L11 Classification Of Acid/Base Status

Question 1

The three lines of defense against acid/base disturbances:

Answer 1

Buffers (mainly HCO3-, Hb and phosphate to lesser extent)

Respiratory compensation - adjusts CO2 levels, very fast but usually incomplete; always active when primary problem is metabolic

Renal compensation - adjusts HCO3- levels, slow but potent; compensates for respiratory problems and metabolic problems if they do not involve the kidney

Question 2

What are normal acid/base values?

Answer 2

pH: 7.35-7.45 (mean = 7.40)

Plasma HCO3-: 22-26 mEq/L (mean = 24)

PaCO2: 35-45 mmHg (mean = 40)

Use these average values for all acid/base assessments

Question 3

How would you classify a condition if the patient has:
pH = 7.52
HCO3- = 22
PCO2 = 28

Answer 3

1) It’s an alkalosis (pH > 7.4)
2) There is a respiratory component (PCO2 is less than 35)
3) Expected HCO3- = 22 (PCO2 is 12 mmHg below normal, which will depress [HCO3-] by 2 mEq/L due to mass action)
4) Actual HCO3- = 22, so there is no renal compensation

Result: It’s an uncompensated (pure) respiratory alkalosis

Question 4

How would you classify a patient with
pH = 7.43
HCO3- = 18
PCO2 = 28

Answer 4

The pH is normal, but the other conditions suggest alkalosis

Primary disturbance is respiratory

Expect [HCO3-] = 22. Actual [HCO3-] = 18; therefore, 4 mEq/L HCO3- has been removed from kidneys

Result: this is completely compensated respiratory alkalosis

Question 5

How would you classify a patient with
pH = 7.25
HCO3- = 12
PCO2 = 28

Answer 5

This is an acidosis (pH < 7.4)

There is a respiratory alkalosis; not primary factor (PCO2 < 40)

Expected HCO3- = 22, actual = 12; a primary metabolic acidosis has therefore reduced [HCO3-] by 10 mEq/L

This is a partly compensated metabolic acidosis

Question 6

How would you classify a patient with
pH = 7.30
HCO3- = 25
PCO2 = 52

Answer 6

This is an acidosis (ph < 7.4)

There is a respiratory acidosis factor (PCO2 > 40)

Expected HCO3- = 25 and it is!

Therefore, this is uncompensated (pure) respiratory acidosis

Question 7

Metabolic alkalosis is defined as

Answer 7

H+ loss or HCO3- gain

Typical causes:

• Ingestion of alkali (ie antacids)
• Hyperaldosterone ( ie - Conn syndrome)

ECF volume contraction:
Vomiting (lose HCl, fluid, and K+)
Nasogastric suction (same as above)
Loop or thiazide diurects (lose fluid and K+)

Question 8

ECF volume contraction due to vomiting or extensive use of diuretics can _______ metabolic alkalosis

Answer 8

Maintain

ECF volume contraction increases H+ loss via RAAS:
• Angiotensin II stimulates Na+/H+ antiporter and HCO3- reabsorption
• Aldosterone stimulates secretion of H+ (H+ ATPase) from type A intercalated cells and K+ from principal cells

These factors can maintain alkalosis even when vomiting has stopped. Critical factor is markedly elevated aldosterone.

Question 9

Treatment for metabolic alkalosis

Answer 9

Administer saline (NaCl or KCl)
• Corrects saline-responsive forms of metabolic alkalosis

MOA for the saline:
Correction of fluid volume deficit —> adjusts the RAAS
Results in excretion of bicarbonate

Question 10

What about saline-resistant metabolic alkalosis?

Answer 10

Due to aldosterone excess (secreting tumor)
—> ECF volume is increased, administering saline does not help as the patient is already volume expanded

Excess aldosterone increases H+ secretion and Na+ reabsorption

Example: Conn Syndrome

Treatment: remove tumor, or aldosterone antagonist (spironolactone)

Question 11

What is the definition of metabolic acidosis

Answer 11

Gain of H+ or loss of HCO3-, typically due to ingestion of acids or acid-forming compounds (salicylate, methanol)

HCO3- is lost from the body (ie from diarrhea)

Non-volatile acid accumulation (lactic acid)

Renal HCO3- recovery is reduced, or excretion of titratable acid and NH4+ is reduced

NOTE: some metabolic acidosis are associated with an increase in teh anion gap

Question 12

In the body, the concentration of anions must equal…

Answer 12

The concentration of cations

Major anions: Cl- (100) and HCO3- (24) = 124
Major cations: Na+ = 140

Anion Gap = [Na+] - [Cl-] - [HCO3-]
Normal gap = 8-16 mM

Question 13

Why does the anion gap exist?

