Lung Function of Adults Born at Very Low Birth Weight.

BACKGROUND: Much remains unknown about the consequences of very low birth weight (VLBW) and bronchopulmonary dysplasia (BPD) on adult lungs. We hypothesized that VLBW adults would have impaired lung function compared with controls, and those with a history of BPD would have worse lung function than those without. METHODS: At age 26 to 30 years, 226 VLBW survivors of the New Zealand VLBW cohort and 100 term controls born in 1986 underwent lung function tests including spirometry, plethysmographic lung volumes, diffusing capacity of the lung for carbon monoxide, and single-breath nitrogen washout (SBN2). RESULTS: An obstructive spirometry pattern was identified in 35% VLBW subjects versus 14% controls, with the majority showing mild obstruction. Compared with controls, VLBW survivors demonstrated significantly lower forced expiratory volume in 1 second (FEV1), FEV1/forced vital capacity (FVC) ratio (FEV1/FVC), forced expiratory flow at 25% to 75% of FVC and higher residual volume (RV), RV/total lung capacity (TLC) ratio (RV/TLC), decreased diffusing capacity of the lung for carbon monoxide, and increased phase III slope for SBN2. The differences persisted after adjustment for sex and smoking status. Within the VLBW group, subjects with BPD showed significant reduction in FEV1, FEV1/FVC, and forced expiratory flow at 25% to 75% of FVC, and increase in RV, RV/TLC, and phase III slope for SBN2, versus subjects without. The differences remained after adjustment for confounders. CONCLUSIONS: Adult VLBW survivors showed a higher incidence of airflow obstruction, gas trapping, reduced gas exchange, and increased ventilatory inhomogeneity versus controls. The findings suggest pulmonary effects due to VLBW persist into adulthood, and BPD is a further insult on small airway function.

The New Zealand 1986 very low birth weight cohort as young adults: mapping the road ahead.

BACKGROUND: Very low birth weight (less than 1500 g) is associated with increased morbidity and costs of health care in childhood. Emerging evidence suggests these infants face a range of health and social problems as young adults. We studied all New Zealand very low birth weight infants born in 1986 (when 58% were exposed to antenatal corticosteroids) in infancy, with later follow-up at 7 to 8 years and 23 to 24 years. We now aim to assess the cohort at 26-28 years compared with controls. METHODS/DESIGN: The case sample will comprise a minimum of 250 members of the 1986 New Zealand national very low birth weight cohort (77% of survivors). Outcomes will be compared with a control group of 100 young adults born at term in 1986. Following written informed consent, participants will travel to Christchurch for 2 days of assessments undertaken by experienced staff. Medical assessments include growth measures, vision, respiratory function, blood pressure and echocardiogram, renal function, dental examination and blood tests. Cognitive and neuropsychological functioning will be assessed with standard tests, and mental health and social functioning by participant interview. A telephone interview will be conducted with a parent or significant other person nominated by the respondent to gain a further perspective on the young person's health and functioning. All those born at less than 28 weeks' gestation, plus a random subset of the cohort to a total of 150 cases and 50 controls, will be offered cranial magnetic-resonance imaging. Statistical analysis will examine comparison with controls and long-term trajectories for the very low birth weight cohort. DISCUSSION: The research will provide crucial New Zealand data on the young adult outcomes for very low birth weight infants and address gaps in the international literature, particularly regarding cardiovascular, respiratory, visual and neurocognitive outcomes. These data will inform future neonatal care, provide evidence-based guidelines for care of preterm graduates transitioning to adult care, and help shape health education and social policies for this high risk group. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12612000995875 . Registered 1 October 2012.

The development of a community-based spirometry service in the Canterbury region of New Zealand: observations on new service delivery.

