Page 331 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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322 ACID-BASE DISORDERS
can be associated with sodium gain in animals with Theadministrationofsubstancescontainingmoresodium
hyperadrenocorticism or in those treated with isotonic than chloride (e.g., NaHCO 3 ) also increases SID, causing
or hypertonic NaHCO 3 because the effective SID of metabolic alkalosis.
NaHCO 3 solutions is high, whereas animals treated with A particular type of hypochloremic alkalosis that does
isotonic or hypertonic NaCl will have hypernatremia and not respond to chloride administration alone (as NaCl) is
decreased SID because the effective SID of NaCl called chloride-resistant metabolic alkalosis and usually is
solutions is 0 mEq/L. 11 Hypernatremia is further caused by hyperadrenocorticism or hyperaldosteronism.
discussed in Chapter 3. Therapy for concentration alkalo- Increased concentrations of cortisol or aldosterone cause
sis should be directed at treating the underlying cause sodium retention by activating the type I renal mineralo-
þ
responsible for the change in [Na ]. If necessary, corticoid receptors. 53 Experimentally, administration of
þ
[Na ] and osmolality should be corrected (see desoxycorticosterone acetate (DOCA) twice daily in
Chapter 3). sodium-supplemented dogs caused a significant increase
in [Na ] and [HCO 3 ] with no change in [Cl ]. 35 When
þ
Hypochloremic Alkalosis NaHCO 3 was added to the diet instead of NaCl, [Na ]
þ
If thereis no changein the watercontent ofplasma, plasma and [HCO 3 ] increased significantly, but [Cl ]
þ
[Na ] will be normal. Other strong cations (e.g., Mg 2þ , decreased. 35 Approximately 30% of dogs with hyperadre-
þ
Ca 2þ ,K ) are regulated for purposes other than acid-base nocorticism have mild hypernatremia. 34,38 In a study of
balance,andtheirconcentrationsneverchangesufficiently 117 dogs with hyperadrenocorticism, 34 only 12 had
to substantially affect SID. Consequently, when water [Cl ] less than 105 mEq/L. However, 25 of these dogs
content is normal, SID changes only as a result of changes had hypernatremia, and the [Cl ], although within the
þ
in strong anions. If [Na ] remains constant, decreases in normal range, could have been low relative to the
þ
[Cl ] can increase SID (so-called hypochloremic alkalosis; [Na ] (i.e., corrected hypochloremia). The mean
þ
Figure 13-6). Primary decreases in [Cl ] unrelated to [Na ] was 150 mEq/L; the mean [Cl ] was 108
increases in plasma water content are recognized by the mEq/L; and the mean [Cl ] after correcting for changes
presence of a low corrected chloride concentration (see in free water was 105 mEq/L. The corrected
Chapter 4). Hypochloremic alkalosis may be caused by hypochloremia that occurs in the presence of high miner-
an excessive loss of chloride relative to sodium or by alocorticoid or glucocorticoid concentrations likely is
administration of substances containing more sodium responsible for the mild metabolic alkalosis observed in
than chloride as compared with normal ECF composition. these patients. The lack of response to NaCl can be
Excessive loss of chloride relative to sodium as compared explained by a resetting of the regulatory mechanism
with normal ECF composition can occur in the urine after and associated increased urinary loss of chloride. 29 Thus
administration of diuretics that cause chloride wasting in so-called chloride-resistant metabolic alkalosis, some-
(e.g., furosemide) or when the fluid lost has a low or nega- thing (e.g., excessive mineralocorticoid activity) prevents
tive SID as in the case of vomiting of stomach contents. chloride retention, and consequently SID cannot be
lowered by chloride administration.
180 Therapy of chloride-responsive hypochloremic alkalo-
sis is directed at correcting the SID with a solution
160
SC HCO 3 SID AG HCO 3 SID HCO 3 SID containing chloride (e.g., 0.9% NaCl, lactated Ringer’s
140
Ionic strength (mEq/L) 120 Na AG SA Cl AG SA expansion of extracellular volume is desired, intravenous
A
solution, K Cl supplemented fluids). In cases in which
SA
A
A
100
infusion of 0.9% NaCl is the treatment of choice.
Corrected hypochloremia and hypochloremic alkalosis
80
are discussed more in Chapters 4 and 10.
Cl
Cl
60
40
20 SID ACIDOSIS
Three general mechanisms can cause SID to decrease,
0 resulting in SID (metabolic) acidosis: (1) a decrease in
Cations Anions Hyperchloremic Hypochloremic þ
(normal) acidosis alkalosis [Na ]; (2) an increase in [Cl ]; and (3) an increased con-
Figure 13-6 Gamblegram of normal plasma and change in ionic centration of other strong anions (e.g., L-lactate in lactic
strength of anions secondary to increases (hyperchloremic acidosis) acidosis, ß-hydroxybutyrate in diabetic ketoacidosis, sul-
or decrease (hypochloremic alkalosis) in chloride (Cl ) content in fate in uremic acidosis). Common causes of SID acidosis
plasma. SID is decreased in hyperchloremic acidosis and increased in are presented in Box 13-3.
hypochloremic alkalosis, whereas anion gap (AG) remains constant
during primary chloride changes. Na , Sodium; SC , other strong Dilutional Acidosis
þ
þ
cations; SA , other strong anions; A , net charge of nonvolatile Dilutional acidosis occurs whenever there is an excess of
buffers; HCO 3 , bicarbonate. water in plasma and is recognized clinically by the