In 1988, Caplan et al. reported 14 unexplained cardiac arrests during spinal anesthesia and, recognizing that hypovolemia played an important role, they suggested that ‘”prompt augmentation of central venous filling might have lessened the damage.”1 Despite this warning, similar arrests have continued to occur with approximately one1 arrest for every 1,000 spinal anesthetics.2-5 The severity of injury has remained high and there are currently 170 cases of cardiac arrest during spinal or epidural anesthesia in the ASA Closed Claims Study database and almost 90% of these claims are for brain damage or death.6
Initial misconceptions about the etiology of these arrests may have delayed progress in treating and preventing these arrests.7-9 It is now rare for these arrests to be attributed to respiratory depression or “high” spinal anesthesia.2,10,11 Evidence for a common circulatory etiology comes from studies using healthy volunteers who have experienced bradycardia or cardiac arrest in settings that mimic the effects of sympathetic blockade. Jacobsen et al.12 studied the effect of sympathetic blockade on left ventricular (LV) diameter with echocardiography in eight unpremedicated volunteers and observed that two of them developed bradycardia and hypotension with epidural anesthetic levels of T8 and T9. These effects coincided with a reduction in LV diameter and were reversed by head-down positioning with rapid infusion of IV fluids. The increased levels of human pancreatic peptide associated these episodes of bradycardia are consistent with vagal activation.
It is well established that vagal responses can be triggered by decreases in preload. In fact, cardiac vagal tone is enhanced primarily through decreased venous return.13 This effect can be profound. Reductions in right atrial pressures of 36% with spinal anesthesia levels below T4 and by 53% after higher levels of blockade have been reported.14 These effects can be attributed to vasodilation with redistribution of central blood volume to the lower extremities and splanchnic beds. With acute blood loss or “third-space” fluid loss, these effects are even more pronounced with decreases in central venous pressure during spinal anesthesia of 66% or higher.15,16
Such decreases in preload may initiate reflexes that cause severe bradycardia. Three such reflexes have been suggested.17 The first involves the pacemaker stretch. The rate of firing of these cells within the myocardium is proportional to the degree of stretch. Decreased venous return results in decreased stretch and a slower heart rate. The second reflex may be attributable to the firing of low-pressure baroreceptors in the right atrium and vena cava. The third is the Bezold-Jarisch reflex in which receptors in the left ventricle are stimulated by a decrease in ventricular volume and cause bradycardia. This reflex slowing should allow time for more complete filling of the heart.
These vagal responses to decreases in preload cause more than bradycardia. A study of negative pressure applied to the lower body to cause functional hypovolemia demonstrated progressive vagal symptoms including sweating, nausea and syncope.18 One subject progressed from vagal symptoms to abrupt sinus arrest. In a separate study, two subjects experienced vagal arrests after 10mL/kg of blood was withdrawn to simulate acute blood loss with epidural block levels of T4 to T6.19
Taken together, these studies demonstrate that hypovolemia can precipitate not only classic vagal symptoms, but also full cardiac arrest in healthy patients. While one might assume that maintaining preload during spinal anesthesia is a consistent priority for anesthetists, the literature demonstrates otherwise. Geffin and Shapiro reported that preloading with a bolus of 300 mL was not practiced during the period when they experienced 12 cases of severe bradycardia or full arrest during spinal anesthesia.4
Even with conventional fluid management during a spinal anesthetic, decreases in preload can occur so quickly with altering patient position, releasing a tourniquet and other common perioperative events that there may not be time to give sufficient volumes of fluid over several minutes. When an abrupt decrease in preload is suspected, elevating the legs while rapidly infusing fluids can be helpful. If this does not rapidly reverse vagal symptoms, then other treatments should be considered. Anticipating an impending cardiac arrest can be difficult because hypovolemia and the subsequent increase in vagal tone may manifest initially as only mild nausea or diaphoresis. Treating the source of these symptoms is appropriate especially if the patient has strong resting vagal tone, a block level above T6 or other risk factors for severe bradycardia and cardiac arrest during spinal anesthesia.11 Multiple simultaneous interventions may be necessary to prevent vagal predominance. Gratadour et al.20 reported that neither volume loading nor infusion of a mixed alpha- and beta-agent during spinal anesthesia was not sufficient to prevent three study patients from experiencing bradycardia and hypotension associated with increased baroreflex activity during spinal anesthesia. When nausea, bradycardia or hypotension are evident during spinal anesthesia, additional volume loading, the use of a vasopressor, and prophylactic treatment with atropine should all be considered.
Atropine is recommended to counteract increased baroreflex activity during spinal anesthesia because glycopyrrolate is ineffective in this setting.5,21 Prophylactic treatment of bradycardia with atropine may decrease the frequency and morbidity of the arrests that occur during spinal anesthesia. Brown et al. reported only three cardiac arrests during a period when 10,080 spinal anesthetics were performed and none of the arrests resulted in “neurologic injury.”9 This was attributed to vigilance and their “willingness to utilize IV atropine (0.4-0.6 mg), ephedrine (25-50 mg), and epinephrine (0.2-0.3 mg) in stepwise escalation of therapy when bradycardia develops following spinal anesthesia.” Similarly, Geffin and Shapiro reported full recovery in all 12 patients treated for bradycardia or asystole following spinal anesthesia.10 This treatment included atropine for 11 of the 12 cases and it was typically used in combination with a vasopressor (ephedrine, epinephrine or phenylephrine). Atropine and a vasopressor (ephedrine) were also utilized in the five successful resuscitations reported by Lovstad et al.22 Taken together this represents 20 successful resuscitations in settings where atropine is used as the first line therapy.
Unfortunately not all of the arrests that occur during spinal anesthesia are successfully treated and fatal arrests still occur in healthy patients.2 With severe bradycardia or full cardiac arrest, the prompt use of epinephrine is recommended.1,9,23 Currently, epinephrine is used in less than one-half of these arrests and up to 25% of the arrests during spinal anesthesia arrests are fatal.2
While many factors can contribute to cardiac arrest during spinal anesthesia, vagal responses to hypovolemia often play a key role. Patients with risk factors for bradycardia or those with other vagal symptoms may be at increased risk for cardiac arrest during spinal anesthesia. This has important implications. Spinal anesthesia may not be the best choice for a patient with vagotonia or for a procedure where rapid blood loss is likely. 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.
Standard regimens for volume preloading may not be sufficient to maintain adequate preload, so a low threshold for administering additional fluid boluses or using a vasopressor may be appropriate. For patients with bradycardia during spinal anesthesia, 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 indicated. For cardiac arrest, full resuscitation doses of epinephrine and atropine, additional volume loading and transcutaneous pacing should all be considered. With the popularity of spinal anesthesia and the reported frequency of these arrests, the potential impact of these interventions on further improving the safety of spinal anesthesia could be substantial.
Dr. Pollard is the Associate Chief of Staff for Education at the VA Palo Alto Health Care System and an Assistant Professor in the Department of Anesthesia, Stanford University, Stanford, California. (John.Pollard@med.va.gov)
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