Focus group interviews to examine the role and development of the clinical nurse specialist.

This paper reports on the use of focus groups to investigate the development of clinical nurse specialist roles. The need for this project was identified during initial research, undertaken in two London Hospital Trusts, to assess the variety and nature of advanced clinical nursing roles already in evidence. From analysis of these data, this second stage of the research developed, in which the future of the clinical nurse specialist role within these two trust settings was explored. The initial steps of grounded theory, analytical techniques and procedures, using a constant comparative method, were used to analyse the findings from five focus groups (composed of a total of 25 nurses from two trusts). From the data, six categories were identified; role components; experience versus education; supportive strategies; personal qualities; future role development and development strategies. These categories provide the framework for discussing the findings of the research, within the context of the available literature. This examination of the clinical nurse specialist role highlights issues for career progression and education strategies. Both will need careful planning, in order for the clinical nurse specialist role to be considered and evolve as part of a potential strategy for the development of nursing roles within the two trusts and on a national level.

The clinical nurse specialist: perceptions of practising CNSs of their role and development needs.

This study was carried out to determine the role and development needs of Clinical Nurse Specialists (CNSs) in two acute hospital trusts. One of the aims was to obtain a detailed understanding of the current professional experience of Clinical Nurse Specialists. Data were collected using focus groups and analysed descriptively. Analysis of the content was qualitative, based on a grounded theory approach, and followed the initial steps of open and axial coding. Role transition and development needs are identified on a continuum of novice to expert.

Warmed humidified inspired oxygen accelerates postoperative rewarming.

STUDY OBJECTIVE: To investigate the efficacy of warmed, humidified inspired oxygen (O(2)) for the treatment of mildly hypothermic postoperative patients. DESIGN: Prospective, randomized, unblinded clinical trial. SETTING: Postanesthesia care unit in a tertiary care hospital. PATIENTS AND INTERVENTIONS: 30 ASA physical status I, II, and III patients following intraabdominal surgical procedures were randomly assigned to receive either routine O(2) therapy (control group, n = 15), or warmed (42 degrees C) humidified O(2) (treatment group, n = 15) for the initial 90 postoperative minutes. MEASUREMENTS: Core (tympanic) temperature, dry mouth score and shivering score. MAIN RESULTS: Tympanic temperature was similar in both groups on admission ( approximately 35.8 degrees C). Rewarming rate in the first postoperative hour was greater in the treatment group (0.7 +/- 0.1 degrees C. hr(-1)) compared to the control group (0.4 +/- 0.1 degrees C. hr(-1)) (p = 0.03). Patients receiving the warmed, humidified O(2) had a lower incidence of dry mouth compared to the control group (p = 0.03). The incidence of shivering was low and similar in both groups. CONCLUSIONS: Warming and humidifying inspired O(2) hastens recovery from hypothermia in postoperative patients.

Response to inspiratory resistive loading during sleep in normal children and children with obstructive apnea.

The response to inspiratory resistance loading (IRL) of the upper airway during sleep in children is not known. We, therefore, evaluated the arousal responses to IRL during sleep in children with the obstructive sleep apnea syndrome (OSAS) compared with controls. Children with OSAS aroused at a higher load than did controls (23 +/- 8 vs. 15 +/- 7 cmH(2)O. l(-1). s; P < 0.05). Patients with OSAS had higher arousal thresholds during rapid eye movement (REM) vs. non-REM sleep (P < 0.001), whereas normal subjects had lower arousal thresholds during REM (P < 0.005). Ventilatory responses to IRL were evaluated in the controls. There was a marked decrease in tidal volume both immediately (56 +/- 17% of baseline at an IRL of 15 cmH(2)O. l(-1). min; P < 0.001) and after 3 min of IRL (67 +/- 23%, P < 0.005). The duty cycle increased. We conclude that children with OSAS have impaired arousal responses to IRL. Despite compensatory changes in respiratory timing, normal children have a decrease in minute ventilation in response to IRL during sleep. However, arousal occurs before gas-exchange abnormalities.

