Use of implantable cardioverter defibrillator and anti-arrhythmic agents in a parturient

A. J. Olufolabi1, G. A. Charlton*,2, S. A. Allen3, I. M. Mettam2 and P. R. Roberts3

1 Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA. 2 Department of Anaesthesia, and 3 Department of Cardiology, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK*Corresponding author

Accepted for publication: May 12, 2002


    Abstract
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
We describe a case of a 36-yr-old patient who presented at 14 weeks gestation with multifocal dysrrhythmic episodes. Despite treatment with anti-arrythmic agents and an implantable cardioverter defibrillator (ICD) in situ, she continued to experience persistent dysrrhythmic episodes. She was delivered by Caesarean section at 34 weeks under general anaesthesia. We discuss some of the anaesthetic challenges of parturients with ICD devices.

Br J Anaesth 2002; 89: 652–5

Keywords: anaesthesia, obstetric; complications, arrhythmia; heart, arrhythmia; heart, pacemakers artificial; pregnancy


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
The introduction of implantable cardioverter defibrillators (ICDs) into clinical practice in the mid 1980s provided a further option for the treatment of cardiac rhythm disorders. We present a case to show the complexity and limitations of these devices. The case also describes the use of anti-arrhythmic agents in pregnancy and following delivery.


    Case report
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 36-yr-old primigravidae (weight 50 kg; height 157 cm) was admitted to the cardiac ward with an unplanned pregnancy at 14 weeks gestation and a history of persistent arrhythmia which required frequent cardioversion. Her past medical history was of surgical correction for double outlet right ventricle, pulmonary stenosis and multiple ventricular septal defects. She had a 4-yr history of episodes of ventricular tachycardia (VT) which were first treated with various anti-arrhythmic agents. An ICD (Mini, Guidant, USA) was implanted 2 yr prior to her pregnancy. In the nine months before she presented, she had numerous (>100 times) ventricular tachycardic episodes despite her anti-arrhythmic treatment with xamoterol 200 mg b.d. and flecanide 50 mg b.d.

She was managed jointly by the Grown Up Congenital Heart (GUCH) Team, electrophysiologists and obstetricians. In the week after presentation, she had further episodes of VT with rates of 194–198 beats min–1. Successful cardioversion treatment restored sinus rhythm but she found each episode distressing. Her ICD was therefore reprogrammed for anti-tachycardia pacing only and disabled from triggering a cardioversion response when it detected a VT rhythm. It would, however, recognize a ventricular fibrillation (VF) signal rate of 240 beat min–1 and respond with a 33 J-defibrillation pulse. Her serum flecanide level (240 µg litre–1) was within the normal range of 200–700 µg litre–1. We noted multi-focal beats with intermittent bigeminy but she was otherwise asymptomatic. She had further intermittent episodes of VT, leading to considerable adjustment to her anti-tachycardia pacing setting and anti-arrhythmic medications. Despite this, she continued to have frequent VTs that predominantly were anti-tachycardia paced but which occasionally had a VT greater than 240 beat min–1 that required a cardioversion from the device. An initial echocardiogram revealed reduced left ventricular function with a dilated right ventricle and mild tricuspid incompetence.

Although maternal weight was unchanged at 51 kg, an ultrasound scan at 18 weeks revealed a normal foetus of appropriate size for its gestation. The patient refused amniocentesis to determine any potential teratogenic effect of the anti-arrhythmic agents. Maternal serum alpha fetoprotein level was, however, normal at 17 ku litre–1. Low-molecular weight heparin was commenced at 22 weeks gestation because of the increased risk of thromboemboli from the combined hypercoagulable state of pregnancy and reduced cardiac output. Because of persistent episodes of VT, her flecanide dose was increased despite a serum concentration of 350 µg litre–1.

The ICD was tested in the third trimester and confirmed to be in good working order. An echocardiogram revealed no changes to previous results. She developed new and frequent episodes of supraventricular tachycardia (SVT). Because the rate of her SVT was similar to her VT, she received inappropriate shock therapy. Thyroid function tests were checked and were normal. The SVT was terminated pharmacologically with intravenous verapamil. Further adjustments to the ICD detection enhancements were made to discriminate the SVT from the VT so that each rhythm could be appropriately treated. Her arterial pressure was not affected by these episodes and she experienced minimal symptoms. A midwife examined the baby after every SVT/VT episode using a cardiotocogram to ensure that the foetal condition remained satisfactory.

