[Show abstract][Hide abstract] ABSTRACT: Objective
Patients with sleep apnea syndrome (SAS) carry a higher stroke risk. The differential stroke risk between sex and among different age groups has not yet been specifically addressed in previous studies.
Using a universal insurance claims database, we identified a large cohort of SAS patients from 1997 to 2010 and assessed the sex- and age-specific stroke risk compared with a control cohort matched for age, sex, and index date. Cox regression analyses were performed to assess the hazard ratio (HR) of stroke and the corresponding 95% confidence interval (CI). Stroke-free probabilities were computed using the Kaplan-Meier method and differences between both cohorts were examined using the log-rank test.
We identified 29,961 patients with SAS and a control cohort of 119,844 subjects without SAS. The overall incidence of stroke in the SAS cohort was 37% higher compared to the non-SAS cohort (54.6 per 10,000 individual-years vs 39.8 per 10,000 individual-years). After controlling for sex and comorbidities, the SAS cohort exhibited a 19% higher risk for stroke compared to the control cohort (adjusted HR, 1.19 [95% CI, 1.09–1.30]). Women with SAS ages 35 years or younger had the highest stroke risk compared to older age groups of the same sex and their risk for stroke was relatively higher compared to their male counterparts.
Women aged 35 years or younger with SAS have a higher stroke risk.
[Show abstract][Hide abstract] ABSTRACT: Long-term oxygen therapy has become standard treatment for patients with chronic respiratory insufficiency. However, patterns of long-term home oxygen therapy have not been well studied in Taiwan. Oxygen concentrator systems are commonly used in Taiwan, but liquid oxygen delivery systems are portable and may provide advantages over the concentrator system. This study compared oxygen usage between patients from a liquid oxygen group (LOG) and an oxygen concentrator group (OCG). The authors also assessed the physiologic responses of patients with chronic obstructive pulmonary disease (COPD) to ambulatory oxygen use at home.
The study used a retrospective, cross-sectional, observational survey design. The LOG comprised 42 patients, and the OCG comprised 102 patients. We recruited participants in northern Taiwan from July 2009 to April 2010. The questionnaire instruments that were used to collect data consisted of three parts: demographic characteristics, devices used in respiratory care, and activity status with portable oxygen. Two-minute walking tests were performed on COPD patients in their homes.
COPD was the most common diagnosis in our study, with more than 50% of patients who received oxygen long term in both groups having received this diagnosis. The LOG used oxygen for an average of 21.7 hours per day, whereas OCG averaged 15.2 hours per day (p<0.001). In the OCG, 92.2% of patients used a concentrator alone, whereas 23.8% of the LOG used liquid oxygen alone (p<0.001). The LOG patients were involved in significantly more outdoors activities (p=0.002) and reported traveling with oxygen more often (p<0.001) than the OCG patients. For patients with the same dyspnea level of COPD severity, those using liquid oxygen had a lower increase in pulse rate after the walking test, in comparison with the concentrator users.
Patients in the LOG used oxygen for longer hours, went on more outings, and were more likely to travel with oxygen than patients in the OCG. Being ambulatory with liquid oxygen might enable patients with COPD to walk more effectively.
Journal of the Formosan Medical Association 01/2014; 113(1):23-32. · 1.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A considerable amount of studies have been conducted to investigate the interactions of biological fluids with nanoparticle surfaces, which exhibit a high affinity for proteins and particles. However, the mechanisms underlying these interactions have not been elucidated, particularly as they relate to human health. Using bovine serum albumin (BSA) and mice bronchoalveolar lavage fluid (BALF) as models for protein-particle conjugates, we characterized the physicochemical modifications of carbon blacks (CB) with 23nm or 65nm in diameter after protein treatment. Adsorbed BALF-containing proteins were quantified and identified by pathways, biological analyses and protein classification. Significant modifications of the physicochemistry of CB were induced by the addition of BSA. Enzyme modulators and hydrolase predominately interacted with CB, with protein-to-CB interactions that were associated with the coagulation pathways. Additionally, our results revealed that an acute-phase response could be activated by these proteins. With regard to human health, the present study revealed that the CB can react with proteins (∼55kDa and 70kDa) after inhalation and may modify the functional structures of lung proteins, leading to the activation of acute-inflammatory responses in the lungs.
