Microvascular effects of oxygen and carbon dioxide measured by vascular occlusion test in healthy volunteers.

BACKGROUND: Changes in near-infrared spectroscopy-derived regional tissue oxygen saturation (StO2) during a vascular occlusion test (VOT; ischemic provocation of microcirculation by rapid inflation and deflation of a tourniquet) allow estimating peripheral tissue O2 consumption (desaturation slope; DS), vascular reactivity (recovery slope; RS) and post-ischemic hyperperfusion (AUC-H). The effects of isolated alterations in the inspiratory fraction of O2 (FiO2) and changes in expiratory CO2 remain to be elucidated. Therefore, in this secondary analysis we determined the effects of standardized isolated instances of hypoxia, hyperoxia, hypocapnia and hypercapnia on the VOT-induced StO2 changes in healthy volunteers (n = 20) to establish reference values for future physiological studies. METHODS: StO2 was measured on the thenar muscle. Multiple VOTs were performed in a standardized manner: i.e. at room air (baseline), during hyperoxia (FiO2 1.0), mild hypoxia (FiO2 ≈ 0.11), and after a second baseline, during hypocapnia (end-tidal CO2 (etCO2) 2.5-3.0 vol%) and hypercapnia (etCO2 7.0-7.5 vol%) at room air. Differences in DS, RS, and AUC-H were tested using repeated-measures ANOVA. RESULTS: DS and RS remained constant during all applied conditions. AUC-H after hypoxia was smaller compared to hyperoxia (963 %*sec vs hyperoxia 1702 %*sec, P = 0.005), while there was no difference in AUC-H duration between hypoxia and baseline. The StO2 peak (after tourniquet deflation) during hypoxia was lower compared to baseline and hyperoxia (92 % vs 94 % and 98 %, P < 0.001). CONCLUSION: We conclude that in healthy volunteers at rest, common situations observed during anesthesia and intensive care such as exposure to hypoxia, hyperoxia, hypocapnia, or hypercapnia, did not affect peripheral tissue O2 consumption and vascular reactivity as assessed by VOT-induced changes in StO2. These observations may serve as reference values for future physiological studies. TRIAL REGISTRATION: This study represents a secondary analysis of an original study which has been registered at ClinicalTrials.gov nr: NCT02561052.

Prognostic effects of arterial carbon dioxide levels in patients hospitalized into the cardiac intensive care unit for acute heart failure.

AIMS: Although both hypercapnia and hypocapnia are common in acute heart failure (AHF) patients, routine assessment of arterial blood gas is not recommended. Additionally, no association between hypercapnia and increased mortality has been found, and the prognostic value of hypocapnia in AHF patients remains to be elucidated. In this observational study, we aimed to investigate the relationship between partial pressure of arterial carbon dioxide (PaCO2), especially low PaCO2, and long-term mortality in AHF patients. METHODS AND RESULTS: Acute heart failure patients hospitalized in the cardiac intensive care unit of our institution between 2007 and 2011 were screened. All eligible patients were divided into two groups based on the inflection point (i.e. 31.0 mmHg) of the 3-knot cubic spline curve of the hazard ratio (HR), with a PaCO2 of 40 mmHg as a reference. The association between PaCO2 levels and all-cause mortality was assessed using Cox proportional hazards regression models. Among 435 patients with a median follow-up of 1.8 years, 115 (26.4%) died. Adjusted analysis with relevant variables as confounders indicated that PaCO2 <31 mmHg was significantly associated with increased all-cause mortality [HR 1.71, 95% confidence interval (CI) 1.05-2.79; P = 0.032]. When PaCO2 was considered as a continuous variable, the lower was the log-transformed PaCO2, the greater was the increased risk of mortality (HR 0.71, 95% CI 0.52-0.96; P = 0.024). CONCLUSIONS: In AHF patients, lower PaCO2 at admission was associated with increased long-term mortality risk.

Neonatal encephalopathy therapy optimization for better neuroprotection with inhalation of CO2: the HENRIC feasibility and safety trial.

