TAILIEUCHUNG - Chapter 048. Acidosis and Alkalosis (Part 6)

Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aerobic disorders (type B)—malignancies, nucleoside analogue reverse transcriptase inhibitors in HIV, diabetes mellitus, renal or hepatic failure, thiamine deficiency, severe infections (cholera, malaria), seizures, or drugs/toxins (biguanides, ethanol, methanol, propylene glycol, isoniazid, and fructose). Propylene glycol may be used as a vehicle for IV medications including lorazepam, and toxicity has been reported in several settings. . | Chapter 048. Acidosis and Alkalosis Part 6 Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion type A circulatory insufficiency shock cardiac failure severe anemia mitochondrial enzyme defects and inhibitors carbon monoxide cyanide or to aerobic disorders type B malignancies nucleoside analogue reverse transcriptase inhibitors in HIV diabetes mellitus renal or hepatic failure thiamine deficiency severe infections cholera malaria seizures or drugs toxins biguanides ethanol methanol propylene glycol isoniazid and fructose . Propylene glycol may be used as a vehicle for IV medications including lorazepam and toxicity has been reported in several settings. Unrecognized bowel ischemia or infarction in a patient with severe atherosclerosis or cardiac decompensation receiving vasopressors is a common cause of lactic acidosis. Pyroglutamic acidemia has been reported in critically ill patients receiving acetaminophen which is associated with depletion of glutathione. D-Lactic acid acidosis which may be associated with jejunoileal bypass short bowel syndrome or intestinal obstruction is due to formation of D-lactate by gut bacteria. Approach to the Patient Lactic Acid Acidosis The underlying condition that disrupts lactate metabolism must first be corrected tissue perfusion must be restored when inadequate. Vasoconstrictors should be avoided if possible since they may worsen tissue perfusion. Alkali therapy is generally advocated for acute severe acidemia pH to improve cardiac function and lactate utilization. However NaHCO3 therapy may paradoxically depress cardiac performance and exacerbate acidosis by enhancing lactate production HCO3- stimulates phosphofructokinase . While the use of alkali in moderate lactic acidosis is controversial it is generally agreed that attempts to return the pH or HCO3- to normal by administration of exogenous NaHCO3 are deleterious. A reasonable approach is to infuse sufficient NaHCO3 to raise the .

• Y học thường thức
• Acidosis and Alkalosis
• bệnh học và điều trị
• bài giảng bệnh học
• tài liệu học ngành y
• Harrisons Internal Medicine
• Respiratory acidosis
• Respiratory alkalosis
• Metabolic acidosis
• Arterial blood gas interpretation
• Metabolic alkalosis
• Compensatory mechanisms
• BMC Pharmacology and Toxicology
• Airway surface liquid pH
• Airway blood flow
• Blood gases
• Case examples
• medical books
• pharmacology
• epidemiologic
• Obstetrics
• anatomy
• Preventing Morbidity
• Multidisciplinary Care
• Handbook of blood gas
• Base interpretation
• Buffer systems
• Carbon dioxide levels
• Gas exchange
• The non invasive monitoring
• Clinical approach
• Diagnose acid–base disorders
• Drinking binge yesterday