- Email: [email protected]
An obstetric patient with neurocadiogenic syncope
International Journal of Obstetric Anesthesia (2009) 18, 396–399 0959-289X/$ - see front matter c 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2008.12.007
CASE REPORT
www.obstetanesthesia.com
An obstetric patient with neurocadiogenic syncope K. Jarvi, N. Osborn, N. Wall Department of Anaesthesia, Heartlands Hospital, Birmingham, UK ABSTRACT We report the peripartum management of a 29-year-old primigravid patient with neurocardiogenic syncope, which had been diagnosed six years previously on tilt-table testing. General principles were applied to minimise the risk of precipitating syncopal episodes. She had an uneventful ventouse-assisted vaginal delivery under epidural anaesthesia in our obstetric high dependency unit. The optimum management of these patients has yet to be established. c 2009 Elsevier Ltd. All rights reserved.
Keywords: Neurocardiogenic syncope; Obstetric anaesthesia
Introduction
Case report
Syncope is a common problem with multiple aetiologies. It is defined as a transient, self limiting loss of consciousness usually leading to collapse. The onset of syncope is relatively rapid. Recovery is spontaneous, complete and usually prompt. The underlying mechanism is transient global cerebral hypoperfusion.1 Neurocardiogenic syncope, also known as vasovagal syncope, vasodepressor syncope, neurally mediated hypotension and bradycardia syndrome,1–3 is a common cause of syncope.4 However, only a minority of individuals suffer severe and/or repeated symptoms. Catastrophic events including prolonged periods of hypotension and cardiac arrest have been reported.5–7 This heterogeneous syndrome is characterised by inappropriate vasodilatation and relative or absolute bradycardia or asystole, resulting in inadequate blood pressure to maintain cerebral perfusion.8 Episodes are triggered by increases in catecholamines or reductions in preload.9 Obstetric patients with neurocardiogenic syncope present an anaesthetic challenge, as there are no clear guidelines regarding their management. We found only two previous case reports on the planned anaesthetic management of these patients.10 We aim to highlight the anaesthetic considerations relevant to this underreported condition.
A 29-year-old primigravid woman presented at 38 weeks of gestation to our obstetric unit for anaesthetic review and formulation of a delivery plan. She had experienced fainting episodes for the last seven years. A cardiologist had diagnosed neurocardiogenic syncope by tilt-table testing six years previously. Her symptoms were precipitated by standing still for periods of time (about ten minutes while pregnant), anxiety and hot baths. A brief prodromal phase of feeling faint usually preceded syncopal episodes, during which she lay still with a vacant gaze. Consciousness was typically regained within seconds, although episodes lasting several minutes had occurred. Management recommended by the cardiologist included advice on avoiding precipitating situations, maintaining a high fluid intake, adopting a sitting or horizontal posture if feeling faint and prescription of the b blocker bisoprolol. Her syncopal episodes had reduced in frequency with this treatment. Bisoprolol was discontinued in early pregnancy due to a risk of intrauterine growth restriction. However, the plan was to resume the bisoprolol if symptoms became problematic. Fortunately, she managed reasonably well with conservative measures, having experienced only two syncopal episodes in pregnancy, with the last nearly two months previously. She was otherwise fit and healthy and there had been no complications in the pregnancy. An anaesthetic plan was made incorporating certain general principles, including minimising pain and anxiety, hunger and dehydration. Aortocaval compression should be avoided as should prolonged standing leading to venous pooling in the lower limbs. Vasodilating drugs should be avoided and prolonged Valsalva manoeuvres kept to a
Accepted December 2008 Correspondence to: Dr. Nicola Wall, Department of Anaesthesia Office, Education Centre, Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS, UK. E-mail address: [email protected]
