Low-frequency Heart Rate Power Research Articles

Circadian rhythms of heart rate and locomotion after treatment with low‐dose acetylcholinesterase inhibitors

This study tested the hypothesis that repeated exposure to low levels of sarin, pyridostigmine bromide (PB) or their combination, at doses equivalent to those possibly experienced by veterans of the 1991 Persian Gulf War, could lead to persistent or delayed autonomic effects and thus help to explain the cause of clinical findings in this population. Male Sprague-Dawley rats were treated for 3 weeks with: saline injection (0.5 ml kg(-1), s.c., 3 times weekly) with tap drinking water (control); saline injection with PB (80 mg l(-1) in drinking water); sarin injection (62.5 microg kg(-1), s.c., 0.5 x LD(50), 3 times weekly) with tap drinking water (sarin); or sarin injection with PB in drinking water (sarin + PB). At 2, 4 or 16 weeks post-treatment, heart rate (HR) and locomotor activity (LA) were studied by radiotelemetry. Two weeks posttreatment, HR in drug-treated animals was significantly lower than in controls. A decrease in low-frequency HR power spectrum (PS) was found at 00:00 h and 08:00 h with sarin + PB and at 00:00 h with sarin, while total power was enhanced with sarin + PB at 22:00 h. Minimal effects of drug treatments on HR and HR PS were detected at 4 and 16 weeks post-treatment. No significant differences in LA between control and other groups were found. Since no consistent long-term effects were found in any of the variables studied, these experiments do not support the hypothesis that repeated administration of low doses of PB and the nerve agent sarin can induce persistent or delayed alterations in autonomic function.

Uncoupling and recoupling of autonomic regulation of the heart beat in pediatric septic shock.

Healthy physiological systems exhibit marked signal variability and complexity, whereas diseased systems generally show a loss of variability, decreased complexity ("decomplexification"), and increased regularity. The goal of this study was to evaluate the uncoupling and recoupling phenomenon in children with septic shock by observing serial changes in heart rate variability metrics. Data were collected from 7 children with septic shock by using the computer system in the Complex Systems Laboratory at Oregon Health Sciences University. Heart rate time series were constructed and analyzed by using the Hales Research System at intervals of 6 h during pediatric intensive care unit (PICU) hospitalization. These power spectral values were then plotted vs. time. Six of seven patients showed an increase over time in low-frequency heart rate power and the low-/high-frequency ratio, whereas high-frequency heart rate power decreased. We also compared the change in mean heart rate, heart rate standard deviation, and power spectral values during the first 24 h of PICU hospitalization vs. the remainder of the PICU stay (for the 5 patients with a PICU length of stay > 48 h). Compared to the initial 24 h in the PICU, low-frequency power and the low-/high-frequency ratio increased, whereas high-frequency power decreased over the course of the illness. This report shows the potential value of monitoring the uncoupling and recoupling phenomenon in patients with septic shock. Our results are in agreement with other investigators who report evidence of decomplexification both in experimental models of sepsis and in clinical studies and provide direction for further work.

Uncoupling of the autonomic and cardiovascular systems in acute brain injury.

We hypothesized that acute brain injury results in decreased heart rate (HR) variability and baroreflex sensitivity indicative of uncoupling of the autonomic and cardiovascular systems and that the degree of uncoupling should be proportional to the degree of neurological injury. We used HR and blood pressure (BP) power spectral analysis to measure neuroautonomic regulation of HR and BP and the transfer function magnitude (TF) between BP and HR as a measure of baroreflex modulation of HR. In 24 brain-injured patients [anoxic/ischemic injury (n = 7), multiple trauma (n = 6), head trauma (n = 5), central nervous system infection (n = 4), and intracranial hemorrhage (n = 2)], neurological injury and survival was associated with low-frequency (0.01-0.15 Hz) HR and BP power and TF. Brain-dead patients showed decreased low-frequency HR power [0. 51 +/- 0.36 (SE) vs. 2.54 +/- 0.14 beats/min2, P = 0.03] and TF [0. 61 +/- 0.16 (SE) vs. 1.29 +/- 0.07 beats . min-1 . mmHg-1, P = 0.05] compared with non-brain-dead patients. We conclude that 1) severity of neurological injury and outcome are inversely associated with HR and BP variability and 2) there is direct evidence for cardiovascular and autonomic uncoupling in acute brain injury with complete uncoupling during brain death.

