side. Other approaches to increasing
vagal tone include having the patient perform a Valsalva maneuver or
(primarily in children) apply an ice pack to the face.
A continuous
12-lead ECG recording of the episode should be obtained during vagal
maneuvers, since the way in which arrhythmias end may provide clues
to their mechanism (Figure 2).9
Adenosine
As with vagal maneuvers, treatment
with intravenous adenosine has both diagnostic and therapeutic
value. Data from randomized trials show that supraventricular
tachycardia
is terminated in 60 to 80 percent of patients treated with 6 mg of
adenosine and in 90 to 95 percent of those treated with 12 mg.10 In patients
with atrial tachycardias, adenosine causes a transient
atrioventricular nodal block or interrupts the tachycardia
(Table 3 and Figure 2).10,11,12 ECG
monitoring is required during the administration of adenosine, and
resuscitation equipment should be available in the event that the
rare complications of bronchospasm or ventricular fibrillation occur.
Adenosine is contraindicated in heart-transplant recipients and
should be used cautiously in patients with severe obstructive lung
disease. Adenosine is also contraindicated in patients with tachycardia
with a wide QRS complex (unless the diagnosis of supraventricular
tachycardia
with aberrancy is certain).
Other Agents
If supraventricular tachycardia
is refractory to adenosine or rapidly recurs, clinical experience
indicates that the tachycardia can usually be terminated by the
administration of intravenous verapamil or a beta-blocker.11,13,14 As a next
step, procainamide, ibutilide, propafenone, or flecainide can be
given intravenously if the patient's blood pressure is stable.15 However,
sequential trials with different antiarrhythmic agents should be
undertaken only after careful consideration of their possible
negative hypotensive, bradycardic, and proarrhythmic effects. At any
point, electrical cardioversion is an alternative, but this technique
is generally considered in patients in hemodynamically stable
condition only if atrioventricular nodal-blocking agents fail. Table 3 reviews
medications used for acute supraventricular tachycardia.
These agents are contraindicated in patients with severe
hypotension, a history of heart block, or congestive heart failure.
Atrial
fibrillation with rapid ventricular conduction can occur spontaneously
in patients with the Wolff–Parkinson–White syndrome or during
treatment for supraventricular tachycardia. Emergency-resuscitation
equipment should be available, since the arrhythmia can degenerate
into ventricular fibrillation if the accessory pathway has a short
refractory period (250 msec or less).16 Treatment
with an electrical shock is a safe option. If the patient's
condition is hemodynamically stable, procainamide, ibutilide,
propafenone, or flecainide may be used; all have a rapid onset of
action, lengthen antegrade refractoriness of the accessory pathway,
and terminate atrial fibrillation in the majority of cases.15
Wide-QRS-Complex Supraventricular
Tachycardia
Supraventricular tachycardia
presents infrequently as a wide-complex tachycardia,
in which there is an associated bundle-branch block or conduction
over an accessory pathway. Wide-QRS-complex, regular tachycardia
should routinely be treated as ventricular tachycardia, unless
the diagnosis of supraventricular tachycardia with aberrancy or
of supraventricular
tachycardia
with preexcitation is certain. Adenosine and other
atrioventricular-nodal–blocking agents are ineffective and
potentially deleterious in patients with ventricular tachycardia.
Long-Term Management
The risk of recurrence after a single
episode of supraventricular
tachycardia
is not well defined, and a single episode is not an indication for
long-term therapy. For patients with recurrent episodes, options for
long-term treatment include medication and ablation therapy.
However, not all patients with recurrent supraventricular
tachycardia
need treatment. The severity of the symptoms and patient preferences
should be considered in decision making. Referral to an
electrophysiologist is warranted for the conditions listed in Table 2 and should
be considered in other cases to assist in decisions regarding
therapy.17,18
Figure 4 shows a
decision algorithm for the long-term care of patients with supraventricular
tachycardia.
In cases in which the precise mechanism of tachycardia
is uncertain, management is based on the presence or absence of
preexcitation on the baseline ECG (Table 3 and Figure 4).
The pharmacologic management of
atrial tachycardias has not been well evaluated in
controlled trials. Depending on the mechanism causing the
arrhythmia, beta-blockers, calcium-channel blockers, and class I or
class III antiarrhythmic drugs may reduce or eliminate symptoms.
"Pill-in-the-Pocket" Approach
For patients with infrequent (i.e.,
no more than a few per year) but prolonged (i.e., lasting more than
one to two hours) episodes of supraventricular tachycardia
that are well tolerated hemodynamically, or for patients who have
had only a single episode of supraventricular tachycardia,
another option is to prescribe single-dose pharmacologic therapy
(the "pill in the pocket") to be taken when needed for an
arrhythmic event. Drugs administered in this fashion include calcium-channel
blockers (e.g., 40 to 160 mg of verapamil), exclusively for patients
without preexcitation; various beta-blockers; flecainide (100 to 300
mg); and propafenone (150 to 450 mg). In one study, 80 percent of
episodes of supraventricular tachycardia
were interrupted within two hours with a combination of diltiazem and
propanolol or with flecainide.23
Supraventricular Tachycardia
with the Wolff–Parkinson–White Syndrome
Verapamil and
digoxin are contraindicated in patients with the Wolff–Parkinson–White
syndrome, unless the accessory pathway has been shown to have a long
refractory period (300 msec or more), because these drugs may
increase the risk of rapid ventricular response, causing ventricular
fibrillation in patients with atrial fibrillation.24,25 Although
catheter ablation is considered the treatment of choice for these
patients, both flecainide and propafenone are effective and have
been approved by the Food and Drug Administration for the prevention
of paroxysmal supraventricular tachycardias
mediated by an accessory pathway (with or without antegrade
conduction).26,27,28
Catheter Ablation
Since the early 1990s, catheter
ablation (Figure 5) has
increasingly been used in the management of supraventricular
tachycardia on the basis of its observed efficacy
and overall safety when performed at centers with experienced
clinicians. Observational studies of catheter ablation of tachycardia
mediated by an accessory pathway indicate that success rates exceed
95 percent and recurrence rates are less than 5 percent during the
first few months after the procedure is performed. Late recurrences
are the exception.29,30,31 In
cases in which the accessory pathway is close to a His bundle, the
application of radiofrequency current can be complicated by
atrioventricular block that requires pacemaker therapy. Data from
observational studies suggest that in this situation, the use of
cryothermal ablation is similarly effective and reduces the
potential for atrioventricular block, although studies directly comparing
these approaches are lacking.32 Other
complications associated with accessory-pathway ablation, occurring
in less than 2 to 3 percent of patients, include damage to an
artery, bleeding, arteriovenous fistula, venous thrombosis,
pulmonary embolism, myocardial perforation, valvular damage,
systemic embolism (in the case of a left-sided accessory pathway),
and rarely, death.33,34
Figure 5. Catheter Ablation of Cardiac
Arrhythmias.
One to four catheter electrodes are introduced into
the cavities of the heart through femoral (or, alternatively, internal jugular
or subclavian) venous access after local anesthesia is administered.
Radiofrequency current — a low-voltage, high-frequency (500 kHz) form of
electrical energy used for electrocautery in surgery — is delivered through a
catheter electrode to create small lesions through thermal injury in the
myocardial tissue, the conduction system, or both, which have been identified
as critical for mediating the cardiac arrhythmia. In patients with arrhythmias
mediated by an abnormal accessory pathway, the catheter is positioned so that
it is in contact with the pathway, and the application of radiofrequency
current blocks conduction over the accessory pathway within a few seconds. For
left-sided accessory pathways, a retrograde approach through the femoral artery
and the aortic valve can be used. Alternatively, a transseptal puncture can be
performed to gain access to the left atrium. Cryothermal ablation is an
effective approach in patients with atrioventricular (AV) nodal reentrant tachycardia or an accessory pathway
close to a His bundle because of the reversibility of the initial effect and
the negligible risk of AV block. Most ablation procedures take one to three
hours. Catheter ablation of supraventricular
tachycardia can be performed as
a one-day outpatient procedure, or it may require overnight hospitalization.
Treatment with aspirin is often recommended for several weeks after ablation
that has been performed in the left side of the heart to reduce the potential
risk of emboli. Patients need no special follow-up after the intervention.
In patients with atrioventricular
nodal reentrant tachycardia, the atrioventricular nodal slow
pathway is targeted by catheter ablation in the posteroseptal region
of the tricuspid annulus.35 Success
rates are higher than 95 percent.34,36 Serious
complications are uncommon but include pulmonary embolism (in up to
0.2 percent of patients) and the development of atrioventricular
block requiring pacemaker therapy (in up to 1 percent of patients).33,34
Tachycardia
recurs in 3 to 7 percent of patients.36
Catheter ablation of focal atrial tachycardias
has slightly lower success rates (about 85 percent) and higher
recurrence rates (about 8 percent).36,37 Procedural
risks are slightly increased for the treatment of left atrial tachycardia,
which requires a transseptal puncture. For reentrant atrial tachycardias,
radiofrequency ablation has high success rates and is often used
as first-line therapy.37,38,39
Areas of Uncertainty
Limited data suggest that, as
compared with antiarrhythmic therapy, catheter ablation improves the
quality of life and is more cost effective in the long term.40,41 However,
there is a lack of large randomized trials with prolonged follow-up
to guide the choice between radiofrequency ablation and medical
therapy.
The appropriate treatment strategy
for patients with asymptomatic preexcitation syndromes is
controversial.42,43,44 The
incidence of sudden death due to rapid conduction of atrial
fibrillation that leads to ventricular fibrillation is estimated at
between 0.15 and 0.45 percent per patient-year.45,46,47 Attempts to
stratify the risk according to the use of noninvasive methods or
invasive measurements of the refractory period of the accessory pathway
have been advocated but may be misleading.17,44,48 A task
force of the American College of Cardiology, the American Heart
Association, and the European Society of Cardiology concluded that
the positive predictive value of invasive electrophysiologic testing
is too low to justify its routine use in asymptomatic patients and
that the decision to ablate accessory pathways in persons with
high-risk occupations or those who engage in high-risk recreational
activities should be made on an individual basis.8
Guidelines
Comprehensive guidelines for the
management of supraventricular tachycardia
were published by an expert committee of the American College of
Cardiology, the American Heart Association, and the European Society
of Cardiology.8 Doses of
antiarrhythmic drugs and their adverse effects are discussed in
these societies' guidelines for the management of patients with
atrial fibrillation.49 The
recommendations in this review are in general agreement with these
guidelines. Generally, radiofrequency ablation is recommended as
primary therapy for patients in whom the preexcitation syndrome or
hemodynamic instability occurs during their arrhythmias. In other
cases, patient preference is an important consideration in the
selection of therapy.
Conclusions and Recommendations
For a patient such as the one
described in the vignette, I would first try carotid sinus pressure
or other vagal maneuvers, followed by intravenous adenosine if the
maneuvers are ineffective.
