Here is a series of articles on medication QT Prolongation. My sense is it is a under recognized problem, although I have no basis for this view, just a feeling. This would make for an interesting CDSS to incorporate wave form analysis.
Drug Induced QT Prolongation - 
September's issue is themed around cardiovascular clinical pharmacology. It includes articles on a range of topics, spanning a review of the role of the renin-angiotensin system in atrial fibrillation [1], through the effect of atorvastatin on high-sensitivity CRP in acute coronary syndrome [2], and the pharmacokinetics and pharmacodynamics of nicorandil in healthy and acute heart failure subjects [3] to the influence of paraoxonase-1 (PON-1) phenotype on the response of paraoxonase activity to statins [4]. Several papers [5–7] relate directly or indirectly to effects of drugs on the electrocardiographic QT interval, and it is on this subject that this Editors' View is focused.
George Ralph Mines identified the 'vulnerable period' within the cycle of the cardiac action potential/pacemaker (or resting) potential [8]. (Mines [9], a contemporary at Cambridge of AV Hill, also described cardiac re-entry and identified the active principle of munchi arrow poison as strophanthin. He was appointed professor of physiology at McGill University in Canada aged 28, but died tragically soon thereafter – of which more later).
A ventricular extra beat falling early in the cardiac cycle, so that it coincides with ventricular repolarisation (the 'R on T' phenomenon), can provoke ventricular tachycardia (VT), and/or ventricular fibrillation (VF). The QT interval is measured from the beginning of the QRS complex (whether Q or R wave) to the end of the T wave. The latter may be difficult to define, especially when a U wave succeeds the T; however, the U wave tends to b...
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