Fundamentals in vibrocardiography : Precordial accelerography and acceleration ballistocardiography

Abstract

Most transducers employed in vibrocardiography give a flat response to acceleration when actuated by means of a vibrator, or they record only the higher precordial frequencies and give tracings which closely resemble an accelerogram. For this reason, vibrocardiography has been more or less identified with precordial accelerography. Moreover, the vibrocardiographic pattern resembles the pattern of acceleration ballistocardiography. The replacement of acceleration ballistocardiography by vibrocardiography has been suggested as a means of avoiding some of the errors introduced into ballistocardiography by limb impedance and by coupling of the patient to the ballistocardiographic bed.

Acceleration ballistocardiography has been used for estimating stroke volume, and it has been related to cardiac “force.” Precordial accelerography was tested with regard to the possibility of estimating both with greater accuracy. In order to do so, the precordial accelerogram was compared with the precordial displacement tracing, of which it is the second derivative.

The initial systolic acceleration complex starts with isometric contraction and continues during the first thrust of ejection. Heaving of the thoracic wall on ventricular contraction, and its deflection caused by cardiac emptying, are both involved in it. So are movements of the precordial soft tissues, which are drawn in around the apex as the tissues over the apex itself are pushed outward. This complexity of precordial movements precludes the possibility of considering precordial acceleration as a measure of the “force” of cardiac contraction. Moreover, the accelerographic amplitudes are favored by sudden changes in the direction of precordial movement, which are more likely to occur in the case of poor ventricular filling and low resistance to ejection than in cardiac overloading. This is but another aspect of the same complexity of precordial motion, which demonstrates the impossibility of using precordial acceleration as a measure of cardiac “force”.

The highest point in the normal apexcardiogram is reached at the summit of the upstroke. The height of the upstroke is conditioned by diastolic aortic pressure and not by stroke volume. In a case of arrhythmia the apex plateaus proved to be of equal height, although stroke volume certainly was larger after a long diastole. If stroke volume is not represented in displacement, it cannot be derived from its second derivative either.

Inasmuch as the purpose of acceleration ballistocardiography is the estimation of stroke volume and of cardiac “force,” precordial accelerography cannot replace it.

Small amplitudes in vibrocardiography, moreover, are not a proof of myocardial damage. They may indicate ventricular hypertrophy. Along the left sternal border a strong right cardiac thrust may give rise to an abnormal vibrocardiographic pattern.* Comparison of vibrocardiographic recordings with the simultaneously recorded displacement tracings over the same precordial area would seem imperative.