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an increased risk to the mother and fetus. Women with preexisting
deaths. One report described the use of an ICD in a woman with
cardiac rhythm disorders are likely to have an exacerbation
ARVC at 21 weeks™ gestation. This life-preserving treatment
of dysrhythmia during pregnancy, which increases the risk
was associated with a normal remainder of the pregnancy and
of adverse fetal complications.35 Women with congenital heart
an uneventful forceps delivery.101 Another case described the
disease, especially those with subpulmonary ventricular systolic
successful use of an epidural anesthetic for labor and C/S in a
woman with ARVC and indwelling ICD.103 dysfunction and/or severe pulmonary regurgitation, may develop
sustained dysrhythmias during pregnancy (3% risk in one study).32
The treatment of the pregnant patient with cardiac dysrhyth-
Postural orthostatic tachycardia
mias may require important modifications of standard dysrhyth-
syndrome (POTS)
mia management. The goal is to protect the mother and her fetus
through delivery, after which chronic or definitive therapy can be
Postural orthostatic tachycardia syndrome encompasses a group
administered.106 New advances, such as ICD, allow immediate
of disorders characterized by orthostatic intolerance. In one case
treatment of dangerous heart rhythms, and fetal magnetocardio-
a parturient had worsening symptoms during pregnancy, which
graphy is a valuable new tool for rhythm diagnosis and for mon-
were managed by increasing the dose of beta-blockers. A labor
itoring maternal and fetal rhythms during therapy.107
epidural was used successfully and optimal postpartum analgesia
was ensured by using neuraxial opioids, NSAIDs, and bilateral
iliohypogastric and ilioinguinal nerve blocks. The aim was to REFERENCES
reduce the risk of triggering a tachycardic response to the stress
1. Palmer, C. M. Maternal electrocardiographic changes in the peripartum per-
of labor and pain.104 iod. Int. J. Obstet. Anesth. 1994; 3: 63“6.
2. Burton, A. & Camann, W. Electrocardiographic changes during cesarean
section: a review. Int. J. Obstet. Anesth. 1996; 5: 47“53.
Cardiopulmonary resuscitation of the parturient
3. Verhaert D. & Van Acker, R. Acute myocardial infarction during pregnancy.
Acta Cardiol. 2004; 59: 331“9.
This topic is well covered in ACLS protocols as a separate sec-
4. Bhanddari, A. & Isher, N. Cardiac arrhythmias and pregnancy. In Gleicher,
tion.105 The standard algorithms are applicable to the pregnant
N. (ed), Principles and Practice of Medical Therapy in Pregnancy, 3rd edn.
woman, including the use of defibrillation. However, because of New York: McGraw-Hill, 1998.
the physiological changes of pregnancy there are some important 5. Shotan, A., Ostrzega, E., Mehra, A., Johnson, J. & Elkayam, U. Incidence of
principles to remember. arrhythmias in normal pregnancy and relation to palpitations, dizziness
and syncope. Am. J. Cardiol. 1997; 79: 1061“4.
 The parturient will undergo oxygen desaturation more rapidly
6. Berlinbrau, R., Yessian, A., Lichstein, E. et al. Maternal arrhythmias of
so supplemental oxygen is required.
normal labor and delivery. Gynecol. Obstet. Inv. 2001; 52: 128“31.
 Successful resuscitation of the mother usually results in a better 7. Marchlinski, F. E., Deely, M. P. & Zado, E. S. Sex-specific triggers
outcome for the fetus. for right ventricular outflow tract tachycardia. Am. Heart J. 2000; 139:
 There is a higher risk of pulmonary aspiration of gastric con- 1009“13.
8. Rodriguez, L-M. & Chillou, C. D. Age at onset and gender of patients with
tents, so the maternal airway should be protected early with
different types of supraventricular tachycardia. Am. J. Cardiol. 1992; 70:
an endotracheal tube. As airway edema is common in the
pregnant woman a smaller endotracheal tube may be required. 9. Nakagawa, M., Katou, S., Ichinose, M. et al. Characteristics of new-onset
 Chest compressions should be performed higher on the ster- ventricular arrhythmias in pregnancy. J. Electrocardiol. 2004; 37: 47“53.
num as the gravid uterus will displace the diaphragm higher 10. Romem, A., Romem, Y., Katz, M. & Battler, A. Incidence and characteristics
of maternal cardiac arrhythmias during labor. Am. J. Cardiol. 2004; 93:
in the chest.
