Peri-partum Cardiomyopathy (PPCM) is a relatively rare disease estimated to occur in 1 in 3000- 4000 pregnancies (1). Criteria for diagnosis include:
1. Development of cardiac failure in the last trimester of pregnancy or within five months of delivery,
2. absence of a determinable aetiology for the cardiac failure, and
3. absence of demonstrable heart disease prior to the last month of pregnancy (2).
The diagnosis therefore, is largely one of exclusion as the disease has no pathognomic features (3, 4). The aetiology of PPCM remains poorly understood with theories generally centred upon viral infection triggering autoimmune mechanisms in susceptible individuals (1, 2, 4).

Considerations for regional anaesthesia in these patients are similar to those with other causes of heart failure. With regard to anaesthesia for caesarean section, general anaesthetic techniques involve either cardiodepressant drugs such as thiopentone and the inhalational anaesthetic agents, or high dose narcotic techniques, which, while they maintain haemodynamic stability, may necessitate post-operative ventilation for both mother and infant. Further considerations with narcotic techniques are the less well defined endpoint at induction of anaesthesia, which may increase the risk of aspiration of gastric contents in this susceptible population. The management of a failed intubation may also be complicated by the longer acting nature of these drugs and the difficulty with mask ventilation that may occur.

Epidural anaesthesia offers several advantages in addition to avoiding these problems. Anaesthesia may be induced in a gradual and controlled manner and if a pulmonary artery catheter is used to guide fluid and inotrope requirements, minimal change in haemodynamic parameters can be achieved. Small bolus doses or an incremental infusion of bupivacaine 0.5% with fentanyl 4-5 mcg/ml is suitable for these purposes. In addition, major neuraxial blockade may actually improve myocardial performance by reducing the afterload on the left ventricle without impairing contractility, although not all authors agree (6).

References:
1. Veille JC. Periparturn Cardiomyopathy - A Review. Am J Obstet Gynecol 148; 805-818, 1984.

2. Demakis JG Rahimtoolas SH. Peripartum Cardiomyopathy. Circulation 44; 964-968, 1971.

3. Demakis JG. Rahimtoolas SH. Sutton GS et al Natural Course of Peripartum Cardiomyopathy. Circulation 44; 1053-1061, 1971.

4. Julian DG, Szekely P. Peripartum Cardiomyopathy Progress in Cardiovasc. Diseases 27; 223-240, 1985.

5. Sanderson JE, Olsen EGJ. Gatei D. Peripartum Heart Disease: An Endomyocardial Biopsy Study. Br. Heart J. 56; 285-91, 1986.

6. Brown G, O'Leary M, Douglas I, Herkes R Perioperative Management of a Case of Severe Peripartum Cardiomyopathy. Anaesth. Intens. Care 20; 80-83, 1992.

7. Hutchinson RC, Ross AW, Severe Peripartum Cardiomyopathy. Anaes. Int. Care. 20; 398 (correspondence) 1992.

8. Scott JR, Wagoner LE, Olsen S. Pregnancy in Heart Transplant Recipients. Management and Outcome. Obstet & Gynecol. 82; 324-327, 1993.

9. Hughes R, Kapur P, Sutton GC, et al A case of fatal Peripartum Cardiomyopathy. Br Heart Jn. 32; 272-276, 1970.

10. Homans DC. Current Concepts. Peripartum Cardiomyopathy NEJM 312; 1432-1437, 1985.

11. Wesley L, Cotton DB. Peripartum Cardiomyopathy: Current Concepts and Clinical Management. Clinical Obstets Gynecol. 20; 54-67, 1989.