Oxyhemoglobin Affinity in Bronchial Asthma: Chronic Stable State, Acute, and Status Asthmaticus

¹ Lung Station (Tufts), Tufts University Medical Services, Boston City Hospital, Boston, and The Department of Respiratory Diseases, St. Vincent Hospital, Worcester
² Hematology Unit (Tufts), Tufts University Medical Services, Boston City Hospital, Boston, and The Department of Respiratory Diseases, St. Vincent Hospital, Worcester

Studies in chronic stable bronchial asthma revealed normal P_50507.40; COLD controls exhibited significantly elevated P_50507.40 and 2,3-DPG levels. In patients with acute asthma, no differences in P_50507.40 or 2,3-DPG were discernible. Subdivision of acute asthma into categories with hyperventilation (PaCO₂ 37.0 mm Hg) and hypoventilation (PaCO₂ 37.1 mm Hg) revealed that hyperventilating patients exhibited a mean P_50507.40 of 27.7 ± 4.3 mm Hg unchanged over normal controls or chronic stable asthma while hypoventilating subjects were significantly left-shifted (P_50507.40 = 25.1 ± 0.7 mm Hg) contrasted with normal and stable asthmatic patients (P < 0.001) despite significant oxyhemoglobin desaturation (80.2 percent). 2,3-DPG data paralleled these observations. The pH was found to influence the P₅₀ change in the hypoventilating population. MCHC measurements, percent HbCO or hemoglobin was not related. While the Bohr effect, reflected in estimates of physiologic in vivo P₅₀ values, tends to temper leftward shifts in asthma associated with respiratory acidosis, the lack of compensatory increase in 2,3-DPG and an associated elevated P_50507.40, in spite of the hypoxic stimulus, may limit maximal oxygen delivery to tissues.