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Biomedical subjects

C E Hunt

Publications and source records attributed to C E Hunt.

At least 91 records · Page 5Linked to original sources
PubMed1984

Electromyographic study of some accessory muscles of respiration in children with obstructive sleep apnea.

To further elucidate the pathogenesis of obstructive sleep apnea (OSA), we recorded sternocleidomastoid (SCM), genioglossal (GG), and abdominal (ABD) muscle activity, using surface electromyograms (EMGs), during 45 polygraphic studies in 39 children referred for possible OSA. For each muscle, an index of electromyographic (EMG) activity was developed, allowing an interpatient regression analysis of EMG amplitude versus highest PACO2 and lowest transcutaneous O2 tension (tcPO2) during sleep. Phasic inspiratory SCM activity was present during more than 50% of sleep time in 16 of 20 patients with OSA versus only 2 of 15 patients without OSA; SCM EMG activity increased with increasing PACO2 (r = 0.45, p less than 0.02) and decreasing tcPO2 (r = 0.51, p less than 0.01). Phasic inspiratory GG activity was present during more than 50% of sleep time in 15 of 18 patients with OSA versus none of 4 without OSA; GG EMG activity increased with increasing PACO2 (r = 0.51, p less than 0.05) and with decreasing tcPO2 (r = 0.60, p less than 0.02). Phasic expiratory ABD activity was present during more than 50% of sleep time in 10 to 20 patients with OSA versus 1 of 12 patients without OSA. These findings suggest the following conclusions: (1) inspiratory (SCM), airway-maintaining (GG), and expiratory (ABD) muscles contract during sleep-related partial airway obstruction in children; (2) augmented GG activity during periods of sleep-related partial airway obstruction suggests that pediatric OSA involves pathogenic mechanisms other than GG hypotonia; (3) expiratory ABD muscle activity suggests that some children with OSA have increased expiratory, as well as inspiratory, airway resistance during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗
PubMed1984

The effect of chloral hydrate on genioglossus and diaphragmatic activity.

A child presented with obstructive sleep apnea (OSA) and a near-fatal airway obstruction and respiratory arrest shortly after receiving chloral hydrate (CH). We, therefore, hypothesize that CH might selectively depress upper airway maintaining muscles such as the genioglossus and so predispose to airway obstruction. Genioglossus (GG) and diaphragmatic (DIA) integrated electromyograms (I EMGs) were recorded in four cats and four rabbits before and after hypnotic doses of CH ranging from 200-1000 mg/kg. Results were similar in both species. Peak GG I EMG decreased within 10-20 min after CH in seven of eight animals. Average peak GG I EMGs were decreased from 100% before CH to as low as 37.0 +/- 27.2% (SD) after CH (P less than 0.001). Minimum GG I EMGs fell from 47.2 +/- 27.2% of peak values before CH to as low as 16.0 +/- 9.7% after CH (P less than 0.01). Phasic GG I EMGs decreased from 53.8 +/- 25.1% of peak control activity to as low as 20.6 +/- 24.6% after CH (P less than 0.05). By contrast, peak and phasic DIA I EMGs after CH were not significantly different from those before CH administration. We conclude that hypnotic doses of CH may preferentially depress GG activity as compared with DIA activity. Selective depression of airway-maintaining muscular contraction by CH may place susceptible patients at risk for life-threatening airway obstruction and may preclude the use of CH to facilitate sleep for polygraphic evaluations in patients suspected of having OSA.

Animals↗
PubMed1983

Phrenic nerve pacing in infants and children: a review of experience and report on the usefulness of phrenic nerve stimulation studies.

