Bi-level positive airway pressure (BiPAP) ventilation in an infant with central hypoventilation syndrome

A 4-month-old baby girl, after a period of apparent good health, began to have aphonia, dyspnea, difficulties with swallowing, cyanosis, apnea, and hypopnea during sleep that resulted in admission to an intensive care unit for intubation and mechanical ventilation. At the age of 9 months she was admitted to our hospital with a possible diagnosis of central hypoventilation syndrome. A polysomnographic study showed apnea and hypopnea (apnea + hypopnea index = 47.1), hypercapnia (mean end-tidal P 89 ± 15.0 mmHg), and arterial desaturation (mean Sa 91 ± 1.7%; lowest Sa < 50%; 68% of total sleep time at Sa below 93%); the study also showed an absent ventilatory response to CO₂, absent cardiac responses to apnea during sleep, and right ventricular hypertrophy. Nocturnal nasal bi-level positive airway pressure (BiPAP), applied initially at 6 cmH₂O and gradually increased to 16 cmH₂O, caused the sleep-related abnormal respiratory events to disappear. End-tidal Pco₂ decreased to 39 mmHg, and Sao₂ increased to 94%. After 6 months of nocturnal BiPAP ventricular right hypertrophy reversed and arrested growth and hypotonia normalized. The child has tolerated and has remained on BiPAP support up to her current age of 3 years and continues to use this form of ventilatory assistance without difficulties. Pediatr. Pulmonol. 1997;24:66–69. © 1997 Wiley-Liss, Inc.     

Ventilatory pump failure in premature newborns

Objective: To determine the prevalence of ventilatory pump failure in premature (<34 weeks gestation) infants. Design: Prospective clinical evaluation of all neonatal intensive care unit (NICU) admissions over a 12 month period in a large, university affiliated hospital. Subjects: A series of 421 consecutive inborn premature infant admissions to the NICU. Methods: Infants were followed for signs and symptoms of respiratory distress and monitored closely for evidence of respiratory failure requiring in tubation and assisted ventilation. The indications for in tubation and assisted ventilation were reviewed, and three such indications were considered clear manifestations of ventilatory pump failure, that is, delivery room resuscitation with CXR negative for evidence of parenchymal lung disease [DR/CXR-1, hypercapnia (P > 55 torr) [ ↑ CO₂], and apnea. Results: A total of 192 premature infants (47% of study sample? required intubations and assisted ventilation. Failure of the ventilatory pump to sustain ventilation (DR/CXR-, ↑ CO₂ apnea) accounted for 70 of these 192 (36%) premature infants. Conclusions: Ventilatory pump failure is a common clinical phenomenon in premature infants. Intensified research on the mechanisms and treatment of ventilatory pump failure might benefit a significant number of such newborns. Pediatr Pulmonol. 1994; 17:231–233. © 1994 Wiley-Liss, Inc.     

The biphasic ventilatory response to hypoxia in preterm infants is not due to a decrease in metabolism

