Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known. When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred. Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated. The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients. The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 70% oxygen is probably safe for 24 hours; and after this time, 45% should be the approximate upper limit to the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen therapy and oxygen toxicity. 641 43

Phosphorus plays an essential role in cellular metabolism, especially in the oxidative phosphorylation process and in the synthesis of 2-3 DPG and membrane phospholipids. Moreover phosphorus is necessary as a buffer, mainly when the organism's principal buffer, the H2CO3/HCO3- system, is working at maximal rate. The authors describe a case of severe hypophosphatemia in a ICU patient with a mixed disorder of the acid-base balance. C.P., a woman, aged 71, obese (IBW 145%), at admission in ICU showed increasing dyspnea, hypoxemia and acidosis. Besides alkaline drugs a Venturi mask with FiO2 = 0.3 alternated to CPAP cycles (7 cm H2O) with facial mask applied. Bading on CVP, MAP and ABG results, a pharmacologic therapy with enoximone, furosemide, bronchodilators, mucolytics, antacids, antibiotics and inotropics was performed. TPN with only essential amino acids was performed, in order to activate lipolysis and ketogenesis; but the ABG showed over again mixed disorder of acid-base balance (metabolic and chronic respiratory acidosis), only partially leading to ketogenesis. The reduction of the hematic HCO3-, without changes of PaCO2, was justified by the blood lactic acid of 6.2 mmol/L. And what about blood lactic acid increase? During patient hospitalization, the hematic phosphorus had decreased to, 0.8 mg/dl. Diuretic therapy together with acidosis tamponage, and reduced phosphorus feed had been responsible of severe hypo-phosphatemia. Therapy adjustments brought the phosphatemia to normal values and to a substantial improvement of clinical conditions.
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PMID:[Severe hypophosphatemia in intensive care]. 761 39