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myocarditis.13
1. Sinus tachycardia occurs when the sinus node discharge rate
is >100 bpm. It is characterized by a gradual onset and offset
and is due to acceleration of Phase 4 diastolic depolarization First-degree AV block
of the sinus node pacemaker cells. Sinus tachycardia may
A prolonged PR interval (>0.20 s) is found in approximately 0.5%
result from a primary disorder of the sinus node (sinus node
of the normal population and may be secondary to increased
reentry). Sinus tachycardia may be seen during pregnancy,
vagal tone, drugs, ischemia, and/or rheumatic heart disease.4
especially in the third trimester (earlier in twin pregnancy)
During pregnancy, first-degree AV block usually results from
and at delivery without any pathological significance. Sinus
rheumatic heart disease, but if there is no underlying pathology
tachycardia is usually a physiological response and treatment
it is usually benign.
is rarely needed. If associated with an underlying pathological
state (e.g. fever, hemorrhage), the underlying problem should
be treated.
Second-degree AV block
2. Sinus bradycardia is defined as a sinus node rate < 60 bpm.
Mobitz type I (Wenckebach) second-degree AV block is charac-
It may be physiologically normal, especially in the physically
terized by a progressive lengthening of the PR interval until an
fit parturient, or abnormal, occurring in association with many
impulse is blocked (i.e. no QRS follows the blocked P wave). The
contributing factors outlined in the Advanced Cardiac Life
Support (ACLS) Bradycardia Algorithm.12 If there is hemody- block is at the AV node, is often transient, and may be asympto-
matic. The condition is relatively benign and may occur during
namic compromise, follow the ACLS bradycardia algorithm
with respect to treatment.12 sleep or whenever vagal tone is increased. It is commonly seen
in association with rheumatic fever, ischemia, and inferior wall
Parturients receiving spinal anesthesia for C/S may develop
MI, and it may result from medication. The block seldom pro-
sudden, severe bradycardia and hypotension. This may be
gresses to complete AV block.4 Treatment with pacing in patients
due to a rapidly ascending sensory block (> T2), with blockade
with Mobitz type I block is indicated only in seriously sympto-
of cardioaccelerator fibers. In some individuals, it seems to
matic patients.
be associated with predominant vagal tone, and atropine
Mobitz type II second-degree AV block is characterized by the
may be required in addition to volume expansion and
sudden stopping of an impulse without previous prolongation
vasopressors.
of the PR interval. The block is most often below the AV node at
3. Wandering pacemaker is the result of shifting of the dominant
the bundle of His or at the bundle branches. The block is often
pacemaker from the sinus node to latent pacemakers in



