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What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
What 2012 lung function ultrasound physiology
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  • 1. WHAT 2012 LUNG FUNCTIONAttilio BonerUniversity ofVerona, Italy
  • 2. Breastfeeding is associated with increased lung function at 18 years of age: a cohort Study Soto-Ramı´rez, Eur Respir J 2012;39:985 Effect of breastfeeding (FVC) (Litres) at 18 yrs of age by height A birth cohort. Breastfeeding duration. Spirometric tests at 10 and 18 yrs.
  • 3. Breastfeeding is associated with increased lung function at 18 years of age: a cohort Study Soto-Ramı´rez, Eur Respir J 2012;39:985 A longer Effect of breastfeeding (FVC) (Litres) at 18 yrs of age by height Aduration of birth cohort. breastfeeding Breastfeeding contributes to duration. lung health in Spirometric and childhood tests adolescence. at 10 and 18 yrs.
  • 4. Redefining Spirometry Hesitating Start Criteria Based on the Ratio of Extrapolated Volume to Timed FEVs. McKibben CHEST 2011;140:164 Volume-time tracing showing cut-off values To investigate defining a hesitating start at 1, 3, and 6 s of exhalation for 1501 workers (n=13025 trials). hesitating start criteria for spirometry maneuvers. 24945 trials. Back extrapolation method: 1) extrapolated volume[EV]/FEV1 2) EV/FEV3 3) EV/FEV6 on EV/FVC were determined.
  • 5. Redefining Spirometry Hesitating Start Criteria Based on the Ratio of Extrapolated Volume to Timed FEVs. McKibben CHEST 2011;140:164 The values for EV/FEV1, EV/FEV3 , and EV/FEV6 To investigate corresponding to the 5% EV/FVC value were determined to be hesitating start criteria 6.62%, 5.59%, and for spirometry maneuvers. 5.25%, respectively. 24945 trials. A new hesitating start criterion using EV/FEV6 of 5.25% Back extrapolation method: is recommended for tracings that do not achieve a plateau or 1) extrapolated when an FEV6 is performed. volume[EV]/FEV1 An EV/FEV3 of 5.59% 2) EV/FEV3 could be incorporated into spirometry 3) EV/FEV6 software as an early warning signal on EV/FVC that could help operators identify trials with were determined. potential hesitating starts.
  • 6. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54What is the key question• We sought to compare lung function at 8-9 and 14-17 yrs in children born late preterm (33-34 and 35-36 weeks gestation) with children of similar age born at term (≥37 weeks gestation).• We also compared children born at 25-32 weeks gestation with children born at term.
  • 7. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54 At 8-9 yrs, all spirometry measures were All births from the lower in the 33-34 Avon Longitudinal Study wk gestation group than in of Parents and Children controls born at (n=14049). term but were Spirometry at 8-9 yrs (n=6705) similar to the spirometry and/or 14-17 yrs (n=4508). decrements observed in the 25-32 wk gestation group. 4 gestation groups. 35-36 wk gestation group and term group had similar values.
  • 8. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54 At 14-17 All births from the yrs, in the late Avon Longitudinal Study preterm of Parents and Children group, FEV1 and (n=14049). FVC were similar to the term group Spirometry at 8-9 yrs (n=6705) but and/or 14-17 yrs (n=4508). FEV1/FVC and FEF25-75% 4 gestation groups. remained significantly lower than term controls.
  • 9. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54 At 14-17 All births from the yrs, in the late Avon Longitudinal Study Some improvements preterm ofin lung function values Parents and Children group, FEV1 and (n=14049). were noted FVC were similar in children born at to the term group Spirometry at 8-9 yrs (n=6705) but 33-34 we gestation and/or 14-17 yrs (n=4508). FEV1/FVC and FEF25-75% by the age 4 gestation groups. remained significantly lower of 14-17 yrs. than term controls.
  • 10. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54 All births from the Children requiring Avon Longitudinal Study mechanical ventilation of Parents and Children in infancy at 25-32 (n=14049). and 33-34 wk gestation Spirometry at 8-9 yrs (n=6705) had lower airway function and/or 14-17 yrs (n=4508). (FEV1 and FEF25-75) at both ages 4 gestation groups. than those not ventilated in infancy.
  • 11. Effect of Late Preterm Birth on Longitudinal Lung Spirometry in School Age Children and Adolescents. Kotecha, Thorax 2012;67:54What is the bottom line• Children born at 33-34 weeks gestation have significantly lower lung function values at 8-9 yrs, similar to decrements observed in the 25-32 weeks group, although these differences were reduced by 14-17 yrs of age.Why read on• The findings from this study suggest that children born at 33-34 weeks gestation may be at risk of decreased lung function at 8-9 yrs of age. By 14-17 yrs there were improvements in FEV1.
  • 12. Low cognitive ability in early adulthood is associated with reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884ObjectiveReduced lung function has been linked to poorer cognitive abilitylater in life.In the present study, the authors examined the converse:whether there was a prospective association betweencognitive ability in early adulthood and lung function in middle age.
  • 13. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 Mean FEV1 by quartile of IQ 4256 male Vietnam-era US veterans. Cognitive ability when partecipants were 20 years old (range 17-34). FEV1 at 3-day medical examination in 1986.
  • 14. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 Not only is Mean FEV1 by quartile of IQ lung function related to subsequent 4256 male Vietnam-era US veterans. ability, cognitive but poor cognitive Cognitive ability when ability earlier in life partecipants were 20 is also associated with years old (range 17-34). reduced lung function in middle age. FEV1 at 3-day medical examination in 1986.
  • 15. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 1.The association between Mean FEV1 by quartile of IQ FEV1 and subsequentcognitive ability is generally 4256 male Vietnam-eraexplained in terms of processes US veterans.such as inflammation, impaired Cognitive ability when fibrinolytic activity, oxidative stress and hypoxia 20 partecipants were associated yearswith (range 17-34). old compromised respiratory function. FEV1 at 3-day medical examination in 1986.
  • 16. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 2.Various pathways that Mean FEV1 by quartile of IQ might link low cognitive ability with subsequent 4256 male Vietnam-era impaired lung function: US veterans. a greater propensity for Cognitive ability when unhealthy partecipants were 20 behaviour, including years old (range alcohol smoking, 17-34). consumption and poorer FEV1 at 3-day medical medical adherence examination in 1986. and surveillance.
