Heart transplant patients seem to be at high risk of this phenomenon while other risk factors may include long-standing autonomic neuropathy, hypersensitivity of immature autonomic nervous system in which the parasympathetic tone dominates, the use of neostigmine, and a paradoxical effect of glycopyrrolate on muscarinic receptors

Heart transplant patients seem to be at high risk of this phenomenon while other risk factors may include long-standing autonomic neuropathy, hypersensitivity of immature autonomic nervous system in which the parasympathetic tone dominates, the use of neostigmine, and a paradoxical effect of glycopyrrolate on muscarinic receptors. after reversibility has been established to avoid adverse patient outcomes. An anticholinergic drug is usually administered followed by a cholinesterase inhibitor or both are given concurrently. The cholinesterase inhibitor prevents the breakdown of acetylcholine, thus increasing its competitiveness on the post synaptic acetylcholine receptors in caparison to the NDMB. Due to their pharmacokinetic properties, the combination of neostigmine and glycopyrrolate or atropine and edrophonium is recommended. The purpose of the anticholinergic drug is to counteract the indirect muscarinic effects of the cholinesterase inhibiting drug, which when given alone can lead to significant bradycardia. We describe a case of heart block that occur following reversal of neuromuscular blockade with clinical doses of neostigmine and glycopyrrolate. We then summarize previous cases that have been reported in the literature and conclude by exploring possible TAK-071 causes of heart block following administration of reversal agents. CASE DESCRIPTION A 20-year-old, 65-kg male was admitted for dental examination, scaling, and multiple teeth extraction under general anesthesia. He had a history of autism, global developmental delay, and well-controlled epilepsy. His medications included lamotrigine and carbamazepine. His previous anesthetic history was unremarkable. The preoperative physical examination revealed a heart rate of 64 beats/min and a blood pressure of 121/65 mm Hg. He was saturating oxygen at 100% on room air. Preoperative laboratory values were unremarkable. A preoperative 12-lead electrocardiogram (ECG) was not performed following institutional guidelines. The patient was brought into the operating room and general anesthesia was induced by inhalation via a firmly placed facemask after the circuit had been primed with 50% N2O, O2 and 8% sevoflurane. With loss of consciousness, O2 was increased and N2O decreased. Intravenous (IV) access was gained and 50 mcg of fentanyl and 30 mg of rocuronium were administered intravenously. The trachea was intubated nasally, and the patient was mechanically ventilated. The patient was maintained with sevoflurane at 1.9 to 2.4%. In addition to standard Canadian Anesthesiologists’ Society (CAS) monitoring, a peripheral nerve stimulator was placed on his left ulnar nerve. The patient was stable throughout the approximately 70-minute operation with a heart rate of 63 to 78 beats/min and systolic arterial blood pressures ranging from 120 to 140 mm Hg. At the end of an uneventful surgery, three successive fading twitches were observed on the left abductor pollicis muscle after ulnar nerve stimulation. TAK-071 A mixture of neostigmine (2.5 mg) and glycopyrrolate (0.4 mg) was given IV to reverse neuromuscular blockade. Two to 3 minutes later, the patient’s heart rate dropped to 32 beats/min and his ECG revealed a Mobitz type I atrio-ventricular (AV) block. Atropine (0.6 mg) was draw but not given as the patient blood pressure and oxygen saturation remained stable. His heart rate gradually returned to a prereversal range of 63 to 70 beats/min over a 6-minute period and remained stable over the next 10 minutes. The trachea was extubated in the operating room, and the patient was transported to the postanesthesia care unit (PACU). A repeat ECG in the PACU revealed normal sinus tracings. He remained hemodynamically stable and was discharged after 4 hours of observation. DISCUSSION AND CONCLUSION In 1986, Triantafillou et al1 described a case (patient 1 in Table) of refractory bradycardia and hypotension requiring epinephrine and external cardiac massage in an elderly male diabetic after reversal of neuromuscular blockade with clinical doses of neostigmine and glycopyrrolate.1 This patient who had chronic renal failure responded to epinephrine and external cardiac massage