Evaluation of the autonomic cardiovascular response in Arnold-Chiari deformities and cough syncope syndrome.

To study the autonomic control of heart rate in patients with Arnold-Chiari deformity types I and II who exhibit the signs and symptoms of cough syncope syndrome. Prospective, clinical descriptive study. University clinical research center. Nine patients with Arnold-Chiari deformity and cough syncope syndrome. None. Changes in heart rate, blood pressure, and electrocardiograms for power spectral analysis of heart rate variability were studied in the supine and standing positions, preoperatively (n = 9) and postoperatively (n = 5). Preoperatively, 8 (89%) of 9 patients increased their heart rate after postural change from supine to standing (mean +/- SD delta = 13 +/- 13 beats per minute [bpm]). Postoperatively, 4 (80%) of the 5 patients exhibited a greater increase in standing heart rate (mean delta = 19 +/- 16 bpm) compared with preoperative values. Changes in systolic, diastolic, and mean blood pressure with postural change were variable. Preoperatively, all patients exhibited abnormal control of heart rate in response to postural change. Three patients (33%) showed an abnormal decrease in low-frequency heart rate power (mean delta = -27 +/- 35 bpm2); the remaining 6 (67%) demonstrated an abnormal increase in high-frequency heart rate power (mean delta = 25 +/- 41 bpm2). All patients were clinically asymptomatic at 2 months after surgery. A normal spectral response to postural change was demonstrated in heart rate power in all 5 patients who were reevaluated postoperatively, with an increase in low-frequency power (mean delta = 33 +/- 21 bpm2) and a decrease in high-frequency power (mean delta = -21 +/- 23 bpm2). Patients with cervicomedullary anatomic abnormalities caused by Arnold-Chiari deformities may exhibit abnormal autonomic control of heart rate, and the autonomic control of their heart rate returns to a normal pattern after surgical palliation in conjunction with resolution of clinical symptoms.

Autonomic control of heart rate after brain injury in children

To study sequential changes in heart rate, respiratory rate, blood pressure, heart rate power spectra, and plasma catecholamine concentrations in patients with acute brain injury and correlate these variables with the severity of neurologic dysfunction and patient outcome. Prospective, clinical study. Pediatric intensive care unit. Thirty-seven pediatric patients with acute brain injury caused by trauma, anoxia/ischemia, hemorrhage, or infection. None. We found significant associations between low-frequency (0.01 to 0.15 Hz) heart rate power and severity of neurologic dysfunction (as assessed by the admission Glasgow Coma Scale) (p < .001) and patient outcome (as assessed by the Glasgow Outcome Scale) (p = .05). The admission (p = .05) and maximum (p < .001) values for low-frequency heart rate power and the minimum value for high-frequency (0.15 to 0.50 Hz) heart rate power obtained during hospitalization (p = .001) predicted an increased likelihood of survival. Ten brain-dead patients had significantly decreased low-frequency heart rate power (p = .008) and plasma norepinephrine (p = .015), epinephrine (p = .03), and dopamine (p = .04) concentrations when compared with six non-brain-dead patients with a Glasgow Coma Scale score of 3. Our results imply that autonomic nervous system control of heart rate is disrupted in proportion to the degree of neurologic insult in children after acute brain injury. Thus, heart rate power spectral analysis and plasma catecholamine concentrations may prove to be useful adjuncts in determining severity of neurologic injury and prognosis for recovery in children suffering from brain injury. In addition, these techniques may aid in the determination of brain death.