  • 17. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 3.Another possibility is Mean FEV1 by quartile of IQ that low cognitive ability might be a marker of 4256 male Vietnam-era poorer „system integrity‟, US veterans.such that various physiological systems mount less Cognitive ability when partecipants were injurious resistance to 20 environmental years old (range 17-34). exposures across the FEV1 atlife course. 3-day medical examination in 1986.
  • 18. Low cognitive ability in early adulthood is associatedwith reduced lung function in middle age: the Vietnam Experience Study Carroll Thorax 2011;66:884 4.Finally, both poor lung Mean FEV1 by quartile of IQ function and low cognitive ability have also been 4256 male Vietnam-eraregarded as markers of early US veterans. life adversity including Cognitive ability when exposure to suboptimal nutrition, poverty,20 partecipants were chronic yearschildhood illness old (range 17-34). FEV1 psychosocial stress. and at 3-day medical examination in 1986.
  • 19. Home – officespirometry
  • 20. Risk associatedwith poor lung function
  • 21. Nature and severity of lung function abnormalities in extremely pre-term children at 11 years of age Lum ERJ 2011;37:1199 Extremely pre-term (EP) % EP children with lung function followed at 11 yrs of age. abnormalities of age 11 yrs Alterations 80 - 78% in the lung periphery 70 - or more centralised airway. 60 - Spirometry, plethysmography, 50 – diffusing 40 – capacity, exhaled nitric oxide, multiple-breath 30 – washout, skin tests and 20 – methacoline challenge. 10 – 49 EP and 52 control children. 0
  • 22. Nature and severity of lung function abnormalities in extremely pre-term children at 11 years of age Lum ERJ 2011;37:1199 Extremely pre-term (EP) % EP children with lung function followed at 11 yrs of age. abnormalities of age 11 yrs Evidence of Alterations 80 - airway 78% in the lung periphery 70 - obstruction, ventilat or more centralised airway. 60 - ion inhomogeneity, Spirometry, plethysmography, 50 – gas trapping diffusing 40 – capacity, exhaled nitric oxide, and multiple-breath 30 – washout, airway skin tests and 20 – hyperresponsiveness. methacoline challenge. 10 – 49 EP and 52 control children. 0
  • 23. Nature and severity of lung function abnormalities in extremely pre-term children at 11 years of age Lum ERJ 2011;37:1199 Extremely pre-term (EP) % EP children with lung function followed at 11 yrs of age. abnormalities of age 11 yrs The prevalence of lung function Alterations 80 - 78% in the lung periphery abnormalities, 70 - or more centralised airway. which is largely obstructive 60 - in nature and likely Spirometry, plethysmography, 50 – to have long-term diffusing 40 – capacity, exhaled nitric implications, remains high oxide, multiple-breath 30 – among 11-yr-old washout, skin tests and 20 – methacoline challenge. EP. children born 10 – 49 EP and 52 control children. 0
  • 24. Nature and severity of lung function abnormalities in extremely pre-term children at 11 years of age Lum ERJ 2011;37:1199 Extremely pre-term (EP) % EP children with lung function followed at 11 yrs of age. abnormalities of age 11 yrs Alterations 80 - Spirometry in the lung periphery proved 78% 70 - or an effective means more centralised airway. 60 - Spirometry, detecting of plethysmography, 50 – these persistent diffusing 40 – capacity, exhaled nitric oxide, abnormalities. multiple-breath 30 – washout, skin tests and 20 – methacoline challenge. 10 – 49 EP and 52 control children. 0
  • 25. Relationship between parental lung function and their children‟s lung function early in life van Putte-Katier ERJ 2011;38:664 A significant positive Lung function was relationship between measured before the infant‟s the age of 2 months respiratory compliance using the single and parental occlusion technique forced expiratory flow in 546 infants. at 25–75% of forced vital Parental data on lung capacity (FEF25–75%), function (spirometry). FEV1, and forced vital capacity.
  • 26. Relationship between parental lung function and their children‟s lung function early in life van Putte-Katier ERJ 2011;38:664 Lung function was measured before A significant the age of 2 months negative relationship using the single was found between the occlusion technique infant‟s respiratory in 546 infants. resistance and parental FEF25–75% Parental data on lung and FEV1 function (spirometry).
  • 27. Relationship between parental lung function and their children‟s lung function early in life van Putte-Katier ERJ 2011;38:664 Lung function was measured before for Adjusting A significant shared environmental the age of 2 months negative relationship using the single was found between the factors infant‟s respiratory occlusion technique did not change in 546 infants. resistance the observed results. and parental FEF25–75% Parental data on lung and FEV1 function (spirometry).
  • 28. Relationship between parental lung function and their children‟s lung function early in life van Putte-Katier ERJ 2011;38:664 Parental lung function levels Lung are predictors of the function was measured before respiratory mechanics of A significant their age of 2 infants, which can the newborn months negative relationship only partially be explained by using the body size. single was found between the occlusion suggests genetic infant‟s respiratory This technique in 546 infants. in familial mechanisms resistance aggregation of lung function, and parental FEF25–75% Parental data on lung which are already detectable and FEV1 function early in life. (spirometry).
  • 29. Increasing Severity of Pectus Excavatum is Associated with Reduced Pulmonary Function Lawson, J Ped 2011;159:256 Spirometry data in 310 patients and lung volumes in 218 patients aged 6 to 21 years. Severity of deformity (based on the Haller index). The Haller index was calculated as the inner transverse thoracic diameter divided by the anteroposterior distance between the anterior thoracic wall and the spine at the narrowest point at CT scan.
