Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention.

Abstract

C ardiac arrests during spinal anesthesia are described as “very rare,” “unusual,” and “unexpected,” but are actually relatively common (1– 3). The two largest prospective studies designed to evaluate the incidence of complications during spinal anesthesia reported two arrests in 1881 patients (4) and 26 arrests in 40,640 patients (5) for an overall incidence of seven arrests for every 10,000 (0.07%) spinal anesthetics. A review of approximately 4000 regional anesthetics revealed six cases of severe bradycardia (pulse of 20 to 40 bpm) and six others (0.15%) with cardiac arrest after spinal anesthesia (3). These rates are high when compared with an incidence of three arrests from any cause for every 10,000 cases (0.03%) reported for patients undergoing noncardiac surgery (6). The incidence of cardiac arrest with spinal anesthesia is also frequent compared with the rate of one cardiac arrest for every 10,000 cases (0.01%) recently reported for epidural anesthesia (5). Auroy et al. (5) reported that all but one of the 26 cardiac arrests that occurred during spinal anesthesia were related to the anesthetic. Advanced age and high ASA physical status could contribute to these arrests, but these factors are often conspicuously absent (1,3). The closed claims analysis by Caplan et al. (1) reported 14 cardiac arrests with a mortality rate that exceeded 40% in healthy patients undergoing minor procedures. 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 spinal anesthesia were ,30 years old (7). The fact that many of these arrests occur in healthy young adults during minor surgery raises the possibility that many of them are avoidable. Keenan and Boyan (8) reviewed all types of anesthesia-related cardiac arrests at a hospital over a 15-yr period and concluded that almost half were related to inadequate ventilation and that two-thirds of the anesthetic cardiac arrests were “avoidable.” Does the same pattern apply to the subset of cardiac arrests that occur during spinal anesthesia? Because sedation is used for over 80% of patients who undergo spinal anesthesia (4,9), the potential role of sedation in these arrests must be considered. The evidence for a respiratory etiology for the arrests that occur during spinal anesthesia is sparse. Spinal anesthesia sensory levels up to T4 do not lead to hypoventilation, but are associated with mild hyperventilation (10,11). Before the widespread use of pulse oximetry, it was argued that oversedation played a key role in the arrests during spinal anesthesia. It is now difficult to invoke hypoxemia as the primary cause of cardiac arrests during spinal anesthesia because they occur in the setting of oxygen saturation readings of 95–100% at the time of the arrests (2,12,13). Studies of the side effects of spinal anesthesia have also failed to corroborate a primary respiratory etiology for these arrests. In fact, none of these prospective studies has found a link between sedation and cardiac arrest during spinal anesthesia (4,5,9). Because the cardiac arrests that occur after spinal anesthesia are not closely linked with sedation or known effects of spinal anesthesia on respiratory drive, alternative mechanisms should be considered. 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 spinal anesthesia (14,15). Most of these effects are directly or indirectly related to the blockade of sympathetic efferents during spinal anesthesia. For example, the level of sympathetic blockade during spinal anesthesia 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 (16). Blockade of these fibers can result in a variety of bradyarrhythmias that are discussed later. Accepted for publication September 26, 2000. Address correspondence to John B. Pollard MD, VA Palo Alto Health Care System, 3801 Miranda Ave #112A, Palo Alto, CA 943041207. Address e-mail to John.Pollard@med.va.gov.