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1 PEFR gradually returned to pretreatment baseline levels
2 PEFR increases over the first 24 h in AHF and could serv
3 PEFR, FVC, FEV1, and FEF25-75 all increased with increas
4 ys-off due to asthma [1.203 (1.148; 1.258)], PEFR<80 [0.76 (0.666; 0.854)], non-use of a self-managem
10 urs was associated with a deficit in evening PEFR (-0.5 liters/minute 95% CI -1.4 to 0.4) and increas
11 ity was associated with a deficit in evening PEFR (-0.5 liters/minute, 95% CI -1.2 to 0.2) and increa
13 time and treatment over 24 h showed greater PEFR improvement after nesiritide compared with placebo
16 6-h postdose average FEV(1) and FVC, and in PEFR, without a significant difference among the differe
17 3 increase in PM10, the estimated decline in PEFR was 13.2 L/min (p = 0.008) for end-of-shift, 9.9 L/
18 steroids group had the greatest declines in %PEFR (1.3%, versus < 0.5% in each of the other three gro
22 ion was associated with a deficit in morning PEFR (-1.0 liters/minute, 95% confidence interval (CI) -
24 Gly/Gly genotype had an increase in morning PEFR during treatment with regularly scheduled albuterol
25 Arg/Arg genotype had an increase in morning PEFR of 23 L/min (p=0.0162); the change in patients with
26 with the Arg/Arg genotype had lower morning PEFR during treatment with albuterol than during the pla
27 .27), normalized FVC (r = -0.22), normalized PEFR (r = -0.27), low-density lipoprotein (r = 0.24), an
31 s of variation for replicate measurements of PEFR, FVC, FEV1, and FEF25-75 were 7.8%, 2.5%, 2.7%, and
33 iritide had a greater effect than placebo on PEFR, and this predicted patients with moderate/marked i
34 75) (-8.12%), and peak expiratory flow rate (PEFR) (-4.65%) as compared with children with less than
35 ines in morning % peak expiratory flow rate (PEFR) (1.8% versus 0.3% per 15 ppb ozone, p < 0.05) and
37 en measured their peak expiratory flow rate (PEFR) every morning and evening, and kept a daily diary
38 addition, morning peak expiratory flow rate (PEFR) improved significantly (mean 9.4%, SEM 3.0%) in th
39 rate (T-PEFR) to peak expiratory flow rate (PEFR) of 10%, 25%, 50%, and 75% (the smaller this ratio
40 We found that peak expiratory flow rate (PEFR) was significantly lower after both a slow inspirat
42 hypothesized that peak expiratory flow rate (PEFR) would increase with acute heart failure (AHF) trea
45 pacity [FVC], and peak expiratory flow rate [PEFR]) normalized for subject's height, plasma lipid lev
49 H2O (mean [SEM], 0.09 [0.08]), but an APRV T-PEFR to PEFR ratio of 75% also promoted alveolar recruit
50 mproved alveolar recruitment using an APRV T-PEFR to PEFR ratio of 75% may be the mechanism of lung p
52 termination of peak expiratory flow rate (T-PEFR) to peak expiratory flow rate (PEFR) of 10%, 25%, 5
55 t than the usual care group (P =.03) and the PEFR monitoring group (P =.001) and were more satisfied
56 n, and after three doses of medication their PEFR still did not exceed 40% of the expected value.
57 r PEEP (5-10 cm H2O) and a decreased EEFR to PEFR ratio (</=50%) demonstrated dynamic heterogeneity b
58 Likewise, APRV with an increased EEFR to PEFR ratio (50%-75%) resulted in alveolar occupancy at i
60 , reducing the time at low pressure (EEFR to PEFR ratio of 75%) in the APRV group provided dynamic ho
62 ostrain was minimized with an APRV T-PEFR to PEFR ratio of 75% (mean [SEM], 0.05 [0.03]) and PEEP of
63 n [SEM], 0.09 [0.08]), but an APRV T-PEFR to PEFR ratio of 75% also promoted alveolar recruitment com
64 alveolar recruitment using an APRV T-PEFR to PEFR ratio of 75% may be the mechanism of lung protectio
66 substudy, 421 patients (37 sites) underwent PEFR testing at baseline, 1, 6, and 24 h after randomiza
67 ; 95% CI: 2.9 to 21.2 L/min) associated with PEFR, but the previous day's ETS exposure was a risk fac
68 2.5 with FEV1 (r = -0.72, p < 0.01), O3 with PEFR (r = -0.75, p < 0.005), and PM2.5 with MMEF (r = -0
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