  • 30. Increasing Severity of Pectus Excavatum is Associated with Reduced Pulmonary Function Lawson, J Ped 2011;159:256 Spirometry data in 310 % of patients with patients and lung volumes in 218 patients aged 15 - 6 to 21 years. 14.5% Severity of deformity 10 – (based on the Haller index). The Haller index was calculated 05 - as the inner transverse thoracic diameter divided by 1.9% the anteroposterior distance 00 obstructive restrictive between the anterior thoracic pattern pattern wall and the spine at the (FEV1/FVC <67%) (FVC and FEV1<80%; narrowest point at CT scan. FEV1/FVC>80%)
  • 31. Increasing Severity of Pectus Excavatum is Associated with Reduced Pulmonary Function Lawson, J Ped 2011;159:256 Spirometry data in 310 patients and lung volumes Relative frequency of reduced FVC in 218 patients aged by Haller index 6 to 21 years. Severity of deformity (based on the Haller index). The Haller index was calculated as the inner transverse thoracic diameter divided by the anteroposterior distance between the anterior thoracic wall and the spine at the narrowest point at CT scan.
  • 32. Increasing Severity of Pectus Excavatum is Associated with Reduced Pulmonary Function Lawson, J Ped 2011;159:256 Spirometry data in 310 patients and lung volumes Relative frequency of reduced FVC Patients with a Haller by Haller index in 218 patients aged index of 7 are >4 6 to 21 years. times more likely to Severity an deformity have of FVC of ≤80% than those with a (based on the Haller index). Haller index of The Haller index was calculated 4, and are also 4 as the inner transverse to times more likely thoracic diameter divided by exhibit a restrictive the anteroposterior distance pulmonary pattern. between the anterior thoracic wall and the spine at the narrowest point at CT scan.
  • 33. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499 The theoretical relationship between airway resistances and airway generation.The x plot tokens indicate the calculation of resistance using the laminar flow equation, length, and total cross-sectional area of all the airways within that generation.
  • 34. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499 The theoretical relationship between airway resistances and airway generation.If the patency of the peripheral airways is compromised or aiways narrowed, then resistance of these small airways might rise (dotted line). However, total resistance would not raise enough to be detected given the normal variation (~10%).
  • 35. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499 The theoretical relationship between airway resistances and airway generation.The finding that respiratory symptom resistance is elevated and resistance is frequency dependent suggests that the site of dysfunction might reside in airways of intermediate size, (double-headed arrow).
  • 36. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499• The significance of this diagram is that small (< 2mm) airways from generation 11 and downward contribute almost nothing (< 10%) to total airway flow resistance.• The human lung has so many small airways that total cross-sectional area in the distal generations of the tracheal bronchial have collectively a very low resistance due to the large cross-sectional area.
  • 37. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499• The significance of this diagram is that small (< 2mm) airways from generation 11 and downward contribute almost nothing (< 10%) to total airway flow resistance.• The human lung has so many small airways that total cross-sectional area in the distal generations of the tracheal bronchial have collectively a very low resistance due to the large cross-sectional area. “The silent zone”
  • 38. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499• Resistance is measured, such as Raw and Sgaw with the body plethysmograph or respiratory symptom resistance with forced oscillations.• Many common lung diseases start or manifest in this “silent zone” of the lung, but the tests developed were either too technically challenging or irreproducible to gain wide acceptance.• The key issue then (and still remaining today) is how best to measure disease in these pesky small airways.• FEV1 is a polyvalent outcome variable affected by many other factors besides airway caliber. In asthma, the fall in FEV1 can be explained by a fall in FVC due to a rise in residual volume (RV ), where RV measures airway closure and hence small airway function and is correlated to symptoms.
  • 39. Will the Small Airways Rise Again? Irvin AJRCCM 2012;184:499• Respiratory symptom resistance (Rrs) is simply not the same thing as FEV1. Yes, there are studies that show the two can be correlated, but nevertheless these two endpoints are in fact very different.• To perform the FEV1 maneuver one must inhale to TLC, which in the normal person abolishes tone of the airway or bronchodilation.• Second, Rrs is measured during quiet breathing and would measure both the structural and tonic components of airway diameter.• Finally, the measurement of Rrs also includes tissue resistance.
  • 40. Relating small airways to asthma control by usingimpulse oscillometry in children Douros, JACI 2012;129:671BackgroundPrevious reports suggest that the peripheralairways are associated with asthma control.Patient history, although subjective, is usedlargely to assess asthma control in childrenbecause spirometric results are many timesnormal values.Impulse oscillometry (IOS) is an objectiveand noninvasive measurement of lung functionthat has the potential to examineindependently both small- and large-airwayobstruction.
  • 41. Relating small airways to asthma control by usingimpulse oscillometry in children Douros, JACI 2012;129:671BackgroundBecause low oscillation frequencies (<15 Hz)can be transmitted more distally in the lungs R5 R5compared with higherfrequencies, R5 reflectsobstruction in both the small R20 R20and largeairways, R20reflects the large airways only, and the R5-R20difference of R5 and R20 (R5-20) is an index R5 – R20of the small airways only.The resistance will become more frequencydependent if peripheral resistance increases.
