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trend? J. Invasive Cardiol. 2003; 15: 725“8. 175. Linter, S. P. & Clarke, K. Caesarean section under extradural analgesia in a
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nancy with coronary artery balloon angioplasty and stenting. Aust. N. Z. J. 176. Walker, E. & Malins, A. F. Anaesthetic management of aortic coarctation in
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ogy. Australas. Ann. Med. 1970; 19: 28“31. 181. Schabel, J. E. & Jasiewicz, R. C. Anesthetic management of a pregnant
153. Hands, M. E., Johnson, M. D., Saltzman, D. H. & Rutherford, J. D. The patient with congenitally corrected transposition of the great arteries for
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pulmonary circulations of pregnant anaesthetized women. Acta Obstet. labour and caesarean section in a parturient with a single ventricle and
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the adult patient with congenital heart disease. Anesthesiol. Clin. North 186. Wilton, N. C., Traber, K. B. & Deschner, L. S. Anaesthetic management for
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158. Mendelson, M. A. Congenital cardiac disease and pregnancy. Clin. Anaesth. 1989; 62: 434“8.
Perinatol. 1997; 24: 467“82. 187. Landau, R., Giraud, R., Morales, M. et al. Sequential combined spinal-
159. Deanfield, J., Thaulow, E., Warnes, C. et al. Management of grown up epidural anesthesia for cesarean section in a woman with a double-outlet
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160. Burn, J., Brennan, P., Little, J. et al. Recurrence risks in offspring of adults 188. Rowbottom, S. J., Gin, T. & Cheung, L. P. General anaesthesia for caesarean
with major heart defects: results from first cohort of British collaborative section in a patient with uncorrected complex cyanotic heart disease.
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161. Lovell, A. T. Anaesthetic implications of grown-up congenital heart dis- 189. Atanassoff, P. G., Schmid, E. R., Jenni, R. et al. Epidural anesthesia for a
ease. Br. J. Anaesth. 2004; 93: 129“39. cesarean section in a patient with pulmonary atresia and ventricular septal
162. Zuber, M., Gautschi, N., Oechslin, E. et al. Outcome of pregnancy in defect. J. Clin. Anesth. 1991; 3: 399“402.
women with congenital shunt lesions. Heart 1999; 81: 271“5. 190. Dob, D. P. & Yentis, S. M. UK registry of high-risk obstetric anaesthesia:
163. Yuh, D. & Reitz, B. Left-to-right shunt defects. In Reitz, B. & Yuh, D. (eds.), report on cardiorespiratory disease. Int. J. Obstet. Anesth. 2001; 10: 267“72.
Congenital Cardiac Surgery. San Francisco: McGraw-Hill, Inc., 2002. 191. Ransom, D. M. & Leicht, C. H. Continuous spinal analgesia with sufentanil
164. Bent, S. Anesthesia for left-to-right shunt lesions. In Andropoulos, D., for labor and delivery in a parturient with severe pulmonary stenosis.
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165. Chia, P., Raman, S. & Tham, S. W. The pregnancy outcome of acyanotic women with and without surgical treatment of congenital heart disease.
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167. Patton, D. E., Lee, W., Cotton, D. B. et al. Cyanotic maternal heart disease 194. Carp, H., Jayaram, A., Vadhera, R. et al. Epidural anesthesia for cesarean
in pregnancy. Obstet. Gynecol. Surv. 1990; 45: 594“600. delivery and vaginal birth after maternal Fontan repair: report of two
168. Burn, J. ˜The next lady has a heart defect™. Br. J. Obstet. Gynaecol. 1987; 94: cases. Anesth. Analg. 1994; 78: 1190“2.
97“9. 195. Cohen, A. M. & Mulvein, J. Obstetric anaesthetic management in a patient
169. Baum, V. C. The adult patient with congenital heart disease. J. with the Fontan circulation. Br. J. Anaesth. 1994; 73: 252“5.
Cardiothorac. Vasc. Anesth. 1996; 10: 261“82. 196. Grunwald, Z., Friedman, L., Hirsch, R. & Doron, K. Anesthetic manage-
170. Weiss, B. M. & Atanassoff, P. G. Cyanotic congenital heart disease and ment of labor and postpartum bleeding in a patient with Fontan physiol-
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Clin. Anesth. 1993; 5: 332“41. 197. Bonnin, M., Mercier, F. J., Sitbon, O. et al. Severe pulmonary hypertension
171. Veldtman, G. R., Connolly, H. M., Grogan, M. et al. Outcomes of preg- during pregnancy: mode of delivery and anesthetic management of 15
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174“80. 198. Blaise, G., Langleben, D. & Hubert, B. Pulmonary arterial hypertension:
172. Ramanathan, J., D™Alessio, J. G., Geller, E. et al. Analgesia and anesthesia pathophysiology and anesthetic approach. Anesthesiology 2003; 99:
during pregnancy. In Elkayam, U. & Gleicher, N. (eds.), Cardiac Problems 1415“32.
in Pregnancy. Wiley-Liss, Inc., 1998. 199. Penning, S., Robinson, K. D., Major, C. A. & Garite, T. J. A comparison of
173. Halpern, S., Gidwaney, A. & Gates, B. Anaesthesia for caesarean section in echocardiography and pulmonary artery catheterization for evaluation of
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Chapter 1