The mechanism underlying the biphasic ventilatory response to hypoxia in neonates is poorly understood. Because alveolar P_CO2 (P_ACO2) decreases and remains low during hypoxia, it has been argued that a decrease in metabolism may occur. We hypothesized that if the late decrease in ventilation during hypoxia is due to a decrease in CO₂ production, an increase in P_ACO2 should abolish it. We studied 27 preterm infants [birth weight, 1,700 ± 41 g (mean ± SEM); study weight, 1,760 ± 36 g; gestational age 32 ± 0.2 weeks; postnatal age, 17 ± 1 days]. A flow-through system and Beckman analyzers were used to measure ventilation and alveolar gases. Metabolism was expressed as changes in oxygen consumption. Infants were studied randomly during hypoxia alone (15% O₂ + N₂, n = 55) and during hypoxia plus CO₂, (0.5% CO₂, n = 30; 2% CO₂, n = 10). Each experiment consisted of 2 minutes of control measurements (21% O₂), 5 minutes of measurements during hypoxia alone or hypoxia plus CO₂, followed by 2 minutes of recovery (21% O₂). We found a biphasic response to hypoxia with or without CO₂ supplementation, the percent change in ventilation from initial peak hyperventilation to late hypoventilation at 5 minutes being -16 ± 2 on 15% O₂; -9 ± 3 on 15% O₂; + 0.5% CO₂ and -15 ± 9 on 15% O₂; + 2% CO₂; (P < 0.05).The decrease in ventilation was primarily due to a significant decrease in frequency; tidal volume increased. Oxygen consumption decreased similarly with the various inspired gas mixtures during hypoxia. These findings indicate that the decrease in ventilation during hypoxia is unlikely to be solely due to a decrease in metabolism since the late decrease in ventilation following initial hyperventilation still occurred despite the elimination of a fall in P_ACO2. We speculate that the mechanism underlying the late decrease in ventilation is likely of central origin, probably mediated through the release of inhibitory neurotransmitters. Pediatr Pulmonol. 1996; 22:287–294. © 1996 Wiley-Liss, Inc.     

BREATHING DURING SLEEP: THE RESPONSES TO ASPHYXIA and PROCHLORPERAZINE IN NORMAL SUBJECTS and PATIENTS WITH OBSTRUCTIVE SLEEP APNEA*

:The effects of sleep and prochlorperazine (12.5 mg intravenous bolus) on the ventilatory and arousal responses to asphyxia were studied in normal subjects and patients with obstructive sleep apnea (OSA). The ventilatory response to asphyxia was reduced during non-rapid eye movement sleep in the six normal subjects studied (1.93 ± 0.181 min^-1. % SaO₂ awake vs. 1.01 ± 0.10 I min^-1. ± SaO₂ asleep; rnean ± SEM; p<0.01) (SaO₂= arterial oxygen saturation). In the two normal subjects studied during sleep following prochlorperazine administration, ventilatory responsiveness was increased (p<0.05) but arousal response to asphyxia was depressed (p<0.025). Although prochlorperazine increased waking ventilatory responsiveness to asphyxia in five of six patients with OSA (2.26 ± 0.44 I min^-1.% SaO₂vs.4.77 ± 1.39 I min^-1.% SaO₂; mean ± SEM; p<0.01), the drug had no clinically significant effect on upper airway obstruction during sleep; in three patients, apnea frequency was slightly reduced but in four of six patients severity of hypoxemia during apnea was increased with drug administration. We conclude that prochlorperazine administration is unlikely to benefit patients with obstructive sleep apnea despite its ventilatory effects during wakefulness and sleep. This lack of effect may be explained by separate effects of the drug on ventilatory and arousal responses to asphyxia. (Aust NZ J Med 1983; 13: 613–620.)     

Assessing ventilatory control in infants at high risk of sleep disordered breathing: A study of infants with cleft lip and/or palate

Neonatal exposure to intermittent hypoxia results in altered ventilatory response to subsequent hypoxia in animal models. The effect of similar exposure in human infants is unknown. Our objective was to determine the impact of sleep disordered breathing (SDB) in early infancy on ventilatory response in infants. We recruited consecutive infants with cleft lip and/or palate (CL/P) to undergo ventilatory response testing using exposure to a hypoxic (15% O₂) gas mixture during sleep. This population is at high risk of SDB because of smaller airway caliber and abnormal palatal muscle attachments predisposing them to airway obstruction of ranging severity from birth. Ventilatory responses were compared between infants with a low apnea–hypopnea index (AHI; AHI < 15 events/hr) and a high AHI (AHI ≥ 15 events/hr). Testing was successfully completed in 22 of 23 infants who underwent testing at 4.4 ± 4.8 months. Infants with high AHI had lower weight z‐scores, higher number of oxygen desaturation events during sleep, but similar oxygen saturation (S_pO₂) nadir compared to infants with low AHI. The pattern of ventilatory response to hypoxia differed between the two groups; infants with high AHI had an earlier ventilatory decline and a blunted maximal ventilatory response to hypoxia. Infants with a high AHI use a different strategy to augment ventilation in response to hypoxia; while infants with a low AHI initially increased respiratory rate, tidal volume was the first parameter to increase in infants with high AHI. These results demonstrate that SDB in infancy is associated with altered ventilatory response to hypoxia. Pediatr Pulmonol. 2013; 48:265–273. © 2012 Wiley Periodicals, Inc.     