BACKGROUND: There is an association between hypocapnia and adverse neurodevelopmental outcome in infants with neonatal encephalopathy (NE). Our aim was to test the safety and feasibility of 5% CO2 and 95% air inhalation to correct hypocapnia in mechanically ventilated infants with NE undergoing therapeutic hypothermia. METHODS: Ten infants were assigned to this open-label, single-center trial. The gas mixture of 5% CO2 and 95% air was administered through patient circuits if the temperature-corrected PCO2 ≤40 mm Hg. The CO2 inhalation was continued for 12 h or was stopped earlier if the base deficit (BD) level decreased <5 mmol/L. Follow-up was performed using Bayley Scales of Infant Development II. RESULTS: The patients spent a median 95.1% (range 44.6-98.5%) of time in the desired PCO2 range (40-60 mm Hg) during the inhalation. All PCO2 values were >40 mm Hg, the lower value of the target range. Regression modeling revealed that BD and lactate had a tendency to decrease during the intervention (by 0.61 and 0.55 mmol/L/h, respectively), whereas pH remained stable. The rate of moderate disabilities and normal outcome was 50%. CONCLUSIONS: Our results suggest that inhaled 5% CO2 administration is a feasible and safe intervention for correcting hypocapnia.

Assessment of cerebral hemodynamic parameters using pulsatile versus non-pulsatile cerebral blood outflow models.

BACKGROUND: Prior methods evaluating the changes in cerebral arterial blood volume (∆CaBV) assumed that brain blood transport distal to big cerebral arteries can be approximated with a non-pulsatile flow (CFF) model. In this study, a modified ∆CaBV calculation that accounts for pulsatile blood flow forward (PFF) from large cerebral arteries to resistive arterioles was investigated. The aim was to assess cerebral hemodynamic indices estimated by both CFF and PFF models while changing arterial blood carbon dioxide concentration (EtCO2) in healthy volunteers. MATERIALS AND METHODS: Continuous recordings of non-invasive arterial blood pressure (ABP), transcranial Doppler blood flow velocity (CBFVa), and EtCO2 were performed in 53 young volunteers at baseline and during both hypo- and hypercapnia. The time constant of the cerebral arterial bed (τ) and critical closing pressure (CrCP) were estimated using mathematical transformations of the pulse waveforms of ABP and CBFVa, and with both pulsatile and non-pulsatile models of ∆CaBV estimation. Results are presented as median values ± interquartile range. RESULTS: Both CrCP and τ gave significantly lower values with the PFF model when compared with the CFF model (p ≪ 0.001 for both). In comparison to normocapnia, both CrCP and τ determined with the PFF model increased during hypocapnia [CrCPPFF (mm Hg): 5.52 ± 8.78 vs. 14.36 ± 14.47, p = 0.00006; τPFF (ms): 47.4 ± 53.9 vs. 72.8 ± 45.7, p = 0.002] and decreased during hypercapnia [CrCPPFF (mm Hg): 5.52 ± 8.78 vs. 2.36 ± 7.05, p = 0.0001; τPFF (ms): 47.4 ± 53.9 vs. 29.0 ± 31.3, p = 0.0003]. When the CFF model was applied, no changes were found for CrCP during hypercapnia or in τ during hypocapnia. CONCLUSION: Our results suggest that the pulsatile flow forward model better reflects changes in CrCP and in τ induced by controlled alterations in EtCO2.

Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial.

