a 39-year - old woman , ( gravida 7 , para 1 , [ weight 67 kg , height 152 cm ] ) at 38 weeks of gestation , was admitted for an elective cesarean section . she had a history of self - limited palpitation , about 3 - 5 times per day . this palpitation began approximately 10 years ago and usually stopped within a few seconds , without other significant symptoms . during pregnancy , she had experienced new symptoms : episodes of sudden nausea , general weakness , and dizziness after prolonged standing . these symptoms were easily relieved by sitting or squatting . the preoperative blood test , urinalysis , chest x - ray , electrocardiogram ( ecg ) , and echocardiogram were all normal . however , her 24 hour holter monitoring revealed one episode of non - sustained ventricular tachycardia ( nsvt ) . five to six hours before the surgery , she felt the same self - limited palpitation , but no other symptoms were observed . we started our routine monitoring with ecg , noninvasive arterial pressure , and oxygen saturation . supplemental oxygen was administrated by a facial mask with a reservoir bag at the rate of 6 l / min . her vital signs were a heart rate ( hr ) of 92 - 95 bpm with normal sinus rhythm , 103 - 104/63 - 64 mmhg of blood pressure ( bp ) , and 100% of oxygen saturation ( spo2 ) . because she had a history of nsvt , a 20-gauge catheter was inserted , at her left radial artery , for continuous arterial pressure monitoring . after positioning the patient to the right lateral decubitus , 8 mg of 0.5% hyperbaric bupivacaine , mixed with 20 g of fentanyl , was injected with a 25-gauge spinal needle at l4 - 5 interspace . her vital signs were 92 bpm of hr , 102/63 mmhg of bp and 100% of spo2 , immediately after spinal anesthesia . then , the patient was put in a supine position with a left lateral tilt , and was given 50 g of prophylactic phenylephrine intravenously for the prevention of hypotension after the spinal anesthesia . the initial block level , 2 minutes after the introduction of spinal anesthesia , was at t10 checked with cold sense using an alcohol swab . as the block height went higher , the patient showed hypotension of 88/40 mmhg with 95 bpm of hr , and complained of nausea . thus far , 700 ml of ringer 's lactated solution had been administrated intravenously . relative hypovolemia , caused by alpha - blocking effect of spinal anesthesia , was the suspected cause of hypotension . therefore , we immediately injected phenylephrine twice ( 50 g each ) , and continued hydration with hydroxyethyl starch ( voluven , fresenius kabi , germany ) . her vital signs were stabilized with 96 bpm of hr and 140/74 mmhg of bp , without showing arrhythmia or reflex bradycardia , after phenylephrine administration , as well as her nausea stopped . sensory level to alcohol swab to the t3 was noticed , 10 minutes after the spinal anesthesia . within 10 minutes of the skin incision , a 3.9 kg female was delivered with apgar scores of 9 at both 1 and 5 minutes . her vital signs were 98 bpm of hr with normal sinus rhythm , 128/68 mmhg of bp , and 100% of spo2 . one gram of cefazolin ( cefamezin , dong - a pharm , korea ) , mixed with 10 ml of normal saline , was administrated intravenously after a confirmation of a negative antibiotic skin test result . then she suddenly deteriorated with cardiovascular collapse , respiratory arrest , and loss of consciousness . the qrs complex disappeared with only p - waves being observed ; eventually asystole occurred . cardio - pulmonary resuscitation ( cpr ) was started immediately with external cardiac compression , manual ventilation with 100% oxygen with ventilator mask , rapid hydration , and trendelenburg position . after the injection of 1 mg of epinephrine , along with 1 minute of cpr , the ecg showed narrow qrs complexes with irregular r - r interval . however , her systolic pressure remained at 30 - 40 mmhg , without external cardiac compression . approximately 3 minutes after cpr , the hr recovered up to 80 - 90 bpm with regular narrow qrs complex and an effective arterial pressure ( 80 - 90/70 - 80 mmhg ) . the patient gradually recovered her consciousness , spontaneous breathing , and orientation within a few minutes , and was placed horizontally with caution . ephedrine 10 mg was administrated twice , when the systolic pressure was lower than 80 mmhg , followed by continuous infusion of dopamine at the rate of 5 g / kg / min . the total operation time was 80 minutes , in addition , 700 ml of hartmann solution and 500 ml of hydroxyethyl starch ( voluven , fresenius kabi , germany ) were infused . after the operation , she was transferred to the surgical intensive care unit ( sicu ) for an intensive cardiovascular monitoring . the postoperative arterial blood gas analysis , complete blood count , electrolyte , and coagulation tests were normal and only serum troponin i was mildly elevated ( 0.298 ng / ml ) . also , the ecg and chest image showed no abnormality . after 27 hours of close observation in the sicu , she was transferred to the general ward . in this case , the possible cause of cardiac arrest includes : vasovagal response ; ventricular arrhythmia ; amniotic fluid embolism ( afe ) ; and anaphylaxis after the administration of cefazolin . we believe that the vasovagal response should be