Effect of Acute β-blocker Withholding on Ventilatory Efficiency in Patients With Advanced Chronic Heart Failure

BackgroundThis is the first study to examine the effect of acute (24-hour) β-blocker withholding on ventilatory efficiency in patients with advanced chronic heart failure (CHF) during maximal incremental treadmill cardiopulmonary exercise test.Methods and ResultsSeventeen CHF patients were studied either 3 hours after administration of β-blocker (BB_ON) or 27 hours after the last β-blocker ingestion (BB_OFF). The ventilatory efficiency was measured via the slope of the linear relationship between ventilation (V′_E) and carbon dioxide production (V′CO₂) (ie, V′_E/V′CO₂ slope). Measurements were also made at rest, anaerobic threshold (AT), maximal end-tidal pressure for carbon dioxide (P_ETCO_2max), respiratory compensation point (RC), and peak exercise. Compared with BB_ON, the V′_E/V′CO₂ slope was significantly increased during BB_OFF (30.8 ± 7.4 vs. 29.1 ± 5.4, P = .04). At peak exercise, oxygen uptake (V′O₂, 16.0 ± 2.7 vs. 15.6 ± 2.8 mL·kg·min) and V′CO₂ (1458 ± 459 vs. 1414 ± 429 mL/min) were not different between the 2 conditions, whereas V′_E was higher during BB_OFF (49.5 ± 10.7 vs. 46.1 ± 9.6 L/min, P = .04). No differences were noted at AT and RC in V′O₂, V′CO₂, V′_E, V′_E/V′O₂, and V′_E/V′CO₂ ratios during the 2 conditions. At P_ETCO_2max, used to noninvasively estimate the CO₂ set point, V′_E was higher (33.9 ± 7.6 vs. 31.7 ± 7.3 L/min, P = .002) and P_ETCO₂ was lower (37.4 ± 4.8 vs. 38.5 ± 4.0 mm Hg, P = .03), whereas V′CO₂ was unchanged (1079 ± 340 vs. 1050 ± 322 mL/min) during BB_OFF.ConclusionAcute β-blocker withholding resulted in decreased ventilatory efficiency mostly from an increase of V′CO₂-independent regulation of V′_E and less likely from a change in ventilation/perfusion mismatching.     

Acetazolamide and Inhaled Carbon Dioxide Reduce Periodic Breathing During Exercise in Patients With Chronic Heart Failure

BackgroundPeriodic breathing (PB) during sleep and exercise in heart failure (HF) is related to respiratory acid-base status, CO₂ chemosensitivity, and temporal dynamics of CO₂ and O₂ sensing. We studied inhaled CO₂ and acetazolamide to alter these factors and reduce PB.Methods and ResultsWe measured expired and arterial gases and PB amplitude and duration in 20 HF patients during exercise before and after acetazolamide given acutely (500 mg intravenously) and prolonged (24 hours, 2 g orally), and we performed overnight polysomnography. We studied CO₂ inhalation (1%–2%) during constant workload exercise. PB disappeared in 19/20 and 2/7 patients during 2% and 1% CO₂. No changes in cardiorespiratory parameters were observed after acute acetazolamide. With prolonged acetazolamide at rest: ventilation +2.04 ± 4.0 L/min (P = .001), tidal volume +0.11 ± 1.13 L (P = .003), respiratory rate +1.24 ± 4.63 breaths/min (NS), end-tidal PO₂ +4.62 ± 2.43 mm Hg (P = .001), and end-tidal PCO₂ −2.59 ± 9.7 mm Hg (P < .001). At maximum exercise: Watts −10% (P < .02), VO₂ −61 ± 109 mL/min (P = .04) and VCO₂ 101 ± 151 mL/min (P < .02). Among 20 patients, PB disappeared in 1 and 7 subjects after acute and prolonged acetazolamide, respectively. PB was present 80% ± 26, 65% ± 28, and 43% ± 39 of exercise time before and after acute and prolonged acetazolamide, respectively. Overnight apnea/hypopnea index decreased from 30.8 ± 83.8 to 21.1 ± 16.9 (P = .003).ConclusionsIn HF, inhaled CO₂ and acetazolamide reduce exercise PB with additional benefits of acetazolamide on sleep PB.     