  • 42. Relating small airways to asthma control by using impulse oscillometry in children Douros, JACI 2012;129:671 Small-airway IOS measurements, including the difference of R5 and R20 [R5- 20], X5, Fres, and AX, of children Asthmatic and with uncontrolled asthma (n=44) healthy children were significantly different from (6-17 years) those of children with controlled asthma (n=57) and healthy children Spirometric and (n=14), especially before the impulse oscillometry administration of a bronchodilator. (IOS) evaluation However, there was no difference in before and after large-airway IOS values (R20). bronchodilator X5 = Reactance of the respiratory system at 5 Hz Fres = Resonant frequency of reactance AX = Reactance area
  • 43. Relating small airways to asthma control by using impulse oscillometry in children Douros, JACI 2012;129:671 Receiver operating characteristic analysis showed cut points for Asthmatic and baseline R5-20 (1.5 cm H2O x L-1 x s) healthy children and AX (9.5 cm H2O x L-1) that (6-17 years) effectively discriminated controlled versus uncontrolled asthma and Spirometric and correctly classified more than 80% impulse oscillometry of the population. (IOS) evaluation before and after bronchodilator AX = Reactance area
  • 44. Relating small airways to asthma control by using impulse oscillometry in children Douros, JACI 2012;129:671 Uncontrolled asthma is Receiver operating characteristic associated with analysis showed cut points for small airways Asthmatic and baseline R5-20 (1.5 cm H2O x L-1 x s) dysfunction, and healthy children and AX (9.5 cm H2O x L-1) that (6-17 years) be a IOS might effectively discriminated controlled reliable and versus uncontrolled asthma and Spirometric and correctly classified more than 80% noninvasive method impulse oscillometry of the population. to assess asthma (IOS) evaluation control in before and after children bronchodilator AX = Reactance area
  • 45. lung functionnon-collaborante
  • 46. Risposta aibroncodilatatori
  • 47. The Relationship of the Bronchodilator Response Phenotype to Poor Asthma Control in Children with Normal Spirometry Galant, J Ped 2011;158:953 OR in BDR ≥10% and ≥12% versus Clinical indexes of negative responses for poorly controlled 4 – asthma. Pre- and post- 3 – 3.4 bronchodilator spirometry. 2 – 2.2 1 – 1.9 1.7 Bronchodilator p<0.05 p<0.01 p<0.01 p<0.001 response (BDR) at 0 ≥8%, ≥10%, and ≥12%. atopy nocturnal β2agonist exercise symptoms use limitation in females
  • 48. The Relationship of the Bronchodilator Response Phenotype to Poor Asthma Control in Children with Normal Spirometry Galant, J Ped 2011;158:953 OR in BDR ≥10% and ≥12% versus The BDR phenotype Clinical indexes of negative responses for ≥10% is significantly poorly controlled 4 – related to poor asthma. asthma control, providing a Pre- and post- 3 – 3.4 potentially useful bronchodilator objective tool in spirometry. naïve 2 – 2.2 controller children even when the 1 – 1.9 1.7 Bronchodilator pre-bronchodilator p<0.05 p<0.01 p<0.01 p<0.001 response (BDR) at spirometry result 0 ≥8%, ≥10%, and ≥12%. is normal. atopy nocturnal β2agonist exercise symptoms use limitation in females
  • 49. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airflow limitation measured as FEV1/FVC% predicted. 77 children with severe asthma. 71 children with nonsevere asthma ages 6 to 17 yrs. Baseline spirometry and plethysmographic lung volumes after a bronchodilation with up to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 50. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airflow limitation measured as FEV1/FVC% predicted. 77 children with severe asthma. 71 children with nonsevere asthma ages 6 to 17 yrs. Baseline spirometry and plethysmographic lung volumes after a bronchodilation with up to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 51. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airflow limitation measured as FEV1/FVC% predicted. Subjects in the 77 children with nonsevere asthma group severe asthma. had modest 71 children with at baseline, airflow limitation nonsevere asthma ages with only 19% having 6 to FEV1/FVC ratio below 17 yrs. Baseline spirometry normal the ower limit of and plethysmographic (<89% predicted for boys and lung volumes afterfor girls) <90% predicted a and no differences bronchodilation with up to 8 between albuterol.4). puff of sexs (p> BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 52. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airflow limitation measured as FEV1/FVC% predicted. The severe asthma group 77 exhibited with children greater airflow severe asthma. the nonsevere limitation than 71 children0.0001) with 54% group (p< with nonsevere asthma ages the of the girls and 73% of 6boys having the FEV1/FVC% to 17 yrs. Baseline spirometrynormal, predicted below and plethysmographic and the boys significantly lung volumes obstructed more after a bronchodilation with up . than the girls (p=0.017) to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 53. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airflow limitation measured as FEV1/FVC% predicted. 77 children with with The subjects severe asthma. asthma nonsevere and the girls with 71 children with nonsevereasthma exhibited severe asthma ages reversal of airflow 6 to 17 yrs. limitation into Baseline spirometry the normal range. and plethysmographic lung volumes after a with However, the boys severe asthma reversed bronchodilation with up incompletely. to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 54. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airtrapping measured as plethysmographic RV/TLC% predicted. The severe asthma group 77 children with exhibited air-trapping severe asthma. compared with the 71 children with nonsevere group nonsevere asthma ages (p <0.0001), and 6 to 17 yrs. the boys had significantly Baseline spirometry more air-trapping and plethysmographic lungthan the after in the volumes girls a bronchodilationgroupup severe with (p =0.023). to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 55. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airtrapping measured as plethysmographic RV/TLC% predicted. 77After bronchodilation, children with severe asthma. severe the girls with 71 children with residual asthma had no nonsevere asthma ages air trapping. 6 to 17 yrs.contrast, In Baseline spirometry the boys with severe and plethysmographic asthma had incomplete lung volumes after a reversal of air-trapping. bronchodilation with up to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 56. Sex dependence of airflow limitation and air trappingin children with severe asthma Sorkness JACI 2011;127:1073 Airtrapping measured as plethysmographic RV/TLC% predicted. Thus, boys with severe 77 children with asthma had greater baseline airflow severe asthma. limitation and 71 children with girls with air-trapping than nonsevere asthma ages severe asthma and, unlike 6 to 17 yrs. had incomplete the girls, Baseline spirometry reversal PstBD, indicating and plethysmographic of that the adult patterns lung volumes after apresent severe asthma are in boys but only partially bronchodilation with up developed in girls. to 8 puff of albuterol. BSLN; baseline * vs respective female, severe asthma subgroup; ** vs respective nonsevere subgroup; PstBD; post bronchodilation *** vs baseline.
  • 57. Pattern of airway physiology in children with severe asthma De Benedictis JACI 2011;128:904• The early pattern of disturbed airway physiology identified in boys with severe asthma in the SARP study may actually be a clue to different lung growth between sexes. The structure of the lung is a crucial determinant of ventilatory function and contributes to the sex differences in airway behavior across the human life span.• Such sex differences are mainly attributable to the different growth patterns of airways in relation to air spaces (dysanapsis).Mead J Dysanapsis in normal lung assessed by the relationship between maximalflow, static recoil, and vital capacity. Am Rev Respir Dis 1980;121:339.
