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Acute Respiratory Failure
Matthew Mellema, DVM, PhD, DACVECC

Applaud Medical, San Francisco, CA, USA

Etiology/Pathophysiology hypercapneic respiratory failure, inadequate time has
passed to allow for generation of maximal compensatory
Acute respiratory failure occurs when an insult to the responses and acidemia is present more often than not.
respiratory system that is sudden in onset or short in The cut‐off value for CO 2 at which hypercapneic res-
duration results in levels of alveolar ventilation or pul- piratory failure is deemed to be present varies, but is
monary oxygen transfer (or both) that are insufficient to typically in the 50–60 mmHg range when arterial or end‐
maintain vital metabolic processes and homeostasis. tidal exhalate sampling is utilized. A PaCO 2 of greater
This term does not imply that chronic respiratory com- than 60 mmHg is often listed among the indications for
promise is not present concurrently. In a subset of cases, mechanical ventilation in the veterinary literature, which
the acute exacerbation of a chronic process or the sud- can thus serve as de facto evidence of respiratory failure
den development of a secondary complication (e.g., res- in many instances.
piratory tract infection) may lead to signs of acute Hypercapneic respiratory failure (and hypercapnia in
deterioration in clinical status. Similarly, chronic pulmo- general) is the result of one or more of the following cir-
nary compromise may lead to fairly abrupt fatigue of the cumstances: (1) inadequate or inappropriate ventilatory
muscles of respiration and provoke an acute crisis. The drive, (2) insufficient ventilatory capacity, or (3) an exces-
proximate cause of the acute crisis in such a case is the sive mechanical or chemical load imposed on the res-
suddenly inadequate ventilatory capacity; however, the piratory system. Inadequate or inappropriate ventilatory
ultimate underlying cause may be an unsustainable drive results from intracranial disease, medications/
workload due to a chronic disease process (e.g., progres- anesthetics/sedatives, or extracranial encephalopathies.
sive dynamic airway collapse, parenchymal fibrosis, etc.). The respiratory centers reside in the medulla with inputs
Categorization schemes for acute respiratory failure from both the pons and cerebrum. Diseases resulting in
are typically multitiered in their organization. The first compromise of these pontine and medullary centers may
level of differentiation is often based on the predominant lead to marked alterations in respiratory pattern (e.g.,
arterial blood gas alteration. With this approach, one Cheyne–Stokes breathing, apneusis, etc.) or alternatively
often finds acute respiratory failure initially divided into a reduction in respiratory rate and/or tidal volume with
three main subcategories: (1) hypercapneic respiratory little alteration in pattern of breathing. In the setting of
failure, (2) hypoxemic respiratory failure, and (3) mixed hypercapneic respiratory failure due to intracranial dis-
respiratory failure. ease, hypercapnia may be both a result and a cause of
elevated intracranial pressure and imminent herniation.
Hypercapneic Respiratory Failure Inadequate or inappropriate respiratory drive is typically
identified in the laboratory setting by determining the
Hypercapneic respiratory failure includes those condi- relationship between minute ventilation and PaCO 2 or
tions that result in a severe, sustained reduction in alveo- PaO 2 . This relationship is rarely defined quantitatively in
lar ventilation. By definition, a respiratory acidosis is the clinical setting, however. Qualitatively, a clinician
present. Acidemia, or a reduction in blood pH, may or may note that a hypoxemic patient has failed to hyper-
may not be present concurrently, depending on a host of ventilate as would be expected. Such a finding would
other factors such as the current capacity of the extracel- suggest altered ventilatory drive or inadequate ventila-
lular hydrogen ion buffering systems. Generally, in acute tory capacity.

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical