Search PubMed⌕ Search

Biomedical subjects

D C Shannon

Publications and source records attributed to D C Shannon.

At least 55 records · Page 3Linked to original sources

A compensation scheme for tape-speed variation in cassette recorders.

A scheme to reduce the data corruption caused by tape-speed variation in cassette recorders used for monitoring infant apnea was developed. Low-frequency timing information is recorded on the tape, under the constraints of the frequency response of the recorder, simultaneously with the other signals. This information is extracted during playback and multiplied to a frequency suitable for data sampling, using an electronic, phase-locked loop. Analog-to-digital conversion of the data is performed at a rate proportional to the tape speed, resulting in compensation for speed variation. No direct modification of the speed-control mechanism of the recorder is required. The scheme was evaluated by comparing interval measurements of recorded timing information with and without compensation. Compensation reduced the error of the measurement by nearly an order of magnitude, which was consistent with theoretical predictions. This allows analysis of clinical value to be performed on signals recorded by systems that lack sophisticated speed-control mechanisms.

Apnea↗

Altered cardiac repolarization in some victims of sudden infant death syndrome.

Abnormal prolongation of cardiac repolarization, as reflected by a long QT interval with respect to the RR interval on the electrocardiogram, is known to be associated with ventricular tachyarrhythmias. To test the hypothesis that prolonged cardiac repolarization may characterize some babies who die of sudden infant death syndrome (SIDS), we studied the dependence of the QT interval on the preceding RR interval in 10 babies with SIDS and 29 healthy control babies. We analyzed approximately 5000 pairs of QT and RR intervals in each subject over a wide range of RR intervals. We found that the QT intervals demonstrated less dependence on the preceding RR intervals in 5 of 10 babies who subsequently died of SIDS than in normal controls. No ventricular arrhythmias were observed, however, during the six-hour recording period. Our data suggest that in some babies with SIDS the ability to shorten the QT interval as the heart rate increases is impaired. These observations are consistent with the hypothesis that relatively prolonged cardiac repolarization may predispose such babies to ventricular arrhythmias.

Electrocardiography↗

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.

Adult↗

Aging of modulation of heart rate.

We postulated that measurements of autonomically mediated fluctuations in heart rate might provide a quantitative probe of biological aging. We used power spectrum analysis of instantaneous heart rate while 33 male subjects matched their breathing to a metronome at 15 breaths/min. Measurements were made in supine and standing position. Total power and its two major components, high- and low-frequency power, declined with age in both positions but at different rates. High-frequency power that represents parasympathetically mediated respiratory sinus arrhythmia declined linearly in supine position only in subjects 9-28 yr with a slope of -0.796, which was significantly different from zero at P = 0.0007. The absolute value of high-frequency power in standing position was approximately 60% of that in supine, a difference that was statistically significant (P = 0.01). Low-frequency power that represents beta-adrenergically mediated heart rate fluctuations, especially in standing position, declined linearly to 62 yr of age (P = 0.0001). Mean heart rate increased 17.2 beats/min, and diastolic blood pressure increased 8 mmHg in the entire group in the standing compared with supine position. There were no significant differences in these changes above and below 30 yr of age. We conclude that the influence of the two major mechanisms that modulate heart rate decline at significantly different rates with aging.

Adolescent↗

Increased respiratory frequency and variability in high risk babies who die of sudden infant death syndrome.

We have tested the hypothesis that autonomic instability, reflected in increased variability of heart rate and respiratory frequency, characterized high risk babies who died of sudden infant death syndrome. Using computer-based methods, we compared the power spectra of instantaneous heart rate and respiration on coded tape recordings from seven asymptomatic siblings and 10 babies with symptomatic apnea who died of sudden infant death syndrome to 34 age- and sex-matched controls. We confirmed our previous observation of increased respiratory bandwidth, an index of variability in respiratory frequency (p = 0.009) but failed to confirm our finding of increased low frequency fluctuations in heart rate (p = 0.18). In addition, we found an increase in mean respiratory frequency during quiet breathing (p = 0.001) and a significant relationship between respiratory bandwidth and mean respiratory frequency (r = 0.604, p = 0.0002). These variables along with those from a previous analysis of the same data base yield a discriminant function with 82% sensitivity and 100% specificity. These results confirm previous suggestions that high risk babies who die of sudden infant death syndrome exhibit autonomic instability.

Autonomic Nervous System↗

A new technique to determine the correlation between the QT interval and heart-rate for control and SIDS babies.

