The St. Paul Infant Apnea Program. An approach to the evaluation and treatment of infantile apnea.
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We examined 17 patients (3 female, 14 male) of 40 to 60 years of age suspected of suffering from sleep apnoea (SA) according to anamnesis and pulse oximetry, using the apnoea check system (AC) and by polysomnography (PS). AC measures the flow at the mouth and nose by means of thermistors and records the apnoea number, maximal duration of apnoea, and mean duration of apnoea (A mean). The PS-measured values: apnoea index (AI), maximal duration of apnoea (A max) and mean duration of apnoea (A mean) were taken to be equal to 100% and the AC-measured values were referred to these. AI (AC) was 76-577% of AI (PS). In 3 patients, AI (AC) was smaller than AI (PS), whereas in 14 patients it was greater. A max (AC) was 83-390% of A max (PS). In 11 patients A max (AC) was greater than A max (PS) and in 6 patients it was smaller. A mean (AC) was 56-223% of A mean (PS). In 9 patients A mean (AC) was greater and in 8 patients smaller than A mean (PS). PS had in 15 patients an AI > 10, in 2 patients < 10. In all patients, AC had an AI > 10. AC enabled identification of all patients suffering from sleep apnoea, and hence it appears to be suitable for screening. Further measurements in patients with AI < 10 will be necessary to examine the specificity.
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OBJECTIVE: Most neonatologists include an apnea-free period in the criteria for the discharge of preterm infants. However, the length of time one should wait after the cessation of apnea before sending an infant home without a monitor is debated. We undertook this study in an attempt to define a minimal and safe observation period between the time of the last apnea episode and discharge. METHODS: We reasoned that in infants with idiopathic apnea of prematurity, the intervals between days on which apnea occurs gradually increase until some point at which clinically significant apnea ceases. Therefore, knowledge about the intervals between days on which apnea occurred just before the last apnea would provide a reasonable estimate of the minimal safe observation interval between the last apnea and discharge. We reviewed the charts of 266 infants born in 1993 and 1994 at </=32 weeks' gestational age or weighing </=1500 g at birth from two institutions to determine the intervals between the day on which the last apnea occurred and the previous two days on which apnea occurred. One hundred seventy-five infants were excluded because they never experienced apnea, or data about the last apnea was missing, or they were on xanthines during the period encompassing the last 3 apnea days, or they weighed <1500 g or were <34 weeks' postmenstrual age at the time of the last apnea. Of the 91 remaining infants, gestational age at birth, birth weight, 1- and 5-minute Apgar scores, and discharge weight were not different between the two institutions. For each infant we determined the longest of the intervals between the 2 days on which apnea occurred previous to the day of the last apnea (MAXINT for maximum interval). The infants were then ordered by MAXINT and, starting at the longest MAXINT, the medical records of each infant were carefully examined for other conditions known to be associated with apnea (eg, recovering from anesthesia, sepsis, chronic lung disease, and so forth). The minimal safe observation period was then defined as the longest MAXINT in which there was at least 1 infant with no other explanation for the apnea other than prematurity. RESULTS: The median duration of the intervals between the 2 days on which apnea occurred previous to the day on which the last apnea occurred were 3. 0 and 2.0 days and the median duration of the MAXINT was 4.0 days. On careful examination of the charts, it was determined that each of 13 infants with a MAXINT preceding the day on which the last apnea occurred of greater than 8 days had some other condition that might result in apnea, including residual lung disease, sepsis, surgery, and so forth. In contrast, among the group of infants with a MAXINT of </=8 days, at least 1 infant at each MAXINT (eg, 1 to 8) had significant apnea with no other explanation other than prematurity. CONCLUSIONS: We conclude that otherwise healthy preterm infants continue to have apneas separated by as many as 8 days before the last apnea before discharge. Conversely, infants with longer apnea intervals often have identifiable risk factors other than apnea of prematurity.