In 2008, as part of the changes to develop integrated health care services in the Canterbury region of New Zealand, the local health board in collaboration with general practitioners, respiratory specialists and scientists introduced a programme for general practices to provide laboratory-quality spirometry in the community. The service adhered to the 2005 ATS/ERS international spirometry standards. The spirometry service was provided by trained practice nurses and community respiratory nurses, and was monitored and quality assured by certified respiratory scientists in the Respiratory Physiology Laboratory, Christchurch Hospital and CISO (Canterbury Initiative Services Organisation). These two organisations were responsible for organising training seminars and refresher courses on spirometry technique and interpretation of results. A total of 10 practices have now become approved spirometry providers, with the number of tests carried out in the primary care setting increasing gradually. Consistently high-quality spirometry tests have been obtained and are now presented on a centrally available results database for all hospital and community clinicians to review. Although the service has proved to be more convenient for patients, the tests have not been delivered as quickly as those carried out by the Respiratory Physiology Laboratory. However, the time scales for testing achieved by the community service is considered suitable for investigation of chronic disease. The success of the service has been dependent on several key factors including hospital and clinical support and a centralised quality assurance programme, a comprehensive training schedule and online clinical guidance and close integration between primary and secondary care clinicians.

Measurement of oxygen concentration delivered via nasal cannulae by tracheal sampling.

BACKGROUND AND OBJECTIVE: Oxygen is used in many clinical scenarios, however the variable performance of nasal cannulae makes determining the precise fraction of inspired oxygen (FiO2 ) difficult. We developed a novel method for measurement of the tracheal FiO2 using a catheter placed via bronchoscopy. We investigate the effects of oxygen delivery, respiratory rate, mouth position and estimated minute ventilation (VE ) on the FiO2 delivered by nasal cannulae. METHODS: The catheter was placed in 20 subjects. Tracheal gas concentrations were analysed during six 5-min treatments controlling for oxygen delivery rate, respiratory rate and mouth position. Ventilation was monitored with respiratory inductive plethysmography (RIP). The FiO2 delivered by nasal cannulae was compared between treatments, and we investigated the relationships among the FiO2 , alveolar partial pressure of oxygen (PA O2 ) and VE . RESULTS: The FiO2 increased by 0.038/L/min of oxygen. Respiratory rate had a significant effect on the FiO2 . A normal respiratory rate of 15 breaths/min and oxygen supplementation via nasal cannula at 2 L/min resulted in an FiO2 of 0.296; however, FiO2 decreased by 0.012 at 20 breaths/min and 0.004 at 10 breaths/min. The mean FiO2 decreased by 0.024 with the mouth open. The FiO2 and PA O2 were observed to decrease with increasing VE . CONCLUSIONS: Continuous measurement of the FiO2 using a transtracheal catheter provides detailed insight into inspiratory changes of the FiO2 delivered by nasal cannulae. Our study confirms that respiratory rate, VE and mouth position significantly influence the inspired oxygen concentration. These parameters should be accounted for when prescribing oxygen.

Effect of salbutamol on the measurement of single-breath diffusing capacity.

BACKGROUND AND OBJECTIVE: The bronchodilation and cardiovascular effects of bronchodilators may alter alveolar ventilation and perfusion distribution, which could subsequently affect single-breath diffusing capacity of the lungs for carbon monoxide (DL ,CO) measurements. The aim of this study was to investigate the effect of salbutamol on DL ,CO in subjects with and without airway obstruction and reversibility. METHODS: Sixty subjects were investigated with 20 in each of the three groups: normal spirometry; irreversible obstruction; and reversible obstruction. Baseline spirometry, plethysmographic lung volumes, DL ,CO, pulse rate and arterial blood gases were measured. The same testing sequence was repeated after administration of a placebo inhaler and again after 400 µg salbutamol. RESULTS: Salbutamol did not affect the mean alveolar volume (VA ) (P > 0.05), transfer coefficient for carbon monoxide (DL ,CO/VA , KCO) (P > 0.05) or DL ,CO (P > 0.05) in the normal and irreversible obstruction groups. In the reversible obstruction group, salbutamol caused an increase in the mean VA compared with placebo (P < 0.001). However, the mean KCO was reduced (P < 0.001). The mean change in DL ,CO was not significant (P > 0.05). A considerable reduction in DL ,CO was found after salbutamol in four subjects in the reversible group as a result of a minor increase in VA and substantial decrease in KCO. No statistical difference in pulse rate or arterial blood gases values was detected. CONCLUSIONS: Salbutamol had no effect on the mean DL ,CO in any group. However, salbutamol may considerably reduce DL ,CO in some individuals with reversibility secondary to its effects on VA and KCO.

