Page 344 - Small Animal Internal Medicine, 6th Edition

316 PART II Respiratory System Disorders

VetBooks.ir 100

O 2 saturation of hemoglobin (%) 60
80

40

20

0
0 20 40 60 80 100
PO 2 (mm Hg)
FIG 20.30
Oxyhemoglobin dissociation curve (approximation).

produces pallor in an animal than cyanosis. Treatment for BOX 20.7
hypoxemia is indicated for all animals with cyanosis. Clinical Correlations of Blood Gas Abnormalities
Determining the mechanism of hypoxemia is useful in
selecting appropriate supportive therapy. These mechanisms Decreased PaO 2 and Increased PaCO 2 (Normal
include hypoventilation, inequality of ventilation and perfu­ A-a Gradient)
sion within the lung, and diffusion abnormality. Hypoventi­ Venous specimen
lation is the inadequate exchange of gases between the Hypoventilation
outside of the body and the alveoli. Both PaO 2 and PaCO 2 are Airway obstruction
affected by lack of gas exchange, and hypercapnia occurs in Decreased ventilatory muscle function
conjunction with hypoxemia. Causes of hypoventilation are • Anesthesia
listed in Box 20.7. • Central nervous system disease
The ventilation and perfusion of different regions of the • Polyneuropathy
lung must be matched for the blood leaving the lung to be • Polymyopathy
̇
fully oxygenated. The relationship between ventilation (V) • Neuromuscular junction disorders (myasthenia
gravis)
̇ ̇
̇
and perfusion (Q) can be described as a ratio (V/Q). Hypox­ • Extreme fatigue (prolonged distress)
̇ ̇
emia can develop if regions of lung have a low or a high V/Q. Restriction of lung expansion
Poorly ventilated portions of lung with normal blood • Thoracic wall abnormality
̇ ̇
flow have a low V/Q. Regionally decreased ventilation occurs • Excessive thoracic bandage
in most pulmonary diseases for reasons such as alveolar • Pneumothorax
flooding, alveolar collapse, or small airway obstruction. • Pleural effusion
The flow of blood past totally nonaerated tissue is known Increased dead space (low alveolar ventilation)
̇ ̇
as a venous admixture or shunt (V/Q of zero). The alveoli • Severe chronic obstructive pulmonary disease/
may be unventilated as a result of complete filling or col­ emphysema
lapse, resulting in physiologic shunts, or the alveoli may End-stage severe pulmonary parenchymal disease
be bypassed by true anatomic shunts. Unoxygenated blood Severe pulmonary thromboembolism
from these regions then mixes with oxygenated blood from Decreased PaO 2 and Normal or Decreased PaCO 2 (Wide
ventilated portions of the lung. The immediate result consists A-a Gradient)
of decreased PaO 2 and increased PaCO 2 . The body responds to Ventilation/perfusion (V/Q) abnormality
̇
̇
hypercapnia by increasing ventilation, effectively returning Most lower respiratory tract diseases (see Box 19.1)
the PaCO 2 to normal or even lower than normal. However,