For patients in whom supraventricular
tachycardia
recurs, preventive therapy is generally warranted if there are
frequent, prolonged, or highly symptomatic episodes that cannot
easily be terminated by the patient's use of vagal maneuvers. If the
tachycardia
is associated with preexcitation or syncope, electrophysiological evaluation
is warranted. In the absence of preexcitation or syncope,
atrioventricular-node–blocking agents are usually recommended as
first-line treatment, even though there is a lack of data from large
trials to compare these drugs with other approaches to management.
However, many patients may have adverse effects or find it
inconvenient to take medication over the long term. For patients in
whom recurrences are infrequent but prolonged, pill-in-the-pocket
treatment (e.g., 100 to 200 mg of flecainide) at the onset of supraventricular
tachycardia
is a reasonable approach. Catheter ablation, when performed at
a center with experienced clinicians, is appropriate for supraventricular
tachycardia
associated with preexcitation or hemodynamic instability or if
antiarrhythmic drugs are not effective or are poorly tolerated.
Catheter ablation may also be used as primary therapy in other cases
if the patients, informed of the risks and benefits, prefer this
approach.
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Approach to wide complex tachycardias
The correct diagnosis of a wide complex tachycardia (WCT)—QRS duration >
120 ms—remains a challenge despite numerous established criteria for
the differentiation of ventricular from supraventricular tachycardia
(SVT) with aberrant conduction. Making the correct diagnosis is
important for the acute as well as long term management of patients
with WCT. The objective of the present review is to discuss the
major causes as well as clinical and electrophysiologic criteria of
WCT in patients without structural heart disease.
Table 1
Causes of wide complex tachycardias (WCTs) in patients without structural
heart disease
|
Broad categories of WCTs include ventricular tachycardia (VT), SVT
with abnormal intraventricular conduction, and ventricular paced
rhythms. A lack of underlying structural heart disease does neither exclude
a VT nor imply a benign prognosis. However, if a patient has had
similar episodes during previous years, SVT is more likely than VT.
Termination of a tachycardia by the Valsalva manoeuvre or adenosine
injection also suggests a supraventricular origin, although some VT
can also be terminated by these manoeuvres (for example, fascicular
VT).
A WCT in a patient who is alert and
haemodynamically stable is not necessarily of supraventricular
origin. The clinical presentation depends on the haemodynamic consequences
it produces. These depend partly on tachycardia rate, the degree of
myocardial dysfunction, the circumstances and suddenness of
initiation, and autonomic factors. Physical examination in a patient
presenting with WCT may indicate haemodynamic distress (low blood
pressure, heart failure or cardiogenic shock). When cardiac output
and blood pressure are maintained and/or when the tachycardia is
short lived, the arrhythmia may present as palpitations, breathlessness
or just discomfort.
WIDE COMPLEX SUPRAVENTRICULAR TACHYCARDIAS
Intraventricular conduction delay can
result from heart rate changes, as well as from fixed pathological
lesions in the conduction system. In patients with pre-existing or
"fixed" (present during the normal baseline rhythm) bundle
branch block (BBB), any SVT results in a broad complex tachycardia. However, rate
related and/or "functional" (present only during
tachycardia) BBB may also result in WCT. Functional aberration
results from sudden increases in cycle length when parts of the
His-Purkinje system are partially or wholly inexcitable. Functional
right bundle branch block (RBBB) occurs more frequently than
functional left bundle branch block (LBBB) because of the longer
refractoriness of the former.1
Sometimes, discrete variations in cycle length change a broad to a
narrow complex
tachycardia and thereby facilitate the correct diagnosis (fig 1
). A sudden
short long cycle length variation lengthens the refractoriness of
the His-Purkinje system and an abrupt long-to-short cycle length
change shortens the refractoriness of the His-Purkinje system
refractoriness.2
Functional BBB may persist for several successive impulses because
the bundle branch that is blocked antegradely may be activated
transseptally via its contralateral counterpart, a process known as
linking phenomenon.3
As the duration of the refractory period is a function of the
immediately preceding cycle length (the longer this cycle length,
the longer the subsequent refractory period), abrupt cycle length
variations (that is, long-to-short or short-to-long) predispose to
the occurrence of functional BBB—for example, in atrial
fibrillation, which is known as Ashman phenomenon4
ELECTROCARDIOGRAPHIC
CLUES IN DIFFERENTIAL DIAGNOSIS: SVT VERSUS VT
QRS criteria
for differential diagnosis in broad complex
tachycardia: ventricular tachycardia (VT) versus supraventricular tachycardia
(SVT) with left (LBBB) or right (RBBB) bundle branch block.
In
general, if an ECG showing a WCT does not look like aberration, it
is most likely a VT If there is any doubt about the origin of a WCT,
the patient should be treated as if the rhythm was VT. The absence
of an RS complex in
any precordial lead or an interval of the R wave onset to the S wave
nadir of more than 100 ms strongly suggest a VT.6
In addition, the following ECG criteria have been suggested to
distinguish between VT and SVT with aberration
- QRS complex
duration—VT is the probable diagnosis when the
QRS duration with RBBB is greater than 140 ms, and greater than
160 ms with LBBB morphology.7
- QRS axis—A frontal axis
between –90° to ±180° cannot be achieved by any
combination of bundle branch block and therefore suggests VT.
Thus, predominantly negative QRS complexes in leads I, II, and
III are a useful criterion for identifying a VT.
- Concordant negative ECG patterns in the precordial leads—If all precordial leads are predominantly
negative, a VT is the likely diagnosis. If all
precordial leads are predominantly positive, the differential
diagnosis is an antidromic tachycardia using a left sided
accessory pathway or a VT.
- QRS morphologies in V1 and V6—In an
RBBB pattern, a monophasic R wave, a broad (> 30 ms)
R, or a qR in V1 strongly suggest VT. A monophasic R
wave, or an S greater than an R in V6, also suggest
VT. In the presence of an LBBB pattern, a broad R wave (usually
greater than 30 ms) and/or a slow descent to the S wave
nadir in V1 and a Q in V6 point towards a VT.
Atrioventricular dissociation
This is one of the most useful criteria for distinguishing VT from
SVT. It occurs in 20–50% of VT and almost never in SVT.
Atrioventricular dissociation may be diagnosed by a changeable pulse
pressure, irregular canon A waves in the jugular veins and a
variable first heart sound. It often demands long 12 lead ECG
recordings and careful ECG analysis. In addition, about 30% of VTs
have 1:1 retrograde conduction. In the presence of AV dissociation,
one may also observe fusion beats which may result from the fusion
of a P wave conducted to the ventricles.
The 12 lead ECG during VT can be
helpful in providing an approximation of the site of origin. In
general, VT that have an LBBB-like morphology in V1 have an exit in
the right ventricle or the interventricular septum. A QRS axis that
is directed superiorly generally indicates an exit in the inferior
wall; an axis directed inferiorly indicates an exit in the anterior
(superior) wall. In V2 to V4, dominant R waves usually indicate an
exit near the base of the ventricle. In idiopathic right ventricular
outflow tract tachycardia (RVOT-VT), the QRS duration during VT is
usually > 140 ms if it originates from the free wall of the RVOT,
and < 140 ms if the arrhythmia originates from the septal site
of the RVOT. Furthermore, the precordial R wave transition in
RVOT-VT usually occurs in leads V2 through V4 and becomes earlier as
the site of origin advances more superiorly along the septum. An R
wave transition in lead V2 suggests a site of origin immediately
inferior to the pulmonic valve or the left ventricular outflow
tract.
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Heart Blocks
Atrioventricular Heart Blocks
1st
degree
PR interval > 0.2 seconds (1
large box), each P is followed by a QRS. PR interval is measured from the
beginning of the P wave to the beginning of the QRS.
Figure: The PR interval is approximately 0.28 seconds.
Definition: 1AVB is a rhythm in which the electrical impulse which leaves the SA
node and travels through the atria, AV node, Bundle of His to purkininjie
fibers is slowed down and takes longer than normal to arrive at its
destination. The normal PR interval is 0.12- 0.20 seconds. A 1AVBT is greater
than 0.20 seconds. The cause ranges from coronary heart disease, inferior wall
MI's, hyperkalemia, congenital abnormalities, and medications such as quinidine, digitalis, beta blockers, and calcium channel blockers.
Rate: The atrial rate or P waves can vary
to any rate. The ventricular rate can also vary. There must be a 1:1 conduction
of the P waves to the QRS waves. Rhythm: Atrial and ventricular rates are
usually regular, but they may also be irregular. P Wave: Usually normally
shaped and occurring with a 1:1 ration with the QRS. PR interval: greater
than0.20 seconds. QRS Complex: Within normal limits or may have a bundle branch
block. ST Segment: Within normal limits for the intrinsic rhythm. T Wave:
Within normal size and configuration.
2nd
degree block - type 1
Also called
"Wenkebach". PR interval gets progressively longer each beat until
finally a QRS is "dropped" (missing).
Figure: Note the increasing PR interval before the QRS is dropped,
then the cycle is repeated.
2nd
degree block - type 2
Also called "Mobitz
II". Look out! A more serious conduction problem than Type 1. PR intervals
are constant and a QRS is "dropped" intermittently.
Figure: Note the dropped QRS after the second and sixth P wave in lead
II (the rhythm strip).
3rd
degree block
The atrial rate is independent
of the ventricular rate (P wave and QRS march out separately. The clue here is
no relationship at all of the P-R intervals). The P-R interval is constantly
changing, the QRS is usually wide and bizarre because it is ventricular origin.
Figure: Note the P waves and QRS waves are independent of each other.
Definition: Second degree AV block is also known as Second Degree Type I, Mobitz
I, or Wenckelbach. This arrhythmia is characterized by a progressive delay
of the conduction at the AV node, until the conduction is completely blocked.
This occurs because the impulse arrives during the absolute refractory period,
resulting in an absence of conduction, and no QRS. The next P wave occurs and
the cycle begins again. Possible causes are acute inferior wall myocardial
infraction, digitalis, beta blockers, calcium channel blockers, rheumatic
fever, myocarditis, or excessive vagal tone.
Rate is ususaly 60-100 beats per
minute. Atrial rhythm is regular. Ventricular rhythm is irregular. P Wave
configuration is normal. PR interval gets longer with each beat until QRS
complex is dropped. QRS complex is normal, but is dropped periodically. ST
Segment and T Wave are normal in configuration.
Mobitz
II is
characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave
will be constant for each QRS. It is usually associated with acute anterior or
anteroseptal myocardial infarction. Other causes are cardiomyopathy, rheumatic
heart disease, coronary artery disease, digitalis, beta blockers, and calcium
channel blockers. Mobitz II has the potential of progressing into a third degree heart block or ventricular standstill
Ventricular
rate will depend on the number of impulses conducted through the AV node, and will
be less than the atrial rate. Rhythm: Atrial and ventricular rate is irregular.