Journal of hazardous materials 11/2013; 264C:127-135. · 4.14 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Considerable evidence shows a key role for protein modification in the adverse effects of chemicals; however, the interaction of diesel exhaust particles (DEP) with proteins and the resulting biological activity remains unclear. DEP and carbon black (CB) suspensions with and without bovine serum albumin (BSA) were used to elucidate the biological effects of air pollutants. The DEP and CB samples were then divided into suspensions and supernatants. Two important goals of the interaction of DEP with BSA were as follows: (1) understanding BSA modification by particles and (2) investigating the effects of particles bound with BSA and the corresponding supernatants on cellular oxidative stress and inflammation. We observed significant free amino groups production was caused by DEP. Using liquid chromatography-mass spectrometry (LC-MS), we observed that BSA was significantly oxidised by DEP in the supernatants and that the peptides ETYGDMADCCEK, MPCTEDYLSLILNR and TVMENFVAFVDK, derived BSA-DEP conjugates, were also oxidised. In A549 cells, DEP-BSA suspensions and the corresponding supernatants reduced 8-hydroxy-2'-deoxyguanosine (8-OHdG) production and increased interleukin-6 (IL-6) levels when compared to DEP solutions without BSA. Our findings suggest that oxidatively modified forms of BSA caused by DEP could lead to oxidative stress and the activation of inflammation.
[Show abstract][Hide abstract] ABSTRACT: Superoxide dismutase (SOD) is a free radical scavenger and a broad-spectrum antioxidant. Its anti-inflammatory and immunomodulatory effects have recently been noted. We studied the effects of this antioxidant on lung damage, oxidative stress, and inflammation in a model of ventilator-induced lung injury (VILI), using 8- to 12-wk-old Sprange-Dawley rats (n = 40). Animals were randomized and evenly divided into two experimental groups, low tidal volume (VT) ventilation (VT = 9 ml/kg) and high VT ventilation (VT = 28 ml/kg). Each group was evenly divided into two subgroups: ten animals were treated with superoxide dismutase (SOD; 10,000 U/kg iv, 2 h prior to the ventilation) and the rests were treated with vehicle. Lung injury was evaluated by histological examination, and cells counts of red blood cells (RBC) and white blood cells (WBC) in the alveoli and the septal wall thickness in lung tissues and serum lactate dehydrogenase (LDH). The lung permeability was assessed by the wet-to-dry weight ratio (W/D), lung weight to body weight ratio (LW/BW) and protein concentration in broncholavage fluid (BALF). Levels of oxidative stress and lipid peroxidation in the lungs were evaluated by tissue malondialdehyde (MDA) and methylguanidine (MG) in BALF, respectively. SOD pretreatment significantly decreased WBC counts in systemic circulation and in alveoli, and effectively attenuated high VT ventilation induced lung injury by reducing hyaline membrane development, septal wall thickness, lung W/D and LW/BW and serum LDH in relation to those of the control. In addition, lung tissue MDA and MG in BALF were also notably reduced.
The Chinese journal of physiology 08/2013; 56(3). · 0.75 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Inhaled cigarette smoke (CS) triggers airway reflexes that are thought to result from the activation of lung vagal C-fiber afferents (LVCAs) via the action of reactive oxygen species in rats. We investigated the role of transient receptor potential vanilloid 1 (TRPV1) and P2X receptors in LVCA activation. Activities of LVCAs were recorded in anesthetized and artificially ventilated rats. Airway challenge of CS produced a concentration-dependent fiber stimulation. Pretreatment with dimethylthiourea [DMTU; a scavenger of hydroxyl radical (•OH)], capsazepine (CPZ; a TRPV1 receptor antagonist) and iso-pyridoxalphosphate-6-azophenyl-2',5'-disulphonate (iso-PPADS; a P2X receptor antagonist) separately reduced the fiber responses by 64, 40 and 44%, respectively, whereas pretreatment with hexamethonium (a nicotinic acetylcholine receptor antagonist) failed to alter the response. A combination of CPZ and iso-PPADS exerted a greater inhibitory effect compared with the effect of either single pretreatment. However, a combination of DMTU, CPZ and iso-PPADS did not further reduce the fiber response compared with the combined effect of CPZ and iso-PPADS. It was concluded that both TRPV1 and P2X receptors, but not nicotinic acetylcholine receptors, participate in the stimulation of LVCAs by inhaled CS, possibly through the action of •OH.
