Page 304 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Respiratory Acid-Base Disorders 295

termed global hypoventilation) or abnormal ventilation- acute respiratory acidosis is not made in small animal
perfusion ratios in the lung. In global hypoventilation, practice. Frequently, the patient dies from hypoxemia
CO 2 is delivered to the lung but ventilation is inadequate before hypercapnia can become severe. Abrupt cessation
and hypercapnia and hypoxemia develop. Global of ventilation is fatal within 4 minutes, whereas severe
hypoventilation results from either an abnormal ventila- hypercapnia would not develop for 10 to 15 minutes in
tory drive or alterations in respiratory pump mechanics. such a setting. 42 Many small animals presented to
In normal animals, carbon dioxide is a marked stimulus veterinarians have been ill long enough to develop a
for ventilation that subsequently increases central respira- chronic steady state (i.e., 2 to 5 days) and their blood
tory drive to offset any potential rise in blood CO 2 levels. gas results reflect adaptation to chronic hypercapnia.
Animals with profound reductions in their drive to However, if a patient with chronic respiratory acidosis
breathing, however, do not respond to such stimuli and acutely decompensates, dyspnea (see Dyspnea section)
become hypercapnic. Conditions that may result in cen- and life-threatening consequences may develop, and the
tral hypoventilation include CNS trauma, neoplasia, patient may die quickly.
infection, inhalant anesthetics, narcotics, and cerebral Although many clinical signs are subtle, especially in
edema. Global hypoventilation also results from failure chronic respiratory acidosis, investigations in humans
of respiratory mechanics. In these cases, the respiratory and experimental animals show that cardiovascular, met-
muscles, chest wall, or both are ineffective in maintaining abolic, and neurologic consequences arise following
adequate ventilation, and the central respiratory drive is acute hypercapnic academia. 80 Hypercapnia stimulates
increased. Examples of diseases that affect respiratory the sympathetic nervous system and causes release of
mechanics are severe obesity, spinal cord injury, and catecholamines. 11,40 Tachyarrhythmias (including ven-
myasthenia gravis. tricular fibrillation) are common and result from
Maintaining normal ventilation to alveolar perfusion increased sympathetic tone, electrolyte fluctuations,
ratios is essential for preserving eucapnia and associated hypoxemia, and academia. 17,35,60 In experi-
normoxemia. 84 Areas of lung that are ventilated but are mental canine models, acute respiratory acidosis increases
ineffectively perfused increase the dead space to tidal vol- heart rate and cardiac output but decreases myocardial
ume ratio (VD/VT). When a normal breathing pattern contractility and systemic vascular resistance with no
shifts to a dyspneic pattern (see Dyspnea section) change in blood pressure. 81 Thus, on physical examina-
consisting of very fast respiratory rates and small, inade- tion of the patient, one sees a hyperdynamic state, with
quate tidal volumes (as that seen in some patients with an increased heart rate and cardiac output, increased or
acute respiratory distress syndrome), the VD/VT normal blood pressure, and “flushed” or “brick-red”
increases. In some disease states, (e.g., shock) there mucous membranes associated with vasodilation. Hyper-
may be areas of the lung with minimal or no alveolar per- capnia also causes a rightward shift of the oxygen-hemo-
fusion. The normal lung has great reserve capabilities, and globin dissociation curve (see Figure 11-3), promoting
unloading of oxygen at the tissues and enhancing oxygen
additional alveoli can compensate to keep the PaCO 2
within normal limits. However, if other alveolar units delivery and carrying capacity. 65
cannot be hyperventilated to remove the CO 2 ,an Metabolic consequences of acute hypercapnia include
increased dead space will result in hypercapnia. Disorders retention of both sodium and water, possibly as a result of
resulting in this type of respiratory acidosis include increased antidiuretic hormone release, increased cortisol
pulmonary thromboembolism, emphysema, and fibrosis. secretion, and activation of the renin-angiotensin sys-
tem. 43 Respiratory, as well as metabolic, acidosis may also
DIAGNOSIS AND CLINICAL FEATURES lead to gastroparesis by altering gastric muscle activity
OF RESPIRATORY ACIDOSIS and fundic tone. 77
Because most clinical signs in animals with respiratory aci- The nature of the neurologic signs seen depends on
dosis reflect the underlying disease process responsible for the magnitude of hypercapnia, rapidity of change in
hypercapnia rather than the hypercapnia itself, subjective CO 2 and pH, and the amount of concurrent hypoxemia.
clinical evaluation of the patient alone is not reliable in Acute hypercapnia causes cerebral vasodilation, subse-
making a diagnosis of respiratory acidosis. In fact, quently increasing cerebral blood flow and intracranial
patients with chronic, compensated respiratory acidosis pressure. 3,36,54,87 Clinically, the CNS effects of hypercap-
may have very mild clinical signs. One should consider nia can result in signs ranging from anxiety, restlessness,
respiratory acidosis in a patient having a disorder likely and disorientation to somnolence and coma, especially
to be associated with hypercapnia (see Box 11-3). when PCO 2 approaches 70 to 100 mm Hg. 1,43,58,80
Definitive diagnosis of respiratory acidosis is established
by arterial blood-gas analysis. TREATMENT OF RESPIRATORY
In extremely acute hypoventilation (e.g., cardiopul- ACIDOSIS
monary arrest, airway obstruction), hypoxemia is the The most effective treatment of respiratory acidosis
immediate threat to life, and a laboratory diagnosis of consists of rapid diagnosis and elimination of the