Page 416 - Clinical Small Animal Internal Medicine

384 Section 5 Critical Care Medicine

to be properly oxygenated despite an adequate alveolar
Box 39.1 Mechanisms of hypoxemia
VetBooks.ir Associated with a normal A‐a gradient (no venous partial pressure of oxygen (PAO 2 ). Calculation of the A‐a
gradient is covered in Chapter 38.
Right‐to‐left shunting (anatomic shunting) is a rela-
admixture)
tively uncommon cause of hypoxemia in veterinary prac-
Hypoventilation
tice relative to other forms of venous admixture. Tetralogy
●
● Decreased PiO 2
of Fallot is perhaps the most common congenital defect
Associated with an increased A‐a gradient (venous in which right‐to‐left shunting occurs routinely. In many
admixture) other conditions, a potential shunting conduit may be
present but right‐to‐left shunting does not occur unless
Right‐to‐left shunting (anatomic shunting)
● cardiac pressures on the right side exceed those on the
Perfusion of nonventilated alveoli (no V–Q; physiologic
● left (e.g., septal defects). Similarly, pathology involving
shunting)
Ventilation–perfusion mismatching (low V–Q) the great vessels such as patent ductus arteriosus would
● not be expected to result in right‐to‐left shunting unless
Diffusion impairment
●
significant pulmonary hypertension, profound systemic
hypotension, or both were present. In such cases, differ-
of oxygen via dilution to a degree, but it is ultimately the ential cyanosis may alert the clinician to the presence of
failure to provide adequate inflow of oxygen to replace this pathology. When significant anatomic right‐to‐left
what has been taken up that reduces PAO 2 . For this rea- shunting is present, hypoxemia may become refractory to
son, hypoxemia due to hypoventilation may be readily correction with supplemental oxygen. When shunt flow
corrected by restoring appropriate levels of alveolar ven- reaches 30% of cardiac output, hypoxemia is largely unre-
tilation, by increasing the proportion of inspired gas that sponsive to supplemental oxygen, with no improvement
is oxygen (i.e., FiO 2 ), or both. Hypoventilation is thus best expected at all when shunt flow approaches 50% of total
considered as a form of hypercapneic respiratory failure blood flow. The shunt equation is slightly cumbersome
rather than a truly hypoxemic form. Hypoventilation is an and a clinically useful shortcut is to estimate 5% extra
implausible mechanism of hypoxemia in patients receiv- shunting (5% is normal so this is additional shunting
ing supplemental oxygen if one excludes complete apnea added to the 5% baseline value) for every 100 mmHg that
from the discussion. the PaO 2 is below the expected value for that FiO2. For
Decreased PiO 2 is an often incorrectly or incompletely example, if a patient has a PaO 2 of 200 mmHg on 100%
categorized cause of hypoxemia. Many authors will list oxygen then one would estimate the shunt fraction to be
decreased FiO 2 instead of PiO 2 as the mechanism. A 20% (expected PaO 2 is 500 mmHg on 100% oxygen).
truly decreased fraction of inspired oxygen is quite rare Physiologic shunting occurs when perfusion is main-
as the proximate cause of hypoxemia and would gener- tained to nonventilated alveoli. This situation could be
ally only be encountered if a patient were on a rebreath- considered a failure of hypoxic pulmonary vasoconstric-
ing circuit with inadequate fresh gas inflow. One would tion. Inflammatory mediators and drug agents can com-
hope that this is a rare occurrence. Low PiO 2 in contrast promise the function of both the sensing and effector
is quite common and occurs any time an animal is taken arms of this response system. As alveolar oxygen ten-
significantly above sea level unless they are maintained sions drop, the expected response is that the local vascu-
in a suitably pressurized environment such as an aircraft. lar resistance to those alveoli will increase, thus diverting
The hypoxemia that develops at elevation is the result of flow to better‐ventilated alveoli. In the case of zero alve-
a decrease in PiO 2 with a normal FiO 2 (i.e., the atmos- olar ventilation, the optimal response would be to reduce
phere is still 21% oxygen, but total pressures and thus all perfusion to that region as well. Failure to do so results in
partial pressures are decreased). For a patient breathing physiologic shunting. The effect is the same as if the lung
room air at sea level, decreased PiO 2 is not a reasonable were not there at all and the blood was passing through
differential diagnosis for hypoxemia. In the case of both an anatomic shunt. This mechanism explains why
hypoventilation and decreased PiO 2 , the hypoxemia that obstruction of ventilation to a lung lobe during lung
is observed is due to a decrease in PAO 2 . This decrease is lobectomy (e.g., during one‐lung ventilation for thoraco-
accompanied by a proportional decrease in PaO 2 and scopic lung lobectomy) results in hypoxemia, but the
thus the A‐a gradient remains within the normal range. subsequent lung lobectomy itself does not. Removal of
As mentioned above, causes of hypoxemia that are an excessive amount of lung tissue (e.g., all the lung lobes
associated with an increased A‐a gradient are those that on the right side) can result in hypoxemia, but this is due
fall under the overarching category of venous admixture. to ventilation–perfusion mismatching (excessive perfu-
Venous admixture includes all mechanisms by which sion relative to ventilation) in the remaining lung lobes
blood passing from the right heart to the left heart fails rather than physiologic shunting. Much as is observed