Chapter 30: Acid-Base Regulation

Guyton and Hall, Textbook of Medical Physiology, 12th 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 basic ion (i.e. OH); the base portion reacts quickly with hydrogen ions and remove them from solution---therefore they act as bases

Acid-Base Regulation

Strong Acid- one that rapidly dissociates and releases large amounts of H+ in solution Strong Base- one that reacts rapidly and strongly with H+ and quickly removes them from solution

Acid-Base Regulation

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

Acid-Base Regulation

Table 30.1 pH and Hydrogen Ion Concentration of Body Fluids

H+ Concentration ECF Arterial Blood Venous blood Interstitial Fluid Intracellular Fluid Urine Gastric HCl 4.0 x 10-5 4.5 x 10-5 4.5 x 10-5 1 x 10-3 to 4 x 10-5 3 x 10-2 to 1 x 10-5 160

pH

7.40 7.35 7.35 6.0-7.4 4.5-8.0 0.8

Defending Against Changes in H+ Three primary systems regulate H+ concentration to prevent acidosis or alkalosis a. Chemical acid-base buffer systems of body fluids (1st line of defense) a. The respiratory center which regulates the removal of CO2 and therefore H2CO3 (2nd line of defense) c. The kidneys which can excrete either acid or alkaline urine

Bicarbonate Buffer System Consists of (1) a weak acid and (2) a bicarbonate salt

Bicarbonate Buffer System

Fig. 30.1 Titration curve for bicarbonate buffer system

Phosphate Buffer System

Addition of a Strong Acid

Addition of a Strong Base

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 in the tubules 2. Tubular fluid usually has a considerably lower pH than extracellular fluid c. Important in intracellular fluid because of the phosphate concentration

Proteins As Important Intracellular Buffers Proteins are the most plentiful buffer due to high concentrations 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 intracellular proteins

Respiratory Regulation of Acid-Base Balance Pulmonary Expiration of CO2 Balances Metabolic Formation of CO2 Increasing Alveolar Ventilation Decreases Extracellular Fluid H+ Concentration and Raises pH

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

Respiratory Regulation (cont.) Increased H+ Concentration Stimulates Alveolar Ventilation

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

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

Respiratory Regulation (cont.) Buffering Power of the Respiratory System a. Acts as a physiologic type of buffering system Impairment of Lung Function Can Cause Respiratory Acidosis

Renal Control of Acid-Base Balance Secretion of H+ and Reabsorption of HCO3- By the Renal Tubules

30.4 Reabsorption of bicarbonate in different segments of the renal tubule

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

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 the tubular epithelium, an HCO3 is also formed and released back into the blood b. HCO3 is titrated against H+ in the tubules

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

Renal Control of Acid-Base Balance Phosphate Buffer System Carries Excess H+ into the Urine and Generates New HCO3

Fig. 30.7

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

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

Quantifying Renal Acid-Base Excretion Regulation of Renal Tubular H+ Secretion

Increase H+ Secretion and HCO3 Reabsorption Increase PCO2 Increase H+ Decrease HCO3

Decrease H+ Secretion and HCO3 Reabsorption Decrease PCO2 Decrease H+ Increase HCO3

Decrease ECF volume Increase Angiotensin II Increase Aldosterone Hypokalemia

Increase ECF volume Decrease Angiotensin II Decrease Aldosterone Hyperkalemia

Renal Correction of Acidosis

Acidosis Decreases the ration of HCO3/H+ in Renal Tubular Fluid

a. In metabolic acidosis, an excess of H+ over HCO3 occurs in the tubular fluid primarily because of decreased filtration of HCO3 b. There is also a decrease in pH and a rise in ECF H+ concentration

Renal Correction of Alkalosis Alkalosis Increases the Ratio of HCO3/H+ in Renal Tubular Fluid
Table. 30.3 Characteristics of Primary Acid-Base Disturbance

pH Normal Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis 7.4

H+ 40 mEq/L

PCO2 40 mm Hg

HCO3 24 mEq/L

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