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commonly seen in patients with severe pulmonary disease. node, and the ventricular rate is irregular at 100“200 bpm. As
Atrial flutter is less common than AF. Paroxysmal forms of atrial with atrial flutter, paroxysmal AF can occur in normal hearts,
flutter may occur in the absence of structural heart disease, while the chronic form is associated with myocardial and
but in its chronic form, atrial flutter is almost always associa- systemic disease (see Table 2.5). In patients with cardiovascu-
ted with underlying structural heart disease.4,30 Atrial flutter is lar disease, AF is associated with doubling of morbidity and
mortality.34
frequently unstable, reverting to sinus rhythm or degenerating
into AF.30 The hemodynamic consequences of AF depend on the sever-
In atrial flutter, the EKG reveals ˜˜saw-tooth™™ morphology in ity of the underlying disease and the ventricular rate. Atrial
the inferior leads. Atrial flutter is classified into two types: type fibrillation is more common in patients with enlarged left atria
I (classic), which shows an atrial rate of 300 bpm and ventricular (> 40 mm). In patients with mitral stenosis, a faster HR shortens
rate of 150 bpm (2:1 AV conduction); and type II, which shows a the diastolic filling time and increases the transvalvular pressure
flat baseline with a positive flutter wave in the inferior leads and gradient. Sudden onset of AF with rapid ventricular rates raises
a rate usually >350 bpm. Type I disease originates close to the left atrial pressure, leading to symptoms of dyspnea and possibly
sinus node and activates the right atrium in a counter-clockwise pulmonary edema. Because normal left atrial contraction con-
direction. Type II disease appears to originate in the lateral atrial tributes up to 30% of the presystolic, transvalvular pressure
wall, and the depolarization wave occurs usually in a clockwise gradient, abrupt loss of atrial contraction can decrease cardiac
direction. output by 20%. Ventricular filling is restricted more by the rapid
HR than by loss of atrial contraction. When LV dysfunction with
reduced ventricular compliance is present, cardiac output may
In pregnancy
drop dramatically.
Relatively few cases of atrial flutter have been reported in preg- Embolic stroke and peripheral embolization are more fre-
nancy.4,15,32 Atrial flutter has been reported in association with a quent in patients with chronic AF and underlying heart dis-
wide variety of conditions including hypertensive heart disease, ease (especially mitral stenosis). Clinically evident emboli
obstructive pulmonary disease, dilated or hypertrophic cardio- develop in approximately 35% of patients with mitral valve
myopathy,4 Graves disease,15 rheumatic heart disease,4 and post- disease, 18% with ischemia and hypertension, and 10% with
surgical correction of congenital heart disease.4,32 hyperthyroidism. Post-mortem examination of patients with
chronic AF demonstrates emboli in 45% of those with valvular
disease and 35% of those with ischemia and hypertension. The
Treatment
risk of embolization is much less in the absence of heart
disease.4
Treatment is dictated by hemodynamic status. Synchronized car-
dioversion of atrial flutter can generally be achieved with a rela-
tively low energy of 10“25 joules, ideally with i.v. access and
In pregnancy
conscious sedation.
In hemodynamically stable patients, beta-blocking agents, cal- Atrial fibrillation and atrial flutter are rare in women of repro-
cium channel blockers, or digoxin4 may control the ventricular ductive age and, therefore, warrant investigation when diag-
rate and occasionally terminate the dysrhythmia. After the ven- nosed during pregnancy. In the past, reported cases of AF
tricular rate is controlled, Class 1A drugs (procainamide, quin- in pregnancy were associated most often with rheumatic heart
disease, especially mitral valve disease. In 1956, Mendelson15
idine) are commonly required to achieve conversion to normal
sinus rhythm. To avoid converting a 2:1 block to 1:1 conduction identified 31 women with AF of whom 29 had rheumatic heart
with an even faster ventricular rate, Class IA antidysrhythmic disease. Nineteen women had New York Heart Association
drugs (e.g. procainamide) should only be administered after the (NYHA) class III and IV disease, and the associated maternal
ventricular rate has been controlled. and fetal mortality was 19% and 58% respectively. Five women
had embolic complications.15 Fifty years ago the prevalence of
When there is hemodynamic instability or drug therapy failure,
direct current cardioversion, starting with low energy of rheumatic heart disease was higher than it is today. Today,
10“25 joules, is the treatment of choice for atrial flutter. The AF occurs more frequently with congenital and valvular heart
need for long-term drug treatment depends on the frequency disease and occasionally with pulmonary embolism, acute
and severity of the dysrhythmia. Beta-blocking agents, calcium myocarditis or pericarditis, cardiomyopathy, rheumatic heart
disease, and alcohol or drug abuse.4 However, AF secondary to
channel blockers (diltiazem, verapamil), or digoxin may be effect-
ive.33 Radiofrequency ablation can potentially cure atrial flutter rheumatic disease still occurs in areas of the world where
with success rates in the 80“90% range.4 women are deprived of health care and sanitary living condi-
tions. In a report of recurrence rates of dysrhythmias during
pregnancy and the early postpartum period,37 AF or atrial flutter
Atrial fibrillation
recurred in 52% of the 23 pregnancies studied.35 In six women
Atrial fibrillation is characterized by totally disorganized atrial with AF or atrial flutter at baseline all remained in that rhythm
depolarization at a rate of 350“600 bpm. Most atrial impulses throughout pregnancy. Adverse fetal events occurred in 20%,
are blocked because of concealed conduction within the AV independent of other maternal or fetal risk factors, and were



