Page 421 - Clinical Small Animal Internal Medicine

39 Acute Respiratory Failure 389

and there is empirical evidence to support both hydro- be salvaged in some cases. Restoring ventilation to alveo-
VetBooks.ir static and inflammatory components. Diuretic usage lar regions that are atelectatic, obstructed, collapsed, or
flooded should improve V:Q ratios. This goal may be
is not considered absolutely contraindicated, but is
unlikely to yield the profoundly beneficial responses
cal ventilation, typically with PEEP), enhancing alveolar
observed with cardiogenic edema. achieved by increasing mean airway pressure (mechani-
Excessive mechanical loads due to chest wall compli- fluid clearance, breath hold recruitment maneuvers, and
ance issues (e.g., flail chest, congenital defects, etc.) may addressing inflammatory or infectious insults to the
be challenging to address unless they are iatrogenic in lower airways with appropriate drug therapy. Diffuse
nature. Iatrogenic alterations in chest wall/diaphragmatic alveolar hemorrhage syndromes should be addressed
compliance can result from excessively tight thoracic and with appropriate drug therapies and blood products
abdominal wraps, splints, and casts. Incremental loosen- when they are the result of a coagulopathy. Note that the
ing of such wraps until chest wall compliance is not exces- majority of therapies that aim to reduce physiologic
sively low is advised. shunting also will generally recruit alveolar surface area
Excessive chemical loads are the result of marked and improve overall V–Q matching. The removal of air or
increases in carbon dioxide production. Malignant hyper- fluid accumulations from the pleural space can result in
thermia (MH) is perhaps the most common cause and is marked improvements in V–Q matching in many cases.
thankfully a rare occurrence. Active cooling, mechanical Early recognition of pleural filling disorders can lead to
ventilation, discontinuance of all volatile inhalational improved outcomes.
anesthetics (or succinylcholine), and the administration Ultrasound is the preferred imaging modality if it is
of dantrolene remain the mainstays of MH therapy. In available in the emergency room. Many of these patients
settings other than MH, excessive CO 2 production is are not stable enough to tolerate radiographic imaging
addressed by minimizing muscle activity (seizures, trem- until after air or fluid has been evacuated from the pleu-
ors) and lowering body temperature when possible. In ral space. Thoracocentesis should be performed until
many instances, active cooling is not required; rather, one negative pressure is achieved. If negative pressure cannot
needs to only not provide active warming therapies. be obtained or if pleural filling rapidly recurs then chest
Maintaining adequate hydration to promote effective tube placement is required.
evaporative heat loss is advised. Increases in the alveolar partial pressure of oxygen
may be achieved by several means. First, the restoration
of ventilation to alveolar regions with limited fresh gas
Hypoxemic Respiratory Failure
flows will raise PAO 2 in those areas. More widespread
As with hypercapneic respiratory failure, the optimal increases in PAO 2 are achieved by providing supple-
therapeutic approach to hypoxemic respiratory failure mental oxygen. Mechanical ventilation with PEEP
will vary with the underlying cause. In cases of hypox- can simultaneously increase alveolar ventilation, recruit
emic respiratory failure in which a normal A‐a gradient underventilated/nonventilated alveolar units, raise mean
is found, therapy should be directed at restoring alveo- airway pressures, and provide supplemental oxygen.
lar ventilation and appropriate inspired gas pressures. Intermittent positive pressure ventilation (IPPV) is fre-
This would entail removing the patient from elevations quently required in hypoxemic respiratory failure cases
above sea level, providing supplemental oxygen, or the and is discussed in Chapter 40. The indication for
measures described above under hypercapneic respira- mechanical ventilation in hypoxemic respiratory failure
tory failure. would be acute, persistent severe hypoxemia (PaO 2
When venous admixture is the underlying cause of <60 mmHg or SpO 2 <90%) that is unresponsive to sup-
hypoxemic failure, the primary goals are as follows: plemental oxygen therapy alone. In chronic disease
states, hypoxemia of this degree of severity may be
reduce anatomic or physiologic shunting if present
● better tolerated and occasionally requires neither supple-
increase alveolar partial pressure of oxygen
● mental oxygen nor IPPV.
correct V–Q inequalities
● Supplemental oxygen is generally required in cases of
recruit alveolar surface area available to participate in
● hypoxemic respiratory failure in which the underlying
gas exchange
cause cannot be immediately addressed. Supplemental
Achieving a reduction in anatomic shunting often oxygen may be sufficient to address hypoxemia in cases
requires an invasive or minimally invasive surgical not requiring mechanical ventilation. Delivery may be
approach to reducing or ablating flow through the shunt via nasal or tracheal cannulae, facemask, intubation/tra-
conduit. Reductions in physiologic shunting may be cheostomy with spontaneous respiration, or via an oxy-
achieved by surgical removal of lung lobes too diseased to gen cage. The lowest FiO 2 required to prevent hypoxemia