Effect of hypobaria on ventilatory and CO2 responses to short-term hypoxic exposure in cats

The effect of hypobaria on the ventilatory response to short-term hypoxia was studied by comparing the respiratory mechanical and inspired CO₂ ventilatory responses to hypobaric hypoxia (438 mmHg) with normobaric hypoxia (11.8% ). Fifteen spontaneously breathing, anesthetized cats were divided into three groups of five: time control, normobaric hypoxia and hypobaric hypoxia. Measurements of ventilation, gas exchange, and responses to intermittent CO₂ rebreathing were collected over a 4 h period. Pa_O2 fell to 44.5±2.7 mmHg, Pa_CO2 fell to 24.8±0.9, and pH rose to 7.49±0.01 in both hypoxic groups. Tidal volume did not change with respect to time or condition, but frequency and ventilation were significantly increased in the hypobaric hypoxic group. The slope of the CO₂ response was unchanged over time or by condition. These results suggest that hypobaric hypoxia may alter the pattern of breathing responses to hypoxia but not the CO₂-response. If metabolic rate remained constant, these results could be explained by a difference in dead space between hypoxic conditions.     

Serotonin is necessary for short-term modulation of the exercise ventilatory response

The exercise ventilatory response is augmented during conditios of increased respiratory dead space (ΔVd), a phenomenon that we refer to as short term modulation (STM). To test the hypothesis that serotonin is necessary in the mechanims underlying STM, experiments were conducted on ten awake goats. Ventilation, CO₂ production and Pa_CO2 were measured at rest and during treadmill exercise (4 km/h, 5% grade), with and without ΔVd (0.25 L), before and after systemic administration of the serotonin receptor antagonist, methysergide maleate (n=6; 1 mg/kg, i.v), or the tryptophan hydroxylase inhibitor, p-chlorophenylalanine (PCPA; n = 4; 100 mg/kg, i.v.). Pre-methysergide: (1) Pa_CO2 decreased from rest to exercise to similar degree with (−1.9mmHg) and without (−1.8mmHg) ΔVd; (2) the exercise ventilatory response increased 59%±13% (p<0.01) with ΔVd, accounting for similar exercise Pa_CO2 regulation and demonstrating STM; and (3) effects of ΔVd on exercise tidal volume and frequency responses were inconsistent. Post-methysergide: (1) there were no significant effects on ventilation or Pa_CO2 at rest or during exercise in control (mask) conditions; (2) the exercise ventilatory response was unaffected by ΔVd, thereby allowing Pa_CO2 to increase 4.1±3.0 mmHg from the rest to exercise (P<0.05); and (3) with ΔVd during exercise, the tidal volume response was increased, but was offset by a decreased frequency response. Following PCPA (16–24 h): (1) hyperventilation was evident at rest and during exercise; (2) the exercise ventilatory response was augmented, indicating STM; and (3) the exercise ventilatory response with ΔVd was not affected further, allowing Pa_CO2 to increase form rest to exercise and indicating an inability to elicit further STM. These data suggest that serotonin is necessary for short term modulation of the exercise ventilatory response with increased respiratory dead space, although the location of relevant serotonin receptors is not yet clear.     

