perioperative vasovagal syncope with focus on obstetric anesthesia

Taiwanese J Obstet Gynecol • September 2006 • Vol 45 • No 3

■ REVIEW ARTICLE ■

208

Introduction

Vasovagal syncope, the most common type of syncope,is a condition known as neurocardiogenic or neurallymediated syncope. It is defined as a complex hemody-namic response characterized by bradycardia, markedhypotension and loss of consciousness. The most com-monly used model for triggering vasovagal syncope is the Bezold–Jarisch reflex [1]. Tilt-table testing, awidely used diagnostic tool, provokes vasovagal syn-cope through the Bezold–Jarisch reflex mechanism.

Vasovagal syncope has a mean prevalence of 22%in the general population [2], and has an enormousmedical, social and economic impact on the generalpopulation. Usually, this episode of bradycardia and

systemic hypotension is self-limiting. During an operation,there are many factors such as hemorrhage, posturalchange, aortocaval compression and regional anesthe-sia that can trigger a vasovagal reaction. Because thesefactors are additive when combined, severe vasovagalsyncope may lead to a lethal outcome. Moreover, encom-passing the triggers of vasovagal reactions, parturientsfor cesarean section might have higher risk [3].

This review summarizes the current knowledge ofvasovagal reflex, emphasizing clinical aspects in obstet-ric anesthesia. The opinions expressed are the resultsof our interpretation of the available data in the litera-ture up to December 2005 in conjunction with ourown clinical experiences.

Mechanism

Vasovagal syncope is one of the reflex-mediated synco-pal syndromes. In each case, the reflex is composed ofa trigger (the afferent limb) and a response (the effer-ent limb) (Figure). Nitric oxide (NO) has recently been

PERIOPERATIVE VASOVAGAL SYNCOPE WITH FOCUS

ON OBSTETRIC ANESTHESIA

Pei-Shan Tsai*, Chih-Ping Chen1, Ming-Song Tsai2

Department of Anesthesiology, Hsinchu Mackay Memorial Hospital, Hsinchu, 1Department of Obstetrics and Gynecology, Mackay Memorial Hospital, and 2Prenatal Diagnosis Center, Cathay General Hospital, Taipei, Taiwan.

SUMMARY

Vasovagal syncope refers to a reflex cardiovascular depression that gives rise to loss of consciousness with brady-cardia and profound vasodilatation. This response commonly occurs during regional anesthesia, hemorrhageor supine inferior vena cava compression in pregnancy. The changes in circulatory response from the normalmaintenance of arterial pressure to parasympathetic activation and sympathetic inhibition may cause severehypotension. This change is triggered by reduced cardiac venous return as well as episodes of emotional stress,excitement or pain. Occasionally, these vasovagal responses may be unpredictable and may dramatically pro-ceed to asystole with circulatory collapse, and may even result in death. In these circumstances, hypotensionmay be more severe than that caused by bradycardia alone, because of unappreciated vasodilatation. Regionalanesthesia, decreased venous return, hemorrhage and abnormal fetal presentation cumulatively increase therisk of vasovagal syncope in cesarean section patients. When a vasovagal response occurs, ephedrine is the drugof first choice because of its combined action on the heart and peripheral blood vessels. Epinephrine must beused early in established cardiac arrest, especially after high regional anesthesia. [Taiwanese J Obstet Gynecol2006; 45(3):208–214]

Key Words: anesthesia, asystole, bradycardia, hemorrhage, vasovagal syncope

*Correspondence to: Dr Pei-Shan Tsai, Department of Anesthesio-logy, Hsinchu Mackay Memorial Hospital, 690, Section 2, GuangfuRoad, Hsinchu 300, Taiwan.E-mail: [email protected]: March 9, 2006

Taiwanese J Obstet Gynecol • September 2006 • Vol 45 • No 3 209

Anesthetic Review of Vasovagal Syncope

implicated in the vasodilatory response associated withvasovagal syncope [4,5]. However, other studies haveshown that infusion of a NO blocker did not preventvasodilatation during syncope [6,7].

