• 
  

  The blood [H⁺] and pH are determined by the strong ion difference (SID), the PCO2, and the total concentration of weak acids, mostly consisting of phosphate and albumin.

  
  
• 
  

  Both acidemia and alkalemia have potentially harmful physiologic effects, and the presence of either is related to mortality.

  
  
• 
  

  Most acid-base derangements do not benefit from specific correction of the abnormal pH; instead, the intensivist should focus on detecting and treating the underlying condition.

  
  
• 
  

  Acid-base disorders are easily characterized using a stepwise approach.

  
  
• 
  

  Lactic acidosis is the most important acid-base abnormality in ICU patients. Inadequate tissue oxygenation underlies the lactic acidosis in some patients (acute hemorrhage, critical hypoxemia, cardiogenic shock) but probably does not in others (such as the resuscitated septic patient).

Acid-base balance and acid-base disorders are imperfect terms for the determining factors and disease processes that lead to a particular hydrogen ion concentration [H⁺] in the blood. The methodology used routinely to determine an acid-base disorder is accurate in defining the disturbance. This methodology does not, however, isolate the variables that have led to a particular [H⁺] in blood. The components of blood that contribute to acid-base balance are

1. 
   

   Water

   
   
2. 
   

   Strong cations (Na⁺, Mg²⁺, Ca²⁺, K⁺) and strong anions (Cl⁻, lactate⁻)

   
   
3. 
   

   Bicarbonate ion (HCO−3)

   
   
4. 
   

   Weak acids and their conjugate bases (HA + A⁻ = A_tot) (A_tot is the total independent variable, and HA + A⁻ are dependent variables.)

   
   
5. 
   

   Partial pressure of carbon dioxide (PCO2)

   
   
6. 
   

   Carbonate ion (CO2−3)

   
   
7. 
   

   Hydroxyl ion (OH⁻)

   
   
8. 
   

   Hydrogen ion (H⁺)

The difference between the strong cations and strong anions (the strong ion difference [SID]), PCO2, and the total amount of weak acids and their conjugate bases ([A_tot]) are the only independent variables.¹ All the other components are, by definition, dependent, including [HCO−3], [HA], [A⁻], [CO2−3], [OH⁻], and [H⁺]. Because the concentrations of each of these six variables are dependent on one or more of the independent variables, we must solve separate equilibrium equations for each. Water itself is minimally dissociated despite the importance of [H⁺] and can be considered a constant. The six equations are as follows:

Water dissociation:

Weak acid dissociation:

Weak acid conservation:

HCO−3 formation:

CO32− formation:

Electrical neutrality:

K₁ through K₄ represent constants for the individual reactions. Now that we have six equations and six unknowns, we can arrange any unknown as a fourth-order polynomial and solve the equation. In acid-base balance, the dependent variable in question is [H⁺]. Stated less elegantly, there is a unique value for each of the six dependent variables once SID, PCO2, and A_tot are known so that all the equations can be solved simultaneously.

By taking logarithms to base 10 of Eq. (100-4) and rearranging, we get the familiar Henderson-Hasselbalch equation:

Since this equation is no more or less correct than any of the other five equations that must be solved simultaneously, there is nothing wrong with using it to determine an acid-base disorder. Indeed, the fact that all three values are readily available from a standard arterial blood gas determination explains the popularity of this equation.

By examining Eq. (100-7) it is possible to determine whether an acid-base disturbance is present and whether it is due to respiratory (PCO2) or metabolic [HCO3−] derangements. One might assume, therefore, that pH is determined by the relationship between PCO2 and [HCO3−]. This presumption is false. Likewise, solving Eq. (100-2) for [H⁺] does not mean that [H⁺] is determined by the HA and A⁻. In truth, [H⁺] and thus pH are determined by PCO2, SID, and A_tot. Since we define respiratory disorders by alterations in PCO2, metabolic disturbances are brought about by changes in SID and A_tot. They are not caused by changes in [HCO3−], but rather, changes in [HCO3−] occur as a result of the disturbance.

As SID becomes less positive, more [H⁺] is released into the solution, and acidemia develops. As SID becomes more positive, more [H⁺] associates with [OH⁻], forming water, and alkalemia develops. By contrast, A_tot, composed of weak acids, is acidifying. As A_tot increases, the pH falls, and as A_tot decreases, such as with hemodilution, the pH increases.

By definition, abnormalities in PCO2 are classified as respiratory disorders. SID (and possibly A_tot) is manipulated by the human body to compensate for chronic respiratory disorders, thus maintaining pH within the normal range (7.35-7.45). SID decreases to compensate for a chronic respiratory alkalosis, and SID increases to compensate for a chronic respiratory acidosis. The physiologic determinants of PCO2 are straightforward:

where VCO2 is CO₂ production and V_a is alveolar ventilation. A change in PCO2 must be explained by one of these factors. Hypercarbia and hypocarbia usually can be explained easily at the bedside.

Even relative extremes of [H⁺] are remarkably well tolerated (eg, pH 7.1-7.7), at least for the short term, in otherwise healthy individuals. However, some authors have even suggested that acidemia itself may be beneficial to critically ill patients.² For example, since acidemia shifts the oxyhemoglobin curve to the right, there is better oxygen delivery under acidemic conditions. Unfortunately, this “benefit” is dubious because acidosis also reduces synthesis of 2,3-diphosphoglycerate (2,3-DPG), and thus chronically, acidosis does not appear to improve oxygen delivery. Acidosis may produce other salutary effects on the circulation that could result in benefit in certain clinical scenarios,² but acidosis also produces numerous undesirable effects on various systems (Table 100-1), and we caution against “permissive acidosis.”