Acidosis, metabolic

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

The regulation of NHE2 is multifactorial. Chronic exposure to nitric oxide and gamma-interferon decrease NHE2 activity, whereas metabolic acidosis and chronic stimulation with epidermal growth factor (EGF) increase activity. 

Metformin is contraindicated in patients with heart failure, renal disease, hypersensitivity to metformin, and acute or chronic metabolic acidosis, including ketoacidosis. The drug is also contraindicated in patients older than 80 years and during pregnancy (Pregnancy Category B) and lactation. 

Administration of protein substrates (amino acids) may result in nausea, fever, flushing of the skin, metabolic acidosis or alkalosis, and decreased phosphorus and calcium blood levels. 

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

Potassium is contraindicated in patients who are at risk for experiencing hyperkalemia, such as those with renal failure, oliguria, or azotemia (file presence of nitrogen-containing compounds in the blood), anuria, severe hemolytic reactions, untreated Addison s disease (see Chap. 50), acute dehydration, heat cramps, and any form of hyperkalemia Potassium is used cautiously in patients with renal impairment or adrenal insufficiency, heart disease, metabolic acidosis, or prolonged or severe diarrhea. Concurrent use of potassium with... 

Metabolic acidosis is caused by the release into the bloodstream of excessive amounts of lactic acid and other acidic byproducts of metabolism. These acids enter the bloodstream, react with hydrogen carbonate ion to produce H2CX)5, and shift the ratio HC03 /H2C03 to a lower value. Heavy exercise, diabetes, and fasting can all produce metabolic acidosis. The normal response of the body is to increase the rate of breathing to eliminate some of the CO,. Thus, we pant heavily when running uphill. 

Metabolic acidosis can also result when a person is severely burned. Blood plasma leaks from the circulatory system into the injured area, producing edema (swelling) and reducing the blood volume. If the burned area is large, this loss of blood volume may be sufficient to reduce blood flow and oxygen supply to all the body s tissues. Lack of oxygen, in turn, causes the tissues to produce an excessive amount of lactic acid and leads to metabolic acidosis. To minimize the decrease in pH, the injured person breathes harder to eliminate the excess C02. However, if blood volume drops below levels for which the body can compensate, a vicious circle ensues in which blood flow decreases still further, blood pressure falls, C02 excretion diminishes, and acidosis becomes more severe. People in this state are said to be in shock and will die if not treated promptly. 

Inhalant intoxication dehrium can occur as a consequence of disturbances in dopaminergic, glutamatergic, and GABAergic neu to transmission secondary to acute, high-level exposure to psychoactive ingredients in solvents such as toluene, trichloroethane, and trichloroethylene. Systemic effects of solvent inhalation such as cerebral hypoxia and/or metabolic acidosis may also be involved (Rosenberg 1982). Under these circumstances, inhalant intoxication dehrium develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. Usually, the delirium resolves as the intoxication ends or within a few hours after cessation of use. 

Metabolic Effects. Severe metabolic acidosis with high anion gap and hyperglycemia was reported in humans after acute poisoning with endosulfan (Blanco-Coronado et al. 1992 Lo et al. 1995). In five of the six cases reported by Blanco-Coronado et al. (1992), the metabolic acidosis was corrected with gastric lavage with activated charcoal and intravenous sodium bicarbonate and diazepam. No further information regarding metabolic effects in humans after exposure to endosulfan was located. 

Excretion into urine of ammonia produced by renal mbu-lar cells facilitates cation conservation and regulation of acid-base balance. Ammonia production from intracellular renal amino acids, especially glutamine, increases in metabolic acidosis and decreases in metabolic alkalosis. 

Phenylephrine 10-1000 pg/minute Seconds Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)... 

Stimulation of basolateral Na /H exchanger transport activity in LLC-PK] cells during chronic metabolic acidosis is accompanied by a parallel increase in NHE-1 transcript abundance [80]. Chronic metabolic acidosis also increases the abundance of Na /H exchanger transcripts in rat renal cortices [81] and SV40-transformed mouse proximal tubule cells [82]. 

Some comatose patients are unconscious for less than 2 hours, do not show signs of severe toxicity, and have few complications. In other patients, coma lasts from 2 to 24 hours, and symptoms are more marked. Patients with severe toxicity, including status epi -lepticus and malignant hyperthermia, may remain in coma for 1 day to 3 weeks. These patients often have respiratory or metabolic acidosis. Comatose patients are susceptible to aspiration pneumonia and rhabdomyolysis. Head injury and intracerebral bleeding should be considered as the cause of the comatose state. 

Propofol infusion syndrome has been described and may result in severe metabolic acidosis, cardiac dysrhythmias, cardiovascular collapse, rhabdomyolysis, and death. The risk may be increased with concomitant catecholamine infusions or when the dose exceeds... 

Chronic or large ingestions of propylene glycol have been associated with the development of hyperosmolar anion-gap metabolic acidosis, renal dysfunction, hemolysis, cardiac arrhythmias, and seizures. 

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

Hyperthermia, metabolic acidosis, arrhythmias, cerebral edema, and rhabdomyolysis... 

Poorly treated hyperthermia may lead to metabolic acidosis, rhabdomyolysis, elevated aminotransferases, seizures, renal failure, and disseminated intravascular coagulation (DIC)... 

Administer if abnormal ECG or pre-existing nonor-ganic metabolic acidosis... 

Hyperchloremic (nonanion gap) metabolic acidosis ° Consumption/loss of bicarbonate... 

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