| Abstract: | Altogether 228 patients with hereditary microspherocytic anemia (HMA), autoimmune hemolytic anemia (AIHA) and hypoplastic anemia (HA) were examined over time for the acid-base state of the arterial blood with the use of the pCO2-buffer bases coordinate system (BE/pCO2 and pCO2/BE diagrams). Prior to surgery the respiratory alkalosis was diagnosed in 60% of HMA patients (of these, 41.7% of patients had a decompensated alkalosis), in 61.7% of AIHA patients (73%), and in 69.7% of HA patients (82.1%). It is shown that the development in the patients of chronic respiratory alkalosis should be regarded as a compensatory mechanisms associated with hemic hypoxia complicated by arterial hypoxemia. During splenectomy, there was an increase in the incidence of decompensated respiratory alkalosis. Mixed respiratory and metabolic alkalosis occurred in 8.3% of AIHA patients and in 19.6% of HA patients because of artificial ventilation of the lungs. Two hours after operation compensated metabolic acytosis was identified in 72% of HMA patients, in 33.3% of AIHA patients, and in 33.9% of HA patients. Twenty-four hours following operation the patients of all the groups had arterial hypoxemia and hypocapnia. In view of this fact the blood acid-base state was determined by the presence of respiratory alkalosis: in 47.5% of patients with HMA, in 60% of patients with AIHA, and in 54% of patients with HA. Analysis of the BE/pCO2 diagram demonstrated that in 2/3 of the patients with HMA and AIHA and in all the patients with HA, respiratory alkalosis was decompensated. It was established that electrolyte imbalance detected in the patients interfered with metabolic compensation for chronic respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS) |
