Acid-Base Problems in Veterinary Medicine

Acid-Base Issues: Objectives and References

Objectives
- Acid-Base Basics (Pun intended)
- Acid-Base analytics (acidytics)
- Evaluating acid-base problems
- Diseases that cause acid-base problems (examples for interpreting coming soon to a class near you!)
References
- Ettinger Ch 128
- Proceedings from VIN

Acid-Base Fundamentals

Cellular/metabolic functions work within a narrow pH range.
Two primary formulas:
- Henderson-Hasselbalch equation: This equation relates the pH of a solution to the concentration of bicarbonate and the partial pressure of carbon dioxide (PCO2).
- Carbonic Acid Equation: This is catalyzed by carbonic anhydrase and proceeds based on the availability of substrates.
Acidifying agents:
- H+ ions: Nonvolatile (fixed) acids produced from protein and phospholipid metabolism, which are excreted by the kidneys.
- CO2: Volatile (fat-soluble) acid produced from carbohydrate and fat metabolism, which is excreted by the respiratory system.
Buffering agents:
- Bicarbonate: Produced by renal tubular cells, in larger amounts, and works via the carbonic acid equation to produce CO2.
- Non-bicarbonate buffers: Include proteins and phosphate.

Other Acid-Base Fundamental Points

TCO2 (Total Carbon Dioxide):
- Not to be confused with PCO2. TCO2 is actually a measure of bicarbonate and reflects metabolic contributions to acid-base balance.
- This is important in the evaluation of acid-base status when PCO2 is abnormal.
Base excess (or base deficit):
- Normal range based on normal temperature (T) and normal PCO2.
- Represents the amount of base above or below the 'normal' base value, generally between -4 and +4.
- More 'negative' base excess indicates a deficit of base (metabolic acidosis), while more 'positive' suggests extra base (metabolic alkalosis).
Anion gap:
- Important in metabolic acidosis; calculated as:
  $ext{AG} = [Na^+ + K^+] - [Cl^- + HCO3^-]$
- Normal value varies (16 mEq/L +/- 4).
- Two general categories:
  - High AG metabolic acidosis: Due to too much acid (causes include DKA, uremia, ethylene glycol toxicity, lactic acidosis).
  - Hyperchloremic (normal AG) metabolic acidosis: Due to loss of bicarbonate (causes include diarrhea, Addison's disease, renal tubular disease).

Advanced Blood Gas Interpretation

Respiratory acidosis: Occurs when the patient is hypoventilating and unable to eliminate CO2.
- Causes:
- Medications that relax thoracic muscles and depress the respiratory center.
- Neuromuscular diseases.
- Upper airway obstructions.
- Pleural space diseases (pneumothorax, effusions, diaphragmatic hernia).
- Gas exchange disorders (pulmonary thromboembolism, pneumonia, pulmonary edema).
Venous Admixture: This occurs when blood travels from the lungs/pulmonary veins, through the left atrium, and to the left ventricle without becoming properly oxygenated, noted during a V/Q mismatch.
- Low V/Q results from diseases such as pneumonia and pulmonary edema.
- No V/Q means no blood gets to ventilated areas, caused by atelectasis or severe pleural effusion.
PaCO2: Indicates ventilation.
- Low PaCO2: Rarely significant, can be caused by fear, stress, pain, or compensation for metabolic acidosis.
- High PaCO2: Indicates hypoventilation caused by various conditions (neurologic diseases, spinal cord injuries, upper airway disease, etc.).

Evaluating Acid-Base Problems

Evaluate via:
- pH
- Normal: neutral range.
- Low: indicates acidemia (acid buildup).
- High: indicates alkalemia (base excess).
- PCO2
- Low: indicates respiratory alkalosis.
- High: indicates respiratory acidosis.
- HCO3- (Bicarbonate)
- Low: indicates metabolic acidosis.
- High: indicates metabolic alkalosis.
- Reference: Silverstein & Hopper, Small Animal Critical Care Medicine.

