Objective: to develop quantitative methods for the clinical interpretation of the ballistocardiogram (BCG), a signal generated by the repetitive motion of the human body due to sudden ejection of blood into the great vessels with each heart beat. Methods: a closed-loop mathematical model of the cardiovascular system is proposed to theoretically simulate the mechanisms generating the BCG signal, which is then compared with the signal acquired via accelerometry on a suspended bed. Results: simulated arterial pressure waveforms and ventricular functions are in very good qualitative and quantitative agreement with those reported in the clinical literature. The simulated BCG signal exhibits the typical I, J, K, L, M and N peaks that characterize BCG signals measured experimentally and its comparison with experimental measurements is very satisfactory both qualitatively and quantitatively. Conclusion: the proposed closed-loop model can reproduce the predominant features of BCG signals on the basis of fundamental mechanisms in cardiovascular physiology. Significance: this work provides a quantitative framework for the clinical interpretation of BCG signals. The present study considers a healthy human body and will be extended to include variability among individuals and to simulate pathological conditions
The ballistocardiogram (BCG) signal represents the movements of the body in response to cardiac ejection of blood. The BCG signal can change considerably under various physiological states; however, little information exists in literature describing how these forces are generated. A physical analysis is presented using a finite element model of thoracic aortic vasculature to quantify forces generated by the blood flow during the cardiac cycle. The traction at the fluid-solid interface of this deformable wall model generates a Central Aortic Force (CAF) which appears of similar magnitude to recorded BCG forces. The increased pulse pressure in an exercise simulation caused a significant increase in CAF, which is consistent with recent BCG measurements in exercise recovery. For more than a century, it has been known that the body recoils each time the heart ejects blood into the arteries. These subtle cardiogenic body movements have been measured with increasingly convenient ballistocardiography (BCG) instruments over the years. A typical BCG measurement shows several waves, most notably the “I”, “J”, and “K” waves. However, the mechanism for the genesis of these waves has remained elusive. We formulated a simple mathematical model of the BCG waveform. We showed that the model could predict the BCG waves as well as physiologic timings and amplitudes of the major waves. The validated model reveals that the principal mechanism for the genesis of the BCG waves is blood pressure gradients in the ascending and descending aorta. This new mechanistic insight may be exploited to allow BCG to realize its potential for unobtrusive monitoring and diagnosis of cardiovascular health and disease. A brief review is given of a mathematical model of the systemic arterial tree that was developed to find a quantitative interpretation of the human longitudinal ballistocardiogram. Derivation and description are presented of an electrical analog of the left ventricle and the systemic arterial tree that has fewer limitations than the mathematical model. Electrical equivalents of blood pressures, blood flows, vascular impedances, plethysmograms, and ballistocardiogram can be easily measured as a function of time, and in absolute value. Samples of such results are reproduced and compared with data reported in the literature.