K. Jarvi et al. minimum. Blood loss should be anticipated and corrected promptly. Delivery was planned to take place in our high dependency room on delivery suite, staffed by specialist midwives trained in obstetric high dependency care. Facilities included immediate access to invasive cardiovascular monitoring (central venous and arterial), in conjunction with a range of standard vasoactive drugs and external cardiac pacing. Our patient presented in early labour at 39+5 weeks of gestation. Her cervix was 2 cm dilated, and the membranes intact. She was not thought to be in established labour, but was admitted for observation. A calm atmosphere with dimmed lights was maintained and the need for analgesia was assessed regularly. She was encouraged to eat and drink freely to avoid hunger and dehydration. When lying in bed, a full left or right lateral position was maintained to prevent aortocaval compression. Prolonged standing was avoided. Graduated compression stockings were fitted to improve venous return. Labour became established with progressively stronger contractions, requiring Entonox. Thereafter her oral intake was restricted to water. Regular antacid prophylaxis of oral ranitidine 150 mg every 6 h was prescribed. Monitoring was established with continuous electrocardiogram (ECG), oxygen saturation and non-invasive blood pressure measurement. Although the designated midwife was not expected to interpret the ECG, it was important that it was immediately available for medical staff to interpret, if needed. Over the next 3.5 h, her cervix dilated to 7 cm. Although early epidural analgesia had been agreed, she continued to decline this as her pain was well controlled with Entonox and she remained asymptomatic. As she was no longer maintaining her oral fluid intake, she was given an infusion of Hartmann’s solution at 200 mL/h through a 16-gauge peripheral venous cannula inserted under local anaesthesia. She progressed well until the second stage of labour, without any symptoms of pre-syncope, and continued to decline epidural analgesia. However, 45 min after full cervical dilatation, she felt unable to continue pushing without feeling faint. She then requested epidural analgesia. Following a 500mL bolus of Hartmann’s solution given over 20 min, the epidural cannula was sited easily in the left lateral position. She was given a 5-mL bolus of 0.125% levobupivacaine, followed 10 min later by a 10-mL top-up of 0.125% levobupivacaine plus fentanyl 100 lg. Her prodromal symptoms were much improved with epidural analgesia and she was able actively to push again. As blood pressure, heart rate and oxygen saturation remained stable, invasive monitoring was not deemed necessary at this point. However, an intravenous oxytocin infusion for augmentation of uterine contraction was required. In accordance with our standard unit guidelines,
397 oxytocin 10 units was added to 500 mL of 0.9% saline. The infusion was initiated at 1 mU/min (3 mL/h), and increased over the next hour and a half to 4 milliunits/ min (12 mL/h). Three hours after epidural insertion, maternal fatigue prompted an assisted ventouse delivery, which resulted in the uncomplicated delivery of a baby boy with Apgar scores of 9 and 10, at 1 and 5 min respectively. Good analgesia for the delivery was achieved with one 5-mL bolus of 0.25% levobupivacaine. The estimated blood loss was 300 mL. The oxytocin infusion rate was then increased to 125 mL/h. After delivery, she remained cardiovascularly stable and asymptomatic with non-invasive monitoring for some four hours after delivery. She was subsequently discharged to our post natal ward. Having remained stable, she was discharged home 5 h later. There were no postpartum complications.
Discussion We found only two previously published case reports on the planned anaesthetic management of obstetric patients with neurocardiogenic syncope.10 Both patients delivered in the same obstetric unit in the UK. Antenatally, one had been managed conservatively in the community, whereas the other had an atrial-based pacemaker in situ. Both had invasive blood pressure monitoring and continuous ECG monitoring in labour. Epidural analgesia was established in both. The first patient required caesarean section, performed under epidural anaesthesia, after a failed attempt at ventouse delivery. Epidural analgesia had the added benefit of controlling blood pressure in the second patient, who had preeclampsia. This woman went on to have an uncomplicated ventouse-assisted vaginal delivery. Neurocardiogenic syncope may be precipitated by central or peripheral stimuli,9 but many episodes have no specific provocation.11 Central triggers include those that increase catecholamine secretion such as emotional stress, pain and unpleasant sights, sounds and smells.3,9 Peripheral triggering occurs due to a reduction of venous return to