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Unit Five: The Body Fluids and Kidneys Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

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Page 1: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Unit Five: The Body Fluids and Kidneys

Chapter 30: Acid-Base Regulation

Guyton and Hall, Textbook of Medical Physiology, 12th edition

Page 2: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Acid-Base Regulation

• Hydrogen Ion Concentration is Precisely Regulated

• Acid- molecules that release H+ in solution

• Base- ion or molecule that can accept an H+

• Alkali- formed by the combination of one or more of the alkali metals (i.e. Na) with a highly basicion (i.e. OH); the base portion reacts quickly with hydrogen ions and remove them fromsolution---therefore they act as bases

Page 3: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Acid-Base Regulation

• Strong Acid- one that rapidly dissociates and releases large amounts of H+ in solution

• Strong Base- one that reacts rapidly and stronglywith H+ and quickly removes them fromsolution

Page 4: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Acid-Base Regulation

The normal H+ concentration is 40nEq/L(0.00000004); therefore, the normal pH is

Page 5: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Acid-Base Regulation

H+ Concentration pH

ECF

Arterial Blood 4.0 x 10-5 7.40

Venous blood 4.5 x 10-5 7.35

Interstitial Fluid

4.5 x 10-5 7.35

Intracellular Fluid 1 x 10-3 to 4 x 10-5 6.0-7.4

Urine 3 x 10-2 to 1 x 10-5 4.5-8.0

Gastric HCl 160 0.8

Table 30.1 pH and Hydrogen Ion Concentration of Body Fluids

Page 6: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Defending Against Changes in H+

• Three primary systems regulate H+ concentrationto prevent acidosis or alkalosis

a. Chemical acid-base buffer systems of body fluids(1st line of defense)

b. The respiratory center which regulates the removal of CO2 and therefore H2CO3 (2nd line of defense)

c. The kidneys which can excrete either acid oralkaline urine

Page 7: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Bicarbonate Buffer System

• Consists of (1) a weak acid and (2) a bicarbonate salt

Page 8: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Bicarbonate Buffer System

Fig. 30.1 Titration curve for bicarbonate buffer system

Page 9: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Phosphate Buffer System

• Addition of a Strong Acid

•Addition of a Strong Base

Page 10: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Phosphate Buffer System

• Role of Phosphate Buffer

a. Relatively insignificant as an extracellular buffer

b. Important in the tubular fluids of the kidney

1. Phosphate becomes greatly concentrated inthe tubules

2. Tubular fluid usually has a considerably lower pH than extracellular fluid

c. Important in intracellular fluid because of thephosphate concentration

Page 11: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Proteins As Important Intracellular Buffers

• Proteins are the most plentiful buffer due to highconcentrations inside cells

• In the rbc, hemoglobin is an important buffer

• Approximately 60-70% of the total chemical buffering of body fluids is inside the cells,and most of this comes from intracellularproteins

Page 12: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Respiratory Regulation of Acid-Base Balance

• Pulmonary Expiration of CO2 Balances MetabolicFormation of CO2

• Increasing Alveolar Ventilation Decreases Extracellular Fluid H+ Concentration and Raises pH

Page 13: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Fig. 30.2 Change in ECF pH caused by increased or decreased rate of alveolar ventilation, expressed as times normal

Page 14: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Fig. 30.3 Effect of blood pH on the rate of alveolar ventilation

Respiratory Regulation (cont.)

• Increased H+ Concentration Stimulates

Alveolar Ventilation

Page 15: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Respiratory Regulation (cont.)

• Feedback Control of H+ Concentration By the

Respiratory System (Negative Feedback)

a. Increased H+ concentration stimulates respiration

b. Increased alveolar ventilation decreases H+ concentration

• Efficiency of Respiratory Control of H+ Concentration- cannot return the

concentrationback to normal when a disturbance outside the respiratory system has altered the pH

Page 16: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Respiratory Regulation (cont.)

• Buffering Power of the Respiratory System

a. Acts as a physiologic type of buffering system

• Impairment of Lung Function Can CauseRespiratory Acidosis

Page 17: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• Secretion of H+ and Reabsorption of HCO3

- Bythe Renal Tubules

30.4 Reabsorption of bicarbonate in different segments of the renal tubule

Page 18: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• H+ is Secreted by Secondary Active Transport in

the Early Tubular Segments

30.5 Cellular mechanisms for (1)active secretion of hydrogen ions into the renal tubule, (2) tubular reabsorption of bicarbonate by formation of carbonic acid, and (3) sodium ion reabsorption in exchange for hydrogen ion secretion

Page 19: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• Filtered HCO3 is Reabsorbed by Interaction with

H+ in the Tubules

a. Each time an hydrogen ion is formed in thetubular epithelium, an HCO3 is also formedand released back into the blood

b. HCO3 is “titrated” against H+ in the tubules

Page 20: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• Primary Active Secretion of H+ in the Intercalated

Cells of Late Distal and Collecting Tubules

Fig. 30.6 Primary active secretion of H ion through the membrane of the intercalated cells

Page 21: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• Phosphate Buffer System Carries Excess H+ into

the Urine and Generates New HCO3

Fig. 30.7

Page 22: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Control of Acid-Base Balance

• Excretion of Excess H+ and Generation of New

HCO3 by the Ammonia Buffer System

Fig. 30.8 Production and secretion of ammonium ion by the proximal tubular cells

Fig. 30.9 Buffering of the hydrogen ion secretion by ammonia in the collecting tubules

Page 23: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Quantifying Renal Acid-Base Excretion

• Bicarbonate excretion is calculate as the urine

flow rate multiplied by urinary HCO3

concentration

• The amount of new HCO3 contributed to the blood

at any given time is equal to the amount of H+

secreted that ends up in the tubular lumen

• The rest of the non-bicarbonate, non-ammmonia

buffer excreted is measured by determining a

value known as titratable acid

Page 24: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Quantifying Renal Acid-Base Excretion

• Regulation of Renal Tubular H+ Secretion

Increase H+ Secretion andHCO3 Reabsorption

Decrease H+ Secretion and HCO3 Reabsorption

Increase PCO2 Decrease PCO2

Increase H+ Decrease HCO3 Decrease H+ Increase HCO3

Decrease ECF volume Increase ECF volume

Increase Angiotensin II Decrease Angiotensin II

Increase Aldosterone Decrease Aldosterone

Hypokalemia Hyperkalemia

Page 25: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Correction of Acidosis

• Acidosis Decreases the ration of HCO3/H+

in Renal Tubular Fluid

a. In metabolic acidosis, an excess of H+ overHCO3 occurs in the tubular fluid primarilybecause of decreased filtration of HCO3

b. There is also a decrease in pH and a rise inECF H+ concentration

Page 26: Chapter 30: Acid-Base Regulation Guyton and Hall, Textbook of Medical Physiology, 12 th edition

Renal Correction of Alkalosis

• Alkalosis Increases the Ratio of HCO3/H+ inRenal Tubular Fluid

pH H+ PCO2 HCO3

Normal 7.4 40 mEq/L 40 mm Hg

24 mEq/L

RespiratoryAcidosis

RespiratoryAlkalosis

MetabolicAcidosis

Metabolic Alkalosis

Table. 30.3 Characteristics of Primary Acid-Base Disturbance

The primary event is indicated by the double arrows. Respiratory acid-base disorders are initiatedBy an increase or decrease in PCO2; metabolic disorders are initiated by an increase or decrease in HCO3