P Wave: Present in two, three or four to one conduction with the QRS. PR
Interval: Constant for each P wave proir to the QRS. QRS: May be within normal
limits for the intrinsic rhythm. ST Segment:
A
third degree atrial ventricular
block is also know as a complete heart block artrioventricular block of 3degree
AV block. It is a problem with electrical conduction. All electrical conduction
from the atria are blocked at the AV junction, therefore, the atria and the
ventricles beat independently from each other. This arrhythmia is dangerous
because it significantly decreases cardiac output, and could lead to asystole.
Possible causes: acute inferior and anterior myocardic infraction, coronary
heart disease, excessive vagal tone, myocarditis, endocarditis, age, edema from
heart surgery, and meditation toxicity from digitalis, beta blockers, calcium
channel blockers
Atrial
rate faster than ventricular rate. Rhythm: Regular, but there is normal
configuration. PR Interval: There is no relationship between P waves and QRS
complexes. QRS Complex: Variates depending on the intrinsic rhythm. ST Segment
and T Wave:
Intervals
Longitudinal Heart Blocks
An interval is a portion of the
baseline and at least one wave. We measure an interval on the horizontal axis
in seconds. The PR, QRS, and QT are the intervals which should be routinely
scanned on each ECG. For measuring intervals, look at the widest form in any
lead.
Figure: Intervals.
4. PR
interval (beginning of P wave to the beginning of the next QRS). Normally, <
.2 seconds or one large box. If it is > .2 seconds, it is a first degree
block. (Note: this concept was introduced under blocks).
Figure: Note the prolonged PR interval (.28 seconds), especially at
the second beat.
5.
QRS interval (beginning of Q to the
end of the S wave) should be < .12 seconds (< 3 small boxes). If QRS
is > .12, check for bundle branch block.
The
QRS complex represents the amount of time required to depolarize the
ventricles. A normal QRS is 0.08-0.12 seconds in length. A length greater than
0.12 seconds is considered a BBB. This means that there may be a block in one
of the bundle branches, or the electrical impulse was conducted through an
abnormal conduction pathway. This can occur in any rhythm. The causes range
from normal to pericarditis, myocarditis, congested heart failure and
congenital heart disease.
Rate: Atrial and ventricular rate can vary depending
on the specific rhythm involved. Any rhythm can have BBB. The P Wave depends on
the intrinsic rhythm involved. The QRS is the determining factor and it must be
greater than 0.12 seconds.
A QRS >
.12 and RR (2 peaks or R waves in QRS) occurring in the right chest leads
(V1-V2) indicates a right bundle branch block.
Figure: RBBB.
If QRS is
> .12 and RR occurs in the left chest leads (V5-V6), this indicates a left
bundle branch block.
Figure: LBBB.
6. QT
interval (beginning of QRS to end of T wave) should be less than half of the
preceding RR interval - this varies with the rate. For normal rates, QT < .4
seconds (2 large boxes). "QT prolongation" (too long) can lead to a
refractory form of ventricular tachycardia called torsades de pointes.
Figure: The QT interval is greater than half the preceding RR
interval. Look at lead I.
|
Rhythm Guidelines |
|
1. Check
the bottom of the rhythm strip for regularity, i.e. - is it completely
regular, mostly regular with a few extra beats, or totally irregular? |
|
2. Check for
a P wave before each QRS, QRS after each P. |
|
3. Check RR
interval (for AV blocks) and QRS interval (for bundle branch blocks). Check for prolonged QT. |
|
4. Continue
to recognize "patterns" such as atrial fibrillation, PVCs, PACs,
escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV
blocks and bundle branch blocks. |
Fasicular
Blocks
Fasicular blocks are blocks of part
of the left bundle, either the posterior or anterior division:
Figure: Divisions of the bundles.
Anterior fasicular block - the most common.
You will see left axis deviation (-30
to -90) and a small Q wave in lead I and an S in lead III (Q1S3). The QRS will
be slightly prolonged (0.1 - 0.12 sec).
Figure: Anterior fasicular block.
Posterior fasicular block - less common.
You will see right axis deviation, an
S in lead I and an Q in lead III (S1Q3). The QRS will be slightly prolonged
(0.1 - 0.12 sec).
Figure: Posterior fasicular block.
Bifasicular block.
This means two (2) of the three (3)
fascicles (in diagram) are blocked. The most important example is a right bundle
branch block and a left anterior fascicular block. Watch out for this. Only one
fascicle is left for conduction, and if that fasicle is intermittently blocked,
the dangerous Mobitz 2 is set up!
Figure: Right bundle branch block and left anterior fascicular block.
"Fasicular Blocks" may seem
a bit complicated - simply remember that axis deviation is the clue.
In your differential, consider posterior fasicular blocks with right axis
deviation and consider anterior fasicular blocks with left axis deviation.
Fascicular blocks cause axis deviations, like infarcts and hypertrophy. If you
see a left or right axis deviation, first look for infarct or hypertrophy. If
neither are present, the remaining diagnosis of fasicular block is usually
correct. Review differential diagnosis of right and left axis deviation.
MANAGEMENT OF
SYMPTOMATIC BRADYCARDIA
CARDIAC PACING
Permanent cardiac pacing remains the only effective treatment
for chronic, symptomatic bradycardia. In recent years, the role of implantable
pacing devices has expanded substantially. At the beginning of the 21st
century, exciting developments in technology seem to happen at an exponential
rate. Major advances have extended the use of pacing beyond the arrhythmia
horizon. Such developments include dual-chamber pacers, rate-response
algorithms, improved functionality of implantable cardioverter defibrillators,
combinations of sensors for optimum physiological response, and advances in
lead placement and extraction. Cardiac pacing is poised to help millions of
patients worldwide to live better electrically. We review pacing studies of
sick-sinus syndrome, neurocardiogenic syncope, hypertrophic obstructive cardiomyopathy,
and cardiac resynchronisation therapy, which are common or controversial
indications for cardiac pacing. We also look at the benefits and complications
of implantation in specific arrhythmias, suitability of different pacing modes,
and the role of permanent pacing in the management of patients with heart
failure.
Introduction
Permanent cardiac pacing is one of
the most important medical innovations of the 20th century.
Although originally designed for management of Stokes-Adams attacks (in patients
with complete heart block), sick-sinus syndrome is now the most common
indication for permanent pacemaker implantation. In the
Recent technical advances in cardiac pacing have
included dual-chamber devices, rate-response algorithms, and progressive
refinement of antibradycardia-pacing function in implantable cardioverter
defibrillators (ICDs). Indications have expanded beyond symptomatic
bradycardia, and now include neurocardiogenic syncope, hypertrophic obstructive
cardiomyopathy, and cardiac resynchronisation therapy (CRT, biventricular
pacing) for congestive heart failure. The role of atrial pacing in the
prevention of atrial fibrillation is being explored.
Pacing modes
The generic pacemaker code of the
North American Society of Pacing and Electrophysiology and the British Pacing
and Electrophysiology Group is used to describe various pacing modes. The first
letter denotes the chamber or chambers that are paced (A=atrial, V=ventricular,
D=dual [atrial and ventricular]). The second letter describes which chambers
detect (sense) electrical signals. The third letter represents the response to
sensed events (I=inhibition, T=triggering, D=dual [inhibition and triggering]).
A fourth letter, R, denotes activation of rate-response features. The most
commonly used pacing modes are: AAI(R) single-chamber atrial pacing without (or
with) rate response, VVI(R) single-chamber ventricular pacing without (or with)
rate response, and DDD(R) dual-chamber pacing without (or with) rate response.
In the latest version of the code, a fifth position
denotes the chamber or chambers in which multisite pacing is delivered.
Single-chamber right atrial pacing might be adequate
for patients with sinus-node dysfunction and intact atrioventricular
conduction. The disadvantage of this pacing modality is that atrioventricular
block develops in 0·6–5·0% of patients with sick-sinus syndrome every year.
Atrial pacing would be inadequate for this type of acquired (natural or
ablation-induced) atrioventricular block. To upgrade to a dual-chamber pacing
system is often more complicated (venous thrombosis/fibrosis, pocket fibrosis)
and might entail more morbidity than a de novo dual-chamber implant. In
patients with sinus-node dysfunction, the presence of bundle-branch block at
implantation is a better predictor of subsequent atrioventricular block than
the atrial rate (Wenckebach cycle length), where Mobitz type I atrioventricular
block occurs.
Single-chamber right ventricular pacing can be
associated with symptoms of pacemaker syndrome. During VVI pacing, this
syndrome is most common in patients with normal (or near normal) left
ventricular function and intact retrograde ventriculoatrial conduction.
Dual-chamber pacemakers that are programmed correctly
assure maintenance of atrioventricular synchrony. Based on pacemaker
programming and the intrinsic rhythm, patients with dual-chamber devices can
show complete inhibition, atrial pacing with intact atrioventricular
conduction, ventricular tracking of a sensed atrial rhythm (P-synchronous
ventricular pacing), or atrioventricular sequential pacing (figure 1).
Figure 1. ECG patterns of
dual-chamber devices
(A) Complete inhibition (sinus rhythm is present
with intact atrioventricular conduction). (B) Atrial pacing with intact
atrioventricular conduction. (C) Ventricular tracking of a sensed atrial rhythm
(P-synchronous ventricular pacing). (D) Atrioventricular sequential pacing. (E)
Single-chamber right ventricular pacing. Arrows point to smaller deflections
occurring at a slower rate, which might represent P waves or baseline artifact.
AS=sensed intrinsic atrial rhythm. VS=sensed intrinsic ventricular rhythm.
AP=paced atrial rhythm. VP=paced ventricular rhythm.
Loss of
atrioventricular synchrony might reduce resting cardiac output by
20–30%.Retrograde ventriculoatrial conduction might also cause a negative
atrial kick, and could result in atrial distention and an autonomically
mediated vasodepressor response. Atrial contraction against closed
atrioventricular valves results in systemic and pulmonary venous regurgitation
and congestion, which might precipitate heart failure.
Symptoms of
pacemaker syndrome include headache, disturbed mentation, neck pulsations,
dyspnoea, chest discomfort, heightened cardiac awareness (transition from
spontaneous to paced beats), fatigue, lethargy, exercise intolerance, and
postural hypotension (lightheadedness, near-syncope, syncope).
Dual-chamber
pacing is traditionally accomplished by lead placement in the right atrial
appendage and right ventricular apex. Development of active fixation technology
has allowed lead placement at various sites within the right heart chambers.
Pacing in the right atrial septum seems to be antiarrhythmic. Haemodynamics can
be improved by pacing in the right ventricular outflow tract; however, in short-term randomised studies, clinical
benefits from outflow tract versus apical pacing have not been shown.
In VDD
pacing, the atrium is sensed but not paced, which is useful for patients with
atrioventricular block and intact sinus nodal function. The main advantage of
VDD pacing is atrioventricular synchrony with a single lead (incorporation of
tip electrodes for ventricular sensing and pacing plus floating atrial
electrodes for P wave sensing). However, there has been concern that long-term
stability of atrial sensing is not as reliable as in DDD systems and about VDD
function under real-life conditions (atrial sensing might be variable). During
atrial undersensing, a VDD system functions as a VVI system. Several recent
studies suggest these concerns are not completely justified.
