Unanticipated cardiac arrest under spinal anesthesia: An unavoidable mystery with review of current literature

Abstract

Cardiac arrest during anesthesia and perioperative period is a matter of grave concern for any anesthesiologist. But such mishaps have been reported for one reason or the other in the literary sciences. We are reporting the occurrence of unanticipated delayed cardiac arrest following spinal anesthesia in two young and healthy patients. Fortunately, these patients were successfully resuscitated with timely and appropriate cardiopulmonary resuscitative measures. Occurrence of such cases needs timely reporting and exploring all the possible causes of these unusual and possibly avoidable events. The present case reports are an important addition to a series of recently published mishaps that occurred during spinal anesthesia in young and healthy patients.

INTRODUCTION

Cardiac arrest during anesthesia and perioperative period is a matter of grave concern for any anesthesiologist. Occasionally, unexpected bradycardia and asystole may develop during the administration of spinal anesthesia in apparently healthy and young patients.[1] Cardiac arrests during spinal anesthesia are described as “very rare,” “unusual,” and “unexpected” but are actually relatively common.[2,3] In the literature, the reported incidence of cardiac arrest is 6.4 ± 1.2 in 1,00,00 patients.[4] We are reporting the occurrence of unanticipated delayed cardiac arrest following spinal anesthesia in two young and healthy patients.

CASE REPORTS

Case 1

The first case pertains to a 26-year-old male weighing 75 kg who was operated for fracture tibia, recently was posted for skin grafting because of extensive skin loss over the fractured site. All the preoperative investigations including routine blood biochemistry, X-ray chest posterior anterior view, and 12 lead electrocardiograms were normal. The patient was premedicated with tablet alprazolam 0.25 mg a night before and in the morning 1 h prior to surgery which was planned under spinal anesthesia. In the operation theater (OT), routine monitoring included heart rate, electrocardiogram, noninvasive blood pressure (BP) and pulse oximetry, and baseline parameters were recorded which were normal. An intravenous (IV) access was secured with cannula and patient was preloaded with 10 mL of lactated Ringer's solution. Under all aseptic precautions, subarachnoid block was performed at L₃ L₄ space in left lateral position with 25 gauge Quincke's needle and 3.2 mL of hyperbaric bupivacaine was injected into subarachnoid space after confirming clear and free flow of cerebrospinal fluid (CSF). Five minutes after turning the patient to supine position, sensory level of block was found to be at T₁₀. During preparation of site for graft and almost 30 min after subarachnoid injection, patient started complaining of difficulty in breathing. Sensory level was rechecked which was found to be at T10. Bolus of injection atropine 0.6 mg was administered as his heart rate suddenly dropped to 38 beats/min, SpO₂ to 72% while BP became unrecordable and peripheral pulses could not be palpated. Owing to diminishing consciousness, patient was immediately intubated with cuffed endotracheal tube (ETT) of 8.5 mm and positive pressure ventilation initiated with Bain's circuit and 100% oxygen was administered. Patient developed cardiac arrest and cardiopulmonary resuscitation (CPR) was started immediately with pharmacological intervention with adrenaline, dopamine, and noradrenaline. Within 3 min, patient responded with a heart rate of 160 bpm, SpO₂-92%, and BP of 90/60 mm Hg but was restless. Patient remained restless even after administration of inj diazepam 10 mg, inj. mannitol 100 mL given and inj. phenytoin 1.5 gm in IV infusion. Considering the poor response to resuscitative measures, patient was administered 150 mg propofol and was paralyzed with 6 mg vecuronium and electively ventilated in OT. Apart from sinus tachycardia, all investigations including serum electrolytes, arterial blood gas analysis [ABG-pH-7.414, pCO2-38, pO₂-103], and chest X-ray were normal. After 4 h of elective ventilation and achievement of hemodynamic stability patient became conscious and started responding to verbal commands with good respiratory efforts and extubation was done after reversing the relaxant effect with standard doses of neostigmine and glycopyrrolate. Postextubation hemodynamic parameters were normal [heart rate (HR) 114 bpm, BP 120/84 mm Hg, and SpO₂-99%) and was transferred to intensive care unit (ICU) for further observation. Patient was discharged on 3^rd day with uneventful course in ICU.