  • 58. Riduzione difunzionalità nel tempo
  • 59. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 % of houses with Participants in the 50 – European Respiratory 50.1% Health Survey initially examined aged 20-45 yrs 40 – 41.3% and 9 yrs later (n=6443). 30 – Dampness (water damage 20 – or damp spots) and indoor mould, ever and in 10 – the last 12 months. 0 Any dampness Indoor mould
  • 60. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the European Respiratory -2.25 Health Survey initially examined aged 20-45 yrs and 9 yrs later (n=6443). -5 Dampness (water damage -7.43 or damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
  • 61. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:396 Additional decline in FEV1 ml/year 0 Participants in the Dampness and Europeanmould growth indoor Respiratory -2.25 Health Survey initially is common in examined aged 20-45 yrs dwellings, and the andpresence of(n=6443). 9 yrs later damp -5 is a risk factor for Dampness (water damage lung function decline, -7.43 orespecially in women. damp spots) and indoor mould, ever and in the last 12 months. -10 Women with In women with dampness observed damp spots at home in the bedroom
  • 62. Lung function decline in relation to mould and dampness in the home: the longitudinal European Community Respiratory Health Survey ECRHS II Norbäck Thorax 2011;66:3961) The additional mean lung function decline, -2.25 ml/year for self- reported dampness and -7.43 ml/year for observed dampness in the bedroom, is of the same order of magnitude as estimated for moderate tobacco smoking in the same ECRHS cohort.2) The reason for the sex difference in effect remains unclear, but could be due to either higher susceptibility or a longer exposure time in the dwelling for women.
  • 63. Longitudinal associations of socioeconomic position in childhood and adulthood with decline in lung functionover 20 years: results from a population-based cohort of British men. Ramsay Thorax 2011;66:1058 FEV1 and FVC declined over time; the decline increased 7735 British men progressively from social aged 40-59 yrs. class I (highest) to V (lowest); p ≤0.0001 for trend Followed-up These differences remained after: from 1978-1980 to 1998-2000. 1) adjustment for age; 2) cigarette smoking; FEV1 and FVC. 3) BMI; Socioeconomic position. 4) physical activity; 5) history of bronchitis.
  • 64. Longitudinal associations of socioeconomic position in childhood and adulthood with decline in lung functionover 20 years: results from a population-based cohort of British men. Ramsay Thorax 2011;66:1058 Mean lung function decline adjusted for age and baseline values according to combined childhood and adult social class
  • 65. Longitudinal associations of socioeconomic position in childhood and adulthood with decline in lung functionover 20 years: results from a population-based cohort of British men. Ramsay Thorax 2011;66:1058 Given that lung function is a strong predictor of mortality and morbidity in later life, the role of socioeconomic position on health in later life is likely to be important. The exact mechanisms underlying the associations between socioeconomic position and decline in lung function merits further research.
  • 66. Longitudinal associations of socioeconomic position in childhood and adulthood with decline in lung functionover 20 years: results from a population-based cohort of British men. Ramsay Thorax 2011;66:1058 Likely contributors to this association are: 1) poor diet; 2) environmental factors (air pollution,housing environment,occupational exposures). Some of these factors could be operating from early in life in addition to maternal undernutrition and low birth weight.
  • 67. physiology
  • 68. Fetal hyperglycemia alters lung structural development in neonatal rat. Koskinen Pediatr Pulmonol 2012;47:275 Maternal hyperglycemia Decreased lung weight, thinner alveolar septa and increased cellular apoptosis
  • 69. Fetal hyperglycemia alters lung structural development in neonatal rat. Koskinen Pediatr Pulmonol 2012;47:275 Barium-filled pulmonary arteriogram. (A) Control lung; (B) lung exposed to maternal hyperglycemia A B
  • 70. Hyperoxia arrests alveolar development through suppression of histone deacetylases in neonatal rats Zhu Pediatr Pulmonol 2012;47:2641) Bronchopulmonary dysplasia (BPD) mainly occurs in preterm infants. It is histopathologically characterized by fewer and larger alveoli and less secondary septa, suggesting an arrested or disordered lung development.2) Histone deacetylase (HDAC) plays an important role by regulating gene transcription.
  • 71. Hyperoxia arrests alveolar development through suppression of histone deacetylases in neonatal rats Zhu Pediatr Pulmonol 2012;47:264 Rats subjected to hyperoxia (85% O2) Arrest of alveolarization, and anSuppression of the HDAC1/HDAC2 elevated expression of the expression and activity, and the cytokine-induced neutrophil overall HDAC activity chemoattractant-1 (CINC-1) in the lungs of newborn rats.
  • 72. Hyperoxia arrests alveolar development through suppression of histone deacetylases in neonatal rats Zhu Pediatr Pulmonol 2012;47:264 Rats subjected to hyperoxia (85% O2) Preservation of HDAC activity by theophylline significantly improved alveolar development Arrest of and attenuated alveolarization, and an CINC-1 release.Suppression of the HDAC1/HDAC2 elevated expression of the expression and activity, and the cytokine-induced neutrophil overall HDAC activity chemoattractant-1 (CINC-1) in the lungs of newborn rats.
  • 73. Hyperoxia arrests alveolar development throughsuppression of histone deacetylases in neonatal rats Zhu Pediatr Pulmonol 2012;47:264 Hyperoxia arrested alveolar development Control Hyperoxia
  • 74. Alveolarization Continues during Childhoodand Adolescence. New Evidence from Helium-3 Magnetic Resonance Narayanan AJRCCM 2012;185:186 The current hypothesis is that human pulmonary alveolarization The is complete by 3 yrs. number of alveoli Using helium-3 (3He) magnetic is estimated to resonance (MR) to assess alveolar size noninvasively increase across between 7 and 21 yrs, during the age range which lung volume nearly quadruples. studied (7-21 yrs). If new alveolarization does not occur, alveolar size should increase to the same extent. 109 healthy subjects aged 7–21 yrs.
  • 75. Alveolarization Continues during Childhoodand Adolescence. New Evidence from Helium-3 Magnetic Resonance Narayanan AJRCCM 2012;185:186 Scatterplot of mean peripheral airspace dimension Xrms against (left panel) age and (right panel) FRC.
  • 76. Alveolarization Continues during Childhoodand Adolescence. New Evidence from Helium-3 Magnetic Resonance Narayanan AJRCCM 2012;185:186 Scatterplot of mean peripheral airspace dimension Xrms against (left panel) age and (right panel) FRC. Green lines indicate the following in a child with an initial FRC of 1 L: top line, predicted change in Xrms with FRC if lung growth was accomplished only by expansion of preexisting alveoli (scenario of no alveolarization); middle line, predicted change if rate of neoalveolarization was 0.54 (predicted from apparent diffusion coefficient vs. FRC multilevel model); lower line, predicted change if all growth of lung was by neoalveolarization.