Does peritoneal mobilization increase laparoscopic acidosis?

PURPOSE: It was hypothesized that laparoscopic colon surgery may be associated with increased absorption of CO₂ resulting from mobilization of lateral peritoneal reflections. METHODS: Six pigs underwent laparotomy with removal of a measured quadrant of peritoneum before insufflation to 15 mmHg with CO₂. Six paired control animals also underwent insufflation with CO₂ to 15 mmHg. Measurements of the end-tidal CO₂ (PetCO₂), arterial blood gas analysis for CO₂(PaCO₂), and pH were performed before insufflation, at 5 and 10 minutes following insufflation, then at successive 15-minute intervals for a total of two hours, and 15 minutes following desufflation. No attempt was made to correct the hypercarbia by increasing minute ventilation. RESULTS: PaCO₂ reached its maximum level at two hours with values of 70.77±5.54 mmHg and 64.62±5.18 mmHg in the peritonectomized and control groups, respectively. PetCO₂ also peaked at two hours to 60±13 mmHg for the study group and 54±11 mmHg for controls. pH reached its nadir at two hours, falling from a baseline of 7.45±0.08 to 7.23±0.09 in the study group, and from 7.42±0.04 to 7.24 ±0.04 in the control group. There were no statistically significant differences between the two groups for any of the parameters measured at each time interval. CONCLUSIONS: The hypothesis that peritonectomy produces greater CO₂ absorption during CO₂ pneumoperitoneum was disproved under these experimental conditions.     

Natural history of primary snoring in children

It is not known whether children with primary snoring (PS) progress to develop obstructive sleep apnea syndrome (OSAS). Therefore, we repeated polysomnography in a cohort of 20 children diagnosed 1–3 years previously with PS. All children initially presented with symptoms suggestive of OSAS. They were diagnosed with PS when initial polysomnography demonstrated snoring, with less than one obstructive apnea per hour, normal gas exchange, and infrequent arousals. Of 75 potential candidates, 20 were available for reevaluation (33 could not be contacted, 8 had undergone tonsillectomy and adenoidectomy, and 14 declined). Mean age was 6 ± 4 (SD) years at the time of the initial study. The initial apnea index was 0.2 ± 0.3, S_pO₂ nadir 95 ± 2%, and peak end-tidal PCO₂ was 47 ± 3 mm Hg. At follow-up, all children were reported by their parents to still be snoring; in 20% snoring had reportedly increased, and in 70% there was no change. Eighty percent were thought to have difficulty breathing during sleep. For the group as a whole, there were no significant changes in apnea index, S_pO₂, or peak end-tidal PCO₂. However, two children had mild OSAS on repeat polysomnography (apnea index of 3). We conclude that, in most children, primary snoring does not progress to OSAS over the course of several years. This study indicates that OSAS in the few individuals who do progress is mild. Parental concern about children's breathing patterns during sleep is a poor predictor of polysomnographic abnormalities. However, because many patients were lost to follow-up in this study, further prospective studies are needed. Pediatr Pulmonol. 1998; 26:6–11. © 1998 Wiley-Liss, Inc.     

Ventilatory Expired Gas at Constant-Rate Low-Intensity Exercise Predicts Adverse Events and is Related to Neurohormonal Markers in Patients With Heart Failure

