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At least 1,207 records · Page 67Linked to original sources
PubMed1977

Respiratory acidosis and alkalosis.

The physiology of respiratory control of acid-base balance is reviewed. The pathophysiological mechanisms during hypercapnia and hypocapnia are discussed in the light of the causes and clinical manifestations of these disturbances. In addition to the role of the kidney in the compensatory processes of these disturbances, renal functional changes during acute and chronic pulmonary acid-base derangement is discussed. Some of the difficulties encountered in the patient with chronic renal disease in whom respiratory abnormalities may be present are also discussed.

Acidosis, Respiratory↗
PubMed1991

[Bulimia, induced vomiting, hypochloremic-hypokalemic alkalosis and fetal distress in the 33rd week of pregnancy. Obstetric and anesthesiologic management].

A 39-year-old primigravida was admitted to the hospital in the 33rd week of pregnancy due to fetal retardation and placental insufficiency, malnutrition, decreased cutaneous turgor, and cardiotocographic (CTG) fetal distress. Body weight had increased subnormally through the 29th week of gestation and had since decreased by 2.5 kg. The following laboratory tests were obtained (normal values for pregnant women in parentheses): serum bicarbonate 50.9 (20-24) mmol/l, pH 7.61 (7.4), PCO2 52.4 (31) mmHg, SaO2 89-91 (greater than 95%); serum sodium 125 (137-145), potassium 1.8 (3.6-5.5), chloride 55 (94-111) mmol/l; colloid osmotic pressure 20.7 (19-22) mmHg. A decompensated hypochloremic-hypokalemic acidosis together with hypovolemic, isotonic hyponatremia was diagnosed and bulimic vomiting that had existed for two decades was discovered as the underlying cause. The acute therapy was aimed at normalization of the fluid-electrolyte status, oxygenation, utero-placental perfusion, and placental-fetal O2 transfer and was carried out under close clinical, biochemical, and CTG surveillance. In addition to the basic measures (lateral tilt position, nasal O2 application, isotonic electrolyte solutions, parenteral nutrition), 158 mmol H+, 240 mmol K+, and 414 mmol Na+ ions were administered. This therapy improved the maternal and fetal parameters continuously (Table 3, Fig. 1). Twenty-six hours following the initiation of treatment, a cesarean section was performed after induction of catheter-epidural anesthesia.

Adult↗
PubMed1990

Intracellular alkalosis induced by increasing extracellular potassium. Ionic dependence and effects of amiloride and DIDS.

The intracellular alkalinization produced when extracellular potassium concentration is increased above its normal levels was studied in the rat diaphragm muscle by determination of the steady-state distribution of [14C]-5,5-dimethyl-2,4-oxazolidinedione (DMO). Replacement of external Na+ with sucrose and Mg2+ or N-methyl-D-glucamine prevented the rise in intracellular pH. Amiloride (1 mM) also abolished the elevation of intracellular pH, while the removal of external Cl- (replaced by gluconate) or addition of 0.1 mM 4-acetamido-4'-diisothyocyanostilbene-2,2-disulfonic acid (DIDS) did not prevent intracellular alkalinization from taking place. These results suggest that in the rat diaphragm muscle a Na(+)-dependent, amiloride-sensitive transport mechanism, perhaps Na+/H+ exchange, plays a major role in the K(+)-induced intracellular alkalinization. This mechanism might account for the metabolic acidosis produced by hyperkalemia.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