the heart, as commonly occurs on standing, when 300-800 mL of blood are displaced to the veins in the lower body.3,9 Central transmission of the afferent stimuli is followed by the vasomotor centre responses of paradoxical withdrawal of peripheral sympathetic tone and a surge in parasympathetic tone, which, in turn, causes vasodilatation and bradycardia.3,9 The exact pathophysiology is unclear and complex. A variant of the Bezold-Jarisch reflex has been widely proposed as a means by which a reduction in venous return may provoke neurocardiogenic syncope. In this reflex pathway the reduction in preload leads to reduced ventricular volume. Subsequent baroreceptormediated sympathetic stimulation leads to increased ventricular inotropy.11,12 Vigorous contraction of the
398 volume-depleted ventricle is believed to stimulate mechanoreceptors (cardiac C fibres), consisting of nonmyelinated fibres that project centrally to initiate the abnormal autonomic responses.2–4 However, evidence from heart transplant recipients in whom re-innervation had not occurred, seems to contradict this theory, or at least to suggest that there are sites other that the heart for the origin of this reflex.9,12 Syncope is often preceded by prodromal symptoms including light-headedness, nausea, vomiting, diaphoresis, visual disturbances, dyspnoea, palpitations and/or paraesthesia.4,11 However, nearly one third of patients (mainly the elderly) experience few, if any, prodromal symptoms before suddenly losing consciousness.11 During a syncopal episode, patients classically appear pale and diaphoretic, with a slow, diminished pulse. Seizurelike activity may occasionally occur during asystole,2 but post-ictal states are rare.11 However, the patient may feel tired.4 In numerous cases, a diagnosis can be made from the history alone, particularly with witnessed accounts.13 A subset of patients require further cardiovascular and neurological examination and investigation. Tilt-table testing is a useful diagnostic tool.2,13 The multiplicity of treatment options for managing these patients in the community gives an indication of the complexity of the condition. Conservative management remains the mainstay of treatment, and includes educating the patient to avoid predisposing stimuli such as extreme heat, dehydration and standing for extended periods of time. Drugs such as alcohol, diuretics and vasodilators may need to be discontinued. A moderate increase in salt intake may be beneficial.2,3,14 A syncopal episode may be aborted by adopting a horizontal position and performing isometric arm and leg muscle contractions to augment venous return.15,16 ‘Tilt training,’ which involves standing against a wall for increasing periods of time each day, surrounded by cushions, has been advocated.17 Medical treatment remains controversial and is reserved for high-risk cases. b blockers continue to be regarded as a first-line pharmacological prophylactic measure.18 Their proposed mechanisms of action include diminished activation of the left ventricular mechanoreceptors (the C fibres described previously) and blunting of the pre-syncopal increase in epinephrine concentration.14 Fludrocortisone, (a synthetic mineralocorticoid), midodrine (an a1 agonist), selective serotonin reuptake inhibitors, disopyramide (a class 1a anti-arrhythmic agent) and scopolamine (an anticholinergic) are also occasionally used.4,14 There is little evidence supporting any pharmacological management of this condition specific to pregnancy. Local cardiologists advised that the following drugs could be considered for use in pregnancy: all b blockers (except atenolol in the first trimester), fludrocortisone and selective serotonin reuptake inhibitors (with the exception of paroxetine). Cardiac pacing is
Neurocardiogenic syncope valuable in certain patients, usually those in whom pharmacological therapy has failed and who have shown a predominantly cardio-inhibitory response during tilt-table testing.3 In the event of an episode of neurocardiogenic syncope, prompt treatment is important. Any delay may result in permanent cerebral damage or death.9 The primary aim must be the re-establishment of an adequate blood pressure and heart rate. The patient should be promptly placed in a lateral position with head down tilt if possible, to improve venous return. Intravenous fluids should be considered if hypovolaemia is suspected, but drug treatment must not be delayed, particularly when venous return is reduced due to redistribution of blood to peripheral compartments during