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Aim: To determine normative data for arterial oxygen saturation, measured by pulse oximetry (SpO2), in healthy full term infants throughout their first 24 hours of life., Methods: Long term recordings of SpO2, pulse waveform, and breathing movements were made on 90 infants. Recordings were analysed for baseline SpO(2), episodes of desaturation (SpO2 /= four seconds, and periodic apnoea (>/= three apnoeic pauses, each separated by /= 20 seconds) were identified in six recordings. Four desaturations fell to

Objective: To assess the response of healthy infants to airway hypoxia (15% oxygen in nitrogen)., Design: Interventional study., Settings: Infants' homes and paediatric ward., Subjects: 34 healthy infants (20 boys) born at term; mean age at study 3.1 months. 13 of the infants had siblings whose deaths had been ascribed to the sudden infant death syndrome., Intervention: Respiratory variables were measured in room air (pre-challenge), while infants were exposed to 15% oxygen (challenge), and after infants were returned to room air (post-challenge)., Main Outcome Measures: Baseline oxygen saturation as measured by pulse oximetry, frequency of isolated and periodic apnoea, and frequency of desaturation (oxygen saturation < or = 80% for > or = 4 s). Exposure to 15% oxygen was terminated if oxygen saturation fell to < or = 80% for > or = 1 min., Results: Mean duration of exposure to 15% oxygen was 6.3 (SD 2.9) hours. Baseline oxygen saturation fell from a median of 97.6% (range 94.0% to 100%) in room air to 92.8% (84.7% to 100%) in 15% oxygen. There was no correlation between baseline oxygen saturation in room air and the extent of the fall in baseline oxygen saturation on exposure to 15% oxygen. During exposure to 15% oxygen there was a reduction in the proportion of time spent in regular breathing pattern and a 3.5-fold increase in the proportion of time spent in periodic apnoea (P < 0.001). There was an increase in the frequency of desaturation from 0 episodes per hour (range 0 to 0.2) to 0.4 episodes per hour (0 to 35) (P < 0.001). In 4 infants exposure to hypoxic conditions was ended early because of prolonged and severe falls in oxygen saturation., Conclusions: A proportion of infants had episodes of prolonged (< or = 80% for > or = 1 min) or recurrent shorter (< or = 80% for > or = 4 s) desaturation, or both, when exposed to airway hypoxia. The quality and quantity of this response was unpredictable. These findings may explain why some infants with airway hypoxia caused by respiratory infection develop more severe hypoxaemia than others. Exposure to airway hypoxia similar to that experienced during air travel or on holiday at high altitude may be harmful to some infants.

Objective: To determine the mechanisms and thereby appropriate management for apparent life threatening events treated with cardiopulmonary resuscitation in infants and young children., Design: Prospective clinical and physiological study., Setting: Royal Brompton Hospital or in patients' homes, or both., Subjects: 157 Patients referred at median age 2.8 months (range 1 week to 96 months), 111 (71%) had recurrent events, 44 were born preterm, 19 were siblings of infants who had died suddenly and unexpectedly, and 18 were over 12 months old., Interventions: Multichannel physiological recordings, including oxygenation, in hospital (n = 150) and at home (n = 61). Additional recordings with electroencephalogram, video, or other respiratory measures were used to confirm diagnoses. Management involved monitoring of oxygen at home, additional inspired oxygen, anticonvulsant treatment, or child protection procedures., Main Outcome Measures: Abnormalities on recordings compared to published normal data and their correlation with clinical events; sudden death., Results: 53 of 150 patients had abnormalities of oxygenation on hospital recordings, 28 of whom had an accompanying clinical event. Home recordings produced physiological data from 34 of 61 patients during subsequent clinical events. Final diagnoses were reached in 77 patients: deliberate suffocation by a parent (18), hypoxaemia induced by epileptic seizure (10), fabricated history and data (Munchausen syndrome by proxy; seven), acute hypoxaemia of probable respiratory origin (40), and changes in peripheral perfusion and skin colour without hypoxaemia (two). Four patients died: three suddenly and unexpectedly (none on home oxygen monitors) and one from pneumonia., Conclusions: Identification of mechanisms is essential to the appropriate management of infants with apparent life threatening events.

Among 818 newborn babies whose electrocardiograms (ECGs) were recorded between April 1975 and April 1976 were 57 babies with recordings that fell outside the accepted normal range. Preliminary observations have identified the need to define more clearly the range of normal variation. Twelve babies showed asymptomatic conduction abnormalities, three of which were thought sufficiently serious to need treatment. Two babies died suddenly, one of whom had abnormal conduction on the ECG and histologically demonstrated abnormalities of the conducting system. This continuing prospective study may indicate a link between conducting tissue abnormalities and the sudden infant death syndrome. Ten babies had congenital cardiac anomalies, four of which were first discovered because of an abnormal screening cardiogram. Electrocardiography, a simple and noninvasive procedure, may be a valuable addition to the routine neonatal examination.

In an unselected population of 2030 newborn infants studied by electrocardiography (ECG) between April 1975 and April 1977, 35 were found to have arrhythmias or other cardiac conduction abnormalities. Further investigation by means of 24-hour ECG monitoring showed that apparently serious tachyarrhythmias, such as ventricular tachycardia and slow heart rates associated with sinoatrial block, may be present without clinical disturbance in some newborn babies. Six infants had both bradycardia and tachycardia in the 24-hour recording, although the screening ECG had shown only one of these abnormalities. The alarming ECG appearance of some of the arrhythmias suggested a possible aetiological link with some unexplained sudden infant deaths: a multicentre study could determine this more readily and is therefore recommended.