The ability of the autonomic nervous system to alter the QT interval in response to heart rate changes is essential to cardiovascular control. An accurate way to determine the relation between QT intervals and their corresponding RR intervals is described. A computer algorithm measures the RR intervals using digital filtering and cross-correlating the QRS sections of consecutive waveforms. The QT intervals is calculated by choosing a section of, the ECG that includes the T wave and cross-correlating it with all the consecutive T waves. At least 4000 pairs of QT-RR intervals are computed for each subject and a best fit correlation function determines the relations between the QT and RR intervals. This technique enables to establish a precise correlation between RR and QT in order to distinguish between control and SIDS babies.

Algorithms↗

Long-term follow-up of children with congenital central hypoventilation syndrome.

The long-term clinical course of six patients with congenital central hypoventilation syndrome is described. During the neonatal period, the patients had prolonged apneas and hypoventilation, in the absence of cardiac, pulmonary, or neuromuscular disease. After an initial period of respirator dependency, they became able to sustain normal gas exchange while awake. During sleep, however, profound hypoventilation developed, and tracheostomy and mechanical ventilation were required. Ventilatory responses to hypercapnia and hypoxia were depressed or absent and did not improve with time. One patient was able, at 2 years of age, to breathe spontaneously during sleep with only moderate hypoventilation. The others, now 4 to 14 years of age, still need ventilatory support during sleep. Complications, such as cardiac failure and hypoxic seizures, mostly occurred early in the course and resolved with correction of insufficient mechanical ventilation. Speech acquisition was possible with the use of a special stoma plug. All patients were managed at home, and with appropriate support, the parents were able to provide safe ventilatory care with low morbidity and no mortality.

Developmental Disabilities↗

Familial occurrence of sudden infant death syndrome and apnea of infancy.

We sought to determine the outcome of infants born to families with multiple victims of sudden infant death syndrome (SIDS) and/or apnea of infancy. Seventy-three infants, born to families who had two or more previous siblings who had either died of SIDS or who were monitored at home for apnea of infancy or for abnormal results on polysomnogram and/or pneumogram recording, were prospectively monitored. The infants underwent polysomnogram and pneumogram recordings and were subsequently monitored at home with a cardiorespiratory monitor. All episodes of apnea were immediately reviewed. Thirteen infants (18%) had subsequent severe episodes of apnea and five other infants (7%) died during a subsequent episode. All deaths occurred in families who had two or more SIDS victims. The outcome for the 17 infants who were half siblings was similar to the outcome for full siblings. Clinical data of the infants and results of evaluation were not predictive of outcome.

Female↗

Bradycardia associated with hiatal hernia and gastroesophageal reflux relieved by surgery.

A man known to have familial dysautonomia presented with a cardiac arrhythmia due to development of hiatal hernia and gastroesophageal reflux. Preoperative symptoms and assessment are described including use of power spectrum analysis of heart rate fluctuations which was consistent with enhanced parasympathetic stimulation. After surgical repair of hiatal hernia and fundoplication, bradycardia resolved, gastroesophageal reflux symptoms subsided, and the power spectrum analysis of heart rate confirmed decreased parasympathetic influence. Power spectrum analysis proved to be a useful adjunct in confirming preoperative autonomic imbalance and assessing the postoperative result. It is concluded that in individuals with disorders such as familial dysautonomia that are associated with autonomic dysfunction, cardiac arrhythmias may be a sign of esophageal pathology. Thus, cardiac evaluations should be accompanied by investigation of gastroesophageal structure and function and appropriate treatment may prevent a catastrophic arrhythmia.

Adult↗

Pneumograms in infants who subsequently died of sudden infant death syndrome.

Victims of sudden infant death syndrome (SIDS) have occasionally been reported to have had prolonged apnea or an increased frequency of short apnea prior to their deaths. To examine the extent of these abnormalities, we compared pneumograms obtained in 17 infants who subsequently died of SIDS (10 with history of apnea) with those of 34 age- and sex-matched controls. The recordings were analyzed by a computer program that avoided observer bias. SIDS infants had significantly greater mean heart rate (P less than 0.05) and periodic breathing during quiet time (P less than 0.003) than control infants had. The apnea in SIDS infants tended to be more periodic than in control infants (P less than 0.002). In addition, the incidence of bradycardia was greater in SIDS (three infants) than in controls (none) (P less than 0.03). These differences suggest a disturbance of autonomic function prior to death in some victims of SIDS.

Apnea↗

Ventilatory effects of almitrine bismesylate in congenital central hypoventilation syndrome.