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symptomatic with the potential to progress to complete (third-
Table 2.4 Congenital complete heart block in pregnancy
degree) AV block. When it occurs in the presence of acute MI, it is
usually associated with larger infarcts and higher morbidity. Incidence ¼ 1:15 000“1:22 000 live births
An accompanying bundle branch block (BBB), frequently involv- ECG criteria for diagnosis (usually narrow QRS)
ing the His-Purkinje system, may be seen on EKG. Permanent Slow pulse from an early age
pacing is recommended for pregnant women with symptomatic No history of infection (diphtheria, rheumatic fever, etc.)
Mobitz type II AV block.4 No evidence of ischemic heart disease or cardiomyopathy
The incidence of second-degree AV block during pregnancy No history of cardiac surgery
is very low. The majority of cases reviewed by Mendelson15 were May present during pregnancy
acquired, occurring in association with rheumatic heart disease
and infection. Among 26 cases of acquired heart block, six
had second-degree AV block. In another study, only 1 of 21 non-
pregnant women with congenital heart block had a second- (>0.12 s), an ˜˜M™™-shaped complex is seen in V1 and V2 and a
degree block.16 broad S wave is present in the LV leads, especially lead I. Right
bundle branch block may be the result of an isolated congenital
lesion, RV hypertrophy or strain, myocardial damage, or disease
Third-degree AV block
of the specialized conducting tissues.
Third-degree AV block (complete heart block) occurs when
no supraventricular impulses are conducted to the ventricles.
Left bundle branch block (LBBB)
The block may occur at the level of the AV node, bundle of
His, or bundle branches. No impulses pass between the atria
In leads V5 and V6, the small negative Q wave normally seen is
and ventricles. Complete AV dissociation is present, with the
replaced by a large, positive R wave and a secondary R wave
atrial and ventricular rates determined by their own independ-
(˜˜M™™-shaped ventricular complex), and QRS > 0.12 s. Left bundle
ent pacemakers. The ventricular rate is usually low (junction-
branch block may occur because of myocardial damage second-
al ¼ 45“50 bpm; idioventricular rate ¼ 35“45 bpm) and the atrial
ary to coronary artery disease or cardiomyopathy, LV hypertro-
rate faster. Congenital third-degree AV block is often nodal,
phy, or disease of the specialized conduction tissues. Left bundle
resulting from an immunologic attack by maternal antibodies on
branch block is rarely seen with an otherwise normal heart and
the fetal AV node.17 Acquired third-degree AV block is usually
can occur intermittently. Recently acquired LBBB has a poor
infranodal, involving the His-Purkinje system. Third-degree heart
prognosis.
block may be permanent, or transient, depending on the under-
lying cause.
The first case of complete heart block in pregnancy was repor- Left anterior and posterior fascicular blocks
ted in 1914. Mendelson15 analyzed 40 reported cases of com- (hemiblocks)
plete heart block in pregnancy. Twenty women had acquired
The anterior and posterior fascicles of the left bundle branch
AV block: secondary to rheumatic heart disease (11), infection (6),
conduct impulses to the anterosuperior and posteroinferior
myocarditis (2), and coronary artery disease (1). In the other 20
areas of the LV respectively. Left anterior and posterior hemi-
women with congenital heart block, 10 had a VSD. The maternal
blocks are common in conduction tissue diseases.
and fetal mortality rates were 13% and 15%, respectively.
Maternal and fetal prognosis for women with complete heart
block is improved due to artificial pacemakers.18 Women with
Management of bradycardia associated
congenital complete heart block (see Table 2.4) and normal QRS
with poor perfusion12
duration are usually asymptomatic and have uneventful pregnan-
cies,19 in contrast to those with acquired heart block.4 Heart Transcutaneous pacing should be used without delay for
block, by itself, rarely affects the course or outcome of pregnancy symptomatic unstable women with high-degree (Mobitz type II
if the ventricular rate remains in the range of 50“60 bpm. If the second-degree or third-degree) block who do not respond to
rate slows suddenly, syncope may occur. Stokes-Adams attacks, oxygen and atropine. While awaiting a pacemaker, second-line
and limited HR responses to stress, may occur and women with drugs, dopamine 5“20 mg/kg/min, epinephrine 2“10 mg/min, or
these symptoms may require a temporary pacemaker for labor isoproterenol 2“10 mg/min, may be helpful. If transcutaneous or
and delivery. Permanent AV sequential pacing is a desirable transesophageal pacing is ineffective because of inconsistent
option in symptomatic women.4 Pregnancy is usually well toler- capture, or if effective pacing does not improve the clinical con-
ated in women with pacemakers. dition because the cardiovascular symptoms are not caused by
the bradycardia, consultation and transvenous pacing are the
next steps. Atropine should be used cautiously in the presence
Right bundle branch block (RBBB)
of coronary ischemia or MI because increased HR may increase
In RBBB there is delay in activation of the RV while septal and left ischemia or the zone of infarction. With the trend for women of
ventricular (LV) activation are normal. The QRS is prolonged advanced maternal age (> 35) to bear children, coronary artery