Investigators have shown maintenance of atrioventricular
synchrony during exercise. Another series of 13 children and 24 adults followed
up for a mean of 3·5 years showed atrial electrogram stability and effective
atrial sensing. Present technology does not allow
reliable atrial pacing via floating electrodes. This accomplishment could
become feasible in the future.
Clinical benefits of physiological
(AAI or dual-chamber) pacing
Despite the apparent advantages of physiological
pacing, recommendations that favoured dual-chamber over single-chamber
ventricular pacing in patients with sick-sinus syndrome or atrioventricular
block were mainly based on observational data and expert opinion, until
recently. A retrospective study of patients with sick-sinus syndrome showed
that development of chronic atrial fibrillation and stroke was strongly
determined by clinical variables and secondarily by ventricular pacing
modality.18 In some instances, atrial fibrillation might be
promoted by ventricular pacing. Data from the same patient population revealed
inconclusive mortality results, and showed that ventricular pacing did not
increase the frequency of progressive or new onset heart failure compared with
physiological pacing.
Andersen and associates published
the first randomised study comparing pacemaker modes in patients with
sick-sinus syndrome. By contrast with the studies noted earlier, patients
assigned to atrial pacing had lower rates of atrial fibrillation, heart
failure, thromboembolic events, and cardiovascular and total mortality than did
ventricularly-paced patients. In the Pacemaker Selection in the Elderly (PASE)
study, very little benefit in quality of life from dual-chamber pacing was
shown in elderly patients. However, patients with sick-sinus syndrome (but not
atrioventricular block) had improvement in quality of life and higher
functional status with dual-chamber pacing. Ellenbogen and colleagues reviewed several variables at pacemaker implantation in
patients from the PASE trial who were randomly assigned
to the VVIR mode. Significant decreases in systolic blood pressure during
ventricular pacing at implantation, β-blocker use
at the time of randomisation, and non-ischaemic cardiomyopathy were the only
variables that predicted crossover to DDDR pacing in the Cox multivariate
regression model.
In the Canadian Trial of Physiologic Pacing (CTOPP),
physiological pacing (AAI or DDD) provided little benefit over ventricular
pacing in prevention of stroke or cardiovascular death.
Further analysis of this large study showed that physiological pacing
significantly reduced the frequency of chronic atrial fibrillation. Patients assigned to physiological pacing had a 27%
relative risk reduction for development of chronic atrial fibrillation compared
with those assigned to ventricular pacing. The yearly
event rate for cardiovascular death or stroke rose steadily with decreased
intrinsic heart rate in the ventricular pacing group. There was no event rate
change in the physiologically-paced group, suggesting a benefit for
pacemaker-dependent patients. The Mode Selection Trial
in sinus-node dysfunction (MOST) showed no difference
between dual-chamber and ventricular pacing in all-cause mortality or non-fatal
strokes. In the Atrial Dynamic Overdrive Pacing Trial (ADOPT), patients with bradycardia-tachycardia syndrome who were
randomly assigned to DDDR with atrial dynamic overdrive pacing had a
significantly higher frequency of atrial pacing than those in the DDDR pacing
alone group (table 1).
Table
1. Pacing trials for sick-sinus syndrome
In the UK
Pacing and Cardiovascular Events study dual-chamber
pacing did not reduce all-cause mortality compared with single-chamber
ventricular pacing (fixed or adaptive) in patients over age 70 years with
high-grade atrioventricular block. Secondary endpoint data also showed no
difference in stroke or transient ischaemic attack, heart failure, and
myocardial infarction. Analyses of quality of life, exercise tolerance, and
other secondary endpoint data are pending.
These studies
consistently showed a decreased frequency of atrial fibrillation with
atrial-based pacing in patients with sinus-node dysfunction (table
1). The findings suggest that some time might be
needed to see potential biological (remodelling) effects of right atrial pacing
for atrial fibrillation prevention. Contrary to all expectations, a reduction
in stroke, heart failure, and mortality has not been consistently shown. High
crossover rates (from single-chamber ventricular to dual-chamber pacing) seen
in MOST and PASE might have limited the value of data assessed by an
intention-to-treat analysis.
Rate-responsive pacing
Inadequate rate response to exercise (chronotropic
incompetence) could be a sign of sick-sinus syndrome. The syndrome might also
be precipitated by drugs (eg, β blockers)
used in the management of coronary disease or heart failure. Rate-responsive
(adaptive) pacing uses sensors to detect physical or physiological indices and
mimic the rate response of the normal sinus node. A rate-control algorithm
affects the overall rate-adaptive characteristics of the pacing system.
Although some features of rate-adaptive pacing are automatic, physicians need
to programme one or more variables to achieve the clinically desired rate
response. Benefits of rate-adaptive pacing for patients with chronotropic
incompetence (eg, sick-sinus syndrome or atrial fibrillation with advanced
heart block) are well established. Many sensors have been developed to modulate
pacing rate (according to metabolic needs) and correct chronotropic incompetence.
Activity, minute-ventilation, QT-interval, and stroke-volume sensors are
commercially available in the
The large number of sensors in clinical or
investigational pacemakers suggests that none is ideal. Characteristics of an
ideal sensor include: compatibility with standard pacing leads, rapid response,
proportionality to workload, sensitivity to non-exercise physiological stimuli
(eg, emotional stress, postural changes, meals, fever), and specificity to
physiological stimuli. Among commonly used sensors, activity sensors have the
fastest response, but have poor proportionality (eg, faster rates when going
downstairs than upstairs), and specificity (eg, inappropriately fast rates when
riding over a bumpy road). Minute ventilation and QT-interval pacemakers have
good proportionality but slow speed of response. Only QT-interval systems
respond to emotional stress. Processing of raw sensor data by refined
algorithms reduces but does not eliminate these limitations. Sensor
strengths and limitations are summarised in table
2.
Table 2. Sensor
strengths and limitations
Sensors using
special lead technology might be unreliable and difficult to implant. Sensors
in the pulse generator are more dependable and only require conventional implant
techniques. Hence, commonly used clinical devices use accelerometers, activity,
QT-interval, and minute-ventilation sensors.
In AAI and
VVI models, single-chamber pacing takes place when the sensed atrial or
ventricular rate falls below a programmed lower rate limit. When rate response
is activated, a sensor-driven rate is recorded. If the sensor-driven rate
exceeds both the intrinsic rate and the lower rate limit, rate-adaptive pacing
occurs. A programmed maximum sensor rate determines the fastest pacing that can
occur.
In
dual-chamber devices programmed in the DDDR mode, rate adaptation might result
from ventricular tracking of the atrial rhythm or be sensor driven (atrial or
atrioventricular sequential pacing). Maximum ventricular tracking and sensor rates
can be programmed separately. If a fast atrial rate during exercise is assumed
to be more likely to represent sinus tachycardia than a fast atrial rate at
rest, a maximum sensor rate (that is programmed faster than the maximum
ventricular tracking rate) helps provide faster ventricular rates during
exertion and limits the ability to track atrial tachyarrhythmias. Dual-chamber
devices also allow rate-responsive atrioventricular delays to be programmed
(which simulates normal shortening of the PR interval).
Rate-response
features could be adapted to individual patients. For instance, activity
sensors can be programmed to various thresholds (high, medium, low), which can
trigger rate-responsive pacing. The slope of acceleration and deceleration of
pacing rate might also be programmed. Recently, different sensors have been
combined to provide a more physiological response to exercise. Sensor
combination aims to improve the speed of rate response, proportionality to
workload, sensitivity to changes induced by exercise-related and
non-exercise-related requirements, and specificity in rate adaptation.
Combinations
of sensors, which exploit strengths and counteract weaknesses of individual
sensors, are a logical step toward optimisation of rate-responsive pacing.
Clinically available combinations include activity/minute ventilation,
accelerometer/minute ventilation, and activity/QT sensors. Combinations have
included a fast reacting activity sensor with a more proportional and specific
metabolic sensor. Initial dual-sensor systems needed time-consuming tailoring
of the individual sensors and their interactions for every patient. Present
systems allow for the automated tailoring of rate response, via self-learning
rate-response algorithms (Vitatron, Arnhem, the Netherlands), or programming of
a target rate histogram on the basis of the patient's activity level and
frequency of exercise (Medtronic, Minneapolis, MN, USA).
Benefits of
rate-adaptive pacing are difficult to gauge in the usual pacemaker recipient.
Most patients already have a quality of life similar to that of age-matched
controls. VVIR pacing seems to be better than VVI pacing in terms of symptoms.
In one study, DDD pacing offered a better quality of life in all patient
subgroups than did dual-sensor VVIR pacing. There is
little evidence to support a major clinical difference between sensors and
their combinations. Cowell and colleagues reported
evidence (in one patient) of potential benefit of a dual-sensor compared with a
single sensor.
Rate
modulation is available in almost all modern pulse generators. In the
Sensors using
special lead technology might be unreliable and difficult to implant. Sensors
in the pulse generator are more dependable and only require conventional
implant techniques. Hence, commonly used clinical devices use accelerometers,
activity, QT-interval, and minute-ventilation sensors.
In AAI and
VVI models, single-chamber pacing takes place when the sensed atrial or
ventricular rate falls below a programmed lower rate limit. When rate response
is activated, a sensor-driven rate is recorded. If the sensor-driven rate exceeds
both the intrinsic rate and the lower rate limit, rate-adaptive pacing occurs.
A programmed maximum sensor rate determines the fastest pacing that can occur.
In
dual-chamber devices programmed in the DDDR mode, rate adaptation might result
from ventricular tracking of the atrial rhythm or be sensor driven (atrial or
atrioventricular sequential pacing). Maximum ventricular tracking and sensor
rates can be programmed separately. If a fast atrial rate during exercise is
assumed to be more likely to represent sinus tachycardia than a fast atrial
rate at rest, a maximum sensor rate (that is programmed faster than the maximum
ventricular tracking rate) helps provide faster ventricular rates during
exertion and limits the ability to track atrial tachyarrhythmias. Dual-chamber
devices also allow rate-responsive atrioventricular delays to be programmed
(which simulates normal shortening of the PR interval).
Rate-response
features could be adapted to individual patients. For instance, activity
sensors can be programmed to various thresholds (high, medium, low), which can
trigger rate-responsive pacing. The slope of acceleration and deceleration of
pacing rate might also be programmed. Recently, different sensors have been
combined to provide a more physiological response to exercise. Sensor
combination aims to improve the speed of rate response, proportionality to
workload, sensitivity to changes induced by exercise-related and
non-exercise-related requirements, and specificity in rate adaptation.
Combinations
of sensors, which exploit strengths and counteract weaknesses of individual
sensors, are a logical step toward optimisation of rate-responsive pacing.
Clinically available combinations include activity/minute ventilation,
accelerometer/minute ventilation, and activity/QT sensors. Combinations have
included a fast reacting activity sensor with a more proportional and specific
metabolic sensor. Initial dual-sensor systems needed time-consuming tailoring
of the individual sensors and their interactions for every patient. Present
systems allow for the automated tailoring of rate response, via self-learning
rate-response algorithms (Vitatron, Arnhem, the Netherlands), or programming of
a target rate histogram on the basis of the patient's activity level and
frequency of exercise (Medtronic, Minneapolis, MN, USA).
