Fetal heart rate patterns preceding death in utero

Four cases of intrauterine fetal demise in term infants are presented. From these cases and other published reports, a sequence of fetal heart rate changes preceding intrapartum death is presented. Late or variable decelerations, if unrelieved or uncorrected, lead to baseline heart rate changes of tachycardia and loss of variability reflecting loss of fetal reserve and fetal distress. This is followed by an unstable heart rate, a sinusoidal pattern, or a rapidly changing fetal heart rate. The final event is a profound bradycardia just prior to fetal demise.     

Metaiodobenzylguanidine and heart rate variability in heart failure

It is assumed that the low-frequency power (LF) of heart rate variability (HRV) increases with progress of congestive heart failure (CHF), therefore positively correlating with cardiac 123I-metaiodobenzylguanidine (MIBG) washout. It is demonstrated here that HRV, including normalized LF, correlated inversely with MIBG washout and positively with the ratio of heart-to-mediastinum MIBG activity in controls and CHF patients, whereas these correlations were not observed within CHF patients. Thus MIBG washout may increase and HRV including normalized LF may decrease with CHF, although the HRV and MIBG measures may not similarly change in proportion to the severity of the cardiac autonomic dysfunction in CHF.     

Variability of the circadian heart rate in diabetes mellitus-related autonomic neuropathy

For assessing the alterations of circadian heart rate variability 66 diabetic patients (age: 52.9 +/- 1.0 years; x +/- SEM) and 23 control subjects (age: 52.7 +/- 1.7 years) were investigated using 24 hours Holter monitoring. Autonomic neuropathy (AN) was evaluated by tests for cardiovascular reflexes and patients were classified as being without AN (n = 26), having mild (n = 25) or definitive (n = 15) signs of AN. Minimal heart rates were significantly higher while maximal heart rates were considerably lower in patients with than without AN (60 +/- 2 min-1 versus 54 +/- 1, min-1, p < 0.05 and 125 +/- 4 min-1 versus 146 +/- 4 min-1, p < 0.01). Diabetic groups were comparable regarding values of averaged heart rates. The difference between the mean waking and sleeping averaged heart rates was the smallest in diabetic patients with definitive signs of AN (9 +/- 2 min-1) differing from those of control subjects (17 +/- 1 min-1, p < 0.01) and diabetic patients without (17 +/- 1 min-1, p < 0.001) or with mild (15 +/- 1 min-1, p < 0.05) signs of AN. Characteristic alteration, i.e. a reduction in circadian heart rate variability could be found in diabetic patients with signs of AN. This phenomenon has primarily been a consequence of more frequent sleeping heart rates due to dominant impairment in cardiac parasympathetic innervation.     

Study of the Lyapunov exponents in heart rate variability signals

Heart rate variability signals obtained from 24 h recordings are analyzed for normal and pathological subjects. This time series contains information about the autonomic nervous system action regulating the beat-to-beat heart rate. Nonlinear contributions to the long period variability have been assessed by the calculation of the entire spectrum of Lyapunov exponents, after the system trajectory reconstruction, starting from the original variability signal. The positivity of Lyapunov exponent values, obtained from an unknown process, can establish whether the structure generating it shows nonlinear chaotic characteristics. This is what happens for the cardiovascular signals. Moreover, the different values obtained for the Lyapunov exponents operate a classification among the considered pathophysiological cases.     

Effects of passive tilt and submaximal exercise on spectral heart rate variability in ventricular fibrillation patients without significant structural heart disease

It has been shown that tilt and exercise elicit significant changes in autonomic activity in normal subjects and that submaximal exercise causes a greater reduction in heart rate variability (HRV) in animals susceptible to ventricular fibrillation (VF). Whether there is an abnormal HRV response to tilt and exercise in patients at risk of sudden cardiac death (SCD) remains unknown. Short-term HRV before and during passive tilt and exercise was studied in 12 survivors of out-of-hospital cardiac arrest with documented VF and compared with 12 age- and sex-matched normal controls. No patient had significant structural heart disease or left ventricular dysfunction. HRV was computed as total-frequency (TF, 0.01 to 1.00 Hz), low-frequency (LF, 0.04 to 0.15 Hz) and high-frequency (HF, 0.15 to 0.40 Hz) components. There was no significant difference between normal controls and SCD survivors in HRV before or during tilt or submaximal exercise testing. The HF component was significantly decreased during tilt compared with that in the supine position in both normal controls (5.85 +/- 0.61 vs 5.08 +/- 0.95 In(msec2), p = 0.005) and patients (5.58 +/- 1.49 versus 4.74 +/- 1.18 In(msec2), p = 0.003). There was again no significant change in the TF or LF components during tilt in either patients or controls. All frequency components were significantly decreased during submaximal exercise testing in both patients and controls. However, there was no significant difference in any of these tilt- and exercise-induced changes in HRV between normal controls and SCD survivors.(ABSTRACT TRUNCATED AT 250 WORDS)     

