6 - Acid Base Regulation by the Kidney II

Question 1

What are the important laboratory values we will see?

Answer 1

• Arterial PCO2
• Arterial pH
• Arterial bicarbonate
• Urinary titratable acid
• Urinary ammonium ion
• Anion gap
• Base excess/deficit (delta base)

Question 2

How do we measure the arterial PCO2?

Answer 2

• measured with a CO2 electrode

- 40 Torr (40 mmHg) considered normal

Question 3

How do we measure the arterial pH?

Answer 3

• measured with a pH electrode

- pH 7.35 - 7.45 considered normal

Question 4

How do we measure arterial bicarbonate?

Answer 4

• typically CALCULATED (not measured) from the concentration of CO2 and the pH
• 24 mmol/L (24 mEq/L) considered normal

It CAN however be measured directly…

• gives total CO2
• sum of dissolved CO2 (~ 1.2 mmol/L) and bicarbonate (~24 mmol/L)

Question 5

How do we determine urinary titratable acid?

Answer 5

• titrate a 24 hr urine collection back to pH 7.4 using standard NaOH solution
• 0 - 20 mmol/day considered normal
• up to 40 mmol/day in acidosis
• may be much higher in ketoacidosis or other conditions where urinary buffers other than phosphate present

Question 6

How do we determine urinary ammonium ion?

Answer 6

• measured chemically, enzymatically, or by ion-specific electrode
• 20 - 40 mEq/day considered normal
• up to 250 mEq/day during an acidosis

Question 7

How do you calculate the anion gap?

Answer 7

[Na+]plasma - ([HCO3-]plasma + [Cl-]plasma)

8 - 12 mEq/L typically accepted as normal

Note: note that K+ is sometimes used in calculation and will alter the normal range

Example:
Na+ 140 mEq/L, Cl– 106 mEq/L, HCO3– 14 mEq/L

Anion gap = 20 mEq/L

Question 8

What does a large anion gap mean?

Answer 8

• large anion gap often observed in metabolic acidosis
• production or ingestion of fixed acid
• conjugate base of acid is an unmeasured anion

Question 9

Describe the measurement of base excess or deficit (delta base)

Answer 9

• largely historical but may come across the term (NOT used clinically)
• difference between measured [HCO3-] and [HCO3-] predicted by the normal buffer slope at that pH
• Would be reported as “Metabolic acidosis with a base deficit of 12 mM”

Question 10

Describe the acid-base imbalance of respiratory acidosis

Answer 10

• pH of blood decreased due to increased PCO2

- ↑ PCO2 results in ↑H2CO3, dissociation yields ↑ H+

Question 11

Describe the recovery of respiratory acidosis

Answer 11

• Recovery requires restoration of normal ventilation but kidney can compensate
• renal compensation requires 5 - 6 days

Question 12

Describe the difference between acute and chronic respiratory acidosis

Answer 12

The fact that renal compensation takes 5-6 days allows us to differentiate between acute and chronic

Allows distinction between acute (uncompensated by kidney) respiratory acidosis and chronic (compensated by kidney) respiratory acidosis

Question 13

What are causes of ACUTE respiratory acidosis?

Answer 13

• severe asthma
• severe pneumonia
• aspiration of foreign body
• drugs that depress respiratory drive
• etc.

Question 14

What are causes of CHRONIC respiratory acidosis?

Answer 14

• emphysema
• chronic bronchitis
• etc.

Question 15

Describe the processes occurring in the body during an ACUTE respiratory acidosis

Answer 15

• [HCO3-] slightly increased and remains on normal buffer slope
• buffering by other blood buffers (hemoglobin) in response to increased [H+]
• ~ 0.1 mmol/L increase in [HCO3-] for every 1 Torr increase in PCO2 (not a lot)

Stays on the normal buffer slope ***

Question 16

Describe the processes occurring in the body during a CHRONIC respiratory acidosis

Answer 16

• increased [H+] stimulates H+ excretion by renal tubule cells
• all filtered HCO3- reabsorbed
• excretion of H2PO4- and NH4+ increases (new HCO3- added to plasma)
• increase in PCO2 partially offset by increase in [HCO3-]
• ~0.35 mmol/L increase in [HCO3-] for every 1 Torr increase in PCO2

The numbers aren’t important, just realize that the kidney is having a LARGER effect in chronic

Question 17

Describe the acid-base imbalance that occurs in respiratory alkalosis

Answer 17

• Decreased PCO2 (hyperventilation)

- pH of blood increased

Question 18

How can we distinguish between acute and chronic conditions?

