Page 302 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Respiratory Acid-Base Disorders 293

TABLE 11-1 Theoretical Effect of Breathing 21% and 100% Oxygen on Mean
PO 2 Values in Alveolar Gas, Arterial Blood, and Mixed Venous Blood
Ideal Gas Exchange V -Q Mismatch Right-to-Left Shunt

FIO 2 21% 100% 21% 100% 21% 100%
PO 2 (venous in mm Hg) 40 51 40 51 40 42
PO 2 (alveolar in mm Hg) 101 673 106 675 114 677
PO 2 (arterial in mm Hg) 101 673 89 673 59 125
(A a) PO 2 gradient in mm Hg 0 0 17 2 55 552

From Murray JF. Gas exchange and oxygen transport. In: Murray JF, editor. The normal lung. Philadelphia: WB Saunders, 1986: 194.

METABOLIC COMPENSATION IN
RESPIRATORY ACIDOSIS BOX 11-2 Predicted Metabolic
Acute Respiratory Acidosis Compensations in
Respiratory Blood Gas
Acute increases in PCO 2 cause intracellular CO 2 levels to
increase. An increase in CO 2 concentration shifts the Disorders
reaction CO 2 þ H 2 O $ H 2 CO 3 $ HCO 3 þ H þ to

the right. Bicarbonate and H þ concentrations slightly Acute Respiratory Acidosis
increase within 10 minutes because of dissociation of [HCO 3 ] increases 0.15 mEq/L for every 1-mm Hg

þ
H 2 CO 3 into HCO 3 and H . Bicarbonate ions are increase in PCO 2 in dogs
released from erythrocytes in exchange for chloride, Same for cats
increasing the plasma strong ion difference (SID). An Chronic Respiratory Acidosis
increase in CO 2 concentration also shifts the general [HCO 3 ] increases 0.35 mEq/L for every 1-mm Hg

buffer reaction ðA þ H $ HAÞ to the left. Intracellu- increase in PCO 2 in dogs
þ
lar buffers (e.g., hemoglobin, hemoglobin þ H þ $ Degree of compensation is not known for cats
reduced hemoglobin) play a critical role in acute buffer- Acute Respiratory Alkalosis
ing of hypercapnia, handling 97% of the H þ load in
dogs. 24,43 Only 3% of the H load is handled by extracel- [HCO 3 ] decreases 0.25 mEq/L for every 1-mm Hg
þ
decrease in PCO 2 in dogs
lular buffers (i.e., plasma proteins). As a result, for each 1-
Same for cats

mm Hg increase in PCO 2 , these buffers increase HCO 3
0.15 mEq/L in dogs 15 and cats 75 (Box 11-2). Presence Chronic Respiratory Alkalosis

of moderate hypoxemia does not alter the adaptive [HCO 3 ] decreases 0.55 mEq/L for every 1-mm Hg
response to acute respiratory acidosis. 44 decrease in PCO 2 in dogs
Degree of compensation is not known for cats, but pH
Chronic Respiratory Acidosis is usually normal or slightly alkalemic
If hypercapnia persists, renal compensation occurs to sta-

bilize plasma HCO 3 at a higher concentration within 5
days. 34,62,69,79, Chronic hypercapnia causes intracellular PCO 2 , HCO 3 will increase 0.35 mEq/L in dogs. 15
þ
H to increase in the renal tubular cells. Upregulation (see Box 11-2). The renal response to chronic hypercap-
þ
of the Na -H þ antiporter of the renal brush border nia is not altered by moderate hypoxemia, dietary sodium
76 44
occurs, and hydrogen ions are exchanged for sodium or chloride restriction, alkali loading, or adrenalectomy.
67,80
and then excreted as NH 4 Cl . Intracellular The renal compensation in chronic respiratory acidosis
þ

HCO 3 is reabsorbed and exchanged for Cl , resulting typically is considered to be incomplete, not returning
in an increase in plasma SID, chloruresis, and negative pH completely to the normal value. 86 In stable human
chloride balance. 20 The chloride lost in the urine patients with chronic respiratory acidosis, however, a
decreases urine SID because the chloride is accompanied 0.51 mEq/L increase in [HCO 3 ] is expected for each

þ
by NH 4 rather than sodium ions. A new steady state is 1 mm Hg increase in PCO 2. 47 Thus arterial pH appears

reached when the increased filtered load of HCO 3 to remain near reference ranges in human patients with
4
resulting from the increased plasma concentration of long-standing respiratory acidosis. Similar results have

HCO 3 is balanced by increased renal reabsorption of been observed in dogs with chronic respiratory acidosis

HCO 3 . The net effect is buffering of the respiratory aci- and no identifiable reason for the increase in [HCO 3 ]

dosis and hypochloremic hyperbicarbonatemia caused by concentration other than renal compensation. 29 These
chronic hypercapnia. For each 1-mm Hg increase in observations suggest that the kidneys may be able to