 After 20 weeks™ gestation, the uterus becomes an abdominal
11. Blomstrom-Lundqvist, C., Scheinman, M. M., Aliot, E. M. et al. ACC/AHA/
organ. As such it can compress the aorta and vena cava inhibiting ESC guidelines for the management of patients with supraventricular
venous return to the heart. This will affect cardiac output limiting arrhythmias “ executive summary: a report of the American College of
the ability to resuscitate the pregnant female. Therefore left uter- Cardiology/American Heart Association Task Force on Practice
Guidelines, and the European Society of Cardiology Committee for
ine displacement should be provided by a wedge under the right
Practice Guidelines. J. Am. Coll. Cardiol. 2003; 42: 1493“531.
hip or by manually displacing the uterus to the woman™s left.
12. ECC Committee, Subcommittees and Task Forces of the American Heart
 If resuscitative efforts are not successful after four minutes the Association. 2005 American Heart Association Guidelines for
fetus should be delivered by C/S in order to relieve aortocaval Cardiopulmonary Resuscitation and Emergency Cardiac Care. Management
compression. This may allow successful maternal resuscitation. of Symptomatic Bradycardia and Tachycardia. Circulation 2005; 112: IV-68.

1 Cardiovascular and respiratory disorders

13. Dauchot, P. & Gravenstein, J. S. Effects of atropine on the ECG in different 39. Chandra, N. C., Gates, E. A. & Thamer, M. Conservative treatment of parox-
age groups. Clin. Pharmacol. Ther. 1971; 12: 272“80. ysmal ventricular tachycardia during pregnancy. Clin. Cardiol. 1991; 14:
14. Schatz, J. W., Fischer, J. A., Lee, R. F. & Lampe, R. M. Pacemaker therapy in 347“50.
pregnancy for management of sinus-bradycardia-junctional tachycardia 40. Field, L. M. & Barton, F. L. The management of anaesthesia for caesarean
syndrome. Chest 1974; 65: 461“3. section in a patient with paroxysmal ventricular tachycardia. Anaesthesia
15. Mendelson, C. L. Disorder of the heartbeat during pregnancy. Am. J. Obstet. 1993; 48: 593“5.
Gynecol. 1956; 72: 1268“301. 41. Navarro, V., Nathan, P. E., Rosero, H. & Sacchi, T. J. Accelerated idioventri-
16. Sobotka, P. A., Mayer, J. H., Bauernfeind, R. A., Kankis, C. & Rosen, K. cular rhythm in pregnancy: a case report. Angiology 1993; 44: 506“8.
Arrhythmias documented in 24 hour continuous electrocardiographic 42. Varon, M. E., Sherer, D. M., Abramowicz, J. S. & Akiyama, T. Maternal ven-
monitoring in young women without apparent heart disease. Am. Heart J. tricular tachycardia associated with hypomagnesemia. Am. J. Obstet.
1981; 101: 753“9. Gynecol. 1992; 167: 1352“5.
17. Ho, S. Y., Esscher, E., Anderson, R. H. & Michaelsson, M. Anatomy of con- 43. Onagawa, T., Ohkuchi, A., Ohki, R. et al. Woman with postpartum ventri-
genital complete heart block and relation to maternal anti-Ro antibodies. cular tachycardia and hypomagnesemia. J. Obstet. Gynaecol. Res. 2003; 29:
Am. J. Cardiol. 1986; 58: 291“4. 92“5.
18. Dalvi, B. V., Chaudhuri, A., Kulkarni, H. L. & Kale, P. A. Therapeutic guide- 44. Iseri, L. T., Chung, P. & Tobis, J. Magnesium therapy for intractable ventri-
lines for congenital complete heart block presenting in pregnancy. Obstet. cular tachyarrhythmias in normomagnesemic patients. West. J. Med. 1983;
Gynecol. 1992; 79: 802“4. 138: 823“8.
19. Mendelson, M. A. & Lang, R. M. Pregnancy and heart disease. In Barron, 45. Chan, T. M. L. C. & Dob, D. P. The anesthetic management of a parturient
W. H. & Lindheimer, M. D. (eds.), Medical Disorders During Pregnancy. with polymorphic catecholamine-sensitive ventricular tachycardia. Int. J.
St. Louis: Mosby, 1995. Obstet. Anesth. 2002; 11: 122“4.
20. Bennett, D. H. Cardiac Arrhythmias “ Practical Notes on Interpretation and 46. Surawicz, B. Prognosis of ventricular arrhythmia in relation to sudden car-
Treatment, 6th edn. London: Arnold, 2002 (ISBN 0340 80731 8). diac death: therapeutic implications. J. Am. Coll. Cardiol. 1987; 10: 435“47.