Dynamic ventilatory responses in rats: normal development and effects of prenatal nicotine exposure.

Infants of smoking mothers are at increased risk of SIDS, one cause of which is thought to be due to impaired ventilatory responses. We tested the hypotheses that prenatal nicotine exposure impairs the development of dynamic carotid chemoreceptor-driven ventilatory responses, and reduces the ability to lower metabolic rate in hypoxia. Osmotic minipumps were implanted into 20 pregnant rats at day 3 of gestation to deliver nicotine (6 mg/kg per day free base) or saline for 4 weeks. Minute ventilation was recorded breath by breath in rat pups at 3, 8 and 18 days (n = 6, 8 and 6) postnatal in response to 5-sec challenges of 100% O2 (Dejours test) and 5% O2 + 5% CO2. Carotid sinus nerve (CSN) responses to hypoxia and CO2 were recorded from 22 control and 17 nicotine-exposed preparations at ages between 3-20 days. Oxygen consumption (V(O)2) was measured in groups of pups at 3 days (n = 7 each for nicotine and control) and 8 days (n = 5 each for nicotine and control) in room air and 10% O2. There was no detectable effect of nicotine exposure on the development of CSN responses. Ventilatory responses to 5% O2-5% CO2 increased with age but did not differ between nicotine and control groups. Ventilatory responses to 100% O2 were unaffected by nicotine exposure at 8 and 18 days. However, the 3-day nicotine group showed no significant response to 100% O2 whereas V(E) was significantly reduced in the control group by 100% O2. There was no significant effect of nicotine exposure on the ability to reduce oxygen consumption in hypoxia at 3 or 8 days, but at 3 days, baseline (room air) variability in oxygen consumption was greater in the nicotine group. We conclude that nicotine exposure appears to result in abnormal ventilatory responses to withdrawal of baseline peripheral chemoreceptor drive during a period of early postnatal life. We speculate that a transient abnormality could contribute to a period of instability and increased vulnerability to challenges.

Chronic hypoxia abolished the postnatal increase in carotid body type I cell sensitivity to hypoxia.

The O2 sensitivity of carotid chemoreceptor type I cells is low just after birth and increases with postnatal age. Chronic hypoxia during postnatal maturation blunts ventilatory and carotid chemoreceptor neural responses to hypoxia, but the mechanism remains unknown. We tested the hypothesis that chronic hypoxia from birth impairs the postnatal increase in type I cell O2 sensitivity by comparing intracellular Ca2+ concentration ([Ca2+]i) responses to graded hypoxia in type I cell clusters from rats born and reared in room air or 12% O2. [Ca2+]i levels at 0, 1, 5, and 21% O2, as well as with 40 mM K+, were measured at 3, 11, and 18 days of age with use of fura 2 in freshly isolated cells. The [Ca2+]i response to elevated CO2/low pH was measured at 11 days. Chronic hypoxia from birth abolished the normal developmental increase in the type I cell [Ca2+]i response to hypoxia. Effects of chronic hypoxia on development of [Ca2)]i responses to elevated K+ were small, and [Ca2+]i responses to CO2 remained unaffected. Impairment of type I cell maturation was partially reversible on return to normoxic conditions. These results indicate that chronic hypoxia severely impairs the postnatal development of carotid chemoreceptor O2 sensitivity at the cellular level and leaves responses to other stimuli largely intact.

Postnatal maturation of carotid body and type I cell chemoreception in the rat.