Apneas in the different sleep states are commonly observed in the full-term healthy newborn infant. Central and short apneas prevail whilst apneas greater than 15 sec. are rare; a marked incidence of short apneas (less than 10 sec.) was observed in active sleep, even though apneas are not exclusive of active sleep. There is a strong inter-individual variability of apnea incidence. Apnea incidence in a state is not positively correlated to apnea incidence in different behavioural states: on the contrary there seems to be an opposite correlation between incidence in AS and QS. Apnea occurrence is positively correlated, in individuals, to the periodic breathing percentage. Apneas number and their duration is markedly lowered already in the second month of life. Periodic breathing must be considered a feature of immaturity. Obstructive apneas are less frequent than central apneas: their survey requires sophisticated technics with the aid of simultaneous recording of several breathing parameters. Relationship between central apneas/ obstructive apneas and mixed apneas is not known. Certainly obstructive and mixed apneas occurrence has been underestimated because of technical difficulties deriving from their survey. The meaning of an incidence of short apneas markedly higher than normal in full-term newborn infants is controversial and not clear, individuals with long apneas and subjects with short apneas in excess have been considered infants at SIDS risk. It is not clear whether periodic breathing and apneas depend on a common pathogenesis; the correlation between high incidence of periodic breathing in postnatal period and SIDS risk is still controversial. Few Authors suggest to treat newborn infants with extended apneas in sleep and considerable percentage of periodic breathing with aminophylline. The relation between gastro-oesophageal reflux and apnea has been recently evidenced. Central apneas and obstructive apneas during breast and bottle feeding have also been documented. Differently from pre-term infant apneas, bradycardia, although not exceptional, is not frequent during apneas in full-term newborn infants.
We examined the influence of apnea type and sleep stage on the severity of apnea-induced desaturations in 32 patients with a sleep apnea syndrome. The individual postapneic desaturations were evaluated by a desaturation curve; this curve was built by plotting the fall in SaO2 after an apnea against this apnea's length for each apneic event during the whole night recording. We considered only apneas where the preapneic SaO2 was greater than 90% and the lowest SaO2 value after the apnea was equal to or greater than 60% (limit of linearity of our oximeter). From the desaturation curve, we determined a desaturation surface defined as the area under the curve between 10s and a variable apnea duration. The upper bound used for the determination of the desaturation curve and the desaturation surface was the maximal length of apnea type with the shortest apnea duration between non-REM obstructive apnea and the other apnea types (i.e., obstructive and central apnea, obstructive and mixed apnea, etc.). The desaturation surface was determined separately for non-REM sleep apneas (obstructive apneas, mixed apneas, central apneas, and obstructive apneas with persistent expiratory flow) and REM sleep apnea (all obstructive in type). Non-REM obstructive apneas served as reference to evaluate the severity of apnea-induced desaturations of the other apneas. We found that the desaturation surface of obstructive apnea (OA) with expiratory flow and of REM sleep OA were significantly greater than for OA in non-REM sleep (p less than or equal to 0.005). The OA-related desaturation was significantly greater than those of central apneas (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
UNLABELLED: Therapeutic decisions in patients with sleep apnea (eg, adjustment of continuous positive airway pressure [CPAP]) depend on differentiating central from obstructive apnea. Obstructive apnea is defined by cessation of airflow in the presence of continued respiratory effort, which is conventionally inferred from chest wall movement or intrathoracic pressure swings. Cardiogenic oscillations in the airflow have been observed during some central apneas, but there is controversy over whether they correlate with airway patency. The present study investigates whether these oscillations are markers of the absence of respiratory effort (central apnea) without regard to airway patency. METHODS: We examined 648 apneas in 52 patients undergoing nocturnal polysomnograms and CPAP titrations. Airflow was measured using the output of the CPAP generator, and apneas were identified from reduction of airflow to < 10% for > 10 s. We used only the presence or complete absence of thoracoabdominal motion to classify apneas: obstructive apnea when motion was present (297 apneas); and central apnea if motion was totally absent (351 apneas). Central apneas most often occurred at sleep onset or followed arousal with a big breath. Using only the flow signal, all apneas were examined for the presence of cardiogenic oscillation by an observer blinded to other signals and apnea types. RESULTS: No obstructive apnea showed definite cardiogenic oscillations. In four cases, there was a suggestion of oscillation that was not regular enough to be called cardiac. Sixty percent of central apneas showed clear, regular oscillations at cardiac frequency. Cardiogenic oscillations also were seen intermittently during quiet exhalation in apnea-free periods. CONCLUSION: The presence of cardiogenic oscillations on the CPAP flow signal is a specific indicator of central apnea and may have a role in self-titrating CPAP algorithms. We speculate that transmission of these cardiac-induced oscillations may relate to the relaxation of thoracic muscles during central apnea and is impeded by high muscle tone during obstructive apnea.