200. Jones, A. M. & Howitt, G. Eisenmenger syndrome in pregnancy. Br. Med. J. 207. Martin, J. T., Tautz, T. J. & Antognini, J. F. Safety of regional anes-
1965; 5451: 1627“31. thesia in Eisenmenger™s syndrome. Reg. Anesth. Pain Med. 2002; 27:
201. Avila, W. S., Grinberg, M., Snitcowsky, R. et al. Maternal and fetal outcome 509“13.
in pregnant women with Eisenmenger™s syndrome. Eur. Heart. J. 1995; 16: 208. Ghai, B., Mohan, V., Khetarpal, M. & Malhotra, N. Epidural anesthesia for
460“4. cesarean section in a patient with Eisenmenger™s syndrome. Int. J. Obstet.
202. Yentis, S. M., Steer, P. J. & Plaat, F. Eisenmenger™s syndrome in pregnancy: Anesth. 2002; 11: 44“7.
maternal and fetal mortality in the 1990s. Br. J. Obstet. Gynaecol. 1998; 105: 209. Spinnato, J. A., Kraynack, B. J. & Cooper, M. W. Eisenmenger™s syndrome in
921“2. pregnancy: epidural anesthesia for elective cesarean section. N. Engl. J.
203. Geohas, C. & McLaughlin, V. V. Successful management of pregnancy in a Med. 1981; 304: 1215“17.
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1170“3. a case report. Anesth. Analg. 1974; 53: 965“8.
204. Goodwin, T. M., Gherman, R. B., Hameed, A. & Elkayam, U. Favorable 211. Cole, P. J., Cross, M. H. & Dresner, M. Incremental spinal anaesthesia for
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205. Lacassie, H. J., Germain, A. M., Valdes, G. et al. Management of 212. Filipovic, M., Seeberger, M. D., Schneider, M. C. et al. Transthoracic echo-
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Obstet. Gynecol. 2004; 103: 1118“20. 2000; 84: 800“3.
206. Smedstad, K. G., Cramb, R. & Morison, D. H. Pulmonary hypertension and 213. Warnes, C. A. Pregnancy and pulmonary hypertension. Int. J. Cardiol.
pregnancy: a series of eight cases. Can. J. Anaesth. 1994; 41: 502“12. 2004; 97: 11“13.