BackgroundVentilatory efficiency (VE/VCO₂ ratio) and the partial pressure of end-tidal carbon dioxide (P_ETCO₂), obtained during moderate to high levels of physical exertion demonstrate prognostic value in heart failure (HF). The present investigation assesses the clinical utility of these variables during low-intensity exercise.Methods and ResultsOne hundred and thirty subjects diagnosed with HF underwent a 2-minute, constant-rate treadmill session at 2 miles per hour. Both the VE/VCO₂ ratio and P_ETCO₂ were recorded during exercise (30-second average) and their change (Δ) from rest. B-type and atrial natriuretic peptide (BNP and ANP) were also determined. Only P_ETCO₂ and ΔP_ETCO₂ emerged from the multivariate Cox regression. Receiver operating characteristic curve analysis revealed the prognostic classification schemes were significant with thresholds of </≥34 mm Hg (hazard ratio: 4.2, 95% CI: 2.2–8.0, P < .001) and </≥1 mm Hg (hazard ratio: 3.5, 95% CI: 1.9–6.6, P < .001) being optimal for P_ETCO₂ and ΔP_ETCO₂, respectively. Moreover, subjects with a P_ETCO₂≥34 mm Hg had a significantly lower BNP (214.1 ± 431.9 vs. 1110.5 ± 1854.0 pg/mL, P=.005) and ANP (108.2 ± 103.6 vs. 246.2 ± 200.4 pg/mL, P < .001).ConclusionsThe results of this pilot study indicate ventilatory expired gas analysis during a short bout of low-intensity exercise may provide insight into prognosis and cardiac stability.     

Ventilatory sensitivity to single breaths of CO2 around the control point in man

We used single inspiratory capacity breaths of 5, 6 or 8% CO₂ in air to obtain ventilatory responses in normal subjects, with ensemble averaging of repeated runs to define stimulus and response (Protocol 1). We also compared the effect of an inspiratory capacity (IC) breath of 8% CO₂ with that of two tidal volumes (TV) at the same concentration (Protocol 2). The ventilatory response was defined first as the ratio of peak changes in ventilation and end-tidal P_CO2, and secondly by the ratio of their integrals. We obtained group mean values of 0.21 L min⁻¹ mmHg⁻¹ for the peak method and 0.80 L min⁻¹ mmHg⁻¹ for integrals (Protocol 1). There was no significant difference between IC and TV response values (Protocol 2) either by the peak method (0.17 vs 0.19 L min⁻¹ mmHg⁻¹) or by integrals (0.47 vs 0.53 L min⁻¹ mmHg⁻¹). A significant decrease in ventilation was seen in the second tidal volume 8% CO₂ breath, even though the stimulus was unperceived by four out of five subjects. CO₂ responses can be obtained from these techniques, but the necessary analysis is too cumbersome for general use. Taking a deep breath had no detectable separate effect, but CO₂ in the airway may depress ventilation even at concentrations which the subject cannot detect.     

Control of breathing in patients with short-term primary hypothyroidism

In 8 patients (3 men and 5 women) with short-term primary hypothyroidism before and during replacement therapy, and in an age-matched control group (9 men and 7 women), we assessed maximal inspiratory muscle force (Pimax) and the ventilatory control system at neural (EMG), muscular (P_0.1), and ventilatory (VE and Vt/Ti) levels. While hypothyroid, patients exhibited a significantly lower Pimax. During a CO₂ rebreathing test, hypothyroid patients exhibited similar diaphragmatic electromyographic (EMGd) and ventilatory (VE) response slopes to increasing end-tidal CO₂ tension (ΔEMGd/ΔPetCO₂ and ΔVE/ΔPetCO₂), but significantly less ΔP_0.1/ΔPetCO₂ (p<0.05) and Δ(Vt/Ti)/ΔPetCO₂ (p<0.05) response slopes. During replacement therapy with L-triiodothyronine (L-T₃), Pimax (p<0.05), ΔP_0.1/ΔPetCO₂, and Δ(Vt/Ti)/ΔPetCO₂ response slopes were found to be significantly increased (p<0.05 for both) while neither EMGd nor VE response changed significantly. We concluded that short-term hypothyroidism does not seem to be associated with blunted neural inspiratory output (EMGd), the respiratory control system seems to be affected mostly at a peripheral (muscular) level, and L-T₃ increases both force (P_0.1 and Pimax) and velocity (Vt/Ti) of inspiratory muscle contraction.     

