Metabolic Acidosis

Introduction

Definition: A process whose primary event is a deficit in body bicarbonate stores. Characterized by a reduction in serum HCO₃- concentration, ß in blood pH, and a compensatory ß in PaCO₂ .

Note: Definition refers to a PROCESS. Can not conclude what the pH is from the term metabolic acidosis, only that there is an increase of arterial [H+].

Etiology: Acidosis is generated by either a gain of acid or a loss of HCO₃-. The processes causing a gain of acid or loss of HCO3 - can be organized by the different effects on ECF electrolytes as measured by the "anion gap"

Anion Gap

important to determine to find cause of metabolic acidosis

Importance: helps differentiate the causes of a metabolic acidosis

Definition: represents Unmeasured Anions in serum: Phosphate, citrate (blood), sulfate, protein

Serum anion gap = [Na+] – ([Cl-] +[HCO₃ -]

Normal value: 12mEq/L

Use: In Metabolic Acidosis (MA), the serum [HCO₃^-] ß as it is depleted in buffering fixed acid. For electroneutrality, the concentration of another anion must Ý to replace [HCO₃ -]. That anion can by Cl^- or an unmeasured anion. For this reason a [HCO₃ -] ß can be manifested as either: normal or Ý anion gap

Etiologies

(1) Normal anion gap: Bicarb loss or Cl gain. Hyperchloremic Metabolic Acidosis

Causes:

Renal tubular acidosis (RTA):

Type I (distal): failure to excrete titratable acid and NH4; failure to acidify urine; inability of tubule to eliminate H+; see hypokalemia and Ý urine Ph

Need 2 things for proper H+ elimination in the distal tubule:

buffers (ammoniagenesis and titratable acids)

pH low enough so that the buffers can work (recall buffers operate optimally 1pH from their pK)

e.g. Amphotericin B (anitfungal): punches holes in wall of distal tubule Þ no H+ gradient Þ Ý urine pH (7) Þ buffers bind no H+ because pH is too high. Titratable buffers (Creatinine, sulfate) bind to K+ instead of H+ Þ hypokalemia

Type II (proximal): impaired proximal tubular HCO₃- reabsorption; renal loss of bicarb

Type IV (hyperkalemic): aldosterone deficiency or unresponsiveness to aldo; failure to excrete NH4; hyperkalemia caused by lack of aldosterone

Massive diarrhea: GI loss of bicarb

Carbonic Anhydrase inhibitors: leads to loss of bicarbonate in the urine

Ammonium Chloride ingestion (ammonia synthesized to urea in the liver, leaving behind HCL)

Pancreatic drainage

Fistulae of small bowel

Treatment: Bicarbonate administration

(2) Increased anion gap: Ý concentration of unmeasured anions and hydrogen ion

Causes: results form either the production of an endogenous acid or the addition of certain exogenous compounds

Endogenous acid:

Lactic acidosis (D or L type): L-type: tissue hypoxia, hypotension; D-type: associated with short-bowel caused by fermentation of incompletely digested carbohydrate by anaerobic bacteria.

Diabetic ketoacidosis: generation of ketoacids from incomplete oxidation of fatty acids

Alcoholic Ketoacidosis: starvation and ethanol accelerate ketogenesis

Uremic acidosis: Severe Renal failure (GFR<20%) Not filtering phosphates from protein metabolism Þ retention of unmeasured anions

Salicylate intoxication: interference with metabolic processes Þ accumulation of organic acids (lactic acid, ketoacids)

Exogenous compounds:

ethylene glycol (antifreeze, radiator fluid)
methanol (metabolized to formic acid)
paraldehyde

Treatment: Treat underlying etiology (DKA with insulin). Treatment with bicarbonate is reserved for only severe acidemia (pH<7.1; bicarb<10mEq/L) because metabolism of organic anions (ketoacids, lactate) yeilds bicarbonate, and treatment with alkali may "overshoot" desired pH inducing a metabolic alkalosis. Also, NaHCO₃ administration may induce iatrogenic hypernatremia, volume overload, Ý intracellular acidosis, cardiovascular compromise

CRF: failure of renal ammoniagenesis Þ impairs ability of kidney to rid body of excess H+; failure to excrete H+ as titratable acid and NH4

Compensation

Respiratory: Immediate but Never returns pH to normal

Metabolic acidosis is a process that causes a primary decrease in [HCO₃ -]. The respiratory compensation (Kussmaul breathing) is an increase in the depth and rate of respiration which reduces alveloar and arterial pCO₂.

Max drop in pCO₂ is down to 10mmHg (normal: 38-42mmHg). Below 10, Ý ventilation will Ý CO₂ Þ ß pH rapidly

PCO₂ decrease of 10mmHg = pH rise of 0.08

ß 1mEq/L [HCO₃ -] = 1.0-1.3mmHG pCO₂ ß

If the magnitude of the respiratory compensation is inappropriate, suspect a mixed acid-base disorder

PCO₂ = 1.5 x (HCO₃-) +8

So, if the measured PCO₂ differs from the this predicted value, a coexisting respiratory disorder is present because pCO₂ is not behaving as expected.

If measured pCO₂ is higher than predicted Þ coexisting respiratory acidosis and vica versa

Allow pCO₂ to be +/- 2mmHg

Renal: excretion of ammonium and titratable acid (phosphate)

Slow: several days