Metabolic acidosis improves airway conductance in patients with asthma.

The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (+/- SD 12) years, forced expiratory volume in 1 second [FEV(1)] 93 [+/-9] % predicted, PC(20) 1.9 (+/-1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (R(aw)), specific airway conductance (sG(aw)), FEV(1), and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC(20)) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (+/-1.4) to -3.9 (+/-1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (+/-0.02) to 7.36 (+/-0.02) (p < 0.01). This caused a statistically significant increase in sG(aw) from 1.15 (+/-0.16) to 1.26 (+/-0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (+/-2.2) versus 8.09 (+/-1.9) (NS, p = 0.10) and in FEV(1) (2.98 (+/-0.9) versus 3.06 (+/-0.9) (NS, p = 0.15). PC(20) did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma.

Underestimation of nocturnal hypoxemia due to monitoring conditions in patients with COPD.

STUDY OBJECTIVES: COPD patients run a risk of developing nocturnal oxygen desaturation. When evaluating patients with nocturnal hypoxemia, an unfamiliar hospital environment and the monitoring equipment may cause sleep disturbances. It was hypothesized that increased sleep disruption will lead to fewer instances of desaturation during a night of monitoring. DESIGN: The following forms of monitoring were evaluated prospectively on 3 nights for each patient: oximetry at home; polysomnography (PSG) at home; and PSG in the hospital. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, The Netherlands. PATIENTS: Fourteen stable COPD patients (7 men; median age, 71.5 years; age range, 59 to 81 years; FEV(1), 32.5% predicted; FEV(1) range, 19 to 70% predicted) participated in the study. All subjects had significant instances of nocturnal arterial oxygen desaturation. Those patients with a sleep-related breathing disorder or cardiac failure were excluded from the study. MEASUREMENTS AND RESULTS: The mean nocturnal arterial oxygen saturation (SaO(2)) level was higher during PSG monitoring at home (89.7%; range, 77 to 93%) than during oximetry monitoring (88.5%; range, 80 to 92%) [p < 0.025]. The fraction of time spent in hypoxemia (ie, SaO(2) < 90%) was lower during PSG monitoring at home (40.8%; range, 5 to 100%) than during oximetry monitoring (59.9%; range, 6 to 100%) [p < 0.01]. Desaturation time (DeltaSaO(2) > 4%) was lower during PSG monitoring at home (22.1%; range, 3 to 63%) during PSG monitoring at home than during oximetry monitoring (50.4%; range, 4 to 91%) [p < 0.01]. A correction for actual sleep during PSG monitoring reduced the differences between PSG monitoring at home and oximetry monitoring, although a difference in the desaturation time remained (PSG monitoring at home, 31.9% [range, 2 to 75%]; oximetry monitoring, 50.4% [range, 4 to 91%]) [p = 0.041]. A comparison of sleep architectures for nights when PSG was being monitored showed a higher arousal index in the hospital than at home (PSG monitoring in the hospital, 5.6 arousals per hour [range, 2 to 16 arousals per hour]; PSG monitoring at home, 2.5 arousals per hour [range, 1 to 6 arousals per hour]) [p < 0.025], but no differences in SaO(2) levels were found between PSG monitoring at home and PSG monitoring in the hospital. CONCLUSION: The artifacts due to sleep-monitoring equipment may cause an underestimation of the degree of nocturnal hypoxemia in COPD patients. The addition of an unfamiliar environment causes more sleep disruption, but this does not affect nocturnal SaO(2) levels further.

Effect of acute metabolic acid/base shifts on the human airway calibre.

Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined by capillary blood gas sampling. Measurements were performed at the maximal acid-base shift, 90 min after intervention. Airway resistance (R(aw)) and specific airway conductance (sG(aw)), were evaluated, as primary variables, pre and post intervention. Secondary variables, including bronchial responsiveness to histamine, maximal respiratory mouth pressures and grip strength, were evaluated post intervention. In alkalosis, base excess (BE) increased from -0.3 (-3.0-1.9) to 3.0 (1.0-4.8) mmol/l and pH increased from 7.41 (7.37-7.43) to 7.44 (7.39-7.47) (both P<0.01), accompanied by an increase in Pa(CO(2)): 4.7 (4.0-5.7) to 5.0 (4.7-6.1) kPa (P<0.05). R(aw) increased from 0.156 (0.134-0.263) to 0.169 (0.132-0.271) kPa s/L (P<0.05), sG(aw) decreased, but this was not statistically significantly. In acidosis, BE decreased from -0.2 (-2.0-2.2) to -3.5 (-6.3-1.1) mmol/l and pH decreased from 7.41 (7.39-7.45) to 7.36 (7.31-7.40) (both P<0.01), accompanied by a non-significant decrease in Pa(CO(2)). Changes in R(aw) and sG(aw) were contrary to those in alkalosis, but did not reach statistical significance. Acute metabolic acid-base shifts mildly influence the airway calibre in healthy human subjects.

Volumetric measurements of peripheral oedema in clinical conditions.