Molecular Medicine Reports 04/2013; 7(4):1300-4. · 1.17 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background
For patients with bronchiectasis, the mechanical mobilization of secretion constitutes a key therapeutic approach. However, the effectiveness of lung expansion therapy to mobilize secretion in bronchiectasis patients has not been investigated extensively. This study compares patients' exercise tolerance and physical assessment outcomes after secretion clearance using intermittent positive pressure breathing (IPPB) or negative pressure ventilation (NPV) as adjuncts to postural drainage.
This prospective, randomized crossover study examined the data for 18 stable outpatients with bronchiectasis. The outcomes were compared for four treatment sessions of either IPPB or NPV, used as adjuncts to postural drainage. The short-term outcomes involved pulmonary functions and a six-minute walk test (6MWT). We also assessed pulmonary functions and physical clinical signs as immediate treatment effects.
Patients' forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and cough efficacy did not change significantly after individual postural drainage sessions using either IPPB or NPV. However, a reduction in the use of accessory muscles was noted after NPV; patients with low baseline FVC might benefit particularly from this reduction (r = 0.699, p < 0.05). No significant differences between two techniques were found for the patient's walking distance. However, the pulse rate after 6MWT was significantly (p < 0.05) lower in the NPV group.
NPV may provide as an effective adjunct to postural drainage as IPPB in weekly lung expansion therapy for outpatients with bronchiectasis. The benefits of NPV might include a reduction in the use of accessory muscles during lung expansion.
Journal of Experimental & Clinical Medicine. 06/2012; 4(3):149–153.
[Show abstract][Hide abstract] ABSTRACT: Background
Dyspnea and related disabling symptoms are common in chronic obstructive pulmonary disease (COPD) patients with chronic hypercapnia. Unfortunately, the indicators during the six-minute walk test (6MWT) for prediction of respiratory functions or exercise intolerance in severe COPD has been little investigated. The relationship between parameters during the 6MWT and respiratory functions was therefore assessed in COPD patients with chronic hypercapnia.
In 2002 and 2003, 37 COPD outpatients with chronic hypercapnia performed the 6MWT, and their respiratory function was measured. Twenty-eight males and nine females with COPD (mean forced expiratory volume in the first second of 26.1% of the predicted value, SD 7.7%) and hypercapnia (mean PaCO2 of 55.5 mmHg, SD 6.4 mmHg) were recruited. All patients were tested to measure pulmonary function, respiratory drive (airway occlusion pressure at 100 ms, P0.1), and respiratory muscle strength on the first day. On the second day, arterial blood gas analysis and the 6MWT were performed. Pearson’s correlation coefficient and regression analysis were used for data analysis.
The study showed that the six-minute walk distance (6MWD) was weakly correlated with the resting arterial oxygen partial pressure (PaO2) (r = 0.349, p = 0.034), expiratory muscle strength (Pemax) (r = 0.358, p = 0.030), and changes of dyspnea sensation (∆Borg) (r = 0.385, p = 0.019); furthermore, ∆Borg was weakly correlated with Pemax (r = 0.377, p = 0.021). The oxygen saturation measured at the end of the 6MWT (ExSpO2) was significantly correlated with FEV1/FVC (r = −0.443, p = 0.006), pH (r = 0.375, p = 0.022), arterial carbon dioxide partial pressure (PaCO2) (r = −0.470, p = 0.003), PaO2 (r = 0.664, p = 0.000) and P0.1 (r = −0.344, p = 0.037). The results of the multiple linear regression with the 6MWD as the dependent variable revealed that PaO2, Pemax, and ∆Borg were significant determinants of the 6MWD (p = 0.018, adjusted R2 = 0.259).