Case 2

The second case was an 18-year-old male, weighing 60 kg, who was posted for orchidopexy. Preanesthetic and routine investigations were normal and patient was prescribed premedication with tablet alprazolam 0.25 mg and ranitidine 150 mg a night before and 1 h prior to surgery. Preoperative hemodynamics were recorded. In the OT, IV access was secured with 18G cannula and preloading was done with 0.9% saline at 10 mL/kg body weight over 20 min.

Intraoperative monitoring included HR, BP, electrocardiography (ECG), and SpO₂. Subarachnoid block was administered under all aseptic conditions in L₃-L₄ interspace with 26G Quincke's needle and 15 mg of 0.5% hyperbaric bupivacaine in left lateral position after confirming free and clear flow of CSF. Sensory blockade up to the level of T10 was attained. We waited for 10 min for complete establishment of neuraxial blockade. Before surgery could be started, just 15 min after the spinal block, patient suddenly developed convulsions with tight jaw and flexural rigidity of both arms. Immediately, inj. midazolam 2 mg and inj. butorphanol 1 mg was given intravenously and patient was ventilated with face mask and 100% O₂ but patient developed sudden cardiac arrest during this short duration. Intubation was done with 7.5 cuffed ETT and ventilation initiated again with 100% O₂. In the meantime, BP and peripheral pulses were unrecordable and CPR started. Heart rate returned to 200/min after 1 min of administration of inj. atropine 0.6 mg and inj. adrenaline 2 mg, but BP remained unrecordable. Infusion of dopamine and noradrenaline started at 10 μg/kg/min. Patient developed ventricular tachycardia (VT) after 5 min and preservative free injection of 100 mg lignocaine was administered intravenously followed by DC shock of 200J as VT did not respond to pharmacological intervention. Rhythm reverted back to sinus rhythm with HR-190/min, BP-86/60 mm Hg, and SPO₂-100%. Injection amiodarone 300 mg in 100 mL saline was given over 20 min and elective ventilation maintained with 100% O₂. Intraoperative ABG and serum electrolytes were normal. After 2 h, BP was 100/60 mm Hg with infusion of dopamine and noradrenaline at 5 μg/kg/min, HR-140/min with regular rhythm and SpO₂ of 100% was recorded. During this period of elective ventilation, chest and cardio-vascular system (CVS) findings became normal. Patient had developed spontaneous respiratory efforts with good tidal volume and started obeying verbal commands. After achieving stable hemodynamic parameters, patient was extubated and shifted to ICU for further monitoring and was discharged on 3^rd day with an uneventful course.

DISCUSSION

Spinal anesthesia is considered to be a safe procedure. However, this anesthetic technique can result in few complications among which the most dreaded though rare is cardiopulmonary arrest.[1] Although the mechanism through which spinal anesthesia induces bradycardia or asystole is not completely known, it is established that the final pathway is the absolute or relative increase in activity of the parasympathetic nervous system.[5] Cardiac arrest has been reported within 12-72 min of spinal anesthesia, while cardiovascular side effects have been reported as late as hours after the administration of spinal anesthesia.[6]

Sudden and unanticipated cardiac arrests have been reported in the literature.[1,2,3,4,5] The explanations and mechanisms related to these mishaps are, however, varied. The common physiological mechanisms probably related to the occurrence of these events are initiated by profound decrease in venous return. Reduction in right atrial pressure has been observed in 36% of the cases after low spinal levels (below T₄) and in 53% of cases with higher blockade levels.[2,5,6] The sudden decrease in preload initiates reflexes (pacemaker, Bezold Jarisch's) that can possibly cause severe bradycardia.[7] Higher neuraxial blockade resulting in hypoxia or hypercarbia can cause profound peripheral vasodilatation leading to significant decrease in venous return and poor atrial filling. The sympathetic blockade decreased venous return and unopposed parasympathetic activity may produce significant degree of bradycardia and hypotension resulting in cardiac arrest.[8,9] The physiological augmentation of these activities can be attributed to blockade of T8-L1 fibers thus leading to decrease catecholamine secretion as a result of blockade of suprarenal glands which can produce refractory cardiac arrest.[10] In the present scenario, the level of sensory blockade was T₁₀ in both the patients so possibility of this being the cause in our cases seems less likely.