Nine infants and children, referred for phrenic nerve pacemakers, had measurements of phrenic nerve conduction times and diaphragmatic action potential amplitudes. In these pediatric patients, phrenic nerve conduction times varied from 2.7 to 7.8 msec, were quite reproducible, and were shorter than phrenic nerve conduction times in adults; phrenic nerve conduction time increased with age and with increasing distance between the stimulating electrode and the diaphragm. Diaphragmatic action potential amplitudes varied from 0.08 to 4.1 mV, roughly equivalent to amplitudes in adults, but were variable between patients and within patients on different days. Lower amplitudes were obtained after percutaneous stimulation than after direct phrenic nerve stimulation. Five patients underwent preoperative, percutaneous phrenic nerve stimulation. Strong diaphragmatic contractions allowed us to advise for pacemaker insertion in three patients; weak or absent diaphragmatic contractions allowed us to advise against pacemaker insertion in two patients. Postoperatively, noninvasive measurements of oxygen, carbon dioxide, tidal volume, and diaphragmatic action potential amplitudes have been used to adjust the phrenic nerve pacemaker settings. Phrenic nerve pacemakers have facilitated discharge from the hospital to a home-based ventilation program in six of the seven patients in whom they were inserted. We conclude that phrenic nerve pacing is a practical method of supporting ventilation in carefully selected infants and children. Phrenic nerve stimulation studies are useful in selecting patients for pacing and in adjusting the pacemaker settings.

Action Potentials↗
PubMed1983

Theophylline improves pneumogram abnormalities in infants at risk for sudden infant death syndrome.

To determine the efficacy of theophylline treatment in infants at increased risk for SIDS, we obtained 24-hour cardiorespiratory recordings (pneumograms) in 80 infants given theophylline in whom the initial pneumogram was abnormal. Fifty-three infants had a clinical diagnosis of near-SIDS, and 27 were asymptomatic siblings with a positive family history for SIDS. The initial pneumogram was obtained at a mean age of 6.9 weeks, and the repeat pneumogram 2.3 weeks later, when the mean theophylline blood concentration was 11.2 +/- 0.5 micrograms/ml. Theophylline treatment resulted in comparable and highly significant improvements in both groups. Among all 80 infants, apnea density decreased from 1.6 +/- 0.2% (SEM) to 0.3 +/- 0.1% (P less than 0.001), periodic breathing episodes/100 minutes decreased from 2.7 +/- 0.4 to 0.3 +/- 0.1 (P less than 0.001), and the longest apneic period decreased from 13.5 +/- 0.7 to 10.1 +/- 0.5 seconds (P less than 0.001). Findings on the pneumogram became completely normal with theophylline therapy in 87% of infants with near-SIDS and 81.5% of asymptomatic siblings. Pneumogram normalization was associated with absence of further symptomatic sleep apnea in the near-SIDS group and with continued absence of any clinical symptoms in the asymptomatic family history group. There were no deaths from SIDS.

Cheyne-Stokes Respiration↗
PubMed1983

Intralipid alterations in pulmonary prostaglandin metabolism and gas exchange.

To assess the role of Intralipid as a prostaglandin (PG) precursor, we infused Intralipid into 40 rabbits with long-term arterial and venous catheters; 24 other rabbits received a control saline infusion. One-half of the rabbits in both experimental and control groups had oleic acid-damaged lungs, and at least 5 in each of the 4 groups (Intralipid/saline in normal/damaged lungs) received indomethacin. Two vasodilating PGs (E2 and 6KF1 alpha) and one vasoconstricting PG (F2 alpha) were measured. Triglyceride levels increased significantly in all Intralipid groups, averaging 580 mg/dl. Intralipid-related alterations in PG levels and arterial oxygen tension (PaO2) were significant only in the lung-damaged group. The mean (+/- sem) decrease in PaO2 was 12 +/- 1.5 torr (p less than .001). For both vasodilating PGs, Intralipid infusion increased the pulmonary arteriovenous gradients for PG E2 and PG 6KF1 alpha by 960 pg/ml (p less than .05) and 697 pg/ml (p less than .10), respectively. Both the PaO2 decrease and the vasodilating PG increases were blocked by indomethacin. In summary, Intralipid infusion in lung-damaged rabbits increased pulmonary production of vasodilating PGs and associated hypoxemia, presumably caused by an unblocking of hypoxic vasoconstriction and resultant increase in intrapulmonary right-to-left shunt.

Animals↗
PubMed1983

Medical and neurobehavioral outcome in low-birthweight infants.