Benefits of
rate-adaptive pacing are difficult to gauge in the usual pacemaker recipient.
Most patients already have a quality of life similar to that of age-matched
controls. VVIR pacing seems to be better than VVI pacing in terms of symptoms.
In one study, DDD pacing offered a better quality of life in all patient
subgroups than did dual-sensor VVIR pacing. There is little evidence to support
a major clinical difference between sensors and their combinations. Cowell and
colleagues reported evidence (in one patient) of potential benefit of a
dual-sensor compared with a single sensor.
Rate
modulation is available in almost all modern pulse generators. In the
Permanent bradycardia pacing
via implantable cardiac defibrillators
Previously, 15–20% of ICD recipients needed separate
pacemakers. Strict criteria for dual-chamber pacing are present in 11–29% of
recipients. This percentage seems certain to rise as
biventricular pacing for heart failure becomes increasingly common. Present
ICDs capable of dual-chamber and triple-chamber, rate-responsive pacing provide
state-of-the-art treatment. Shortcomings in early-generation devices have been
corrected. However, addition of full-featured pacing is technically complex,
and the final product is not merely the sum of a DDDR or DDDRV pacemaker and a
tiered-therapy ICD. A tiered-therapy ICD includes antitachycardia pacing,
cardioversion, and defibrillation capabilities. Emphasis on safe and reliable
defibrillation can result in suboptimum pacemaker function.
If present and future trials expand indications for
prophylactic defibrillator implantation, a large number of patients needing
pacemakers for bradycardia or heart failure might instead receive (at least in
the most developed countries) an ICD.39,40
Cost considerations aside, substituting ICDs would have a profound effect on
how cardiac rhythm management devices are designed, marketed, implanted, and
followed up. Panel 1 shows the limitations of ICDs as pacemakers.
Panel
1: Limitations of ICD pacing function
·
Increased incidence of hardware and
software design problems
·
Uncertain long-term reliability of
presently available defibrillation leads (compared with standard pacing leads)
·
Increased current drain that reduces
device longevity
·
Heightened susceptibility to
oversensing of endogenous (eg, diaphragmatic myopotentials) or exogenous (eg,
electromagnetic interference) signals
·
Pacing at rapid rates might delay or
prevent detection of ventricular tachyarrhythmias
·
Complicated pacing algorithms could result
in inappropriate detection of ventricular tachyarrythmias by ICDs
Frequent right ventricular pacing could be detrimental
to ICD patients without indications for antibradycardia pacing. In the Dual
chamber and VVI Implantable Defibrillator (DAVID) trial,41
dual-chamber ICDs were programmed VVI 40 beats per minute or DDDR with a lower
rate limit of 70 beats per minute. 1-year survival free of the composite
endpoint (time to death or first admission for heart failure) was 89·3% in the
VVI-40 group compared with 73·3% for the DDDR-70 group (p < 0·03). Although
the VVI-40 group had less congestive heart failure and death than did the DDDR-70
group, these differences for these individual endpoints were not significant.
Nearly 60% of ventricular beats were paced in the DDDR-70 group compared with
1% in the VVI-40 patients. Andersen and colleagues22 noted an improvement in cardiovascular and total
mortality with AAI pacing. Dual-chamber pacing has not shown similar benefits.23,25,29,31 Data from
MOST42 suggested that increased admission for heart failure was
not associated with pacing mode, but with a prevalence of right ventricular
pacing exceeding 40%. DAVID investigators suggested that right ventricular
pacing (and the resultant left ventricular conduction delay) increases heart
failure by creating ventricular desynchronisation.41
From the DAVID trial, single-chamber ICDs seem to be
the device of choice. However, many ICD recipients will develop sinus-node
dysfunction and atrial tachyarrhythmias. The diagnostic and therapeutic
features of dual-chamber devices would be more suitable for these patients.
Instead, the message from the DAVID trial should be that, when a dual-chamber
ICD is chosen, the programming of a long atrioventricular delay (to reduce or
avoid right ventricular pacing) should be considered for patients with intact
atrioventricular conduction and narrow QRS complexes.
Pacing to terminate
ventricular tachyarrhythmias
Antitachycardia pacing might
terminate, accelerate, or have no effect on ventricular tachycardia. Because
acceleration can turn a haemodynamically stable tachyarrhythmia into lethal
ventricular fibrillation, this treatment requires backup defibrillation
capabilities via an ICD. ICD treatment aims to prevent syncope and sudden death
with minimum shock delivery. Antitachycardia pacing has traditionally been used
to treat monomorphic ventricular tachycardias with rates up to 200 beats per
minute. Only re-entrant monomorphic ventricular tachycardia (usually associated
with clinically significant structural heart disease) can be ended by
antitachycardia pacing. Ventricular tachycardia rates exceeding 200 beats per
minute might be more likely to be accelerated by antitachycardia pacing and
deteriorate into ventricular fibrillation. Adjuvant antiarrhythmic treatment
might slow ventricular tachycardia rates and help with pace termination.43 Various pacing techniques can be used or combined to
find a regimen that works consistently without arrhythmia acceleration (figure 2).
Figure 2. Antitachycardia
pacing for ventricular tachycardia
(A) Ventricular tachycardia at cycle lengths of
310–20 ms (188–94 beats/minute). (B) Simulated ventricular tachycardia
(courtesy of Medtronic) with cycle lengths of 330–70 ms (162–82 beats/minute).
(C) Ventricular tachycardia at cycle lengths of 340–50 ms (rate 171–76
beats/minute). EGM1 Vtip to Vring=intracardiac ventricular electrogram recorded
from pacing electrodes. EGM2=intracardiac ventricular electrogram recorded from
high voltage (shock electrodes). TS=tachycardia sensing. TD=tachycardia
detection. TP=tachycardia pacing. VS=sensing of intrinsic ventricular rhythm.
V-V interval=ventricular cycle length (ms).
Antitachycardia
pacing requires pacing faster than each tachycardia. Figure
2A shows burst pacing at 290 ms (fixed rate of 207
beats per minute), which terminates ventricular tachycardia. In scanning burst
pacing (figure
2B), successive bursts are paced at fixed and
faster rates. The second attempt ends another ventricular tachycardia. More
aggressive ramp pacing (rate increase or cycle length decrement between beats)
is required to terminate the tachyarrhythmia in figure
2C.
Termination
success rates of 80% or more can be achieved in heart disease. Termination
rates of induced ventricular tachycardia with biventricular or right
ventricular antitachycardia pacing are much the same.
Careful programming can result in acceleration rates as low as 1%. Almost all
slow ventricular tachycardia episodes are pace terminable. However, in some
patients antitachycardia pacing is unsuccessful and low-energy shocks are
effective. Both treatments have comparable success, failure, and acceleration
rates. Almost all patients describe shocks of 1 J or more as uncomfortable. By
contrast, effective and painless pacing can be achieved with μJ
and is therefore more tolerable and less energy-consuming than cardioversion.
Additionally, appropriately delivered pacing is unlikely to result in atrial
proarrhythmia.
Antitachycardia
pacing treatment might be guided by electrophysiological test results or chosen
empirically. New data suggest that ventricular tachycardia faster than 200
beats per minute can respond to empirical antitachycardia pacing.46
Pacing to prevent ventricular
tachyarrhythmias
Algorithms that prevent ventricular tachyarrhythmias
use continuous or intermittent (rate smoothing or stabilisation) pacing (with
ventricular capture) to suppress triggering of ectopic beats, prevent re-entry,
decrease dispersion of refractoriness, and eliminate pauses that might induce
tachyarrhythmia. Various pacing techniques have been thought to prevent
ventricular tachyarrhythmias; most are not very effective.
In the acquired long-QT syndrome, torsades de pointes is invariably preceded by
pauses or bradycardia.
We reviewed publications of acquired torsades de
pointes in patients with permanent pacing. Studies providing documentation of
tachycardia onset and pacemaker programming were included in our analysis, and
events occurring less than 1 month after atrioventricular nodal ablation were
excluded. 18 cases were identified. No patients developed the tachyarrhythmia
with an effective pacing rate of more than 70 beats per minute. Programmed
lower rates of up to 70 beats per minute were not protective. At programmed
lower rates of over 70 beats per minute, torsades de pointes occurred only by
programmable pause-promoting features or oversensing. Whether rate-smoothing
algorithms can prevent the condition when the baseline rate is programmed to
less than 70 beats per minute remains to be seen. Viskin
and colleagues reported most pauses leading to torsade
de pointes were unequivocally longer than the preceding basic cycle length
(ventricular rate). The shortest culprit pause was 760 ms. They recommended
pacing at a cycle length of 750 ms (ventricular rate of 80 beats per minute).
We agree that this is reasonable. A detailed review of pacing in the long-QT
syndrome has been published.
Acute and chronic congestive heart failure contribute
to the need for tachyarrhythmia treatment in ICD recipients. Although small
trials (93 patients in total) have shown that biventricular pacing treatment
diminished ventricular arrhythmias, these results were not confirmed in larger
trials.
Pacing for neurally-mediated
syncope
Case history, physical examination,
and a 12-lead electrocardiogram (ECG) are most important in the assessment of a
patient with syncope. With these investigations, the diagnosis can be
ascertained or suspected in 40% of patients. Although echocardiography is
commonly requested, little evidence supports its use if the physical
examination and ECG are normal. Myocardial ischaemia rarely causes syncope, and
stress testing is low yield unless there is a high index of suspicion (ie,
angina pectoris). Holter monitoring is also low yield. If another diagnosis is
not established or suspected, patients without evidence of structural heart
disease are generally referred for assessment of neurally-mediated syncope
(carotid sinus massage, head-up tilt table testing [HUT]). Those with
structural heart disease or known cardiac arrhythmias are usually referred for
electrophysiological testing.
Benefit from pacing in patients with severe symptoms
or unexplained falls and evidence of cardioinhibitory carotid sinus
hypersensitivity has been recorded. Carotid
hypersensitivity is common in elderly patients with unexplained falls. Although
empiric pacing is generally used, whether bradycardia causes these episodes is
uncertain. The Syncope and Falls in the Elderly—Pacing
and Carotid Sinus evaluation (SAFE-PACE) randomly
selected patients to clinical observation or pacemaker implantation. After
follow-up, paced patients had a lower incidence of recurrent falls than did
controls. A second study (SAFE-PACE 2) is an ongoing
multicentre trial in which similar patients are randomly assigned to permanent
pacing or an implantable loop recorder. Table 3 summarises the pacing trials for carotid sinus
hypersensitivity.
Table
3. Pacing trials for carotid sinus hypersensitivity
The role of
permanent pacing in management of neurocardiogenic (vasovagal) syncope remains
controversial. A predominant cardioinhibitory (bradycardic <40 beats per
minute or asystolic) response during HUT testing has been proposed as a means
to identify patients with neurocardiogenic syncope who may respond to permanent
pacing.
