acid-base
25.5 Acid-Base Balance
Acid-base balance (pH balance) is essential for homeostasis in the body.
Normal pH range: 7.35 to 7.45 (slightly alkaline).
Proper pH balance is critical for various body functions.
Factors altering H+ concentration:
Input of acid and base.
Output of acid and base by the kidneys.
Respiratory rate variations.
Chemical buffers.
25.5a Categories of Acid
1. Relationship of pH and H+ Concentration
The pH is inversely related to H+ concentration.
Adding an acid increases H+ concentration; a base reduces it.
2. Types of Acids in the Body
Fixed Acids:
Non-volatile, metabolic acids.
Produced as waste products from metabolic processes.
Examples include:
Lactic acid from glycolysis.
Phosphoric acid from nucleic acid metabolism.
Ketoacids from fat metabolism.
Regulation occurs primarily by the kidneys.
Volatile Acids:
E.g., Carbonic acid, formed when carbon dioxide combines with water.
This reaction is facilitated by the enzyme carbonic anhydrase.
Called "volatile" because it can evaporate (expired gas).
Regulation is achieved via the respiratory system.
25.5b The Kidneys and Regulation of Fixed Acids
1. Increase in Blood H+ Concentration
Conditions leading to increased blood H+:
Major inputs of acid can occur from:
Nutrients absorbed from the gastrointestinal (GI) tract, particularly in a diet high in animal protein and wheat.
Metabolic waste products such as lactic acid, phosphoric acid, and ketoacids.
Consequence of diarrhea.
Kidneys respond to maintain normal pH:
Reabsorbs all filtered bicarbonate (HCO3−) along the nephron.
Synthesizes and absorbs new bicarbonate.
Excretes H+ into the filtrate.
2. Decrease in Blood H+ Concentration
Conditions leading to decreased blood H+:
Rare occurrences such as antacid ingestion or loss of HCl through vomiting.
Kidney response:
Do not reabsorb all filtered HCO3− throughout the nephron tubule.
Secrete HCO3− from blood into the filtrate.
Reabsorb H+ in exchange.
Role of the kidneys:
Act as a physiological buffering system.
Eliminate excess acid or base, though this process may take several hours to days, making it the most powerful method of pH regulation.
25.5c Respiration and Regulation of Volatile Acid
The respiratory system regulates the level of carbonic acid in the body.
At Rest:
CO2 is eliminated from the lungs at the same rate it is produced.
During Exercise:
Changes in CO2, H+, and O2 levels are detected by chemoreceptors.
Signals are relayed to the respiration center to alter breathing rates.
Key variable:
CO2 is the most significant factor influencing respiratory changes.
Carbonic acid levels are dependent on CO2 levels, and fluctuations are typically stable, thus not usually impacting acid-base balance.
25.5d Chemical Buffers
1. Function of Chemical Buffers
Chemical buffering systems act within minutes to provide temporary prevention of pH changes.
Systems are composed of one or two types of molecules capable of binding and releasing H+ ions very rapidly.
Composition:
Involves a weak acid and a weak base.
A weak base can bind excess H+, while a weak acid can release H+.
Known for their temporary and limited action until more permanent physiological buffering systems take over.
2. Types of Chemical Buffering Systems
Three primary systems in the body:
Protein Buffering System:
Found within cells and blood.
Accounts for approximately 75% of the chemical buffering in body fluids.
Involves intracellular protein, plasma proteins, and hemoglobin.
Helps to minimize pH changes.
Amine groups act as weak bases, while carboxylic acids act as weak acids.
Phosphate Buffering System:
Located in intracellular fluid (ICF).
Efficient in buffering metabolic acids produced by cells.
Composed of weak base (hydrogen phosphate, HPO₄²⁻) and weak acid (dihydrogen phosphate, H₂PO₄⁻).
Buffering results in strong acids producing weak acids and strong bases producing weak bases.
Bicarbonate Buffering System:
The most significant buffering system in extracellular fluid (ECF).
Composed of weak base (bicarbonate, HCO₃⁻) and weak acid (carbonic acid, H₂CO₃).
Operates similarly to the phosphate system regarding strong acid/base interactions.
3. Buffering Capacity
Chemical buffering systems have limited capacities to balance excess acid or base, which necessitates the involvement of physiological systems over time.
Section 25.5 Review Questions
Define acid-base balance in the body.
What distinguishes fixed acids from volatile acids?
Explain how the kidneys regulate fixed acids to maintain blood pH when blood H+ concentration rises.
Discuss the reasons respiration typically does not influence acid-base balance.
