No. 4—Evidence of inefficient gas exchange
Inefficient gas exchange is confirmed by the presence of hypoxemia and, occasionally, hypercapnia. The best way to determine
whether a patient has hypoxemia is to obtain an arterial blood gas sample for analysis (see sidebar titled "How to obtain arterial samples for blood gas analysis"). Many bench-top and point-of-care analyzers are reliable sources of blood gas information. The partial pressure of oxygen
in arterial blood (PaO2) provides information about blood oxygenation. A normal PaO2 should be about 80 to 110 mm Hg if the patient is breathing room air.9 If the patient is receiving oxygen supplementation, the PaO2 should be about five times the percentage of oxygen being supplemented. For example, a patient receiving 40% oxygen in an
oxygen cage should be expected to have a PaO2 around 200 mm Hg (40 x 5), while an anesthetized patient receiving 100% oxygen should have a PaO2 near 500 mm Hg (100 x 5).
If blood gas analysis is not available in a practice, pulse oximetry measurement can be performed to get a general idea of
blood oxygenation. However, blood gas analysis is necessary for true diagnosis of acute lung injury or ARDS; it is also necessary
to distinguish between these two conditions.
. Other parameters that may help define a patient's respiratory status include the partial pressure of carbon dioxide in arterial
blood (PaCO2) and the percent of hemoglobin that is saturated with oxygen (SaO2). The PaCO2 provides information about carbon dioxide production and elimination. Normal values are between 32 and 43 mm Hg in dogs and
26 and 36 mm Hg in cats.9 Elevation in PaCO2 represents hypoventilation, while values below normal suggest hyperventilation. The SaO2 should be near 100% when a patient has a PaO2 of 100 mm Hg or more. An SaO2 of 96% corresponds to a PaO2 of 80 mm Hg or above, while an SaO2 of 91% corresponds to a PaO2 of 60 mm Hg.9 SaO2 is not as effective of a measurement of arterial oxygenation as PaO2 is when a patient is receiving oxygen supplementation because of the small change in percentage once PaO2 exceeds 100 mm Hg.9
SpO2. Pulse oximetry is a widely available noninvasive tool that can also be used to provide a quick assessment of oxygenation
by indirectly measuring the oxygen saturation of hemoglobin (SpO2). This tool may be useful when blood gas analysis is not available, but it has several disadvantages. SpO2 measurement can be difficult to perform in animals with a thick coat, pigmented skin, or poor perfusion. SpO2 results may also be inaccurately low in these circumstances. The best ways to ensure accurate readings include minimizing
movement of the patient, using the probe on thin skin that is adequately perfused, comparing the measured heart rate to the
actual heart rate of the patient, and taking several consistent SpO2 readings. Finally, SpO2 cannot differentiate PaO2 values > 100 mm Hg; the results will all be 99% to 100%. Therefore, animals receiving oxygen supplementation that have significant
lung dysfunction may still have a SpO2 of 99% to 100% as long as their PaO2 remains above 100 mm Hg.
PaO2/FiO2 ratio. Arterial blood gas results can be further analyzed to determine the ratio of PaO2 to the fraction of inspired oxygen (FiO2). FiO2 is equal to 21% (or 0.21) when the patient is breathing room air. Most oxygen cages supplement up to at least 40% oxygen,
so the FiO2 is 40%, or 0.4.10 Oxygen (100%) delivered through bilateral nasal cannulas can supplement an FiO2 of 50% if the patient is not panting.10 An anesthetized patient is receiving 100% oxygen, barring any leak in the system, so the FiO2 is 100%, or 1. However, in nonventilated dogs it can be difficult to determine FiO2 because of wide variation in the character of respiration demonstrated by the patient.
The PaO2/FiO2 ratio is used to determine the severity of respiratory compromise and is the one factor that distinguishes acute lung injury
from ARDS. A ratio of < 300 indicates acute lung injury, and a ratio < 200 is diagnostic of ARDS.2 The PaO2/FiO2 ratio also allows accurate comparison between different arterial samples taken when different levels of oxygen (FiO2) were being supplemented to the patient. The ratio is calculated by dividing the PaO2 by the FiO2 percentage (expressed as a decimal). A normal animal should have a value > 400. For example, an animal breathing room air
with a PaO2 of 60 mm Hg would have a PaO2/FiO2 ratio of 60/0.21, which = 285 and is consistent with acute lung injury when other criteria that indicate acute lung injury
Because ARDS is a more severe form of acute lung injury, distinguishing between these two respiratory disorders might indicate
the severity of the disease and provide prognostic information for the owner.