BACKGROUND: Controversy exists as to the risk for postoperative apnea in former preterm infants. The conclusions of published studies are limited by the small number of patients. METHODS: The original data from eight prospective studies were subject to a combined analysis. Only patients having inguinal herniorrhaphy under general anesthesia were included; patients receiving caffeine, regional anesthesia, or undergoing other surgical procedures were excluded. A uniform definition for apnea was used for all patients. Eleven risk factors were examined: gestational age, postconceptual age, birth weight, history of respiratory distress syndrome, bronchopulmonary dysplasia, neonatal apnea, necrotizing enterocolitis, ongoing apnea, anemia, and use of opioids or nondepolarizing muscle relaxants. RESULTS: Two hundred fifty-five of 384 patients from eight studies at four institutions fulfilled study criteria. There was significant variation in apnea rates and the location of apnea (recovery room and postrecovery room) between institutions (P < 0.001). There was considerable variation in the duration and type of monitoring, definitions of apnea, and availability of historical information. The incidence of detected apnea was greater when continuous recording devices were used compared to standard impedance pneumography with alarms or nursing observations. Despite these limitations, it was determined that: (1) apnea was strongly and inversely related to both gestational age (P = 0.0005) and postconceptual age (P < 0.0001); (2) an associated risk factor was continuing apnea at home; (3) small-for-gestational-age infants seemed to be somewhat protected from apnea compared to appropriate- and large-for-gestational-age infants; (4) anemia was a significant risk factor, particularly for patients > 43 weeks' postconceptual age; (5) a relationship to apnea with history of necrotizing enterocolitis, neonatal apnea, respiratory distress syndrome, bronchopulmonary dysplasia, or operative use of opioids and/or muscle relaxants could not be demonstrated. CONCLUSIONS: The analysis suggests that, if it is assumed that the statistical models used are equally valid over the full range of ages considered and that the average rate of apnea reported across the studies analyzed is accurate and representative of actual rates in all institutions, the probability of apnea in nonanemic infants free of recovery-room apnea is not less than 5%, with 95% statistical confidence until postconceptual age was 48 weeks with gestational age 35 weeks. This risk is not less than 1%, with 95% statistical confidence, for that same subset of infants, until postconceptual age was 56 weeks with gestational age 32 weeks or postconceptual age was 54 weeks and gestational age 35 weeks. Older infants with apnea in the recovery room or anemia also should be admitted and monitored. The data do not allow prediction with confidence up to what age this precaution should continue to be taken for infants with anemia. The data were insufficient to allow recommendations regarding how long infants should be observed in recovery. There is additional uncertainty in the results due to the dramatically different rates of detected apnea in different institutions, which appear to be related to the use of different monitoring devices. Given the limitations of this combined analysis, each physician and institution must decide what is an acceptable risk for postoperative apnea.
The effects of periodic obstructive apneas on systemic and myocardial hemodynamics were studied in nine preinstrumented sedated pigs under four conditions: breathing room air (RA), breathing 100% O2, breathing RA after critical coronary stenosis (CS) of the left anterior descending coronary artery, and breathing RA after autonomic blockade with hexamethonium (Hex). Apneas with RA increased mean arterial pressure (MAP; from baseline 103.0 +/- 3.5 to late apnea 123.6 +/- 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 +/- 22.9% of baseline, P < 0.001) but decreased cardiac output (CO; from baseline 2.97 +/- 0.15 to late apnea 2.39 +/- 0.19 l/min, P < 0.001). Apneas with O2 increased MAP (from baseline 105.1 +/- 4.6 to late apnea 110.7 +/- 4.8 Torr, P < 0. 001). Apneas with CS produced similar increases in MAP as apneas with RA but greater decreases in CO (from baseline 3.03 +/- 0.19 to late apnea 2.1 +/- 0.15 l/min, P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 +/- 1.5 to late apnea 7.6 +/- 2.0%, P < 0.01) and regional intramyocardial pH (baseline 7.05 +/- 0.03 to late apnea 6.72 +/- 0. 11, P < 0.001) during apneas with CS but under no other conditions. Apneas with Hex increased to the same extent as apneas with RA. Myocardial O2 demand remained unchanged during apnea relative to baseline. We conclude that obstructive apnea-induced changes in left ventricular afterload and CO are secondary to autonomic-mediated responses to hypoxemia. Increased CBF during apneas is related to regional metabolic effects of hypoxia and not to autonomic factors. In the presence of limited coronary flow reserve, decreased O2 supply during apneas can lead to myocardial ischemia, which in turn adversely affects left ventricular function.