21. Rotmensch, H. H., Rotmensch, S. & Elkayam, U. Management of cardiac 47. Prystowsky, E. N. Antiarrhythmic therapy for asymptomatic ventricular
arrhythmias during pregnancy. Current concepts. Drugs 1987; 33: 623“33. arrhythmias. Am. J. Cardiol. 1988; 61: 102A.
22. Meller, J. & Goldman, M. E. Cardiovascular disease in pregnancy, In Cherry, 48. Rally, C. R. & Walters, M. B. Paroxysmal ventricular tachycardia without
S. H. & Merkatz, I. R. (eds.), Complications of Pregnancy: Medical, Surgical, evident heart disease. Can. Med. Assoc. J. 1962; 86: 268“73.
Gynecologic, Psychosocial and Perinatal, 5th edn. Philadelphia: Lippincott, 49. Shah, D. M. & Sunderji, S. G. Hypertrophic cardiomyopathy and pregnancy:
Williams & Wilkins, 2000. report of a maternal mortality and review of literature. Obstet. Gynecol.
23. Szekely, P. & Snaith, L. Paroxysmal tachycardia in pregnancy. Br. Heart J. Surv. 1985; 40: 444“8.
1953; 15: 195“8. 50. Vetter, V. L. & Horowitz, L. N. Electrophysiologic residua and sequelae of
24. Kjer, J. J. & Pedersen, K. H. Persistent supraventricular tachycardia follow- surgery for congenital heart defects. Am. J. Cardiol. 1982; 50: 588“604.
ing infusion with ritodrine hydrochloride. Acta Obstet. Gynecol. Scand. 1982; 51. Drenthen, W., Pieper, P. G., Ploeg, M. et al. Risk of complications during
61: 281“2. pregnancy after Senning or Mustard (atrial) repair of complete transposi-
25. Cummins, R. O. (ed). Textbook of Advanced Cardiac Life Support. Dallas, TX: tion of the great arteries. Eur. Heart J. 2005; 26: 2588“95.
American Heart Association, 1994. 52. Gallagher, J. J., Pritchett, E. L., Sealy, W. C., Kasell, J. & Wallace, A. G. The
26. Lim, S. H., Ananatharaman, V., Teo, W. S., Goh, P. P. & Tan, A. T. Comparison preexcitation syndromes. Prog. Cardiovasc. Dis. 1978; 20: 285“327.
of treatment of supraventricular tachycardia by Valsalva maneuver and 53. Cowles, T. & Gonik, B. Mitral valve prolapse in pregnancy. Sem. Perinatol.
carotid sinus massage. Ann. Emerg. Med. 1998; 31: 30“5. 1990; 14: 34“41.
27. Cybulski, J., Kulakowski, P., Makowska, E. et al. Intravenous amiodarone is 54. Widerhorn, J., Widerhorn, A. L. M., Rahimtoola, S. H. & Elkayam, U. WPW
safe and seems to be effective in termination of paroxysmal supraventri- syndrome during pregnancy: increased incidence of supraventricular
cular tachyarrhythmias. Clin. Cardiol. 1996; 19: 563“6. arrhythmias. Am. Heart J. 1992; 123: 796“8.
28. Mariani, P. J. Pharmacotherapy of pregnancy-related SVT (letter). Ann. 55. Kanjwal, Y., Kosinski, D., Kanj, M., Thomas, W. & Grubb, B. Successful
Emerg. Med. 1992; 21: 229. radiofrequency catheter ablation of left lateral accessory pathway using
29. Mason, B. A., Ricci-Goodman, J. & Koos, B. J. Adenosine in the treatment of transseptal approach during pregnancy. J. Interv. Card. Electrophysiol.
maternal paroxysmal supraventricular tachycardia. Obstet. Gynecol. 1992; 2005; 13: 239“42.
80: 478“80. 56. Klepper, I. Cardioversion in late pregnancy. The anaesthetic management
30. Brown, C. E. & Wendel, G. D. Cardiac arrhythmias during pregnancy. Clin. of a case of Wolff-Parkinson-White syndrome. Anaesthesia 1981; 36: 611“16.
Obstet. Gynecol. 1989; 32: 89“102. 57. Afridi, I., Moise, K. J., Jr. & Rokey, R. Termination of supraventricular tachy-
31. Hidaka, N., Chiba, Y., Kurita, T., Satoh, S. & Nakano, H. Is intrapartum cardia with intravenous adenosine in a pregnant woman with Wolff-
temporary pacing required for women with complete atrioventricular Parkinson-White syndrome. Obstet. Gynecol. 1991; 80: 481“3.
block ? An analysis of seven cases. BJOG 2006; 113: 605“7. 58. Robinson, J. E., Morin, V. I., Douglas, M. J. & Wilson, R. D. Familial hypoka-
32. Khairy, P., Ouyang, D. W., Fernandes, S. M. et al. Pregnancy outcomes in lemic periodic paralysis and Wolff-Parkinson-White syndrome in preg-
women with congenital heart disease. Circulation 2006; 113: 517“24. nancy. Can. J. Anesth. 2000; 47: 160“4.