Measurement of the 6MWT demonstrated that a stronger association of exercise limitation is the value of ∆Borg in COPD patients with chronic hypercapnia. Ventilation constraints, hypoxemia, hypercapnia, and respiratory drive might be associated with oxygen desaturation during the 6MWT in COPD patients with chronic hypercapnia.
Journal of Experimental & Clinical Medicine. 02/2012; 4(1):47–51.
[Show abstract][Hide abstract] ABSTRACT: Early physical training is necessary for severely deconditioned patients undergoing prolonged mechanical ventilation (PMV), because survivors often experience prolonged recovery. Long-term outcomes after physical training have not been measured; therefore, we investigated outcome during a 1-year period after physical training for the PMV patients.
We conducted a prospective randomized control trial in a respiratory care center. Thirty-four patients were randomly assigned to the rehabilitation group (n = 18) and the control group (n = 16). The rehabilitation group participated in supervised physical therapy training for 6 weeks, and continued in an unsupervised maintenance program for 6 more weeks. The functional independence measurement (FIM) was used to assess functional status. Survival status during the year after enrollment, the number of survivors discharged, and the number free from ventilator support were collected. These outcome parameters were assessed at entry, immediately after the 6 weeks physical therapy training period, after 6 weeks unsupervised maintenance exercise program, and 6 months and 12 months after study entry.
The scores of total FIM, motor domain, cognitive domain, and some sub-items, except for the walking/wheelchair sub-item, increased significantly in the rehabilitation group at 6 months postenrollment, but remained unchanged for the control group. The eating, comprehension, expression, and social interaction subscales reached the 7-point complete independence level at 6 months in the rehabilitation group, but not in the control group. The 1-year survival rate for the rehabilitation group was 70%, which was significantly higher than that for the control group (25%), although the proportion of patients discharged and who were ventilator-free in the rehabilitation and control groups did not differ significantly.
Six weeks physical therapy training plus 6 weeks unsupervised maintenance exercise enhanced functional levels and increased survival for the PMV patients compared with those with no such intervention. Early physical therapy interventions are needed for the PMV patients in respiratory care centers.
Journal of the Formosan Medical Association 09/2011; 110(9):572-9. · 1.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The effectiveness of noninvasive ventilation (NIV) after extubation in preventing post-extubation respiratory failure is still controversial.
We conducted a prospective, multicenter randomized controlled study involving patients on mechanical ventilation for > 48 hours who tolerated a 2-hour spontaneous breathing trial and were subsequently extubated. The patients were randomized to NIV or standard medical therapy. Re-intubation rate within 72 hours was the primary outcome measure. Multivariable logistic regression analysis was used to determine predictors for extubation failure.
We randomized 406 patients to either NIV (no. = 202) or standard medical therapy (no. = 204). The 2 groups had similar baseline clinical characteristics. There were no differences in extubation failure (13.2% in control and 14.9% in NIV), intensive care unit or hospital mortality. Cardiac failure was a more common cause of extubation failure in control than in NIV. There was no difference in rapid shallow breathing index (RSBI) in extubation failure patients between control (80) and NIV (73). When using data from all patients, we found Acute Physiology and Chronic Health Evaluation (APACHE II) scores (odds ratio [OR] 1.13, 95% CI 1.07-1.20, P < .001), maximal inspiratory pressure (OR 1.04, 95% CI 1.00-1.08, P = .03), and RSBI (OR 1.03, 95% CI 1.02-1.05, P < .001) to be predictors of extubation failure. Abundant secretions were the most common reason (35.1%) for extubation failure identified by attending physicians.
Preventive use of NIV after extubation in patients who passed spontaneous breathing trial did not show benefits in decreasing extubation failure rate or the mortality rate.