The site of postnatal maturation of carotid body chemoreception is unclear. To test the hypothesis that maturation occurs synchronously in type I cells and the whole carotid body, the development of changes in the intracellular Ca2+ concentration responses to hypoxia, CO2, and combined challenges was studied with fluorescence microscopy in type I cells and compared with the development of carotid sinus nerve (CSN) responses recorded in vitro from term fetal to 3-wk animals. Type I cell responses to all challenges increased between 1 and 8 days and then remained constant, with no multiplicative O2-CO2 interaction at any age. The CSN response to hypoxia also matured by 8 days, but CSN responses to CO2 did not change significantly with age. Multiplicative O2-CO2 interaction occurred in the CSN response at 2-3 wk but not in younger groups. We conclude that type I cell maturation underlies maturation of the CSN response to hypoxia. However, because development of responses to CO2 and combined hypoxia-CO2 challenges differed between type I cells and the CSN, responses to these stimuli must mature at other, unidentified sites within the developing carotid body.

Resetting and postnatal maturation of oxygen chemosensitivity in rat carotid chemoreceptor cells.

1. Carotid chemoreceptor sensitivity is minimal immediately after birth and increases with postnatal age. In the present study we have investigated the peri- and postnatal developmental time course of [Ca2+]i responses to hypoxia in clusters of type I cells isolated from near-term fetal rats and rats that were 1, 3, 7, 11, 14 and 21 days old, using the Ca2+-sensitive fluoroprobe fura-2. 2. In type I cells from all age groups a graded increase in [Ca2+]i occurred in response to lowering the PO2 from 150 mmHg to 70, 35, 14, 7, 2 and 0 mmHg. The graded [Ca2+]i response to hypoxia was hyperbolic at all ages. 3. Type I cells from rats near-term fetal to 1 day old exhibited small [Ca2+]i responses, mainly to the most severe levels of hypoxia. After day 1, an increase in the [Ca2+]i responses to submaximal hypoxia stimulation resulted in a rightward shift in the O2 response curve. Using the Delta[Ca2+]i between 35 and 2 mmHg PO2 as an index of O2 sensitivity, type I cell O2 sensitivity increased approximately 4- to 5-fold between near-term fetal to 1 day old and 11 to 14 days of age. 4. Exposure to elevated extracellular potassium (10, 20 and 40 mM K+) caused a dose-dependent [Ca2+]i rise in type I cells from all age groups. There were no age-related changes in [Ca2+]i responses to any level of K+ between near-term fetal and 21 days. 5. We conclude that the maximal type I cell [Ca2+]i response to anoxia, as well as the sensitivity to submaximal hypoxic stimulation, of rats aged from near-term fetal to 21 days depends on the level of postnatal maturity. The lack of an age-related increase in the [Ca2+]i response to elevated K+ during the timeframe of maximal development of O2 sensitivity suggests that resetting involves maturation of O2 sensing, rather than non-specific developmental changes in the [Ca2+]i rise resulting from depolarization.

Arousal and ventilatory responses during sleep in children with obstructive sleep apnea.

Abnormal central regulation of upper airway muscles may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). We hypothesized that this was secondary to global abnormalities of ventilatory control during sleep. We therefore compared the response to chemical stimuli during sleep between prepubertal children with OSAS and controls. Patients with OSAS aroused at a higher PCO2 (58 +/- 2 vs. 60 +/- 5 Torr, P < 0.05); those with the highest apnea index had the highest arousal threshold (r = 0.52, P < 0.05). The hypercapnic arousal threshold decreased after treatment. For all subjects, hypoxia was a poor stimulus to arousal, whereas hypercapnia and, particularly, hypoxic hypercapnia were potent stimuli to arousal. Hypercapnia resulted in decreased airway obstruction in OSAS. Ventilatory responses were similar between patients with OSAS and controls; however, the sample size was small. We conclude that children with OSAS have slightly blunted arousal responses to hypercapnia. However, the overall ventilatory and arousal responses are normal in children with OSAS, indicating that a global deficit in respiratory drive is not a major factor in the etiology of childhood OSAS. Nevertheless, subtle abnormalities in ventilatory control may exist.