Name the three chemical buffering systems and their locations.
Outline the relative time required for maintaining pH by chemical buffering systems, respiratory adjustments, and renal function.
25.6a Overview of Acid-Base Disturbances
Acidosis: A condition where arterial blood pH falls below 7.35.
Alkalosis: Arterial blood pH rising above 7.45.
Acid-base disturbances occur when the buffering capacity is exceeded.
Transient changes in H+ lead to significant pH changes beyond normal ranges.
25.6b Respiratory-Induced Acid-Base Disturbances
1. Respiratory Acidosis
Most prevalent type of acid-base disturbance.
Results from impaired CO2 elimination by the respiratory system, leading to
Elevation of arterial blood PCO2 above 45 mm Hg.
Increased H+ levels, influencing blood pH.
At-Risk Population: Infants due to smaller lung capacity.
Causes include:
Hypoventilation caused by trauma or infection affecting the respiratory center.
Respiratory muscle or nerve disorders.
Airway obstructions (asthma, bronchitis).
Impaired pulmonary gas exchange (e.g., emphysema, pneumonia).
2. Respiratory Alkalosis
Occurs when PCO2 levels fall below 35 mm Hg due to hyperventilation.
Reduced H+ concentration, indicating alkaline blood conditions.
Causes include:
Severe anxiety.
Hypoxia relating to altitude, congestive heart failure, or severe anemia.
Aspirin overdose which stimulates increased respiratory activity.
25.6c Metabolic-Induced Acid-Base Disturbances
1. Metabolic Acidosis
Characterized by loss of bicarbonate (HCO3−) or gain of H+.
More frequently arises from excess H+.
Levels drop below 22 mEq/L.
At-Risk Population: Infants who generate more acidic metabolic waste.
Causes include:
Production of more fixed acids, such as ketoacidosis, lactic acid accumulation, or acetic acid from alcohol metabolism.
Decreased renal elimination of acids.
Severe diarrhea leading to loss of HCO3−.
2. Metabolic Alkalosis
Defined by arterial HCO3− concentrations exceeding 26 mEq/L.
Results from H+ loss or HCO3− gain.
Common Causes include:
Loss of H+ through vomiting.
Diuretic-induced acid losses.
Increased base from excessive antacid intake.
3. Clinical View on Lactic Acidosis and Ketoacidosis
Lactic Acidosis: Caused by accumulated lactic acid during hypoxic conditions.
Ketoacidosis: Occurs from increased ketoacids during fat metabolism under insulin deficiency in uncontrolled diabetes type 1.
25.6d Compensation
1. Definition and Mechanism
Compensation: Refers to the body's physiological response to an acid-base disturbance affecting blood CO2 or HCO3−.
Possible outcomes:
Complete Compensation: Blood pH returns to normal.
Incomplete Compensation: Blood pH does not normalize fully.
Uncompensated: No physiological attempts to correct imbalance; persistent acid-base disturbance.
2. Renal Compensation Mechanisms
Response to Elevated Blood H+: Type A intercalated cells
Excrete H+ and reabsorb HCO3− more than under normal conditions.
Result: Higher blood HCO3− levels; lower urine pH.
Response to Decreased Blood H+: Type B intercalated cells
Reabsorb H+ and excrete HCO3− more than in standard conditions.
Outcome: Lower blood HCO3−; higher urine pH.
This mechanism effectively neutralizes acid-base disturbances unrelated to renal dysfunction.
3. Respiratory Compensation
Triggered by metabolic acidosis or alkalosis:
Increased respiratory rate in response to elevated H+; excess CO2 is expelled.
Decreased respiratory rate in metabolic alkalosis leads to carbon dioxide retention.
Efficiency is lower than renal compensation due to the limits imposed by potential hypoxia.
4. Clinical Application: Arterial Blood Gas (ABG) Analysis
ABG tests help diagnose and monitor acid-base disturbances and the body’s compensatory mechanisms.
Key indicators: pH, arterial PCO2, HCO3− levels.
Examples of Compensation:
Respiratory Acidosis with Renal Compensation: Increased CO2, leading to increased H2CO3 with kidneys compensating through enhanced secretion of H+ and reabsorption of HCO3−.
Respiratory Alkalosis with Renal Compensation: Decrease in CO2, prompting similar renal adjustments in fluid levels.
Metabolic Acidosis with Respiratory Compensation: Increased H+ leads to decreased HCO3−, prompting respiratory drive increases to clear CO2.
Metabolic Alkalosis with Respiratory Compensation: Elevated HCO3− relative to subdued respiratory action results in compensatory changes in CO2 exhalation.