Page 306 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Respiratory Acid-Base Disorders 297

represents effective compensation, and the pH is BOX 11-4 Causes of Respiratory
normal or near normal in dogs with chronic respiratory
alkalosis. However, normalization of pH may take up Alkalosis
to 4 weeks to be achieved. 13 Cats chronically exposed
to a hypoxic environment (FIO 2 ¼ 10%) for 28 days also Hypoxemia (Stimulation of Peripheral
7
were able to maintain a normal arterial pH. Expected Chemoreceptors by Decreased Oxygen
compensation in cats cannot be inferred from this study, Delivery)
but based on the ability to maintain a normal pH, it may Right-to-left shunting
be reasonable to assume that cats can compensate to Decreased PIO 2 (e.g., high altitude)
chronic respiratory alkalosis, as well as dogs and humans. Congestive heart failure
Severe anemia
As a result, abnormal PCO 2 and HCO 3 concentration
with normal pH does not necessarily imply a mixed Severe hypotension
acid-base disorder in both dogs and cats. Decreased cardiac output
Pulmonary diseases with ventilation-perfusion mismatch
Pneumonia
CAUSES OF RESPIRATORY ALKALOSIS Pulmonary thromboembolism
Pulmonary fibrosis
Common causes of respiratory alkalosis include stimula- Pulmonary edema
tion of peripheral chemoreceptors by hypoxemia, Acute respiratory distress syndrome (ARDS)
primary pulmonary disease, direct activation of the Pulmonary Disease (Stimulation of Stretch/
brainstem respiratory centers, overzealous mechanical Nociceptors Independent of Hypoxemia)
ventilation, and situations that cause pain, anxiety, or fear.
In addition, respiratory alkalosis can occur during recov- Pneumonia
Pulmonary thromboembolism
ery from metabolic acidosis because hyperventilation Interstitial lung disease
persists for 24 to 48 hours after correction of metabolic Pulmonary edema
acidosis. A more detailed list of causes is found in Acute respiratory distress syndrome (ARDS)
Box 11-4.
When PO 2 decreases to less than 60 mm Hg, the Centrally Mediated Hyperventilation
Liver disease
peripheral chemoreceptors mediate an increase in rate
Hyperadrenocorticism
and depth of breathing, resulting in hypocapnia.
Gram-negative sepsis
Decreased oxygen delivery also results in hypocapnia
Drugs
(e.g., severe anemia, cardiovascular shock). The effect Salicylates
of the resulting hypocapnia and decreased [H ] on the Corticosteroids
þ
central chemoreceptors is to negatively feedback on the Progesterone (pregnancy)
respiratory control system and blunt this initial hyperven- Xanthines (e.g., aminophylline)
Recovery from metabolic acidosis
tilation. As renal compensation occurs, plasma HCO 3
þ
decreases, [H ] increases, and central inhibition of fur- Central neurologic disease
ther hyperventilation is removed. A steady-state results Trauma
when the peripherally mediated hypoxemic drive to ven- Neoplasia
Infection
tilation is balanced by the central effect of the alkalemia
Inflammation
resulting from renal adaptation to hypocapnia. If PCO 2
Cerebrovascular accident
is held constant in the presence of hypoxemia (as seen
Exercise
in patients with pulmonary disease), the dampening effect Heatstroke
of hypocapnia does not occur, and a lesser degree of
hypoxemia may stimulate ventilation. Muscle Metaboreceptor Overactivity
Pulmonary diseases such as pneumonia, diffuse inter- Heart failure
stitial lung disease, and thromboembolism may cause Overzealous Mechanical Ventilation
respiratory alkalosis. The hyperventilation seen with pri-
mary lung disease may be a result, at least in part, of the Situations Causing Pain, Fear, or Anxiety
concurrent hypoxemia. However, pulmonary diseases
may cause hyperventilation without hypoxemia as a result
of stimulation of stretch receptors and nociceptive
receptors. 23,68 The stretch receptors are located in the
smooth muscle of the tracheobronchial tree. The noci- (J receptors) lining capillaries in the interstitium. These
ceptive receptors include irritant receptors in the epithe- receptors respond to stimuli such as irritants, interstitial
lium of small airways and juxtacapillary receptors edema, fibrosis, or pulmonary capillary congestion.