Respiratory care 07/2011; 57(2):204-10. · 2.03 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: There is growing evidence that increased expression of cyclooxygenase-2 (COX-2) in the lungs of patients is a key event in the pathogenesis of lung diseases. In this study, we investigated the involvement of the extracellular signal-regulated kinase (ERK), IkappaB kinase alpha/beta (IKKalpha/beta), and nuclear factor-kappaB (NF-kappaB) signaling pathways in thrombin-induced COX-2 expression in human lung fibroblasts (WI-38). Treatment of WI-38 cells with thrombin caused increased COX-2 expression in a concentration- and time-dependent manner. Treatment of WI-38 cells with PD 98059 (2-[2-amino-3-methoxyphenyl]-4H-1-benzopyran-4-one, a MEK inhibitor) inhibited thrombin-induced COX-2 expression and COX-2-luciferase activity. Stimulation of cells with thrombin caused an increase in ERK phosphorylation in a time-dependent manner. In addition, treatment of WI-38 cells with Bay 117082, an IkappaB phosphorylation inhibitor, and pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor, inhibited thrombin-induced COX-2 expression. The thrombin-induced increase in COX-2-luciferase activity was also blocked by the dominant negative IkappaBalpha mutant (IkappaBalphaM). Treatment of WI-38 cells with thrombin induced IKKalpha/beta and IkappaBalpha phosphorylation, IkappaBalpha degradation, and kappaB-luciferase activity. The thrombin-mediated increases in IKKalpha/beta phosphorylation and kappaB-luciferase activity were inhibited by PD 98059. Taken together, these results suggest that the ERK-dependent IKKalpha/beta/NF-kappaB signaling pathway plays an important role in thrombin-induced COX-2 expression in human lung fibroblasts.
European journal of pharmacology 08/2009; 618(1-3):70-5. · 2.59 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A previous report showed that transforming growth factor-beta1 (TGF-beta1) can induce heme oxygenase-1 (HO-1) expression, attenuate cellular injury, and maintain tissue homeostasis. In this study, we investigated the involvement of phosphoinositide-3-OH-kinase (PI3K)/Akt and the nuclear factor-kappaB (NF-kappaB) signaling pathway in TGF-beta1-induced HO-1 expression in human lung epithelial cells (A549). Treatment of A549 cells with TGF-beta1 caused HO-1 to be expressed in a concentration- and time-dependent manner. Treatment of A549 cells with LY 294002 (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, a PI3K inhibitor), an Akt inhibitor, and the dominant negative mutant of Akt (Akt DN) inhibited TGF-beta1-induced HO-1 expression and HO-1-luciferase activity. Stimulation of cells with TGF-beta1 caused an increase in Akt phosphorylation in a time-dependent manner, which was inhibited by wortmannin and LY 294002 (PI3K inhibitors). In addition, treatment of A549 cells with Bay 117082 ((E)-3-[4-methylphenylsulfonyl]-2-propenenitrile, an IkappaB phosphorylation inhibitor), pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibitor), and the dominant negative mutant of IkappaBalpha (IkappaBalphaM) inhibited TGF-beta1-induced HO-1 expression and HO-1-luciferase activity. Treatment of A549 cells with TGF-beta1-induced IkappaB kinase alpha/beta (IKKalpha/beta) phosphorylation, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 Ser536 phosphorylation, and kappaB-luciferase activity. The TGF-beta1-mediated increases in IKKalpha/beta phosphorylation, p65 Ser536 phosphorylation, and kappaB-luciferase activity were inhibited by LY 294002, an Akt inhibitor, and Akt DN. Taken together, these results suggest that the PI3K/Akt dependent IKKalpha/beta/NF-kappaB signaling pathway plays an important role in TGF-beta1-induced HO-1 expression in A549 cells.
European Journal of Pharmacology 05/2007; 560(2-3):101-9. · 2.59 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study assessed how positive expiratory pressure (PEP) affected pulmonary function, functional capacity, and subjective cough difficulty in individuals with chronic obstructive pulmonary diseases (COPD).
