The electrical conductivity of human cerebrospinal fluid (CSF) from seven patients was measured at both room temperature (25 degrees C) and body temperature (37 degrees C). Across the frequency range of 10 Hz-10 kHz, room temperature conductivity was 1.45 S/m, but body temperature conductivity was 1.79 S/m, approximately 23% higher. Modelers of electrical sources in the human brain have underestimated human CSF conductivity by as much as 44% for nearly two decades, and this should be corrected to increase the accuracy of source localization models.

We performed this study to test whether the denervated human heart has the ability to manifest respiratory sinus arrhythmia (RSA). With the use of a highly sensitive spectral analysis technique (cross correlation) to define beat-to-beat coupling between respiratory frequency and heart rate period (R-R) and hence RSA, we compared the effects of patterned breathing at defined respiratory frequency and tidal volumes (VT), Valsalva and Mueller maneuvers, single deep breaths, and unpatterned spontaneous breathing on RSA in 12 normal volunteers and 8 cardiac allograft transplant recipients. In normal subjects R-R changes closely followed changes in respiratory frequency (P less than 0.001) but were little affected by changes in VT. On the R-R spectrum, an oscillation peak synchronous with respiration was found in heart transplant patients. However, the average magnitude of the respiration-related oscillations was 1.7-7.9% that seen in normal subjects and was proportionally more influenced by changes in VT. Changes in R-R induced by Valsalva and Mueller maneuvers were 3.8 and 4.9% of those seen in normal subjects, respectively, whereas changes in R-R induced by single deep breaths were 14.3% of those seen in normal subjects. The magnitude of RSA was not related to time since the heart transplantation, neither was it related to patient age or sex. Thus the heart has the intrinsic ability to vary heart rate in synchrony with ventilation, consistent with the hypothesis that changes, or rate of changes, in myocardial wall stretch might alter intrinsic heart rate independent of autonomic tone.

SUMMARY The genesis of gallop sounds was investigated in 12 patients by simultaneous measurement of external apexcardiographic (ACG) and left ventricular (LV) pressure, dP/dt, and sound using infinite time constant piezo-resistive pressure transducers with identical sensitivity and frequency responses. Absolute intensity of internal and external sound was quantified. The external transducer was applied to the chest wall with a pressure of 200-400 mm Hg. Six patients had a third heart sound (S,), eight had a fourth heart sound (S4) and one patient had a summation gallop. Left atrial (LA) pressure, dP/dt, and sound were also recorded in one S.and four S4 patients. The dP/dt of the rapid filling wave (RFW) and "a" wave of both apexcardiogram and left ventricle were measured. Similar data were obtained in 10 control patients without gallop sounds.The intensity of gallop sounds was uniformly greater over the chest wall than inside the left ventricle or left atrium. In addition, the dP/dt of RFW and "a" wave tended to be higher in the apexcardiogram than the left ventricle of control patients. Also, the dP/dt of the LV RFW in S, patients and "a" wave in S4 patients tended to be higher than ihose in control subjects, but there was overlap. The dP/dt of ACG filling waves in patients with gallop sounds was significantly greater (p < 0.01) than the respective filling wave of the left ventricle. The ACG dP/dt of the RFW in all S, patients and "a" wave in all S, patients was increased above the maximal values of the respective ACG filling waves in the control subjects.The data suggest that the higher intensity of gallop sounds and the higher dP/dt of the filling waves over the chest cannot be caused by passive transmission of sound or pressure changes in the left ventricle. Therefore, we postulate that the greater vibratory energy of gallop sounds recorded over the precordium is caused by the impact of the heart on the chest wall. The strength of the impact is a function of several interacting mechanisms, including the momentum transfer and coupling between the heart and the chest wall.SINCE POTAIN'S original description of gallop sounds in 1885,1 several mechanisms have been proposed to explain their genesis. From studies using phonocardiograms in association with the apexcardiograms with short-time constants, Benchimol et al. concluded that the third heart sound (S3) occurs at the peak of the rapid ventricular filling wave (RFW), and that the fourth heart sound (S4) appears at the peak of the "a" wave of the ACG.'On the basis of these findings and hemodynamic observations made by means of fluid-filled catheters, several investigators proposed that the S3 is caused by the sudden deceleration of the RFW and that the S4 was produced by an exaggerated "a" wave generated by the left atrium in an attempt to fill a noncompliant left ventricle.3-' However, Arevalo et al." found in animals that the S3 occurs when left ventricular (LV) pressure ceases to fall during relaxation. At this instant, the dP/dt of LV pressure is almost 0 ...

Several investigators have noted external gallop sounds to be of higher amplitude than their corresponding internal sounds (S3 and S4). In this study we hoped to determine if S3 and S4 are transmitted in the same manner as S,. In 11 closed-chest dogs, external (apical) and left ventricular pressures and sounds were recorded simultaneously with transducers with identical sensitivity and frequency responses. Volume and pressure overload and positive and negative inotropic drugs were used to generate gallop sounds. Recordings were made in the control state and after the various interventions. S3 and S4 were recorded in 17 experiments each. The amplitude of the external S, was uniformly higher than that of internal S, and internal gallop sounds were inconspicuous. With use of Fourier transforms, the gain function was determined by comparing internal to external S,. By inverse transform, the amplitude of the internal gallop sounds was predicted from external sounds. The internal sounds of significant amplitude were predicted in many instances, but the actual recordings showed no conspicuous sounds. The absence of internal gallop sounds of expected amplitude as calculated from the external gallop sounds and the gain function derived from the comparison of internal and external Sl make it very unlikely that external gallop sounds are derived from internal sounds. Circulation 71, No. 5, 987-993, 1985 24, 1985. Presented in part at the 56th Scientific Sessions of the American Heart Association, Anaheim, CA, November 1983.Vol. 71, No. 5, May 1985 contribute to this phenomenon: (1) chest wall-transducer resonance, which might vary depending on type, method of applicaticn, and pressure of application of the transducers, and (2) the fact that a small external transducer applied with significant pressure and causing obvious indentation of the chest wall may perceive greater pressure because of stretching (shear forces) of the surrounding structures. It is not easily possible to define the degree to which these and other factors contribute to the relatively high amplitude of external gallop sounds. However, if we compare the sounds produced internally to the external recordings, the gain function of the total system could be derived.2 We have therefore used first heart sound as a reference to calculate the gain function of the total system. Since the gain function could vary with varying frequencies, the sounds have been analyzed in the frequency domain and then compared to determine the gain function of the system. If the externally recordable gallop sounds exhibit higher amplitude than corresponding internal sounds in spite of correction for the gain function, then it can be assumed that these sounds are not generated within the ventricular cavity.This experimental study was undertaken to answer amplitude of intracardiac diastolic sounds was calculated from external gallop sounds. Intracardiac gallop sounds were reconstructed in time domain from the calculated intensity frequency spectra (figure 4). Amplitude...