Lack of induction of substance P gene expression by hypoxia and absence of neurokinin 1-receptor mRNAs in the rat carotid body.

Peripheral chemoreceptors are commonly thought to respond to hypoxia by releasing neurotransmitters from the type 1 cells of the carotid body; these molecules then bind to post-synaptic receptors on the carotid sinus nerve. The tachykinin substance P (SP) may act as an important neurotransmitter/neuromodulator in hypoxic chemotransmission in peripheral arterial chemoreceptors. In order to elucidate the role of SP in modulating hypoxic chemotransmission, we have used quantitative in situ hybridization histochemistry, to determine the effect of hypoxia on SP gene induction, and the localization of neurokinin 1 (NK-1) receptor mRNA in the carotid body and petrosal ganglia complex in rats at 21 days post-natal age. For comparison, we also determined: (1) the effect of hypoxia on tyrosine hydroxylase (TH) gene induction and (2) the localization of the mRNA encoding the D2-dopamine receptor. SP mRNA was not detected in the rat carotid body during normoxia and its expression was not induced after a 1 h of exposure to hypoxia (10% O2/90% N2), a stimulus that was sufficient to cause a significant increase (P < 0.01) in TH mRNA levels in the carotid body. Both SP and TH mRNAs were abundantly expressed in multiple cells in the petrosal and the jugular ganglia. However, these mRNAs were not co-localized and SP and TH mRNA levels were not affected by hypoxia in these ganglia. Although D2-dopamine receptor mRNA was abundantly expressed in the rat carotid body, we found no evidence of NK-1 receptor mRNA in the carotid body. In contrast, both NK-1 receptor mRNA and D2-dopamine receptor mRNA were present in petrosal ganglion cells. In the rat, SP does not appear to modulate hypoxic chemotransmission by being made in and released from type 1 cells in the carotid body, and neither does SP modulate the activity of type 1 cells by binding to NK-1 receptors on these cells.

The cardiorespiratory response to anoxia: normal development and the effect of nicotine.

Maternal smoking increases the risk of the sudden infant death syndrome (SIDS) 2-4-fold. The mechanism is unknown but may be related to hypoxia responses. Recovery from hypoxic apnea by young mammals depends on gasping and bradycardia. We asked whether prenatal nicotine exposure, reported to reduce hypoxic survival in 2 day old rat pups, acted by impairing gasping or bradycardia. Pregnant rats were infused throughout gestation and 1 week postnatally with nicotine tartrate (NIC) 12 mg/kg per day or saline (CON). Maternal plasma nicotine was 134.4 +/- 42 ng/ml, significantly reducing pup body weight. Pups at 3-28 days were exposed to anoxia (97% N2/3% CO2) until gasping ceased, while breathing and heart rate were recorded. NIC and CON groups were not significantly different at any age, in baseline heart rate, respiratory rate, the time course for bradycardia, time to gasp onset, duration of gasping, or number of gasps, although most of these variables declined significantly with age. We conclude that responses to anoxia are not affected by prenatal high-dose nicotine.

Developmental expression of tyrosine hydroxylase, D2-dopamine receptor and substance P genes in the carotid body of the rat.