Afferent limb activitySome chemical stimuli within the left ventricular wallcan activate unmyelinated afferent type C fibers thatpass via the vagus nerve to the brainstem. These fibersreflexively increase parasympathetic tone [8] and causea vasodepressor response, the classic Bezold–Jarischreflex [9]. Other unmyelinated afferents are activatedby mechanoreceptors that are usually sensitive to leftventricular distension, but may also respond to hypo-volemia [10]. An alternative mechanism of triggeringvasodepressor reflexes could be via arterial barorecep-tors other than the cardiac route. Baroreceptor activa-tion, secondary to increased blood pressure, decreasessympathetic outflow and increases parasympatheticactivity, and subsequently leads to vasodilatation andbradycardia.

Central transmissionArterial baroreceptor and cardiac afferents enter thebrain via the glossopharyngeal and vagus nerves, andsynapse in the nucleus tractus solitarius and the ven-trolateral medulla [11]. Some syncopal reactions areinitiated by emotional factors. The limbic system of thebrain is known to be associated with emotions. In someanimal species, stimulation of the limbic sympathoinhi-bitory center causes hypotension and bradycardia [12].Strong emotions also stimulate the sympathetic nerv-ous system to increase concentrations of circulatingepinephrine [3].

Efferent limb activityDuring vasovagal syncope, the efferent responses notonly increase vagal activity to the heart, but also decreasesympathetic activity. The resulting combination ofbradycardia and vasodilatation causes significant hypo-tension. Stroke volume and cardiac output generallydecline further [13]. The decrease in sympathetic nerveactivity is followed by decreased concentrations ofnorepinephrine [3,12]. However, epinephrine concen-trations increase, causing muscle vasodilatation andtending to reduce systemic vascular resistance further[3,12].

Predisposing Factors

HemorrhageDuring World War II, cardiovascular responses to trau-matic and experimental hemorrhage were observed.When venous blood was progressively lost, blood pres-sure was initially maintained by vasoconstriction. Thiswas followed by a sudden fall in blood pressure, heartrate and peripheral resistance [14]. Barcroft et al foundthat the incidence of “fainting” increased as blood lossincreased, from 4% after loss of 440 mL to 50% afterloss of 1,000–1,200 mL [15].

Regional anesthesiaIn the blocked segments, reflex vasoconstriction canbe prevented by regional anesthesia. Hypotension maydevelop if venous return is inadequate because ofreduced blood volume or head-up tilting after highregional anesthesia. Then, syncope and abrupt brady-cardia or asystole may follow [16].

Stimulus Efferent responseAfferent pathway

Pain, emotion

Decreasedvenous return

Bradycardia

↓Norepinephrine— vasodilatation in resistance vessels

↑Epinephrine— vasodilatation in skeletal muscles

Ventricularafferents

Other viscerae.g. bladder

Vagus

Sympathetic

Sympathetic

Medullaryvasomotor

center

Highercenters

Aorticbaroreceptors

Vagus

Unmyelinated C fibersResponse to chemicaland mechanical stimuli

Figure. Mechanisms of vasovagal syncope.

OrthostasisIndividuals with vasovagal syncope have a normal ini-tial response to upright positioning. Van Lieshout et alfound that 300–800 mL of blood is redistributed fromthe intrathoracic capacitance vessels to the veins in thelower body when a supine individual stands. Compen-sation is required to maintain venous return to the heartand systemic arterial pressure [13]. Vasovagal syncopeis more likely to occur in subjects with a smaller bloodvolume [17].

Compression of inferior vena cava during pregnancyHansen noted that 12% of term women had severehypotension and collapsed while in a supine position[18]. Kinsella and Lohmann reported that somewomen suffered from an acute circulatory collapse,severe enough to mimic hemorrhagic shock, in thesupine position [19]. Reducing venous return resultingfrom compression of the inferior vena cava by the graviduterus was thought to be responsible for this phenom-enon [20]. Lees et al suggested that this “supine hypoten-sive syndrome of pregnancy” referred to vasovagalfainting [20].