33. Cosio, F. G. Atrial flutter update. Cardiac Electrophysiology Review 2002; 59. Peters, R. W. & Gold, M. R. The influence of gender on arrhythmias.
6: 356“64. Cardiology in Review 2004; 12: 97“105.
34. Kannel, W. B., Abbott, R. D., Savage, D. D. & McNamara, P. M. 60. Locati, E. H., Zareba, W., Moss, A. J. et al. Age and sex-related differences in
Epidemiologic features of chronic atrial fibrillation: the Framingham clinical manifestations in patients with congenital long-QT syndrome.
study. N. Engl. J. Med. 1982; 306: 1018“22. Circulation 1998; 97: 2237“44.
35. Silversides, C. K., Harris, L., Haberer, K. et al. Recurrence rates of arrhyth- 61. Ackerman, M. J. The long QT syndrome: ion channel diseases of the heart.
mias during pregnancy in women with previous tachyarrhythmia and Mayo Clin. Proc. 1998; 73: 250“69.
impact on fetal and neonatal outcomes. Am. J. Cardiol. 2006; 97: 1206“12. 62. Daley, S. M., Tranebjaerg, L., Samson, R. A. & Green, G. E. Jervell and Lange-
36. Khan, I. A., Nair, C. K., Singh, N., Gowda, R. M. & Nair, R. C. Acute ventricular Nielsen syndrome. Gene Reviews. (last update 29 July
rate control in atrial fibrillation and atrial flutter. Int. J. Cardiol. 2004; 97: 7“13. 2004).
37. Braverman, A. C., Bromley, B. S. & Rutherford, J. D. New onset ventricular 63. Vincent, G. M. Romano-Ward Syndrome. Gene Reviews.
tachycardia during pregnancy. Int. J. Cardiol. 1991; 33: 409“12. (last update 7 July 2005).
38. Brodsky, M., Doria, R., Allen, B. et al. New-onset ventricular tachycardia 64. Al-Refai, A., Gunka, V. & Douglas, J. Spinal anesthesia for cesarean section
during pregnancy. Am. Heart J. 1992; 123: 933“41. in a parturient with long QT syndrome. Can. J. Anesth. 2004; 51, 10: 993“6.

Chapter 2

65. Booker, P. D., Whyte, S. D. & Ladusans, E. J. Long QT syndrome and 86. Lau, C. P., Lee, C. P., Wong, C. K., Cheng, C. H. & Leung, W. H. Rate respon-
anesthesia. Br. J. Anaesth. 2003; 90: 349“66. sive pacing with a minute ventilation sensing pacemaker during preg-
66. Bhandari, A. K., Nguyen, P. T. & Scheinman, M. M. Congenital and acquired nancy and delivery. Pacing Clin. Electrophysiol. 1990; 13: 158“63.
long QT syndromes. In Chatterjee, K., Chemlin, M. D., Karliner, J., Parmley, 87. Matorras, R., Diez, J., Saez, M. & Montoya, F. Repeat pregnancy associated
W. W., Rapaport, E., Scheinman, M. (eds.), Cardiology an Illustrated Text/ with cardiac pacemaker. Int. J. Gynecol. Obstet. 1991; 36: 323“7.
Reference, Vol. I, Philadelphia: J.P. Lippincott Co, 1991. 88. Jaffe, R., Gruber, A., Fejgin, M., Altaras, M. & Ben-Aderet, N. Pregnancy
67. Molnar, J., Zhang, F., Weiss, J., Ehlert, F. S. & Rosenthal, J. E. Diurnal pattern with an artificial pacemaker. Obstet. Gynecol. Surv. 1987: 42: 137“9.
of QTc interval: how long is prolonged? Possible relation to circadian 89. Terhaar, M. & Schakenbach, L. Care of the pregnant patient with a pace-
triggers of cardiovascular events. J. Am. Coll. Cardiol. 1996; 27: 76“83. maker. J. Perinat. Neonatal Nurs. 1991; 5: 1“12.