27
DISORDERS OF CARDIAC CONDUCTION
2
Jean E. Swenerton, Ravishankar Agaram, and Victor F. Huckell




Introduction autonomic tone, and hormonal fluxes.6,7 Cardiac dysrhythmias
are more common in parturients with structural cardiac defects
Disorders of cardiac conduction seen in pregnancy are those
(e.g. atrial (ASD) and ventricular septal defects (VSD)), or with
involving abnormal impulse generation or propagation (supra-
abnormal conduction pathways. These dysrhythmias may occur
ventricular, ventricular dysrhythmias, heart blocks) and specific
for the first time or be exacerbated by the cardiovascular changes
conduction disorders (preexcitation syndromes, long QT syn-
of pregnancy. Long QT syndrome (LQTS), more common in
drome). The clinical implications and current management
young women compared to the general population, may be asso-
of some familiar disorders of conduction during pregnancy are
ciated with ventricular dysrhythmias. Right ventricular (RV) out-
discussed but there is an emphasis on the more uncommon
flow tract dysrhythmias7 and supraventricular tachycardias (SVT)
disorders of cardiac conduction.
with reentry are more common in women,8,9 and may occur
during pregnancy. Other causes of cardiac dysrhythmias during
Physiologic heart rate and rhythm changes pregnancy include electrolyte imbalance (hypokalemia, hyperka-
in pregnancy (see Table 2.1) lemia), drug interactions (anesthetic drugs, antidysrhythmic
drugs, cocaine), and hypo- or hyperthyroidism.
In conjunction with the antepartum rise in blood volume, resting
Premature ectopic atrial and ventricular depolarizations (PAD,
heart rate (HR) increases steadily by 10“15% throughout preg-
PVD) and sinus tachycardia are the most common dysrhythmias
nancy, reaching a peak of 10 to 20 beats above baseline during
during pregnancy. Premature atrial beats, generally benign and
the third trimester. During labor and delivery, sinus tachycardia
well tolerated, occur in approximately 50% of women.
is seen, with maximal HR occurring peripartum.1 Parturients with
Palpitations, dizziness or light-headedness, dyspnea, presyn-
more labor pain may have higher sympathetic tone and higher
cope and syncope, and chest pain are presenting complaints of a
peripartum HR.
cardiac dysrhythmia (in descending order of frequency). Shotan
Electrocardiogram (EKG) changes during pregnancy include
et al.5 compared the incidence of dysrhythmias in 110 pregnant
shift of QRS axis in any direction, the appearance of small q
women without structural heart disease who had palpitations,
waves in Lead III, T wave inversion and, commonly, ST-T changes.
dizziness, or syncope with 54 pregnant women with an asympto-
ST segment depression, coinciding with maximal HR and usually
matic functional precordial murmur. Both groups had a high
asymptomatic, has been reported during nonoperative and opera-
incidence of dysrhythmias on Holter monitoring (PAD in 56%
tive deliveries. ST changes may result from tachycardia, hormonal
of symptomatic women vs. 58% of asymptomatic women).
milieu, heart position changes, venous air emboli, hypokalemia,
Simple and multifocal PVD were higher in symptomatic women.
and hyperventilation.2 It is unclear whether the sympathectomy
There was no correlation between symptoms and the incidence
produced by regional anesthesia affects the ECG but both ST seg-
of dysrhythmias (only 10% of symptomatic episodes had a dys-
ment depression (> 1 mm) and ST elevation have been reported
rhythmia). Six weeks™ postpartum, there was significant decrease
during cesarean section (C/S).2 The clinical significance of ST
in the incidence of dysrhythmia in nine parturients with docu-
changes remains uncertain. An uncomplicated nonQ wave ante-
mented multiple premature beats,5 consistent with reports of an
rolateral myocardial infarction (MI) was reported in a primigravida
increased propensity for tachydysrhythmias during pregnancy.
receiving ritodrine and nifedipine for preterm labor at 28 weeks™
Although dyspnea severe enough to limit activity and syncope
gestation.3 Coronary angiography was normal two days later
with exertion may be normal during pregnancy, these symptoms
and she had an uncomplicated spontaneous vaginal delivery at
warrant careful evaluation.
40 weeks™ gestation.
During labor and delivery, nearly all parturients have some
form of dysrhythmia10 (see Table 2.2), which usually has no
Dysrhythmias during pregnancy hemodynamic consequences and rarely requires treatment.
Hemodynamically significant dysrhythmias are uncommon
There may be an increased propensity for tachydysrhythmias
(mainly supraventricular) during pregnancy.4,5 As the circulation and life-threatening dysrhythmias during pregnancy and labor
are rare.
becomes more hyperdynamic some women become more aware
As the fetus is vulnerable to the effects of maternal dysrhy-
of the heart beat, changes in HR, and skipped beats. Proposed
thmias and their treatment, fetal well-being is a vital considera-
mechanisms for pregnancy-induced dysrhythmias include
tion in the decision to treat a dysrhythmia and in the choice of
changes in cardiac ion channel conduction, increase in cardiac
treatment.
size (atrial stretch, increased end-diastolic volume), changes in