Anesthesia

General anesthesia“Fainting” or asystole before induction of general anes-thesia is not uncommon and has been previously repor-ted [21–23]. Vasovagal reactions have been describedto be associated with anxiety and pain during venepunc-ture [21,24]. They occur particularly in the young or inpatients with a history of syncopal attack during vene-puncture or minor surgery [21,22,25]. The therapeuticuse of sevoflurane as an induction agent to avoid thepotentially fatal complications of malignant vasovagalsyndrome in an adult has been reported [21].

Ketamine, an old anesthetic drug, is believed to havesympathomimetic effects, although the central mecha-nism remains unclear. In contrast, other modern anes-thetic agents lack anticholinergic or sympathomimeticside effects. Simple vagal reflexes with bradycardia andtransient asystole are more common, especially dur-ing anesthesia for ophthalmic or pelvic surgery [3,26].However, hypotension will occur only if bradycardia isextreme. It is presumed that there is no component ofvascular dilatation [27]. The event resolves quickly whenthe stimulus ceases.

Spinal and epidural anesthesiaPain and anxiety may cause fainting during induction ofregional anesthesia as with general anesthesia [28,29].

A history of fainting as well as the added influence oforthostatic stress may cause vasovagal syncope duringneedle insertion or after postural change duringregional anesthesia [28,29]. Caplan et al reviewed adatabase of over 900 closed insurance claims duringthe period 1978–1986 and found 14 cases of cardiacarrest leading to death or severe brain damage inpatients having spinal anesthesia [10]. They indicatedthat the landmark associated with a risk of fatality, notonly in elderly and those with comorbidity but also inhealthy patients, was T4 as the average upper limit ofsensory block. Two other prospective studies pointedout that dermatomal block to T5/6 or higher is the mostimportant factor causing the complication during spinalanesthesia [30,31].

In the time leading up to cardiac arrest, bradycardia,hypotension, cyanosis or loss of consciousness developin descending order of frequency. However, in somecases, a sudden decrease in heart rate will occur duringstable anesthesia. According to our experiences,reduced blood supply to the brain may trigger focalconvulsions.

Caplan et al also suspected two aspects of manage-ment that might have been responsible for these devas-tating outcomes [10]. The first was the use of centraldepressant drugs in addition to the regional anesthesia.They pointed out that patients given at least one butusually more than one intravenous opioid or sedative,including fentanyl, diazepam, droperidol and thiopen-tone, developed a sleep-like state. Besides, the circula-tory changes associated with high sympathetic blockplayed an important role in unappreciated respiratorydepression. Furthermore, spinal and epidural anesthe-sia prevented reflex vasoconstriction in the blockedsegments so that a critical reduction in venous returnafter vasovagal reactions was sustained. Hypertensionand tachycardia in response to hypoxia do not occurduring epidural anesthesia in dogs, probably becauseof sympathetic block [32]. Coronary perfusion pres-sure gradient during ventricular fibrillation in dogs wassignificantly reduced after high spinal anesthesia [33].In general, vasovagal reactions occur during spinal anes-thesia at an upper thoracic level and during epiduralanalgesia induced by large doses of local anesthetic[34,35]. Deep sedation is not suggested [34,35]. Anaspect of management that might have contributed to the event in some cases was the use of infusions ofepinephrine to maintain cardiac output and sodiumnitroprusside to induce hypotension [35]. Decreasesin cardiac filling pressure were recorded or surmised inseveral cases. Both β-stimulants [36] and nitroprus-side [37] have been implicated in inducing vasovagalreactions.


P.S. Tsai, et al



When the vasovagal reactions occurred, bradycardiawas reversed with atropine initially in all subjects, butephedrine, epinephrine and external cardiac massagewere also required in some cases. The immediate treat-ment of bradycardia or asystole is crucial and usuallyleads to successful outcome. However, delay in insti-tuting corrective treatment and resuscitation may causepermanent cerebral damage or death [10]. The risk ofasystole extends into the postoperative phase [35].