Alterations in the level of putative neurotransmitters/neuromodulators and corresponding receptors may be a possible mechanism involved in changes in chemosensitivity of peripheral chemoreceptors in the carotid body during development. Using quantitative in situ hybridization histochemistry, levels of messenger RNAs encoding tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, the D2-dopamine receptor and substance P of newborn rats at postnatal days 0, 2, 14 and 21 were determined. For comparison, during the same time points during development, we also determined the level of expression of these messenger RNAs in the cells of the superior cervical ganglion which are not chemosensitive. Tyrosine hydroxylase and D2-dopamine receptor messenger RNAs were co-localized in many of the cells in both the carotid body and the superior cervical ganglion. In the carotid body, the level of tyrosine hydroxylase messenger RNA expression was greatest at birth, significantly decreased by 48 h postnatal age and remained decreased at 14 and 21 postnatal days. In contrast, D2-dopamine receptor messenger RNA levels significantly increased with postnatal age in the carotid body. This profile of an D2-dopamine receptor was not observed in the superior cervical ganglion where tyrosine hydroxylase and D2-dopamine receptor messenger RNAs levels did not significantly change from postnatal days 0 to 21. Lastly, in the rat carotid body, substance P messenger RNA was not detected. However, substance P messenger RNA was abundant in the nodose and petrosal ganglion. The increasing contribution of carotid body on ventilation with increasing postnatal age is associated with changes in levels of gene expression for tyrosine hydroxylase and D2-dopamine receptor in the carotid body.

Effect of nicotine exposure on postnatal ventilatory responses to hypoxia and hypercapnia.

The risk of SIDS is increased up to fourfold by maternal smoking, by an unknown mechanism. We tested the hypothesis that prenatal nicotine exposure can cause abnormal postnatal development of breathing control. Osmotic minipumps were implanted into pregnant rats to deliver either nicotine bitartrate (6 mg kg-1 day-1) (NIC) or saline (CON) throughout gestation and for 1 week postnatal. NIC and CON rat pups from 4 age groups (means 3, 8, 18 and 34 days) were studied. Ventilation was recorded at 30 degrees C in air and after 10 min at FIO2 = 0.1 and 0.15, and at FICO2 = 0.05. Ventilatory responses to FIO2 = 0.1 and FICO2 = 0.05 showed significant changes with age but were unaffected by NIC at all ages. The weak respiratory responses to FIO2 = 0.15 were unaffected by NIC or age. Oxygen consumption in normoxia and hypoxia, and hypoxic depression of oxygen consumption, declined with age but were not affected by NIC. We conclude that NIC exposure alone has no detectable effect on the postnatal development of respiratory responses to moderate levels of hypoxia or hypercapnia for short periods. However, effects of NIC on the responses to more severe or prolonged stimuli cannot be ruled out.

Mechanisms of carotid chemoreceptor resetting after birth. In vitro studies.

The results of these studies are consistent with the hypothesis that carotid chemoreceptor type-I cell resetting occurs, at least in part, at the level of the type-I cell. Furthermore, we have developed an in vitro model of newborn type-I cell resetting, in which freshly isolated glomus cells from newborns exhibit small, immature [Ca2+]i response to anoxia, but-after 72 hours in culture-[Ca2+]i responses convert to adult magnitude and profile. Finally, work so far suggests that glomus cell resetting in this model is modulated by oxygen tension. The mechanisms of glomus cell resetting remain unknown. Resetting of O2 sensitivity could result from withdrawal of tonic inhibitory influences present in vivo, changes in the oxygen sensor itself, changes in ion channel expression, modulation, and function, or other mechanisms occurring around the time of birth. Additional work is needed to determine the mechanisms of glomus cell resetting at the cellular level, and the role of O2 tension and other potential modulators of resetting.

Supplemental oxygen during sleep in children with sleep-disordered breathing.

Supplemental O2 is sometimes used to treat children with the obstructive sleep apnea syndrome (OSAS). However, its effects have not been studied. We therefore evaluated the use of supplemental O2 during sleep in children with OSAS. Oxygen and room air were delivered via nasal cannula at 1 L/min for 4 h each in a randomized, double-blind fashion. Twenty-three children were studied (mean age, 5 +/- 3 [SD] yr). Patients had a higher mean SaO2 and higher SaO2 nadir when breathing O2. There was no difference in the number (10.9 +/- 20.6/h on O2 versus 13.5 +/- 19.3 on room air) or duration of obstructive apneas. Although there was no overall change in end-tidal PCO2 when patients breathed O2, two children showed a significant increase. We conclude that breathing supplemental O2 during sleep in children with OSAS results in improved oxygenation and in most cases does not exacerbate sleep-disordered breathing. However, end-tidal PCO2 should be monitored in children with OSAS receiving O2 therapy. We speculate that supplemental O2 does not depress the ventilatory drive during sleep in most children with OSAS.

