metabolic acidosis and alkalosis
the following is a brief summary. for additional information visit: e-medicine (christie thomas)
there are many causes of primary metabolic acidosis and they are commonly classified by the anion gap
- metabolic acidosis with a normal anion gap:
- longstanding diarrhea (bicarbonate loss)
- pancreatic fistula
- renal tubular acidosis
- intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants
- renal failure
- metabolic acidosis with an elevated anion gap:
- lactic acidosis
- chronic renal failure (accumulation of sulfates, phosphates, uric acid)
- intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, inh, toluene, sulfates, metformin.
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treating severe metabolic acidosis.
the ideal treatment for metabolic acidosis is correction of the underlying cause. when urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. the best measure of the level of metabolic acidosis is the standard base excess (sbe) because it is independent of pco2. if it is decided to administer bicarbonate, the sbe and the size of the treatable space are used to calculate the dose required:
primary metabolic alkalosis may occur from various causes including:
prolonged metabolic alkalosis
- loss of acid via the urine stools, or vomiting
- transfer of hydrogen ions into the cells
- excessive bicarbonate administration, e.g. alkali given to patients with renal failure.
- contraction of the extracellular space due to excessive diuretic treatment
may be caused by a number of different mechanisms:
- decrease in renal perfusion: occurs in dehydration, cardiac failure, or cirrhosis, stimulates the renin-angiotensis system which increases sodium reabsorption in the nephron.
- chloride depletion: may occur via vomiting or through the use of loop diiuretics and this enhances bicarbonate reabsorption with associated hydrogen ion loss.
- hypokalemia: metabolic alkalosis may be associated with hypokalemia which can then maintain metabolic alkalosis by various mechanisms:
- shift of hydrogen ions intracellularly which enhances bicarbonate reabsorption in the collecting duct.
- stimulation of the h+/k+ atpase in the collecting duct: this leads to potassium ion reabsorption and hydrogen ion secretion. the net gain of bicarbonate maintains the metabolic alkalosis.
- renal ammonia genesis: ammonium ions (nh4+) are produced in the proximal tubule from glutamine metabolism. alpha-ketoglutarate is produced the metabolism generates bicarbonate.
- impaired chloride ion reabsorption in the distal nephron increases luminal electronegativity with enhanced hydrogen ion secretion.
- lowered glomerular filtration rate (gfr). hypokalemia may decrease gfr, which in turn decreases the filtered load of bicarbonate. in volume depletion this impairs excretion of the excess bicarbonate.
treating severe metabolic alkalosis
adequate hydration normally allows the kidneys to correct the problem. however, in severe cases accompanied by hypokalemia, correction of the hypokalemia may be necessary first.
as with metabolic acidosis
, ideal treatment is the correction of the underlying abnormality. more active intervention is occasionally required and various techniques are available. a common transient cause is iatrogenic; correction of acute metabolic acidosis with sodium bicarbonate leaves a residual metabolic alkalosis. time, hydration, and renal function should gradually correct this.
is one of the easier causes to understand and treat. dehydration concentrates the body's electrolytes. as the extracellular fluid (ph = 7.4) is on the alkaline side of neutral (ph = 6.8), the relative alkaline mixture of electrolytes is concentrated and shifts the ph to more alkaline value. rehydration, e.g., with oral fluids or intravenous ringer's lactate, restores the normal electrolyte concentration and, therefore, the ph.
intravenous dilute hydrochloric acid is occasionally used but carries the risk of hemolysis. potassium chloride may also be used unless there is kidney failure. in severe cases which are unresponsive to other measures ammonium chloride may be given (1 to 2 g orally every 4 to 6 hours up to 4 g every 2 hours. it may also given by intravenous infusion (100 to 200 meq dissolved in 500 to 1000 ml of isotonic saline) in addition to potassium replacement. in severe unresponsive metabolic alkalosis it may be necessary to administer hydrochloric acid or institute peritoneal dialysis.
specific therapy depends on the underlying pathology. for details visit: e-medicine (christie thomas)
the body's metabolism produces respiratory (carbonic) acid and, in ischemia or cardiorespiratory failure, metabolic (lactic) acid. in emergencies, therefore, urgent correction is most commonly required for metabolic or respiratory acidosis.
calculating the bicarbonate dose.
(move mouse over the diagram)
the diagram shows an example of a patient with a (pure) metabolic acidosis, sbe = -18 meq/l. to achieve complete correction for someone weighing 70 kg:
dose (meq) = 0.3 x wt (kg) x sbe (meq/l)
378 = 0.3 x 70 x 18
this assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters. our intention , of