Page 305 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

296 ACID-BASE DISORDERS

underlying cause of alveolar hypoventilation. For exam- production. NaHCO 3 itself is not innocuous. NaHCO 3
ple, airway obstruction should be identified and relieved, may alter hemodynamics, causing hypotension, decreased
whereas medications that depress ventilation should be contractility, and cardiac arrest, 57 as well as decreased
discontinued if possible. Pleurocentesis should be cerebral blood flow and cerebrovenous oxygen tension. 5
performed to remove fluid or air when pleural effusion Thus NaHCO 3 treatment is not warranted. In addition,
or pneumothorax is present. Although at times it is not the use of the strong organic base tris(hydroxymethyl)
possible to remove the underlying cause of aminomethane (THAM) has been investigated. 17 THAM
hypoventilation (e.g., chronic pulmonary disease), appro- promotes CO 2 removal as HCO 3 is generated. How-
priate treatment of the primary disease should still be ever, the amount of CO 2 removed is very small, and thus
initiated along with supportive therapeutic measures. THAM has marginal clinical benefit, at best.
The primary goal is to remove the CO 2 , and consequently Administration of a parenteral solution with adequate

mechanical ventilation is often necessary. amounts of Cl facilitates recovery from chronic hyper-
According to the alveolar gas equation, a patient capnia and prevents the development of metabolic alkalo-
breathing room air at sea level (PIO 2, approximately sis after PaCO 2 has returned to normal. Dogs recovering
150 mm Hg) will develop life-threatening hypoxia from chronic hypercapnia and receiving a low-salt diet
(PaO 2 <55 to 60 mm Hg) before life-threatening hyper- had persistently increased plasma HCO 3 levels. 70 Addi-

capnia. Thus supplemental oxygen and assisted ventila- tion of sodium or potassium chloride to the diet allowed
tion is needed in treating acute respiratory acidosis. full correction of the acid-base disturbances. Provision of

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Although oxygen therapy may aid in the treatment of sufficient Cl allows the kidney to reabsorb Na in con-

acute respiratory acidosis, in patients with chronic hyper- junction with Cl and excrete the excess HCO 3 retained
capnia, oxygen may suppress the drive for breathing in during compensation for chronic hypercapnia.
patients with chronic hypercapnia. In chronic hypercap-
nia, the central chemoreceptors become progressively RESPIRATORY ALKALOSIS
insensitive to the effects of CO 2 , and O 2 becomes the pri-
mary stimulus for ventilation. As a result, oxygen therapy Respiratory alkalosis or primary hypocapnia is
may further suppress ventilation, worsening the respira- characterized by decreased PCO 2 , increased pH, and a
tory acidosis. If oxygen is administered, PaO 2 should be compensatory decrease in HCO 3 concentration in the

kept between 60 and 65 mm Hg because the hypoxic blood. Respiratory alkalosis occurs whenever the magni-
drive to breathing remains adequate up to this level. 67 tude of alveolar ventilation exceeds that required to
In respiratory acidosis, the goals of treatment are to eliminate the CO 2 produced by metabolic processes in
ensure adequate oxygenation and provide adequate alve- the tissues.
olar ventilation. Patients approaching respiratory muscle
fatigue or respiratory failure or those experiencing pro- METABOLIC COMPENSATION IN
gressive acidemia or hypoxemia will need mechanical or RESPIRATORY ALKALOSIS
assisted ventilation to accomplish these objectives. Respi- Acute Respiratory Alkalosis
ratory failure in the face of concurrent hypoxemia is
diagnosed when the PaCO 2 is more than 50 mm Hg in When PCO 2 is acutely decreased, CO 2 leaves the cells to
a nonsedated or nonanesthetized patient, when PaO 2 is achieve a new equilibrium point. Chloride ions leave red

less than 50 mm Hg with FIO 2 of 0.21, or when PaO 2 is blood cells in exchange for HCO 3 ,causingadecrease

8
less than 50 mm Hg with a FIO 2 of more than 0.5. When in plasma HCO 3 concentration. This results in decreased
mechanical or assisted ventilation is begun, care must be plasma SID and increases intracellular SID. Furthermore,
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taken to decrease PaCO 2 slowly. In human patients, rapid H translocation into the extracellular space in exchange
decreases in PCO 2 can result in cardiac arrhythmias, for sodium and potassium also decreases plasma SID.
decreased cardiac output, and reduced cerebral blood As in respiratory acidosis, intracellular phosphates
flow. 43 A sudden decrease in blood PCO 2 may also result and proteins are the major buffers in the acute adaptive
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in posthypercapnic metabolic alkalosis and rapid diffusion response. Extracellular buffering by release of H from
of CO 2 from cerebrospinal fluid into blood, thus quickly plasma proteins constitutes only 1% of the acute response,
increasing cerebrospinal pH. whereasintracellularbufferingaccountedfor theremaining
24
Therapy with NaHCO 3 or other alkalinizing solutions 99%. In dogs and cats, a compensatory decrease of
concentration for each 1-mm
is not indicated in respiratory acidosis. Administration of 0.25 mEq/L in HCO 3 15,28
NaHCO 3 increases SID and may decrease [H ] and ven- Hg decrease in PCO 2 is expected (see Box 11-2).
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tilatory drive, thus worsening hypoxemia. The resulting
Chronic Respiratory Alkalosis
decrease in respiratory drive as a result of NaHCO 3
administration additionally may increase CO 2 and worsen During chronic respiratory alkalosis, a 0.55 mEq/L
respiratory failure, especially if alveolar ventilation cannot decrease in HCO 3 is expected for each 1-mm
Hg decrease in PCO 2 in dogs 15 (see Box 11-2). This
be increased to balance out the increased CO 2