Fully successful resuscitation despite prolonged cardiac arrest.

Sudden cardiac arrest following spinal anesthesia is a relatively common and often fatal complication. Careful patient selection, appropriate dosing of the local anesthetic, volume loading, close monitoring and prompt intervention at the first sign of cardiovascular instability should improve outcomes.

INTRODUCTION

Cardiac arrest following spinal anesthesia typically responds quickly to the administration of epinephrine. In the series reported by caplan et al.[1] “Spontaneous rhythm and independent perfusion” returned within an average of 3 minutes after intravenous epinephrine was administered. We report a more delayed response to rapidly escalting doses of epinephrine with a good outcome.

CASE REPORT

A 19-year-old American society anesthesiologists (ASA) physical Status I male was admitted to operating room for knee manipulation. Spinal anesthesia (SA) was selected in part because he had a good experience of SA with a previous surgery. SA was conducted with 3 cc hyperbaric bupivacaine 0.5% injected at the L5-S1 interspace. This dose was selected because it was possible that positive findings could lead to a two-hour procedure. The patient received 350 cc of Ringer's lactate and his blood pressure (BP) was 100/60 mmHg and the pulse rate was 80/min at the beginning of procedure. The BP was monitored every 3 min, while the pulse and oxygen saturation were continuously monitored. There was a slow decline in BP to 70/40 mmHg during the first 10 min which was treated with fluid during the 30-min procedure. The BP stabilized between 85-95/50-60 mmHg with a pulse rate of 90 beats per min and an oxygen saturation of 99% (oxygen via face mask). During the case there was close verbal communication between the surgeon and the patient. At the end of surgery, his BP was 86/56 and PR = 90/min and the patient was transferred to the recovery room. On arrival he was asked the question: “Are you OK?” and he answered: “Very well”. Initially, he was monitored with pulse oximetry and received about 400 cc Ringer's lactate in recovery (1500 cc from the beginning of anesthesia). Less than 5 min after arrival and before measuring his BP, a sudden cardiac arrest occurred with unconsciousness, apnea and no carotid pulse. Cardiopulmonary resuscitation (CPR) was initiated with endotracheal intubation and ventilation with 100% oxygen. The electrocardiogram EKG monitor showed ventricular fibrillation. This cardiac arrest required prolonged CPR with multiple defibrillation attempts (360j times 6), 20 mg of adrenaline (1, 3 and 5 mg), atropine 0.5 mg times 4, bicarbonate, lidocaine, bretylium and amiodarune.

During the resuscitation nearly 2 liters of crystalloid were administered. Later, bloody foamy fluid from the endotracheal tube was observed and diagnosed as pulmonary edema. This was treated with 100 mg of lasix and 10 mg morphine. After approximately 45 min of CPR, the patient had sinus rhythm with blood pressure of 170/110. He was then transferred to the intensive care unit (ICU) where he was supported with mechanical ventilation. His pulmonary edema resolved with a second dose of lasix 100 mg. His complete blood count CBC, and electrolytes were normal but the arterial blood gas revealed a severe mixed acidosis (primarily metabolic) which was treated. His BP stabilized between 120-100/70-80 mmHg during the next hour. Three hours after admission to the ICU, the patient gradually regained consciousness. First he began reacting to the endotracheal tube and later opened his eyes and attempted to sit. Within 4 h of admission to the ICU he was extubated and asked about his surgery. Fortunately, the patient was discharged to the ward the next day without any sequelae and with a normal brain computer aided tomography (CT) scan.

DISCUSSION

This arrest occurred in an otherwise healthy patient with a relative limited procedure. The patient had close monitoring and stable cardiopulmonary status during anesthesia without any IV medication during anesthesia. Cardiac arrests during spinal anesthesia are described as “very rare” but are actually relatively common.[1-3] In large studies, the incidence of arrests following spinal anesthesia has been 0.07% in comparison with 0.03% when general anesthesia is utilized for noncardiac surgery.[4-6] The outcome from these arrests can be very poor. The closed claim analysis by Caplan et al.[1] reported 14 intraoperative cardiac arrests, all of which were resuscitated, but six suffered such severe neurologic injury that they died in hospital (40% mortality). Of the eight survivors, only one exhibited sufficient recovery to allow independence in daily safe-care. Comparable outcomes were reported in young patients in a study of 20.000 consecutive spinal anesthetics. One-half of the patients who experienced cardiac arrest in the operating room during SA were less than 30 years old.[7] The fact that many of these arrests occurred in healthy young adults during minor surgery raises the possibility that many of them are avoidable.[8]

Before the widespread use of pulse oximetery, it was argued that oversedation and hypoxemia played a key role in these arrests, but studies show that they occur in the setting of oxygen saturation readings of 95-100% at the time of arrests.[2910] In this patient, no sedation was given so it too was unlikely precipitated by hypoventilation. The evidence for a circulatory etiology for these cardiac arrests comes from physiology studies using healthy volunteers who have experienced bradycardia and cardiac arrest in settings that mimic the effects of SA.[1112] Most of these effects are directly or indirectly related to the block of sympathetic efferent during SA. For example, the level of sympathetic blockade during SA is often two to six levels higher than the sensory level, so a patient with a T4 sensory block may have completely blocked cardiac accelerator fibers that originate from T1 to T4.[13] Blockade of these fibers can result in a variety of bradyarrhythmias and more importantly a significant decrease in venous return to the heart.[14] Decreases in preload can occur so quickly with altering position, releasing a tourniquet, and other common perioperative events that there may not be time to give sufficient volumes of fluid over several minutes. Decreases in preload can precipitate not only classic vagal symptoms, but also full cardiac arrest.

When a spinal anesthetic is selected, maintaining preload should be a priority, and prophylactic preloading with a bolus of IV fluid should not be omitted before initiating SA. Standard regimens for volume preloading may not be sufficient to maintain adequate preload so a low threshold for administering additional fluid boluses, using vasopressors or repositioning the patient to augment venous return (e.g. Trendelenberg), may be appropriate. For patients with bradycardia during SA, the stepwise escalation of treatment of bradycardia with atropine (0.4-0.6 mg), ephedrine (25-50 mg), and, if necessary, epinephrine (0.2-0.3 mg) may be appropriate. When the bradycardia is profound or a full cardiac arrest occurs, early and full resuscitation doses of epinephrine can be critical and should be promptly administered. The fully successful outcome in this case may be largely attributable to the high doses of adrenaline that were utilized.

In contrast, more limited dosing of the spinal anesthetic might have decreased the chance of precipitating this arrest. Higher doses of local anesthetic are associated with higher levels of block and a higher risk of cardiovascular collapse. The package insert for hyperbaric marcaine recommends a maximum of 12 mg for SA. In this case 15 mg of hyperbaric marcaine were utilized while a more limited the dose (12 mg or less) would have been more appropriate. When it is anticipated that surgery will be prolonged, the use of moderate doses of longer-acting agents such as tetracaine should be considered in place of using large doses of a shorter-acting agent. Alternatively, general anesthesia may be preferable when the time needed to complete surgery is very uncertain as it was in this case. Table 1 shows the factors that have been linked with bradycardia during SA.[8] These risk factors may help identify patients who are more susceptible to vagal predominance leading to circulatory collapse and asystole during SA.

Table 1

Risk factors for moderate bradycardia (Pulse, 50 bpm) during spinal anesthesia