The superiority of bicarbonate dialysis (Bi HD) over acetate dialysis (Ac HD) using a high sodium dialysate has not been established to our knowledge. We compared to Bi HD to Ac HD over 6 weeks each in ten stable patients using a double-blind crossover design and a dialysate sodium concentration of 140 mEq/liter. The dialyzer, delivery system, and disalysate constituents were identical except for the substitution of Bi or Ac. Interdialytic weight gain, pre- and post-HD blood pressures, and heart rates were also comparable in the two protocols. Beginning of the week pre-HD serum Bi was greater during Bi HD than Ac HD (19.1 +/- 0.9 vs. 15.1 +/- 0.8 mEq/liter, P less than 0.001); post-HD Bi values were also higher during Bi HD. Similarly, pre-HD pH was also greater with Bi HD 7.40 +/- 0.012 vs. 7.35 +/- 0.001 U, P less than 0.01). The number of adverse symptoms and signs were similar during each protocol (2.0 +/- 0.65 for Bi HD vs. 2.5 +/- 0.5 for Ac HD episodes/patient/6 weeks, NS). However, fewer therapeutic interventions were required during the Bi HD protocol (1.5 +/- 0.43 vs. 3.1 +/- 0.6 treatments/patient/6 weeks, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
Recent studies have suggested that oxygen consumption (VO2) may be dependent on systemic oxygen transport (SOT) in patients with the adult respiratory distress syndrome. To evaluate this relationship in patients with chronically impaired SOT, 2 groups underwent control right heart catheterization. Twenty-six patients with pulmonary hypertension (Group I) were then reevaluated after 48 h of treatment with a vasodilator, either hydralazine or nifedipine. Nine patients with refractory left ventricular failure (Group II) were first studied using nitroprusside, and 24 h later were begun on a double-blind drug protocol using either minoxidil or hydralazine. A significant correlation existed between control SOT and VO2 in both groups (r = 0.65, p less than 0.001). There were no changes in either group, however, in VO2 with vasodilator therapy, despite significant increases in cardiac output and SOT. We conclude that although resting oxygen consumption may be correlated with systemic oxygen transport when SOT is at low levels in stable patients with chronically impaired SOT, VO2 appears to be independent of SOT when oxygen delivery is increased by the administration of vasodilators.
The purpose of these experiments was to quantify stagnant intrapulmonary blood caused by a pulmonary arterial occlusion (PAO). The hypothesis was that the diffusing capacity of the lung for CO (DLCO) would be altered little by PAO when measured with the usual inspired concentrations (0.3%) of CO, since stagnant blood distal to the occlusion takes up CO for 20 s or more before significant CO backpressure would develop. However, higher levels of CO (i.e., greater than or equal to 3%) would equilibrate faster with capillary blood (within 5-10 s), and DLCO measured 10-20 s subsequent to the high CO exposure would reflect only the DLCO in the unoccluded regions. Thus the fractional reduction in DLCO measured with 3% CO, with respect to that measured with 0.3% CO, should be related to the fractional occlusion of the pulmonary artery in a predictable way. We occluded the right pulmonary artery (RPAO), the left pulmonary artery (LPAO), or the left lower lobar artery (LLPAO) and found that DLCO measured during rebreathing a 0.3% CO mixture was 80, 87, and 94%, respectively, of the preocclusion value, whereas the DLCO measured during rebreathing a 3.3% CO mixture was 59, 73, and 87% of the preocclusion value. A computer model was developed to predict the reduction in DLCO at different levels of CO exposure that would be caused by varying fractions of PAO. Our data indicated that RPAO corresponded to a 42% vascular occlusion, LPAO a 35% occlusion, and LLPAO a 20% occlusion. Measurement of DLCO using low and high concentrations of CO might be useful in assessing the fraction of vascular bed occluded and in following noninvasively the course of vascular occlusion in a variety of pulmonary diseases.
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