Pattern of breathing and carbon dioxide retention in chronic obstructive lung disease

Carbon dioxide (CO₂) retention occurs in some but not all patients with obstructive pulmonary disease. In order to assess if the pattern of ventilation modulates CO₂ retention, 15 normocapnic (group 1) and 15 hypercapnic (group 2) patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 second (FEV₁ ≤ 1.0 liter) were studied retrospectively. Utilizing clinical information, anion gap and acid-base nomogram, subjects with superimposed acid-base disturbances were eliminated. Therefore, only patients who exhibited steady state ventilatory patterns were studied. In group 1, mean arterial carbon dioxide tension (PaCO₂) was 40 ± 2 torr and mean arterial pH (pH_a) was 7.410 ± 0.004. In group 2, mean PaCO₂ was 52.5 ± 1.2 torr and pH_a was 7.390 ±0.007. No statistically significant differences between groups were present with respect to age, height, sex, lung volumes and flow rates, diffusing capacity and CO₂ production. Minute ventilation was similar in both groups (7.631 liters and 7.81 liters). In group 2, the patients had a significantly higher respiratory rate per minute (22 versus 16.5) and smaller tidal volume (355 versus 463 cc) than the patients in group 1. This pattern of ventilation resulted in a larger dead space ventilation (3.98 liters versus 2.95 liters) and a lower alveolar ventilation (3.82 liters versus 4.61 liters) with consequent CO₂ retention. The higher respiratory frequency in the patients in group 2 may be due to vagal stimulation from the lungs since this group had a fivefold greater incidence of chronic bronchitis and a seven-fold greater incidence of cor pulmonale than the patients in group 1.     

Polysomnographic characteristics in patients with mucopolysaccharidoses

To evaluate the prevalence of obstructive sleep apnea (OSA) and to clarify sleep characteristics in patients with mucopolysaccharidoses (MPS), we performed overnight polysomnographic studies in 24 patients (22 males and 2 females; 3 with MPS I, 15 with MPS II, 1 with MPS III, 1 with MPS IV, and 4 with MPS VI; mean age, 10.8 ± 6.0 years; age range, 2.0–23.7 years; 2 patients ≥18 years of age). The nadir arterial oxygen saturation (SaO₂) was 74.5 ± 12.3%, and the average percentage of sleep time with an SaO₂ of <95% was 39.4%. The percentages of total sleep time spent in sleep stages N1, N2, N3, and R were 18.6 ± 10.8%, 50.3 ± 7.6%, 14.8 ± 8.1%, and 15.3 ± 4.6%, respectively. The respiratory disturbance index (RDI) was 21.8 ± 20.4/hr, and obstructive apnea–hypopnea index (OAHI) and central apnea index were 21.4 ± 19.9/hr and 0.4 ± 0.6/hr, respectively. The desaturation index was 17.6 ± 17.8/hr. All patients had some degree of OSA. For 22 children, the disorder was mild (OAHI 1.5–5) in 2, moderate (OAHI 5–10) in 7, and severe (OAHI > 10) in 13. Two patients with MPS II who received enzyme replacement therapy had reductions in RDI after treatment (38.9–10.8 and 3.5–2.0, respectively). The prevalence of moderate to severe OSA was 88% (21/24) in patients with MPS. The overnight polysomnography will help to determine the abnormalities of breathing during sleep more precisely and urge the clinicians to take necessary action for patients with severe manifestations. Pediatr Pulmonol. 2010;45:1205–1212. © 2010 Wiley‐Liss, Inc.     

Exercise Ventilatory Efficiency in Older and Younger Heart Failure Patients With Preserved Ejection Fraction

Background

Patients with heart failure with preserved ejection fraction (HFpEF) exhibit pulmonary abnormalities, but the studies to date have reported wide variability in the ventilatory equivalent for carbon dioxide (V?_E/V?CO₂) slope. It is possible that aging may contribute to that variability. We sought to compare ventilatory efficiency and its components in older and younger HFpEF patients during exercise.

