Witnessed asystole during spinal anesthesia treated with atropine and ondansetron: a case report

Abstract

P Pu ur rp po os se e: : To present a case of asystole during spinal anesthesia that responded to atropine and ondansetron and to discuss the possible pathophysiology with special emphasis on the Bezold-Jarisch reflex and the role of 5-HT 3 receptors in mediating bradycardia and sympathoinhibition.C Cl li in ni ic ca al l f fe ea at tu ur re es s: : A 50-yr-old, 97-kg, healthy male presented for elective left high tibial osteotomy. Spinal anesthesia was induced uneventfully at L3-4 with 11.25 mg of hyperbaric 0.75% bupivacaine and morphine 0.25 mg. Thirteen minutes after induction, the incision site was infiltrated with 20 mL of 0.5% bupivacaine with epinephrine 5 µg·mL -1 for intraoperative hemostasis, resulting in an increase in heart rate from 74 to 90 beats·min -1 . Three minutes after infiltration of the incision site, the patient's heart rate dropped to 48 beats·min -1 , accompanied by a blood pressure of 107/51 mmHg, SpO 2 97%, and a sinus bradycardia on the electrocardiogram. The electrocardiographic complexes suddenly disappeared with loss of the pulse oximeter waveform. Pre-drawn atropine 0.6 mg iv and ondansetron 4 mg iv were administered within seven seconds of the event. After an asystolic period of 30 to 40 sec, but before chest compressions were initiated, vital signs returned to normal with no other sequelae. C Co on nc cl lu us si io on n: : Exogenous epinephrine may have triggered the Bezold-Jarisch reflex and subsequent asystole. It is postulated that the combination of atropine and ondansetron may have played a key role in resuscitation by blocking the serotonergic and cholinergic receptors in the afferent and efferent limbs of this vagally-mediated reflex. HE risk of sudden cardiac arrest in healthy patients during spinal anesthesia is well documented 1-4 with a quoted incidence of seven per 10,000 spinal anesthetics. Objectif

Reduction in spinal-induced hypotension with ondansetron in parturients undergoing caesarean section: A double-blind randomised, placebo-controlled study

“…18,19 Thus, spinal anaesthesia causes vasodilatation, hypotension, and bradycardia by sympathetic blockade, the BJR and stimulation of 5-HT3 receptors in vagal nerve endings. 5 Although we were unable to find reports of direct effects of 5-HT3 antagonist administration on cardiac output, we believe our results indicate that ondansetron prevented the serotonin-induced BJR, suppressed venodilatation, augmented venous return to the heart and resulted in lesser reductions in SBP and MAP. Blockade of the 5-HT3 receptor antagonizes the BJR induced by serotonin.…”

“…12,13 In response to hypovolaemia, stimulation of cardiac sensory receptors in the left ventricle induces the BJR and results in reflex bradycardia, vasodilation and hypotension. [12][13][14] Chemoreceptors are activated in response to decreased blood volume by serotonin, 5,13 which is released from activated thrombocytes. 5,15,16 Activation of 5-HT3 receptors, which are G protein coupled, ligand-gated fast-ion channels, results in increased efferent vagal nerve activity, 13 frequently producing bradycardia.…”

“…[12][13][14] Chemoreceptors are activated in response to decreased blood volume by serotonin, 5,13 which is released from activated thrombocytes. 5,15,16 Activation of 5-HT3 receptors, which are G protein coupled, ligand-gated fast-ion channels, results in increased efferent vagal nerve activity, 13 frequently producing bradycardia. 17 However, bradycardia occurs less frequently than hypotension following spinal anaesthesia, 4 ranging from 2.1-4.9% vs. 36.8-52%, respectively.…”

“…3 Owczuk et al observed that intravenous ondansetron attenuated spinal-induced hypotension. 4 Animal studies suggest that 5-HT (serotonin) may be an important factor associated inducing the BJR in the setting of decreased blood volume [5][6][7][8] ; this effect can be blocked at the 5-HT3 receptor. 9 We hypothesized that spinal-induced hypotension and bradycardia could be minimized with the use of intravenous ondansetron, a 5-HT3 receptor antagonist, in non-labouring obstetric patients undergoing caesarean section.…”

Adrenaline infiltration in proximal tibial osteotomy: is there evidence for safety?

“…Accidental intravenous injection of epinephrine can lead to serious adverse cardiovascular events such as cerebral haemorrhage, pulmonary oedema, ventricular arrhythmia or cardiac ischemia and arrest. Several cases of such complications are reported in the literature even after low dose of local epinephrine inWltration [3,4]. To illustrate, patients are routinely exposed to high-dose epinephrine inWltration during large volume liposuction.…”