SUDDEN cardiac arrest during spinal anesthesia can occur in otherwise healthy patients. 1–6Although respiratory depression secondary to excessive sedation is responsible in some cases, sudden cardiac arrest can occur without overt signs of respiratory depression in hemodynamically stable patients. 1
Vasovagal reactions have been reported to cause cardiac arrest during spinal and epidural anesthesia. 5,6Increased vagal tone, or vagotonia, is present in approximately 7% of the population. 7Such individuals frequently have a history of recurrent reactions precipitated by emotional or physical stress. Vagotonic manifestations can include nausea, sweating, pallor, bradycardia, hypotension, and syncope. 7,8If a patient who is prone to have vasovagal reactions is exposed to emotional stress during spinal anesthesia, what might otherwise be a benign or transient reaction may progress to cardiac arrest. 5,6Two incidents of syncope and asystole, during two separate spinal anesthetics, are described in a patient with a history of recurrent vasovagal reactions.
A 37-yr-old, 170-cm, 67-kg, 14-weeks-pregnant patient was scheduled to undergo cerclage for cervical incompetence. Medications included prenatal vitamins, and no allergies were reported. An electrocardiogram was not available. The remainder of the history and physical examination were unremarkable, except for a history of “passing out” if exposed to needles. Three years earlier, the patient fainted during a spinal anesthetic for a similar procedure. Medical records from the first cerclage were received only after discharge from this admission. Then, the patient was 12 weeks pregnant and scheduled for her first cervical cerlage. She was given 50 mg of 5% lidocaine without epinephrine in the sitting position. Soon thereafter, she fainted, but she recovered spontaneously after 30–60 s. Blood pressure (130/80 mmHg) and heart rate (85 beats/min) were reported as stable during the syncopal episode. The anesthesiologist did not record or recall the sensory level achieved by the spinal anesthetic, except that the level was not high and sensory and motor function of the upper extremities was intact. No sedation was administered. Despite the patient's fear of needles, she consented to a spinal anesthetic for the second procedure.
Upon arrival in the operating room, standard monitors were applied, including a pulse oximeter and a nasal cannula with an end-tidal carbon dioxide sampling port. Midazolam, 2 mg intravenously, was given to reduce her anxiety during placement of the spinal anesthetic. Before the intrathecal injection, 1,500 ml of Ringer's lactated solution was administered intravenously. An intrathecal injection of 80 mg of 5% lidocaine in dextrose was performed using a 25-gauge needle, with the patient in the left lateral decubitus position. Immediately after the injection of the anesthetic, the patient was moved to the supine position. The operating table was tilted so that the patient's head was elevated slightly. Blood pressure and heart rate decreased slightly from 120/70 to 105/65 mmHg and 80 to 70 beats/min, respectively, after injection of the anesthetic. A stable T4 level was achieved 10 min after the lidocaine injection. The patient was awake and breathing comfortably. Twenty minutes after administration of the spinal anesthetic, the patient complained of left hand and arm pain as an antibiotic was given intravenously. Immediately after verbalizing these complaints, bradycardia was noted, which progressed to asystole with loss of consciousness and no palpable blood pressure. The patient was given 100% oxygen by mask, chest compressions were begun, and 1 mg of atropine was administered intravenously. Approximately 30 s later, a sinus rhythm and palpable pulse were noted, and chest compressions were discontinued. Blood pressure and heart rate were 115/70 mmHg and 90 beats/min, respectively; the patient was awake, alert, and breathing without difficulty. Hand strength was not diminished, and the sensory level remained at T4. The patient stated, “I guess that I passed out again.”
The balance of parasympathetic and sympathetic activity is not equal in approximately 7% of the population who have increased vagal tone, or vagotonia. 7Although vagotonia can occur at any age, it frequently is observed in young, athletic individuals and typically is precipitated by an emotionally or physically stressful event. Pallor, weakness, sweating, nausea, and retching frequently precede unconsciousness. Physiologic studies have demonstrated that vagal stimulation decreases heart rate, cardiac output, blood pressure, and systemic vascular resistance. 8Electrophysiologic studies have demonstrated that conduction across the atrioventricular node is prolonged or dissociated, and resting electrocardiograms frequently reveal first- or second-degree atrioventricular block. 7Significant bradycardia, hypotension, and syncope for up to 20 min can occur, even in the absence of anesthesia. Patients with severe or frequent syncope may be treated long-term with atropine, a sympathomimetic agent, or a permanent pacemaker. 7In most other cases, symptoms usually are transient and resolve spontaneously, as the balance between sympathetic and parasympathetic activity is restored.