PURPOSE: We assessed the effects of targeting low-normal or high-normal arterial carbon dioxide tension (PaCO2) and normoxia or moderate hyperoxia after out-of-hospital cardiac arrest (OHCA) on markers of cerebral and cardiac injury. METHODS: Using a 23 factorial design, we randomly assigned 123 patients resuscitated from OHCA to low-normal (4.5-4.7 kPa) or high-normal (5.8-6.0 kPa) PaCO2 and to normoxia (arterial oxygen tension [PaO2] 10-15 kPa) or moderate hyperoxia (PaO2 20-25 kPa) and to low-normal or high-normal mean arterial pressure during the first 36 h in the intensive care unit. Here we report the results of the low-normal vs. high-normal PaCO2 and normoxia vs. moderate hyperoxia comparisons. The primary endpoint was the serum concentration of neuron-specific enolase (NSE) 48 h after cardiac arrest. Secondary endpoints included S100B protein and cardiac troponin concentrations, continuous electroencephalography (EEG) and near-infrared spectroscopy (NIRS) results and neurologic outcome at 6 months. RESULTS: In total 120 patients were included in the analyses. There was a clear separation in PaCO2 (p < 0.001) and PaO2 (p < 0.001) between the groups. The median (interquartile range) NSE concentration at 48 h was 18.8 µg/l (13.9-28.3 µg/l) in the low-normal PaCO2 group and 22.5 µg/l (14.2-34.9 µg/l) in the high-normal PaCO2 group, p = 0.400; and 22.3 µg/l (14.8-27.8 µg/l) in the normoxia group and 20.6 µg/l (14.2-34.9 µg/l) in the moderate hyperoxia group, p = 0.594). High-normal PaCO2 and moderate hyperoxia increased NIRS values. There were no differences in other secondary outcomes. CONCLUSIONS: Both high-normal PaCO2 and moderate hyperoxia increased NIRS values, but the NSE concentration was unaffected. REGISTRATION: ClinicalTrials.gov, NCT02698917. Registered on January 26, 2016.

Association Between Arterial Carbon Dioxide Tension and Outcome in Patients Admitted to the Intensive Care Unit After Coronary Artery Bypass Surgery.

OBJECTIVES: The aim of this study was to determine the association between PaCO2 and patient outcome in patients admitted to the intensive care unit (ICU) after coronary artery bypass grafting (CABG). DESIGN: A retrospective cohort study. SETTING: Single-institutional, university hospital. PARTICIPANTS: All patients admitted to the ICU after CABG between January 2009 and December 2012. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Based on PaCO2 status during the first 24 hours after CABG, 1,011 patients were classified into 4 groups: normocapnia, hypocapnia, hypercapnia, and dual hyper/hypocapnia. The 30-day mortality rate was 0.7% (n = 4) for normocapnia, 1.5% (n = 4) for hypocapnia, 2.2% (n = 3) for hypercapnia, and 7.5% (n = 4) for the dual-exposure group. The extubation times were 13.3±21.7 hours, 15.8±21.37 hours, 21.79±39.70 hours, and 42.29±75.35 hours, respectively. After adjusting for confounding variables, the dual hypocapnia and hypercapnia exposure group was associated with increased 30-day mortality (odds ratio [OR] = 8.08; 95% confidence interval [CI], 1.82-35.86; p = 0.006) and delayed extubation (OR = 2.40; 95% CI, 1.24-4.64; p = 0.010). CONCLUSIONS: Exposure to both hypocapnia and hypercapnia within 24 hours after CABG was associated independently with increased risk of 30-day mortality and delayed extubation. Exposure to either hypocapnia or hypercapnia alone was not associated with patient outcome.

Hypocapnia and hyperoxia induction using a hyperventilation protocol in electroconvulsive therapy. / Inducción de hipocapnia e hiperoxia con maniobras de hiperventilación reglada en la terapia electroconvulsiva.

INTRODUCTION: Hyperventilation in electroconvulsive therapy sessions has been associated with seizure threshold, seizure characteristics, and cognitive effects. There is no consensus on the optimal procedure of applying hyperventilation manoeuvres during electroconvulsive therapy. MATERIAL AND METHODS: Prospective evaluation of the effects of systematic use of hyperventilation manoeuvres with facial mask and capnography (protocolized hyperventilation [pHV]), on ventilation parameters and on seizures. The study included a sample of 130 sessions (65 performed according to hyperventilation standard practice and 65 successive sessions, with pHV) of 35 patients over a period of 10 weeks. RESULTS: The pHV manoeuvres reduced exhaled CO2 and increased O2 saturation significantly (P<.001). The average CO2 reduction achieved was 6.52±4.75mmHg (95% CI -7.7 to -5.3). The CO2 values after pHV correlated significantly with seizure duration and O2 values, with other electroencephalographic quality indices. In pHV sessions, compared with sessions performed according to hyperventilation standard practice, the average lengthening of the motor and electroencephalographic seizure was 3.86±14.62 and 4.73±13.95s, respectively. No differences were identified in other ictal quality parameters. CONCLUSIONS: The proposed pHV manoeuvres significantly modify ventilation parameters. The hypocapnia and hyperoxia obtained by applying these manoeuvres lengthen the duration of seizures without worsening the quality of the electroencephalographic trace. The use of pHV is generalisable and might improve electroconvulsive therapy procedure without adding costs.