regional anaesthesia. In the normal population, anticholinergic drugs are often used initially in the treatment of bradycardia. However, in a neurocardiogenic response, where bradycardia is accompanied by profound vasodilatation, increasing the heart rate alone may not correct hypotension.9,19,20 For this reason, anticholinergic drugs or pacing alone may not be effective. Ephedrine, with its effects on both heart rate and vascular resistance, is the most logical first line pharmacological agent in an acute attack.18 If hypotension persists despite adequate doses of ephedrine, then a agonists such as metaraminol or phenylephrine may be considered, bearing in mind their potential to decrease the heart rate. In a cardiac arrest, epinephrine must be given without delay.9 The management of our patient raises some discussion points. Although the benefits of early epidural analgesia had been explained, and it was offered on more than one occasion when labour was established, our patient agreed to its insertion only in the second stage, on developing prodromal symptoms while straining. Perhaps we could have ensured that the epidural catheter was sited earlier. Also, as the woman became fatigued during a prolonged second stage, earlier intervention with an assisted delivery might have been more appropriate. Invasive arterial blood pressure monitoring provides a continuous record of heart rate and blood pressure. In our case this was to be considered if she became symptomatic, or if the progress of labour indicated that an operative delivery was likely to be required. The timing of any introduction of invasive techniques remains difficult, as the act of siting an arterial line can, in itself, constitute a stimulus to cardiovascular events. In our case, we did not establish invasive blood pressure monitoring as our patient was asymptomatic with her epidural in situ, and our obstetric colleagues were confident that minimal assistance at delivery would be sufficient. Our plan in the event of operative delivery was to apply the general principles of avoiding any fall in pre-
K. Jarvi et al. load and minimising catecholamine release. Invasive arterial pressure monitoring was to be instituted and a 250–500-mL crystalloid preload was to be administered. Other appropriate measures included left lateral tilt to avoid aortocaval compression, meticulous replacement of intraoperative blood loss, and a continuous infusion or boluses of ephedrine to keep the blood pressure within 20% of the preoperative baseline. In order to avoid uterine atony after delivery of the baby, oxytocin was to be given as an i.v. infusion (5 units over 15 min) rather than a bolus, followed by a 2040-unit infusion in 500 mL 0.9% saline at a rate of 125 mL/h. Adequate postoperative analgesia and continuation of maintenance fluids were important, with postoperative care to continue in our high dependency unit. Our proposed anaesthetic options for operative delivery included incremental top-up of an existing epidural, ideally over 15 to 20 min and guided by cardiovascular responses, or a cardiostable general anaesthetic. Spinal anaesthesia, including a combined spinal-epidural technique was to be avoided, as any spinal component would be likely to increase the risk of cardiovascular instability. Options for general anaesthesia would need to be guided by the clinical condition of the patient. Several techniques would be possible. All options would need to minimise the cardiovascular responses to laryngoscopy, surgical incision and emergence. This could be achieved by techniques using opioids such as alfentanil or remifentanil, or total intravenous anaesthesia. If using volatile agents, we would have chosen sevoflurane rather than isoflurane for increased haemodynamic stability. Adequate analgesia into the postoperative period would be essential. The specific techniques used for anaesthesia and analgesia would depend on both the clinical condition of the patient and the preference of the duty anaesthetist. Neurocadiogenic syncope has important implications for anaesthetists, particularly in the obstetric patient. A joint anaesthetic, obstetric and midwifery delivery plan should be formulated well in advance. Early involvement of cardiology colleagues is also recommended. Certain general principles are always relevant to the care of these patients, regardless of the mode of delivery. Avoidance of precipitating factors and prompt treatment of syncopal episodes is essential.
399