A flat decelerative fetal heart rate tracing with normal fetal heart rate variability

We report two cases for which computer interpretation of nonstress test indicated a flat decelerative trace in spite of normal fetal heart rate variability. Fetal behavioral state in the first case and signal loss in the second case were possibly responsible for this computerized interpretation of the tracings in the absence of fetal distress.     

The influence of premedication on heart rate variability

Analysis of heart rate variability has been used to study the effects of midazolam, morphine and clonidine on the autonomic nervous system, when administered to patients for premedication. Ninety-five patients were studied 60 min before and 60 min after premedication. Normal saline (n = 25), midazolam 0.08 mg.kg-1 (n = 24), morphine 0.15 mg.kg-1 (n = 23), or clonidine 2 micrograms.kg-1 (n = 23) were administered intramuscularly by random allocation. A Holter device was connected to the patient during the study period. Using power spectral analysis the low-frequency and high-frequency components were calculated from the Holter recordings. These are markers for sympathetic and parasympathetic activity respectively; the low- to high-frequency ratio was also calculated, a ratio of > 1 signifying sympathetic dominance. A significant reduction was noticed in both low-frequency and high-frequency power in the three premedicated groups, whereas no changes were observed in the normal saline group. In the case of midazolam, both the low and high frequencies were decreased but the low- to high-frequency ratio did not change significantly. Morphine and clonidine depressed the low-frequency component more than the high-frequency component and the low- to high-frequency ratio was decreased, suggesting parasympathetic dominance. We conclude that heart rate variability may be a useful tool for investigating the effect of drugs on the autonomic nervous system.     

Autonomic control of heart rate during physical exercise and fractal dimension of heart rate variability

The objectives of the present study were to investigate autonomic nervous system influence on heart rate during physical exercise and to examine the relationship between the fractal component in heart rate variability (HRV) and the system's response. Ten subjects performed incremental exercise on a cycle ergometer, consisting of a 5-min warm-up period followed by a ramp protocol, with work rate increasing at a rate of 2.0 W/min until exhaustion. During exercise, alveolar gas exchange, plasma norepinephrine (NE) and epinephrine (E) responses, and beat-to-beat HRV were monitored. HRV data were analyzed by "coarse-graining spectral analysis" (Y. Yamamoto and R. L. Hughson. J. Appl. Physiol. 71: 1143-1150, 1991) to break down their total power (Pt) into harmonic and nonharmonic (fractal) components. The harmonic component was further divided into low-frequency (0.0-0.15 Hz) and high-frequency (0.15-0.8 Hz) components, from which low-frequency and high-frequency power (Pl and Ph, respectively) were calculated. Parasympathetic (PNS) and sympathetic (SNS) nervous system activity indicators were evaluated by Ph/Pt and Pl/Ph, respectively. From the fractal component, the fractal dimension (DF) and the spectral exponent (beta) were calculated. The PNS indicator decreased significantly (P < 0.05) when exercise intensity exceeded 50% of peak oxygen uptake (VO2 peak). Conversely, the SNS indicator initially increased at 50-60% VO2peak (P < 0.05) and further increased significantly (P < 0.05) at > 60% VO2peak when there were also more pronounced increases in NE and E.(ABSTRACT TRUNCATED AT 250 WORDS)     

Disopyramide in ventricular tachycardia

A procedure for the measurement of free erythrocyte protoporphyrin (FEP) in a drop of blood collected on filter paper is described. The method is useful as a screening test for lead poisoning in children. Based on the FEP finding and blood lead tests, asymptomatic children are classified into four major categories. A course of action is suggested for each category.     