68. Jervell, A. & Lange-Nielsen, F. Congenital deaf-mutism, functional heart 90. Exner, D. V., Muzyka, T. & Gillis, A. M. Proarrhythmia in patients with the
disease with prolongation of the QT interval and sudden death. Am. Heart J. Wolff-Parkinson-White syndrome after standard doses of intravenous
1957; 54: 59“68. adenosine. Ann. Intern. Med. 1995; 122: 351“2.
69. Ratshin, R. A., Hunt, D., Russell, R. O., Jr. & Rackley, C. E. QT-interval pro- 91. Strickberger, S. A., Man, K. C., Daoud, E. G. et al. Proarrhythmic effects of
longation, paroxysmal ventricular arrhythmias, and convulsive syncope. adenosine: a review of the literature. Emerg. Med. J. 2004; 21: 408“10.
Ann. Int. Med. 1971; 75: 919“24. 92. Camm, A. J. & Garratt, C. J. Adenosine and supraventricular tachycardia. N.
70. Schwartz, P. J. Idiopathic long QT syndrome: progress and questions. Am. Engl. J. Med. 1991; 325: 1621“9.
Heart J. 1985; 109: 399“411. 93. Lerman, B. B. & Belardinelli, L. Cardiac electrophysiology of adenosine.
71. Moss, A. J., Zareba, W., Hall, W. J. et al. Effectiveness and limitations of Basic and clinical concepts. Circulation 1991; 83: 1499“509.
b-blocker therapy in congenital long-QT syndrome. Circulation 2000; 101: 94. Gowda, R. M., Khan, I. A., Mehta, N. J., Vasavada, B. C. & Sacchi, T. J.
616“23. Cardiac arrhythmias in pregnancy: clinical and therapeutic considera-
72. Wilde, A. A. Is there a role for implantable cardioverter defibrillators in long tions. Int. J. Cardiol. 2003; 88: 129“33.
QT syndrome? J. Cardiovasc. Electrophysiol. 2002; 13: S110“3. 95. Podolsky, S. M. & Varon, J. Adenosine use during pregnancy. Ann. Emerg.
73. M¨ nnig, G., K¨ be, J., L¨ her, A. et al. Implantable cardioverter-defibrillator
o o o Med. 1991; 20: 1027“8.
therapy in patients with congenital long-QT syndrome: a long-term follow- 96. Harrison, J. K., Greenfield, R. A. & Wharton, J. M. Acute termination
up. Heart Rhythm 2005; 2: 497“504. of supraventricular tachycardia by adenosine during pregnancy.
74. Freshwater, J. V. Anaesthesia for caesarean section and the Jervell, Lange- Am. Heart J. 1992; 123: 1386“8.
Nielson syndrome (prolonged Q-T interval syndrome). Br. J. Anaesth. 1984; 97. Leffler S. & Johnson, D. R. Adenosine use in pregnancy: lack of effect on
56: 655“7. fetal heart rate. Am. J. Emerg. Med. 1992; 19: 548“9.
75. Bruner, J. P., Barry, M. J. & Elliott, J. P. Pregnancy in a patient with idiopathic 98. Matfin, G., Baylis, P. & Adams, P. Maternal paroxysmal supraventricular
long QT syndrome. Am. J. Obstet. Gynecol. 1984; 149: 690“1. tachycardia treated with adenosine (letter). Postgrad. Med. J. 1993; 69: 661“2.
76. Ryan, H. Anaesthesia for caesarean section in a patient with Jervell, Lange- 99. Mason, B. A., Ogunyemi, D., Punla, O. & Koos, B. J. Maternal and fetal
Nielsen syndrome. Can. J. Anaesth. 1988; 35: 422“4. cardiorespiratory responses to adenosine in sheep. Am. J. Obstet.
77. Rashba, E. J., Zareba, W., Moss, A. J. et al. Influence of pregnancy on the risk Gynecol. 1993; 168: 1558“61.
for cardiac events in patients with hereditary long QT syndrome. 100. Wheeler, C. P. D. & Yudilevich, D. L. Transport and metabolism of adeno-
Circulation 1998; 97: 451“6. sine in the perfused guinea pig placenta. J. Physiol. 1988; 405: 511“26.
78. Wilkinson, C., Gyaneshwar, R. & McCusker, C. Twin pregnancy in a patient 101. Doyle, N. M., Monga, M., Montgomery, B. & Dougherty, A. M.
with idiopathic QT syndrome. Case report. Br. J. Obstet. Gynaecol. 1991; 98: Arrhythomogenic right ventricular cardiomyopathy with implantable car-
1300“2. dioverter defibrillator placement in pregnancy. J. Matern. Fetal Neonatal
79. Heradien, M. J., Goosen, A., Crotti, L. et al. Does pregnancy increase cardiac Med. 2005; 18: 141“4.
risk for LQT1 patients with the KCNQ1-A341 V mutation? J. Am. Coll. 102. Lee, L. C., Bathgate, S. L. & Macri C. J. Arrhythmogenic right ventricular
Cardiol. 2006; 48: 1410“15. dysplasia in pregnancy: a case report. J. Reprod. Med. 2006; 51: 725“8.