Patients with congenital central hypoventilation syndrome (CCHS) lack hypercapnic and hypoxic stimulation of ventilation but have demonstrated carotid body function in response to hyperoxia and to pharmacological stimulation with doxapram. This study investigated the ventilatory effects of almitrine bismesylate, a carotid body stimulant, in 12 patients with CCHS. Measurements of minute ventilation, tidal volume (VT), respiratory rate (RR) and transcutaneous PO2 (TCPO2) were taken before and after administration of 4.5 mg/kg and 6 mg/kg of almitrine. Twenty-four hour pharmacokinetic studies were performed in 7 patients who received 4.5 mg/kg and in 6 patients who received 6 mg/kg almitrine. There was no significant improvement in ventilatory and gas exchange parameters at either dose of almitrine despite appropriate peak serum concentration of the drug at the time of the studies. These results suggest that almitrine is not a useful ventilatory stimulant in children with CCHS.

Almitrine↗

Analysis of heart rate and respiratory patterns in sudden infant death syndrome victims and control infants.

Retrospective analyses of patterns of breathing and heart rate variability obtained by visual inspection and spectral analysis of ECG and respiratory activity have provided markers associated with subsequent death in a referred population of infants at high risk for sudden infant death syndrome (SIDS). Such markers include breathing patterns characterized by excessive apneic pauses and periodic breathing, heart rate spectra characterized by increased low frequency oscillations, and respiratory activity spectra characterized by a widened "bandwidth" during regular breathing. To test whether such measurements could distinguish SIDS cases and randomly selected controls from a population study the data from 10 cases and 100 age-matched control subjects were analyzed blind. The code was disclosed after completion of the analysis. We found that none of the markers served to distinguish the SIDS cases from the controls in the population at large. This observation may indicate important physiological differences between infants destined to die in the referred high risk population and infants who die of SIDS at large. The possible reasons for our inability to identify the group of SIDS in the general population, as compared to the group of deaths in the referred high risk group are: (1) different disease processes in the two groups, (2) difference responses to the same disease process in the two groups, (3) a response reflecting the psychosocial setting of the referred high risk population, (4) methodological differences between this and previous studies. We conclude that these markers are not of value in screening the population at large.

Heart Rate↗

Identification of a high-risk group for sudden infant death syndrome among infants who were resuscitated for sleep apnea.

Of the 1,153 infants who completed monitoring by Aug 1, 1984, through our program at Massachusetts General Hospital, 76 infants had an initial apnea spell during sleep which was characterized by a change in tone and color, was unresponsive to repeated vigorous stimulation, and was terminated only after mouth to mouth resuscitation. The infants were hospitalized for observation and evaluation, and no cause could be identified. All were discharged on a home apnea or cardiorespiratory monitor, and subsequent episodes of apnea and/or bradycardia were reviewed. We grouped infants based on the intervention used to terminate subsequent episodes: Group 1, resuscitation; group 2, vigorous stimulation; and group 3, neither resuscitation or vigorous stimulation. There was no significant difference in clinical features or in the results of the initial evaluation in groups 1 and 2, compared with group 3. However, the mortality rate was significantly higher in group 1 (4/13) and group 2 (3/12) than in group 3 (3/51) (P less than .007). Siblings of victims of sudden infant death syndrome (n = 8) were at a significantly higher risk of an adverse outcome (two deaths and four resuscitations) than nonsiblings (P less than .02). A seizure disorder that developed during monitoring was associated with a high mortality (4/11 v 6/65, P less than .02). We conclude that these relatively rare infants who have sleep-onset apnea that responded only to resuscitation and have a subsequent similar episode or are siblings of victims of sudden infant death syndrome or develop a seizure disorder during monitoring have a very high risk of dying (31%, 25%, and 36% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Bradycardia↗

Assessment of autonomic function in humans by heart rate spectral analysis.

Spectral analysis of spontaneous heart rate fluctuations were assessed by use of autonomic blocking agents and changes in posture. Low-frequency fluctuations (below 0.12 Hz) in the supine position are mediated entirely by the parasympathetic nervous system. On standing, the low-frequency fluctuations increase and are jointly mediated by the sympathetic and parasympathetic nervous systems. High-frequency fluctuations, at the respiratory frequency, are decreased by standing and are mediated solely by the parasympathetic system. Heart rate spectral analysis is a powerful noninvasive tool for quantifying autonomic nervous system activity.

Adult↗

Hemodynamic regulation: investigation by spectral analysis.

We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.

Animals↗