This was a prospective, randomized, controlled study. Subjects were recruited from an outpatient department at a university hospital. Thirty-two patients with COPD were allocated to either PEP + FET (forced expiratory technique) group (n = 16) or FET only group (n = 16). Subjects in PEP + FET and FET groups were in a clinically stable condition before and during the study. Subjects in the PEP + FET group received PEP breathing using a mouth adjunct to FET, and the FET group was administered FET for 4 weeks only. Patients received weekly follow-up during the study period. Pulmonary function, 6-minute walk tests, and subjective cough difficulty scores were measured before and after the 4-week interventions.
Subjects in the PEP + FET group had a significantly increased diffusing capacity (DLCO) compared to preintervention (p < 0.05) and after intervention in the FET group (p < 0.05). DLCO significantly increased in the PEP + FET group from 18.0 +/- 7.3 to 20.1 +/- 7.2 mL/min/mmHg. The 6-minute walking distance (6MWD) also increased significantly from 516.8 +/- 94.1 to 570.6 +/- 60.4 m in the PEP + FET group (p < 0.001) after intervention, compared to that for the FET group (p < 0.05). Additionally, the PEP + FET group had significantly lower cough difficulty scores compared to those at baseline and in the FET group.
Four-week PEP therapy as an adjunct to FET further enhanced DLCO and 6MWD, and reduced cough difficulty compared to FET only in COPD patients with mucus hypersecretion.
Journal of the Formosan Medical Association 04/2007; 106(3):204-11. · 1.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Patients requiring prolonged mechanical ventilation (PMV) are frequently deconditioned because of respiratory failure precipitated by the underlying disease, the adverse effects of medications, and a period of prolonged immobilization. The effects of 6 weeks of physical training on the strength of respiratory and limb muscles, on ventilator-free time, and on functional status in patients requiring PMV were examined.
Thirty-nine patients with PMV were initially enrolled in the study and were assigned to either a treatment group (n=20) or a control group (n=19). Three subjects in the treatment group and 4 subjects in the control group died during the 6-week intervention period and thus their data were excluded from the final analysis.
Subjects in the treatment group received physical training 5 days a week for 6 weeks. Strength of respiratory and limb muscles, ventilator-free time, and functional status, which was measured by the Barthel Index of Activities of Daily Living (BI) and Functional Independence Measure (FIM), were examined at baseline and at the third and sixth weeks of the study period.
Respiratory and limb muscle strength improved significantly at the third and sixth weeks in the treatment group compared with baseline measurements. Total BI and FIM scores increased significantly in the treatment group and remained unchanged in the control group. Effect sizes of the BI and FIM scores were 2.02 and 1.93, respectively, at the sixth week.
The results show that a 6-week physical training program may improve limb muscle strength and ventilator-free time and thus improve functional outcomes in patients requiring PMV.
[Show abstract][Hide abstract] ABSTRACT: This study was designed to investigate the effects of 6 months of nocturnal nasal positive pressure ventilation (NNPPV) on respiratory muscle function and exercise capacity in patients with chronic respiratory failure.
A prospective, randomized, controlled design was used. Twenty-nine patients with chronic respiratory failure were enrolled and allocated to either the NNPPV (n = 14) or control group (n = 15). Patients in the NNPPV group received bi-level positive pressure ventilation via nasal mask for 6 consecutive months. Arterial blood gas, respiratory muscle assessment and 6-minute walk test (6MWT) were performed before and after the 6-month NNPPV intervention. Respiratory muscle function was assessed using the variables of maximal inspiratory pressure (Pimax), maximal expiratory pressure (Pemax), and maximum voluntary ventilation (MVV).
Subjects in the NNPPV group showed a significant improvement in blood gas exchange and increased 6-minute walk distance (6MWD) compared to baseline and the control group. The 6MWD was significantly increased from 257.1 +/- 114.1 to 345.2 +/- 109.9 m (34.3%) in the NNPPV group. NNPPV also significantly improved MVV and Pimax relative to baseline. MVV was significantly increased from 19.2 +/- 6.5 to 22.3 +/- 7.1 L/min (16.1%) in the NNPPV group (p < 0.05). Furthermore, there was a significant correlation between the magnitude of MVV improvement and 6MWD change.