At 30 weeks gestation, and with a maternal weight of 59 kg, she was transferred to a high-dependency unit. A series of abnormal rhythms consisting of VT, SVT, and atrial fibrillation persisted and required further adjustment of her drugs (flecanide, xamoterol, digoxin and magnesium). At 34 weeks gestation, an episode of heart block required reduction of the flecanide and verapamil doses. A decision was made to deliver the baby and three doses of dexamethasone were given to promote foetal lung maturation.

She was transferred to the obstetric theatre. General anaesthesia was planned as the patient refused regional anaesthesia. Experienced obstetric and cardiac anaesthetists, and an electrophysiologist familiar with the ICD functions were present. The device was programmed to ‘monitor only’ mode by the electrophysiologist for the duration of the Caesarean section. Venous and arterial canulae were placed under local anaesthesia. Following routine anti-reflux prophylaxis, the patient underwent a rapid sequence induction with thiopental 325 mg and succinylcholine 100 mg. Anaesthesia was maintained with 50% oxygen in nitrous oxide and isoflurane 1%. A female 2.1-kg baby was delivered with Apgar scores of 8 and 9 at 1 and 5 min. Oxytocin infusion was started post delivery and intravenous morphine was administered. Blood loss was approximately 600 ml. Postoperative Hb was 10.8 g dl–1 (preoperative Hb 11 g dl–1). She had no dysrrhythmic episodes throughout the delivery. A bipolar electrocautery was used intermittently for surgical haemostasis.

After surgery, heparin, digoxin and flecanide were continued and the verapamil dose was reduced. She developed a cough and breathlessness 48 h after delivery. On auscultation, bilateral lung crepitations were heard. An enlarged right ventricle with moderate function was seen by echocardiography. Left ventricular contractility was normal. Her symptoms improved after furosemide. Episodes of recurring SVT occurred on the 6th postpartum day. Digoxin and verapamil treatment was reduced. Varying episodes of bundle branch block occurred that responded to doses flecanide. During her second and third postpartum week, she had numerous cardiac dysrrhythmias that required changes of her anti-arrhythmia drugs. Hypotension accompanied some of these episodes. With episodes of refractory SVT and VT and new evidence of cardiovascular compromise, she underwent cardiac ablation of identified accessory pathways using local anaesthesia with sedation. A new dual chamber ICD (Medtronic 7250) was also inserted. This device is more capable of discriminating between SVT and VT, so that inappropriate therapy is less likely. She also started taking oral amiodarone. Her cardiac rhythm became stable with no further rhythm disturbance. She was discharged after a very long hospital stay (200 days).


    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
Cardiac arrhythmia is more frequent during pregnancy. Metabolic and hormonal changes increase cardiac excitability.1 The patient also has to compensate for the physiological requirements of the developing pregnancy. These changes, which develop in the first trimester before becoming stable in the middle and third trimester, include: increased cardiac output, increased intravascular volume, increased total body water; increased glomerular filtration and renal clearance, increased hepatic enzyme function, and reduced plasma protein.2 These changes alter the pharmacokinetics and pharmacodynamics of many drugs and consequently their doses. Changes in absorption, volume of distribution, and elimination can make serum levels difficult to predict. Observation of drug serum levels and clinical effects are often required for adequate management.

The risk of teratogenic effects during organogenesis in the first trimester, and effects on growth and development in the second and third trimesters demands caution in the use of medication in pregnancy. Most cardiac drugs appear safe and are classified as category C according to the US Food and Drug Administration, that is, some risk has been found in animals but not in humans.3 However, phenytoin and amiodarone should be avoided because significant congenital abnormalities are associated with their use.4

Most anti-arrhythmic drugs are also safe for nursing mothers. The concentration of the drug in breast milk does not usually exceed maternal plasma concentration, and the amount of drug taken by the baby rarely reaches therapeutic levels.5 Drugs with a proven record of safe use during pregnancy should be chosen for first line treatment.4

The ICD provides both stored and real-time telemetry information that aids the diagnosis of complex rhythm disturbances. It also treats life-threatening cardiac events. Our report describes a limitation of these devices, since single chamber devices may not differentiate between SVTs, VTs and VF, resulting in inappropriate treatment. Only after a dual chamber system was placed were the unstable cardiac rhythms in by our patient correctly identified and appropriately treated.