The other mechanisms involved in cardiac arrest after spinal anesthesia include administration of excessive doses of local anesthetics in a previously hypovolemic patient which can be secondary to preoperative fasting, malnutrition, dehydration, use of diuretics or vasodilators. Even the perioperative events such as bleeding, changes in patient's positioning, placement of bone cement, light nature of anesthesia in the background of comorbidities and others can be responsible for cessation of cardiac activity. It is generally recommended that the level of blockade should be limited to T₆ and hemodynamic reserves should be evaluated and monitored for any complication. The degree of bleeding should be observed regularly and replaced with blood whenever necessary, so as to reduce the morbidity and mortality.[11] The present case reports pertains to young ASA grade I patients, who were preloaded with adequate fluid before administration of anesthesia. Then, the surgery did not start so all the above-mentioned causes do not seems to offer any plausible etiology.

Local anesthetics are widely used in modern medical procedures. Though the incidence of reported adverse effects of local anesthetics is low, occasional severe toxicity and deaths have been reported.[12] Among all, bupivacaine is considered to be 4-16 times more cardio-toxic than lignocaine.[13] Delayed cardiac arrests have been reported after 20 min of spinal anesthesia.[12,13] This possibility cannot be ruled out comprehensively in the present scenario as one of the patient developed convulsions before cardiac arrest, while another patient had uneasiness and difficulty in breathing almost 20 min after administration of spinal anesthesia.

Circulatory or respiratory insufficiency can occur after inducing sedation for the purpose of giving comfort and relieving anxiety related to surgical procedure. The sedated state can result in loss of spontaneous verbalization for a brief period of time before detection of cardiac arrest. Major hypoxic events (SpO₂ <85% for >30 s) have been reported without apparent cyanosis or changes in the respiratory pattern. Thus it is possible that respiratory insufficiency may have been present but clinically unrecognized.[14] It has been suggested recently that the combination of sympathetic blockade produced by high spinal anesthesia and vagolytic effect of fentanyl might account for the sudden appearance of bradycardia.[15] Drugs such as droperidol can also lead to severe hypotension and sudden cardiac arrest during spinal anesthesia on account of their α-blocking effect.[16] Patients on β blockers and other alternative medicines provide another challenging situations as the cardiac arrest in these patients can be refractory as vasoconstriction mechanisms in the peripheral vasculature may be impaired.[2,5,17] But in the present clinical situation, both the patients were neither receiving any β blockers or other medications nor any sedation was administered before the occurrence of cardiac arrest.

The term “vagotonia” describes the clinical situation of resting bradycardia, AV block or complete AV dissociation that is normally present in 7% of the population.[18] In such population, incidence of asystole is higher during performance of procedures which can enhance vagolytic activity.[19,20] Cardiac arrest is more common in young individuals with an established fact that vagal tone is greater in these patients and increase in parasympathetic activity further enhances exaggerated vagal tone.[5,21] This could be one of the plausible causes in our patients. Unexpected cardiac arrest has been reported after small postural changes of the patient including placing a leg in the holder and turning the patient to the left lateral or prone position and in some cases the arrest has been reported even after the surgical procedure had already finished.[22] It seems difficult to explain these situations based only on preload changes. May be, they are due to reflex phenomena similar to those of autonomic dysfunction or hyperreflexia described in patients with a spinal cord section. Thus, there should be minimal movement or mobilization of the patient after spinal anesthesia. However, in the present clinical scenario, patients had cardiac arrest in supine position which excludes the above-mentioned plausible cause.

The possibility of pulmonary embolism in the first case also does not seem to be a cause of cardiac arrest, because typical clinical presentation apart from shortness of breath such as chest pain, (pleuritic in nature) cough, and hemoptysis were absent. Moreover, intraoperative investigations such as ABG, ECG, and CXR were also normal. Chest and CVS findings were also normal and no features suggestive of pulmonary edema were observed in either of the patients. Further, early recovery in our patients without any cardiac or central neurological sequelae does not favor the possibility of any pulmonary embolism episode.

Finally, the significance and management of such clinical situations depends upon anesthesiologist's acumen and attitude while detecting that something is “going wrong”. The experience-based empirical anesthesia practice should always consider evidence-based approach in such clinical situations.[23] The best clinical pearl in such situation is to believe and treat immediately what is happening in front of you. Disbelief and insecurity are common patterns of this situation and may influence the final outcome.

We wish to emphasize that a caution must be exercised when administering spinal anesthesia in high- risk patients. The knowledge of the physiological changes caused by spinal anesthesia and its complications, as well as adequate patient selection, respecting the contraindications of the procedure are extremely important. When a decision to use spinal anesthesia is made adequate monitoring and constant vigilance are of paramount importance. Epinephrine should be considered early in the treatment of sudden bradycardia, especially if conventional doses of atropine or ephedrine are not effective.