Overall, bradycardia and hypotension are not infre-quently noted during spinal and epidural anesthesia. Therisk of life-threatening vasovagal reactions during regionalanesthesia may be in the order of three per 1,000 [34],compared with 5% of patients who have both bradycar-dia and hypotension during spinal anesthesia [30].

Obstetric anesthesiaThe pregnant woman experiences physiologic changesin every organ system. The normal changes in the cardio-vascular system during pregnancy can simulate organicheart disease [38]. A 35% increase in blood volume anda 45% increase in plasma volume generate the physio-logic anemia of pregnancy [39]. The great veins of thepelvis and lower extremities hold a large portion of thisexpanded blood volume. Aortocaval compression by theenlarging uterus can significantly impair venous return bythe mid-second trimester [34]. Therefore, regional anes-thesia combined with inferior vena cava compressionmay cause profound hypotension, triggering vasovagalsyncope.

Holmes reviewed the literature from the 1930s tothe 1950s on maternal mortality during cesarean sectionwith spinal anesthesia. Sudden bradycardia occurredsoon after the patient was moved into the supine posi-tion, as the sympathetic block developed [40,41].Holmes pointed out that unappreciated compressionof the vena cava was the likely cause, rather than otherpossibilities such as respiratory insufficiency [40]. Leftlateral tilt during cesarean section was suggestedbecause of the improvement in venous return by reliefof inferior vena cava compression [39].

Anatomic and physiologic changes of pregnancyincrease the risk of failed intubation and the risk foraspiration of gastric contents. Pulmonary aspirationof gastric contents and failed endotracheal intubationduring general anesthesia are the main causes of mater-nal morbidity and mortality [42]. In some circumstan-ces, the stimuli of a direct laryngoscope, desaturationinduced by failed ventilation or specific anestheticssuch as propofol and suxamethonium [43,44], maycause bradycardia and even asystole during generalanesthesia. The syncopal reaction is hard to diagnosebecause of anesthetic drugs given simultaneously.

Compensated hypovolemia may become evident afterinduction of anesthesia [45].

Regional anesthesia is preferred to general anesthe-sia for cesarean section, because regional anesthesia isassociated with lower maternal mortality. We usuallyuse general anesthesia only for emergency cesarean deliv-ery of a severely distressed fetus.

Emergency cesarean sectionIndications for emergency cesarean section includemassive bleeding, umbilical cord prolapse and severefetal distress. Parturients with placenta previa, pla-centa accreta, abruptio placentae or uterine rupturehave the potential risk of profound hemorrhage thatcould initiate a vasovagal reaction. Moreover, regionalanesthesia is contraindicated in severely hypovolemicor hypotensive patients.

Abnormal fetal presentations and positionsAbnormal fetal positions and presentations increasematernal and fetal morbidity and mortality. In thesecases, intrauterine manipulation is inevitable. In ourexperience, vasovagal reaction is not uncommonlynoted during manual rotation of the fetus from transverse lie to the breech presentation. We alsoencountered vasovagal syncope combined with facialconvulsion during spinal anesthesia for cesarean sec-tion. Compression of the inferior vena cava induced bymanipulation was thought to be responsible for theevent.

Amniotic fluid embolismAlthough amniotic fluid embolism is rare, it is a truenightmare for both obstetricians and anesthesiolo-gists. Entry of amniotic fluid into the maternal circula-tion can occur through a break in the uteroplacentalmembranes. Such breaks may occur during normaldelivery or cesarean section or following placentalabruption, placenta previa, or uterine rupture. Whenthis occurs during cesarean section, it often presentsas sudden vasovagal syncope with acute circulatorycollapse. Thereafter, the response will persist becausethe following shock, hypoxemia and disseminatedintravascular coagulation are sustained. Mortalityexceeds 50% in the first hour [42].

Anesthetic Management

General anesthesiaThe vasovagal syncope mostly occurs during the induc-tion period of general anesthesia. The syncopal episodesare specifically related to needle phobia and some


P.S. Tsai, et al

induction agents. Previous fainting history contributesto the occurrence of vasovagal reaction. Topical localanesthetic cream for the venepuncture site [23] or inhal-ational induction of anesthesia [21] may be tried. Drugsimplicated in the genesis of asystole include propofol,fentanyl, suxamethonium and vecuronium.