Hydrocarbon anaesthetic agents such as halothane and enflurane are known to depress the cardiac atrio-ventricular node and thus can initiate or ameliorate dysrrhythmic events.6 Halothane sensitizes the heart to adrenaline-induced atrial arrhythmias, an effect potentiated by thiopentone.7 There is, however, no reported evidence of pacing or ICD thresholds affected directly by anaesthetic drugs. Anti-arrhythmic drugs can, however, alter pacing or defibrillation thresholds.8 This is more relevant in parturients already on antiarrhythmic agents in whom appropriate dosing is already uncertain.

All cardiac devices should be assessed before and after surgery. Pacemaker output failure has been attributed to suxamethonium-induced fasciculations.9 Although there are previous reports of pacemaker malfunction caused by high voltage intraoperative electrocautery or by magnets,10 11 modern devices are unlikely to be reprogrammed because specific sequences of information are needed to alter programming. However, electrocautery can directly damage circuitry or the tissue–lead interface, resulting in increased pacing thresholds or inadequate sensing. Bipolar diathermy should therefore be used.

Because of her extreme anxiety, our patient opted for general anaesthesia. General anaesthesia allows use of more invasive monitoring such as a pulmonary artery catheter or transoesophageal echocardiogram. However, there is no clear contraindication to regional anaesthesia. An epidural may be preferable to a subarachnoid block since a more controlled onset of effect is possible. Complex cardiac patients have undergone Caesarean section using regional anaesthesia with good outcome.12 Regional anaesthesia can give good analgesia and reduce the sympathetic response to surgery. The arrythmogenic and depressant effects of volatile agents are avoided so that perioperative cardiac rhythm disturbances can be reduced.

Better treatment of complex cardiac patients increases the frequency of treatment in pregnancy and challenges all involved in their care, requiring a multidisciplinary approach from cardiologists, obstetricians, anaesthetists, and electrophysiologists.


    References
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Ostrzega E, Mehra A, Widerhorn J, et al. Evidence of increased incidence of arrhythmias during pregnancy: a study of 104 pregnant women with symptoms of palpitations, dizziness or syncopy. J Am Coll Cardiol 1999; 19: 125A

2 Sibai BM, Frangieh A. Maternal adaptation to pregnancy. Curr Opin Obstet Gynecol 1995; 7: 420–6

3 Drugs Facts and Comparisons. St Louis, MO: Facts and Comparisons, 1997

4 Joglar JA, Page RL. Treatment of cardiac arrhythmias during pregnancy: safety considerations. Drug Safety 1999; 20: 85–94[ISI][Medline]

5 Committee on drugs. Transfer of drugs and other chemicals into human milk. Pediatrics 1994; 93: 137–50[ISI][Medline]

6 Hantler CB, Wilton NC, Knight PR. Comparative effects of halothane, enflurane, and isoflurane on atrioventricular conductivity and subsidiary pacemaker function in dogs. Anesth Analg 1994; 79: 455–9[Abstract]

7 Atlee JL, Malkinson CE. Potentiation by thiopental of halothane–epinephrine-induced arrhythmias in dogs. Anesthesiology 1982; 57: 285–8[ISI][Medline]

8 Kowey PR, Marinchak RA, Rials SJ, Bharucha DB. Classification and pharmacology of antiarrhythmic drugs. Am Heart J 2000; 140: 12–20[ISI]

9 Finfer SR. Pacemaker failure on induction of anaesthesia. Br J Anaesth 1991; 66: 509–12[Abstract]

10 Domino KB, Smith TC. Electrocautery-induced reprogramming of a pacemaker using a precordial magnet. Anesth Analg 1983; 62: 609–12[ISI][Medline]

11 Bierman PQ, Roche DA, Carlson LG. Abnormal permanent pacemaker inhibition by a magnet: a case study. Heart Lung 1993; 22: 148–50[ISI][Medline]

12 Lockhart EM, Penning DH, Olufolabi AJ, Bell EA, Booth JV, Kern FH. SvO2 monitoring during spinal anesthesia and cesarean section in a parturient with severe cyanotic congenital heart disease. Anesthesiology 1999; 90: 1213–5[ISI][Medline]