The 6-month NNPPV treatment significantly decreased the partial pressure of carbon dioxide and improved daytime respiratory muscle function, thus contributing to exercise-capacity increase in patients with chronic respiratory failure.
Journal of the Formosan Medical Association 07/2006; 105(6):459-67. · 1.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The study objective was to investigate the efficacy of 6 months of nocturnal nasal positive pressure ventilation (NNPPV) on arterial blood gas, exercise capacity, respiratory muscle function, and the frequency of hospital admission in hypercapnic patients with severe obstructive lung diseases.
This was a prospective, randomized, controlled study. Twenty-seven patients with hypercapnic obstructive lung diseases were randomized to either the NNPPV group (N = 13) or the control group (N = 14). Arterial blood gas, exercise capacity and respiratory muscle function were measured before and after 6 months of NNPPV intervention. The number of hospital admissions and the length of stay during the 6-month period before and after NNPPV intervention were recorded.
Subjects in the NNPPV group showed a significant reduction in arterial carbon dioxide partial pressure (PaCO2). bicarbonate (HCO3-), and base excess (BE), compared with those before intervention and of the control group. Six-minute walk distance (6MWD) also increased significantly from 232.2 +/- 79.3 m to 333.4 +/- 81.3 m in the NNPPV group after 6 months of intervention. The maximum voluntary ventilation (MVV) also increased significantly after NNPPV intervention. Moreover, the NNPPV group had significantly lower frequency of admission and fewer days of hospital stay during the intervention period compared with those before intervention and of the control group.
Six months of NNPPV improved the arterial blood gas, increased exercise capacity and respiratory muscle endurance, and helped to reduce the frequency and the length of hospitalization in hypercapnic patients with severe obstructive lung disease.
[Show abstract][Hide abstract] ABSTRACT: Oxygen supplementation is the treatment most commonly used to relieve dyspnea in chronic obstructive pulmonary disease (COPD). There is a lack of data, however, on the response of the respiratory drive to low flow oxygen in severe stable COPD. The purpose of this investigation was to evaluate the magnitude of chemoresponsiveness to low flow supplemental oxygen in patients with COPD of variable severity in terms of mouth occlusion pressure at 100 msec (P0.1), P0.1 and minute ventilation (MV) response to CO2 stimulation, and blood gas tension.
Twenty-six patients with stable COPD of variable severity were divided into two groups: those with mild airway obstruction and normocapnia (n = 14) and those with hyperinflation and hypercapnia (n = 12).
Arterial oxygen tension, oxygen saturation, and arterial CO2 tension were significantly increased after oxygen therapy in COPD patients with or without hypercapnia (all p < 0.01). COPD patients with hypercapnia had a significantly higher P0.1 (0.7 +/- 0.07 kPa) than those with normocapnia (0.3 +/- 0.03 kPa, p < 0.01). Oxygen significantly decreased the P0.1 adjusted by end tidal CO2 pressure (delta P0.1/PETCO2) only in patients with hyperinflation and hypercapnia, from 0.2 +/- 0.05 to 0.1 +/- 0.03 kPa (p < 0.05). There was a weak correlation between P0.1/PETCO2 and forced vital capacity (FVC; r = 0.41, p < 0.05) or forced expiratory volume in 1 second (FEV1; r = 0.45, p < 0.05). In addition, the arterial CO2 tension (PaCO2) was inversely related to P0.1/PETCO2 (r = -0.57, p < 0.01). The MV with 6% CO2 (MVCO2) was also significantly decreased in the hypercapnic group from 17.9 +/- 3.7 to 14.8 +/- 4.9 L after oxygen therapy (p < 0.01). The maximum inspiratory pressure did not change after oxygen usage in either group.
We conclude that short-term oxygen therapy may blunt respiratory response to CO2 in COPD with chronic hypercapnia. Cautious observation of respiratory response is needed during oxygen therapy in COPD patients with a higher magnitude of air-trapping and hypercapnia.
Journal of the Formosan Medical Association 09/2002; 101(9):607-15. · 1.00 Impact Factor