Page 301 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

292 ACID-BASE DISORDERS

hemoglobin dissociation curve, the effect of increasing Final blood gas tensions are determined by the mixing
alveolar ventilation on arterial oxygen saturation is mini- of gas contents from different gas units. Thus V-Q mis-
mal above a PaO 2 of 55 to 60 mm Hg. 27,46 Clinically, match will produce hypoxemia based on the actual O 2
important causes of hypoventilation include CNS disease, and CO 2 levels in each lung area and the amount of blood
respiratory depressant pharmacologic agents, neuromus- flow to each unit. 59,85 The severity of V-Q mismatch can
cular diseases affecting the respiratory muscles, chest wall be assessed using the (A a) O 2 gradient as both
injury, upper airway obstruction, and severe diffuse abnormally low and high V-Q ratios increase the gradient.
pulmonary disease. Patients with V-Q mismatch usually are hypoxemic but
have normal or decreased PaCO 2 because chemoreceptors
DIFFUSION IMPAIRMENT respond to, and minute ventilation is altered by, changes
Diffusion impairment occurs whenever there is incom- in carbon dioxide levels. 58,85 Hypoxemia resulting from
plete equilibration of alveolar gas and pulmonary end- V-Q mismatch can be corrected by increasing the fraction
capillary blood. Equilibration of oxygen between the of inspired oxygen (FIO 2 ) by use of 100% O 2 .
alveolus and the erythrocyte is extremely rapid under nor-
mal conditions, and this type of hypoxemia infrequently is RIGHT-TO-LEFT SHUNT
observed in small animal medicine. However, a diffusion Right-to-left shunting is a severe form of V-Q mismatch
impairment leading to hypoxemia may be seen with and results when mixed venous blood completely
thickening of the alveolar-capillary membrane (e.g., bypasses ventilated pulmonary alveoli and returns to
“alveolar-capillary block” seen in diffuse pulmonary the arterial circulation. A small amount (2% to 3%) of
interstitial disease), or loss of alveolar or capillary surface shunting is present in normal animals through the bron-
area (e.g., emphysema or vasculitis). Although hypox- chial and thesbian circulations. In pathologic states, shunt
emia from a diffusion impairment may occur as a conse- results from perfusion of lung areas that receive no venti-
quence of the aforementioned disease states, it also may lation because of atelectasis or consolidation (V-Q ¼ 0) or
be detected under certain circumstances of high cardiac from deoxygenated blood flow through anatomic right-
output that markedly decrease transit time of red cells to-left channels. Thus shunting is the main cause for hyp-
(e.g., exercise). In any case, its contribution to hypoxemia oxemia in pulmonary edema, atelectasis, pneumonia, and
is usually negligible and a diffusion impairment seldom is in congenital abnormal cardiac communications between
the limiting factor in oxygen transfer to arterial blood. the systemic and pulmonary circulations (e.g., patent
ductus arteriosus, ventricular or atrial septal defect, tetral-
VENTILATION-ALVEOLAR ogy of Fallot) with right-to-left blood flow bypassing
PERFUSION MISMATCH (V-Q the lungs.
MISMATCH) Even small amounts of shunt result in clinically rele-
Despite regional differences in V-Q ratios throughout the vant hypoxemia because venous blood oxygen content
mammalian lung, the heterogeneity of individual lung is extremely low and mixed venous blood is being added
units is relatively limited, resulting in a V-Q ratio of directly to arterial blood without alveolar gas exchange.
approximately 0.8. 46 This ratio enables the mixed venous Similar to V-Q mismatch, patients with right-to-left
blood to become fully oxygenated and the CO 2 to be shunting have a decreased PaO 2 with a normal or
eliminated without increases in minute ventilation. 85 decreased PaCO 2 and widened (A a) O 2 gradients.
V-Q mismatch is one of the most commonly encoun- However, one major difference is that the PaO 2 levels in
tered causes of hypoxemia. It is present in areas of the animals with increased shunting fail to return to normal
lung where there are perturbations in ventilation or per- even with 100% O 2 supplementation. In contrast, animals
fusion resulting in inefficient gas exchange. For example, with V-Q mismatch, hypoventilation, or diffusion
low V-Q units have a low PaO 2 and high alveolar PCO 2 , impairment exhibit pronounced increases in PaO 2 with
resulting in hypercapnic and hypoxemic blood. In fact, oxygen enrichment (Table 11-1).
when breathing room air, the blood leaving a gas
exchange unit with a V-Q ratio of less than 0.1 is essen- RESPIRATORY ACIDOSIS
tially unoxygenated. Low V-Q units (poorly ventilated,
adequately perfused) can be found in patients with Respiratory acidosis, or primary hypercapnia, results
increased airway resistance (e.g., asthma, bronchitis, when carbon dioxide production exceeds elimination
chronic obstructive pulmonary disease). High V-Q units via the lung*. Respiratory acidosis is almost always a result
of respiratory failure with resultant alveolar
(poorly perfused, adequately ventilated) have a high PaO 2
and a low PaCO 2 . In lung areas with V-Q ratios greater hypoventilation and is characterized by an increase in
than 1, additional increases in ventilation do not improve PaCO 2 , decreased pH, and a compensatory increase in
oxygenation. 59,85 High V-Q ratios are found in diseases blood HCO 3 concentration.

with increased compliance (e.g., emphysema) or low out-
46
put states (e.g., pulmonary embolism). *For reviews see: Epstein and Singh, 2001 17 and Markou et al. 2004 .