References 1. Fitzpatrick AP, Cooper P. Diagnosis and management of patients with blackouts. Heart 2006;92:559–68. 2. Nelson SD, Boudoulas H, Schaal SF, Lewis RP. Diagnosis and management of syncope. In: Fuster V, Alexander RW, O’Rourke RA, editors. The Heart. 11th edition. New York: McGraw-Hill, Inc.; 2004 p. 1033–50. 3. Calkins H, Zipes DP. Hypotension and syncope. In: Braunwald E, Zipes DP, Libby P, editors. Heart Disease, a Textbook of Cardiovascular Medicine. Philadelphia: W. B. Saunders; 2001. p. 932–40. 4. Scarabelli-Chen C, Scarabelli TM. Neurocardiogenic syncope. BMJ 2004;329:336–41. 5. Watkins EJ, Dresner M, Calow CE. Severe vasovagal attack during regional anaesthesia for Caesarean section. Br J Anaesth 2000;84:118–20. 6. Firth P. Vasovagal syncope: an unusual cause of postpartum collapse. J Obstet Gynaecol 1997;17:491. 7. Sprung J, Schoenwald PK. Vasovagal cardiac arrest during the insertion of an epidural catheter and before the administration of epidural medication. Anesth Analg 1998;86:1263–5. 8. Robertson RM, Medina E, Shah N, Furlan R, Mosqueda-Garcia R. Neurally mediated syncope: pathophysiology and implications. Am J Med Sci 1999;317:102–9. 9. Kinsella SM, Tuckey JP. Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold-Jarisch reflex. Br J Anaesth 2001;86:859–68. 10. Saqr L, Saqr M, Kumar M. Neurocardiogenic syncope in the obstetric patient. Anaesthesia 2007;62:79–84. 11. Grubb BP. Neurocardiogenic syncope and related disorders of orthostatic intolerance. Circulation 2005;111:2997–3006. 12. Fenton AM, Hammill SC, Rea RF, Low P, Shen W. Vasovagal syncope. Ann Intern Med 2000;133:714–25. 13. Parry SW, Kenny RA. The management of vasovagal syncope. Q J Med 1999;92:697–705. 14. Grubb BP. Neurocardiogenic syncope. N Engl J Med 2005;352:1004–10. 15. Brignole M, Croci F, Menozzi C et al. Isometric arm counterpressure manoeuvres to abort impending vasovagal syncope. J Am Coll Cardiol 2002;40:2053–9. 16. Krediet CTP, van Dijk N, Linzer M, van Lieshout JJ, Wieling W. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation 2002;106:1684–9. 17. Ector H, Willems R, Heidbuchel H, Reybrouck T. Repeated tilt testing in patients with tilt-positive neurally mediated syncope. Europace 2005;7:628–33. 18. Sweeney B, Jaffer M. Treatment of neurocardiogenic syncope. Anaesthesia 2007;62:632–3. 19. Abboud FM. Neurocardiogenic syncope. N Engl J Med 1993;328:1117–20. 20. Morillo CA, Eckberg DL, Ellenbogen KA et al. Vagal and sympathetic mechanisms in patients with orthostatic vasovagal syncope. Circulation 1997;96:2509–13.
CASE REPORT
www.obstetanesthesia.com
An obstetric patient with neurocadiogenic syncope K. Jarvi, N. Osborn, N. Wall Department of Anaesthesia, Heartlands Hospital, Birmingham, UK ABSTRACT We report the peripartum management of a 29-year-old primigravid patient with neurocardiogenic syncope, which had been diagnosed six years previously on tilt-table testing. General principles were applied to minimise the risk of precipitating syncopal episodes. She had an uneventful ventouse-assisted vaginal delivery under epidural anaesthesia in our obstetric high dependency unit. The optimum management of these patients has yet to be established. c 2009 Elsevier Ltd. All rights reserved.
Keywords: Neurocardiogenic syncope; Obstetric anaesthesia
Introduction
Case report
Syncope is a common problem with multiple aetiologies. It is defined as a transient, self limiting loss of consciousness usually leading to collapse. The onset of syncope is relatively rapid. Recovery is spontaneous, complete and usually prompt. The underlying mechanism is transient global cerebral hypoperfusion.1 Neurocardiogenic syncope, also known as vasovagal syncope, vasodepressor syncope, neurally mediated hypotension and bradycardia syndrome,1–3 is a common cause of syncope.4 However, only a minority of individuals suffer severe and/or repeated symptoms. Catastrophic events including prolonged periods of hypotension and cardiac arrest have been reported.5–7 This heterogeneous syndrome is characterised by inappropriate vasodilatation and relative or absolute bradycardia or asystole, resulting in inadequate blood pressure to maintain cerebral perfusion.8 Episodes are triggered by increases in catecholamines or reductions in preload.9 Obstetric patients with neurocardiogenic syncope present an anaesthetic challenge, as there are no clear guidelines regarding their management. We found only two previous case reports on the planned anaesthetic management of these patients.10 We aim to highlight the anaesthetic considerations relevant to this underreported condition.
