ECG-Derived Respiratory Frequency Estimation

The respiratory signal is usually recorded with techniques like spirometry, pneumography, or plethysmography. These techniques require the use of cumbersome devices that may interfere with natural breathing, and which are unmanageable in certain applications such as ambulatory monitoring, stress testing, and sleep studies. Nonetheless, the joint study of the respiratory and cardiac systems is of great interest in these applications and the use of methods for indirect extraction of respiratory information is particularly attractive to pursue. One example of application would be the analysis of the influence of the respiratory system in heart rate variability (HRV) during stress testing, since it has been observed that the power in the very high frequency band (from 0.4 Hz to half the mean heart rate expressed in Hz) exhibits potential value in coronary artery disease diagnosis [1], and HRV power spectrum is dependent on respiratory frequency. Another field of application would be sleep studies, since the diagnosis of apnea could be based on fewer and simpler measurements, like the ECG, rather than on the polysomnogram, which is expensive to record. It is well known that the respiratory activity influences electrocardiographic measurements in various ways. During the respiratory cycle, chest movements and changes in the thorax impedance distribution due to filling and emptying of the lungs cause a rotation of the electrical axis of the heart which affects beat morphology. The effect of respiration-induced heart displacement on the ECG was first studied by Einthoven et al. [2] and quantified in further detail in [3, 4]. It has been experimentally shown that “electrical rotation” during the respiratory cycle is mainly caused by the motion of the electrodes relative to the heart, and that thoracic impedance variations contribute to the electrical rotation just as a second-order effect [5]. Furthermore, it is well known that respiration modulates heart rate such that it increases during inspiration and decreases during expiration [6, 7]. It has also been shown that the mechanical action of respiration results in the same kind of frequency content in the ECG spectrum as does HRV [8]. Figure 8.1 displays an ECG lead as well as the related heart rate (HR) and respiratory signals in which the ECG amplitude is modulated with a frequency similar to that of the respiratory signal. It seems that the ECG amplitude modulation is not in phase with the respiratory signal. It can also be seen that the HR and the

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