Water-displacement volumetry can be used for quantifying the volume of the leg. However, not much is known about its application in patients with peripheral oedema of cardiopulmonary origin. We measured the reproducibility of a water-displacement apparatus with a solid object and in ten non-oedematous clinical patients (group A). The day-to-day variability of the leg volume was assessed in the same group. The diurnal variability was assessed in ten patients with persisting peripheral oedema (group B). The effect of treatment on the severity of peripheral oedema was evaluated in another nine patients with peripheral oedema, who were in need of diuretic treatment (group C). Volumetric results were compared to the ankle circumference method and the body weight method. The coefficient of variation was 0.16% in the fixed object and 0.47% in group A. The day-to-day variability was 1.52% after 1 day and 1.76% after a mean interval of 4.8 days. In group B, leg volume and circumference increased during the day (5.9%, P<0.001, and 2.4%, P<0.01, respectively), while body weight remained unchanged. In group C, leg volume, circumference and body weight decreased significantly after treatment (13.1%, P<0.01, 7.1%, P<0.05, and 5.9%, P<0.05). The correlation between the changes in volume and body weight was poor (r=0.37, P=0.33). In conclusion, (1) water-displacement volumetry is highly reproducible, (2) a diurnal variability of peripheral oedema was found, and (3) volumetry is a suitable tool for monitoring peripheral oedema, while the body weight method appears to be less accurate.

Outcome analysis of patients with vasculitis associated with antineutrophil cytoplasmic antibodies.

BACKGROUND: Objective scoring systems of disease activity and disease-associated damage have proven useful in the management of patients with systemic vasculitis. PATIENTS AND METHODS: We used the recently designed Birmingham vasculitis activity score (BVAS; maximum score 63) and vasculitis damage index (VDI; maximum score 59) to assess initial activity and long-term damage, respectively, in ANCA positive patients from one center over a 3-year period. Thirty-two patients with ANCA vasculitis were identified and analyzed as an historic cohort. The median BVAS for all vasculitis patients at first presentation was 19 (range 6 - 36). Patients with Wegener's granulomatosis had a significantly higher total score and respiratory BVAS score compared to the 15 with microscopic polyangiitis. The majority of patients received standard cyclophosphamide/steroid treatment. RESULTS: At the end of follow-up (mean 24.9 months), 4 patients had died; all patients had evidence of permanent organ damage. The median total VDI score at last follow-up was 4.0 (range 0-11), with no differences between patients with Wegener's granulomatosis and microscopic polyangiitis. The VDI was not associated with the number of relapses. A high initial BVAS was found to correlate with a later high vasculitis damage index (r = 0.56). Initial renal or respiratory involvement was also associated with longterm damage in the same organ system. CONCLUSION: Although mortality from ANCA-associated vasculitis has decreased, morbidity remains a common problem. High early-disease activity may identify patients at high risk of long-term organ damage, allowing more effective individualized therapy. This hypothesis requires validation in a prospective, controlled study.

[Use of noninvasive mechanical ventilation to avoid intubation during acute respiratory insufficiency]. / Niet-invasieve beademing ter voorkoming van intubatie tijdens acute respiratoire insufficiëntie.

OBJECTIVE: To determine the value of noninvasive mechanical ventilation in patients with acute respiratory insufficiency. DESIGN: Descriptive. METHODS: Noninvasive mechanical ventilation was considered in all patients with acute respiratory insufficiency in the intensive care unit of the Rijnstate Hospital, Arnhem, the Netherlands, between 1 June 1998 and 31 January 1999. Indication for mechanical ventilation was: respiratory frequency > or = 28/min, and PaCO2 > 6.0 kPa, pH < 7.35, and/or PaO2 < 8.0 kPa. Patients were intubated immediately in case of systolic blood pressure < 90 mmHg, cardiac or respiratory arrest, coma or a severely diminished consciousness. The other patients received noninvasive mechanical ventilation by nasal or full face mask (pressure support: 10-20 cmH2O; positive end expiratory pressure (PEEP): 0-5 cmH2O). Patients were intubated if the respiratory frequency or the level of consciousness or a blood gas value deteriorated. RESULTS: Of the 97 patients who needed ventilation support, 67 were immediately intubated. Noninvasive mechanical ventilation was administered in the other 30 (31%) patients, 22 men and 8 women with a mean age of 67 years (SD: 15). Causes for acute respiratory failure were: chronic obstructive pulmonary disease (COPD) (n = 12); pneumonia (n = 6); heart failure (n = 4); and other (n = 8). Median characteristics at baseline in the noninvasive mechanical ventilation group: acute physiology and chronic health evaluation (APACHE) II score: 17 (range: 1-25); respiratory frequency: 30/min (28-59); pH: 7.33 (6.99-7.54); PaCO2: 9.3 kPa (3.2-18.7); PaO2: 7.4 kPa (4.2-13.4); SaO2: 85% (63-95). Intubation was avoided in 9/30 (30%) of all patients and in 7/12 (58%) of the patients with COPD. Intubation was needed in 21/30 patients (70%): in 8/30 (27%) immediately because of clinical deterioration within 2 hours and in 13/30 (43%) after a mean period of stabilisation of 6 hours (2-16). CONCLUSION: Noninvasive mechanical ventilation prevented intubation in over half of the selected patients presenting with acute respiratory failure due to an exacerbation of COPD. The method appears to be less successful in acute respiratory failure due to other causes.