Acid-Base Balance and Disorders

Acid-Base Balance

  • Definition: Maintenance of homeostasis between acidity and alkalinity within body systems.

  • Human Body pH Range: Should be between 7.35 to 7.45.

  • Acidosis:

    • Definition: Accumulation of acid or loss of base (Acidemia).

    • pH < 7.35.

  • Alkalosis:

    • Definition: Accumulation of base or loss of acid (Alkalemia).

    • pH > 7.45.

Acids

  • Definition: Substances that give up hydrogen ions.

  • Types of Acids:

    • Volatile Acids: e.g., carbonic acid (H2CO3) which is converted to CO2 and eliminated by the lungs.

    • Non-volatile/Fix Acids: e.g., phosphoric acid, lactic acid, etc., which must be excreted by the kidneys.

  • Largest Source of Acid:

    • Carbonic acid (H2CO3).

    • Acid concentration measured using CO2, represented as PaCO2PaCO2.

Bases

  • Definition: Substances that accept or neutralize hydrogen ions.

  • Largest Source of Base:

    • Bicarbonate (HCO3^-), primarily regulated by the kidneys.

  • Other Sources: Ingestion of fruits, vegetables, milk products, and egg whites.

Buffers

  • Function: Substances that decrease the effect of acids or bases on the pH of a solution.

  • Defenses Against Hydrogen Ions:

    • Chemical Buffers: Increase or decrease in hydrogen ions.

    • Respiratory Regulation: Lungs alter CO2 levels to maintain pH.

    • Renal Regulation: Kidneys manage H+ and HCO3^- balance.

Chemical Buffers

  • Bicarbonate-Carbonic Acid Buffer System:

    • Reacts with acids to produce H2CO3, which dissolves into CO2 and H2O.

  • Disodium/Monosodium Phosphate Buffer: Used within red blood cells (RBC) and kidneys.

    • Prevents damage from acidic urine by accepting H+ ions.

  • Protein Buffers:

    • Proteins in plasma act as buffers (Intracellular Fluid - ICF).

    • Hemoglobin binds H+ ions and assists in balancing pH changes.

Respiratory Regulation of pH

  • Mechanism: Lungs change respiratory rate and depth to control CO2 release/retention.

  • Response to pH Changes:

    • Acidosis: Increased respiratory rate (hyperventilation) to expel more CO2.

    • Alkalosis: Decreased respiratory rate, leading to CO2 retention and pH normalization.

Renal Regulatory Control

  • Role of Kidneys: Manage H+ and HCO3^- levels for pH homeostasis.

  • Compensation Mechanisms:

    • In acidosis: Reduced H+ secretion and increased HCO3^- reabsorption.

    • In alkalosis: Reduced HCO3^- reabsorption.

  • Timeframe: Renal control takes longer than respiratory regulation, up to 24 hours.

    • Ammonium Formation: Combines free H+ with NH3 to form ammonium.

    • Bibasic phosphate and sulfur: accepts H+ to control acid-base balance

Electrolyte Balance and Acid-Base Disorders

  • Electrolytes Involved: Hydrogen (H+) and bicarbonate (HCO3^-).

    • Must maintain electroneutrality between Extracellular Fluid (ECF) and Intracellular Fluid (ICF).

    • Chloride (Cl^-) moves in the opposite direction of HCO3^-.

    • Changes in K, Cl, and Na may accompany acid-base disorders

Types of Acid-Base Disorders

  • Respiratory Acidosis:

    • Decreased pH & increased PCO2.

    • Caused by CO2 retention due to respiratory dysfunction leading to hypercapnia.

    • Acute: kidney regulatory systems don’t have time to compensate (more acute onset = more severe symptoms)

    • Chronic: less critical, kidneys have more time to compensate

  • Respiratory Alkalosis:

    • Increased pH & decreased PCO2 due to hyperventilation

    • Acute response: shift of acid from ICF to ECF

    • Chronic: renal compensation: reduce H+ secretion and increase HCO3 excretion

  • Metabolic Acidosis:

    • Decreased pH & decreased PCO2. Due to loss of base (HCO3^-) or excessive gain of fixed acids.

    • All types of acidosis that are not caused by excess CO2 (either excessive loss of base or excessive gain of fixed acids)

    • Loss of base: This can occur due to conditions such as diarrhea, renal tubular acidosis, or excessive use of diuretics, chronic renal failure.

    • Increased acid: ketoacidosis (increased betahydroxybuterate production, inability to metabolize ketones), poisoning, lactic acidosis (inc. production of lactate of ketoacids)

  • Metabolic Alkalosis:

    • Increased pH & increased PCO2. Results from excessive base (HCO3^-) or loss of H+.

    • Alkalotic agents (base meds in excess), loss of H+ via vomiting or excess aldosterone inducing Na retention and H+ excretion, hypokalemia (K shifts out, H+ shifts into cells), contraction alkalosis (diuretics, chloride diarrhea)

Specific Acid-Base Disorders

  • Respiratory Acidosis:

    • Symptoms: Hyperventilation, decreased O2 leading to restlessness, confusion, and possibly coma. Lethargy, muscle twitching, tremors, breathing changes, inc. depth of respiration

    • Treatment: Correct the underlying issue, improve oxygenation (via O2 or mechanical ventilation if needed). Chronic: bronchodilators and corticosteroids, CPAP or BiPAP, supplemental o2 prescribed

  • Respiratory Alkalosis:

    • Symptoms: Anxiety, confusion, seizures, tingling/numbness, deeper breathing, cold/clammy extremities.

    • Treatment: Correct the underlying cause, provide supplemental oxygen (if hypoxemia present).

  • Metabolic Acidosis:

    • Symptoms: Headaches, nausea, vomiting, fatigue, Kussmaul breathing, potential for arrhythmias and coma.

    • Treatment: Manage underlying cause, may require dialysis for severe cases.

  • Metabolic Alkalosis:

    • Symptoms: Weakness, muscle pain, polyuria, hypocalcemia (jitters, tingling, muscle spasms), hypoventilation due to respiratory center inhibition.

    • Treatment: Two types: chloride responsive, chloride resistant

    • Chloride responsive: correct volume imbalance with IV of NaCl, usually associated with hypokalemia, use KCl to correct

    • Chloride resistant: treat underlying cause, if severe or electrolytes can’t be given d/t RF, HCl for rapid correction, dialysis, mon