Page 415 - Clinical Small Animal Internal Medicine

39 Acute Respiratory Failure 383

mechanical load. Many commonly diagnosed diseases in An excessive chemical load on the respiratory system
VetBooks.ir small animal practice can lead to excessive airway resist- can also manifest as hypercapneic respiratory failure. In
this context, the high chemical load is in the form of
ance, which is the resistance to the flow of gases during
inhalation and exhalation. Airway resistance can impact
that which any healthy respiratory system might be able
both total gas flow into the system as well as intrapulmo- excessive carbon dioxide and this CO 2 burden exceeds
nary redistribution of gas after bulk flow has ceased to eliminate. An excessive CO 2 load can be the result of an
(pendelluft). Many common diseases in small animal abrupt and marked increase in carbon dioxide produc-
practice can cause life‐threatening increases in airway tion (VdotCO 2 ) as is seen in malignant hyperthermia or
resistance at the level of the extrathoracic (e.g., laryngeal status epilepticus. Alternatively, the excessive CO 2 load
paralysis, brachycephalic syndrome) or intrathoracic can be the result of rebreathing exhaled carbon dioxide.
(e.g., feline asthma, tracheobronchial malacia) airways. Rebreathing may occur in several clinically relevant set-
These conditions are often chronically active with sud- tings such as a maintaining a patient in a poorly venti-
den deterioration resulting from additional factors such lated, confined space (e.g., anesthetic induction box),
as increased environmental temperatures, inhaled par- excessive apparatus dead space (e.g., end‐tidal monitor-
ticulates and antigens, respiratory tract infections, or ing and other devices attached to orotracheal tubes in
atypical activity/exertion. Alternatively, disease progres- very small patients), or exhausted soda lime in a rebreath-
sion may lead to a new manifestation that represents an ing anesthetic circuit. The greater density of carbon diox-
intolerable burden (e.g., the onset of new, or higher ide relative to oxygen and nitrogen has raised concerns
grade, laryngeal or pharyngeal collapse). that a gradient may develop over time when animals are
Focal/localized intrathoracic airway narrowing or col- delivered supplemental oxygen via an improvised oxygen
lapse typically needs to be quite proximal to significantly hood or nonpurpose‐built oxygen cage (i.e., Elizabethan
impair ventilation (e.g., tracheal or lobar bronchial col- collar with plastic wrap cover). Convention is often to
lapse). Diffuse collapse or narrowing of large intratho- place the venting site upwards (12 o’clock) so that heat
racic airways can severely impair ventilation and limit may readily escape; however, periodic shifting of the vent
expiratory flow substantially. Narrowing or collapse of site to a downward location (6 o’clock) may be useful to
smaller intrathoracic airways generally needs to be dif- reduce carbon dioxide accumulation. Typically, patient
fuse in nature to significantly impair ventilation. Feline movement is sufficient to periodically shift the vent ori-
asthma and bronchiolitis in dogs (e.g., secondary to entation without clinician intervention, but active reposi-
canine adenovirus infection) serve as examples of dis- tioning may be required in moribund patients.
eases encountered in small animal practice that result in
diffuse small airway narrowing. Hypoxemic Respiratory Failure
Increased alveolar dead space ventilation also repre-
sents a form of excessive mechanical load. In this setting, Respiratory failure that is categorized as hypoxemic
an atypically high proportion of respiratory muscular largely results from venous admixture in various forms.
work is being devoted to ventilating alveolar units that Venous admixture is a term for the co‐mingling of deox-
are not participating in gas exchange. The effective alve- ygenated venous blood with arterialized blood during
olar ventilation is reduced although total minute ventila- flow from the right heart to the left heart. Some authors
tion may be normal (or more likely increased). This prefer to use the term true venous admixture to describe
reduction in alveolar ventilation is identified (and right‐to‐left shunting through an abnormal anatomic
defined) by the accompanying rise in alveolar and arte- conduit (e.g., right‐to‐left patent ductus arteriosus). In
rial carbon dioxide tensions. However, end‐tidal concen- such frameworks, the mixing of deoxygenated venous
trations become dissociated and reduced. This increase blood with arterialized blood that occurs in the pulmo-
in the gradient between arterial and alveolar carbon nary veins in conditions such as increased ventilation–
dioxide tensions is due to the simultaneous emptying of perfusion mismatching is termed venous admixture‐like
those alveolar units that did and those that did not par- in nature. Such distinctions offer little advantage in the
ticipate in gas exchange. Thus dead space gases dilute the author’s opinion. A more clinically relevant approach
carbon dioxide in the exhalate from perfused alveoli. might be to define venous admixture as those conditions
Increased alveolar dead space may result from pulmo- which produce hypoxemia with an accompanying
nary vascular occlusion (e.g., pulmonary thromboembo- increase in alveolar‐to‐arterial PO 2 gradient (A‐a gradi-
lism) or from decreased pulmonary capillary hydrostatic ent). The predominant mechanisms resulting in hypox-
pressures in hypovolemia and other forms of severe car- emia are listed in Box 39.1.
diovascular impairment when intraluminal pressures are Hypoventilation results in hypoxemia by reducing
below alveolar pressures (i.e., extraluminal pressures alveolar oxygen tensions. The retention of carbon dioxide
exceed intraluminal pressures). within the alveolar spaces reduces the partial pressure