Acid Base Balance Flashcards
What pH indicates alkalemia and acidemia?
Alkalemia: >7.42
Acidemia: <7.38
What is one danger of having an alkaline plasma?
since calcium is only soluble in acidic solutions, hypocalcemia can result in abnormal muscle firings producing twitches and tetany
What can happen to the heart in acidemia?
Acidic conditions means there is an increase in H+ which will want to enter the cell. The only way to move H+ into the cell is to transport K+ out, and increasing K+ means pacemaker cells will repolarise too quickly = causing an arrhythmia
What does plasma pH depend on? Which 2 organs are responsible for maintaining this balance?
The ratio of [HCO3-] to dissolved CO2, the ratio should be 20:1. This ratio is controlled by the lungs and the kidneys
What can the kidneys compensate and correct for?
What can ventilation compensate and correct for?
Kidneys compensate for a respiratory pH imbalance and correct for a metabolic pH imbalance
Ventilation will compensate for a metabolic pH imbalance and correct for a ventilation pH imbalance
How does metabolic acidosis occur? How does the body compensate AND correct for this?
- Tissues produce acid metabolically, which enters the blood and dissociates into H+ and an anion
- H+ reacts with HCO3- in the capillaries to produce CO2 and water
- CO2 travels back to the lungs and is lost
Therefore, for every mole of H+, you lose one mole of HCO3- and the net effect is acidic. The body has 2 options…
Correct: kidneys will reabsorb/make more HCO3-
Compensate: Ventilation increases to eliminate more CO2
How does metabolic alkalosis occur? How can you partially compensate for this?
HCO3- is produced as a byproduct of creating acid in the stomach and immediately travels into the bloodstream. Normally it can recombine with H+ in the duodenum and neutralize, BUT if you’re vomiting up H+ it never makes it to the duodenum and there’s nothing to neutralize the HCO3- in the blood
Can only partially compensate as you can’t decrease ventilation without putting the patient at risk of hypoxia
How do the kidneys replace lost HCO3- in the PCT? List both ways
- In the PCT the kidneys can metabolize amino acids (N containing compounds):
Glutamine gets broken down to produce alpha-ketoglutarate which makes HCO3- and NH4 (ammonia), ammonia reacts with H+ to make ammonium and neutralize the pee - Na combines with HCO3- in the filtrate, NaHCO3- dissociates into Na and HCO3- :
The HCO3- combines with H+ in the filtrate to form H20 and CO2, which diffuses across the luminal membrane and reforms H+ and HCO3-
The Na+ enters the Na/H+ exchanger and is resorbed into the cell and helps drive H+ movement into the filtrate
How do the kidneys replace lost HCO3- in the alpha intercalated cells of the DCT?
Since the kidneys are highly metabolic they produce large quantities of CO2: CO2 reacts with water to produce
- HCO3- enters the plasma
- H+ which goes into the urine via 2 pumps: the H+ ATPase and the H+-K+ exchanger which uses K+ excreted by the principal cells via ROMK
Once in the filtrate H+ binds with phosphate or ammonia and is excreted
Where is HCO3- recovered in the nephron?
80-90% is recovered in the PCT and the rest in the LOH
What must the body do in general to compensate for lost HCO3-?
It must be replaced by another anion, so acids that are produced metabolically dissociate into an H+ and an anion; e.g; ketones, lactate, etc
In summary, give 3 cellular responses in the kidney to acidosis
- enhanced Na/H exchange so more HCO3- gets recovered from the filtrate in the PCT and LOH
- Enhanced ammonium production in the PCT
- Increased activity of H+ ATPase in DCT
Why can’t excretion of H+ from the DCT use the Na gradient like the rest of the nephron?
Because most HCO3 has been reabsorbed by the time it reaches the DCT so there’s no dissociation of NaHCO3- into Na and HCO3-. Therefore Na cannot be used in the sodium hydrogen exchanger and the H+ cannot be exported to the lumen, therefore you need active secretion of H+ ions
What does the anion gap account for?
Determines whether HCO3- has been replaced by an anion other than Cl- by measuring the difference between anions and cations: [Na+] + [K+] – [Cl-] + [HCO3-]
What does it mean if the anion gap is high? Name 3 examples of when this could occur and explain one in detail
Means the unmeasured anions account for a greater proportion of the serum’s (-) charge than usual
E.g; lactic acidosis, diabetic ketoacidosis, methanol poisoning
Lactic acidosis: H+ and the anion lactate increase in the plasma, excess H+ is buffered by HCO3- to form CO2 and H2O - lowering the HCO3- levels in the plasma: SO there’s more lactate and less HCO3-
What is meant by a normal anion gap?
Means the patient’s HCO3-, Cl-, Na+ and K+ levels are all normal
What could it mean if there’s low HCO3- and an increased anion gap?
