Acid+Base+Balance
Title: Acid-Base Balance Notes
Introduction
Source: Marieb EN, Koehn K. Anatomy and Physiology. Acid-Base Balance. 4th ed. Pearson Education Inc; 2011
Slides by Janice Meeking, Mount Royal College: Acid-Base Balance
pH and Its Importance
pH impacts functional proteins and biochemical reactions.
Normal pH levels:
Arterial blood: pH 7.4
Venous blood: pH 7.35
Intracellular fluid (ICF): pH 7.0
Conditions:
Alkalosis (alkalemia): arterial blood pH > 7.45
Acidosis (acidemia): arterial pH < 7.35
pH levels below 6.8 or above 8.0 are lethal.
Production of Hydrogen Ions (H+)
Major sources of H+ in the body include:
Metabolism of phosphorus-containing proteins leading to phosphoric acid in extracellular fluid (ECF).
Lactic acid produced during anaerobic respiration of glucose.
Fatty acids and ketone bodies from fat metabolism.
H+ released when CO2 is converted to bicarbonate (HCO3-) in blood.
Regulation of H+ Concentration
Sequential regulation mechanisms include:
Chemical buffer systems: Rapid response, first line of defense.
Brain stem respiratory centers: Act within 1-3 minutes.
Renal mechanisms: Most potent but take hours to days to alter pH.
Acid-Base Properties
Strong Acids:
Fully dissociate in water, greatly affect pH.
Weak Acids:
Partially dissociate, effective at stabilizing pH.
Strong Bases:
Dissociate easily to tie up H+ quickly.
Weak Bases:
Accept H+ more slowly.
Chemical Buffer Systems
Chemical buffer: A system to resist pH changes in the presence of strong acids or bases.
Bicarbonate buffer system
Phosphate buffer system
Protein buffer system
Bicarbonate Buffer System
Mixture of bicarbonate (H2CO3) and salts.
Buffers both ICF and ECF; vital for ECF buffering.
If a strong acid is added:
HCO3- combines with H+ to form H2CO3.
pH decreases slightly until HCO3- is exhausted.
If a strong base is added:
H2CO3 dissociates to donate H+, neutralizing the base.
pH increases minimally.
Phosphate Buffer System
Similar functioning as the bicarbonate buffer system:
Uses dihydrogen phosphate (H2PO4-) and monohydrogen phosphate (HPO4^2-) as buffers.
Effective in urine and ICF due to high phosphate concentration.
Protein Buffer System
Intracellular proteins are the most abundant buffers; plasma proteins are also significant.
Protein molecules can act as both weak acids and bases.
When pH increases, carboxyl (COOH) groups release H+.
When pH decreases, amine (NH2) groups bind H+.
Respiratory System Regulation
The respiratory system has a slower response but larger capacity for altering acid-base balance:
Eliminates CO2.
Blood equilibrium: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-.
CO2 unloading shifts equilibrium left; CO2 loading shifts it right.
Effects of pH Imbalance
Hypercapnia activates medullary chemoreceptors, resulting in less CO2 and reduced H+.
Alkalosis depresses the respiratory center, causing decreased respiratory rate.
Impairments lead to:
Hypoventilation: Respiratory acidosis
Hyperventilation: Respiratory alkalosis
Renal Regulation of Acid-Base Balance
The kidneys control acid-base balance by:
Conserving or generating HCO3-.
Excreting HCO3-.
Secretion of H+ occurs primarily in the proximal convoluted tubule (PCT) and alpha intercalated cells.
H+ comes from H2CO3 formed by carbonic anhydrase reactions.
Mechanisms of HCO3- Regulation
Tubule cells are impermeable to HCO3-; CO2 forms H2CO3 in PCT cells, leading to H+ secretion and HCO3- reabsorption.
Intercalated cells actively secrete H+ into urine, buffered by phosphates, and generate new HCO3-.
Body Responses During Alkalosis
Type B intercalated cells secrete HCO3- and reclaim H+ to acidify blood.
The process differs from bicarbonate ion reabsorption in type A cells.
Acid-Base Imbalance Conditions
Respiratory and Metabolic Imbalances:
Respiratory acidosis and alkalosis.
Metabolic acidosis and alkalosis.
Evaluating Respiratory Function
PCO2 level is the key indicator of respiratory adequacy (normal range: 35-45 mm Hg).
Elevated PCO2 (> 45 mm Hg) → respiratory acidosis due to poor ventilation.
Low PCO2 (< 35 mm Hg) → respiratory alkalosis typically caused by hyperventilation.
Causes of Metabolic Acidosis
Results from:
Excess alcohol ingestion (producing acetic acid).
Loss of HCO3- (e.g., persistent diarrhea).
Lactic acid accumulation from shock, diabetic crisis, starvation, kidney failure.
Metabolic Alkalosis
Less common than acidosis:
Indicated by rising blood pH and HCO3-.
Caused by vomiting or excess base intake (e.g., antacids).
Consequences of Extreme pH Levels
Blood pH below 7: CNS depression, leading to coma and death.
Blood pH above 7.8: Nervous system excitation, muscle tetany, convulsions, respiratory arrest.
Compensation Mechanisms
If a physiological buffer system fails, compensation occurs:
The respiratory system attempts to correct metabolic imbalances.
The kidneys work to correct respiratory imbalances.
Respiratory Compensation for Metabolic Imbalances
In metabolic acidosis, high H+ levels stimulate increased respiratory rate and depth, leading to lower CO2.
In metabolic alkalosis, respiration slows to allow CO2 accumulation, maintaining high pH and HCO3- levels.
Summary of Responses to Acid-Base Disturbances
Hypoventilation indicates elevated PCO2 (respiratory acidosis) and can show renal compensation via high HCO3- levels.
Respiratory alkalosis is marked by low PCO2 and high pH, with renal compensation indicated by decreasing HCO3- levels.