Cardiac arrest during epidural anesthesia has been attributed to local anesthetic and opioid overdose , intravascular injection of local anesthetic , sympathetic blockade especially in the presence of hypovolemia, excessive sedation in the presence of hypoxemia , hypercarbia , or autonomic imbalance during recovery from neuraxial blockade . Cardiac arrest due to psychogenic causes during extensive sympathetic blockade  or during establishment of spinal anesthesia  has rarely been described. In both reports, the patients had already received local anesthesia. In the first case , the patient experienced vasovagal asystole after the surgeon informed him about the poor prognosis of his vascular surgery. In the second patient , a presumed vasovagal arrest occurred immediately after the administration of local anesthetic. We report a patient who experienced cardiac arrest due to a vasovagal syncope that occurred during insertion of an epidural catheter and before any medication was administered epidurally.
A 54-yr-old male patient (weight 78 kg, height 184 cm) was admitted for repair of an abdominal aortic aneurysm. His medical history included a vasovagal episode 3 yr before the present surgery, which occurred during proctosigmoidoscopy, and which was triggered by an emotional reaction after the endoscopist commented that he had noticed a "lesion consistent with tumor." The patient did not recall any other details about the incident, except that he was lying in the left lateral position and that he had "passed out." A review of this incident in his medical record indicated a "fainting spell" during sigmoidoscopy without any electrocardiographic or blood pressure documentation.
Preoperatively, the patient's baseline electrocardiogram (ECG) was normal. A dobutamine echo stress test was negative for myocardial ischemia at 88% of maximal predicted heart rate, and left ventricular function was normal. He was taking no medications. Preoperatively, the patient appeared nervous; therefore, 1 mg of midazolam was given IV. In preparation for epidural anesthesia, the usual monitors were placed, and the patient was then positioned sitting. Oxygen was administered via a nasal cannula at a rate of 3 L/min, and 0.2 mg of glycopyrrolate was given IV. We asked the patient to warn us if he experienced any sign of lightheadedness or felt that he might faint. Epidural anesthesia was attempted at the T8-9 spinal level, and the epidural space was identified without difficulty using a loss of resistance technique. The patient's blood pressure (BP) was 134/80 mm Hg, and the heart rate was 78 bpm. During the insertion of an epidural catheter through the Touhy needle, the patient felt a paresthesia and immediately said, "I feel dizzy. I will faint." The ECG went abruptly from a normal sinus rhythm at a rate of 76 bpm to asystole; the pulse oximeter tracing ceased, and the patient had a short, generalized myoclonic movement. His eyes rolled upward; he was pale, became unresponsive, and collapsed. We quickly withdrew the epidural needle and left the catheter in, placed the patient supine, and assessed his vital signs within 30 s. At the same time, we administered 1 mg of atropine and 20 mg of ephedrine IV. As we prepared to initiate cardiopulmonary resuscitation, the ECG showed several ventricular escape beats, followed by a normal sinus rhythm. Several seconds after regaining spontaneous ECG activity, the patient awakened and asked what had happened. He did not have any neurologic deficits or stool or urine incontinence. Analysis of the ECG disclosed a 42-s period of asystole. We continued to monitor him for another 20 min. A repeat 12-lead ECG was normal; therefore, we continued with the planned surgery, which was accomplished uneventfully.
Vasovagal syncope, also known as "the common faint," is a clinical disorder that is often not taken seriously by either patients or physicians. However, this condition may be serious, and syncope due to unexplained causes has been associated with a 6% mortality rate . We describe a patient with severe vasovagal syncope with cardiac arrest that occurred during the insertion of an epidural catheter and before any medication was injected epidurally. This vasovagal presentation is unique in two ways. First, this is the first case reported of such a severe syncopal episode associated with epidural catheter placement. Second, the vasovagal attack was very serious, and the accompanying asystole was of unusually long duration (42 s). The patient regained consciousness and simultaneously resumed normal sinus rhythm in the supine positioning before IV atropine reached the central circulation.
