acid-base balance clinical application

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RENAL MODULE SOLA AOUN BAHOUS Acid-Base Balance: Clinical Application

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Page 1: Acid-Base Balance Clinical Application

RENAL MODULE

SOLA AOUN BAHOUS

Acid-Base Balance: Clinical Application

Page 2: Acid-Base Balance Clinical Application

Learning Objectives

Discuss renal contribution to acid-base maintenance and compensation

Calculate the amount of filtered bicarbonate given the GFR and plasma concentration

Calculate the amount of secreted H+ given GFR, plasma bicarbonate concentration, titratable acidity and urine bicarbonate concentration

Calculate titratable acidity from urinary and plasma parameters

Page 3: Acid-Base Balance Clinical Application

Outline

Quantitation of renal acid-base compensation

Exercises

Page 4: Acid-Base Balance Clinical Application

Outline

Quantitation of renal acid-base compensation

Exercises

Page 5: Acid-Base Balance Clinical Application

Relationship between the arterial pH and [H+] in the physiologic range

pH [H+], nanomol/L

7.80 16

7.70 20

7.60 26

7.50 32

7.40 40

7.30 50

7.20 63

7.10 80

7.00 100

6.90 125

6.80 160

Page 6: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

How much bicarb is excreted?

How much new bicarb is added to the plasma through phosphate buffer?

How much new bicarb is contributed by glutamine?

Page 7: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

How much bicarb is excreted? Ubicarb x V

How much new bicarb is added to the plasma through phosphate? We titrate the urine with NaOH to a pH of 7.4 (plasma pH). The number of milliequivalents of OH-

required to reach this pH must equal the number of milliequivalents of H+ that were added to the tubular fluid. This value is the titratable acid.

How much new bicarb is contributed by glutamine?

UNH4+ x V

wiam
Textbox
mainly this happens in the distal tubule coz bil proximal bikoon we r still returning the hco3-
Page 8: Acid-Base Balance Clinical Application

HCO3- loss = negative

contribution

HCO3- reabsorption

prevents further loss

H+ secretion and binding

to phosphate yields

titratable acidity

H+ excretion in the form of

ammonium contributes to

correction of acidosis

Page 9: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Titratable acid excreted + NH4+ excreted – HCO-

3

excreted = contribution of the kidney to acid-base regulation

Total = net HCO-3 gain or loss

Negative value loss

Positive value gain

Page 10: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Page 11: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

• The glutamine-NH4+ mechanism for new HCO3-

generation becomes the preeminent renal process for opposing the acidosis mainly the 1st few days of an acidosis

• Many inputs exist that affect tubular H+ secretion: PCO2, pH, volume, ionic composition of the plasma, renal sympathetic nerves and many hormones

Page 12: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Renal compensation for respiratory acidosis and alkalosis

Respiratory acidosis CO2 retention and plasma pH

Respiratory alkalosis CO2 loss and plasma pH

Page 13: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

By HCO-3 the acidosis will be compensated

Low pH and high PCO2 stimulate the kidneys to excrete H+ and NH4

+, consequently, blood pH returns toward normal

In respiratory alkalosis the opposite occurs

Page 14: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Renal compensation for metabolic acidosis and alkalosis:

• Metabolic disturbance acid-base disturbance not caused by a primary disturbance in PCO2

• Metabolic acidosis = addition to the body (by ingestion, infusion or production) of increased amounts of any acid other than carbonic acid, or alternatively, the loss from the body of HCO-

3 (as in diarrhea)

• The pH and HCO-3

Page 15: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

The lungs will try to compensate for metabolic acidosis by hyperventilation to decrease PCO2

The kidneys, to compensate, must reabsorb all the HCO-

3 and add new bicarb to the blood through increased formation and excretion of NH4

+ and titratable acid

Page 16: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

The kidneys may be a cause of metabolic acidosis or alkalosis or may fail to compensate for a metabolic disturbance

Page 17: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Page 18: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Factors causing the kidneys to generate or maintain a metabolic alkalosis:

1- extracellular volume contraction:

EC volume contraction stimulates Na+ reabsorption and H+ secretion by stimulating aldosterone secretion, Ang II formation and SNS activity

Page 19: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Aldosterone stimulates luminal H+-ATPase