80. McCurdy, C. M., Jr., Rutherford, S. E. & Coddington, C. C. Syncope and 103. Frost, D. A. & Dolak, J. A. Cesarean section in a patient with familial
sudden arrhythmic death complicating pregnancy. A case of Romano- cardiomyopathy and a cardioverter-defibrillator. Can. J. Anaesth. 2006;
Ward syndrome. J. Reprod. Med. 1993; 38: 233“4. 53: 478“81.
81. Behl, S. & Wauchob, T. D. Long QT syndrome: anaesthetic management at 104. Corbett, W. L., Reiter, C. M., Schultz, J. R., Kanter, R. J. & Habib, A. S.
delivery. Int. J. Obstet. Anesth. 2005; 14: 347“50. Anaesthetic management of a parturient with the postural orthostatic
82. Sen, S., Ozmert, G., Turan, H. et al. The effects of spinal anesthesia on QT tachycardia syndrome: a case report. Br. J. Anaesth. 2006; 97: 196“9.
interval in preeclamptic patients. Anesth. Analg. 2006; 103: 1250“5. 105. EEC Committee, Subcommittees and Task Forces of the American Heart
83. Salukhe, T. B., Dob, D. & Sutton, R. Pacemakers and defibrillators: anaes- Association. 2005 American Heart Association Guidelines for
thetic implications. Br. J. Anaesth. 2004; 93: 95“104. Cardiopulmonary Resuscitation and Emergency Cardiac Care. Cardiac arrest
84. Gudal, M., Kervancioglu, C., Oral, D. et al. Permanent pacemaker implanta- associated with pregnancy. Circulation 2005; 112:IV-150“3.
tion in a pregnant woman with the guidance of ECG and two-dimensional 106. Trappe, H. J. Acute therapy of maternal and fetal arrhythmias during
echocardiography. Pacing Clin. Electrophysiol. 1987; 10: 543“5. pregnancy. J. Intensive Care Med. 2006; 21: 305“15.
85. Holdright, D. R. & Sutton, G. C. Restoration of sinus rhythm during two 107. Campbell, J. Q., Best, T. H., Eswaran H. & Lowery, C. L. Fetal and maternal
consecutive pregnancies in a woman with congenital complete heart magnetocardiography during flecainide therapy for supraventricular
block. Br. Heart J. 1990; 64: 338“9. tachycardia. Obstet. Gynecol. 2006; 108: 767“71.

David R. Gambling

Introduction oxygen saturation (SaO2). When SaO2 is greater than 63%, three-
year survival is 55%. When SaO2 is less than 63%, three-year survi-
Maternal vascular lesions that become apparent during preg-
val is only 17%.7 Sudden death in primary pulmonary hypertension
nancy may be present before conception but only become symp-
may be caused by tachycardia and loss of effective atrial systole,
tomatic as a result of the physiologic changes of pregnancy. Blood
acute pulmonary embolism from deep venous thromboses, or
vessels are weakened by an increase in blood volume and cardiac
from RV ischemia or infarction.3 A rapid increase in venous return
output (CO); a decrease in systemic vascular resistance (SVR); and
to the right heart, and subsequently to the lungs, may produce a
hormonal changes. Hence, aneurysms can expand and rupture,
vagally-mediated bradycardia and fall in CO, which can be lethal.8
or arteriovenous (AV) malformations can grow and, if present in
In most cases, postmortem microscopic examination of the
the pulmonary circulation, can worsen a preexisting shunt. Some
lungs reveals that both lungs are affected by diffuse pulmonary
of the rare conditions described in this chapter affect blood ves-
vascular changes characterized by intimal proliferation, medial
sels in discrete areas of the body whereas others affect all blood
hypertrophy, and perivascular lymphocytic cuffing, described as
vessels. Often the disorders described are part of an autoimmune
plexogenic arteriopathy.9 Others have reported that thrombotic
disease process that impacts other organ systems. Many of the
pulmonary arteriopathy is a more likely cause of pulmonary hyper-
vascular disorders are associated with high maternal and neona-
tension.7 Primary pulmonary hypertension caused by pulmonary
tal mortality. For example, rupture of an enlarging aneurysm can
veno-occlusive disease with intimal proliferation and fibrosis of
cause abrupt, catastrophic blood loss and poor peripartum out-
intrapulmonary veins and venules occurs less frequently.3
comes. Likewise, pulmonary hypertension worsens during preg-
nancy and is often associated with maternal and/or neonatal
Signs and symptoms
death. This chapter discusses the clinical implications for the
obstetric anesthesiologist of most vascular lesions seen during
The signs and symptoms of primary pulmonary hypertension
pregnancy. Intracranial aneurysms during pregnancy are dis-
relate to RV compromise and failure. Dyspnea is caused by
cussed in Chapter 9.
