A novel heart rate control model provides insights linking LF-HRV behavior to the open-loop gain.
BACKGROUND
Low-frequency heart rate variability (LF-HRV) at rest has already been successfully modeled as self-sustained oscillations in a nonlinear control loop, but these models fail to simulate LF-HRV decreases either during aerobic exercise or in heart failure patients. Following control engineering practices, we assume the existence of a biological excitation (dither) within the heart rate control loop that softens the nonlinearity and studied LF-HRV behavior in a dither-embedded model.


METHODS
We adopted the Ottesen model with some revisions and induced a dither of high-frequency stochastic perturbations. We simulated scenarios of a healthy subject at rest and during aerobic exercise (by decreasing peripheral vascular resistance) and a heart failure patient (by decreasing stroke volume).


RESULTS
The simulations resembled physiological LF-HRV behavior, i.e., LF-HRV decreased during aerobic exercise and in the heart failure patient. The simulations exhibited LF-HRV dependency on the open-loop gain, which is related to the product of the feedback gain and the feed forward gain.


CONCLUSIONS
We are the first to demonstrate that LF-HRV may be dependent on the open-loop gain. Accordingly, reduced open-loop gain results in decreased LF-HRV, and vice versa. Our findings explain a well-known but unexplained observed phenomenon of reduced LF-HRV both in heart failure patients and in healthy subjects performing aerobic exercise. These findings have implications on how changes in LF-HRV can be interpreted physiologically, a necessary step towards the clinical utilization of LF-HRV.
School of Electrical Engineering, Tel Aviv University, Tel Aviv, Israel.
Hila
H
Dvir
Ben Zion
BZ
Bobrovsky
Uri
U
Gabbay
D001794:Blood Pressure / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D006329:Heart Conduction System / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008955:Models, Cardiovascular; D012146:Rest / Q000502:physiology*