  • 77. Alveolarization Continues during Childhoodand Adolescence. New Evidence from Helium-3 Magnetic Resonance Narayanan AJRCCM 2012;185:186 Number of alveoli in the developing human The current hypothesis is that lung estimated by morphometry from human pulmonary alveolarization previously published studies. is complete by 3 yrs. Using helium-3 (3He) magnetic resonance (MR) to assess alveolar size noninvasively between 7 and 21 yrs, during which lung volume nearly quadruples. If new alveolarization does not occur, alveolar size should increase to the same extent. 109 healthy subjects 7 21 aged 7–21 yrs.
  • 78. Alveolarization Continues during Childhoodand Adolescence. New Evidence from Helium-3 Magnetic Resonance Narayanan AJRCCM 2012;185:186 Conclusions Our observations are best explained by postulating that the lungs grow partly by neo-alveolarization throughout childhood and adolescence. This has important implications: developing lungs have the potential to recover from early life insults and respond to emerging alveolar therapies. Conversely, drugs, diseases, or environmental exposures could adversely affect alveolarization throughout childhood.
  • 79. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219• The emergency management of hypoxaemic patients requires clinicians to avoid the hazard of dangerous hypoxaemia due to under-treatment with oxygen, whilst also avoiding the hazards of hypercapnic respiratory failure (iatrogenic hypercapnia) and oxygen toxicity, which may be caused by over-treatment with oxygen.• Some patient groups, particularly those with chronic obstructive pulmonary disease (COPD), are especially vulnerable to uncontrolled oxygen therapy and mortality in this patient group was doubled when high-concentration oxygen was used compared with controlled oxygen therapy.• Hyperoxaemia is associated with increased mortality in patients with stroke, and in survivors of cardiac resuscitation and critically ill patients in the intensive care unit (ICU).• The British Thoracic Society (BTS) guidelines for emergency oxygen use recommend a target oxygen saturation range of 94–98% for most emergency medical patients and a lower target range of 88–92% for those at risk of hypercapnic respiratory failure.
  • 80. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219 % samples with 30 – Database of blood gas 26.9% analysis results from 20 – 3,524 specimens. 19% were said to be 10 – breathing air at the time of sampling and 81% were on 0 5.6% oxygen therapy Hypercapnia with PCO2>6.0 kPa PO2 < 8.0 kPa or ranging 24–100%. or 45 mmHg consistent with 60 mmHg with normal PCO2 type 2 respiratory failure (type 1 respiratory failure)
  • 81. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219 % samples with 40 – Database of blood gas 41.3% analysis results from 30 – 3,524 specimens. 30% 20 – 19% were said to be breathing air at the 10 – time of sampling and 10% 81% were on 0 oxygen therapy hyperoxaemic grossly hyperoxaemic oxygen ranging 24–100%. saturation >98% with PO2 >15.0 kPa with PO2 ≥20 kPa (112 mmHg) (≥150 mmHg)
  • 82. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219 % samples with 10.2% samples 40 – had oxygen Database of blood gas saturation <90% 41.3% analysis results from but only 2.7% 30 – 3,524 specimens. were severely 30% 20 – hypoxaemic withbe 19% were said to oxygen breathing air at the 10 – saturation <80% time of sampling and 10% 81% were on 0 oxygen therapy hyperoxaemic grossly hyperoxaemic oxygen ranging 24–100%. saturation >98% with PO2 >15.0 kPa with PO2 ≥20 kPa (112 mmHg) (≥150 mmHg)
  • 83. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219 % samples with Hypercapnic (type blood gas 40 Database of2) – 41.3% respiratory failure analysis results from 30 – was 5X more 3,524 specimens. common than pure 30% 20 – 19%hypoxaemia be were said to breathing air at the 10 – (type 1 time of sampling and respiratory 10% 81% were on failure) 0 oxygen therapy hyperoxaemic grossly hyperoxaemic oxygen ranging 24–100%. saturation >98% with PO2 >15.0 kPa with PO2 ≥20 kPa (112 mmHg) (≥150 mmHg)
  • 84. An audit of hypoxaemia, hyperoxaemia, hypercapnia and acidosis in blood gas specimens O‟Driscoll B.R, Eur Respir J 2012;39:219 % samples with These 40 – Database of blood gas findings 41.3% analysis results from suggest 30 – 3,524 specimens. that oxygen 30% needs saidbe be 20 – 19% were to to used with breathing air at the 10 – more caution time of sampling and 10% 81% were on in hospitals 0 oxygen therapy hyperoxaemic grossly hyperoxaemic oxygen ranging 24–100%. saturation >98% with PO2 >15.0 kPa with PO2 ≥20 kPa (112 mmHg) (≥150 mmHg)
  • 85. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937 Proportion of patients with a rise 106 patients with severe in PtCO2 ≥ 4 mm Hg at 60 minexacerbations of asthma 50 -FEV1 ≤ 50% pred. High concentration oxygen 40 – 44%(8 l/min via mediumconcentration mask) or 30 – RR=2.3 p < 0.006titrated oxygen (to achieveoxygen saturations between 20 –93% and 95%) for 60 min. 19% 10 – Transcutaneous partialpressure of carbon dioxide 000(PtCO2) was measured at High Titrated oxygen0, 20, 40 and 60 min. concentration O2 group
  • 86. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937 Proportion of patients with a rise in PtCO2 ≥ 4 mm Hg at 60 min 106 patients with severe 50 -exacerbations of asthma. High concentration oxygen 40 – 44%(8 l/min via mediumconcentration mask) or 30 – RR=2.3titrated oxygen (to achieve p < 0.006oxygen saturations between 20 –93% and 95%) for 60 min. 19% 10 – Transcutaneous partialpressure of carbon dioxide(PtCO2) was measured at 000 High Titrated oxygen0,20,40 and 60 min. concentration O2 group
