6 - Acid Base Regulation by the Kidney II Flashcards
What are the important laboratory values we will see?
- Arterial PCO2
- Arterial pH
- Arterial bicarbonate
- Urinary titratable acid
- Urinary ammonium ion
- Anion gap
- Base excess/deficit (delta base)
How do we measure the arterial PCO2?
- measured with a CO2 electrode
- 40 Torr (40 mmHg) considered normal
How do we measure the arterial pH?
- measured with a pH electrode
- pH 7.35 - 7.45 considered normal
How do we measure arterial bicarbonate?
- 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)
How do we determine urinary titratable acid?
- 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
How do we determine urinary ammonium ion?
- measured chemically, enzymatically, or by ion-specific electrode
- 20 - 40 mEq/day considered normal
- up to 250 mEq/day during an acidosis
How do you calculate the anion gap?
[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
What does a large anion gap mean?
- large anion gap often observed in metabolic acidosis
- production or ingestion of fixed acid
- conjugate base of acid is an unmeasured anion
Describe the measurement of base excess or deficit (delta base)
- 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”
Describe the acid-base imbalance of respiratory acidosis
- pH of blood decreased due to increased PCO2
- ↑ PCO2 results in ↑H2CO3, dissociation yields ↑ H+
Describe the recovery of respiratory acidosis
- Recovery requires restoration of normal ventilation but kidney can compensate
- renal compensation requires 5 - 6 days
Describe the difference between acute and chronic respiratory acidosis
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
What are causes of ACUTE respiratory acidosis?
- severe asthma
- severe pneumonia
- aspiration of foreign body
- drugs that depress respiratory drive
- etc.
What are causes of CHRONIC respiratory acidosis?
- emphysema
- chronic bronchitis
- etc.
Describe the processes occurring in the body during an ACUTE respiratory acidosis
- [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 ***
Describe the processes occurring in the body during a CHRONIC respiratory acidosis
- 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
Describe the acid-base imbalance that occurs in respiratory alkalosis
- Decreased PCO2 (hyperventilation)
- pH of blood increased
How can we distinguish between acute and chronic conditions?
Slow renal compensation allows distinction between acute (uncompensated by the kidney) and chronic (compensated by the kidney) conditions
Describe the causes of an ACUTE respiratory alkalosis
Causes include fear, anxiety, trauma, salicylate intoxication
[HCO3-] decreases slightly due to buffering
Describe the causes of a CHRONIC respiratory alkalosis
Causes include mechanical hyperventilation, many cardiopulmonary disorders (early/intermediate stages)
Describe the compensation seen in chronic respiratory alkalosis
- 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
Describe the acid-base imbalance seen in a metabolic acidosis
Metabolic acidosis produces a BASE DEFICIT
- decrease in plasma [HCO3-]
Describe the causes of base deficit seen in metabolic acidosis
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
Describe the high anion gap seen in metabolic acidosis
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
Describe the hyperchloremic state of metabolic acidosis
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
Describe the acid-base imbalance that occurs in metabolic alkalosis
Metabolic alkalosis produces a base excess ***
How does a metabolic alkalosis occur?
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
Describe how aldosterone release can lead to volume contraction and interfere with acid-base control
- 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
Describe the compensation we see in metabolic alkalosis
Decreased ventilation
- This leads to increased PCO2, decreased pH
Decreased HCO3- reabsorption, active HCO3- secretion by B-type intercalating cells of collecting duct
Describe the effect of accidental ingestion of excess antacids (Tums)
Surprisingly common cause of metabolic alkalosis
Take 10 packs of tums/day for heartburn, become alkalotic
Describe “combined acidosis”
Patient with respiratory difficulties and renal failure
- cannot effectively ‘blow off’ CO2
- the number of functioning nephrons insufficient to cope with net acid production
Describe “combined alkalosis”
A patient receiving mechanical ventilation and nasogastric suction
- hyperventilation decreases PCO2
- removal of gastric acid
Describe respiratory acidosis with metabolic alkalosis
Patient with chronic lung disease who is undergoing diuretic therapy
- cannot effectively ‘blow off’ CO2
- volume contraction
Describe metabolic acidosis with respriatory alkalosis
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
Give an example of a triple acid-base disturbance
Patient with metabolic acidosis due to alcoholic ketoacidosis
- vomiting may lead to metabolic alkalosis
- hyperventilation of alcohol withdrawal may produce respiratory alkalosis