Maloney and
colleagues described a patient who had 73 s of asystole provoked by HUT. After
the investigators acknowledged that vasovagal spells were usually benign, they
defined long episodes (that could alter lifestyle or threaten health) of
cardiac standstill during vasovagal spells as malignant vasovagal syncope. Even
with a dual-chamber pacemaker, the patient had severe symptomatic hypotension
on repeat HUT. Maloney and co-workers recommended
permanent dual-chamber pacing as adjuvant treatment for such patients. Sra and
colleagues subsequently assessed 22 patients with
bradycardia (or asystole) and hypotension provoked by HUT. Temporary pacing did
not prevent a substantial decline in mean arterial pressure during repeat HUT.
During long-term follow-up (median 16 months), of 19 patients treated with
drugs alone, 18 did not have presyncope or syncope. Sra and co-workers
concluded that drug treatment was often effective for prevention of
cardioinhibitory neurocardiogenic syncope, whereas permanent pacing was not.
Baron-Esquivias and colleagues reported a study
including 1322 patients and concluded that neither pacing nor drug treatment
affected the outcome of patients with tilt-induced asystole. They also
concluded that the patients' clinical course was affected mainly by the
frequency of pretreatment events.
Two new
pacing modalities—search hysteresis and rate-drop response—could be more
effective than conventional pacing. Search hysteresis allows the patient's
heart rate to fall to a low value before pacing begins at a much faster rate.
When search hysteresis is turned on, the escape interval automatically
continues for an extra cycle to allow spontaneous sinus rhythm to resume. In
rate-drop response, a substantial drop in spontaneous rate triggers rapid
pacing (90–100 beats per minute) for a programmable period. In the Vasovagal
Syncope International study, dual-chamber permanent
pacing with search hysteresis was compared with no treatment. During follow-up,
syncope occurred significantly more often in untreated patients than in those
with permanent pacing.
Two
controlled studies compared permanent pacing with drug treatment in patients
with vasovagal syncope. In the North American Vasovagal Pacemaker Study (VPS), a large treatment effect for permanent pacing with
rate-drop response versus medical treatment resulted in the study finishing
early: a greatly reduced risk of syncope was seen in paced patients. Syncope
Diagnosis and Treatment compared dual-chamber permanent
pacing (with rate-drop response) with atenolol treatment in patients with recurrent
vasovagal syncope. This study was also ended early after an interim analysis
showed significant benefit from permanent pacing. Rate-drop response seems to
be more effective than search hysteresis. New syncope
sensors such as monitoring QT interval, right ventricular pressure, and other
indicators of contractility are under investigation.
Results of
the second Vasovagal Pacemaker Study (VPS II) were not as encouraging as the
first VPS: cumulative risk of recurrent syncope did not differ significantly in
patients with dual-chamber pacemakers with either ODO (control group, not
actively pacing) or DDD (with rate-drop response). Because of a lower than
expected event rate in the control group, the study lacked sufficient
statistical power to prove that pacemaker treatment prevents recurrent
vasovagal syncope. This unexpectedly low event rate
could represent a placebo effect that resulted from device implantation in the
control group. Flevari and associates recently compared
the effects of propranolol, nadolol, and placebo in 30 patients with recurrent
vasovagal syncope and positive HUTs. All three treatments significantly reduced
spontaneous presyncope and syncope, although no differences in recurrence rates
were seen between treatment arms. The vasovagal syncope and pacing trial
(SYNPACE) randomised 29 patients to pacemaker on versus
pacemaker off modes and was unable to show a benefit from active pacing in
prevention of recurrence in patients with severe recurrent tilt-induced
syncope.
We believe
that neurocardiogenic syncope is generally a benign condition and can usually
be managed without permanent pacing. Pure or predominantly vasodepressor
episodes do not need pacing. At present, we believe that dual-chamber pacing
should be regarded as an adjunctive treatment for patients with frequent and
severe cardioinhibitory spells, especially for those who are drug refractory or
intolerant or have asystole exceeding 5 s that can be shown clinically or
during HUT.
Pacing in hypertrophic
obstructive cardiomyopathy
Dual-chamber pacing has been proposed as an
alternative to septal myotomy-myectomy for patients with hypertrophic
obstructive cardiomyopathy (that is refractory to drug treatment). DDD pacing
is used because patients with the condition often cannot tolerate loss of
atrioventricular synchrony. Placement of the right ventricular electrode at the
apex pre-excites the right-sided septum. Reduced inward septal motion (during
systole) augments left ventricular outflow tract diameter and diminishes
obstruction, which allows further systolic emptying.
Appropriate timing of the atrioventricular interval is
essential for effective pacing. The programmed delay must be less than the
native PR interval (to ensure full ventricular capture), but long enough to
allow adequate atrial contribution to ventricular filling (to avoid falls in
cardiac output and systemic blood pressure). Paced, sensed, and rate-adaptive
atrioventricular delays help to maintain optimum atrioventricular intervals
during daily activities. Correctly programmed dual-chamber pacing results in a
30–60% acute reduction in the left ventricular outflow tract gradient without
systemic compromise.
Several investigations have been undertaken to assess
the clinical benefits of pacing in hypertrophic obstructive cardiomyopathy (table 4). These studies have generated
much controversy. Some investigators have suggested that responders tend to be
older and more symptomatic than non-responders. The balance between gradient
reduction and impaired diastolic relaxation during ventricular pacing might
determine clinical response. Pacing might be more favourable in patients with
slight (or well compensated) diastolic dysfunction. Attempts to objectively
assess functional capacity could be frustrated by the intrinsic heterogeneity
of disease in hypertrophic obstructive cardiomyopathy. Much attention has been
drawn to the consistent placebo effect noted in randomised pacing trials.72
Table 4. Summary
of hypertrophic obstructive cardiomyopathy studies
Surgery
is still regarded as the gold standard intervention for medically refractory
hypertrophic obstructive cardiomyopathy. Patients should be aware that
percutaneous transluminal septal myocardial ablation (PTSMA) is a treatment
option. These procedures are associated with a risk of atrioventricular block,
which needs subsequent permanent pacing. Permanent
dual-chamber pacing might be considered in patients who are not candidates for
surgery or PTSMA. Pacing might also be a reasonable adjunct for patients who
use drugs that greatly impair their native conduction system.
Pacing to palliate, prevent,
and interrupt atrial fibrillation
Complete atrioventricular junction ablation and
permanent pacing was introduced in 1982 as an alternative treatment for
patients with medically refractory supraventricular tachycardia. When radio-frequency currents were used as the energy
source for ablation, this technique became a popular and effective method for
palliative treatment of atrial fibrillation with a rapid ventricular response. In atrioventricular nodal modification, radio-frequency
current is used to reduce ventricular rates. Energy is initially delivered to
the posterior atrioventricular nodal imputs (near the ostium of the coronary
sinus) and, if needed, gradually applied anteriorly (toward the compact
atrioventricular node and bundle of His) until the desired effect is achieved.
Attempts to modify the atrioventricular node have been successful in achieving
long-term rate control in over 70% of patients. Inadvertent high-grade
atrioventricular block (that needs permanent pacing) is seen in 10–20% of
patients. Both nodal ablative techniques substantially
improve symptoms, left ventricular function, and quality of life. However,
complete atrioventricular junction ablation had a significantly greater effect
on frequency of major symptoms and quality of life than did node modification.
Use of these palliative techniques has waned, as
curative procedures (ie, pulmonary vein isolation and left atrial ablation)
continue to develop. Atrioventricular junction ablation and permanent pacing
might still be useful in elderly patients with clinically significant
underlying structural heart disease, and those with persistent or chronic
atrial fibrillation.
Atrial pacing has been investigated
for prevention (and reduced frequency) of atrial fibrillation. Theoretical
explanations are: (1) prevention of bradycardia-induced dispersion of
refractoriness, which reduces the likelihood for re-entry; (2) overdrive
suppression of spontaneous atrial ectopy that could trigger atrial
fibrillation; and (3) change in atrial excitation patterns and prevention of
intra-atrial re-entry, in response to premature atrial beats. As previously
noted, the benefit of atrial-based pacing (compared with ventricular-based
pacing) in reduction of atrial fibrillation (over time) in patients with
sick-sinus syndrome has been well established in several randomised studies.
Clinical data have suggested that right atrial pacing
is less effective for atrial fibrillation prevention in patients with right
atrial conduction delays or increased dispersion of refractoriness.
Site-specific pacing from the atrial septum or Bachmann's bundle could shorten
atrial conduction time and help to prevent atrial fibrillation.
Intra-atrial conduction delay can be diagnosed in the
presence of P waves longer than 120 ms. Right atrial pacing could produce
delayed left atrial activation with a suboptimum left-sided atrioventricular
conduction time, which could result in left atrial mechanical systole close to,
or simultaneous with, left ventricular systole. Loss of the atrial contribution
to left ventricular filling could be haemodynamically deleterious. Simultaneous
biatrial pacing (right atrium and proximal or distal coronary sinus),
manifested by normalisation of P-wave configuration and duration, improves
haemodynamics.
Multisite atrial pacing has been investigated for
prevention of atrial flutter and fibrillation. Some investigators have combined
high right atrial and distal coronary sinus pacing. Saksena and co-workers paced the right atrium and the coronary sinus ostium. In
another small study, no difference was recorded in atrial fibrillation
frequency or duration between right atrial and dual-site atrial pacing.
Long-term results of multisite atrial pacing in heterogeneous atrial
fibrillation populations have not been uniformly favourable.
Benefits of dual-site pacing over right atrial pacing seem to be, at best,
modest and clinical enthusiasm for this technique has waned.
The value of atrial pacing to prevent atrial
fibrillation in patients without bradycardia remains controversial. Trials have
been small and undertaken in individuals with frequent, drug-refractory atrial
fibrillation and in populations in which effective treatments are difficult to
find. In the Atrial Pacing Peri-Ablation for Prevention of Atrial Fibrillation
study, the investigators concluded that in patients with
drug–refractory, paroxysmal fibrillation who were candidates for ablation,
right atrial pacing did not prevent atrial fibrillation. In a subsequent
randomised crossover comparison of DDDR and VDD pacing modalities in patients
with paroxysmal atrial fibrillation, the time to first recurrence did not
differ between groups and the atrial fibrillation burden (h/day) increased
significantly over time in both. In the New Indications
for Pacing Prevention of Atrial Fibrillation study,
although time to first recurrence was extended by dual-site pacing compared
with high right atrial pacing in conjunction with a consistent atrial-pacing
algorithm, total atrial fibrillation burden was much the same in the two
groups.
New pacemaker pulse generators will include
antitachycardia pacing modalities. Studies in patients receiving dual-chamber
ICDs show that atrial tachyarrhythmias are common. Antitachycardia or
high-frequency burst pacing could end two-thirds of these episodes. Whether
these episodes indicate true pace termination will need further investigation.
Although we are skeptical that atrial fibrillation can be reliably
pace-terminated, arrhythmias that trigger atrial fibriallation (such as atrial
flutter or tachycardia) can be readily pace-terminated.