Developmental changes in intracellular Ca2+ response of carotid chemoreceptor cells to hypoxia.

The carotid chemoreceptor response to hypoxia is weak just after birth and increases during postnatal development. The mechanisms underlying chemoreceptor maturation are unknown. We tested the hypothesis that carotid chemoreceptor maturation occurs at the glomus cell level by measuring intracellular calcium ([Ca2+]i) mobilization in response to hypoxia, anoxia, and NaCN in freshly dissociated cells from newborn vs. adult rabbit carotid bodies. Cells were loaded with fura 2 and superfused at 37 degrees C with balanced salt solution equilibrated with 5% CO2. [Ca2+]i mobilization in response to 3-min challenges of hypoxia (PO2 approximately 15 mmHg), anoxia (PO2 approximately 0 mmHg), and NaCN (1 mM) was measured using a digital imaging microscope. The fluorescence intensity ratio was used to calculate [Ca2+]i. Peak [Ca2+]i responses to all three challenges were three- to fivefold greater in glomus cells from adult compared with newborn carotid chemoreceptors. In addition, the average normoxic [Ca2+]i baseline was approximately threefold higher in the adult glomus cells. These results suggest that carotid chemoreceptor glomus cell sensitivity to natural stimuli, as reflected by the [Ca2+]i response, depends on the level of postnatal maturity.

Correlation of cervical auscultation with physiological recording during suckle-feeding in newborn infants.

Pharyngeal swallows during infant suckle-feeding are associated with a characteristic sequence of sounds audible by stethoscope or by an accelerometer or microphone held over the larynx. In rhythmically feeding term-born neonates, the delineating acoustic elements are discrete sounds which precede and succeed pharyngeal swallows. Digital signal processing shows similarities in morphological detail between the discrete sounds preceding swallows and between those succeeding swallows; those succeeding swallows are more variable in temporal relation to swallows, amplitude and morphological detail. Variations in the pattern of interswallow respiration, including apnea, are correlated with variations in the discrete sounds. Specification of physiological correlates of these internal feeding sounds increases the utility of cervical auscultation as a method of investigation and of clinical observation of feeding.

Effects of domperidone on neonatal and adult carotid chemoreceptors in the cat.

It has been postulated that the weak carotid chemoreceptor responses of neonatal mammals may be due to inhibition produced by high levels of endogenous dopamine release or exaggerated sensitivity to dopaminergic inhibition. This was studied by measuring the effect of domperidone, a selective dopamine D2-receptor antagonist, on the carotid chemoreceptor response to O2 and CO2 in anesthetized neonatal and adult cats. The animals were exposed to four levels of isocapnic O2 (arterial PO2 of approximately 35-45, 55-65, 80-90, > 300 Torr) and four levels of isoxic CO2 (end-tidal PCO2 of approximately 21, 40, 58, and 78 Torr) before and after D2-receptor blockade. Whole nerve activity was recorded from the carotid sinus nerve (CSN). Both neonatal and adult cats increase CSN activity during hypoxia and hypercapnia (P < 0.001). Domperidone caused an increase in CSN activity at all O2 levels in adults (P < 0.01) but only during hypoxia in neonates (P < 0.001). Domperidone caused an increase in CSN activity during normo- and hypercapnia in adults but only during hypercapnia in neonates (P < 0.001). Domperidone approximately doubled an index of hypoxic sensitivity in the normoxia-hypoxia range (100 to 40 Torr) in the neonatal group but had little effect on sensitivity to hypoxia in adults. We conclude that the inhibitory role of endogenous dopamine in the carotid chemoreceptors changes with postnatal development.