Metabolic acidosis decreased bicarbonate

Metabolic acidosis (decreased serum phosphate, serum bicarbonate) Glucosuria... 

Advanced stages Increased potassium, phosphorus, and magnesium decreased bicarbonate (metabolic acidosis) calcium levels are generally low in earlier stages of CKD and may be elevated in stage 5 CKD, secondary to the use of calcium-containing phosphate binders. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

As kidney function declines, bicarbonate reabsorption is maintained, but hydrogen excretion is decreased because the ability of the kidney to generate ammonia is impaired. The positive hydrogen balance leads to metabolic acidosis, which is characterized by a serum bicarbonate level of 15 to 20 mEq/L (15 to 20 mmol/L). This picture is generally seen when the GFR declines below 20 to 30 mL/minute.38... 

The answer is c. (Hardman, pp 6917 693 J Acetazolamide is a carbonic anhydrase inhibitor with its primary site of action at the proximal tubule of the nephron. Acetazolamide promotes a urinary excretion of Na, K, and bicarbonate There is a decrease in loss of Cl ions The increased excretion of bicarbonate makes the urine alkaline and may produce metabolic acidosis as a consequence of the loss of bicarbonate from the blood. None of the other diuretic drugs promote a reduction in the excretion of the Cl ion... 

Metabolic acidosis is characterized by decreased plasma bicarbonate concentrations (HC03 ), whereas metabolic alkalosis is characterized by increased HC03T... 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations higher than 50 mg/dL are thought to be an absolute indication for hemodialysis and treatment with fomepizole or ethanol, although formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase-independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. Nevertheless, carbonic anhydrase inhibition causes significant bicarbonate losses and hyperchloremic metabolic acidosis. Because of this and the fact that HCO3" depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, the diuretic efficacy of acetazolamide decreases significantly with use over several days. 

Baseline and periodic serum bicarbonate levels to monitor for hyperchloremic, nonanion gap metabolic acidosis (i.e., decreased serum bicarbonate below the normal reference range in the absence of chronic respiratory alkalosis)... 

CAIs alter renal function primarily by inhibiting carbonic anhydrase in the proximal tubule, which results in decreased bicarbonate reabsorption. The net effect of the renal actions of acetazolamide therapy is alkaliniza-tion of the urine and metabolic acidosis. Metabolic acidosis results from the initial bicarbonate loss and persists with continued acetazolamide use. Moderate metabolic acidosis develops in most patients. Reabsorption of bicarbonate independent of carbonic anhydrase prevents severe acidosis. Initially, acetazolamide produces diuresis, but urinary output decreases with the development of metabolic acidosis. In addition, decreased urinary citrate excretion follows acetazolamide therapy and has been attributed to the metabolic acidosis it produces. A high urinary pH and low urinary citrate concentration are conducive to precipitation of calcium phosphate in both the renal papillae and the urinary tract. 

The pH value in the portal vein drops in the case of increased urea synthesis. This decrease corresponds to the consumption of HC03. At the same time, intra-and extrahepatic glutamine synthesis is reduced. When the pH value falls in the blood, corresponding amounts of bicarbonate must be made available for the compensation of metabolic acidosis. This amount of HC03 is then not available for urea synthesis, which results in a curbing of the urea cycle. Additionally, the glutaminase... 

Acid-base disorders Initial metabolic alkalosis (resulting from decreased urea synthesis with reduced bicarbonate consumption) may be superimposed by respiratory alkalosis as an outcome of disorders in lung function. During the further course, metabolic acidosis (with renal insufficiency) and respiratory acidosis (with pulmonary insufficiency) can be expected. In advanced or severe stages of the disease, lactate acidosis may develop in some 50% of all comatose patients owing to restricted gluconeogenesis. 

Treatment for salicylate intoxication is directed toward (1) decreasing further absorption, (2) increasing elimination, and (3) correcting add-base and electrolyte disturbances. Activated charcoal binds aspirin and prevents its absorption. Elimination of salicylate may be enhanced by alkaline diuresis and in severe cases by hemodialysis." Sodium bicarbonate may be given to alleviate metabolic acidosis. Indications for hemodialysis include serum salicylate >1000 mg/L, severe CNS depression, intractable metabolic acidosis, hepatic failure with coagulopathy, and renal failure. ... 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

Metabolic acidosis is readily detected by decreased plasma bicarbonate (or a negative extracellular base excess), the primary perturbation in this acid-base disorder. Bicarbonate is lost in the buffering of excess acid. Causes include the foUowing ... 

The answer is d. (Murray, pp 238-249. Scriver, pp 2165-2194. Sack, pp 121-144. Wilson, pp 287-324.) Propionic acidemia (232000) results from a block in propionyl CoA carboxylase (PCC), which converts propionic to methylmalonic acid. Excess propionic acid in the blood produces metabolic acidosis with a decreased bicarbonate and increased anion gap (the serum cations sodium plus potassium minus the serum anions chloride plus bicarbonate). The usual values of sodium (-HO meq/L) plus potassium ( 4 meq/T) minus those for chloride (-105 meq/L) plus bicarbonate (—20 meq/L) thus yield a normal anion gap of -20 meq/L. A low bicarbonate of 6 to 8 meq/L yields an elevated gap of 32 to 34 meq/L, a gap of negative charge that is supplied by the hidden anion (propionate in propionic acidemia). Biotin is a cofactor for PCC and its deficiency causes some types of propionic acidemia. Vitamin B deficiency can cause methylmalonic aciduria because vitamin Bn is a cofactor for methylmalonyl coenzyme A mutase. Glycine is secondarily elevated in propionic acidemia, but no defect of glycine catabolism is present. 