Renal nerves and Ang II stimulate Na+/H+ antiporter in the proximal tubule

Net result = all the filtered bicarb is reabsorbed and not excreted

Page 20: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

Page 21: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

2- Chloride depletion:

Chloride depletion stimulates H+ secretion and/or inhibits HCO-

3 secretion

Page 22: Acid-Base Balance Clinical Application

Quantitation of renal acid-base compensation

3- Aldosterone excess and K+ depletion:

Excessive diuretic use

ECV contraction

aldosterone secretion

K+ depletion

Creation or maintenance of metabolic alkalosis

Page 23: Acid-Base Balance Clinical Application
Page 24: Acid-Base Balance Clinical Application

Outline

Quantitation of renal acid-base compensation

Exercises

Page 25: Acid-Base Balance Clinical Application

Exercise 1

1. The daily H+ load is excreted in the urine as titratableacidity and NH4

+. Would H+ retention leading to metabolic acidosis occur if there were:

a. A marked reduction in titratable acid excretion, as a result of a decrease in the plasma phosphate concentration?

b. A marked reduction in NH4+ formation?

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Page 26: Acid-Base Balance Clinical Application

Exercise 2

2. Two patients with a normal GFR of 180 L/day are studied, one with normal acid-base balance and one with metabolic acidosis. The following laboratory data were obtained:

Parameter Patient 1 Patient 2

Plasma [HCO3-] 24 meq/L 6 meq/L

Titratable acidity 30 meq/day 75 meq/day

NH4+ excretion 50 meq/day 140 meq/day

Urine pH 5.5 5.0

Page 27: Acid-Base Balance Clinical Application

Exercise 2

Assuming that all the filtered bicarbonate is reabsorbed, calculate:

Net acid excretion in any form

Total H+ secretion

wiam
Callout
30+50 la patient A
wiam
Callout
24*gfr + titratable acid only
Page 28: Acid-Base Balance Clinical Application

Exercises

3. Is NH4+ excretion included in the measurement of

titratable acidity?

4. A patient with persistent vomiting develops metabolic alkalosis as a result of the loss of HCl in gastric juice. Why isn’t the condition corrected spontaneously by excretion of the excess bicarbonate in the urine?

wiam
Callout
no bas l hpo4
wiam
Callout
volume is low so we have reabsorbtion of na secretion of h secretion of k reabsorbtion of bicarb
Page 29: Acid-Base Balance Clinical Application

Exercises 5 and 6

5. The following results were obtained on a patient under normal physiological conditions: plasma HCO-

3 = 22 mmol/L, GFR = 7.5 L/hour, urinary HCO-

3 = 8 mmol/d, titratable acid = 24 mmol/d.

What is the amount of HCO-3 filtered?

a.24 mmol/d

b.180 mmol/d

c.3960 mmol/d

d.4328 mmol/d

e.4340 mmol/d

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3960
wiam
Oval
Page 30: Acid-Base Balance Clinical Application

Exercises 5 and 6

6. What is the total amount of hydrogen ion secreted?

a. 8 mmol/d

b. 24 mmol/d

c. 3312 mmol/d

d. 3976 mmol/d

e. 4339 mmol/d

wiam
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wiam
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gfr thingy - excereted + l titratable
Page 31: Acid-Base Balance Clinical Application

Exercise 7

7. Hypoventilation is associated with which acid-base disturbance?a. Increased plasma pH, increased plasma HCO-

3 , alkaline urine

b. Increased plasma pH, decreased plasma HCO-3 ,

alkaline urinec. Decreased plasma pH, increased plasma HCO-

3 , acidic urine

d. Decreased plasma pH, decreased plasma HCO-3 , acidic

urinee. Decreased plasma pH, decreased plasma HCO-

3 , alkaline urine

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Page 32: Acid-Base Balance Clinical Application

Exercise 8

8. Choose the correct statement describing the reabsorption or the addition of new bicarbonate to the blood.

a. When secreted H+ binds to HCO-3 in the tubular

lumen, addition of new HCO-3 occurs

b. When secreted H+ binds to non HCO-3 buffers in the

tubular lumen, addition of new HCO-3 occurs

c. When NH4+ is produced and excreted, reabsorption of filtered HCO-

3 occurs

d. When H+ binds to phosphate in the tubular lumen, reabsorption of HCO-

3 occurs

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