Influence of heart rate on stroke volume variability in atrial fibrillation in patients with normal and impaired left ventricular function

Both resting tachycardia and irregular ventricular rhythm may contribute to impaired cardiac performance in atrial fibrillation (AF). This study assesses the relation between resting heart rate and beat-to-beat changes in left ventricular (LV) ejection and filling in patients with normal and impaired LV systolic function. Beat-to-beat variation in LV outflow and inflow velocity-time integral was measured using pulsed Doppler ultrasound in 39 patients with chronic AF and normal (n=22) or impaired (n=17) LV systolic function. Aortic velocity-time integral variability increased with mean heart rate (p=0.003) even though RR interval variability decreased (p <0.001). Aortic velocity-time integral was more sensitive to the duration of both the preceding (p <0.001) and prepreceding (p <0.001) RR intervals at higher heart rates. These relations were similar for patients with normal and impaired LV systolic function. The sensitivity of the filling velocity-time integral to RR interval variability also increased with heart rate (p <0.001). However, at higher heart rates the filling velocity-time integral (p=0.009) and filling time (p=0.005) were less sensitive to change in RR intervals in patients with impaired LV function. We conclude that beat-to-beat stroke volume variability in AF increases with heart rate. Stroke volume variability was not influenced by LV systolic function.     

Analysis of heart rate variability demonstrates effects of development on vagal modulation of heart rate in healthy children

OBJECTIVES: Analysis of heart rate variability (HRV) has been found to be a useful method of assessing cardiovascular autonomic control, but normal values for standard HRV measures in children have not been established. We analyzed HRV in 60 healthy children aged 3 to 15 years to determine normal values and to assess the effects of development on cardiac autonomic control with the use of ambulatory electrocardiographic monitoring. RESULTS: The high-frequency (HF) component, an index of cardiac autonomic tone, increased significantly with age from 3 to 6 years (p < 0.01) and decreased with age from 6 to 15 years (p < 0.01), and the magnitude of HF correlated significantly with the R-R intervals. Thus the changes in cardiac autonomic tone could be described as a simple equation using age and heart rate. CONCLUSIONS: We present normal values and changes in the cardiac autonomic system during childhood after HRV analysis, which could lead to a better understanding and treatment of cardiac disease in children.     

Termination of ventricular tachycardia in the human heart. Insights from three-dimensional mapping of nonsustained and sustained ventricular tachycardias

BACKGROUND: To define the electrophysiological basis for the termination of ventricular tachycardia (VT), three-dimensional cardiac mapping and analysis of the terminal beats of nonsustained VT and beats of sustained VT were performed in six patients with healed myocardial infarcts. METHODS AND RESULTS: Termination of VT was due to activation from multiple initiation sites that were discordant from those responsible for the maintenance of sustained VT in 45% of cases, to repetitive activation from single sites that were discordant from those responsible for the maintenance of sustained VT in 24% of cases, or to activation from sites concordant with the sites of repetitive activation during sustained VT in 31% of cases. Sustained VT was characterized by occasional shifting of initiation sites, even after the tachycardia entered the stable monomorphic phase. Mapping was of sufficient density to define the mechanisms for 21 terminating beats of VT. In 5 cases, termination was due to intramural reentry, which initiated with the total activation time of the preceding beat of 204 +/- 11 milliseconds (ms) but terminated primarily because of a decrease in total activation time (144 +/- 23 ms, P = .03) that was associated with the development of intramural conduction block or with significant changes in the activation sequence along the reentrant circuit. In 16 cases, terminal beats were initiated by a focal mechanism on the basis of the absence of intervening electrical activity from the termination of the preceding beat to the initiation of the terminating beat (172 +/- 9 ms). Focal activation was associated with less conduction delay of the preceding beat (115 +/- 6 ms) than terminating reentrant beats (P < .001) and usually terminated suddenly without oscillations in cycle length or total activation time. CONCLUSIONS: Termination of VT is associated with alterations in initiation sites that are most often discordant from those maintaining sustained VT and is due to either reentrant or focal mechanisms.     