Examples of Primary Acid-Base Disturbances

Metabolic acidosis: Most common issue.
- Causes: Lactic acidosis, renal failure, diabetic ketoacidosis (DKA), gastrointestinal loss of HCO3-.
- Remember H+ and K+ shifts!
- Treatment with bicarbonate is appropriate only if respiratory function is maintained.
Respiratory acidosis: Second most common issue, possibly mixed with metabolic acidosis.
- Increased PCO2 (hypercapnia).
- Caused by poor ventilation, decreased circulation/perfusion, reduced respiratory rate (RR), or V/Q mismatches.
- Common conditions include circulatory failure, neurological diseases, respiratory muscle failure, and upper airway obstructions.
- DO NOT USE bicarbonate in treating respiratory acidosis.
Metabolic alkalosis: Generally characterized by an acid loss or bicarbonate gain.
- Often hypochloremic due to acid loss from upper GI issues (like pyloric obstruction/vomiting), diuretics, renal diseases, potassium deficiencies, or poor perfusion impacting HCO3- reabsorption.
Respiratory alkalosis: Caused by hyperventilation leading to hypocapnia and alkalemia.
- Often involved with hypoxemia from various pulmonary or systemic issues causing excitement, exercise, or pain.
- Ventilation issues occur independently of hypercapnia (normal CO2 levels but increased ventilation).

Potential Adverse Effects Associated with Sodium Bicarbonate Administration

Increased hemoglobin affinity for oxygen.
Increased blood lactate concentration.
Paradoxical intracellular acidosis.
Hypercapnia.
Hypervolemia.
Hyperosmolality.
Hypernatremia.
Hypocalcemia (ionized).
Hypomagnesemia (ionized).
Hypokalemia.
Phlebitis.

Other Acid-Base Fundamental Points

A-a Gradient (Alveolar-Arterial Gradient):
- Normal value < 15. An abnormal value (>15) indicates potential pulmonary parenchymal issues.
- If hypoxia and abnormal blood gas occur with a normal A-a gradient, hypoxia is unlikely caused by lung disease.
V-Q Mismatch and Oxygenation:
- PaCO2 demonstrates ventilation; low ventilation reflects high CO2 levels.
- When tissue perfusion (Q) is adequate, SpO2 = SaO2.
- PaO2 is necessary when measuring SpO2 for accuracy in poorly perfused tissues.
- Goals include SpO2 > 90%; PaO2 > 60 mm Hg; SaO2 is critical for determining arterial oxygen content.
Compensation Mechanisms:
- The body shifts pH toward normal by compensating with the 'other' system but does not return to the normal range.
- Respiratory compensation for metabolic issues occurs quicker than metabolic compensation for respiratory issues (immediate response seen in blood gas analysis vs days for metabolic adjustments).

Pulmonary Pathophysiology

Diffusion Impairment: Occurs with decreased diffusion across the blood-gas membrane (common in interstitial edema), preventing complete oxygen diffusion and causing respiratory failure.
Reasons for Hypoxemia:
- Low inspired oxygen content (low FiO2): Rare in emergency settings unless exposed to a hypoxic environment.
- Generally during anesthesia due to equipment failure.
- Arterial partial pressure of oxygen should be about five times the FO2 (FiO2 expressed as a percent).
- Hypoventilation: Decreased fresh gas reaching the blood-gas membrane, often due to central nervous system or airway obstructions.
- Can result in both hypoxemia and hypercapnia needing oxygen administration.
- In severe cases, positive pressure ventilation may be necessary.
- V/Q Mismatch: Anytime ventilation and blood flow are not matching. Low V/Q results from hypoventilation, impacting arterialization.
- Shunt: Extreme form of V/Q mismatch wherein blood flows from the right side of the heart to the left without diffusion.
- Anatomic shunt occurs normally due to circulation; physiologic shunt typically surfaces during alveolar collapse.
Hemoglobin Disorders: Conditions that impair hemoglobin can cause hypoxemia despite normal PaO2 (e.g., anemia, carbon monoxide toxicity).

Summary of Respiratory Component V/Q Mismatch

Issues with ventilation and perfusion can significantly affect arterial oxygen content.
Inspired oxygen levels and respiration inhibitors are crucial in maintaining oxygen saturation.
Many issues improve with oxygen therapy, emphasizing the importance of measuring A-a gradients to evaluate respiratory effectiveness.
Comparison of alveolar oxygen levels to arterial oxygen levels is essential to identify pulmonary issues.