The primary physiologic mechanism responsible for the syncope and cardiac arrest in this patient could be (1) uniquely related to the underlying vagotonia, (2) caused by a combination of the underlying vagotonia and the autonomic disturbances caused by the spinal anesthesia, (3) caused solely by the autonomic perturbations of the spinal anesthesia, or (4) related to either the underlying vagotonia or the autonomic disturbances but unable to make a distinction.
We believe that the syncopal incident during the first cerclage was uniquely related to the underlying vagotonia. Our patient was young and athletic and had a history of “passing out” if exposed to needles. Considering her underlying vagotonia it is not surprising that a reaction occurred in a hospital setting with ample exposure to needles and other stressful circumstances. The sensation of the spinal needle as it entered or exited the skin, or exposure to a sensory-level testing needle, was probably the precipitating event.
The cardiac arrest during the second cerclage resulted from a combination of the underlying vagotonia and the autonomic changes accompanying the spinal anesthesia. If the sympathetic system is blocked by a spinal anesthetic, and a vasovagal reaction occurs, then the balance between the parasympathetic and sympathetic systems may be disturbed even further. The additional vagal stimulation may lead to bradycardia and cardiac arrest. 3,5,6Blood pressure and heart rate were stable for over 20 min before asystole suddenly occurred after a painful intravenous injection. This stress event produced additional vagal stimulation, which in the presence of a sympathetic blockade led to cardiac arrest. In the absence of either contributing factor, the autonomic disturbances of the spinal anesthesia or the vagotonia, symptoms may been mild or unappreciated.
The autonomic changes that accompany spinal anesthesia can cause significant bradycardia and hypotension and could have been the sole cause of either the syncope or cardiac arrest. However, the syncope during the first episode occurred almost immediately after the intrathecal injection, before the local anesthetic had time to have an effect, and blood pressure and pulse were stable, and motor and sensory function in the upper extremity were intact before and after the cardiac arrest. For these reasons, it seems unlikely that the described events were solely related to the spinal anesthesia.
Although reported, 1respiratory depression is an unlikely explanation for either described incident. The patient received no sedation during the first anesthetic and received only 2 mg intravenous midazolam before cardiac arrest and was responsive, without change in pulse oximetry or end-tidal carbon dioxide readings.
Treatment of sinus arrest during spinal anesthesia depends upon the mechanisms responsible. Because most vagally mediated syncopal episodes resolve rapidly and spontaneously, treatment may be unnecessary. However, if the hypotension, bradycardia, or sinus arrest do not resolve quickly, then a vagolytic agent, such as atropine, or a sympathomimetic agent may be appropriate. Because the bradycardia and sinus arrest were felt to be vagally mediated during the second cerclage, atropine was administered intravenously and proved to be effective. If no response was observed with atropine, epinephrine would have been the next best choice. Administering a potent sympathomimetic agent as the first line of treatment, particularly if there is any doubt as to the cause of the cardiac arrest, has its advantages. Alpha-adrenergic stimulation raises systemic vascular resistance essential for coronary and cerebral blood flow during cardiopulmonary resuscitation, and β-stimulation opposes the negative chronotropic and the inotropic effects of vagal stimulation.
Prompt treatment is important. In a closed-claim study, Caplan et al. 1attributed significant neurologic injury or death to delayed treatment of cardiac arrest during spinal anesthesia. Prophylactic treatment also may be warranted. A history of syncope after exercise or noxious stimuli and first- or second-degree atrioventricular block indicate a state of vagotonia. Prophylactic administration of atropine should be considered, and an external pacemaker readily available.
Otherwise healthy patients can experience sudden cardiac arrest during spinal anesthesia. Vasovagal reactions can occur during spinal anesthesia, may exacerbate the adverse hemodynamic consequences of spinal anesthesia, and led to bradycardia, syncope, and cardiac arrest. Our report suggests that a history of vasovagal reactions may indicate an increased risk of cardiac arrest during spinal anesthesia. In such patients, the clinician should consider administration of prophylactic atropine and be prepared to provide prompt and appropriate resuscitative measures.