This is the condition where someone is systemically too acid. The extracellular plasma fluid has a low pH wherein the H+ concentration is high and the bicarbonate level is low.
Just as in metabolic alkalosis, metabolic acidosis engages first the body’s acid-base second to second chemical buffering system, and if more assistance is required it turns to the minute by minute buffering ability of the lungs. So here we see a compensatory rise in breath rate as the body says “hey, I’ve got to get rid of some of this acid so let’s blow off some CO2”. But you will recall that the lungs are only good for about 50-75% of the job at which point the kidneys will engage.
So first clue to metabolic acidosis is a rise in breath rate.
Recall normal breath rate is at about 14 breaths per minute. When you start moving much above this start looking at the urine and saliva pH pattern. Here we are blowing off CO2 – so low CO2 means low carbonic acid which means a rise in saliva pH.
Now what are the kidneys up to…
The kidneys will dump as much H+ as they can, and it will be going out with ammonium ions (NH4+). Sodium ions are conserved in this process. The rate of ammonium secretion depends on the pH of the urine and the duration of the acidosis. pH is the independent variable, ammonium is the dependent variable , i.e. NH4+ going out depends on urine pH value and how long acidosis as been around.
If pH is lowered, ammonium output increases, if urine pH is raised, ammonium decreases. The magnitude of the response depends on the duration of acidosis. If the duration has been severe, more ammonium will be excreted at a given pH.
An example from Davenport’s text The ABC of Acid Base Chemistry :
A normal man excretes 30 millimoles of ammonium a day when his urine pH is 5, but he may excrete 200 millimoles a day at the same pH if he has had severe metabolic acidosis for two or three days. However, if something is done to raise his urine pH abruptly to 7.5, his ammonium excretion drops to zero, just as it would if he were normal.
Recall also the need for electric neutrality. H+ goes out, Cl- (chloride) goes out. Anions and cations going out together. But if an anion goes out, an anion is held back. So here we see chloride going out (an acidifying anion which is what the body wants to get rid of) and a reciprocal anion will be held back which is bicarbonate.
Recall also the preference of the kidneys to hang onto sodium, so here as H+ goes out as well as the ammonium ions as mentioned earlier the sodium is conserved. Sodium in fact can move into the intracellular compartment along with H+ while potassium moves out. This increases serum potassium with a concurrent decrease of potassium in saliva and urine as well as decreased extracellular plasma fluid volume.
With metabolic acidosis there arises a dissolution of cellular phosphorous and that phosphorous is lost in the urine with concurrent lowering of phosphorous in the cells, blood and saliva.
The pH pattern for metabolic acidosis is a high saliva pH and low urine pH with a concurrent high breath rate (low breath hold) which puts the pH pattern into context for an acidosis situation. An increased pulse will be seen as the oxygen carrying capacity of the blood is reduced, and when standing from a supine position you will get a large pulse rate jump. There could be a cold sweat to the palms and a dry mouth. Urine output will be decreased.
Now as we had seen with metabolic alkalosis, a loss of potassium could occur resulting in a further manifestation of the alkaline situation leading to potassium depletion alkalosis. The same can occur with metabolic acidosis only in reverse – a potassium excess acidosis.
Remember that the kidneys want to preferentially hang onto sodium. In metabolic acidosis the kidneys are releasing the acid, H+, which is desired, but if potassium increases in serum, the kidneys can shift to exchanging the potassium for the sodium instead of H+ and the H+ backs up and is retained allowing the body fluids to become even more acid.
Dietary intake of excess potassium can engage the kidney to let it go but as in this case it is over the benefit of releasing H+. Also, the cells themselves have buffering action by taking in the H+ and releasing K+ leaving the serum K+ high as previously mentioned.
The same effects are here as seen in metabolic acidosis: a decreased extracellular plasma fluid volume and a dissolution of cellular phosphorous with concurrent lowering of phosphorous in the cells, blood and saliva and the phosphorous will show up in the urine at increased levels – until it has been depleted.
Renal complications can occur (called renal acidosis) in association with the adrenal’s aldosterone production (which regulates the removal of both sodium and potassium) and if this adrenal insufficiency exists potassium retention will increase leaving less going out the urine but in turn increasing the release of sodium and chloride while decreasing their retention. This renal complication will see phosphorous being retained as opposed to excreted, thereby increasing blood and saliva phosphorous.
What’s the pattern for potassium excess or renal acidosis?
The urine will be alkaline due to decreased H+ excretion but the saliva can be variable. It could be high as with metabolic acidosis due to low CO2 as lungs compensating actions result in less carbonic acid in the saliva, but with the accumulation of organic acids the saliva pH can become depressed. Breath rate will be increased with short breath hold, pulse can be increased but if adrenal insufficiency then it can be lower. A big jump in pulse will be seen and when standing from a supine position. There will be a dry mouth and low urine output. Decreased O2 carrying capacity in the blood.
Maybe there’s a little bit more to this acid/base stuff and overall health than telling people the cause of their problem is too much acid and all they need to do is alkalize.