Autonomic modulation of heart rate variability during endotoxin shock in rabbits

Gram-negative septic shock is associated with severe hypotension and autonomic cardiovascular dysfunction. We hypothesized that in an anesthetized rabbit model of endotoxin shock, autonomic modulation of cardiac activity, as measured by power spectral analysis of heart rate (HR) variability, would be decreased compared with the anesthetized control rabbits. Experimental, comparative study. Laboratory of a university hospital. Fourteen adult male New Zealand white rabbits (2.7 to 3.1 kg body weight) were studied under anesthesia. None. We studied the absolute and temporal changes in HR power spectra and plasma catecholamine concentrations in eight experimental and six control New Zealand white rabbits during Escherichia coli endotoxin-induced shock. HR, respirations, arterial blood pressure (BP), HR power spectra, and plasma catecholamine concentrations were measured at 5- to 10-min intervals for 60 mins in control rabbits or until the mean arterial pressure (MAP) decreased by > or = 20 mm Hg in experimental rabbits. There were no differences in basal HR, respiratory rate, BP, HR power spectra, or catecholamine concentrations between groups. After endotoxin administration, MAP decreased (82 +/- 7 vs. 62 +/- 5 mm Hg; p < .05) as did log low-frequency HR power (-2.14 +/- 2.46 vs. -2.20 +/- 2.48 beats/min2; p < .05). Low-frequency HR power and MAP remained unchanged in control animals. Log high-frequency HR power decreased in control and experimental rabbits (-1.02 +/- 1.34 vs. -1.69 +/- 2.12 [control], p < .05; -1.53 +/- 2.19 vs. -2.19 +/- 2.85 beats/min2 [experimental], p < .05). While there was an inverse relationship between low- and high-frequency HR power and MAP, the direction of change was opposite in six of six rabbits in the control group and in six of eight rabbits in the experimental group. Plasma catecholamine concentrations did not change during the experiment in either group. Sympathetic modulation of cardiac activity decreased, while the sympathomedullary response remained unchanged during endotoxin shock. We speculate that a concomitant decrease in low-frequency HR power as MAP decreases may prove to be an early marker for impending shock.

Spectral analysis of heart rate dynamics in elderly persons with postprandial hypotension

Prior studies suggest that postprandial hypotension in elderly persons may be due to defective sympathetic nervous system activation. We examined autonomic control of heart rate (HR) after a meal using spectral analysis of HR data in 13 old (89 ± 6 years) and 7 young (24 ± 4 years) subjects. Total spectral power, an index of overall HR variability, was calculated for the frequency band between 0.01 and 0.40 Hz. Relatively low-frequency power, associated with sympathetic nervous system and baroreflex activation, was calculated for the 0.01 to O.15 Hz band. High-frequency power, representing parasympathetic influences on HR, was calculated for the O.15 to 0.40 Hz band. Mean arterial blood pressure declined 27 ± 8 mm Hg by 60 minutes after the meal in elderly subjects, compared with 9 ± 8 mm Hg in young subjects (p ≤0.0001, young vs old). The mean change in low-frequency HR power from 30 to 5O minutes after the meal was +19.4 ±25.3 U in young subjects versus −0.1 ± 1.5 U in old subjects (p ≤0.02). Mean change in total power was also greater in young (19.0 ± 26.6 U) subjects compared with old subjects (0.0 ± 1.6 U, p ≤0.02). Mean ratio of low:high-frequency power increased 3.1 ± 3.3 U in young subjects vs O.5 ± 2.7 U in old subjects (p ≤0.01). The increase in low-frequency HR power and in the low:high frequency band ratio in young subjects is consistent with sympathetic activation in the postprandial period. Absence of this finding in elderly subjects with postprandial hypotension is consistent with defective baroreflex compensation after a meal.

Evaluation of autonomic dysfunction in familial dysautonomia by power spectral analysis

We examined the nature and extent of the autonomic control defect in patients with autonomic dysfunction using power spectral analysis of heart rate fluctuations. Heart rate variability and respiratory patterns were monitored and discrete blood pressure measurements were made during supine and standing positions in 10 ambulatory patients with familial dysautonomia and in controls. Postural hypotension without compensatory tachycardia was confirmed in the patients upon standing. The balance between sympathetic and parasympathetic activity was compared in both positions by quantifying the power of the low (0.04–0.095 Hz) and high (respiratory) frequency fluctuations in instantaneous heart rate. After changing from supine to standing position there was a small decrease in the low frequency power of heart rate fluctuations in the patients as opposed to a significant increase in controls. The mean power of fluctuations occurring at high frequency decreased only slightly in the patients compared to a marked decrease in the controls. We conclude that the fall in blood pressure, lack of appropriate heart rate modulation, and failure to increase low frequency heart rate power which occurred in the patients upon standing, are all due to lack of increased sympathetic output under the influence of gravity. The failure to decrease power in the respiratory frequency peak in the patients, suggests an abnormal retention of parasympathetic activity. This may be explained by parasympathetic compensation for the substantial sympathetic loss, or by a lack of appropriate inhibition of parasympathetic tone from baroreceptors or supraspinal structures.