Quetiapine Toxicity Overview

Clinical Features
  • Quetiapine (a second-generation atypical antipsychotic) is a leading cause of toxic coma in Australia.
  • Main toxic effects in overdose include coma, anticholinergic delirium, prolonged QTc and a brisk sinus tachycardia.
  • Doses > 3g are associated with coma.
  • Despite the prolonged QTc, Torsades de Pointes does not occur (see below).
  • A similar pattern of clinical and ECG features is seen with other atypical antipsychotics, such as olanzapine or clozapine.

Drug-Induced QT-Prolongation And Torsades
  • In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by the absolute rather than corrected QT.
  • More precisely, the risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate (i.e. on the same ECG tracing).
  • These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP.
  • A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP.
  • From the nomogram, you can see that QTc-prolonging drugs that are associated with a relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that are associated with a relative bradycardia (e.g. amisulpride).
QT nomogram risk stratification for torsades de pointes

ECG Example

ECG quetiapine overdose 2

This ECG (taken following a 6g quetiapine overdose) with characteristic features of quetiapine toxicity

Advanced Reading



LITFL Further Reading


Emergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner

One comment

  1. Hi There. I don’t know if I understand this incorrectly but your statements about QT prolongation and HR, in drug induced qt prolongation, above doesn’t make sense. You said that if the HR is rapid and QT prolonged this plots below the nomogram curve and makes one less likely to have TdP. However if my HR is 40 and my Qt is 400 I’m still below the curve, but if my HR is 140 and my qt is 400 I’m above the curve and at then should be at higher risk of TdP. Thus, drugs that cause tachycardia should be associated with a higher risk of TdP? Please let me know if I’m missing something somewhere. Thanks.

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