An optimized method for the estimation of the respiratory rate from electrocardiographic signals: implications for estimating minute ventilation.

It is well-known that respiratory activity influences electrocardiographic (ECG) morphology. In this article we present a new algorithm for the extraction of respiratory rate from either intracardiac or body surface electrograms. The algorithm optimizes selection of ECG leads for respiratory analysis, as validated in a swine model. The algorithm estimates the respiratory rate from any two ECG leads by finding the power spectral peak of the derived ratio of the estimated root-mean-squared amplitude of the QRS complexes on a beat-by-beat basis across a 32-beat window and automatically selects the lead combination with the highest power spectral signal-to-noise ratio. In 12 mechanically ventilated swine, we collected intracardiac electrograms from catheters in the right ventricle, coronary sinus, left ventricle, and epicardial surface, as well as body surface electrograms, while the ventilation rate was varied between 7 and 13 breaths/min at tidal volumes of 500 and 750 ml. We found excellent agreement between the estimated and true respiratory rate for right ventricular (R(2) = 0.97), coronary sinus (R(2) = 0.96), left ventricular (R(2) = 0.96), and epicardial (R(2) = 0.97) intracardiac leads referenced to surface lead ECGII. When applied to intracardiac right ventricular-coronary sinus bipolar leads, the algorithm exhibited an accuracy of 99.1% (R(2) = 0.97). When applied to 12-lead body surface ECGs collected in 4 swine, the algorithm exhibited an accuracy of 100% (R(2) = 0.93). In conclusion, the proposed algorithm provides an accurate estimation of the respiratory rate using either intracardiac or body surface signals without the need for additional hardware.

A novel pacing method to suppress repolarization alternans in vivo: implications for arrhythmia prevention.

BACKGROUND: Repolarization alternans (RA), a pattern of ventricular repolarization that repeats on an every other beat basis, has been closely linked with the substrate associated with ventricular tachycardia/ventricular fibrillation. OBJECTIVE: To evaluate a novel method to suppress RA. METHODS: We have developed a novel method to dynamically (on R-wave detection) trigger pacing pulses during the absolute refractory period. We have tested the ability of this method to control RA in a structurally normal swine heart in vivo. RESULTS: RA induced by triggered pacing can be measured from both intracardiac and body surface leads and the amplitude of R-wave triggered pacing-induced alternans can be locally modulated by varying the amplitude and width of the pacing pulse. We have estimated that to induce a 1 µV change in alternans voltage on the body surface, coronary sinus, and left ventricle leads, a triggered pacing pulse delivered in the right ventricle of 0.04±0.02, 0.05±0.025, and 0.06±0.033 µC, respectively, is required. Similarly, to induce a 1 unit change in Kscore (ratio of alternans peak to noise), a pacing stimulus of 0.93±0.73, 0.32±0.29, and 0.33±0.37 µC, respectively, is required. We have been able to demonstrate that RA can be suppressed by R-wave triggered pacing from a site that is within or across ventricles. Lastly, we have demonstrated that the proposed method can be used to suppress spontaneously occurring alternans in the diseased heart. CONCLUSION: We have developed a novel method to suppress RA in vivo.