and he was subsequently found to have severe diabetic vagal neuropathy. The authors suggested this unusual occurrence to be due to hypersensitivity of the vagal postsynaptic receptor to the dose of the anticholinergic administered for reversal.1 Five cases (Table), including our case, have recently been described in which patients developed AV block following administration of clinical doses of a combination of neostigmine and glycopyrrolate for neuromuscular block reversal. Patient 2 was a.The trachea was intubated nasally, and the patient was mechanically ventilated. neuromuscular blocking drugs (NDMB), appropriate reversal of the effect of these drugs at the neuromuscular junction (NMJ) is essential after reversibility has been established to avoid adverse patient outcomes. An anticholinergic drug is usually administered followed by a cholinesterase inhibitor or both are given concurrently. The cholinesterase inhibitor prevents the breakdown of acetylcholine, thus increasing its competitiveness on the post synaptic acetylcholine receptors in caparison to the NDMB. Due to their pharmacokinetic properties, the combination of neostigmine and glycopyrrolate or atropine and edrophonium is recommended. The purpose of the anticholinergic drug is to counteract the indirect muscarinic effects of the cholinesterase inhibiting drug, which when given alone can lead to significant bradycardia. We describe a case of heart block that occur following reversal of neuromuscular blockade with clinical doses of neostigmine and glycopyrrolate. We then summarize previous cases that have been reported in the literature and conclude by exploring possible causes of heart block following administration of reversal providers. CASE DESCRIPTION A 20-year-old, 65-kg male was admitted for dental exam, scaling, and multiple teeth extraction under general anesthesia. He had a history of autism, global developmental delay, and well-controlled epilepsy. His medications included lamotrigine and carbamazepine. His earlier anesthetic history was unremarkable. The preoperative physical exam revealed a heart rate of 64 beats/min and a blood pressure of 121/65 mm Hg. He was saturating oxygen at 100% on space air. Preoperative laboratory values were unremarkable. A preoperative 12-lead electrocardiogram (ECG) was not performed following institutional guidelines. The patient was brought into TAK-071 the operating space and general anesthesia was induced by inhalation via a securely placed facemask after the circuit had been primed with 50% N2O, O2 and 8% sevoflurane. With loss of consciousness, O2 was improved and N2O decreased. Intravenous (IV) access was gained and 50 mcg of fentanyl and 30 mg of rocuronium were given intravenously. The trachea was intubated nasally, and the patient was mechanically ventilated. The patient was taken care of with sevoflurane at 1.9 to 2.4%. In addition to standard Canadian Anesthesiologists’ Society (CAS) monitoring, a peripheral nerve stimulator was placed on his remaining ulnar nerve. The patient was stable throughout the approximately 70-minute operation having a heart rate of 63 to 78 beats/min and systolic arterial blood pressures ranging from 120 to 140 mm Hg. At the end of an uneventful surgery, three successive fading twitches were observed within the remaining Col11a1 abductor pollicis muscle mass after ulnar nerve activation. A mixture of neostigmine (2.5 mg) and glycopyrrolate (0.4 mg) was given IV to reverse neuromuscular blockade. TAK-071 Two to 3 minutes later on, the patient’s heart rate fallen to 32 beats/min and his ECG exposed a Mobitz type I atrio-ventricular (AV) block. Atropine (0.6 mg) was draw but not given as the patient blood pressure and oxygen saturation remained stable. His heart rate gradually returned to a prereversal range of 63 to 70 beats/min over a 6-minute period and remained stable over the next 10 minutes. The trachea was extubated in the operating room, and the patient was transported to the postanesthesia care unit (PACU). A repeat ECG in the PACU exposed normal sinus tracings. He remained hemodynamically stable and was discharged after 4 hours of observation. Conversation AND Summary In 1986, Triantafillou et al1 explained a case (patient 1 in Table) of refractory bradycardia and hypotension requiring epinephrine and external cardiac massage in an seniors male diabetic after reversal of neuromuscular blockade with medical doses of neostigmine and glycopyrrolate.1 This individual who had chronic renal.