Effects of serotonin re-uptake inhibition on ventilatory control in goats

Fluoxetine (Prozac^®) inhibits serotonin (5-HT) re-uptake, thereby enhancing serotonergic effects. Since serotonin is known to affect ventilation in a variety of circumstances, we investigated the effects of chronic serotonin re-uptake inhibition with fluoxetine on selected ventilatory responses including: (1) eupnea; (2) the hypercapnic ventilatory response at rest; (3) the exercise ventilatory response and (4) repeated trials of hypercapnic exercise. Ventilatory and arterial blood gases were measured in goats (n=5) at rest, during steady-state treadmill exercise, and during successive rest/exercise trials with increased respiratory dead space (0.4–0.6 L). Fluoxetine was administered (≥4 weeks, 1 mg/kg, SQ, SID) and protocols were repeated. Following fluoxetine, Pa_CO2 was increased in most conditions studied; however, no differences were seen in exercise Pa_CO2 regulation or ventilatory responses pre- versus post-fluoxetine. We conclude that chronic fluoxetine slightly depresses respiratory control at rest, but, has minimal effects during exercise or with mild hypercapnia during rest or exercise in goats.     

Acute respiratory failure and obesity with normal ventilatory response to carbon dioxide and absent hypoxic ventilatory drive

We measured hypoxic and hypercapnic ventilatory drive in a 64 year old woman with acute respiratory failure, congestive heart failure and obesity when she was in remission. She had a ventilatory response to carbon dioxide (CO₂) comparable to that in six obese women without hypoventilation but no ventilatory response to hypoxia or to vital capacity breaths of 15 per cent CO₂ in N₂- Following weight loss, her ventilatory response to CO₂ increased but hypoxic ventilatory drive remained absent. These findings indicate that attenuation of hypoxic ventilatory drive caused by loss of peripheral chemoreceptor function can be a predisposing factor in the development of acute respiratory failure associated with obesity.     

Home testing for pediatric obstructive sleep apnea syndrome secondary to adenotonsillar hypertrophy

The objective of this study was to determine the accuracy and practicality of home testing for pediatric obstructive sleep apnea syndrome (OSAS) secondary to adenotonsillar hypertrophy. Twenty-one children aged 2-12 years and referred for possible OSAS were studied twice, once at home and once in the sleep laboratory. The home test consisted of two parts: (1) a cardiorespiratory recording of saturation (SaO₂), pulse rate, pulse waveform, electrocardiogram, and respiratory inductive plethysmography; and (2) an 8-hour videotape recording of the sleeping child. In the laboratory, standard nocturnal polysomnography including electroencephalography was performed. Experiences with another 62 children who underwent home testing alone were also reviewed and are reported. At home, saturation, respiratory, and video data were obtained 96.4 ± 13.3% (mean ± SD) 99.4 ± 1.6%, and 90.0 ± 7.8% of the time, respectively. The sleep efficiency was greater at home than in the laboratory, 91.1 ± 3.9% vs. 86.1 ± 7.2%, with a mean difference of 5.0% (P < 0.01). The median environmentally induced movement/arousal index was lower in the home than in the laboratory, 0.0 (inter-quartile range, 0.0-0.3) vs. 2.4/hr (inter-quartile range 1.2–4.2), with a median difference of 2.4/hr (P < 0.001). Study duration, apne/dhypopnea index, desaturation index, respiratory and spontaneous movement/arousal indices, and oxygen saturation during sleep were similar for home and laboratory studies. Although neither sleep state nor PCO₂, (transcutaneous or end-tidal) was measured in the home, this information would have modified patient management in, at most, one case. In the second group of 62 children, exclusively studied at home, all studies were successfully recorded despite a wide range of sleep efficiencies, apne/dhypopnea indices, and desaturation indices. We conclude that home testing, using a simplified cardiorespiratory montage plus video recording, is accurate and of practical use in the routine evaluation of OSAS in patients with adenotonsillar hypertrophy. Pediatr Pulmonol. 1995; 20:241–252 . © 1995 Wiley-Liss, Inc.