Answer 13

Due to the omission of several anions from routine blood chemistry analysis (ie sulphate, phosphate etc). K+ also typically omitted from the anion gap calculations.

Question 14

Anion gap is often normal in acidosis due to …

Answer 14

Simple bicarbonate loss

Cl- increases to meet the drop in HCO3- (maintains the anion balance), ex: diarrhea, RTAs

Question 15

The anion gap _______ in acidosis where there is an excess of other non-volatile (fixed) acids

Answer 15

Increases

Fixed acids liberate H+ which is buffered by HCO3- w/o changing Cl- levels; this increases the anion gap.

Question 16

Disorders that increase the anion gap generate _________ which reduce HCO3- concentrations.

Answer 16

Non-volatile acids (ie lactic acid, oxalic acid)

Anions associated with these acids (lactate, oxalate) take the place of HCO3-; Cl- levels do not change

Question 17

Metabolic acidosis from diminished tubular H+ secretion

Answer 17

Renal Tubular Acidosis (RTA)

Three types:
Type I (distal) - H+ ATPase activity is reduced
Type II (proximal) - Na+/H+ antiporter activity is reduced
Type IV - reduced formation of NH4+, often due to hyperkalemia secondary to aldosterone deficiency; inhibits enzymes that degrade glutamine

Question 18

How does Distal/Type I RTA happen?

Answer 18

Due to impaired H+ secretion by H+ ATPase in the distal nephron, or generalized failure of type A intercalated cells

Presenting symptoms are metabolic acidosis and HYPOkalemia

Anion gap is NORMAL

Question 19

How does Proximal/Type II RTA happen?

Answer 19

Due to defect in Na+/H+ exchanger in the proximal convoluted tubule —> leads to impairment of H+ secretion and bicarbonate recovery (reabsorption)

Several causes (ie - toxins, hereditary conditions etc)

Results in loss of bicarbonate (less H+ in lumen)

Anion gap is NORMAL

Question 20

Which is usually more severe, Type I or Type II RTA?

Answer 20

Type I (distal)

Question 21

Type IV RTA includes several disorders w/ these common features:

Answer 21

• Impaired bicarbonate generation
• Metabolic acidosis
• Hyperkalemia

Defect in urinary acidification due to inhibition of renal glutamine season which impairs formation of NH4+

Correlated w/ aldosterone deficiency —> leads to hyperkalemia (inhibits renal glutaminase)

Anion gap is NORMAL

Question 22

Which type of RTA is correlated with aldosterone deficiency?

Answer 22

Type IV RTA

Question 23

What are some examples of metabolic acidoses with INCREASED anion gap?

Answer 23

Lactic acidosis (due to lactic acid)

Ketoacidosis (ie diabetic - due to acetoacetic acid)

Renal failure (due to accumulation of phosphoric, sulphuric, and other non-volatile metabolic acids)

Salicylate poisoning (aspirin)

Ethylene glycol poisoning (converted to glycolic and oxalic acids)

Methanol poisoning (converted to formic acid)

Question 24

Respiratory alkalosis is due to a …

Answer 24

Decrease in PaCO2 via increased alveolar ventilation

Causes:
High Altitude
Anxiety
Hypoxemia

In some cases, the lack of oxygen leads to increased production of lactic acid, which partially counters the respiratory alkalosis

Question 25

Respiratory acidosis is due to…

Answer 25

Impaired pulmonary excretion of CO2

Chronic respiratory acidosis occurs when alveolar ventilation is reduced by:
Impairment of central respiratory regulation
Chest wall dysfunction
Impaired airway mechanics
Impaired gas exchange

Focus of treatment is to correct underlying ventilators disorder