ABG Interpretation
Regulation of Acid Base Balance
Normal serum pH is 7.35-7.45
Seriously bad things start happening when pH falls to 7.2 or rises to 7.55
Three physiologic systems act interdependently to maintain a normal serum pH
Chemical buffering of excess acid or base by buffer systems in blood plasma and cells
Excretion of acid by lungs
Excretion of acid or regeneration of base by the kidneys
Important blood buffers = proteins such as hemoglobin in RBCs and albumin in the plasma
Important intracellular buffers = negatively charged ions such as phosphate and carbonate
The status of the bicarbonate buffer is representative of acid-base homeostasis within the body as a whole
Lungs and kidneys eliminate acid/base...buffers do not eliminate!
Regulation of Volatile Acids by the Lungs
Volatile acids are those that can be converted to gases (like CO2)
Recall the hydrolysis reaction we went over in respiratory physiology:
In the tissues, the addition of CO2 to the blood drives hydrolysis to teh RIGHT forming H+ and HCO3-.
The H+ is buffered by hemoglobin
The HCO3- diffuses into plasma
Chloride moves in to maintain electroneutrality (the chloride shift)
In the lungs. CO2 diffues into alveoli and is exhaled.
This drives hydrolysis reaction in reverse
In a reversal of the chloride shift, HCO3- reenters the RBCs, and chloride exits. HCO3- combines with H+ (which
has been released from its buffers), regenerating CO2 and H2O. Isn't this exciting?
Regulation of Fixed Acids and Bicarbonate by the Kidneys
Acids that cannot be converted to gases must be eliminated by the kidneys (fixed acids)
Sulfuric, phosphoric and other acids produced by protein metabolism
Ketones produced by lipid metabolism and in diabetic ketoacidosis
Lactic acid produced by CHO metabolism and in conditions which cause the accumulation of increased metabolic rates and
accelerated anaerobic glycolysis (such as in shock and hypoxemia)
Occasionally things like ingested toxins (salicylate, drugs and methanol)
The kidneys regulate serum pH by secreting H+ into urine and be regenerating HCO3- for reabsorption into blood.
Three buffer systems in the renal tubules:
Bicarbonate buffer: for every molecule of H+ secreted, a molecule of HCO3- is returned to the blood to restore
components of the plasma bicarbonate buffer system
Ammonia buffer: NH3 diffuses into tubular lumen where it binds with H+ to form NH4+ which is large and cannot be
reabsorbed. This means the H+ is now trapped in the tubule where it is excreted in urine as ammonium.
Phosphate buffer: operates similarly to the ammonia one. The result is the formation of weak acids that are excreted in
urine...sodium and bicarb are reabsorbed.
Electroneutrality
Potassium and Hydrogen
When serum K+ is elevated, renal tubular cells secrete more K+ but retain H+ to maintain electroneutrality, leading
to acidosis.
Low serum K+ promotes renal secretion of H+ (leading to alkalosis)
When serum H+ is high, renal tubular cells will secrete more H+, but retain K+...leading to hyperkalemia
At tissue level, H+ moves into cells to be buffered by intracellular proteins and K+ moves out...contributes to
clinical manifestations of hyperkalemia (though it does not indicate a "true" excess of K+)
When serum H+ is low, renal cells retain H+ and secrete more K+, and cellular proteins release H+ to extracellular
fluid while K+ shifts intracellularly.
Sodium and Chloride
Active reabsorption of Na+ from the renal tubules drives secretion of H+ and reabsorption of anions such as
chloride and HCO3-.
JG cells sense low extracellular volume, triggering renin-angiontensin-aldosterone system...aldosterone stimulates
renal reabsorption of Na+. H+ and K+ are excreted to maintain electroneutrality, and HCO3- is reabsorbed.
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