Pathophysiology of central sleep apneas.

The transition from wake to sleep is accompanied by a host of physiologic changes, which result in major alterations in respiratory control and may result in sleep-related breathing disorders. The central sleep apneas are a group of sleep-related breathing disorders that are characterized by recurrent episodes of airflow reduction or cessation due to a temporary reduction or absence of central respiratory drive. The fundamental hallmark of central sleep apnea (CSA) disorders is the presence of ventilatory control instability; however, additional mechanisms play a role in one or more specific manifestations of CSA. CSA may manifest during conditions of eucapnia/hypocapnia or chronic hypercapnia, which is a useful clinical classification that lends understanding to the underlying pathophysiology and potential therapies. In this review, an overview of normal breathing physiology is provided, followed by a discussion of pathophysiologic mechanisms that promote CSA and the mechanisms that are specific to different manifestations of CSA.

Comparison of end-tidal CO2 measured by transportable capnometer (EMMA™ capnograph) and arterial pCO2 in general anesthesia.

An end-tidal CO2 monitor (capnometer) is used most often as a noninvasive substitute for PaCO2 in anesthesia, anesthetic recovery, and intensive care. Additionally, the wide spread on-site use of portable capnometers in emergency and trauma situations is now observed. This study was conducted to compare PaCO2 measurement between the EMMA™ portable-capnometer and sidestream capnometry. End-tidal CO2 (portable capnometer: EMMA™ capnograph, side stream capnometry module: Datex-Ohmeda S5 Anesthesia Monitor) levels were recorded at the time of arterial blood gas sampling of patients undergoing general anesthesia. Data were compared using the Bland and Altman method, and by evaluating the clinical significance performed by calculating the percent error (%). A total of 100 data were obtained from 35 patients. The bias of PaCO2 and portable capnometer was 6.0 mmHg, where the upper and lower limits of the agreement were 11.8 and 0.3 mmHg, respectively. The percent error was 18.0 %. The bias of side stream capnometry and portable capnometer was 2.2 mmHg, where the upper and the lower limits of the agreement were 6.0 and -1.6 mmHg, respectively. The percent error was 13.0 %. Significant differences between the PETCO2 and PaCO2 values of the EMMA™ portable-capnometer were not observed for patients undergoing general anesthesia. ClinicalTrials.gov identifier NCT02184728.

Effect of mild hypocapnia on hemodynamic and bispectral index responses to tracheal intubation during propofol anesthesia in children.

The purpose of this study was to investigate the effect of mild hypocapnia on hypertension and arousal response after tracheal intubation in children during propofol anesthesia. Forty-four children, American Society of Anesthesiologists physical status I-II patients, aged 3-9 years were randomly allocated to either the normocapnia group [end-tidal carbon dioxide tension (ETCO2=35 mmHg, n=22)] or the hypocapnia group (ETCO2=25 mmHg, n=22). Anesthesia was induced with propofol 2.5 mg/kg. Five minutes after the administration of rocuronium 0.6 mg/kg, laryngoscopy was attempted. The mean arterial pressure (MAP), heart rate (HR), SpO2 and bispectral index (BIS) were measured during induction and intubation periods. The maximal change in the BIS with tracheal intubation (ΔBIS) was defined as the difference between the baseline value and the maximal value within the first 5 min after intubation. Before tracheal intubation, the change in BIS over time was not different between the groups. After tracheal intubation, the changes in the MAP, HR and BIS over time were not significantly different between the groups. The mean value±SD of ΔBIS was 5.7±5.2 and 7.4±5.5 in the normocapnia and hypocapnia groups, respectively, without any intergroup difference. This study showed that mild hypocapnia did not attenuate hemodynamic and BIS responses to tracheal intubation in children during propofol anesthesia. Our results suggested that hyperventilation has no beneficial effect on hemodynamic and arousal responses to tracheal intubation in children.