37
1 Cardiovascular and respiratory disorders


Wide-complex tachycardia
more common in women who developed recurrent antepartum
dysrhythmias.35
Ventricular tachycardia
Electrocardiographic features of VT include bizarre QRS com-
Treatment
plexes longer than 120 ms, fusion beats, capture beats, and AV
Initially, correct any contributing or underlying cause, followed dissociation occurring at a rate of 100“250 bpm. Fifty percent
by either conversion of the dysrhythmia to sinus rhythm, have retrograde conduction to the atria. Occasionally, differentia-
or slowing of the ventricular response when conversion does tion from a wide-QRS tachycardia of supraventricular origin may
not occur. Intravenous drugs used to convert acute AF include be difficult and expert consultation is advisable. For example,
esmolol, procainamide, and amiodarone. Esmolol and amiodar- rapid AF with conduction over a bypass tract appears as a grossly
one are pregnancy category C and D drugs, respectively, meaning irregular, rapid (200“300 bpm), wide-QRS tachycardia on EKG.
they should only be given if the potential benefit justifies the Vagal maneuvers or drug therapies that slow conduction over
potential risk to the fetus. Digitalis, calcium channel blockers, the AV node may help in the differential diagnosis. Occasionally,
and/or beta-blockers are given to control the HR in chronic electrophysiologic testing may be required. Wide-QRS tachycar-
AF that does not convert to sinus rhythm. In the operating room dia of uncertain origin should be considered as VT until proven
and intensive care unit, i.v. calcium channel blockers and beta- otherwise, and it should be treated accordingly (i.v. amiodarone,
blocking drugs are useful because they quickly slow ventricular synchronized cardioversion). Nonsustained VT is defined as
response, although they do not restore normal sinus rhythm. VT that does not cause hemodynamic compromise and stops
Beta-blockers are the preferred drugs for acute ventricular rate con- spontaneously in < 30 s. Sustained VT is defined as VT that
trol in women with AF during pregnancy. 36 Digoxin is not as lasts >30 s or that which causes hemodynamic compromise and
requires immediate termination.4
effective in the acute setting, because it requires more than one
hour to slow ventricular response significantly. Adenosine slows Ventricular tachycardia develops by one of three mechanisms:
ventricular response briefly, aiding in the diagnosis but not the (1) reentry; (2) abnormal automaticity; and (3) triggered activity.
treatment of AF. If AF is part of a tachycardia“bradycardia syn- Triggered activity occurs when the impulse is the result of early
drome, pacing may be required in addition to drug therapy. or delayed after-depolarizations. Calcium ions and slow, inward
Electrical cardioversion (100“360 joules) is reserved for patients calcium channels are involved in the latter, and calcium channel
who are unstable or unresponsive to drug therapy.36 The decision blocking drugs (e.g. verapamil) may be helpful. Triggered activity
to proceed to electrical cardioversion should be made after care- also may be involved in dysrhythmias associated with congenital