Answer 18

Slow renal compensation allows distinction between acute (uncompensated by the kidney) and chronic (compensated by the kidney) conditions

Question 19

Describe the causes of an ACUTE respiratory alkalosis

Answer 19

Causes include fear, anxiety, trauma, salicylate intoxication

[HCO3-] decreases slightly due to buffering

Question 20

Describe the causes of a CHRONIC respiratory alkalosis

Answer 20

Causes include mechanical hyperventilation, many cardiopulmonary disorders (early/intermediate stages)

Question 21

Describe the compensation seen in chronic respiratory alkalosis

Answer 21

• increase in pH decreases secretion of H+ by renal tubular cells
• lack of H+ secretion prevents complete reabsorption of HCO3-
• HCO3- lost in urine

Also…

• B-type intercalated cells of collecting tubule
• actively secrete HCO3- into filtrate

Question 22

Describe the acid-base imbalance seen in a metabolic acidosis

Answer 22

Metabolic acidosis produces a BASE DEFICIT

- decrease in plasma [HCO3-]

Question 23

Describe the causes of base deficit seen in metabolic acidosis

Answer 23

HIGH USE of HCO3- in buffering reactions

• inability to excrete normal daily acid load
• increase in acid load e.g. diabetic ketoacidosis

LOSS of HCO3- from body
- diarrhea

Question 24

Describe the high anion gap seen in metabolic acidosis

Answer 24

Increased acid load

• HCO3- consumed by buffering reactions
• Anions (e.g. acetoacetate, lactate) accumulate in ECF

Rapid respiratory response
- hyperventilation decreases PCO2 and increases pH

Renal response

• reabsorption of all filtered HCO3-
• increased titratable acid and ammonia excretion

Question 25

Describe the hyperchloremic state of metabolic acidosis

Answer 25

NO ANION GAP ***

Occurs with gastrointestinal or renal loss of HCO3-

• Kidney retains NaCl to maintain extracellular volume
• Net exchange of HCO3- for Cl-

Yields reciprocal changes in [HCO3-] and [Cl-]

• Sum of [HCO3-] and [Cl-] remains constant
• No anion gap

This is one of the reasons clinicians check the anion gap - to see if the kidney is retaining NaCl

Question 26

Describe the acid-base imbalance that occurs in metabolic alkalosis

Answer 26

Metabolic alkalosis produces a base excess ***

Question 27

How does a metabolic alkalosis occur?

Answer 27

Loss of protons from the body

• vomiting, nasogastric suction
• proton replacement by body involves generation of bicarbonate

Volume contraction

• water and NaCl lost through diuretic use but AMOUNT of HCO3- unchanged
• so, CONCENTRATION of HCO3- increased
• aldosterone can do this

Question 28

Describe how aldosterone release can lead to volume contraction and interfere with acid-base control

Answer 28

• aldosterone release promotes Na+ reabsorption and H+ secretion
• increased H+ secretion increase HCO3- reabsorption and secretion of acid urine
• interferes with effective compensation for alkalosis

Question 29

Describe the compensation we see in metabolic alkalosis

Answer 29

Decreased ventilation
- This leads to increased PCO2, decreased pH

Decreased HCO3- reabsorption, active HCO3- secretion by B-type intercalating cells of collecting duct

Question 30

Describe the effect of accidental ingestion of excess antacids (Tums)

Answer 30

Surprisingly common cause of metabolic alkalosis

Take 10 packs of tums/day for heartburn, become alkalotic

Question 31

Describe “combined acidosis”

Answer 31

Patient with respiratory difficulties and renal failure

• cannot effectively ‘blow off’ CO2
• the number of functioning nephrons insufficient to cope with net acid production

Question 32

Describe “combined alkalosis”

Answer 32

A patient receiving mechanical ventilation and nasogastric suction

• hyperventilation decreases PCO2
• removal of gastric acid

Question 33

Describe respiratory acidosis with metabolic alkalosis

Answer 33

Patient with chronic lung disease who is undergoing diuretic therapy

• cannot effectively ‘blow off’ CO2
• volume contraction

Question 34

Describe metabolic acidosis with respriatory alkalosis

Answer 34

Salicylate intoxication

Salicylates stimulate respiratory center
- respiratory alkalosis

Salicylates inhibit various metabolic processes

• increased lactate and ketone body production
• may produce renal insufficiency
• leads to metabolic acidosis

Question 35

Give an example of a triple acid-base disturbance

Answer 35

Patient with metabolic acidosis due to alcoholic ketoacidosis

• vomiting may lead to metabolic alkalosis
• hyperventilation of alcohol withdrawal may produce respiratory alkalosis