Supplemental oxygen effect on hypoxemia at moderate altitude in patients with COPD.

INTRODUCTION: Altitude exposure will cause moderate to severe hypoxemia in patients with chronic obstructive pulmonary disease (COPD). Supplemental oxygen can be used to attenuate this hypoxemia; however, individual response is variable and difficult to predict. The aim of this study was to assess the efficacy of oxygen supplementation in patients with COPD at a barometric pressure similar to that of a commercial aircraft cabin. METHODS: Following sea-level (40 m) arterial blood gases measurements, 18 patients with COPD were driven to altitude (2086 m), where blood gases were repeated at rest and while on 2 L x min(-1) of supplementary oxygen (altitude O2). RESULTS: Ascent from sea level to altitude caused significant hypoxemia (75 +/- 9 vs. 51 +/- 6 mmHg), which was partially reversed by supplemental oxygen (64 +/- 9 mmHg). Oxygen supplementation did not significantly alter PaCO2 levels (vs. altitude PaCO2). There was a significant relationship between the sea-level CaO2 versus the altitude O2 CaO2 (r = 0.89, P < 0.001). There was a significant relationship (r = 0.81, P < 0.001) between altitude-induced desaturation and resaturation with the administration of oxygen. There was a significant negative correlation (r = -0.74, P < 0.001) between baseline K(CO) and the improvement in CaO2 with the administration of oxygen. CONCLUSION: Low-flow supplemental oxygen during acute altitude exposure will partially reverse altitude-induced hypoxemia in patients with COPD. Patients with diffusion impairments are likely to experience the greatest altitude desaturation, but will gain the most benefit from supplemental oxygen. Supplemental oxygen, delivered at 2 L x min(-1), should maintain clinically acceptable oxygenation during commercial air travel in patients with COPD.

Resting and exercise response to altitude in patients with chronic obstructive pulmonary disease.

INTRODUCTION: Exposure to altitude invariably involves some form of physical activity. There are limited data available to help predict the response to activity at altitude in patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the response to acute altitude exposure at rest and during exercise in patients with COPD. METHODS: Sea level measures of cardio-pulmonary function were compared to the resting and exercise hypoxemic response at the summit of the Mt. Hutt ski field (2086 m), New Zealand, in 18 patients with COPD. RESULTS: Ascent from sea level to altitude caused significant hypoxemia at rest (PaO2: 75 +/- 9 vs. 51 +/- 6 mmHg), and during a walk test (41 +/- 7 mmHg). At altitude, the walk test distance was reduced by 52%. Sea level PaO2 and SaO2 correlated with resting PaO2 (r = 0.69) and SaO2 (r = 0.79) at altitude. Diffusion capacity corrected for alveolar volume (K(CO)) correlated with resting SaO2 (r = 0.74) and exercise PaO2 (r = 0.75) at altitude. Aerobic capacity correlated with the walk test distance at altitude (r = 0.70). Spirometry, lung volumes, and ventilatory reserve did not correlate with the hypoxemic response to altitude. DISCUSSION: Baseline arterial oxygen levels and K(CO) are key measures in predicting the hypoxemic response to acute altitude exposure in patients with COPD. The impairment in gas exchange associated with COPD is a significant mechanism causing altitude-related hypoxemia in this group.