The prevention and treatment of severe metabolic acidosis in patients with kidney disease is also important to prevent the development of renal bone disease, fatigue, decreased exercise tolerance, reduced cardiac contractility, and increased ventricular irritability. Metabolic acidosis also appears to stimulate protein catabolism, which can contribute to a negative nitrogen balance and lower albumin concentrations, as well as cause growth retardation in children. Lower serum bicarbonate levels in peritoneal dialysis patients have also been associated with a higher hospitalization rate and longer hospital stays. Severe acidemia (blood pH <7.1 to 7.2) suppresses myocardial contractility, predisposes patients to cardiac arrhythmias, and may lead to a decrease in total peripheral vascular resistance and blood pressure, reduced hepatic blood flow, and impaired oxygen delivery. ... 

In hyperchloremic metabolic acidosis, bicarbonate losses from the ECF are replaced by chloride and the SAG remains normal. This decrease in bicarbonate results from losses from the gastrointestinal tract, dilution of bicarbonate in the ECF space by the addition of sodium chloride solutions, or the addition of chloride-containing acids to the ECF. Common causes of metabolic acidosis with an increased or a normal SAG are listed in Table 51-5. 

The patient s primary means to compensate for metabolic acidosis is to increase carbon dioxide excretion by increasing respiratory rate. This results in a decrease in PaC02. This ventilatory compensation results from stimulation of the respiratory center by changes in cerebral bicarbonate concentration and pH. For every 1 -mEq/L decrease in bicarbonate concentration below the average of 24, the PaC02 decreases by about 1 to 1.5 mm Hg from the normal value of 40 (see Table 51 ). 

In mixed respiratory and metabolic acidosis, there is a failure of compensation. The respiratory disorder prevents the compensatory decrease in PaC02 expected in the defense against metabolic acidosis. The metabolic disorder prevents the buffering and renal mechanisms from raising the bicarbonate concentration as expected in the defense against respiratory acidosis. In the absence of compensatory mechanisms, the pH decreases markedly. 

This mixed disorder is often seen in patients with advanced liver disease, salicylate intoxication, and pulmonary-renal syndromes. The respiratory alkalosis decreases the PaC02 beyond the appropriate range of the respiratory compensation for metabolic acidosis. The plasma bicarbonate concentration also falls below the level expected in compensation for a simple respiratory alkalosis. In a sense, the defense of pH for either disorder alone is enhanced thus the pH may be normal or close to normal, with a low PaC02 and a low [HCOj]. Treatment of this disorder should be directed at the underlying cause. Because of the enhanced compensation, the pH is usually closer to normal than in either of the two simple disorders. 

Metabolic acidosis, a common complication of ESKD, is associated with increased protein degradation and decreased synthesis of albumin. Correction of acidosis in ESKD patients may be associated with increases in serum albumin, body weight, and midarm muscle circumference, and fewer hospitabzations. Appropriate stabilization of serum bicarbonate concentrations (>22 mEq/L) via alteration of the dialysate bicarbonate concentration or administration of oral bicarbonate salts thus seems a prudent nutritional intervention in these patients (see Chap. 44 and 51). 

Metabolic acidosis. The primary disorder is a decrease in bicarbonate concentration. 

Ifihe [H l is elevated, decide what is the primary cause of the acidosis. Look at the pro,. If this is elevated, then there is a respiratory acidosis. Look at the bicarbonate. I f this is decreased, there is a metabolic acidosis. 

The phase of primary respiratory alkalosis rarely is recognized in children with salicylate toxicity. They usually present in a state of mixed respiratory and renal acidosis, characterized by a decrease in blood pH, a low plasma bicarbonate concentration, and normal or nearly normal plasma PCO2. Direct salicylate-induced depression of respiration prevents adequate respiratory hyperventilation to match the increased peripheral production of CO2- Consequently, plasma PCO2 increases and blood pH decreases. Because the concentration of bicarbonate in plasma already is low due to increased renal bicarbonate excretion, the acid-base status at this stage essentially is an uncompensated respiratory acidosis. Superimposed, however, is a true metabolic acidosis caused by accumulation of acids as a result of three processes. First, toxic concentrations of salicylates displace 2-3 mEq/L of plasma bicarbonate. Second, vasomotor depression caused by toxic doses of salicylates impairs renal function, with consequent accumulation of sulfuric and phosphoric acids. Third, salicylates in toxic doses may decrease aerobic metabolism as a result of inhibition of various enzymes. This derangement of carbohydrate metabolism leads to the accumulation of organic acids, especially pyruvic, lactic, and acetoacetic acids. 

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