Page 307 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

298 ACID-BASE DISORDERS

DIAGNOSIS AND CLINICAL FEATURES TREATMENT OF RESPIRATORY
OF RESPIRATORY ALKALOSIS ALKALOSIS
It is difficult to attribute specific clinical signs to respira- Treatment should be directed towards relieving the
tory alkalosis in the dog and cat. The clinical signs usually underlying cause of the hypocapnia; no other treatment
are caused by the underlying disease process and not by is effective. Respiratory alkalosis severe enough to cause
the respiratory alkalosis itself. However, in humans, head- clinical consequences for the animal is uncommon.
ache, light-headedness, confusion, paresthesias of the Hypocapnia itself is not a major threat to the well being
extremities, tightness of the chest, and circumoral numb- of the patient. Thus the underlying disease responsible for
23,1
ness have been reported in acute respiratory alkalosis. hypocapnia should receive primary therapeutic attention.
In any case, clinical signs in small animals are uncommon
due to efficient metabolic compensation and tachypnea DYSPNEA
may be the only clinical abnormality found, especially
with chronic hypocapnia. In small animal practice, dyspnea is an important clinical
If the pH is greater than 7.6 in respiratory sign associated with acute or severe respiratory dysfunc-
alkalosis, neurologic, cardiopulmonary, and metabolic tion and abnormal acid-base regulation. In animals, dys-
1
consequences may arise. Such a pH can only be achieved pnea is defined as difficult or labored breathing.
in acute respiratory alkalosis before renal compensation However, dyspnea in humans is further described as an
ensues. Alkalemia results in arteriolar vasoconstriction unpleasant sensory experience of breathing discomfort
that can decrease cerebral and myocardial perfusion. In or “pain.” With the recent advances in veterinary pain rec-
addition, hyperventilation (PCO 2 <25 mm Hg) causes ognition and management, it is appropriate to assume
decreased cerebral blood flow, potentially resulting in veterinary patients have similar negative sensory
clinical signs such as confusion and seizures. experiences associated with disorders that result in dys-
Hypocapnia decreases blood pressure and cardiac out- pnea in humans. There are at least three types of dyspnea
put in anesthetized but not awake subjects, possibly that are pertinent to veterinary patients: air hunger,
because anesthetics blunt reflex tachycardia. For example, increased work of breathing, and thoracic tightness*.
in anesthetized dogs, acute hypocapnia decreased blood Air hunger results from an imbalance in the perception
pressure as a result of reduced cardiac output together of an increased drive to breathe from chemoreceptors
with an ineffective increase in total peripheral resistance (e.g., hypoxemia and hypercapnia) relative to the afferent
and no change in heart rate. 39,52 Although alkalemia signaling from stretch receptors in the thoracic cavity and
exerts a small positive inotropic effect on the isolated lungs. 51 Although air hunger does not require abnormal
heart, alkalemia also predisposes to refractory supraven- arterial concentrations of oxygen or carbon dioxide, it is
tricular and ventricular arrhythmias, especially in patients the balance of the patient’s actual alveolar ventilation
with preexisting cardiac disease. 1 compared with the ventilation needed to maintain normal
Acute alkalemia shifts the oxygen-hemoglobin dissoci- acid-base regulation of the patient that determines if dys-
ation curve to the left, reducing the release of oxygen to pnea occurs. A second type of dyspnea occurs with an
the tissues by increasing affinity of hemoglobin for oxy- increased work or effort of breathing. Increased respira-
gen 31 (see Figure 11-3). However, chronic alkalemia tory pressures generated to breathe in the face of
negates this effect by increasing the concentration of decreased pulmonary compliance, airway obstruction,
2,3-DPG in red cells. 30,23,66 or alterations in respiratory muscle length result in dys-
Hypokalemia may occur due to the translocation of pnea. 21,71 A common example of this type is seen in
potassium into cells and renal and extrarenal losses in dynamic upper airway obstructions in which cognitive
patients with acute respiratory alkalosis. 23,30,66 In awareness of the inability to breathe can reach distressing
anesthetized, hyperventilated dogs, potassium is expected levels. Lastly, in humans, and presumably in animals,
to decrease 0.4 mEq/L for each 10-mm Hg decrease in asthmatic chest tightness results in dyspnea secondary
PCO 2 . 52 Similar changes (0.6 mEq/L for each 10-mm to bronchoconstriction. The primary afferent signals
Hg decrease in PCO 2 ) were observed in awake dogs with responsible for this type of dyspnea are generated from
acute respiratory acidosis induced by hypoxemia 32 or by intrapulmonary afferent receptors and not respiratory
simulating a high altitude environment (30,000 feet). 72 muscle afferents. 9,45
Hypokalemia can result in neuromuscular weakness, sen- Treatment specifically directed at relieving dyspneic
sitization to digitalis-induced arrhythmias, polyuria, and sensations associated with respiratory disorders is chal-
increased ammonia production that amplifies the effects lenging. Although therapy should initially be directed
1
of hepatic encephalopathies. However, the hypokalemia at removing the inciting cause, newer treatments such
induced by respiratory alkalosis is mild and short-lived.
Hypokalemia is not present in patients with chronic
respiratory alkalosis. 2,22,25
*For review see Mellema, 2008. 48