This process results in net secretion of H and net reabsorption of newly synthesized HC03

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Lumen Cell Blood

Lumen Cell Blood

Figure 5-19. Mechanism for excretion of H* as titratable acid. CA = carbonic anhydrase.

(3) As a result of H+ secretion, the pH of urine becomes progressively lower. The minimum urinary pH is 4.4.

(4) The amount of H+ excreted as titratable acid is determined by the amount of urinary buffer and the pK of the buffer.

- The amount of H+ excreted as NH4+ depends on both the amount of NH3 synthesized by renal cells and the urine pH.

(1) NH3 is produced in renal cells from glutamine. It diffuses down its concentration gradient from the cells into the lumen.

(2) H+ and HC03" are produced in the cells from C02 and H20. The H+ is secreted into the lumen via an H+-ATPase and combines with NH3 to form NH4+, which is excreted (diffusion trapping). The HCOs- is reabsorbed into the blood ("new" HC03).

(3) The lower the pH of the tubular fluid, the greater the excretion of H+ as NH4+; at low urine pH, there is more NH4+ relative to NH3 in the urine, thus increasing the gradient for NH3 diffusion.

(4) In acidosis, an adaptive increase in NH3 synthesis occurs and aids in the excretion of excess H+.

D. Acid-base disorders (Tables 5-8 and 5-9 and Figure 5-21)

Lumen Cell Blood

Lumen Cell Blood

Figure 5-20. Mechanism for excretion of H* as NIV. CA = carbonic anhydrase.
Table 5-8. Summary of Acid-Base Disorders

Disorder

I (respiratory compensation)

T

Hyperventilation

Renal Compensation t H+ excretion t "new" HC03" reabsorption

Metabolic alkalosis

T (respiratory compensation)

i

t

Hypoventilation

T HC03" excretion

Respiratory acidosis

t

T

T

None

T H+ excretion t HCCV reabsorption

Respiratory alkalosis

*

I

1

None

i H+ excretion 4- HC03" reabsorption

Heavy arrows indicate primary disturbance.

Heavy arrows indicate primary disturbance.

- The expected compensatory responses to simple acid-base disorders can be calculated as shown in Table 5-10. If the actual response equals the calculated (predicted) response, then one acid-base disorder is present. If the actual response differs from the calculated response, then more than one acid-base disorder is present. 1. Metabolic acidosis a. Overproduction or ingestion of fixed acid or loss of base produces an increase in arterial [H+] (acidemia).

b. HC03" is used to buffer the extra fixed acid. As a result, the arterial [HC03~] decreases. This decrease is the primary disturbance.

c. Acidemia causes hyperventilation (Kussmaul breathing), which is the respiratory compensation for metabolic acidosis.

d. Renal compensation for metabolic acidosis consists of increased excretion of the excess fixed H+ as titratable acid and NH4+, and increased reabsorption of "new" HCO:i~, which replenishes the HC03" used in buffering the added fixed H+.

- In chronic metabolic acidosis, an adaptive increase in NH3 synthesis aids in the excretion of excess H+.

e. Serum anion gap = [Na+] - ([CI ] + [HCO,]) [Figure 5-22]

- The serum anion gap represents unmeasured anions in serum. These unmeasured anions include phosphate, citrate, sulfate, and protein.

- The normal value of the serum anion gap is 8 to 16 mEq/L.

- In metabolic acidosis, the serum [HC03~] decreases as it is depleted in buffering fixed acid. For electroneutrality, the concentration of another anion must increase to replace HCOs". That anion can be CI" or an unmeasured anion.

(1) The serum anion gap is increased if the concentration of an unmeasured anion (e.g., phosphate, lactate, 3-hydroxy butyrate, formate) is increased to replace HC03~.

(2) The serum anion gap is normal if the concentration of CI" is increased to replace HC03" (hyperchloremic metabolic acidosis).

Table 5-9. Causes of Acid-Base Disorders

Accumulation of p-OH-butyric acid and acetoacetic acid T anion gap

Accumulation of lactic acid during hypoxia t anion gap

Failure to excrete H+ as titratable acid and NH4+ t anion gap

Also causes respiratory alkalosis T anion gap Produces formic acid T anion gap

Produces glycolic and oxalic acids T anion gap GI loss of HCOs" Normal anion gap Renal loss of HC03" Normal anion gap

Failure to excrete titratable acid and NH4+; failure to acidify urine Normal anion gap

Hypoaldosteronism; failure to excrete NH4+

Hyperkalemia caused by lack of aldosterone Normal anion gap

Metabolic alkalosis

Vomiting

Hyperaldosteronism Loop or thiazide diuretics

Loss of gastric H+; leaves HC03~ behind in blood

Worsened by volume contraction Hypokalemia

May have Î anion gap because of production of ketoacids (starvation) Increased H+ secretion by distal tubule Volume contraction alkalosis

Respiratory acidosis

Opiates; sedatives; anesthetics

Guillain-Barre syndrome; polio; ALS; multiple sclerosis Airway obstruction Adult respiratory distress syndrome; COPD

Inhibition of medullary respiratory center

Weakening of respiratory muscles i C02 exchange in pulmonary capillaries

Respiratory alkalosis

Pneumonia; pulmonary embolus High altitude Psychogenic Salicylate intoxication

Hypoxemia causes Î ventilation rate Hypoxemia causes T ventilation rate

Direct stimulation of medullary respiratory center; also causes metabolic acidosis

ALS = amyotrophic lateral sclerosis; COPD = chronic obstructive pulmonary disease; GI = gastrointestinal; RTA = renal tubular acidosis.