decreased CO and ventilation/perfusion mismatch. Syncope is
due to a fixed CO with the inability of the heart to respond to a
demand for increased output. Angina is common, and probably
Primary pulmonary hypertension
results from RV ischemia and increased RV afterload. Other signs
Primary pulmonary hypertension is a progressive disease that and symptoms include fatigue, edema, and peripheral cyanosis.
produces a sustained rise of at least 25 mmHg in mean pulmonary Occasionally hoarseness may develop due to the pressure of an
artery pressure and an increase in pulmonary resistance, in the enlarging pulmonary artery on the recurrent laryngeal nerve,
absence of an identified pulmonary or cardiac lesion.1,2 This which is known as Ortner syndrome.3
inevitably leads to right ventricular (RV) dilatation and RV hyper- During physical examination of the parturient with pulmonary
trophy progressing to RV failure and death.1,3 The course of pri- hypertension, a RV heave may be present and an ejection click
mary pulmonary hypertension usually is slow, but unrelenting, may be heard over the pulmonic area. The second heart sound
with death occurring 4“6 years after the initial diagnosis. usually is split, with accentuation of the pulmonic component.
However, its course may be as short as six months from first There may be an ejection murmur and a regurgitant murmur over
symptoms to death. This condition is covered in other major the pulmonary valve. Jugular venous distension and prominent A
textbooks of obstetric anesthesia4,5 and the following represents waves usually are evident. Chest radiography (CXR) demonstrates
a brief outline of the importance of primary pulmonary hyperten- RV enlargement, hilar enlargement, and pruning of the peripheral
sion to the obstetric anesthesiologist. Discussion of the manage- vasculature. Electrocardiogram shows RV hypertrophy, and right-
ment of women with Eisenmenger syndrome (pulmonary axis deviation (see Figure 3.1). Pulmonary function tests may
hypertension secondary to a chronic, uncorrected left-to-right indicate restrictive disease due to decreased lung compliance
resulting from elevated pulmonary vascular pressure.3
cardiac shunt) is found in Chapter 1.
Primary pulmonary hypertension affects women four to five
times more often than men. It may arise at any age, but is most
Association with pregnancy
prevalent in the third and fourth decades6 with a mean age of
27 years at diagnosis.7 Among the prognostic indicators of survival, Among women of reproductive age, approximately 8% of primary
pulmonary hypertension is associated with pregnancy.9 It is
the most powerful and easily obtainable is the systemic arterial

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

Figure 3.1 EKG from a patient with severe pulmonary hypertension. Note the deep S waves in leads I, II, V5, and V6 plus a prominent R wave in V1 (all circled). Provided
by Dr Renaldo Beyer, Cardiologist, Sharp Rees-Stealy Medical Group, San Diego, California.

