Long QT Syndrome and Perioperative Torsades de Pointes: What the Anesthesiologist Should Know

Life-Threatening Cardiac Arrhythmias during Anesthesia and Surgery

“…Although dexmedetomidine may cause mild prolongation of QT interval, it is unlikely to cause TdP. It should also be prudent to use dexmedetomidine with caution, especially in patients with bradyarrhythmias tendencies where the risk of QT prolongation is increased [12][13][14][15].…”

Effect of lipid emulsion on acute clozapine poisoning-induced QT prolongation

“…1 Acute toxicity of clozapine, which is used to treat schizophrenia, can prolong the QT interval, leading to Torsade de pointes, ventricular fibrillation, and sudden cardiac arrest. 3,4 Additionally, toxicity of other antipsychotic drugs, including risperidone, quetiapine, haloperidol, and droperidol, can cause Torsade de pointes. 4 Repolarization of phase 3 of action potential in cardiac myocytes normally occurs when calcium channels are inactivated and conductance through potassium channels is increased, which include mainly rapid delayed rectifier potassium current, slow delayed rectifier potassium current, and inward rectifying potassium current.…”

“…3,4 Additionally, toxicity of other antipsychotic drugs, including risperidone, quetiapine, haloperidol, and droperidol, can cause Torsade de pointes. 4 Repolarization of phase 3 of action potential in cardiac myocytes normally occurs when calcium channels are inactivated and conductance through potassium channels is increased, which include mainly rapid delayed rectifier potassium current, slow delayed rectifier potassium current, and inward rectifying potassium current. 4 QT prolongation of phase 3 of action potential in the cardiac myocytes, associated with Torsade de pointes, may be induced in decreased outward potassium current or increased inward calcium or sodium current.…”

“…4 Repolarization of phase 3 of action potential in cardiac myocytes normally occurs when calcium channels are inactivated and conductance through potassium channels is increased, which include mainly rapid delayed rectifier potassium current, slow delayed rectifier potassium current, and inward rectifying potassium current. 4 QT prolongation of phase 3 of action potential in the cardiac myocytes, associated with Torsade de pointes, may be induced in decreased outward potassium current or increased inward calcium or sodium current. The following discussion may help understand the potential mechanisms underlying the lipid emulsion-mediated inhibition of QT prolongation induced by clozapine poisoning.…”

“…1 Drug-induced prolonged QT interval causing Torsade de Pointes is due to the inhibition of human Ether-à-go-go-Related Gene (hERG)encoded rapid delayed rectifier potassium channels, leading to the inhibition of potassium efflux. 4 Local anesthetics including bupivacaine, ropivacaine, and mepivacaine inhibit hERG potassium channel encoding rapid delayed rectifier potassium channels, which is correlated with the lipid solubility of local anesthetics. 5 Bupivacaine toxicity induces transmural dispersion of repolarization, which is responsible for QT prolongation.…”