The sleep state characteristics of infant sleep apnea were studied in 36 twins examined by polygraphy at 40, 44, and 52 weeks after conception. The definition of sleep apnea is dependent upon the length of apnea, sleep state, and post-conceptional age. None of the infants had apnea longer than 20 seconds and apnea of 10 seconds or longer was uncommon. The attack rates for apneas 2 to 4.9 seconds long were highest in REM and lowest in qliet sleep. The attack rates for apneas 5 to 9.9 seconds long were equal in REM and indeterminate and lowest in quiet sleep. The percentage of infants with apnea of 10 seconds or longer at 40 weeks was highest in REM (27%) and indeterminate sleep (42%) and lowest in quiet sleep (12%). At 52 weeks, apnea 10 seconds or longer during REM decreased to 0%. The effect of maturation on apnea varies with sleep state. Over the period from 40 to 52 weeks, quiet sleep apnea was unchanged and indeterminate sleep apnea decreased only between 40 and 44 weeks. Although REM apnea 2 to 4.9 seconds long was unchanged, REM apnea 5 to 9.9 seconds long decreased between 40 and 44 weeks, and REM apnea of 10 seconds or longer decreased from 27% at 40 weeks to 0% at 52 weeks. This suggests that semi-independent apnea turn-on and turn-off mechanism operate during REM sleep. A correlation between brief apneas and the longer apneas was seen only during REM sleep. For all sleep states, there was no correlation between the levels of apnea of 5 seconds or longer at 40, 44, and 52 weeks.
STUDY OBJECTIVE: To evaluate the effect of a mandibular advancement device in patients with supine-dependent sleep apnea and patients with non-supine-dependent sleep apnea. DESIGN: Prospective study. SETTING: Department of Respiratory Medicine, University Hospital, Umeå, Sweden. PATIENTS: Twenty-six patients with obstructive sleep apnea. INTERVENTION: Individually fabricated and adjusted mandibular advancement devices. MEASUREMENTS: Overnight polysomnographic sleep recordings with and without the device. Supine-dependent sleep apnea was defined when the supine apnea-hypopnea index was > or = 10, together with a lateral apnea-hypopnea index of < 10. Non-supine-dependent sleep apnea was considered when the lateral apnea-hypopnea index was > or = 10. RESULTS: In 12 patients with supine-dependent sleep apnea, the device reduced the supine apnea-hypopnea index from a median of 41 (range, 16 to 70) to 5.9 (range, 0.0 to 15) (p < 0.01). In 14 patients with non-supine-dependent sleep apnea, the treatment reduced the supine apnea-hypopnea index from 44 (range, 1.8 to 73) to 21 (range, 6.3 to 60) (p < 0.05) and the lateral apnea-hypopnea index from 21 (range, 12 to 70) to 4.5 (range, 0.0 to 31) (p < 0.01). The odds ratio for a successful apnea reduction to an apnea-hypopnea index of < 10 in both the supine and the lateral positions was 30 for supine-dependent sleep apnea adjusted for age, obesity, mandibular advancement, and mandibular opening (p < 0.01). CONCLUSION: Successful apnea reduction with a mandibular advancement device is highly related to supine-dependent sleep apnea.
STUDY OBJECTIVE: To evaluate the tolerability and to find predictors of treatment success for an individually adjusted, one-piece mandibular advancement device in patients with snoring and obstructive sleep apnea. DESIGN: Prospective study. SETTING: Departments of Respiratory Medicine and Orthodontics, Umeå University. PATIENTS: Six hundred nineteen of 630 patients (98%), who consecutively received treatment for sleep apnea and snoring from February 1989 to August 2000, were followed up. They had a mean apnea-hypopnea index of 16 (range, 0.0 to 76) and a mean body mass index of 28 (range, 19 to 42). MEASUREMENTS: Interviews, questionnaires, and overnight sleep apnea recordings. Patients with an apnea-hypopnea index of >or=10 in the supine and/or lateral position were considered to have obstructive sleep apnea. A lateral apnea-hypopnea index of < 10, together with a supine apnea-hypopnea index of >or= 10, defined supine-dependent sleep apneas. RESULTS: One hundred forty-eight of the 619 patients (24%) discontinued treatment. Female gender predicted treatment success, defined as an apnea-hypopnea index of < 10 in both the supine and lateral positions, with an odds ratio of 2.4 (p = 0.01). In the women, the odds ratios for treatment success were 12 for mild sleep apnea (p = 0.04), and 0.1 for complaints of nasal obstruction (p = 0.03). In the men, the odds ratios for treatment success were 6.0 for supine-dependent sleep apneas (p < 0.001), 2.5 for mild sleep apnea (p = 0.04), 1.3 for each millimeter of mandibular advancement (p = 0.03), and 0.8 for each kilogram of weight increase (p = 0.001). CONCLUSIONS: The mandibular advancement device is recommended for women with sleep apnea, for men with supine-dependent sleep apneas defined by a lateral apnea-hypopnea index of < 10, and for snorers without sleep apnea. Men who increase in weight during treatment reduce their chance of treatment success and are advised to be followed up with a new sleep apnea recording with the device.