or acquired LQTS or excess catecholamines.4 Ventricular tachy-
ful evaluation of underlying heart disease, duration of AF, left
atrial size, and condition of the mother and fetus. Successful con- cardia may occur in the absence of any obvious structural cardiac
version and sustained sinus rhythm are most likely in patients with abnormalities (primary electrical disease). Ventricular tachy-
small left atria and AF of less than several months™ duration. cardia in pregnancy usually fits into this category with some
episodes arising for the first time during pregnancy.37,38,39,40,41
Administration of procainamide or quinidine (after digitalization)
for a few days before electrical cardioversion is recommended, Typically, VT originates from the RV outflow tract or LV septal
because 10“15% of cases convert to sinus rhythm during this region.
time. Despite successful conversion, hemodynamic improvement Factors known to precipitate paroxysmal VT include physical
may not be seen immediately as left atrial contraction may remain exertion, emotional upset, fear, exercise, caffeine, smoking, alco-
depressed for several weeks.20 Long-term therapy with flecainide, hol, trauma, changes in posture, hypokalemia, hypomagnese-
mia,42,43,44 and imbalance of the autonomic system.45 Clinically,
sotalol, disopyramide, propafenone, and amiodarone may be
required to prevent recurrence of AF.22 Calcium channel blockers VT usually presents with symptoms of rapid palpitations, chest
that affect the AV node are deleterious in patients with AF or flutter discomfort, and dizziness. Syncope or sudden death may be the
associated with preexcitation (e.g. WPW). initial manifestation, especially in the presence of structural heart
The incidence of embolization during cardioversion is 1“3%. disease and/or a very rapid VT rate.
If elective cardioversion is planned, consideration should be Some catecholamine-sensitive, nonsustained VT can be pre-
given to thromboembolic prophylaxis. Anticoagulation is recom- vented by treatment with beta-blocking drugs and avoidance
mended in the presence of mitral stenosis; in recent-onset AF of of exercise and other triggers. Ventricular tachycardia in the
more than four days™ duration; and in association with a history of presence of underlying structural heart disease has a poorer
recurrent and recent emboli, prosthetic mitral valve, and dilated prognosis.
cardiomyopathy. If not contraindicated, anticoagulation for two
weeks before and four weeks following cardioversion signifi-
In pregnancy
cantly decreases systemic embolization.4 Long-term anticoagula-
tion is recommended for individuals with persistent AF. Warfarin Ventricular tachycardia is rare in pregnancy and usually occurs in
is associated with spontaneous abortion in 10“50% of pregnan- the absence of structural heart disease. Ventricular tachycardia
cies and multiple teratogenic effects.4 As a result, low molecular has been reported with structural heart disease including congen-
weight heparin has become a commonly used anticoagulant ital heart disease, RV dysplasia, MVP, LQTS, acute myocarditis,
cardiomyopathy, cardiac tumors, and coronary artery disease.4
during pregnancy.