Regional anesthesiaPreexisting hypovolemia before induction of regionalanesthesia leads to cardiovascular collapse [16]. If theblock extends above the midthoracic region, the inci-dence of vasovagal reaction increases. All parturientsshould receive a 1,500–2,000mL bolus of lactated Ringer’sinjection before neural blockade because cesarean sec-tion requires a T4 sensory level [42]. Smaller volumes(250–500 mL) of colloid solutions, such as hetastarch,are also effective [42]. However, block height of regionalanesthesia cannot be precisely controlled. The anes-thesiologists can only control the drug dose, baricityand patient positioning [46]. The lateral position forinsertion of a spinal or epidural needle is thought to besafer than the sitting position [28,29]. Prophylactic oxy-gen administration should also be considered becausehypoxemia occurs during high regional anesthesia. Pulseoximetry is helpful.

Intraoperative blood loss must be carefully replaced.Changing from a head-down to a horizontal positioncan precipitate cardiac arrest [47], whereas asystole[28] may be reversed by tilting back to a head-downposition. The necessity of using a slight head-downposition during spinal-induced hypotension has beenemphasized [3,48].

Sedation may be beneficial to parturients duringregional anesthesia, but oversedation must be preven-ted. A patient who is able to communicate symptomsmay give an early warning of the development of avasovagal reaction. Therefore, hypnotic drugs should begiven to obtain anxiolysis rather than deep sedation.

Drug treatmentAnticholinergic drugs are often the first treatment forslow heart rate during anesthesia, especially generalanesthesia. Atropine has been used as the only anti-cholinergic agent to treat asystole during regionalanesthesia [49]. But if bradycardia is combined withvasodilatation it may not be the best single agent.Hypotension during vasovagal syncope persists afterthe relief of bradycardia by atropine [50]. Ephedrine, acommonly used sympathomimetic agent, has the vaso-dilatory effect of β2 agonist in addition to the vaso-constrictive effect of α1 and β1 agonists. Unlikedirect-acting α-agonists, ephedrine does not decreaseuterine blood flow [39]. This makes it the preferred

vasopressor for most obstetric uses. Ephedrine has alsobeen reported to possess antiemetic properties, partic-ularly in association with hypotension following spinalanesthesia. Phenylephrine, a noncatecholamine withpredominantly direct α1-agonist activity, increases sys-temic vascular resistance and arterial blood pressureeffectively.

Restoration of venous return as well as drug treat-ment is urgent and must not be delayed. Head-down tiltor leg elevation should be used [10], and compressionof the vena cava should be relieved in obstetric cases[40,41].

In 1997, Liguori and Sharrock [35] reported the suc-cessful use of thump pacing for a case of asystole duringregional anesthesia. However, the most recent trial,the Vasovagal Pacemaker Study II, did not support theimplantation of dual-chamber pacemaker in vasovagalsyncope [51]. Pacing was not recommended as first-linetherapy in the vasovagal type of syncope patient popula-tion, but pacing may be useful in patients refractory topharmacologic agents and with documented vasovagalbradycardia during an episode [18]. Once persistentcardiac arrest occurs, external cardiac massage must bestarted to ensure circulation of resuscitation drugs andperfusion of vital organs [3]. Prompt treatment withepinephrine has been emphasized as crucial for suc-cessful recovery [10,35]. For asystole or persistent severebradycardia, epinephrine should be used early [52].

Conclusion

Simple vagal reactions are not uncommon during general anesthesia. During regional anesthesia, the car-diovascular change of a vasovagal reaction is augmentedby original vasodilatation resulting from sympatheticblocks. Significant hypotension may persist even afterthe relief of bradycardia or asystole. In parturients forcesarean section, the vasovagal response triggered by the compression of the inferior vena cava may lead toa lethal outcome. Early detection and early treatment arerecommended.

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perioperative vasovagal syncope with focus on obstetric anesthesia

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