[Lactic acidosis in a child with acute severe asthma]. / Acidose lactique chez un nourrisson au cours d'une crise d'asthme grave.

Lactic acidosis is a recognized event in adult patients with acute severe asthma (ASA). Only a few cases have been reported in children. Hereinafter is reported the case of a 2-year-old girl hospitalized in the pediatric intensive care unit for ASA, which was treated with high-flow oxygen therapy and intravenous methylprednisolone and salbutamol. During hospitalization, she had metabolic acidosis with a 7.29 pH, a 26mmHg hypocapnia, and a decrease in bicarbonates to 12 mmol/L. The anion gap was increased to 20 mmol/L and lactates to 8 mmol/L. The work-up for a congenital metabolic disease was normal. Progression was propitious with spontaneous improvement of lactic acidosis, and the child was discharged from the intensive care unit after 72 h. The origin of lactic acidosis during ASA seems to be multifactorial. Although its recovery can be spontaneous, it is important to know how to identify it because it can worsen respiratory symptoms and can lead to incongruous therapeutic escalation.

Hypo- and hypercapnia predict mortality in oxygen-dependent chronic obstructive pulmonary disease: a population-based prospective study.

BACKGROUND: The prognostic role of the arterial blood gas tension of carbon dioxide (PaCO2) in severe Chronic Obstructive Pulmonary Disease (COPD) remains unknown. The aim of this study was to estimate the association between PaCO2 and mortality in oxygen-dependent COPD. METHODS: National prospective study of patients starting long-term oxygen therapy (LTOT) for COPD in Sweden between October 1, 2005 and June 30, 2009, with all-cause mortality as endpoint. The association between PaCO2 while breathing air, PaCO2 (air), and mortality was estimated using Cox regression adjusted for age, sex, arterial blood gas tension of oxygen (PaO2), World Health Organization performance status, body mass index, comorbidity, and medications. RESULTS: Of 2,249 patients included, 1,129 (50%) died during a median 1.1 years (IQR 0.6-2.0 years) of observation. No patient was lost to follow-up. PaCO2 (air) independently predicted adjusted mortality (p < 0.001). The association with mortality was U-shaped, with the lowest mortality at approximately PaCO2 (air) 6.5 kPa and increased mortality at PaCO2 (air) below 5.0 kPa and above 7.0 kPa. CONCLUSION: In oxygen-dependent COPD, PaCO2 (air) is an independent prognostic factor with a U-shaped association with mortality.

Application of transcutaneous carbon dioxide tension monitoring with low electrode temperatures in premature infants in the early postnatal period.

OBJECTIVE: The aim of this article is to evaluate the accuracy, precision, and safety of transcutaneous carbon dioxide tension (TcPCO2) monitoring at different electrode temperatures in preterm infants in the early postnatal period. STUDY DESIGN: A total of 26 neonates with a median birth weight of 974 g (432-1,694 g) and gestational age of 28.0 weeks (26.1-31.3 weeks) were studied in the first 5 days of life. A total of 252 simultaneous pairs (TcPCO2 and arterial carbon dioxide tension [PaCO2]) were analyzed at 38, 39, and 40°C at 26 and 27 weeks, and at 38, 39, 40, and 42°C at 28 to 31 weeks. RESULTS: The mean difference of TcPCO2 and PaCO2 (bias) increased from 3.93 mm Hg at 42°C to 5.64 mm Hg at 40°C, 6.58 mm Hg at 39°C, and 6.07 mm Hg at 38°C. Standard deviation (SD) of the bias increased from 4.17 mm Hg at 42°C to 4.76 mm Hg at 40°C, 5.29 mm Hg at 39°C, and 5.07 mm Hg at 38°C. Adverse skin lesions were not observed. CONCLUSION: TcPCO2 measurements are the most accurate and precise at an electrode temperature of 42°C. However, in premature babies, monitoring at 38, 39, and 40°C is possible provided a bias correction of 6 mm Hg and SD of 5 mm Hg are applied.