Alveolar-arterial gradient. The alveolar-arterial gradient represents the difference in alveolar and arterial oxygen and is useful to help determine
lung function over time. It can help distinguish hypoxemia due to hypoventilation from true pulmonary disease. The gradient
is increased in animals with acute lung injury or ARDS. The alveolar-arterial gradient is based on barometric pressure at
sea level, but if a hospital's location is not extremely above or below sea level, this equation can be simplified and used
with routine arterial blood gas information (Table 3). Normal is < 15, with higher values representing decreased lung function. Normal alveolar-arterial gradient values in the
face of hypoxemia are supportive of respiratory failure.9 To ensure accuracy, this equation should be used when a patient is breathing room air.
Table 3: Alveolar-Arterial Gradient Calculation*
No. 5—Evidence of pulmonary inflammation
The last criterion for diagnosing acute lung injury or ARDS, and the only criterion that is optional, is evidence of pulmonary
inflammation. Transtracheal wash or bronchoalveolar lavage samples taken from animals with acute lung injury or ARDS demonstrate
characteristic types of inflammation. Cytologic examination of respiratory fluid reveals a predominance of neutrophils (suppurative
inflammation).2 When these diagnostic samples are tested for inflammatory cytokines such as tumor necrosis factor alpha and interleukin-beta,
these substances are also increased from normal values.2,6 However, performing these diagnostic tests in a dyspneic animal may be contraindicated because of the risks associated with
anesthesia or the procedure itself. So while these diagnostic procedures may provide useful information, they are not currently
a requirement in diagnosing acute lung injury or ARDS. These tests might be more practical if a dog is already being ventilated
or if samples are necessary for diagnosis and treatment of pneumonia.
A variety of treatment strategies have been attempted, but strong clinical evidence for the best approach to these patients
is lacking. In general, managing acute lung injury and ARDS should focus on early recognition with treatment of the underlying
disease and supportive care for the respiratory system. The underlying disorder (risk factor) should be fully evaluated and
treated aggressively and specifically, if possible. In patients that require transfusions, use blood products cautiously because,
in people, transfusion-related acute lung injury is another cause of noncardiogenic pulmonary edema.
Fluid therapy. Supportive care should include maintaining organ perfusion with appropriate fluid therapy. Some clinicians advocate the conservative
use of fluids since the lung vasculature is already more permeable than normal and it might be easy to cause fluid overload
in these patients. Additionally, the hope is that mild dehydration may help pull some of the interstitial lung fluid back
into the vasculature.3,4,7 But if you use this conservative approach to fluid therapy, monitor blood pressure closely to make sure the patient does
not become hypotensive, which is especially likely in septic patients. If the patient has been sufficiently volume-loaded
and hypotension is still present, use vasopressors such as dobutamine, dopamine, vasopressin, or norepinephrine to stabilize
systemic blood pressure and achieve adequate organ perfusion. Other clinicians advocate aggressive fluid management to maximize
oxygen delivery and organ perfusion as a more appropriate approach, but no consensus has been reached at this time.
A recent study in people evaluated these two philosophies of fluid therapy, placing patients in either a conservative or liberal
fluid management group. No difference in 60-day mortality was seen between the groups, but patients in the conservative fluid
group had significantly more days alive, ventilator-free, and spent outside of the intensive care unit.11 These findings suggest that providing as small a fluid volume as possible while maintaining organ perfusion may be the most
appropriate fluid plan for patients with acute lung injury or ARDS. Colloid therapy may help improve systemic blood pressure
by increasing the volume of fluid in circulation, but it should generally be avoided in patients with suspected pulmonary
capillary leaks. The colloid may leak from the capillary into the pulmonary interstitium, worsening the existing pulmonary
Oxygen therapy. Oxygen therapy is also a vital part of treatment for these patients. Oxygen may be provided by intranasal cannulas or nasal
prongs, an enclosed hood, or an oxygen cage (Figure 2). Animals can tolerate up to 60% oxygen without concern for oxygen toxicosis,4 but high concentrations may be difficult to obtain unless a tightly sealed oxygen cage is available. Closely monitor the
patient for response, and consider obtaining samples for serial blood gas analysis to check for hypoxemia. If a patient persistently
has a PaO2 < 60 mm Hg, a PaCO2 > 60 mm Hg, or increased respiratory effort despite receiving oxygen therapy, consider ventilator therapy.9
Other therapies. Other supportive care measures that have been attempted in people include antibiotic therapy, gastric ulcer prophylaxis,
nitric oxide administration, surfactant replacement, specific cytokine therapy, glucocorticoid therapy, and nutritional management.13,14 While no strong evidence supports or negates some of these treatment options, we do know that early nutritional interventions
are important in human critical care and are probably equally important in our veterinary patients.15 Nutrition can be provided either enterally or parenterally. Most patients with dyspnea will be unwilling to eat on their
own, so parenteral therapy may be necessary. If the patient must be anesthetized, consider placing a feeding tube to provide
enteral nutrition since early enteral nutrition improves gastrointestinal mucosal barrier function and may decrease the incidence
of bacterial translocation.16