The prognosis for normal medical and neurobehavioral outcome in NICU survivors has been progressively improving during the past few years. Prematurity per se does not reduce the potential for normal outcome, especially in greater than 1,500-gm preterm infants. For infants less than or equal to 1,500-gm birthweight, the potential for normal outcome is somewhat diminished, but is nevertheless very encouraging unless complicated by significant IVH. Improved survival and improved neurobehavioral outcome in less than 1,000-gm preterm infants remain as major challenges, especially in respect to the prevention of IVH. Although further improvements in neonatal care can be expected to yield modest additional improvements in neurobehavioral outcome, drastic further improvements will likely depend primarily on preventive measures, ie favorable trends in birthweight distribution related to improved methods for the prevention of prematurity.

Bronchopulmonary Dysplasia↗
PubMed1982

Abnormalities of breathing control and airway maintenance in infants and children as a cause of cor pulmonale.

Respiratory control abnormalities may result in cor pulmonale. This report summarizes the clinical history, diagnostic evaluation, treatment, and outcome of 16 infants and children presenting with cor pulmonale subsequently found to be due to sleep-dependent hypoventilation. Eleven patients had cardiomegaly and electrocardiographic evidence of right ventricular hypertrophy (RVH) while 5 had only severe RVH or biventricular hypertrophy (BVH). Four infants with central hypoventilation syndrome (CHS)--absence of sleep-related ventilatory drive--had severe sleep-dependent asphyxia and resultant acute respiratory failure; all were ultimately treated with phrenic nerve pacing. One patient with alveolar hypoventilation syndrome (AHS)--a partial deficit in ventilatory drive during sleep--presented with severe pulmonary hypertension and ultimately died despite symptomatic relief with respiratory stimulants. Eleven patients presented with obstructive sleep apnea (OSA) and sleep-dependent asphyxia secondary to intermittent complete or to prolonged partial upper airway obstruction. Localized airway obstruction due to an anomalous innominate artery in 1 child was corrected by arteriopexy. Four children underwent adenotonsillectomy (T&A) with disappearance of symptoms in 1, clinical improvement in 2 and no clinical improvement in another. This unimproved patient and the 6 remaining OSA children improved dramatically after tracheostomy to bypass the sleep-dependent airway obstruction; none presently has evidence of cor pulmonale. In summary, early recognition and appropriate treatment of respiratory control disorders will improve sleep ventilation, eliminate asphyxia during sleep, and prevent the development of cor pulmonale.

Cardiomegaly↗
PubMed1982

Arousal responses in near-miss sudden infant death syndrome and in normal infants.

Hypercarbic and hypoxic arousal responses were measured in 22 normal and 11 near-miss sudden infant death syndrome infants during natural sleep. End-tidal PCO2, (PACO2), transcutaneous PO2, electrocardiogram and heart rate, and thoracic and abdominal circumference were continuously recorded. The essential behavioral criteria for arousal were eye opening and crying. For each hypercarbic arousal test, step increases in FICO2 were made until arousal occurred or until PACO2 reached 65 mm Hg. For each hypoxic arousal, step decreases in FIO2 were made until arousal occurred or until FIO2 = 0.15 had been maintained for 20 minutes. The hypercarbic arousal threshold was significantly higher in near-miss SIDS than in normal infants, 54.9 +/- 2.3 vs 48.4 +/- 1.4, respectively ((P less than 0.05). An arousal response to hypoxia occurred in only 9% of near-miss SIDS infants compared to 70% of normal infants (P less than 0.01). The level of respiratory chemostimulation required to produce an arousal response from sleep is significantly greater in near-miss SIDS than in normal infants. We speculate that deficient arousal responsiveness, especially to hypoxia, may prevent potential SIDS victims from responding appropriately to apneic asphyxia.

Arousal↗
PubMed1982

Obstructive sleep apnea in infants and children.

