Acid–Base Disorders

Owais Bhatti

Steven Cheng

General Principles

The body maintains acid–base homeostasis through three primary mechanisms:

Chemical buffering by extracellular and intracellular buffers.
Controlling pCO₂ through modulation of alveolar ventilation.
Altering net acid excretion or the reabsorption of HCO₃⁻.

Definitions

An acid is a substance that donates H⁺ ions and a base is a substance that accepts H⁺ ions.
- Physiologic balance of the acid–base status can be described by the following equation:
  
  Acids and bases may be “strong” or “weak” depending on the degree of ionization in the human body.
- The Henderson–Hasselbalch equation shows the pH as a mathematical relationship between HCO₃⁻ and pCO₂.
- Acidemia is an increase in the [H⁺] and a decrease in the pH.
- Alkalemia is a decrease in the [H⁺] and a rise in the pH.

Classification

Acid and base disturbances are generally classified by the genesis of the disorder.
- Changes in the pCO₂ are referred to as “Respiratory” processes.
  - A decrease in pH due to an increase in pCO₂ is termed “Respiratory Acidosis.”
  - An increase in pH due to a decrease in pCO₂ is termed “Respiratory Alkalosis.”
- Changes in the [HCO₃⁻] are referred to as “Metabolic” processes.
  - A decrease in pH due to a decrease in [HCO₃⁻] is termed “Metabolic Acidosis.”
  - An increase in pH due to an increase in [HCO₃⁻] is termed “Metabolic Alkalosis.”

Pathophysiology

Acid–base homeostasis is under constant challenge. For example, the typical Western diet generates 1 mEq of acid/kg/day. The human body is well adapted to maintain pH within a narrow range (please see Fig. 6-1).
Buffering:
- HCO₃⁻ is the most important physiologic buffer in the extracellular fluid (ECF) space.
- HCO₃⁻ can combine with free H⁺ to form H₂CO₃, which can subsequently convert to CO₂ and H₂O (see ventilatory response, below)
- Intracellular buffers include proteins, phosphates, and hemoglobin.
- Bone can also absorb a significant acid load and, on dissolution, release buffer compounds such as calcium carbonate and calcium bicarbonate.
FIGURE 6-1. Physiologic response to acid load.
Ventilatory response:
- The ability to sense changes in pH and control pCO₂ via alveolar ventilation allows the body to further respond to the acid–base imbalance.
- In response to an acid load, a reduction in pCO₂ attenuates the change in pH by shifting the equation toward the generation of CO₂ and H₂O.
  - The normal pCO₂ is 40 mm Hg.
  - The level falls with increased ventilation, and rises with decreased ventilation.
Excretion:
- Ultimately, net acid excretion and reabsorption/regeneration of HCO₃⁻ is required to return the system to balance.
- This is accomplished through the renal elimination of titratable acids (dihydrogen phosphate) and nontitratable acids (ammonium).
- Bicarbonate reabsorption must also be maximized to excrete the daily acid load.
  - The majority of bicarbonate reabsorption occurs at the proximal tubule.
  - Bicarbonate reabsorption is regulated by plasma HCO₃⁻ levels and effective circulating volume.
Acid–base disorders arise when the capacity for resisting change in pH is exceeded or when mechanisms used to maintain physiologic pH are impaired (see Fig. 6-2).

Acidosis can occur from any of the following:

Metabolic insults:
- A large acid load
- Exogenous sources, such as ethylene glycol or other alcohols
- Endogenous sources during conditions such as lactic acidosis or ketoacidosis

A loss of bicarbonate buffer

Gastrointestinal (GI) loss (diarrhea).

Renal loss (proximal renal tubular acidosis [RTA]).

FIGURE 6-2. Acid–base map. HCO₃⁻, bicarbonate; pCO₂, partial pressure of CO₂; resp., respiratory. (Adapted from DuBose TD, Cogan MG, Rector FC Jr. Acid-base disorders. In: Brenner BM, ed. Brenner and Rector’s The Kidney. 5th ed. Philadelphia, PA: WB Saunders; 1996:949.)

An inability to excrete the acid load (distal RTA).
Respiratory failure causes acidosis through the elevation of pCO₂.

Alkalosis can occur from any of the following:
- Metabolic insults:
  - Loss of H⁺-rich fluids
  - Alkali ingestion
  - Renal bicarbonate reabsorption
  - Volume contraction, hypochloremia, and hypokalemia all impair renal excretion of excess alkali and contribute to the perpetuation of the alkaline state
- A decrease in pCO₂ due to hyperventilation (respiratory alkalosis).
Compensation:
- Compensatory responses minimize the change in pH by minimizing the alteration in the [HCO₃⁻] to [pCO₂] ratio.
- Expected values for compensatory responses are found in Table 6-1.

TABLE 6-1 EXPECTED COMPENSATORY RESPONSES FOR PRIMARY ACID–BASE DISTURBANCES

Disorder	Primary Change	Compensatory Response
Metabolic acidosis	Decreased HCO₃⁻	1.2 mm Hg decrease in pCO₂ for every 1 mEq/L fall in HCO₃⁻
Metabolic alkalosis	Increased HCO₃⁻	0.7 mm Hg increase in pCO₂ for every 1 mEq/L rise in HCO₃⁻
Acute respiratory acidosis	Increased pCO₂	1 mEq/L increase in HCO₃⁻ for every 10 mm Hg rise in pCO₂
Chronic respiratory acidosis	Increased pCO₂	3.5 mEq/L increase in HCO₃⁻ for every 10 mm Hg rise in pCO₂
Acute respiratory alkalosis	Decreased pCO₂	2 mEq/L decrease in HCO₃⁻ for every 10 mm Hg fall in pCO₂
Chronic respiratory alkalosis	Decreased pCO₂	4 mEq/L decrease in HCO₃⁻ for every 10 mm Hg fall in pCO₂

Metabolic Acidosis

General Principles

Metabolic acidosis is a clinical disorder characterized by low pH and low HCO₃⁻.
The appropriate respiratory compensation is hyperventilation resulting in low pCO₂.

Diagnosis

Metabolic acidosis is further categorized into those that have an increased anion gap (AG, also known as an AG acidosis) and those that have a normal AG (also known as a non-AG acidosis).

Diagnostic Testing

Differentiating the various forms of metabolic acidosis is critical for management.
Step 1: AG versus non-AG
- In patients with an AG acidosis, the acid dissociates into H⁺ and an “unmeasured” anion.
- Detection of this “unmeasured anion” is possible through the AG, a simple difference between the measured cations and anions that predominate in the ECF space.
  - AG = [Na⁺] − ([Cl⁻] + [HCO₃⁻])
  - Normal AG is 10 ± 3 mEq/L
    - This normal AG typically reflects the presence of unmeasured negative charges from plasma albumin.
    - Because of this, a fall in serum albumin of 1 g/dL (from normal of 4 g/dL) decreases the AG by 2.5 mEq/L.
- An increase in the AG reflects an accumulation of other unmeasured anions, such as lactate and acetate, from the various causes of an AG acidosis.
- The amount by which the AG increases (ΔAG) typically approximates the amount by which the serum HCO₃⁻ decreases (ΔHCO₃).
  - The relationship between ΔAG/ΔHCO₃ is often referred to as the delta ratio.
  - A significant disparity between the ΔAG and the ΔHCO₃ suggests a superimposed metabolic disorder.
    
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