38
Chapter 2


About 30 case reports of VT in pregnancy appeared in the litera-
Table 2.6 Dysrthythmias associated with congenital
ture between 1942 and 1992.4 Overall, maternal outcome is
heart disease in pregnancy
good but cardiac deaths have occurred.46,47 Careful evaluation
to determine the cause of VT may identify a correctable cause Heart defect Dysrhythmia
such as hypomagnesemia-induced recurrent sustained VT.42,43
Atrial septal defect Supraventricular dysrhythmias
One woman with VT died during her sixth month of pregnancy,
Congenital heart block Bradydysrhythmias
three weeks after initiation of procainamide,48 and another with
Ebstein anomaly Supraventricular dysrhythmias
hypertrophic cardiomyopathy died from VT at 39 weeks™ gesta-
Eisenmenger syndrome Sudden death
tion.49 Paroxysmal VT in women without demonstrable heart
Mitral valve prolapse Atrial & ventricular dysrhythmias
disease is reported to be more frequent in pregnancy but evid-
Tetralogy of Fallot Conduction system disorders
ence is limited. It also is unclear as to whether there is a pattern
Heart block
of variability during different trimesters.4
Bradycardia
Ventricular dysrhythmias
Treatment Transposition of the Loss of sinus rhythm
53
great arteries Supraventricular dysrhythmias
If VT is well tolerated hemodynamically, the drug of choice
Heart block
in current ACLS12 protocols is amiodarone. There are concerns
Tricuspid atresia Atrial fibrillation
about the safety of amiodarone in pregnancy. It currently is
Double outlet right Sinus bradycardia
classified as a Food and Drug Administration (FDA) Class D
ventricle or
drug. Lidocaine (FDA Class B) and procainamide (FDA Class
Single ventricle Complete AV block
C), considered safer during pregnancy, successfully terminate
the majority of VT. If VT is unresponsive to drug therapy or is AV ¼ atrioventricular
associated with hemodynamic compromise, direct-current
cardioversion (50“300 joules) is indicated. Low-energy synchro-
Specific lesions
nized shock (20“50 joules) is often successful in restoring normal
sinus rhythm. In those individuals with a history of sustained VT
Ebstein anomaly
or who are symptomatic with frequent episodes of nonsustained
VT, correction of an identified precipitating factor or long-term Women with Ebstein anomaly are at risk for reentrant paroxysmal
antidysrhythmic medication may be necessary.4 Some antidys- tachycardia, often via a bypass tract as seen in WPW syndrome.
rhythmic medications increase the propensity to other dysrhy- The course of the pregnancy is determined by the severity of the
thmias (prodysrhythmia), and these may increase the risk of tricuspid regurgitation, stenosis, and right-to-left shunting across
sudden death. Drugs currently considered to have less prodysrhy- the ASD. This anomaly is usually mild in adults and some women
thmic potential include beta-blockers and amiodarone. The risks remain asymptomatic, successfully completing pregnancy.
and benefits of each medication must be assessed on an indivi- Cyanosis may appear for the first time during pregnancy. Right
dual basis. ventricular failure can occur from an increase in tricuspid regur-
gitation. After surgical tricuspid valve reconstruction, pregnancy
may result in worsening of residual tricuspid regurgitation,
Ventricular fibrillation
dysrhythmias, and endocarditis. Epidural anesthesia has been
Ventricular fibrillation (VF) should be treated according to the used successfully for C/S and labor analgesia in women with
current ACLS protocol,12 always with care to maintain left uterine Ebstein anomaly (see Chapter 1).
displacement to ensure adequate venous return.

Eisenmenger syndrome and pulmonary
Dysrhythmias associated with heart disease hypertension
Heart disease is classified as either congenital or acquired. Death may occur suddenly in patients with Eisenmenger syn-
Advances in the medical and surgical management of children drome, although symptomatic dysrhythmias generally occur
with congenital heart disease (CHD) have resulted in an increasing late in the natural history of the disease. Pregnancy is not toler-
number of affected females reaching childbearing age (see ated well (50% maternal mortality; > 40% fetal mortality), and
Chapter 1). From 1970 to 1983, CHD increased from 20% to 42% consideration may be given to first trimester termination of
as a cause of heart disease complicating pregnancy. A dysrhythmia pregnancy.
during pregnancy may be the presenting complaint that leads to a
diagnosis of previously unrecognized CHD. Women with uncor-
Surgically repaired Tetralogy of Fallot (TOF)
rected ASD may develop supraventricular dysrhythmias during
pregnancy. Dysrhythmias associated with CHD50,51 are outlined Important postoperative electrophysiologic sequelae, including
in Table 2.6 and those associated with acquired structural heart bradycardia, conduction system disease, heart block, ventricular
disease are outlined in Table 2.7. dysrhythmias, and sudden death, have been reported following



39
1 Cardiovascular and respiratory disorders


repair of TOF.50 Affected patients should be evaluated periodi-
Table 2.7 Dysrhythmias associated with structural cally for the presence of serious dysrhythmias.
heart disease in pregnancy

