Search

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.

Six pulse oximeters with finger probes were studied in three groups of 17 hypoxemic patients with COPD aged 50 to 75 years. Transcutaneous arterial oxygen saturation (SpO 2 ) was measured with the Nellcor N101 (oximeter 1a), the Ohmeda Biox III (oximeter 1b), the Nellcor N200 (oximeter 2a), the Critikon Oxyshuttle (oximeter 2b), the Radiometer Oxi100 (oximeter 3a), and the Ohmeda Biox 3700 (oximeter 3b). The SpO 2 was compared with SaO 2 measured in simultaneously withdrawn samples of arterial blood (Radiometer OSM2) at three 20-minute steady-state levels of Flo 2 ranging from 0.21 to 0.40 (SaO 2 , 62 to 100 percent). The bias (mean SpO 2 -SaO 2 difference) and the error in precision (SD of the differences) were both below 4 percent for instruments 1a and 1b and remained below 1.2 and 3 percent, respectively, for the others. A good agreement between SpO 2 and SaO 2 , as reflected by the Bartko intraclass correlation coefficient, was observed in instruments 2a, 3a, and 3b. The individual relationships between SpO 2 -SaO 2 differences and SaO 2 appeared to be linear and parallel. With four instruments (1a, 1b, 2a, and 2b), the mean slope of this relationship was negative, showing a systematic instrumental error: the lower the SaO 2 , the larger the overestimation of SaO 2 . The scattering of the data (precision) principally reflects a subject source of error. In most instruments a technical adjustment could greatly improve instrumental errors and accuracy. The correction of the errors due to between-subject variation would require a system of calibration adjustable by the users to each individual.

This study was undertaken in 23 patients with chronic lung disease to determine whether local wedge pressure variability is related to the state of the local perfusion as observed in distal wedge angiograms. We also compared the variability of the pressures obtained after distal (mechanical) and proximal (balloon inflation) wedging of a catheter in three to six different sites in each patient. When the wedge pressure measurements were repeated in the same site (n = 7), the mean of the absolute differences was below 1 mm Hg. In individual patients, the maximal pressure difference between sites ranged from 0 to 6 mm Hg for Ppw and from 1 to 12 mm Hg for Pdw. The range in Pdw increased from normal to abnormal angiograms. These results suggest that when Pdw is high in one region, it may correspond to local perfusion abnormalities. When the wedge pressure is measured repeatedly or under different conditions, it should be determined after wedging the catheter in the same location for all of the periods of observation. (Chest 1988; 94:491-95)

This study aimed to assess the effect of hypoxemia on theophylline disposition. Ten patients with a mean (+/- SEM) of 58 +/- 3 years with COLD (PaO2 55 +/- 1 mm Hg, PaCO2 46 +/- 2 mm Hg, and pH of 7.39 +/- 0.01) were hospitalized to have oxygen therapy. Before starting O2, they received intravenously, 4 mg/kg of theophylline over a 20-minute period; blood samples and urine were collected for six hours. The results suggested that hypoxia does not influence the disposition of theophylline or its metabolites.