  • 87. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937 106 patients with severe Proportion of patients with a rise inexacerbations of asthma PtCO2 ≥ 8 mm HgFEV1 ≤ 50% pred. 40 – High concentration oxygen(8 l/min via medium 30 –concentration mask) ortitrated oxygen (to achieveoxygen saturations between 20 – 22%93% and 95%) for 60 min. 10 – RR=3.9 Transcutaneous partialpressure of carbon dioxide 0 6% High(PtCO2) was measured at concentration Titrated oxygen0, 20, 40 and 60 min. oxygen group
  • 88. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937 Proportion of patients with a rise in 106 A titrated oxygen patients with severe PtCO2 ≥ 8 mm Hg regime is recommendedexacerbations of asthma. in the treatment of 40 – High concentration oxygen severe asthma, in(8 l/minwhich oxygen is via medium 30 –concentration mask) or administered only totitrated oxygen (to achieve patients withoxygen saturations between 20 – 22%93%hypoxaemia, 60 a dose and 95%) for in min. that relieves 10 – hypoxaemia without RR=3.9 Transcutaneous partial causing hyperoxaemiapressure of carbon dioxide 0 6%(PtCO2) was measured at High0, 20, 40 and 60 min. concentration Titrated oxygen oxygen group
  • 89. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937 106 patients with severeexacerbations of asthma 100 – % patients admitted toFEV1 ≤ 50% pred. 90 – the hospital 80 – High concentration oxygen 70 –(8 l/min via medium 60 – p<0.042concentration mask) or 50 –titrated oxygen (to achieveoxygen saturations between 40 – 52%93% and 95%) for 60 min. 30 – 20 – 32% Transcutaneous partial 10 –pressure of carbon dioxide(PtCO2) was measured at 00, 20, 40 and 60 min. High O2 Titrated group O2 group
  • 90. Randomised controlled trial of high concentrationversus titrated oxygen therapy in severe exacerbations of asthma Perrin Thorax 2011;66:937It is well recognised that:1. high concentration oxygen therapy may lead to carbon dioxide (CO2) retention when administered to patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) Westlake EK, Q J Med 1955;94:155e73. Murphy R, Emerg Med J 2001;18:332e9.2. that worsening ventilation-perfusion mismatch due to release of hypoxic pulmonary vasoconstriction with a resulting increase in physiological dead space is one of the major mechanisms causing this effect. Aubier M, Am Rev Respir Dis 1980;122:747e54. Dick C, Am J Respir Crit Care Med 1997;155:609e14. Robinson TD, Am J Respir Crit Care Med 2000;161:1524e9. Sassoon CS, Am Rev Respir Dis 1987;135:907e11.
  • 91. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 1) Hypocarbia and/or hypercarbia are implicated as a causative factor in periventricular leukomalacia, intra-ventricular hemorrhage, and chronic lung disease. 2) Extreme fluctuations in partial pressure of arterial carbon dioxide (PaCO2) and higher max PaCO2 are associated with worse neurodevelopmental outcomes. Prevention of extreme hypocarbia and/or hypercarbia in preterm infants is essential.
  • 92. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 3) Though arterial blood gas analysis is the gold standard of monitoring partial pressure of arterial oxygen (PaO2) and PaCO2, it leads to blood loss and iatrogenic anaemia, may cause procedural pain, and each sample is only a snapshot view of the sampling moment. 4) End-tidal carbon dioxide (ETCO2) measurement is a continuous and non-invasive indirect measurement of blood carbon dioxide tensions with fast response time to changes in blood CO2. 5) The principal determinants of ETCO2 are alveolar ventilation, pulmonary perfusion (cardiac output), and CO2 production.
  • 93. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 Scatterplot (with identity line) of end-tidal CO2 and PaCO2 relationship r=0.69 p<0.0001 Simultaneous end-tidal and arterial CO2 pairs. 143 ventilated low birth weight infants (VLBWI).
  • 94. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 Scatterplot (with identity line) of end-tidal CO2 and PaCO2 relationship r=0.69 p<0.0001 Simultaneous end-tidal There was a significant and arterial CO2 pairs. correlation 143(r = 0.69; P < 0.0001) ventilated low birth between ETCO2 and weight infants (VLBWI). PaCO2 values.
  • 95. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 Bland-Altman plot of the difference between the end-tidal and arterial CO2 versus the average of the two simultaneous readings r=0.16 p=0.06 Simultaneous end-tidal and arterial CO2 pairs. 143 ventilated low birth weight infants (VLBWI).
  • 96. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 Bland-Altman plot of the difference between the end-tidal and arterial CO2 versus the average of the two simultaneous readings r=0.16 p=0.06 But the ETCO2 value Simultaneous end-tidal andwas lower than the arterial CO2 pairs. corresponding PaCO2 143 ventilated low birth value in 94% weight infants (VLBWI). pairs, with a mean bias of 13.5 ± 8.4 mmHg
  • 97. End-tidal carbon dioxide monitoring in very low birthweight infants: Correlation and agreement with arterial carbon dioxide. Trevisanuto Pediatr Pulmonol 2012;47:367 Bland-Altman plot of the difference between the end-tidal and arterial CO2 versus the average of the two simultaneous readings ETCO2 should not Simultaneous end-tidal r=0.16 p=0.06 replace PaCO2 and arterial CO2 pairs. measurements in 143ventilated VLBWI, ventilated low birth weight may have a role but infants (VLBWI). to detect trends of PaCO2.
  • 98. Effects of maternal food restriction on offspring lungextracellular matrix deposition and long term pulmonary function in an experimental rat model Rehan Pediatr Pulmonol 2012; 47:167 Intrauterine growth restriction (IUGR) increases the risk of respiratory compromise throughout postnatal life. However, the molecular mechanism(s) underlying the respiratory compromise in offspring following IUGR is not known. We hypothesized that IUGR following maternal food restriction (MFR) would affect extracellular matrix deposition in the lung, explaining the long-term impairment in pulmonary function in the IUGR offspring.
