Page 418 - Clinical Small Animal Internal Medicine

386 Section 5 Critical Care Medicine

This explanation seems insufficient to explain clinical hypoxemia in the absence of alveolar flooding in this
VetBooks.ir experiences with this disease process, however. Surgically species. Many clinicians have reported the experience
of managing congestive heart failure patients in which
removing a similarly sized region of lung would presum-
ably produce the same level of overperfusion, but does
thoracic radiographs still demonstrate persistent inter-
not typically result in hypoxemia. The missing portion of clinical signs of respiratory distress have resolved yet
the mechanism for hypoxemia in this setting is likely to stitial edema. Such experiences may reflect resolution
be altered bronchomotor tone. It was first demonstrated of hypoxemia prior to clearance of excessive fluid accu-
in 1942 that pulmonary thromboembolism (or external mulation in the pulmonary interstitium.
mechanical occlusion of a pulmonary artery) results in Diffusion impairment may be overcome by increasing
bronchospasm in the dog. The hypoxemia seen in PTE, the partial pressure gradient by raising PAO 2 or instead
but not following lung lobectomy, is likely the result of by recruiting additional surface area (or both). The
overperfusion combined with regional decreases in ven- recruitment of additional surface area can involve both
tilation. Relief in sensations of dyspnea in humans is recruitment maneuvers (breath hold) and the applica-
reported following theophylline administration. This tion of PEEP during mechanical ventilation.
may be due to a reduction in bronchospasm or reduced
activation of pulmonary C‐fibers via adenosine receptor
antagonism. Epidemiology
Diffusion impairment is a common contributor to
hypoxemia in small animal patients, but rarely a sole or The epidemiology of respiratory failure in small animal
primary cause of such. Fick’s law of diffusion details the patients is largely unknown. The epidemiology of res-
major contributing factors to gas or solute flux via diffu- piratory failure in human medicine is also poorly under-
sion: (1) concentration or partial pressure difference, (2) stood. Most definitions of respiratory failure are based
length of the diffusion pathway, and (3) surface area on arterial blood gas values. In human pediatrics, nonin-
available for diffusion. With these factors in mind, both vasive tools are widely employed for the assessment of
hypoventilation and low PiO2 represent a reversible pulmonary function (e.g., pulse oximetry, cutaneous gas
form of diffusion impairment. Many of the diseases listed monitoring systems, etc.). Conservative estimates sug-
above under V–Q mismatch result in alveolar flooding gest that as many as 35% of respiratory failure patients in
or collapse which represents a loss of surface area for dif- pediatrics are excluded because noninvasive monitoring
fusion. In a similar manner, PTE results in the formation methods were employed. Similar concerns are raised in
of excessive alveolar dead space, which also represents a studies of the epidemiology of respiratory failure in adult
loss of surface area for diffusion. Among the diseases humans to a lesser degree. Between 2001 and 2009, hos-
common to small animal practice, chronic congestive pitalizations for acute respiratory failure rose from 1 mil-
heart failure likely represents the best example of lion cases to 1.9 million cases per year in the United
increased diffusion distance. Remodeling of the alveolar States alone. The associated healthcare costs rose from
epithelial–capillary endothelial interface in chronic con- $30 billion to $54 billion. A decrease in mortality has
gestive heart failure can result in thickening of this bar- been observed over this period despite overall rates of
rier and an increased diffusion distance. mechanical ventilation remaining unchanged.
Despite these many examples of means by which Attempts could be made to estimate the prevalence
common disease processes can compromise the pro- or incidence of small animal respiratory failure based
cess, diffusion limitation is considered to be a primary on previously published large retrospective studies
cause of hypoxemia on only rare occasion. In human of mechanical ventilation in small animal patients.
medicine, emphysema can result in a massive sustained However, such data are heavily biased and likely poorly
loss of surface area and diffusion limitation is consid- represent small animal patient populations as a whole.
ered a more significant cause of hypoxemia in that Patients in such studies represent only those with the fol-
species. The limited role of diffusion impairment in lowing characteristics: (1) patients that were presented
producing hypoxemia in small animal species is per- to a secondary or tertiary care center that offers long‐
haps best illustrated in the setting of chronic congestive term (>24 h) mechanical ventilation, (2) patients in
heart failure. In this syndrome, some degree of diffu- whom respiratory failure was recognized by the attend-
sion limitation is likely chronically present yet hypox- ing clinician, (3) cases in which mechanical ventilation
emia is rarely noted in the absence of pulmonary edema was offered, (4) cases in which clients elected to pursue
with alveolar flooding and V–Q mismatch. Pioneering this therapeutic option, and (5) cases which were not
work by Norman Staub has previously demonstrated in excluded from the analysis. Such reports almost cer-
acute models of canine congestive heart failure that tainly document only a small fraction of respiratory fail-
interstitial pulmonary edema is insufficient to produce ure cases cared for by small animal practitioners.