the most probable cause of her cardiac arrest . firstly , although the history of nsvt , of course , was one issue for abnormal cardiac activity , it was not the direct cause of cardiac arrest . in addition , the progressively slowing hr , immediately before the cardiac arrest , suggests their supraventricular origin . secondly , unique characteristics of afe , such as disseminated intravascular coagulation , pulmonary edema , and heart failure , were not observed . her postoperative coagulation test , chest radiography , and echocardiography were all within normal limits . also , the patient had a good response to cpr and recovered without complication , while cardiac arrest originated from afe usually has a poor response to cpr , and thus , exhibits a high mortality rate . anaphylaxis is a severe systemic allergic reaction , and is typically presented with multi - organ system involvement . nausea is a common gastrointestinal symptom of anaphylaxis , and acute anaphylactic shock can trigger bezold - jarisch reflex . however , her preoperative allergy skin test ( ast ) result was negative for cefazolin , and there was no other evidence of anaphylaxis ; itchiness , flushing , or swelling of the skin and mucosa , as well as wheezing or stridor in the respiratory system . on the other hand , many factors in this case support vasovagal response , as the cause of sudden cardiac arrest ( fig . 1 ) . the patient was a full term woman , and had several vasovagal episodes before the surgery ; she was more susceptible for vasovagal response . term pregnant women experience aortocaval compression in the supine position , followed by a decrease in the right atrial filling pressure . in about 8% of the pregnant women , cardiovascular system can not compensate for severe abrupt drops in venous return , and hence , the supine hypotensive syndrome develops . furthermore , term pregnant women present significant decrease in systemic vascular resistance ( -25% ) by the development of a low resistance vascular bed in the placenta and vasodilation caused by prostacyclin , estrogens , and progesterone . not only an increase in the plasma volume ( + 50% ) , but also a compensatory sympathetic activation with increased hr ( + 25% ) , stroke volume ( + 25% ) , and cardiac output ( + 50% ) maintain hemodynamic stability . however , this compensatory sympathetic activity is blocked during neuraxial anesthesia . in cesarean section , due to a lower maternal mortality and complication rate a mid- or high - thoracic level block ( t4 ) is necessary to comfort the patient . therefore , the incidence of hypotension ( 63% ) and severe bradycardia ( 6.7% ) are much higher . introduction of the left lateral tilting position , and a massive pre - hydration before neuraxial anesthesia ( 10 - 20 ml / kg of crystalloid solution or 250 - 500 ml of colloid solution ) have reduced the incidence of hypotension and cardiac arrest during a cesarean section . the patient 's block level was t3 ; in this block level , the sympathetic vasomotor tone , arising from t5 to l1 , is completely blocked , while the sympathetic cardiac accelerator fibers that are arising from t1-t4 are only partially blocked . when the patient showed nausea and mild hypotension after a spinal anesthesia , judging from the hr , we administrated crystalloid and phenylephrine . it was effective , and she showed stable vital signs , until the beginning of placental expulsion . however , similar to that of the previous reports , this case showed an abrupt onset of severe sinus bradycardia , and cardiac arrest in a patient who was hemodynamically stable , well oxygenated , and comfortable . we suggest an inversion and traction of the uterus , during the placental expulsion , as the triggers of catastrophic vasovagal response . a transient uterine inversion occurred during the placental expulsion , and immediately after that , cardiac arrest occurred . there are some case reports of hemodynamic instability , during the placental expulsion , due to an inversion or traction of the uterus . during a uterine manipulation , stretching of the peritoneal and broad ligaments around the uterus can result in a secondary stretching of infundibulopelvic ligaments ; which then can cause vasovagal reflex via the afferent nerve stimulation . in these cases , patient 's hemodynamic status improved dramatically , immediately after the reposition of the uterus , which suggests a vasovagal response . our patient 's cardiovascular system could not compensate for this vasovagal response , potentiated by a high neuraxial anesthesia with impaired reflex tachycardia and vasoconstriction in blocked segment ; eventually leading to a cardiac arrest . acute hemorrhage , during placental expulsion , may have played a role in vasovagal response , which decreased the venous return . however , it does not seem to be the main cause of vasovagal cardiac arrest . the total estimated blood loss of this case was about 500 ml ; which is less than the average blood loss during a cesarean section . anxiety and fear make the management of a patient difficult , and can cause vasovagal response . on the other hand , due to the risk of maternal desaturation , neonatal sedation and respiratory problem , our hospital provides intraoperative sedation , after the