Pacing for heart failure
Two small studies have
suggested that DDD pacing with a short atrioventricular delay might benefit
patients with dilated cardiomyopathy and a prolonged baseline PR interval. CRT
refers to pacing techniques that alter the degree of atrial or ventricular
electromechanical asynchrony in patients with major conduction disorders, and
is usually done by pacing more than one atrial or ventricular site (biatrial or
biventricular pacing, respectively). Bifocal pacing refers to two sites in the
same anatomic cardiac chamber (ie, right ventricular apex and outflow tract).
CRT can also be achieved by pacing from an atypical site (such as single-site
left ventricular pacing). The Pacing Therapies in Congestive Heart Failure II
study group showed that left ventricular pacing
significantly improved exercise tolerance in patients with left ventricular
systolic dysfunction, chronic heart failure, and a QRS duration of more than
150 ms. At least 20–30% of class III and IV chronic heart failure patients have
major left ventricular conduction disorders that make them potential candidates
for ventricular CRT.
Ventricular CRT has had far greater effect on
improvement of heart failure than biatrial pacing has had on atrial
fibrillation. Several studies have shown beneficial
effects from biventricular or left ventricular pacing in patients with severe
left ventricular systolic dysfunction and major left-sided intraventricular
conduction disorders, such as complete left bundle-branch block. These conduction
delays result in inefficient left ventricular contraction, shortened diastole
(or overlap of systole and diastole), and worsened functional mitral
regurgitation. CRT improves the sequence of left ventricular contraction and
reduces functional mitral regurgitation. By contrast to inotropic agents, this
treatment reduces myocardial oxygen consumption.
Atrioventricular optimisation might be needed to
ensure continuous ventricular pacing. Patients with chronic atrial fibrillation
might respond to biventricular pacing. Atrioventricular
junction ablation might be needed to maintain pacemaker-controlled ventricular
depolarisation. Biventricular pacing is technically complex. Until recently,
CRT was accomplished with modified use of conventional hardware. The left ventricular lead is usually placed over the
epicardial left ventricular surface via a tributary of the coronary sinus.
Lateral and posterolateral cardiac veins seem to provide the best haemodynamic
benefit (figure 3, figure 4), but could result in
diaphragmatic (phrenic nerve) stimulation. Access to these lateral veins might
be limited by variation in anatomy.
Figure 3. Diagrammatic presentation of
heart showing positions for coronary venous lead placement
Figure 4. Chest
radiographs showing lead placements
(A)
Posteroanterior and (B) lateral chest radiographs showing tip of a left
ventricular lead (arrows) in a tributary of the middle cardiac vein. Despite
proximity of the lead to the left hemidiaphragm, phrenic nerve stimulation did
not take place. The right ventricular lead points anteriorly toward the rib
cage.
Success rates
of implantation are dependent on experience, and experienced implanters achieve
initial success in about 90% of patients. Median time for implantation has been
reported to be 2·7 h. Lead dislodgment occurs in 5–10%
of cases. Other potential complications include: increased left ventricular
pacing thresholds, cardiac sinus dissection, cardiac tamponade, and various
sensing problems. As mentioned earlier, cardiac venous anatomy is more variable
than coronary artery anatomy. Leads and lead delivery systems likewise vary in
length, shape, and stiffness. We can now choose from an increasing variety of
catheters, sheaths, guidewires, and leads, to assist left ventricular
epicardial pacing. Recent addition of leads designed specifically for cardiac
venous pacing (including models that can be advanced over wires used for
percutaneous transluminal coronary angioplasty) helps to reduce procedure times
and increase success rates. Some older biventricular pacing ICDs might sense
every conducted QRS twice, because ventricular activation is detected at
different times by the right and left ventricular leads. In newer devices,
detection of tachyarrhythmias based on right ventricular sensing prevents the
triggering of inappropriate shocks related to sequential ventricular sensing.
In several
trials, CRT has improved 6-min walking distance, quality of life score, left
ventricular ejection fraction, functional class, exercise time, and peak oxygen
consumption.
The less
impressive results from the CONTAK CD study might relate to less stringent QRS
duration and New York Heart Association (NYHA) functional class requirements.
The US Food and Drug Administration felt that the CONTAK CD studydid not fully
establish the effectiveness of CRT as a treatment for heart failure. In the
Focused Confirmatory Study, 127 patients with class III or IV heart failure
received the CONTAK CD system. In about half the patients, only the
defibrillator component was turned on. In the other half, both defibrillator
and CRT components were turned on. These results established the effectiveness
of CRT for heart failure. Additional supporting evidence showed reduced left
ventricular intracavitary dimensions and improved left ventricular ejection
fraction in patients on CRT. In the InSync ICD trial, patients given CRT had
significantly improved quality of life, NYHA functional class, peak VO2 (oxygen consumption), exercise
duration, left ventricular intracavitary dimensions, and ejection fraction.
In a
meta-analysis of four controlled CRT studies (Multisite Stimulation in
Cardiomyopathy trial [MUSTIC], CONTAK CD, InSync ICD
[MIRACLE ICD], and MIRACLE;
1634 patients) CRT significantly reduced death from progressive heart failure
and admission for heart failure, at follow-up. Total mortality was reduced by
23%, although this was not significant. In a meta-analysis, nine CRT trials
were analysed for efficacy. All-cause mortality was significantly reduced by
21%. This result was largely driven by a reduction in progressive heart
failure. A non-significant increase in sudden cardiac death was noted. A
metaregression showed no difference in all-cause mortality benefit between CRT
patients an CRT-D patients. Data from the Comparison of Medical Therapy,
Pacing, and Defibrillation in Chronic Heart Failure trial (companion) were not
included in the metaregression. The companion trial was stopped prematurely
because of the significant benefit of CRT and CRT defibrillators (CRT-D) in the
combined primary endpoint of all-cause mortality and admission. The
investigators recorded a non-significant 24% relative reduction in all-cause
mortality with CRT alone. However, a significant relative reduction in
all-cause mortality with CRT-D was reported.
The MIRACLE
ICD trial showed that at 6 months, patients assigned to
CRT-D had a greater improvement in quality of life and functional class than
controls. Treadmill exercise duration increased in the CRT-D group and
decreased in the control group. No significant changes in left ventricular size
or function, survival, or rates of admission were noted. Proarrhythmia was not
seen and arrhythmia termination was likewise not impaired.
Which
patients are the best candidates for CRT? Presently, those with drug-refractory
NYHA class III or IV congestive heart failure, left ventricular ejection
fraction up to 35%, left ventricular end-diastolic diameter equal to or more
than
Because right
ventricular pacing might lead to ventricular asynchrony, patients who are
dependent on ventricular pacing are candidates for biventricular pacing.
Preliminary data from a subanalysis of the biventricular pacing after ablate
compared with right ventricular study (PAVE) suggests
that CRT might benefit patients with left ventricular ejection fractions of 35%
or less and chronic atrial fibrillation who undergo ablation of the
atrioventricular junction. Controversy exists over whether patients with right
bundle-branch block should be candidates for CRT. Few with this condition have
been included in clinical trials. Some cardiac electrophysiologists believe
that the type of bundle-branch block does not predict clinical response and
advocate biventricular pacing for advanced heart failure and any QRS duration
of 130 ms or longer. Others have suggested that there might be a benefit in
patients with right bundle-branch block accompanied by a substantial
concomitant left-sided intraventricular conduction delay (assessed by
echocardiography).
We cautiously
offer biventricular pacing to patients with right bundle-branch block after
counselling them that the benefits for their patient group are uncertain.
Achilli and co-workers have shown that CRT might be
helpful in patients with severe heart failure and narrow and incomplete left
bundle-branch block QRS complexes who show echocardiographic evidence of
intraventricular and interventricular asynchrony. Larger studies will be needed
to confirm these preliminary results. A recent analysis of CRT cost-effectiveness
suggested that CRT should not be considered in patients with comorbidities that
are likely to reduce life expectancy. Table
5 summarises some of the data from
CRT studies.
Table 5. Summary
of CRT studies
Percutaneous lead extraction
Advances in cardiac pacing have spurred the use of
percutaneous techniques for permanent lead extraction. Formal methods for
transvenous extraction of permanent pacing leads have been available since
1988. Although new methods are still being developed, currently available
techniques are generally safe and very effective.
All lead extractions need some degree of direct
traction (pulling). Simple direct traction on the proximal portion of the lead
might be sufficient to remove newly implanted leads. Some evidence has shown
that infected leads respond to direct traction alone more often. The tensile strength of fibrous lead encapsulation
increases over time. Passive fixation leads are generally more difficult to
remove than active fixation leads. Traction alone is often ineffective and
unsafe in leads implanted for more than 4–6 months. A variety of locking
stylets (inserted into the proximal conductor coil and bound to its tip at the
distal pacing electrode) has greatly simplified the application of direct traction.
Most operators begin with a superior vena caval
(subclavian) approach and switch to an inferior vena caval (transfemoral)
approach if needed. The ability to use snares and basket catheters makes the
inferior venal caval approach more versatile than the superior approach. A
transfemoral approach is recommended when a subclavian insertion site is
grossly infected and when leads are broken or free-floating.
Many sheath systems are available for extraction.
Sheaths provide counterpressure (forward movement to break adhesions) as they
are advanced, and countertraction (opposition to movement of the myocardial
wall) as the extractor pulls to remove the lead. The Pacemaker Lead Extraction
with the Excimer Sheath trial showed that excimer laser sheaths (which vaporise
fibrous adhesions) improved the effectiveness of lead extraction and reduced
procedure time. Complete lead removal was achieved in 94% of patients with
laser sheaths compared with 64% of those using conventional telescoping
non-laser sheaths. In a more recent study, extraction of 2561 pacing and
defibrillator leads was attempted with three sizes of laser sheaths. Complete
removal took place in 90% of leads, 3% were partially removed, and the
remaining 7% were failures. Multivariate analysis showed that implant duration
was the only preoperative independent predictor of failure; female sex was the
only multivariate predictor of complications.128
Indications for lead extraction are evolving. We believe that decisions on lead
removal should be guided by parallel hierarchies that assess procedural timing
(emergent, urgent, elective) and the risk benefit ratio (ie, whether extraction
is mandatory, necessary, or discretionary; panel 2). Success is inversely related to duration of
implantation and patient age.
Panel
2: Assessment of risk benefit ratios for lead
removal
Mandatory
•Life-threatening
condition, leads must be removed
•Indications
include septicaemia (endocarditis), migration (causing emboli, arrhythmia, or perforation),
device interference (ie, abandoned ICD lead), and occlusion of all usable
vessels
Necessary
•Great
potential for morbidity or mortality, leads should be removed
•Indications
include pocket infection, chronic draining sinus, erosion, potential device
interference, venous thrombosis, and lead replacement (extract and reimplant
via thrombosed vein)
Discretionary
•Lead
removal is optional
•Indications
include pain, malignant disease, and replacement of leads abandoned for less
than 3–4 years (not advisable to remove non-infected leads that have been
implanted for more than 8–10 years)
Major complications of lead extraction can be expected
in up to 2% of patients, and happen more often during an operator's early
experience. These problems include low cardiac output,
lead breakage, pulmonary embolism, lead migration (consequences depend on size
and ultimate destination of the debris), avulsion of
veins or myocardial tissue, venous or myocardial tears (resulting in
haemothorax, cardiac tamponade, or death), and failure to remove an infected
lead. The
Complications of permanent
pacing
Expanding indications and the relative ease of
percutaneous implantation have fuelled enthusiasm for permanent pacing devices.