ALS = amyotrophic lateral sclerosis; COPD = chronic obstructive pulmonary disease; GI = gastrointestinal; RTA = renal tubular acidosis.

Example

Metabolic Ketoacidosis acidosis

Lactic acidosis Chronic renal failure

Salicylate intoxication

Methanol/formaldehyde intoxication

Ethylene glycol intoxication

Diarrhea

Type 2 RTA

Type 1 distal RTA

Type 4 RTA

co b o

Figure 5-21. Acid-base map with values for simple acid-base disorders superimposed. The relationships are shown between arterial Pco2, [HC03~], and pH. The ellipse in the center shows the normal range of values. Shaded areas show the range of values associated with simple acid-base disorders. Two shaded areas are shown for each respiratory disorder: one for the acute phase and one for the chronic phase. (Adapted with permission from Cohen JJ, Kassirer JP: Acid/Base. Boston, Little, Brown, 1982.)

2. Metabolic alkalosis a. Loss of fixed H+ or gain of base produces a decrease in arterial [H+] (alkalemia).

b. As a result, arterial [HC03~] increases. This increase is the primary disturbance.

-For example, in vomiting, H+ is lost from the stomach, HC03~ remains behind in the blood, and the [HC03~] increases.

c. Alkalemia causes hypoventilation, which is the respiratory compensation for metabolic alkalosis.

d. Renal compensation for metabolic alkalosis consists of increased excretion of HC03~ because the filtered load of HC03" exceeds the ability of the renal tubule to reabsorb it.

- If metabolic alkalosis is accompanied by ECF volume contraction (e.g., vomiting), the reabsorption of HCO:f increases (secondary to ECF volume contraction), worsening the metabolic alkalosis.

3. Respiratory acidosis

- is caused by a decrease in respiratory rate and retention of C02.

a. Increased arterial Pco2, which is the primary disturbance, causes an increase in [H+] and [HC03"] by mass action.

b. There is no respiratory compensation for respiratory acidosis.

Table 5-10. Calculating Compensatory Responses to Simple Acid-Base Disorders

Acid-Base Disturbance

Metabolic acidosis

Metabolic alkalosis

Respiratory acidosis Acute

Chronic

Respiratory alkalosis Acute

Chronic

Primary Predicted Compensatory

Disturbance Compensation Response

-I Pco2 T Pco2

1 mEq/L decrease in HCO:) —> 1.3 mm Hg decrease in Pc&2

1 mEq/L increase in H CO./ 0.7 mm Hg increase in Pco2

1 mm Hg increase in Pco2 —> 0.1 mEq/L increase in HCO:i

1 mm Hg increase in Pco2 0.4 mEq/L increase in HCO:f

1 mm Hg decrease in Pco2 —> 0.2 mEq/L decrease in HCO:)-

1 mm Hg decrease in Pco2 —> 0.4 mEq/L decrease in HCO;,

Anion gap

HCOg-

Na+

} Unmeasured anions = protein, phosphate, citrate, sulfate

Cations Anions

Figure 5-22. Serum anion gap.

c. Renal compensation consists of increased excretion of H as titrat-able H' and NH.,\ and increased reabsorption of "new" HCO:! . This process is aided by the increased Pco2, which supplies more H' to the renal cells for secretion. The resulting increase in serum fHCO.~] helps to normalize the pH.

- In acute respiratory acidosis, renal compensation has not yet occurred.

- In chronic respiratory acidosis, renal compensation (increased HCO:; reabsorption) has occurred. Thus, arterial pH is increased toward normal (i.e., a compensation).

4. Respiratory alkalosis

- is caused by an increase in respiratory rate and loss of COj.

a. Decreased arterial Pco2, which is the primary disturbance, causes a decrease in [H ] and [HCO:f] by mass action.

b. There is no respiratory compensation for respiratory alkalosis.

c. Renal compensation consists of decreased excretion of H as titrat-able acid and NH,*, and decreased reabsorption of "new" HC03~. This process is aided by the decreased Peo2, which causes a deficit of H* in the renal cells for secretion. The resulting decrease in serum [HCO;f] helps to normalize the pH.

- In acute respiratory alkalosis, renal compensation has not yet occurred.

- In chronic respiratory alkalosis, renal compensation (decreased HCO:i reabsorption) has occurred. Thus, arterial pH is decreased toward normal (i.e., a compensation).

d. Symptoms of hypocalcemia may occur because H' and Ca-" compete for binding sites on plasma proteins. Decreased [ H * J causes increased protein binding of Ca2" and decreased free ionized Ca1'".

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