Aortic valve Ventricular dysrhythmias
Transposition of the great arteries
disease PVD (84%)
Most people with transposition of the great arteries (TGA) undergo
Multifocal PVD, couplets, runs of ventricular
surgical repair before reaching childbearing age. Although atrial
tachycardia (73%)
switch is rarely performed today except as part of a ˜˜double switch™™
Aortic stenosis " risk of severe hemodynamic
operation, there continues to be interest in pregnancy outcome in
problems with atrial fibrillation or junctional
Mustard and Senning repair survivors who are at risk from heart
rhythm (loss of atrial contraction)
block, ventricular dysrhythmias, and sudden death. In a large
Avoid volatile anesthetic-induced junctional
report from Holland looking at the risk of complications during
rhythms
pregnancy after a Mustard or Senning repair, there was a high
Supraventricular dysrhythmias with atrial
incidence of obstetric complications and mortality in the off-
dilation
spring.51 The most important cardiac complication was clinically
CHF þ dilated cardiomyopathy
significant dysrhythmia (22% of subjects) especially if there was
“ PVD (80%)
a prior history of dysrhythmia. Preterm delivery was common
“ Nonsustained ventricular tachycardia
and 22% of the offspring were small for gestational age. However,
(50%)
no recurrence of congenital heart disease was documented in the
“ Decreasing heart chamber size may
offspring.51
decrease atrial and ventricular dysrhythmias
IHSS Sudden death
Ventricular tachycardia
Tricuspid atresia, double-outlet right
Ischemic heart Ischemia/coronary vasospasm
ventricle, and single ventricle
disease Atrial dysrhythmias
Ventricular dysrhythmias The electrophysiologic sequelae of surgical repairs include AF,
Anti-ischemic therapy (nitroglycerin) may be sinus bradycardia, and complete AV block.50 In preconception
therapeutic and more efficacious than counselling, these women should know that dysrhythmias may
antidysrhythmics increase during pregnancy.
Mitral stenosis Atrial fibrillation
Decreased LV filling/cardiac output
Mitral valve prolapse (MVP)
Increased LAP & LA volume ! CHF
Thrombus formation atrial appendage
Mitral valve prolapse is usually benign. However, atrial and ven-
Mitral valve Atrial dysrhythmias (PSVT)
tricular dysrhythmias occur with greater frequency in women
prolapse Ventricular dysrhythmias
with MVP, especially if there are resting ST segment and T
Prolonged Q-T
wave abnormalities (see Table 2.8). Paroxysmal supraventricular
Avoid hypovolemia and vasodilatation
tachycardia involving AV nodal reentry or accessory AV connec-
(decrease LV size; " prolapse)
tions (see later) is the most common tachydysrhythmia. A very
Pericarditis Atrial dysrhythmias
small subset of patients with a diagnosis of MVP and LQTS
ECG changes:
may have a predisposition to VT, which can result, rarely, in
“ Low voltage QRS complexes
sudden death.
“ Electrical alternans
“ ST segment elevation (diffuse)
“ T wave inversion Dysrhythmias associated with cardiac
“ PR segment depression transplantation
Peripartum Dysrhythmias common
The transplanted heart is denervated (see Chapter 22). Although
cardiomyopathy ECG:
the transplanted heart shows an increased sensitivity to catecho-
“ Nonspecific ST-T changes
lamines, normal vagal tone and reflex activity are lacking.
“ Infarct pattern
Normal contractility is present, but chronotropic responses to
Avoid hyperkalemia (can exacerbate
stress and exercise are altered. The HR increase with exercise
dysrhythmias)
may be delayed and initial adaptation occurs as a result of the
PVD ¼ premature ventricular depolarization; CHF ¼ congestive heart Frank-Starling mechanism. The usual decrease in HR during
failure; IHSS ¼ idiopathic hypertrophic subaortic stenosis; LAP ¼ left recovery is attenuated. Dysrhythmias may result from the
atrial pressure; LA ¼ left atrial; PSVT ¼ paroxysmal supraventricular increased sensitivity to catecholamines or be a manifestation of
tachycardia
rejection. Only direct-acting agents will exert inotropic or chron-
otropic effects. Atropine should be used with caution and



40
Chapter 2



Table 2.8 Mitral valve prolapse in pregnancy

Associated conditions Clinical importance Course

Accessory AV connections (WPW syndrome Prolapse aggravated by hypovolemia and Benign
and variants) vasodilatation Progressive degeneration of mitral valve
ASD Atrial dysrhythmias (PSVT) Mitral regurgitation
Ebstein anomaly of tricuspid valve Ventricular dysrhythmias Complex dysrhythmias
Hypertrophic cardiomyopathy
Marfan syndrome
Ostium secundum
Long Q-T syndrome (" risk VT)