However, complications vary in clinical significance (and patient effect) from
benign to life-threatening. An acute pacemaker implant might be associated with
a complication rate of 4–5%.Incidence of acute complications is related to
operator experience. In MOST, the incidence of late complications was 2·7%.
Some investigators believe this incidence correlates with the number of leads
implanted, but this opinion is debatable. However, the direct correlation
between procedure duration and the patient's risk for system infection is
generally accepted.
Complications related to venous access include
pneumothorax, haemothorax, and air embolism. In MOST, the incidence of
pneumothorax was 1·5%. Risk of pneumothorax is associated with the experience
of the implanter, plus the number and difficulty of subclavian punctures. This
risk can be eliminated by the cephalic vein cutdown technique. Pneumothorax is
often small, asymptomatic, and noted incidentally on follow-up chest
radiography; however, tension pneumothorax should always be part of the differential
diagnosis when hypotension or pulseless electrical activity ensues during an
implantation. Haemothorax results from trauma to the great vessels. Arterial
puncture must be promptly recognised and treated with manual compression.
Arterial cannulation (with a sheath or lead) can be avoided by advancing a
guide wire to the inferior vena cava before any introducer insertion. Patients
are surprisingly tolerant of air emboli. The air is filtered, absorbed in the
lungs, and treatment is generally not needed. However, large emboli can result
in respiratory distress, oxygen desaturation, and hypotension. Treatment with
100% oxygen, inotropic agents, or aspiration of the embolus from the right
heart might be needed.
Lead-related complications include perforation,
dislodgment, diaphragmatic stimulation, and malposition.132 Perforation can involve the great vessels, right
atrium, or right ventricle. Most perforations do not result in major sequelae.
Cardiac tamponade, usually the result of chamber perforation, is the most
ominous implant complication and should be suspected whenever hypotension
occurs. The diagnosis is supported by enlargement of the cardiac silhouette and
weak contractions, and can be confirmed by emergent 2D echocardiography.
Definitive treatment via emergent pericardiocentesis should not be delayed.
Surgical intervention might be needed if the bleeding persists and pericardial fluid
reaccumulates. Trauma to the great vessels is more common with lead extraction
than implantation and might result in direct bleeding into the mediastinum,
which is an indication for emergent open chest surgery. Lead dislodgment takes
place in 2·5% of implants, usually in the first 24–48 h postimplant. If the patient is not dependent on pacing in that
chamber, a different pacing mode could be reprogrammed to manage dislodgement.
Definitive correction needs lead repositioning or replacement.
Diaphragmatic stimulation results from phrenic nerve
stimulation. Right atrial leads can stimulate the right phrenic nerve, whereas
right and left (cardiac venous leads) ventricular leads stimulate the left
phrenic nerve and left hemidiaphragm. Screening for this complication by pacing
at maximum outputs is a requisite part of correct implantation procedure.
Presence of an atrial or ventricular septal defect can
allow passage of a lead to the left heart. Passage into the left heart is more common
with ventricular leads. Confirmation of lead position by use of a left anterior
oblique fluoroscopic projection of equal to or more than 40° should identify
this problem during implantation. A lateral chest radiograph usually provides
definitive diagnosis (figure 5). A paced right bundle-branch
block configuration on surface ECG might result from left ventricular pacing.
However, this configuration can be present in up to 8% of patients with
properly placed right ventricular leads. Coman and Trohman have developed an
algorithm to distinguish right versus left ventricular lead positions when
pacing produces a right bundle-branch block configuration.
Figure 5. Lateral
chest radiograph of lead passing through atrial septum
This ventricular lead points posteriorly and its tip
is in the left ventricular endocardium. The lead passed through a patent
foramen ovale, the left atrium, and the mitral valve into the left ventricle.
This abnormal position is emphasised by comparison with figure
4B in which the right ventricular lead points
anteriorly and the left ventricular epicardial lead points posteriorly.
Pocket-related
complications include haematoma, wound pain, pocket erosion, and infection.
Haematomas are usually managed conservatively. Evacuation is required in 1–2%
of implants. Risk of bleeding is increased in anticoagulated patients,
especially in those receiving heparin. Simple analgesics usually control wound
pain. Pain that initially improves and then recurs or is temporally remote from
the implant suggests infection.
The frequency
of pacemaker implant infection ranges from 1–19%. We believe that laboratory or
surgical-suite infection rates greater than 7–8% suggest (potentially
correctable) contamination or technical problems that need thorough
investigation. Manifestations of pacemaker infection range from mild local pain
and erythema to life-threatening septicaemia. Early infection tends to be more
clinically evident than the often indolent course of late infection. In one
large series of patients with infected implantable antiarrhythmic devices,137 the most common pathogens were coagulase-negative
staphylococci (68%), Staphylococcus aureus (24%), and gram-negative
enteric bacilli (17%). 16 of 123 (13%) infected patients had polymicrobial
infections. When infection is strongly suspected, the entire system should be
regarded as contaminated. The treatment of choice is complete system removal
(pulse generator explant plus transvenous lead extraction), and antimicrobial
therapy. Reimplantation should be undertaken at a different site. Morbidity due
to persistent infection (ie, when infected leads are not removed) can be as
high as 66%. Erosion is associated with a high risk of infection and complete
extraction of the device-lead system is likewise advised.
Delayed
complications of permanent pacing leads include venous thrombosis, exit block,
insulation failure, and conductor fracture. Late lead damage might be reduced
by use of axillary or cephalic venous access. Symptomatic venous thrombosis
takes place in up to 5% of patients. Treatments depend on the site and symptoms
associated with thrombosis, and vary from heparin (followed by warfarin) or
thrombolysis to angioplasty or open surgery. Exit block manifests as increased
pacing thresholds. Insulation failure results in decreased lead impedance.
Conduction fracture manifests as increased lead impedance. Definitive treatment
for these complications is lead replacement.
We postulated
that the design of bipolar coaxial leads from modern endocardial pacemakers
might be susceptible to a high failure rate. We analysed the long-term survival
of bipolar coaxial leads and unipolar leads implanted at the Cleveland Clinic,
OH,
Most modern
pulse generators have an expected longevity of 5–9 years. Unexpected pulse
generator (electrical) failure is rare. Many problems
discovered in new models can be corrected by software upgrades. Lead-related
problems (increased thresholds, decreased impedance) resulting in increased
current drain are the most common causes of premature battery depletion.
Stepwise changes in pacing or magnet pacing rates, changes in pacing mode,
pulse-width stretching, and telemetered battery voltages or impedances are
clinical indicators used to measure the time for elective generator replacement
and battery end-of-life.144 Lithium-iodine batteries used in current pulse
generators are not rechargeable and surgical replacement of the entire
generator is needed.
SYSTEMATIC INTERPRETATION GUIDELINES for
Electrocardiograms
RATE
Rate calculation
Common method: 300-150-100-75-60-50
Mathematical method: 300/# large boxes between R waves
Six-second method: # R-R intervals x10
RHYTHM
Rhythm Guidelines:
1. Check the bottom rhythm strip for regularity, i.e. - regular, regularly
irregular, and irregularly irregular.
2. Check for a P wave before each QRS, QRS after each P.
3. Check PR interval (for AV blocks) and QRS (for bundle branch blocks). Check
for prolonged QT.
4. Recognize "patterns" such as atrial fibrillation, PVC's, PAC's,
escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks
and bundle branch blocks.
AXIS
|
|
Lead I |
Lead aVF |
|
1. Normal axis (0 to +90 degrees) |
Positive |
Positive |
|
2. Left axis deviation (-30 to -90)
Also check lead II. To be true left axis deviation, it should also be down in
lead II. |
Positive |
Negative |
|
3. Right axis deviation (+90 to +180) |
Negative |
Positive |
|
4. Indeterminate axis (-90 to -180) |
Negative |
Negative |
|
|
|
|
Left axis deviation differential:
LVH, left anterior fasicular block, inferior wall MI.
Right axis deviation differential: RVH, left posterior fascicular block,
lateral wall MI.
HYPERTROPHY
1. LVH -- left ventricular hypertrophy = S wave in V1 or V2 + R wave in V5 or
V6 > 35mm or aVL R wave > 12mm.
2. RVH -- right ventricular hypertrophy = R wave > S wave in V1 and gets
progressively smaller to left V1-V6 (normally, R wave increases from V1-V6).
3. Atrial hypertrophy (leads II and V1)
Right atrial hypertrophy -- Peaked P wave in lead II >
Left atrial hypertrophy -- Notched wide (> 3mm) P wave in II. V1 has increase in the terminal negative
direction.
INFARCT
|
Ischemia |
Represented by symmetrical T wave
inversion (upside down). Look in leads I, II, V2-V6. |
|
Injury |
Acute damage -- look for elevated
ST segments. |
|
Infarct |
"Pathologic" Q waves. To
be significant, a Q wave must be at least one small square wide or one-third
the entire QRS height. |
Certain leads represent certain areas
of the left ventricle:
|
V1-V2 |
anteroseptal wall |
II, III, aVF |
inferior wall |
|
V3-V4 |
anterior wall |
I, aVL |
lateral wall |
|
V5-V6 |
anterolateral wall |
V1-V2 |
posterior wall (reciprocal) |
References.
A
- Basic:
1. Davidson’s Principles and practice
of medicine (21st revised ed.) / by Colledge N.R., Walker B.R., and
Ralston S.H., eds. – Churchill Livingstone, 2010. – 1376 p.
2.
3. The Merck Manual of Diagnosis and Therapy (nineteenth
Edition)/ Robert Berkow, Andrew J. Fletcher and others. – published by Merck
Research Laboratories, 2011.
4. Web
-sites:
a)http://emedicine.medscape.com/
b) http://meded.ucsd.edu/clinicalmed/introduction.htm
B – Additional:
1.
Braunwald’s Heart Disease: a textbook of cardiovascular medicine (9th
ed.) / by Bonow R.O., Mann D.L., and Zipes D.P., and Libby P. eds. – Saunders,
2012. – 2048 p.
2.
Braunwald’s Heart Disease: review and assessment (9th ed.) / Lilly
L.S., editor. – Saunders, 2012. – 320 p.
3.
Cardiology Intensive Board Review. Question Book (2nd ed.) / by Cho
L.,
4.
5.
Hurst’s the Heart (13th ed.) / by Fuster V., Walsh R.A., Harrington
R., eds. – McGraw-Hill, 2010. – 2500 p.
5.