We believe that a vasovagal attack provoked by anxiety and nociception caused the cardiac arrest in our patient. We base this assumption on the fact that he had no history of heart disease, he had had a similar episode in the past in response to a situational stimulus, and his apparent preoperative anxiety culminated when the epidural catheter elicited paresthesia. The presentation of the syncope was typical, with a brief prodrome of dizziness, nausea, diaphoresis, and pallor, followed by sudden loss of consciousness and myoclonic movement. We also believe that cases like this are more frequent in our clinical practice than they are reported to be.
Syncope most often results from a transient episode (8-10 s) of insufficient cerebral blood flow  The lack of an identifiable cause characterizes as much as half of recurrent syncopal attacks . Situational vasovagal episodes are often described in association with injury, pain, the sight of blood, hunger, crowding, long periods of standing, fear, and/or anxiety. Any of those triggering events can cause a transient catecholamine surge that enhances myocardial contractility enough to stimulate the myocardial mechanoreceptors (C-fibers) . Activation of these afferent nonmyelinated C-fibers through vigorous contraction of a relatively empty left ventricle induces bradycardia and vasodilation (Bezold-Jarisch reflex) [12,13]. Despite a substantial decrease in BP at the time of induced syncope, norepinephrine levels do not increase, whereas epinephrine levels increase severalfold . Therefore, even in patients with bradycardia or asystole, hypotension is likely the primary event, whereas vagally mediated bradycardia may play only a secondary role in the pathogenesis of vasovagal syncope . The cardiac mechanoreceptors erroneously sense that there is an increase in BP, and they therefore produce a neurohormonal response that causes the body's autonomic system to respond as if the individual was hypertensive, when the opposite is true. Another theory is that these individuals have hypersensitive mechanoreceptors and that any slight increase in contractility and/or pressure early during neuroautonomic compensation induced by the baroreceptors allows the body to mistakenly believe it has become fully compensated [11,14].
A standard pharmacologic treatment for the prevention of neurocardiogenic (vasovagal) syncope has not been established. However, several drug modalities have been used with success, including disopyramide (negative myocardial inotropic activity, anticholinergic, peripheral vasoconstrictive properties), beta-adrenergic blockers (to lower the discharge frequency of mechanoreceptors and to allow unopposed activation of alpha-receptors), anticholinergics, theophylline (blocking the uptake of adenosine that causes presynaptic inhibition and release of transmitters from peripheral adrenergic nerves), and selective serotonin uptake inhibitors (suppression of baroreceptor reflex) [10,15]. A mineralocorticoid, fludrocortisone, has also been used with success as a pharmacotherapy for neurocardiogenic syncope. The presumed mechanism is maintenance of intravascular volume and venous return, which can prevent the vigorous contraction of a hypovolemic ventricle that results in activation of mechanoreceptors . Permanent placement of a dual chamber pacemaker has also been suggested; however, in patients with neurocardiogenic syncope, drug therapy is often effective in preventing syncope, whereas artificial pacing is not . This can be explained by the pathogenesis of neurocardiogenic syncope, whereas bradycardia or asystole are secondary events. Finally, avoidance of situations that may precipitate the vasovagal episode may be advisable.
Attention to a history of syncopal episodes may help to identify patients at risk of recurrent vasovagal attacks. If such an event is anticipated based on the history, one should try to prevent it with proper communication before the procedure. This may alleviate the patient's anxiety and reduce the risk imposed by the triggering event. Although performing the neuraxial blockade in the recumbent position should decrease the incidence of severe vasovagal cardiovascular collapse, our patient experienced his initial episode during a sigmoidoscopy performed in the recumbent position. In addition, adequate sedation and generous subcutaneous local anesthesia to relieve anxiety and/or pain may be a useful adjunct to successful regional block in these patients. In patients who are prone to neurogenic vasovagal attack of a malignant nature, close monitoring and liberal sedation should be used before attempting regional anesthesia. Finally, as in our case, a general anesthetic with more liberal sedative and anticholinergic premedication may be an option for avoiding any situational triggers.
In conclusion, we describe a patient who experienced a vasovagal cardiac arrest during the placement of an epidural catheter. Although we anticipated the possibility of a vasovagal reaction in our patient and pretreated him with glycopyrrolate and light sedation, these medications were not sufficient to suppress the excessive vagal tone caused by our patient's anxiety, which culminated in a cardiac arrest.
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