Clinical disturbance characterized by relative increase in total body acid.
A low plasma bicarbonate is present and may be primary or secondary to a respiratory alkalosis.
Induced by the underlying mechanisms: an inability of the kidneys to excrete dietary hydrogen load (H+) and an increase in the generation of H+ such as with lactic acidosis or ketoacidosis, or the loss of bicarbonate (HCO3) by wasting via the kidney or the gastrointestinal tract.
When H+ increases in the body it responds with extracellular buffering by carbonic acid (H2CO3), with compensation via respiratory CO2 by varying the respiratory rate and renal HCO3 handling which serve to maintain equilibrium.
H+ +HCO3=H2CO3=CO2+H2O.
The sum of the positive and negative ion charges in plasma are equal in Vigo:NA +K +Ca2+Mg2+H+ unmeasured cations= Cl+HCO3+CO3+OH +albumin +phosphate +sulfate+lactate + unmeasured anions.
The kidney regenerates HCO3- by combining H+ with urinary buffers NH3 and HPO4 and are excreted in the distal tubule while HCO3 is regenerated and added to the intravascular space.
Results in the stimulation of the central and peripheral chemoreceptors that control respiration causing an increase in alveolar ventilation, resulting in a compensated respiratory alkalosis.
Intracellular and bone buffering also provide improvement by taking up High+ ions which enter the cells and be taken up by bone protein, phosphates and carbonates which act as bone buffers.
Initial evaluation involves the determination of the anion gap.
Classified by the anion gap, even normal or increased.first
The anion gap represents the difference between unmeasured cations and anions in the plasma.
Major unmeasured cations or calcium, magnesium, gamma globulin’s, and potassium.
Major unmeasured cations are albumin, phosphate, sulfate, lactate, and other organic ions.
The normal anion gap is 12 +/- 4 mEq per liter
A normal gap characterized by a lowered bicarbonate concentration, which in the presence of a normal sodium concentration is counterbalanced by an equivalent increase in plasma chloride concentration-hypercholoremic metabolic acidosis.
High-anion-gap metabolic acidosis most commonly caused by glycols, five-oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, rhabdomyolysis , and ketoacidosis.
The anion gap increases when bicarbonate concentration decreases relatively to levels of sodium and chloride because of overproduction of acid, underexcretion of acid, cell lysis, or other circumstances.
Metabolic acidosis has been shown to have deleterious effects on protein balance, leading to:
Negative nitrogen balance
Increased protein degradation
Increased essential amino acid oxidation
Reduced albumin synthesis
Lack of adaptation to a low-protein diet