Acid-base balance and disorders

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.
Last modified: Wednesday, 22 February 2012, 4:50 AM