Twenty-two infants and children were found to have clinically significant obstructive sleep apnea. A history suggesting complete or partial airway obstruction during sleep was obtained on all patients, and physical examination of the sleeping patient revealed snoring, retractions, or OSA in 21 patients. Nevertheless, the mean delay in referral for 20 patients first seen after the neonatal period was 23 +15 (+ SD) months. Sixteen of 22 patients (73%) developed serious sequelae: cor pulmonale in 12 (55%), failure to thrive in six (27%), permanent neurologic damage in two (9%), and behavioral disturbances, hypersomnolence, or developmental delays in five (23%). Clinical and radiologic evaluations revealed anatomic abnormalities which narrowed the upper airway in 21 patients; enlarged tonsils and/or adenoids in 14, micrognathia in three,generalized facial abnormalities in three, and cleft palate repair/tonsillar hypertrophy in one. In five patients, upper airway fluoroscopy was performed and was helpful in establishing the site and mechanism of obstruction. Polygraphic monitoring was utilized to quantify the frequency and duration of OSA. Prolonged partial airway obstruction during sleep resulted in significant hypercarbia in 11 patients and hypoxemia in five. Twenty patients improved after surgery which relieved or bypassed the pharyngeal airway obstruction; two cases are pending. Increased awareness of OSA and examination of the sleeping patient should result in earlier treatment and less morbidity for infants and children with OSA.

Adenoids↗
PubMed1982

Experimental effects of chloral hydrate in ventilatory response to hypoxia and hypercarbia.

The effect of chloral hydrate (CH)-induced sleep on inspiratory drive has not been systematically assessed. To determine the effects of CH on the ventilatory responses to hypercarbia and to hypoxia, nine unanesthetized adult rabbit with chronic tracheostomy were studied. We compared awake ventilatory measurements before CH to non-REM sleep assessments at 30, 60, 90, and 120 min after administration of 250 mg/kg of CH. There were no significant differences between any of these assessment intervals for respiratory rate, PACO2, PAO2, tidal volume (VT), minute volume, Ti/Ttot, or VT/Ti. Hypercarbic ventilatory response to slopes were not diminished at any of the CH-sleep intervals compared to the awake mean slope. In addition, the ventilatory response to hypoxia at PAO2=70 mm Hg (V70) and the hypoxic response slope demonstrated no significant decrease at any of the CH-sleep intervals. In summary, absence of any significant decrease in either hypercarbic or hypoxic ventilatory response after CH administration indicates absence of any CH effect on chemical inspiratory drive.

Animals↗
PubMed1981

Indomethacin inhibition of intralipid-induced lung dysfunction.

Intralipid-related pulmonary alterations have been attributed to hyperlipemia. To better quantitate and explain these alterations, Intralipid (0.4 gm/kg over one hour) was infused into three groups of rabbits and saline into a fourth group. Group I had normal lung function; Groups II-IV were pretreated with oleic acid and Group III also received indomethacin. Serum triglyceride (TG) levels, arterial (a) and end-tidal (A) PCO2 and PO2 were measured at baseline and then hourly for six hours. There was no ventilatory deterioration in Group I despite a peak TG level of 638 mg/dl. In Group II there was an Intralipid-related PaO2 decrease of 11-13 mmHg (p less than .01) and a delta AaPO2 increase of 16 mmHg (p less than .01); both returned to baseline without significant TG normalization. Since indomethacin prevented these PaO2 and delta AaPO2 changes despite a significant TG increase, the effects of Intralipid appear not to be TG-related but rather to be related to PG-mediated alterations in pulmonary vasomotor tone. Our results are most consistent with a net increase in vasodilating prostaglandins and resultant hypoxemia secondary to unblocking of baseline hypoxic vasoconstriction.

Animals↗
PubMed1981

Diaphragm pacing in infants and children: report of a simplified technique and review of experience.

Diaphragm pacing was used for treating 6 infants with congenital hypoventilation syndrome at the Children's Memorial Hospital, Chicago. All patients had inadequate sleep-related ventilation and absent ventilatory response to hypercarbia. A single incision was utilized to implant both the electrode and receiver. The phrenic nerve was isolated with a piece of pericardium to minimize injury. All infants required bilateral nerve pacing to obtain satisfactory ventilation (normal transcutaneous measurements of partial pressure of oxygen and end-tidal pressure of carbon dioxide). The technical details described here are helpful in achieving successful phrenic nerve pacing in infants with results comparable to those reported in adults.

Carbon Dioxide↗