33
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disease and ischemia should be considered in the differential heart disease, myocardial ischemia and MI, myocarditis, car-
diomyopathy, rheumatic heart disease, long QT syndrome, 4
diagnosis.
and a variety of medications, including digoxin.
Indications for treatment of PVD during pregnancy include
Ectopic beats PVD with hemodynamic compromise, sustained symptomatic
PVD, and PVD with an underlying structural abnormality, possi-
The terms ectopic beat, extrasystole, and premature contraction
bly predisposing to life-threatening dysrhythmia (controversial).
are synonymous. They refer to an impulse arising from the atria,
Correction of underlying causes and avoidance of stimulants may
AV junction (AV node or bundle of His), or ventricles, which arises
reduce or eliminate PVD and, generally, pharmacologic therapy is
prematurely in the cardiac cycle.
avoided. Quinidine and procainamide (Vaughan Williams Class
IA) have a good safety record in pregnancy (FDA Pregnancy Risk
Classification “ Class C) although the side effects are undesirable.
Premature atrial depolarizations (PAD)
Low-level beta-blockade is as effective as quinidine in suppres-
A diagnosis of PAD is made on the ECG when a premature P wave sing symptoms. Among Class IB antidysrhythmic drugs, the safest
is noted with a P“R interval >120 milliseconds (msec). The inter- appears to be lidocaine (Class IB), provided serum levels are
val between the ectopic beat and the preceding beat (coupling monitored and maternal and fetal effects followed closely.
interval) is shorter than the cycle length of the dominant rhythm. A small subset of women with MVP and LQTS is predisposed to
Usually the contour of a premature P wave differs, indicating a ventricular tachycardia, which, if sustained, may be associated
different focus of origin.20 Sometimes PAD are not conducted to with embolic events and sudden death. A history of PVD and,
the ventricles or may be conducted with a BBB pattern. Premature MVP or LQTS may warrant prophylactic antidysrhythmic treat-
atrial depolarizations occur in 20“40% of young healthy indivi- ment. Chronic PVD, which are frequent, multifocal, ˜˜R on T™™, or
duals4 and they may be found during routine prenatal examination that occur in salvos, are associated with increased cardiovas-
or an investigation of ˜˜palpitations™™. Isolated PAD were found cular mortality, but there is no evidence that their suppression
in 90% of 30 healthy women studied during labor.8 Contributing improves prognosis.20
factors include stress, anxiety, fatigue, infection, nicotine, caffeine,
alcohol, and sympathomimetic asthma preparations or deconge-
stants. Normally, PAD do not require therapy, and avoidance or Tachydysrhythmias
removal of precipitating factors is often therapeutic. Occasionally,
Based on the appearance of the QRS complex, the tachycardias
PAD reflect occult heart failure or excessive adrenergic tone
are classified into sinus tachycardia, narrow-complex (supra-
when appropriate treatment is diuretics, analgesics, sedatives, or
ventricular) tachycardia, and wide-complex tachycardia. Most
beta-blockade. If PAD are frequent, they may trigger sustained
wide-complex tachycardias are ventricular in origin. Narrow-
supraventricular or ventricular tachydysrhythmias that require
complex tachycardias, which are irregular, are usually atrial
treatment.
fibrillation (AF), or possibly atrial flutter, or multifocal atrial
tachycardia.
Premature ventricular depolarizations (PVD)
The QRS complex of PVD is premature, broad ( >0.12 sec), Narrow-QRS-complex tachycardias (SVT)
abnormal in shape, and is not preceded by a premature
Supraventricular tachycardia encompasses a variety of tachy-
P wave. The most common cause of ˜˜palpitations™™ or ˜˜awareness
dysrhythmias originating in the sinoatrial (SA) node, atria, and
of skipped beats™™ during pregnancy is PVD as they tend to be
AV junction. Supraventricular tachycardia is characterized by a
noticed more than those caused by PAD. Premature ventricular
narrow QRS (< 0.12 s) complex (except for cases of preexisting
depolarizations are followed by a compensatory pause only if
BBB or aberrant conduction) with a regular R“R interval and a
they are not conducted to the atria. Occasionally, PVD produce
rate between 150“250 bpm (see Table 2.5) Atrial depolarization
distressing symptoms from the increased myocardial contract-
is retrograde, resulting in inverted P waves in EKG leads II, III,
ility associated with the postectopic beat. Clinically, PVD are
and aVF. The P wave may occur just before, during, or after the
accompanied by a giant ˜˜a™™ (cannon) wave, visible in the neck
QRS complex, and it is not seen if it arises during the QRS
as the PVD occurs against a closed tricuspid valve. Sudden
complex. Reciprocating tachycardias involving anomalous
distension of the pulmonary veins may elicit an associated
(accessory) AV or nodal-ventricular pathways are included
spontaneous cough.
even though the atrium and ventricle are part of the reentrant
Premature ventricular depolarizations occur frequently in the
circuit.
general population. In a Holter monitor study of 50 healthy
women, 54% had PVD (6% had >50 beats in 24 hours).16 Most
pregnant women with PVD have no underlying heart disease.
Paroxysmal supraventricular tachycardia (PSVT)
Premature ventricular depolarizations may be associated with
anxiety, intake of stimulants, infection, electrolyte abnormalities, If a dysrhythmia is recurrent, starts and stops suddenly, it is
hypoxia, mitral valve prolapse (MVP), hypertension, congenital designated paroxysmal. Paroxysmal supraventricular tachycardia



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Table 2.5 Supraventricular dysrhythmias in pregnancy