Cardiac conduction disorders caused sudden serious illnesses in six infants that might have been fatal if diagnosis and treatment had been delayed. These cases provide circumstantial evidence to support a link between cardiac conduction disorders and some sudden infant deaths. A further potential long-term effect of these disorders is illustrated in one child in whom psychomotor retardation seemed to develop after an episode of cerebral hypoxia that was probably by an arrhythmia associated with the Wolff-Parkinson-White syndrome. Cardiac conduction disorders may be detected by routine neonatal ECG screening, and it may therefore be appropriate to start prophylactic antiarrhythmic treatment in certain children before clinical signs develop.

From a prospective study in which 24 hour recordings of the electrocardiogram and respiratory activity (abdominal wall movement) were made on a population of full term infants, 22 recordings were obtained from 16 infants who later were victims of the sudden infant death syndrome. The average heart rate, average heart rate variability, average breath to breath interval, and average breath to breath interval variability over the whole of each recording for the 22 recordings were compared with those from a control group of 324 infants selected at random from the rest of the population. No significance was found in the number of recordings from those infants who suffered the sudden infant death syndrome which lay outside the 5th-95th percentile range of the control group for the four variables studied. In a group comparison no difference was found between the sudden infant death syndrome group and the controls either in terms of the respiratory variables studied or in terms of the average heart rate variability. The results did, however, suggest that there may be a group difference in terms of the average instantaneous heart rate.

Objective: To assess the efficacy of a newly developed system for applying continuous or intermittent negative (subatmospheric) extrathoracic pressure in respiratory failure., Design: Uncontrolled clinical trials in infants deteriorating or failing to improve despite standard medical treatment., Setting: Paediatric and neonatal intensive care units and paediatric wards., Patients: 88 Infants and young children aged 1 day to 2 years with respiratory failure due to bronchopulmonary dysplasia, the neonatal respiratory distress syndrome, bronchiolitis, myopathy, the congenital hypoventilation syndrome, pneumonitis, and postoperative phrenic nerve palsy. At the start of treatment 59 were receiving greater than or equal to 50% inspired oxygen and 40 positive airway pressure ventilation., Intervention: Treatment was provided within purpose built Perspex chambers of appropriate size. The chamber incorporated safe and effective latex neck seals; facilities for access, monitoring, and observation; and a heater to control the ambient air temperature., Main Outcome Measures: Inspired oxygen concentration and carbon dioxide pressure before application of negative extrathoracic pressure and two and 48 hours afterwards; duration of treatment; and final outcome (discharge home or death)., Results: While arterial oxygen saturation was maintained at constant values 75 infants showed reductions in inspired oxygen concentrations (range 4-50%, median 15%) two hours after starting treatment and 74 showed reductions at 48 hours (2-79%, median 20%). Of 59 infants who had carbon dioxide pressure measured before and after starting negative extrathoracic pressure, 21 showed a reduction (range 0.6-8.9 kPa, median 2.0), 30 no change (+/- 0.5 kPa), and eight a rise (range 0.6-5.1 kPa, median 2.1). In 28 patients extubation was facilitated, 54 patients were discharged home, where six continued treatment, and 34 died. Treatments lasted for between two and 236 days (median 13 days)., Conclusion: Negative pressure respiratory support is a non-invasive yet effective treatment for respiratory failure. It may avoid the need for intubation, reduce the pathophysiological consequences of positive airway pressure ventilation, and aid extubation.

Two ambulances from the existing fleet in Brighton and one in Hove are equipped with portable defibrillator-oscilloscope units. Selected attendants have been trained not only to defibrillate patients but also to perform endotracheal intubation and administer intravenous atropine and lignocaine for carefully defined indications. In the two years up to December 1975 the ambulances responded to 2253 calls which were considered possible emergencies. Retrospective analysis showed that half of these had been for patients with myocardial infarction, coronary insufficiency, or angina. The ambulances took a median time of five minutes to reach a patient. Attempts at resuscitation were made in 207 patients with circulatory arrest, of whom 160 had ventricular fibrillation. Coordinated rhythm was restored at least transiently in 66 patients, and 27 of them survived to leave hospital. Sixteen of the survivors had been in ventricular fibrillation before the arrival of the ambulance. The delay before admission to hospital was reduced: over 50% of patients carried in the ambulances were admitted within two hours of the onset of major symptoms. No extra ambulance staff have been employed for the scheme. The increased load on hospital services has been limited by encouraging a rational admission policy and also by early discharge.

Recurrent cyanotic episodes associated on some occasions with loss of consciousness due to cerebral hypoxia were investigated by long term tape recordings of breathing activity, oxygen saturation, air flow, electrocardiographic activity, and in some cases electroencephalographic activity. In 51 infants and children the mechanisms for the cyanotic episodes were identified (prolonged expiratory apnoea in 45, sleep related airway obstruction in three, seizure induced apnoea in one, behaviour induced apnoea in one). In one child apnoea was suspected as being caused by suffocation (smothering) by the mother. This was confirmed after enlisting the help of the police, who undertook covert video surveillance during cyanotic episodes. Each cyanotic episode was associated with a pattern of disturbance on the multichannel tape recordings which may be pathognomonic of this type of apnoea. A second infant with cyanotic episodes in whom smothering was suspected was referred for similar investigation after the availability of video recordings became established. Maternal smothering was again supported by specific patterns on multichannel tape recordings and confirmed by video surveillance. Diagnosis by video surveillance produces unequivocal evidence in these cases and avoids the need for medical and nursing staff to confront the mother with a possibly incorrect suspicion or in a court of law.