AV ¼ atrioventricular; WPW ¼ Wolff“Parkinson“White; ASD ¼ atrial septal defect; VT ¼ ventricular tachycardia; PSVT ¼ paroxysmal supraventricular
tachycardia




Preexcitation syndromes
appropriate monitoring; however, it is likely to be ineffective
because the transplanted heart lacks vagal innervation.
Definition
Paradoxical slowing and high-degree AV block have been
reported.12 Preexcitation results when an impulse, originating in the atrium,
activates (depolarizes) the ventricular myocardium (whole or in
part) earlier than expected. The clinical syndromes that accom-
Dysrhythmias associated with electrolyte pany short PR intervals and anomalous QRS complexes are
abnormalities shown in Table 2.9. Collectively they constitute the preexcitation
syndromes.52 The incidence of preexcitation in the normal popu-
Potassium
lation is 0.01% to 0.3%, but it occurs with increased frequency
Ventricular dysrhythmias may occur with serum potassium (Kþ)
in MVP 53 and Ebstein anomaly. In the majority of cases there is
levels < 3.0 mEq/l. Hypokalemia and hypomagnesemia may
no evidence of underlying heart disease. Ten percent of indivi-
attenuate the effects of antidysrhythmic drugs. The serum Kþ level
duals with recurrent PSVT have WPW syndrome.
should be kept > 4.0 mEq/l.

Magnesium
Pathophysiology
Low serum magnesium (Mg2þ) levels reduce sodium (Naþ)“
potassium (Kþ) pump activity. This results in increased Naþ/ Normally the atria become electrically isolated from the ventri-
calcium (Ca2þ) exchange, raises intracellular Ca2þ levels, and cles during fetal development. Incomplete separation leads to an
reduces intracellular Kþ concentrations. It is difficult to restore accessory AV pathway, which may be situated anywhere across
intracellular Kþ in the presence of low Mg2þ levels. Chronic Mg2þ the groove between the atria and ventricles. The most common
site is the left free wall of the heart, but other locations include
depletion may occur with diuretic and aminoglycoside therapy,
posteroseptal, right free wall and anteroseptal. In a minority,
alcohol abuse, secondary aldosteronism, and malabsorption
syndromes. Serum Mg2þ levels may not accurately reflect intra- there is more than one accessory pathway.20
cellular Mg2þ levels, especially in chronic depletion. Reduced To facilitate the most common form of AV reentrant tachy-
intracellular Mg2þ decreases extrusion of Ca2þ (via the calcium“ cardia it is only necessary for the accessory pathway to conduct
adenosine triphosphatase pump), resulting in increased Ca2þ in a retrograde direction, from ventricles to atria. Many indivi-
duals with AV reentrant tachycardia have an accessory AV path-
currents, which are dysrhythmogenic in triggered automaticity
way, which is only capable of ventriculoatrial conduction. In
models.
Clinical reports suggest that Mg2þ deficiency is linked with those with WPW syndrome, the pathway is also capable of
anterograde conduction, that is from atria to ventricles. Unlike
cardiac rhythm disturbances including PVD, supraventricular and
ventricular dysrhythmias, and Torsade de Pointes.43 Magnesium the AV node, the accessory connection does not delay conduc-
tion between atria and ventricles. During sinus rhythm, an
therapy reduces the incidence of supraventricular and ventricular
atrial impulse reaches the ventricles by both the accessory
dysrhythmias following MI and cardiac bypass surgery.
pathway and the AV node. The AV node conducts relatively
Magnesium is also beneficial in digitalis toxic dysrhythmias,
slowly. Initial ventricular activation is due to conduction via
Torsade de Pointes, and refractory ventricular dysrhythmias, even
when the serum Mg2þ level is within normal limits. Two grams the accessory pathway, resulting in a shortened PR interval
(ventricular preexcitation). Because the accessory pathway is
of magnesium sulfate i.v., given over two to three minutes, can

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