Veterinary Clinical Medicine-I (General and Systemic)

ACID-BASE BALANCE AND DISORDERS

Major concepts

• Acidosis and alkalosis refer to the pathophysiologic process that cause net accumulation of acid or alkali (base) in the body
• Acidemia and alkalemia refer specifically to the pH of the blood
• Buffer - a substance that is able to take up or release H+ so that drastic changes in [H+] are minimized; a depot for H+.

Physiologically relevant buffer systems

• Bicarbonate (HCO3-/H2CO3) – most important quantitatively; easily measured;
• Can be effectively regulated in response to acidosis or alkalosis through Mmtabolic (renal) or respiratory (lung) compensation
• Red cell hemoglobin
• Plasma and intracellular proteins
• Organic and inorganic phosphates (HPO42-, / H2PO4-)
• Bone carbonate (CO32-)

Bicarbonate system

CO2 + H2O → H2CO3 → H+ + HCO3-

Respiratory Metabolic
Component Component

• Measurements of the above components, and more, are performed on a blood gas analyzer
• CO2 - Respiratory Acid; HCO3- - Metabolic Base
• Samples are collected in a heparinized syringe with the needle closed with a rubber stopper to prevent exposure to air
• Analysis should be done within minutes
• Analytes of a standard blood gas include pH, pCO2, HCO3-, TCO2, pO2, and Base Excess (BE)

pH

• pH is necessary to determine if the patient is acidemic or alkalemic
• Remember that small changes in pH represent large changes in [H+] since it is measured on an logarithmic scale

pCO2

• Partial pressure of CO2 dissolved in plasma (mmHg)
• Respiratory component – regulated by the lungs
• Respiratory acidosis is characterized by ↑ pCO2 (hypercapnia) caused by alveolar hypoventilation
• Respiratory alkalosis is characterized by ↓ pCO2 (hypocapnia) caused by alveolar hyperventilation

HCO3-

• Bicarbonate concentration (mmol/L)
• Metabolic component – regulated by the kidney
• Metabolic acidosis is characterized by ↓ [HCO3-], due either to HCO3- loss or HCO3- buffering of acid (titration)
• Metabolic alkalosis is characterized by ↑ [HCO3-], due to H+ loss or rarely iatrogenic HCO3- administration
• pH [H+] Primary Compensatory
• Metabolic acidosis ↓ ↑ ↓ [HCO3-] ↓ pCO2
• Metabolic alkalosis ↑ ↓ ↑ [HCO3-] ↑ pCO2
• Respiratory acidosis ↓ ↑ ↑ pCO2 ↑ [HCO3-]

Respiratory alkalosis ↑ ↓ ↓ pCO2 ↓ [HCO3-]

Total CO2 (TCO2)

• TCO2 ~ HCO3- ; TCO2 ≠ pCO2
• TCO2 is the sum of all substances in serum which can be converted to CO2 gas after the addition of a strong acid; dissolved CO2, H2CO3, and HCO3-
• Approximately 95% of TCO2 is HCO3-
• Can be performed on serum/plasma and may be run several hours after collection; however, values will decrease over longer periods

Anion gap (AG) = (Na+ + K+) − (HCO3- + Cl-)

• Represents the major electrolytes in serum
• Law of electroneutrality → all anionic charges = all cationic charges
• AG measures the major electrolytes and compares to reference range

Abnormal AG - change in an ion(s) not normally present to that degree or at all in health

In practice is used to detect unmeasured anions :

• lactic acid
• ketoacids
• uremic acids (PO42-, SO42-, and citrate)
• ethylene glycol metabolites (glycolate and oxalate)
• massive rhabdomyolysis (PO42- and lactic acid)
• ↓ AG is rare and not likely of clinical significance; substantial hypoalbuminemia can lower AG somewhat.

Metabolic Acidosis

• Addition of H+ (unmeasured acids):
  • ↑AG, normochloremic -
  • organic acids:
  • lactic acidosis (hypoxia)
  • ketoacidosis (DKA, ketosis)
  • anionic toxins: (ethylene glycol, salicylate, methanol, paraldehyde, etc.)
• Decreased removal of H+:
  • inorganic acids:
  • PO42-, SO42-, citrate (renal failure, urinary obstruction, uroabdomen)
  • renal distal tubular acidosis
• HCO3- loss:
  • normal AG, hyperchloremic
  • GI (diarrhea, vomiting, sequestration, salivation in ruminants)
  • renal proximal tubular acidosis

respiratory compensation (immediate) → hyperventilation → ↓ pCO2

Metabolic Alkalosis

• Loss of H+:
  • hypochloremic
  • GI (vomiting, pyloric obstruction, abomasal displacement)
• Addition of HCO3-:
  • iatrogenic with fluid administration (NaHCO3, lactate, citrate)

respiratory compensation (immediate) → hypoventilation → ↑ pCO2

Respiratory acidosis

↑ pCO2 from hypoventilation: Iinhibition or dysfunction of medullary respiratory center

• drugs (anesthetics, sedatives, narcotics)
• brain stem disease
• alkalemia
• inhibition or dysfunction of respiratory muscles (tick paralysis, tetanus, botulism, myasthenia gravis, hypokalemia, succinylcholine
• upper airway dysfunction (foreign body, vomitus)
• impaired gas exchange (lung/thoracic disease)
• inappropriate mechanical ventilation

metabolic compensation (days) → ↑ H+ secretion and ↑ HCO3- production

Respiratory Alkalosis

• ↓ pCO2 from hyperventilation
  • altered respiratory control (fear, convulsions, fever, heat exposure, hepatic encephalopathy)
  • hypoxemia (lung disease, hypotension)
  • inappropriate mechanical ventilation
• Metabolic compensation (days) → ↓ H+ secretion and ↓ HCO3- production
• Mixed acid/base - coexistence of multiple primary acid/base abnormalities
• Compensating responses to simple acid-base disturbances do not correct pH to normal

First type

• A normal pH with abnormal HCO3- and/or pCO2 represents a mixed acid/base disturbance. e.g. HBC → uroabdomen + extremely painful (panting):
  • Low normal pH
    ↓ [HCO3-]
    ↓ pCO2
    ↑ AG
  • Uroabdomen → primary metabolic acidosis
  • Panting → primary respiratory alkalosis
• An extremely high or low pH can occur if the [HCO3-] and pCO2 levels go in opposite directions, i.e. both representing primary acidoses or both representing primary alkaloses.
• These can be grave situations.