A 29-year-old primigravid woman presented at 38 weeks of gestation to our obstetric unit for anaesthetic review and formulation of a delivery plan. She had experienced fainting episodes for the last seven years. A cardiologist had diagnosed neurocardiogenic syncope by tilt-table testing six years previously. Her symptoms were precipitated by standing still for periods of time (about ten minutes while pregnant), anxiety and hot baths. A brief prodromal phase of feeling faint usually preceded syncopal episodes, during which she lay still with a vacant gaze. Consciousness was typically regained within seconds, although episodes lasting several minutes had occurred. Management recommended by the cardiologist included advice on avoiding precipitating situations, maintaining a high fluid intake, adopting a sitting or horizontal posture if feeling faint and prescription of the b blocker bisoprolol. Her syncopal episodes had reduced in frequency with this treatment. Bisoprolol was discontinued in early pregnancy due to a risk of intrauterine growth restriction. However, the plan was to resume the bisoprolol if symptoms became problematic. Fortunately, she managed reasonably well with conservative measures, having experienced only two syncopal episodes in pregnancy, with the last nearly two months previously. She was otherwise fit and healthy and there had been no complications in the pregnancy. An anaesthetic plan was made incorporating certain general principles, including minimising pain and anxiety, hunger and dehydration. Aortocaval compression should be avoided as should prolonged standing leading to venous pooling in the lower limbs. Vasodilating drugs should be avoided and prolonged Valsalva manoeuvres kept to a
Accepted December 2008 Correspondence to: Dr. Nicola Wall, Department of Anaesthesia Office, Education Centre, Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS, UK. E-mail address: [email protected]
K. Jarvi et al. minimum. Blood loss should be anticipated and corrected promptly. Delivery was planned to take place in our high dependency room on delivery suite, staffed by specialist midwives trained in obstetric high dependency care. Facilities included immediate access to invasive cardiovascular monitoring (central venous and arterial), in conjunction with a range of standard vasoactive drugs and external cardiac pacing. Our patient presented in early labour at 39+5 weeks of gestation. Her cervix was 2 cm dilated, and the membranes intact. She was not thought to be in established labour, but was admitted for observation. A calm atmosphere with dimmed lights was maintained and the need for analgesia was assessed regularly. She was encouraged to eat and drink freely to avoid hunger and dehydration. When lying in bed, a full left or right lateral position was maintained to prevent aortocaval compression. Prolonged standing was avoided. Graduated compression stockings were fitted to improve venous return. Labour became established with progressively stronger contractions, requiring Entonox. Thereafter her oral intake was restricted to water. Regular antacid prophylaxis of oral ranitidine 150 mg every 6 h was prescribed. Monitoring was established with continuous electrocardiogram (ECG), oxygen saturation and non-invasive blood pressure measurement. Although the designated midwife was not expected to interpret the ECG, it was important that it was immediately available for medical staff to interpret, if needed. Over the next 3.5 h, her cervix dilated to 7 cm. Although early epidural analgesia had been agreed, she continued to decline this as her pain was well controlled with Entonox and she remained asymptomatic. As she was no longer maintaining her oral fluid intake, she was given an infusion of Hartmann’s solution at 200 mL/h through a 16-gauge peripheral venous cannula inserted under local anaesthesia. She progressed well until the second stage of labour, without any symptoms of pre-syncope, and continued to decline epidural analgesia. However, 45 min after full cervical dilatation, she felt unable to continue pushing without feeling faint. She then requested epidural analgesia. Following a 500mL bolus of Hartmann’s solution given over 20 min, the epidural cannula was sited easily in the left lateral position. She was given a 5-mL bolus of 0.125% levobupivacaine, followed 10 min later by a 10-mL top-up of 0.125% levobupivacaine plus fentanyl 100 lg. Her prodromal symptoms were much improved with epidural analgesia and she was able actively to push again. As blood pressure, heart rate and oxygen saturation remained stable, invasive monitoring was not deemed necessary at this point. However, an intravenous oxytocin infusion for augmentation of uterine contraction was required. In accordance with our standard unit guidelines,
397 oxytocin 10 units was added to 500 mL of 0.9% saline. The infusion was initiated at 1 mU/min (3 mL/h), and increased over the next hour and a half to 4 milliunits/ min (12 mL/h). Three hours after epidural insertion, maternal fatigue prompted an assisted ventouse delivery, which resulted in the uncomplicated delivery of a baby boy with Apgar scores of 9 and 10, at 1 and 5 min respectively. Good analgesia for the delivery was achieved with one 5-mL bolus of 0.25% levobupivacaine. The estimated blood loss was 300 mL. The oxytocin infusion rate was then increased to 125 mL/h. After delivery, she remained cardiovascularly stable and asymptomatic with non-invasive monitoring for some four hours after delivery. She was subsequently discharged to our post natal ward. Having remained stable, she was discharged home 5 h later. There were no postpartum complications.
