Page 333 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

324 ACID-BASE DISORDERS

should be given to plasma pH. Sodium bicarbonate can the patient and treatment of the primary disorder. Sodium
be administered whenever plasma pH is less than 7.20 bicarbonate may help patients in renal failure with acidosis
because it has a high effective SID. Corrected but its efficacy remains controversial in patients with lactic
hyperchloremia and hyperchloremic acidosis are further acidosis or ketoacidosis. The efficacy of NaHCO 3 therapy
discussed in Chapters 4 and 10. in renal failure is because the increase in plasma sodium
concentration results in an increase in plasma SID (strong
SID Acidosis Caused by an Increase in ion alkalosis); expansion of the extracellular fluid volume,
Unmeasured Strong Anions (Organic which is the distribution space for phosphorus; and
Acidosis) increased urine production. The combined effect of these
Accumulation of metabolically produced organic anions changes is to decrease the plasma phosphorus concentra-
(e.g., L-lactate, acetoacetate, citrate, ß-hydroxybutyrate) tion. The initial goal in acidemic patients with renal failure
or addition of exogenous organic anions (e.g., salicylate, is to increase systemic pH to more than 7.20. Sodium
glycolate from ethylene glycol poisoning, formate from bicarbonate should be used cautiously in lactic acidosis
methanol poisoning) will causemetabolicacidosisbecause or ketoacidosis because subsequent metabolism of
these strong anions decrease SID (Figure 13-8). Accumu- accumulated organic anions will further increase
2
lation of some inorganic strong anions (e.g., SO 4 in [HCO 3 ], potentially leading to excessive alkalinization.
renal failure) will resemble organic acidosis because these Organic acidoses are further discussed in Chapter 10.
substances decrease SID. The pK values for the clinically
most important organic anions are as follows: lactate ¼ CLINICAL APPROACH
3.9, acetoacetate ¼ 3.6, citrate ¼ 4.3, and ß-
hydroxybutyrate ¼ 4.4. Thus the pK values of these ions Three simplified approaches have been developed to
are at least 3 pH units below normal plasma pH, and at a allow the clinical use of Stewart’s strong ion approach:
pH of 7.4, the concentrations of their dissociated forms the effective SID method also known as the Stewart-
are at least 1000 times greater than the concentrations Figge methodology, 25 the BE approach, or Fencl-Stewart
of the nondissociated forms. For example, at a pH of 7.4 algorithm, 23 and Constable’s simplified strong ion equa-
5
for each molecule of lactic acid, there are approximately tion. Clinical application of these approaches has been
3200 molecules of lactate. Thus it can be assumed that helpful in identifying complex metabolic derangements
4
43
these organic acids are completely dissociated within the in critically ill humans, dogs, 19 calves, 13 and pigs ; how-
pH range of body fluids compatible with life and conse- ever, the clinical utility of these approaches has not appear
quently behave as strong ions. The most frequently to have been extensively investigated in cats.
encountered causes of organic acidosis in dogs and cats
are renal failure (uremic acidosis), diabetic ketoacidosis, EFFECTIVE SID MODEL
lactic acidosis, and ethylene glycol toxicity. Management Figge et al 25 developed and successfully tested in humans
of organic acidosis should be directed at stabilization of a mathematical approach to evaluate metabolic acid-base

disorders. Unmeasured strong ions (XA ) are estimated
180 by subtracting the “effective SID” (SID eff ), an approxi-
mation of the “real” SID, from the “apparent SID”
160

SC (SID app )as XA ¼ SID app – SID eff . The SID app is calcu-
SID AG HCO 3 SID lated using electrolytes measured in the serum (SID app ¼
HCO 3
140
Ionic strength (mEq/L) 100 Na SA SA [Na ] þ [K ] þ [Mg ] þ [Ca ] – [Cl ]), and SID eff is
A
A
AG
120
2þ
2þ

þ
þ
a satisfactory approximation of the “real SID.” Despite
being a very promising model for assessment of metabolic
80
acid-base disorders, Stewart-Figge’s model was devel-

Cl
Cl
60
40
and has not been tested in dogs or cats. Moreover, calcu-
lation of SID eff is not simple and may be clinically imprac-
20 oped using protein behavior based on human albumin
0 tical, and the approach has been shown to be less accurate
Normal Normal Organic in human plasma than calculating the SIG using
(cations) (anions) acidosis 49
(anions) Constable’s simplified strong ion equation.
Figure 13-8 Gamblegram of normal plasma and change in ionic
strength of anions secondary to increases in unmeasured strong BASE EXCESS ALGORITHM
anions (organic acidosis) in plasma. SID is decreased in organic BE has been used to assess changes in the metabolic com-
acidosis, whereas anion gap (AG) is increased because of increase in ponent because SID is synonymous with buffer base. BE is
unmeasured strong anions. Na , Sodium; SC , other strong cations; a measurement of the deviation of buffer base (and there-
þ
þ
SA , other strong anions; A , net charge of nonvolatile buffers; fore SID) from normal values, assuming nonvolatile buffer

HCO 3 , bicarbonate.

ion concentrations (albumin, phosphate, globulin) are