Dysrhythmias Rate/rhythm P wave/PR QRS Clinical importance Treatment

PAD Regular with P wave contour Normal Common (64%) Reassurance
˜˜skipped™™ beats abnormal; Occasionally may trigger Avoid stimulants
PR >120 ms sustained PSVT or VT Usually no drugs
Underlying heart disease required
uncommon;
Precipitating factors: stress,
infection, alcohol, caffeine
(tea, coffee, colas), nicotine
(cigarettes), stimulant
drugs (sympathomimetic
asthma medications,
decongestants); occult
heart failure (very
occasionally)
Normal or "
PSVT AR 140“220 bpm ? P waves (inverted 2.6% pregnancies Goal: slow AV
2:1 AV block (usual) P in II, III, AvF) Usually well tolerated conduction:
PR normal or "
regular rhythm Serious sequelae can occur 1. Vagal
Can mimic VT if aberrant QRS 2. Drugs
Abrupt onset & offset 3. Cardioversion
Atrial tachycardia: AV block P wave in or follows “ Multifocal AT frequently
a. Nonparoxysmal QRS RP > PR associated with respiratory
b. Multifocal interval failure
Atrial flutter Type I (classic): AR Sawtooth flutter Normal Less common than AF 1. Rapid atrial pacing
300, VR 150; 2:1 waves Underlying heart disease (Type I)
AV conduction; usual 2. Drugs (Type II)
Type II: AR >350 3. Cardioversion
Atrial fibrillation AR 350“600 No P waves Narrow Uncommon in 1. Convert to SR: Drugs
VR 100“200 complexes pregnancy Cardioversion
Irregular Can occur in structurally Pacemaker
normal hearts (paroxysmal 2. Slow VR drugs
form) 3. Prevent recurrence
Chronic form associated with Drugs
myocardial and systemic
disease

PAD ¼ premature atrial depolarizations; PR ¼ pulse rate; PSVT ¼ paroxysmal supraventricular tachycardia; VT ¼ ventricular tachycardia; AT ¼ atrial
tachycardia; AR ¼ atrial rate; AV ¼ atrioventricular; SR ¼ sinus rhythm; VR ¼ ventricular rate; AF ¼ atrial fibrillation



is a distinct clinical syndrome characterized by repeated episodes and rapidly, along a circuit consisting of the AV node junction
(paroxysms) of tachycardia with an abrupt onset, lasting from and the additional AV connection. Additional connections
a few seconds to several hours. Paroxysmal supraventricular may occur between atria and ventricles. In atrioventricular
tachycardia may stop spontaneously, or it may stop when nodal reentrant tachycardia (AVNRT), the AV node and its adja-
another ectopic supraventricular beat interrupts the circitous cent atrial tissues are functionally dissociated into fast and slow
movement.20 AV nodal pathways. In AVNRT, the additional connection is an
accessory AV pathway “ a strand of myocardium that straddles the
groove between atria and ventricles and bypasses the AV node.
General mechanisms
If the accessory AV pathway can conduct in an anterograde
Electrophysiologically, SVT is caused by two main mechanisms: direction (atria to ventricles), the features of Wolff“Parkinson“
(1) reentry; or (2) rapid, abnormal atrial activity (atrial tachycardia, White (WPW) syndrome are present (see later). More than 90%
atrial flutter, AF). With reentrant tachycardias, there is an addi- of PSVT are due to reentry, and the initial event is frequently a
tional electrical connection between atria and ventricles, so that PAD. Details of the mechanisms involved can be found in stan-
an impulse can circulate between atria and ventricles, repeatedly dard cardiology texts.



