Pulmonary oedema in two parturients with hypertrophic obstructive cardiomyopathy (HOES)TwoHypertrophic obstructive cardiomyopathy (HOES) is a relatively recently described abnormality which appears to be increasing in frequency.' It is observed in all races, at all ages, in both sexes and can be lethal, z-4Hypertrophic obstructive cardiomyopathy presents a major challenge to the anaesthetist managing parturients. Women in labour are stressed by the pain of labour and its associated increase in catecholamine secretion. 5 Cardiac output normally increases as a result of the catecholamine-induced increase in heart rate and stroke volume. 6 However, in patients with HOES, elevated circulating catecholamines can lead to decreased forward flow. Increased contractility leads to greater obstruction of the left ventricular outflow tract and tachycardia limits diastolic filling which reduces left ventricular enddiastolic volume. 7 The Valsalva manoeuvre, used to help the fetus descend in the second stage of labour, can also impair cardiac output in these patients through reducing preload. 2Many authors have stated that regional anaesthesia (spinal or epidural) is relatively contraindicated in the patient with HOES. 9-'1 General anaesthesia with halothane to reduce myocardial contractility and heart rate is the recommended form of anaesthesia. 9 This cannot be applied absolutely to the parturient in labour and lumbar epidural analgesia is often administered. I~ Two patients with HOCM who presented for delivery are reported. Each was managed with a different anaesthetic technique yet both developed pulmonary oedema. The discussion will focus on the pathophysiological changes in HOCM and their implications for management once pulmonary oedema has occurred.
Case 1A 27-yr-old female, G3P2 was admitted to the antepartum ward at 37 weeks gestation and was scheduled for elective Caesarean section the following morning. She had had CAN J ANAESTH 1990/ 37:4 /pp469-73
A 24-year-old black female presented for repeat elective Caesarean section. The procedure was performed under epidural anaesthesia. Sufentanil 25 micrograms, intended for postoperative analgesia, was inadvertently diluted to 10 ml with 15 per cent potassium chloride (KCl) instead of preservative-free normal saline (0.9 per cent NaCl). This solution was then injected via an epidural catheter into the epidural space at the conclusion of surgery. Two hours after injection of the sufetanil-KCl mixture, the patient had a level of sensory blockade to T1 and diaphoresis above this level. Painful muscle spasms had also developed below T1. One hour later she developed hypertension which required hydralazine 10 mg and labetalol 25 mg IV for treatment. The patient was treated supportively with oxygen. Dexamethasone 10 mg was administered intravenously to reduce spinal cord oedema. Intravenous diazepam 10 mg and meperidine 75 mg were given for sedation and analgesia. Complete recovery occurred within 12 hours.
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