confirmation of an uneventful childbirth and placental expulsion . alert patients can give us important information by complaining their symptoms that can not be obtained by monitoring vital signs . also , alert patients can experience and remember the moment of childbirth and the first contact between mother and baby . in this case , the patient did not let out her feelings through the operation ; she did not seem to be anxious , nervous or restless . however , cesarean section in an unfamiliar environment would have put an extremely heavy burden on the patient , and childbirth may cause huge emotional change . after childbirth , she smiled at her baby being examined by the nurses , and consequently , began to tear . anxiety and emotional change may have played an important role in triggering or exaggerating a vasovagal response . aggressive treatments , during cpr , including intravenous administration of epinephrine , rapid hydration and trendelenburg position , were effective in this case , and no postoperative complications were observed . similar rapid recovery and relatively satisfactory outcomes were reported in the previous cases of vasovagal cardiac arrest . their treatment included early recognition , chest compression , manual ventilation with 100% oxygen , rapid hydration , and administration of atropine , ephedrine , phenylephrine and epinephrine . firstly , a careful history taking regarding fainting or syncope , and proper preoperative evaluations , such as head - up tilt test would have reduced the risk of unprepared vasovagal reaction . secondly , a careful and slow induction of epidural anesthesia would have reduced the risk of high neuraxial anesthesia . thirdly , maintenance of adequate preload with sufficient hydration , before neuraxial anesthesia , and placental expulsion would have prevented sudden decrease in the venous return . fourthly , intravenous administration of ephedrine , rather than phenylephrine , after neuraxial anesthesia induced hypotension would have prevented severe reflex bradycardia , by stimulating both alpha- and beta - adrenergic receptor systems . finally , appropriate intraoperative sedation would have reduced the anxiety of the patient , and possibility of a vasovagal response . vasovagal response is just a reflex , making it difficult to predict ; hence , hard to prevent . the hemodynamic collapse during a severe vasovagal response takes place in an instant ; in the present case , asystole occurred in less than 5 - 10 seconds . without constant and careful attention , and appropriate preparation , early recognition and treatment are unlikely to be achieved . fortunately , we continuously monitored the patient 's invasive arterial pressure in preparation for ventricular arrhythmias , so that immediate assessment and treatment were possible . however , monitoring of an invasive arterial pressure is not indicated for routine cesarean section , and pain and/or anxiety , during arterial cannulation , can trigger the vasovagal response . thus , the risks and benefits of invasive pressure monitoring should be considered , carefully , before making any clinical decision , based on the individual patient 's condition and characteristics of previous vasovagal episodes . in conclusion , we described a patient with severe vasovagal cardiac arrest , during the spinal anesthesia for cesarean section . in korea , this is the first case report of vasovagal cardiac arrest , during a spinal anesthesia for cesarean section . this case illustrates a serious potential risk of vasovagal response superimposed on neuraxial anesthesia , during a cesarean section . vasovagal response should be suspected , among the many potential causes of cardiac arrest during a cesarean section , especially when cardiac arrest occurs during placental expulsion . careful history taking and preoperative evaluation , appropriate preload management , early recognition of vasovagal response by vigilant monitoring , and prompt treatment of hemodynamic collapse , were important lessons we have learned in this case .
the vasovagal response is characterized by an inappropriate combination of bradycardia and paradoxical vasodilation . during a general or neuraxial anesthesia - induced sympathectomy , a sudden vagal activation and/or 
 an acute reduction in sympathetic tone can cause serious vasovagal responses . 
 neuraxial anesthesia for cesarean section may trigger vasovagal response , due to multiple risk factors ; high neuraxial block , sudden hemorrhage , aortocarval compression , peritoneal manipulation , and emotional stress . 
 a 39-year - old pregnant woman , at 38 weeks of gestation with episodes of non - sustained ventricular arrhythmia and newly developed vasovagal syncope during pregnancy , was scheduled to undergo a spinal anesthesia for an elective cesarean section . immediately after the placental expulsion , a sudden severe bradycardia , followed by a cardiac arrest occurred . 
 the patient fully recovered after prompt cardiopulmonary resuscitation with chest compression , manual ventilation with oxygen , rapid injection of epinephrine and hydration . 
 this case illustrates a serious potential risk of vasovagal response superimposed on neuraxial anesthesia , during a cesarean section , especially during placental expulsion .