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does not respond to vagal maneuvers, current ACLS guidelines12
Clinical presentation
recommend adenosine (Class I). Calcium channel blockers
Supraventricular tachycardia has a heterogeneous clinical presenta-
(verapamil is more effective than propanolol)29 have a similar
tion most often occurring in the absence of detectable heart disease
SVT conversion rate to adenosine, but adenosine tends to be
in younger individuals.11 Patients with paroxysmal dysrhythmias
more rapid with fewer side effects than verapamil.12 If the
are often asymptomatic at the time of evaluation. A clinical history,
rhythm converts, it was most likely reentry SVT. The woman
describing the pattern in terms of number of episodes, duration,
should be observed for recurrence, and any recurrence treated
frequency, mode of onset, and possible triggers, is important.
again with adenosine or a longer-acting AV nodal blocking agent
Paroxysmal supraventricular tachycardia-related symptoms
such as diltiazem or a beta-blocker. Amiodarone can achieve
include syncope, or near-syncope, distressing palpitations, angina,
nearly 100% efficacy in the inhibition of induced sustained
dyspnea, fatigue, anxiety, and polyuria. Some women with PSVT
reentrant SVT.27
may be asymptomatic or be aware of palpitations that are not
Irregular palpitations are probably due to premature depolar-
distressing. Syncope occurs in approximately 15% of patients with
izations, AF, atrial flutter, or multifocal atrial tachycardia.11
SVT, usually just after initiation of rapid SVT or during a prolonged
Expert consultation is recommended. The rate may be controlled
pause after abrupt termination of the tachycardia. Syncope may be
using diltiazem and/or beta-blockers.
associated with AF, with rapid conduction over an accessory AV
If someone is hemodynamically unstable with narrow-complex
pathway, or structural abnormalities such as valvular aortic steno-
tachycardia, adenosine can be administered while preparations
sis, hypertrophic cardiomyopathy, or cerebrovascular disease.11
are made for synchronized cardioversion (10“50 joules, Class IIb).
Angina and pulmonary edema may occur in women with heart
Current recommendations are to proceed quickly to synchro-
disease, the symptoms reflecting myocardial ischemia and heart
nized cardioversion and to not delay in order to establish i.v.
failure, respectively. These latter hemodynamic events result from
access and administer drugs.12 Various drugs, including adeno-
decreased LV filling and cardiac output.21 Pulmonary edema is
sine, verapamil, beta-blockers, and Class IA antidysrhythmic
most likely to occur if SVT lasts longer than six hours or in the
drugs, will successfully terminate SVT 21,28,29 with adenosine
presence of underlying heart disease, such as mitral stenosis.
the drug of choice.12,28 Cholinergic agents (e.g. edrophonium)
Physical examination does not usually lead to a definitive diag-
and pressor agents (e.g. phenylephrine) are other classes of
nosis. If irregular cannon waves and/or irregular variation in the
drugs that are used to stop PSVT in the presence of normal or
first heart sound intensity are present, then a ventricular origin of
low blood pressure (BP), respectively.30 Rapid atrial pacing is also
a regular tachycardia is strongly suggested. The presence of asso-
effective in stopping PSVT and may be useful for those cases
ciated heart disease should be sought, and an echocardiogram
refractory to drug therapy.31
may be helpful.
If someone with irregular, narrow-complex tachycardia is stable,
there is time to obtain a 12-lead EKG and evaluate the rhythm,
In pregnancy await consultation, and determine the best treatment option.
Irregular narrow-complex tachycardia is probably AF, or possibly
The estimated incidence of PSVT during pregnancy is as high
atrial flutter, or multifocal atrial tachycardia. Attempts to control
as 2.6% but in those with a prior history, episodes may be more
the rate with diltiazem or beta-blockers may be successful. It can
frequent and severe.4,22,23 Often, a diagnosis of PSVT is made
be difficult to differentiate supraventricular ectopic beats or SVT
for the first time during pregnancy. Paroxysmal supraventricular
with aberrant conduction, from ventricular ectopic beats or
tachycardia occurs more often during pregnancy in women
ventricular tachycardia (VT). The typical narrow QRS complex
with a prior history of PSVT, or with WPW syndrome-associated
of PSVT is not seen if a preexisting, or rate-dependent, BBB is
dysrhythmias,4,22 or in those treated with beta-agonists.24 The most
present, or if anterograde conduction to the ventricles occurs over
common cause of a sustained dysrhythmia in pregnancy is reentrant
an accessory AV nodal pathway, such as a Kent bundle. The clinical
SVT. Paroxysmal supraventricular tachycardia is often called par-
importance of differentiating PSVT and VT is considerable. Treat-
oxysmal auricular, atrial, or supraventricular tachycardia with the
ment of rapid, wide, regular QRS tachycardias with agents such
underlying electrophysiologic mechanism rarely defined.4
as verapamil, in the belief that the rhythm is SVT with aberrant
conduction, can have disastrous consequences (precipitate ventri-
cular fibrillation) if the tachycardia is ventricular.
Treatment
Prevention of PSVT depends on the frequency and severity
In the absence of coexisting heart disease, the majority of SVT of attacks. Beta-blockers, amiodarone, or verapamil may be
of the atrioventricular nodal reentrant type (AVNRT) are well given. In some, pacemaker implantation may be necessary. When
tolerated in young people.25 When treatment is required for appropriate, ablation procedures that destroy part of an accessory
reentrant pathway are done and can result in a long-term cure.25
termination of stable reentry SVT, vagal maneuvers and adeno-
sine are preferred. If the tachycardia has a regular narrow-
complex QRS, vagal maneuvers alone (carotid sinus massage,
Atrial tachycardia and atrial flutter
Valsalva maneuver, or gagging) will terminate about 20“25%
of reentry SVT.26 Eyeball massage should never be performed Atrial tachycardia may be classified as nonparoxysmal atrial
because it may result in retinal detachment.25 If reentry SVT tachycardia and multifocal atrial tachycardia, with the latter



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