  • 99. Effects of maternal food restriction on offspring lungextracellular matrix deposition and long term pulmonary function in an experimental rat model Rehan Pediatr Pulmonol 2012; 47:167 IUGR pups Rat model with At postnatal day 21, and at 9 months (9M) maternal food of age the expression and abundance of restriction elastin and alpha smooth muscle actin (αSMA), two key extracellular matrix proteins, were increased in IUGR lungs when compared to controls (P < 0.05)
  • 100. Effects of maternal food restriction on offspring lungextracellular matrix deposition and long term pulmonary function in an experimental rat model Rehan Pediatr Pulmonol 2012; 47:167 Compared to controls, the MFR group did have significantly decreased IUGR pups pulmonary compliance Rat 9M (P < 0.05) vs andpostnatal day 21, and at 9 months (9M) at model with At increased food maternal responsiveness age the expression and abundance of of restriction to methacholine challenge.elastin and alpha smooth muscle actin (αSMA), two key extracellular matrix proteins, were increased in IUGR lungs when compared to controls (P < 0.05)
  • 101. Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation Structural changes started to appear around postnatal day 42, that is, 3 weeks after weaning and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
  • 102. Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation Rich source of antioxidants such as lycopene, will prevent Structural changes the effects of started to appear around nicotine on the lungs postnatal day 42, that of the offspring. is, 3 weeks after weaning and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
  • 103. Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Maternal nicotine exposure during pregnancy and lactation All these nicotine- induced structural changes were Structural changes prevented by started to appear around supplementing the postnatal day 42, that mothers diet with is, 3 weeks after weaning tomato juice and thus the onset of nicotine withdrawal. Structural integrity of the lungs of the offspring
  • 104. Tomato juice protects the lungs of the offspring offemale rats exposed to nicotine during gestation and lactation. Maritz Pediatr Pulmonol 2011;46:976 Nicotine + tomato juice Nicotine. Arrows = emphysema
  • 105. Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 1) Ageing has been described as the accumulation of oxidative damage that is incompletely repaired by the body‟s antioxidant defences. 2) This damage is caused by free radicals produced in the body via normal metabolic processes and inflammation, and by exogenous free radicals, such as from smoking and noxious gases. 3) In the lungs, ageing is associated with declining lung function, and rate of decline increases with advancing age.
  • 106. Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and vegetables were associated with a slower rate of FEV1decline compared with a lower intake 1,443 participants 0 – completed a food frequency questionnaire. p=0.003 -10 – Self-reported smoking history. + FEV1 at both baseline -20 – and after 4 yrs of -24mL/yr followup. -30 -
  • 107. Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and In quitters vegetables were associated with a slower rate (a current smoker at of FEV1decline compared with a lower intake study participants had 1,443 baseline who 0 – completed a food quit during follow-up), frequency questionnaire. higher intake was p=0.003 associated with an -10 – Self-reportedrate of attenuated smoking history. decline for each + nutrient studied -20 – FEV(1p≤0.003 for all at both baseline and after 4 yrs of -24mL/yr models). followup. -30 -
  • 108. Dietary antioxidants and forced expiratory volumein 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and vegetables were associated with a slower rate of FEV1decline compared with a lower intake 1,443 participants In nonsmoking 0 – completed a food participants, frequency questionnaire. there was little or p=0.003 no association Self-reported -10 – smoking history.rate of diet and + of decline FEV1 at both baseline -20 – in FEV1. -24mL/yr and after 4 yrs of followup. -30 -
  • 109. Dietary antioxidants and forced expiratory volume in 1 s decline: the Health, Aging and Body Composition study Bentley, Eur Respir J 2012;39:979 In continuing smokers higher intake of fruit and The intake of vegetables were associated with a slower rate of FEV1decline compared with a lower intake nutrients with 1,443 participants 0 – completed a food antioxidant frequency questionnaire. properties may p=0.003modulate lung function Self-reported -10 – decline in older smoking history. adults exposed to + FEV1 at bothsmoke. -20 – cigarette baseline -24mL/yr and after 4 yrs of followup. -30 -
  • 110. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385ABSTRACT: Wine intake is associated with a better lung functionin the general population, yet the source of this effect is unknown.Resveratrol, a polyphenol in wine, has anti-inflammatory propertiesin the lung, its effects being partially mediated via induction ofSirtuin (SIRT)1 activity.We assessed the impact of wine and resveratrol intake, andSIRT1 single-nucleotide polymorphisms (SNPs) on lungfunction in the general population.
  • 111. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 • Resveratrol intake was Effects of red and associated with white wine and higher FVC levels. resveratrol intake. FEV1, FVC and FEV1/FVC. • White wine intake with Population-based cohort higher FEV1 levels and (n=3,224). lower risk of airway obstruction.
  • 112. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according tothe average intake of white wine and total resveratrol FEV1 white FEV1 total resveratrol wine FVC white wine FVC total resveratrol
  • 113. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according to Polyphenolicthe average intake of white wine and total compounds present in white resveratrol wine may exert beneficial FEV1 total resveratrol FEV1 white effects on lung function. wine Plausible candidates in this respect are tyrosol and hydroxytyrosol, polyphenolic white wine molecules FVC total resveratrol FVC white wine that, similar to resveratrol, exhibit antioxidant and cardioprotective effects
  • 114. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385 Mean adjusted FEV1 and FVC for the subjects according tothe average intake The white wine and total of positive resveratrol we observed between association FEV1 white white FEV1 total resveratrol wine intake and higher wine FEV1 reflects a very modest average consumption of 1.0–1.5 glasses of white wine per week (i.e. 7.4 g·day-1) and, thus, we FVC white wine by no meanstotal to suggest that FVC aim resveratrol more than moderate white wine drinking could be considered as beneficial health behaviour.
  • 115. Dietary factors and lung function in the general population: wine and resveratrol intake Siedlinski M , Eur Respir J 2012;39:385Beneficial effects of wine consumption are postulated to account for the„„French paradox‟‟, the observation of lower mortality due to coronaryheart disease in the French population despite thispopulation‟s relatively high consumption of a cholesterol- andsaturated fat-rich diet.The proposed mechanism includes the inhibition of platelet reactivity bywine and resveratrol is a prominent candidate responsible for the vascularprotection provided by wine.However, our study shows that white wine intake and not redwineintake, the major dietary resveratrol source, is associated with a lowerrisk of airway obstruction and with higher FEV1, both of which are indicesof COPD.This is of great importance given the fact that reduced lung function is amarker for cardiovascular-related mortality.

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