Discussion We found only two previously published case reports on the planned anaesthetic management of obstetric patients with neurocardiogenic syncope.10 Both patients delivered in the same obstetric unit in the UK. Antenatally, one had been managed conservatively in the community, whereas the other had an atrial-based pacemaker in situ. Both had invasive blood pressure monitoring and continuous ECG monitoring in labour. Epidural analgesia was established in both. The first patient required caesarean section, performed under epidural anaesthesia, after a failed attempt at ventouse delivery. Epidural analgesia had the added benefit of controlling blood pressure in the second patient, who had preeclampsia. This woman went on to have an uncomplicated ventouse-assisted vaginal delivery. Neurocardiogenic syncope may be precipitated by central or peripheral stimuli,9 but many episodes have no specific provocation.11 Central triggers include those that increase catecholamine secretion such as emotional stress, pain and unpleasant sights, sounds and smells.3,9 Peripheral triggering occurs due to a reduction of venous return to the heart, as commonly occurs on standing, when 300-800 mL of blood are displaced to the veins in the lower body.3,9 Central transmission of the afferent stimuli is followed by the vasomotor centre responses of paradoxical withdrawal of peripheral sympathetic tone and a surge in parasympathetic tone, which, in turn, causes vasodilatation and bradycardia.3,9 The exact pathophysiology is unclear and complex. A variant of the Bezold-Jarisch reflex has been widely proposed as a means by which a reduction in venous return may provoke neurocardiogenic syncope. In this reflex pathway the reduction in preload leads to reduced ventricular volume. Subsequent baroreceptormediated sympathetic stimulation leads to increased ventricular inotropy.11,12 Vigorous contraction of the
398 volume-depleted ventricle is believed to stimulate mechanoreceptors (cardiac C fibres), consisting of nonmyelinated fibres that project centrally to initiate the abnormal autonomic responses.2–4 However, evidence from heart transplant recipients in whom re-innervation had not occurred, seems to contradict this theory, or at least to suggest that there are sites other that the heart for the origin of this reflex.9,12 Syncope is often preceded by prodromal symptoms including light-headedness, nausea, vomiting, diaphoresis, visual disturbances, dyspnoea, palpitations and/or paraesthesia.4,11 However, nearly one third of patients (mainly the elderly) experience few, if any, prodromal symptoms before suddenly losing consciousness.11 During a syncopal episode, patients classically appear pale and diaphoretic, with a slow, diminished pulse. Seizurelike activity may occasionally occur during asystole,2 but post-ictal states are rare.11 However, the patient may feel tired.4 In numerous cases, a diagnosis can be made from the history alone, particularly with witnessed accounts.13 A subset of patients require further cardiovascular and neurological examination and investigation. Tilt-table testing is a useful diagnostic tool.2,13 The multiplicity of treatment options for managing these patients in the community gives an indication of the complexity of the condition. Conservative management remains the mainstay of treatment, and includes educating the patient to avoid predisposing stimuli such as extreme heat, dehydration and standing for extended periods of time. Drugs such as alcohol, diuretics and vasodilators may need to be discontinued. A moderate increase in salt intake may be beneficial.2,3,14 A syncopal episode may be aborted by adopting a horizontal position and performing isometric arm and leg muscle contractions to augment venous return.15,16 ‘Tilt training,’ which involves standing against a wall for increasing periods of time each day, surrounded by cushions, has been advocated.17 Medical treatment remains controversial and is reserved for high-risk cases. b blockers continue to be regarded as a first-line pharmacological prophylactic measure.18 Their proposed mechanisms of action include diminished activation of the left ventricular mechanoreceptors (the C fibres described previously) and blunting of the pre-syncopal increase in epinephrine concentration.14 Fludrocortisone, (a synthetic mineralocorticoid), midodrine (an a1 agonist), selective serotonin reuptake inhibitors, disopyramide (a class 1a anti-arrhythmic agent) and scopolamine (an anticholinergic) are also occasionally used.4,14 There is little evidence supporting any pharmacological management of this condition specific to pregnancy. Local cardiologists advised that the following drugs could be considered for use in pregnancy: all b blockers (except atenolol in the first trimester), fludrocortisone and selective serotonin reuptake inhibitors (with the exception of paroxetine). Cardiac pacing is