Obstetric Anesthesia and Uncommon Disorders, eds. David R. Gambling, M. Joanne Douglas and Robert S. F. McKay. Published by Cambridge University Press.
# Cambridge University Press 2008.
1 Cardiovascular and respiratory disorders


preexisting dysrhythmia on established drug therapy. In both
Table 2.1 Physiological cardiovascular changes of pregnancy cases, knowledge of the dysrhythmia, antidysrhythmic drugs,
and other methods used to treat dysrhythmias is needed to for-
Cardiac Begins early pregnancy
mulate a safe anesthetic plan. A cardiologist should be consulted
" 2nd and 3rd trimesters
output
as early as possible; however, this is not always possible.
Interindividual variability a
In the acute situation, assess the woman while supporting her
Further " during labor and delivery b
airway and breathing, administering oxygen, obtaining a 12-lead
" steadily through pregnancy
Heart rate
ECG to identify the rhythm, and monitoring blood pressure (BP)
Peak 10“20 bpm above baseline 3rd trimester
and oxygen saturation. In general, dysrhythmias in parturients
" with pain and stress
can be assessed by asking the following questions:
Rhythm PAD and PVD common
 Is the woman hemodynamically stable?
ECG Shift of QRS axis in any direction
 Is fetal well-being compromised?
Small rightward deviation of average mean QRS axis
 Are there any causative or potentiating factors?
(1st trimester)
 Is the dysrhythmia likely to progress into a more dangerous
Small leftward deviation due to progressive elevation
dysrhythmia?
of left hemidiaphragm (3rd trimester)
 Is treatment required immediately?
Lead III: small Q-T wave inversion
 Is treatment appropriate in pregnancy and will it affect the fetus?
Transient ST-T changes common
General principles of management (see Figure 2.1)
a
See text 1. When there is no identifiable precipitating factor, no under-
b
Depends on physiological changes, blood loss, stress of delivery lying heart disease, and no hemodynamic compromise, reas-
PAD ¼ premature atrial depolarizations; PVD ¼ premature ventricular surance may be appropriate.
depolarizations; bpm ¼ beats per minute 2. Successful management may require identification and elim-
ination of precipitating factors only.
3. Clinically significant dysrhythmias requiring treatment most
Table 2.2 Dysrhythmias recorded during labor among often occur in those who have underlying structural heart
30 women8 disease and/or a history of preexisting dysrhythmia. In the
absence of clinically overt cardiac disease, the dysrhythmia
no. (%)
may be the initial manifestation of a congenital or acquired
Sinus node dysfunction structural heart abnormality (see Chapter 1).
tachycardia 30 (100) 4. Identification and evaluation of underlying heart disease and
bradycardia 15 (50) choice of appropriate treatment are critical for a normal
Supraventricular dysrhythmia maternal and fetal outcome.
isolated PAD 27 (90) 5. If there is hemodynamic compromise, a sustained dysrhyth-
nonconducted P waves 4 (13) mia, or one predisposing to a ventricular dysrhythmia, immedi-
ectopic atrial tachycardia 3 (10) ate synchronized cardioversion is indicated. Serious signs and
wandering atrial pacemaker 2 (7) symptoms are uncommon if the ventricular rate is < 150 bpm
sinus pause 1 (3) (beats per minute) in women with healthy hearts. If impaired
retrograde P waves 1 (3) cardiac function or significant comorbid conditions are pre-
AV junctional dysrhythmia sent, symptoms may occur at lower HRs. Definitive and pro-
accelerated idioventricular rhythm 1 (3) phylactic treatment in the form of drug therapy, cardioversion,
Ventricular dysrhythmia or pacemaker therapy (temporary or permanent) is required
isolated PVD 15 (50) while monitoring the mother and fetus. Oxygen and left uterine
multifocal PVD 5 (17) displacement should be ensured.
couplet 2 (7) 6. Diagnosing and treating serious dysrhythmias promptly and
aberrant intraventricular block 3 (10) appropriately minimizes the risk of embolic events.
AV block 7. Avoid myocardial ischemia and electrolyte imbalance in
first degree 1 (3) women susceptible to dysrhythmias.
second degree, type I 1 (3)

Cardiac assessment of conduction disorders
PAD ¼ premature atrial depolarizations; PVD ¼ premature ventricular
during pregnancy
depolarizations; AV ¼ atrioventricular

Cardiology consultation11 is requested frequently when a preg-
nant woman has palpitations of uncertain etiology or signifi-
Diagnosis and management of dysrhythmias
cance, or a specific conduction disorder.
Noninvasive diagnostic investigations (ECG, Holter event moni-
A parturient may present with a new acute dysrhythmia during
tor, echocardiogram) are preferred over radiographic studies,
labor where urgent diagnosis and treatment is required, or with a



30
Chapter 2


DYSRHYTHMIA


Precipitating factor(s)?