Hypocapnia in patients with chronic neck pain: association with pain, muscle function, and psychologic states.

OBJECTIVE: The aim of this study was to investigate whether patients with chronic neck pain have changes in their transcutaneous partial pressure of arterial carbon dioxide (PtcCO2) and whether other physical and psychologic parameters are associated. DESIGN: In this cross-sectional study, 45 patients with chronic idiopathic neck pain and 45 healthy sex-, age-, height-, and weight-matched controls were voluntarily recruited. The participants' neck muscle strength, endurance of the deep neck flexors, neck range of movement, forward head posture, psychologic states (anxiety, depression, kinesiophobia, and catastrophizing), disability, and pain were assessed. PtcCO2 was assessed using transcutaneous blood gas monitoring. RESULTS: The patients with chronic neck pain presented significantly reduced PtcCO2 (P < 0.01). In the patients, PtcCO2 was significantly correlated with strength of the neck muscles, endurance of the deep neck flexors, kinesiophobia, catastrophizing, and pain intensity (P < 0.05). Pain intensity, endurance of the deep neck flexors, and kinesiophobia remained as significant predictors into the regression model of PtcCO2. CONCLUSIONS: Patients with chronic neck pain present with reduced PtcCO2, which can reach the limits of hypocapnia. This disturbance seems to be associated with physical and psychologic manifestations of neck pain. These findings can have a great impact on various clinical aspects, notably, patient assessment, rehabilitation, and drug prescription.

Sleep apnea in precapillary pulmonary hypertension.

OBJECTIVES: Pilot studies have described the occurrence of sleep apnea in patients with precapillary pulmonary hypertension (PH). However, there are no data on the prevalence of sleep-related breathing disorders in larger patient cohorts with PH. METHODS: 169 patients with a diagnosis of PH confirmed by right heart catheterisation and clinically stable in NYHA classes II or III were prospectively investigated by polygraphy (n = 105 females, mean age: 61.3 years, mean body mass index: 27.2 kg/m(2)). Recruitment was independent of sleep-related symptoms and the use of vasodilator drugs or nasal oxygen. RESULTS: 45 patients (i.e. 26.6%) had an apnea-hypopnea-index (AHI) >10/h. Of these, 27 patients (i.e. 16%) had obstructive sleep apnea (OSA) and 18 patients (i.e. 10.6%) had central sleep apnea (CSA). The mean AHI was 20/hour. As a polygraphy had been performed with nasal oxygen in half of the patients without evidence for sleep apnea, the frequency of CSA was probably underestimated. Patients with OSA were characterized by male gender and higher body mass index whereas, those with CSA were older and hypocapnic. CONCLUSIONS: At least every fourth patient with PH suffers from mild-to-moderate sleep apnea. Considering the anthropometric characteristics of the patients studied, the prevalence of both OSA and CSA seem to be higher in PH than in the general population.

Continuous integrated distal capnography in infants ventilated with high frequency ventilation.