Neurocardiogenic syncope valuable in certain patients, usually those in whom pharmacological therapy has failed and who have shown a predominantly cardio-inhibitory response during tilt-table testing.3 In the event of an episode of neurocardiogenic syncope, prompt treatment is important. Any delay may result in permanent cerebral damage or death.9 The primary aim must be the re-establishment of an adequate blood pressure and heart rate. The patient should be promptly placed in a lateral position with head down tilt if possible, to improve venous return. Intravenous fluids should be considered if hypovolaemia is suspected, but drug treatment must not be delayed, particularly when venous return is reduced due to redistribution of blood to peripheral compartments during regional anaesthesia. In the normal population, anticholinergic drugs are often used initially in the treatment of bradycardia. However, in a neurocardiogenic response, where bradycardia is accompanied by profound vasodilatation, increasing the heart rate alone may not correct hypotension.9,19,20 For this reason, anticholinergic drugs or pacing alone may not be effective. Ephedrine, with its effects on both heart rate and vascular resistance, is the most logical first line pharmacological agent in an acute attack.18 If hypotension persists despite adequate doses of ephedrine, then a agonists such as metaraminol or phenylephrine may be considered, bearing in mind their potential to decrease the heart rate. In a cardiac arrest, epinephrine must be given without delay.9 The management of our patient raises some discussion points. Although the benefits of early epidural analgesia had been explained, and it was offered on more than one occasion when labour was established, our patient agreed to its insertion only in the second stage, on developing prodromal symptoms while straining. Perhaps we could have ensured that the epidural catheter was sited earlier. Also, as the woman became fatigued during a prolonged second stage, earlier intervention with an assisted delivery might have been more appropriate. Invasive arterial blood pressure monitoring provides a continuous record of heart rate and blood pressure. In our case this was to be considered if she became symptomatic, or if the progress of labour indicated that an operative delivery was likely to be required. The timing of any introduction of invasive techniques remains difficult, as the act of siting an arterial line can, in itself, constitute a stimulus to cardiovascular events. In our case, we did not establish invasive blood pressure monitoring as our patient was asymptomatic with her epidural in situ, and our obstetric colleagues were confident that minimal assistance at delivery would be sufficient. Our plan in the event of operative delivery was to apply the general principles of avoiding any fall in pre-
K. Jarvi et al. load and minimising catecholamine release. Invasive arterial pressure monitoring was to be instituted and a 250–500-mL crystalloid preload was to be administered. Other appropriate measures included left lateral tilt to avoid aortocaval compression, meticulous replacement of intraoperative blood loss, and a continuous infusion or boluses of ephedrine to keep the blood pressure within 20% of the preoperative baseline. In order to avoid uterine atony after delivery of the baby, oxytocin was to be given as an i.v. infusion (5 units over 15 min) rather than a bolus, followed by a 2040-unit infusion in 500 mL 0.9% saline at a rate of 125 mL/h. Adequate postoperative analgesia and continuation of maintenance fluids were important, with postoperative care to continue in our high dependency unit. Our proposed anaesthetic options for operative delivery included incremental top-up of an existing epidural, ideally over 15 to 20 min and guided by cardiovascular responses, or a cardiostable general anaesthetic. Spinal anaesthesia, including a combined spinal-epidural technique was to be avoided, as any spinal component would be likely to increase the risk of cardiovascular instability. Options for general anaesthesia would need to be guided by the clinical condition of the patient. Several techniques would be possible. All options would need to minimise the cardiovascular responses to laryngoscopy, surgical incision and emergence. This could be achieved by techniques using opioids such as alfentanil or remifentanil, or total intravenous anaesthesia. If using volatile agents, we would have chosen sevoflurane rather than isoflurane for increased haemodynamic stability. Adequate analgesia into the postoperative period would be essential. The specific techniques used for anaesthesia and analgesia would depend on both the clinical condition of the patient and the preference of the duty anaesthetist. Neurocadiogenic syncope has important implications for anaesthetists, particularly in the obstetric patient. A joint anaesthetic, obstetric and midwifery delivery plan should be formulated well in advance. Early involvement of cardiology colleagues is also recommended. Certain general principles are always relevant to the care of these patients, regardless of the mode of delivery. Avoidance of precipitating factors and prompt treatment of syncopal episodes is essential.
399
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