pulmonary arterial hypertension.13 However, bosentan is not
possible that pregnancy initiates primary pulmonary hyperten-
sion in some women, but more likely symptoms of preexisting approved for use during pregnancy. Perioperative therapies
used during pregnancy have included nitroglycerin infusion,14
disease are unmasked by the increased hemodynamic stress of
pregnancy.9 When symptoms arise during pregnancy, the diag- inhaled nitric oxide (which is very expensive),15 or inhaled or
intravenous (i.v.) epoprostenol (prostacyclin).16,17,18
nosis is made only after excluding other causes of pulmonary
hypertension. These include amniotic fluid embolism, tropho-
blastic embolism, thromboembolism, obliterative hypertension,
Anesthetic management of women with primary
and Eisenmenger syndrome.9
pulmonary hypertension
Primary pulmonary hypertension and pregnancy is an omi-
nous combination. Maternal mortality ranges from 30“56%1,7,10 The principal goals of anesthetic management of primary pul-
with death often occurring during delivery, or from four days to monary hypertension include avoiding increases in pulmonary
five weeks following delivery despite intensive postoperative vascular resistance and pulmonary artery pressure, preventing
management.11 Death usually is sudden, precipitated by acute changes in RV preload, and maintaining left ventricular afterload
and RV contractility.19,20 Potent titratable drugs should be readily
RV failure. Absolute pulmonary artery pressure is a poor indicator
of the extent of the disease. However, a poor prognosis in available in the event of hemodynamic instability. The need for
pregnancy is associated with the presence of RV hypertrophy, inotropes (dopamine or dobutamine), pressors (phenylephrine or
low cardiac index (2“2.5 l/min/m2), increased right atrial ephedrine), or afterload reducers (nitroprusside or phentola-
pressure (>10 mmHg) and high pulmonary vascular resistance mine) during labor and delivery or cesarean section (C/S) should
(>1500 dynes.sec.cmÀ5).1 Other maternal risk factors include be anticipated. In one report, a vasopressin infusion was used to
late diagnosis and late hospital admission.11 Neonatal survival prevent systemic hypotension in a patient with primary pulmon-
was reported as 88% in one series.11 ary hypertension having surgery under spinal anesthesia.21
Prior to the onset of labor, the severity of pulmonary hyperten-
sion can be assessed by pulmonary artery catheterization, which
Treatment of primary pulmonary hypertension
also allows an assessment of the response of the pulmonary vascu-
lature to vasoactive drugs.19,22 Preoperative adenosine and nifedi-
A number of therapies have been tried to treat primary pulmon-
pine have been shown to reduce pulmonary vascular pressure23
ary hypertension. These include calcium channel blockers and
anticoagulation, prostacyclin, and, ultimately, lung transplanta- and may be useful adjuncts to oxygen therapy at the time of parturi-
tion.12 More recently, the successful use of the endothelin antago- tion. It is important to measure right- and left-sided pressures
nist, bosentan (Tracleer’), has been described in the treatment of continuously during labor and delivery. However, multiple

Chapter 3

pulmonary capillary wedge pressure (PCWP) measurements should described the use of general anesthesia and extracorporeal mem-
be discouraged because of the risk of pulmonary artery rupture. brane oxygenation support for termination of pregnancy in a
woman with primary pulmonary hypertension.41
During delivery an increase in pulmonary vascular resistance
can occur as a result of hypercarbia, acidosis, hypoxia, stress, and Spinal anesthesia is contraindicated due to the risk of rapid-
pain.22 Epidural analgesia provides excellent pain control and onset deleterious hemodynamic changes. However, even when
attenuates many of these adverse effects. Investigators have general anesthesia is used in the presence of a pulmonary artery
reported successful management of labor and C/S using various catheter, and successful intraoperative control of pulmonary
doses of epidural local anesthetics, with and without fenta- artery pressure is achieved using iNO, nebulized iloprost, and a
nyl.1,8,22,24,25,26,27,28 The addition of fentanyl to labor epidural prostacyclin infusion, a patient can still die in the first few weeks
following surgery.42
infusions is a theoretical concern because of the potential to
cause myocardial depression in patients with compromised In summary, pregnancy should be discouraged in women with
hearts.29 However, it is unlikely that 2 mg/ml fentanyl at primary pulmonary hypertension and therapeutic abortion
10“15 ml/h would produce serum levels that would be clinically should be offered, especially with early clinical deterioration. A
important in this regard. Care should be taken to titrate the level multidisciplinary approach to the management of a parturient is
of analgesia to avoid hypotension and a reduction in RV preload. important, but mortality is high even with the most modern
treatment options.43
Excellent pain relief has also been obtained in patients with
pulmonary hypertension using intrathecal morphine.30,31
However, unless vaginal delivery is imminent, a neuraxial cathe-
Pulmonary arteriovenous malformations
ter technique is recommended. Forceps or vacuum extraction is
often used to help prevent the untoward hemodynamic effects
caused by maternal pushing.
Pulmonary arteriovenous malformations (PAVM) are rare, thin-
Cesarean section can be performed after careful extension of an
walled vascular lesions that may complicate pregnancy because
epidural block to T4“5. The risk of severe hypotension is minimal
of rapid enlargement or rupture (see Figures 3.2 and 3.3). Most
as long as provisions to support blood pressure (BP) have been
PAVM are congenital but many patients are not diagnosed until
taken. Epidural anesthesia,32,33 combined spinal“epidural (CSE)
the second decade. They usually occur singly and grow slowly.
anesthesia,34 and general anesthesia all have been used success-
However, they can occur as discrete or multiple lesions, in one or
fully for C/S25,35 and tubal ligation36 in patients with primary
more lobes, and in one or both lungs,44,45 and many small AVM
pulmonary hypertension. Invasive monitoring was used during
may be scattered throughout the lungs.45,46 The mortality rate in
these procedures. If epidural anesthesia is used, it is uncertain if

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