Genesis of the normal T-U wave: A slice model of the left ventricular myocardium

Abstract

Augmentation in the amplitude of ECG QRS complexes (AUQRS) has been described in patients treated for heart failure (HF), but the underlying mechanism has remained enigmatic. We assessed the effect of diuresis-based fluid loss in patients treated for HF on the AU-QRS. Twenty-one patients aged 70.512.7 years, 13 with ischemic and 8 with non-ischemic cardiomyopathy, received diuresis in the hospital for exacerbated HF, and had standard ECGs recorded prior to the initiation of therapy, and at 24, and 48 hours. Percent change (%) over the course of observation in the sums of the amplitude of QRS complexes from 12 leads (QRS12), 6 limb leads (QRS6), and leads 1 2( QRS2) in mm were correlated with net fluid loss, corrected for admission weight in mL/Kg. Fluid loss amounted to 3,204.91,399.5 mL, and QRS12 was 160.942.3 mm before and 170.050.7 mm after diuresis (p 0. 024). % in QRS12, QRS6, and QRS2 correlated well with the net fluid loss (r 0.70, 0.82, 0.61, and p 0.002, 0.0005, 0.001), correspondingly. AU-QRS correlates well with net fluid loss from shortterm diuresis in patients with HF, and can be used as an easily obtainable and universally available bedside index of the net fluid loss, experienced by bed-ridden patients with exacerbated HF. undergoing therapy.