Page 263 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

254 ACID-BASE DISORDERS

Mechanism concentration by two mechanisms: the effect of the
Acid load of buffering administered HCl on body buffers and a reduction in
renal HCO 3 reabsorption that accompanies secondary

Na + hyperventilation. In this study, serum potassium concen-
36% HPr H + tration decreased during development of chronic HCl
HPi acidosis (contrary to what is typically described for acute
Proteins 57%
Pr – metabolic acidosis caused by mineral acids), whereas
Pi – (including Hb in RBC) Intracellular 147
and phosphates buffering serum sodium concentration was unchanged.
K +
HPr H + RENAL RESPONSE TO AN ACUTE
15% HPi –
Pr ACID LOAD
Pi – –
+
H Cl or
6% Cl – The role of the kidneys is to excrete the fixed acid load
HCO 3 – imposed by the underlying disease process responsible for
metabolicacidosis.Thekidneysaccomplishthistaskprimar-
þ
ily by augmenting its excretion of NH 4 .Titratable acidity
Plasma and changes little unless there is a change in the filtered load of
interstitial bicarbonate 43% þ
+ – Extracellular phosphate. Chloride ions accompany the NH 4 into urine
42% H + HCO 3 ⇔ H 2 CO 3 ⇔ H 2 O + ↑CO 2
buffering while HCO 3 is regenerated and reabsorbed into extracel-

lular fluid(ECF)torestoreHCO 3 thatwastitratedduring
theacutefixedacidload.Within48hoursofafixedacidload,
Plasma proteins approximately 25% of the added acid has been excreted in
1% H + Pr ⇔ HPr the urine, and the remainder is excreted during the next 4
–
+
days. 232 The kidney can increase its NH 4 þ excretion
Metabolic acidosis as much as fivefold to tenfold during chronic metabolic
Figure 10-1 Distribution of buffer response to a fixed acid acidosis. 219,235,238 There is some evidence that cats do
load. (Drawing by Tim Vojt. Adapted from Pitts RF. Physiology of the not adapt to metabolic acidosis by enhanced renal
kidney and body fluids, 2nd ed. Chicago: Year Book Medical, 1968: ammoniagenesis. 137 The role of the kidneys in regulation
171.)
of acid-base balance is discussed further in Chapter 9.
CLINICAL FEATURES OF METABOLIC
response is an approximately 0.7-mm Hg decrement in

per 1-mEq/L decrement in plasma HCO 3 concen- ACIDOSIS
P CO 2
*
tration. Inthesestudies,thesmallestobservedrespiratory The clinical signs in small animals with metabolic acidosis
response was an approximately 0.5-mm Hg decrement in are more likely to be caused by the underlying disease
per milliequivalents per liter decrement in plasma responsible for metabolic acidosis than by the acidosis
P CO 2 3
HCO 3 concentration, and the largest response was a itself. In humans, respiratory compensation for metabolic

per milliequivalents per acidosis leads to characteristic hyperventilation,
1.1-mm Hg decrement in P CO 2

liter decrement in plasma HCO 3 concentration. 66 Data recognized by a deep, rhythmic breathing pattern (i.e.,
are limited on the respiratory response of cats to metabolic Kussmaul respirations). Such a characteristic respiratory
acidosis, but there is some evidence that the cat fails to pattern has not been described in small animal patients,
develop respiratory compensation to the same extent as and metabolic acidosis is usually suspected by observation
observed in the dog in spontaneous 236 and NH 4 Cl- of a low total CO 2 content on a biochemical profile and
induced metabolic acidosis. 43,85,137,211,212 confirmed by blood gas analysis.
The classic explanation of the respiratory response to Severe acidosis has serious detrimental effects on car-
metabolic acidosis is that the increase in [H ] (decrease diovascular function, including decreased cardiac output,
þ
in pH) stimulates ventilation, and the resultant decrease decreased arterial blood pressure, and decreased hepatic
ratio and pH toward and renal blood flow. 4 Myocardial contractility is
in P CO 2 returns the HCO 3 /P CO 2
normal. This is true in acute metabolic acidosis, but the decreased when blood pH falls below 7.20. 161,180
resultant secondary hypocapnia has been observed to Impaired contractility may result from a decrease in
decrease plasma HCO 3 concentration further in chronic myocardial intracellular pH (pH i ) and displacement of

metabolic acidosis, presumably by reducing renal HCO 3 calcium ions from critical binding sites on contractile
reabsorption. This secondary hypocapnia contributes to proteins. Acidosis may predispose the heart to ventricular

40% of the observed decrease in plasma HCO 3 concen- arrhythmias or ventricular fibrillation. Acidosis has a
tration during chronic HCl acidosis. 147 Thus, chronic direct arterial vasodilating effect that is offset by increased
metabolic acidosis decreases plasma HCO 3 release of endogenous catecholamines. However, the
inotropic response to catecholamines is impaired, and this
*References 3, 49, 54, 66, 141, 147–149 may be associated with a reduction in the number of