• Anxiety • Drug (therapeutic/abuse)
• Alcohol • Electrolyte abnormalities
• Caffeine • Endocrine/metabolic abnormalities
• Cigarettes • Pulmonary disease



NO Structural heart disease? YES
Fewer implications Important
implications



Diagnosis

• History
• Physical examination
• ECG/Holter monitoring
• Echo
• Chest x-ray
• Electrophysiologic testing
• Cardiac catheterization




Hemodynamic compromise?
Dysrhythmia sustained?
NO YES
Dysrhythmia predisposing to
ventricular dysrhythmia?




• Treat underlying disease/problem
• Definitive/prophylactic treatment
• Reassure • Follow appropriate algorithm
• Do not treat
• DRUG
• Proven safety record/“safest drug”
• Smallest effective dose
• Periodic assessment

• CARDIOVERSION

• PACEMAKER

• ELECTRICAL/SURGICAL ABLATION


Figure 2.1 Management of dysrhythmias during pregnancy.


cardiac catheterization, and electrophysiologic investigations in risk of childhood malignancy, particularly leukemia. Serial echo-
order to avoid ionizing radiation exposure, procedure-induced cardiographic assessments are useful with minimal maternal and
dysrhythmias, and/or hemodynamic compromise. Some radio- fetal risk (see Table 2.3). Chest radiographs are not ordered rout-
graphic procedures, especially in the first eight weeks of preg- inely but, if required, appropriate pelvic shielding keeps fetal radia-
nancy, may cause abnormal fetal organogenesis and increased tion below minimally acceptable levels. When necessary, right



31
1 Cardiovascular and respiratory disorders


the atria or atrioventricular junction. It rarely requires
Table 2.3 Noninvasive echocardiography assessment treatment.
during pregnancy 4. Sinus node dysfunction/sick sinus syndrome (SSS) incorpor-
ates a range of abnormalities of sinus node impulse forma-
Two-dimensional Evaluation of LA dilation or thrombus
tion and conduction including sinus bradycardia, sinus arrest,
echocardiography
sinus exit block, sinoatrial and atrioventricular conduction
Doppler Transmitral gradients
disorders, paroxysms of alternating rapid, regular, or irregular
echocardiography Mitral valve areas
atrial tachydysrhythmias with bradydysrhythmias. Although
Using atrioventricular pressure gradient
more usual in the elderly, SSS may occur in patients under
half-time
age 30.13 The incidence of SSS during pregnancy is unknown.
Two-dimensional exam technically
Treatment depends on the dysrhythmia. Permanent pacing
inadequate
may be necessary for bradydysrhythmias, and drug therapy
Previous commissurotomy
may be required for tachydysrhythmias. Schatz and colleagues
Densely calcified leaflets
described a primigravida with Ebstein anomaly who had a
Intracardiac pressures (RV and PAP)
severe bradycardia-junctional tachycardia syndrome requir-
if tricuspid regurgitation
ing multiple drug treatments and temporary transvenous
Transesophageal Visualization of thrombi (usually in
pacing during delivery.14 Mendelson described a 32-year-old
echocardiography LA appendage)
woman who had occasional syncope associated with sinus exit
LA ¼ left atrium; RV ¼ right ventricle; PAP ¼ pulmonary artery pressure block. Pregnancy did not affect the frequency of syncopal
episodes and no therapy was required. She had three normal
term deliveries.15

heart catheterization can be performed without fluoroscopy, using
a flow-directed catheter. Nuclear studies have little place in preg- Atrioventricular (AV) blocks
nant women.
Atrioventricular blocks, (first-, second-, third-degree), may be
caused by medications, electrolyte abnormalities, or structural
problems such as those resulting from acute MI and
Sinus node dysrhythmias

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