What does it mean if there’s low HCO3- and a normal anion gap?
A high anion gap and low HCO3-: means there’s been acid produced metabolically
If HCO3- is low and there’s a normal anion gap: A normal anion gap indicates there’s no high amounts of metabolic anions, but since HCO3- is STILL low it could mean there’s a renal problem that the kidney has compensated for with Cl-.
Why is it hard for the kidney to correct the pH when someone is excessively vomiting?
That being said, how should you rebalance the pH of a patient who is excessively vomiting?
Normally a rise in intracellular pH means the kidney would secrete more HCO3- and preserve more H+, BUT when someone is excessively vomiting the patient becomes dehydrated and the kidney is preoccupied with retaining solutes and water and is less able to excrete the excessive HCO3-.
In order to treat the patient, you must rehydrate them so the kidney is able to focus on excreting more HCO3-.
What is the normal range of extracellular and intracellular [K+]?
Extracellular: 3.5-5 mmol/L
Intracellular: 130 mmol/L
What is the danger of hypokalemia?
Not enough K+ prolongs the AP/QT interval in pacemaker cells, this can trigger an after depolarisation and cause an arrhythmia; bradycardia
Name 2 medium-long term factors that affect the ECF [K+]
- Ingestion of K+, as 90% of ingested K+ gets resorbed
- K+ loss through the body occurs in the kidneys which is relatively slow, and some K+ is lost in the gut (which increases when you vomit or have diarrhea)
How is ECF [K+] controlled short term?
K+ is quickly moved in and out of cells via different pumps and with the help of insulin
Name 2 pumps that move K+ in and out of cells and how K+ can leave cells without a pump
- Na+/K+ ATPase pump moves K+ into the cell and na+ out to maintain membrane potential
- K+ can leave the cell through the K+/H+ exchanger: when plasma is acidic more H+ enters the cell and is exchanged for K+ and a rise in plasma [K+] means more H+ is exported from the cell and K+ brought in
K+ can also leak out of cells or move out of excitable cells during APs
Where in the nephron is K+ resorbed?
The PCT, LOH and DCT
What 3 things can stimulate K+ excretion?
K+ movement into the lumen is stimulated by:
- High ECF [K+]
- Aldosterone: by increasing Na+ resorption (Na+/K+ ATPase)
- High ECF pH: Body should be excreting more K+ so more H+ is retained
At which part of the DCT is K+ resorbed?
How does the ECF pH influence this resorption?
In the alpha intercalated cells K+ is resorbed in exchange for H+.
This is driven by the pH of the ECF:
- A low ECF pH will mean more H+ is excreted and K+ resorbed
- A high ECF pH will mean more K+ is excreted and more H+ retained
What are the consequences of an acidic or alkaline pH in terms of [K+]?
Acidic pH: means more K+ is excreted and can lead to hyperkalemia
Alkaline pH: less K+ resorbed which can lead to hypokalemia
Why doesn’t the body go into acidosis or hyperkalemia when K+ is ingested?
K+ is absorbed and insulin secreted, moving K+ rapidly into cells preventing hyperkalemia.
Some H+ is excreted via H+/K+ exchanger, but since there’s now extra HCO3- in the blood coming from the stomach (as more acid is synthesized to breakdown the food) it neutralizes the H+.
Why doesn’t the body go into hyperkalemia after lactic acidosis?
Lactic acidosis means H+ will move into cells and K+ into the plasma. Although the ECF [K+] tends to rise, other mechanisms are rapidly excreting H+ from the body, such as:
1. Respiration increases: which lowers pCO2 and H+
2. Kidney exports more H+
(and H+ is neutralized by HCO3- in the plasma)
So soon after, K+ is able to go back into the cells and hyperkalemia doesn’t occur
How does the body avoid hypokalemia when someone is excessively vomiting or has diarrhea? How should you treat this?
The ECF [HCO3-] increases and [H+] falls, so more K+ moves into the cells.
BUT the kidney is also trying to compensate for dehydration by retaining more H+ so it should never fully drop, (and plasma [K+] shouldn’t drop)
Usually correcting the dehydration will sort it all out
What happens to the ECF [K+] in diabetic ketoacidosis?
- No insulin in the body means the cells produce ketones and less K+ enters cells
- The ECF [H+] is also rising (due to ketones), so more H+ will enter the cells and K+ will leave
BUT the ECF [K+] never rises as the kidneys will lose the extra electrolytes in the urine along with extra water that followed the solutes
What are the pros and cons of giving insulin to treat diabetic ketoacidosis?
If you give insulin:
Pro: Move more K+ back into the cells and ketone production will reduce
Con: Since the body has already excreted most of its K+, giving insulin may make the body go into hypokalemia