OBJECTIVE: To assess within a feasibility study the correlation, agreement, and trending of continuous integrated distal capnography (dCap) with PaCO(2) in infants on HFV. STUDY DESIGN: Sixteen premature infants [median (range) gestational age: 26.5 (24.7-34.7) weeks], ventilated with HFV (mean ± SD airway pressure: 8.1 ± 2.1 cmH(2) O, FiO(2) : 0.39 ± 0.21) for RDS, intubated with a double-lumen endotracheal-tube and whose data were recorded on a bedside computer participated in the study. Side-stream dCap was measured via the extra-port of a double-lumen endotracheal-tube by a Microstream capnograph, with a specially designed software for HFV and compared with simultaneous PaCO(2) . Integrated time-window analysis of the data was performed retrospectively on data collected prospectively. RESULTS: Analysis included 195 measurements. The correlation of dCap with PaCO(2) (r = 0.68, P < 0.0001) and the agreement (bias ± precision: -2.0 ± 10.7 mmHg) were adequate. Area under the ROC curves for dCap to detect high (>60 mmHg) or low (<35 mmHg) PaCO(2) was 0.79 (CI: 0.70-0.89) and 0.87 (CI: 0.73-1.00), respectively; P < 0.0001. Changes in dCap and in PaCO(2) for consecutive measurements within each patient were adequately correlated (r = 0.65, P < 0.0001). CONCLUSIONS: Continuous integrated dCap is feasible in premature infants ventilated with HFV and can be helpful for trends and alarm for unsafe levels of PaCO(2) .

Episodes of hypocarbia and early-onset sepsis are risk factors for cystic periventricular leukomalacia in the preterm infant.

BACKGROUND: Septic episodes in preterm infants recently have been reported to be associated with periventricular leukomalacia (PVL). The role of hypocarbia as an independent risk factor for PVL in clinical studies raises many questions without conclusive answers. AIMS: To evaluate risk factors for cystic PVL focussing on the influence of hypocarbia. STUDY DESIGN: Retrospective single centre case-control study. SUBJECTS: Preterm infants 24 to 35 weeks of gestational age and matched (1:2 for gender, birth year, gestational age and birth weight) controls. OUTCOME MEASURES: Multivariate analysis of perinatal factors being associated with cystic PVL diagnosed by serial ultrasound examinations. RESULTS: Univariate analysis of risk factors revealed lower 5 and 10 min Apgar scores, and higher rates of neonatal seizures, early-onset sepsis, neonatal steroids, respiratory distress syndrome with surfactant replacement therapy, and episodes of hypocarbia significantly being associated with PVL. Multivariate analysis using a logistic regression model revealed early-onset sepsis and hypocarbia being significantly associated with PVL (p=.022 and .024, respectively). Lowest PaCO(2) values did not differ as did not the duration of hypocarbia, but the onset of hypocarbia was significantly later in PVL cases compared to controls (mean 26 vs. 15 h, p=.033). Neurodevelopmental follow-up at a median time of 46 months was poor showing 88% of the cases having an adverse neurological outcome. CONCLUSION: We found early-onset sepsis and episodes of hypocarbia within the first days of life being independently associated with PVL.

The effect of physiotherapy-based breathing retraining on asthma control.

BACKGROUND: The mechanism of the breathing retraining effect on asthma control is not adequately based on evidence. OBJECTIVE: The present study was designed to evaluate the effect of physiotherapy-based breathing retraining on asthma control and on asthma physiological indices across time. STUDY DESIGN: A 6-month controlled study was conducted. Adult patients with stable, mild to moderate asthma (n = 40), under the same specialist's care, were randomized either to be trained as one group receiving 12 individual breathing retraining sessions (n = 20), or to have usual asthma care (n = 20). The main outcome was the Asthma Control Test score, with secondary outcomes the end-tidal carbon dioxide, respiratory rate, spirometry, and the scores of Nijmegen Hyperventilation Questionnaire, Medical Research Council scale, and SF-36v2 quality-of-life questionnaire. RESULTS: The 2 × 4 ANOVA showed significant interaction between intervention and time in asthma control (F = 9.03, p < .001, η(2) = 0.19), end-tidal carbon dioxide (p < .001), respiratory rate (p < .001), symptoms of hypocapnia (p = .001), FEV1% predicted (p = .022), and breathlessness disability (p = .023). The 2 × 4 MANOVA showed significant interaction between intervention and time, with respect to the two components of the SF-36v2 (p < .001). CONCLUSION: Breathing retraining resulted in improvement not only in asthma control but in physiological indices across time as well. Further studies are needed to confirm the benefits of this training in order to help patients with stable asthma achieve the control of their disease.