Spectral analysis of heart rate variability during isoflurane anesthesia

The autonomic nervous system is an important neural control system for maintaining cardiovascular stability in humans. Analysis of heart rate variations may provide important clinical information on the influence of anesthesia on the autonomic nervous system and the central nervous system. Therefore, the effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane anesthesia on beat-to-beat heart rate variations were studied in ten patients (ASA Physical Status 1). Spectral analysis was used to determine the intensity of the variations. For each power spectrum, the frequency components were identified as follows: 1) the parasympathetically mediated respiratory component (0.15-0.4 Hz) and 2) both parasympathetically and sympathetically mediated components (0.04-0.15 Hz). The latter was subdivided into the low-frequency component (0.04-0.09 Hz) of vasomotor origin and the mid-frequency component (0.09-0.15 Hz) of baroreceptor origin. Marked reductions in the power of heart rate variations, at all frequencies, were found during isoflurane anesthesia, indicating isoflurane decreased total autonomic nervous system activity. Isoflurane decreased the high-frequency and mid-frequency components in a concentration-dependent manner. The low-frequency component increased transiently at 1.5 minimum alveolar concentrations concomitant with the burst suppression in the electroencephalogram. The ratio of mid-frequency to high-frequency components did not change significantly during isoflurane anesthesia compared with the awake period. These frequency characteristics of heart rate variations during isoflurane anesthesia suggest there are dose-related decreases in autonomic nervous system activity in both the vagus and the cardiac sympathetic nerves.     

Age-dependent influence on heart rate variability in salt-sensitive hypertensive subjects

OBJECTIVE: The known association between systemic arterial hypertension in its initial stages and increased sympathetic nervous system drive prompted us to evaluate the influence of age on autonomic nervous system function in subjects with salt-sensitive arterial hypertension. DESIGN: In a randomized study, autonomic nervous system function was assessed by power spectral analysis of heart-rate variability calculated with an autoregressive algorithm in salt-sensitive hypertensives and controls at baseline and under sympathetic stress (passive head-up tilt). For 1 week before the study, all subjects kept to a diet supplying 120 mEq sodium. Sodium sensitivity was assessed by measuring and comparing arterial pressures after a 7-day controlled dietary sodium intake of 20 mEq per day after a 7-day period on 220 mEq sodium/day. SETTING: Geriatric division at the I Medical Clinic of the University of Rome "La Sapienza". PARTICIPANTS: Sixty-five patients with salt-sensitive hypertension (age range 19 to 89 years) and 64 age-matched normotensive controls, divided for data comparison into three age-groups: < 44 years; 44 to 64 years; and > or = 65 years. MEASUREMENTS: With an autoregressive algorithm in a power spectral analysis of heart rate variability, we detected four spectral frequency-domains: total power (0.0033 to 0.40 Hz), high-frequency power (0.16 to 0.40 Hz), low-frequency power (0.04 to 0.15 HZ) and very-low-frequency power (0.0033 to 0.04 Hz). To determine sodium sensitivity, for 1 week before the study all subjects kept to a diet supplying 120 mEq sodium. Sodium sensitivity was assessed by measuring and comparing arterial pressures after a 7-day controlled dietary intake of 20 mEq per day and after a 7-day period of 220 mEq sodium/day. RESULTS: Results were expressed as natural logarithms of power and normalized units. The hypertensive patients of all ages had significantly lower total power of heart rate variability than the normotensive controls (P < .05). At baseline, the youngest hypertensives had lower natural logarithms and low-frequency normalized units than controls (P < .001). After tilt, only their low-frequency normalized units exceeded those of controls (P < .001). The middle-aged hypertensive group had higher low-frequency normalized units than controls at baseline (P < .05) and after tilt (P < .001). At baseline and after tilt, the oldest hypertensives had lower low-frequency natural logarithms than controls (P < .05) and normalized units equal to those of controls. But the hypertensives of all ages were less able than controls (P < .001) to increase low-frequency power after head-up tilt. In the less than 44-year-old hypertensives, diastolic pressure correlated significantly with low-frequency power of heart rate variability, expressed in normalized units, at baseline (P < .05) and after head-tilt (P < .05). A significant inverse correlation was found between age and the natural logarithm of low-frequency power at baseline (r = -.682, P < .001) and after tilt (r = -.800; P < .001). Also, a significant inverse correlation was found to exist in normotensive subjects between the natural logarithm of low-frequency at baseline (r = -.595; P < .001) and after tilt (r = -.391; P < .001). The two regression line coefficients for age correlated significantly (P < .001) with the natural logarithm of low-power frequency after tilt. CONCLUSION: Whereas sodium chloride-sensitive hypertension appears to be associated with sympathetic hyperactivity in young and middle-aged subjects, in older people it is not. Sympathetic activity diminishes with age, declining faster in hypertensive subjects.