Page 414 - Clinical Small Animal Internal Medicine

382 Section 5 Critical Care Medicine

Insufficient ventilatory capacity is the second general respiratory failure, or limited to select lines of highly
VetBooks.ir mechanism for hypercapneic respiratory failure and is inbred animals (e.g., Duchenne muscular dystrophy, thy-
rotoxicosis, myxedema, hyperadrenocorticism, systemic
typically the result of compromise of the respiratory
muscles or the neural input to them. Respiratory drive
num or chest wall may compromise diaphragmatic func-
may be sufficient (although it is difficult to assess in this lupus erythematosus). Severe abnormalities of the ster-
setting), while the transmission or end‐effector systems tion by placing it at an unfavorable orientation or resting
are dysfunctional. The problem may lie anywhere along length.
the myoneural axis. High cervical myelopathies (cranial An excessive mechanical or chemical load imposed on
to the C5 spinal segment) can disrupt transmission at a the respiratory system is the third general mechanism of
level cranial to the formation of the phrenic nerve roots. acute hypercapneic respiratory failure. In this case, the
Low cervical myelopathies may impair the intercostal respiratory system may be functioning at a high level but
nerves while sparing phrenic nerve transmission (which has been required to perform its duties in the face of a
is usually sufficient on its own to maintain ventilatory mechanical or chemical load that would exceed the
status). The nerve roots may be impacted by disease as is capacity of any healthy respiratory system. Mechanical
seen in polyradiculoneuritis (coon hound paralysis). loads that are excessive may be the result of reductions in
Similar forms of ascending paralysis (tick paralysis, botu- compliance of the chest wall or pulmonary parenchyma,
lism, some snake envenomations) may result in hyper- increases in respiratory system resistance, or both.
capneic respiratory failure that appears quite similar in Reductions in compliance can result from alterations in
nature although occurring via different mechanisms. the biomechanical properties of the structural elements
The phrenic nerve itself may become compromised themselves or alterations in surface tension forces. In the
(phrenic neuropathy) due to trauma (surgical or exter- former instance, such alterations are typically the result
nal), demyelinating diseases, disruption by tumor of chronic disease processes and excessive fibrosis.
growth, or idiopathic causes. Unilateral phrenic neurop- However, acute changes can be superimposed iatrogeni-
athy is often well tolerated, while bilateral dysfunction cally in the form of tight wraps on the trunk at either
can require mechanical ventilatory support. the thoracic or abdominal level (e.g., spica splints, etc.).
Disorders of the neuromuscular junction can lead to Elevated intraabdominal pressure (intraabdominal
hypercapneic respiratory failure. Junctionopathies may hypertension, abdominal compartment syndrome) can
be subclassified as presynaptic, synaptic, or postsynap- secondarily result in reduced respiratory system compli-
tic in nature. Presynaptic disorders include those that ance and can develop acutely in the setting of hemoab-
increase (e.g., low serum magnesium and some enveno- domen or other forms of rapid peritoneal fluid
mations such as black widow spider bites) as well as accumulation. Likewise, pleural filling disorders can
decrease (e.g., hypocalcemia, botulism, tick paralysis, compromise the tidal volume achieved with a given
aminoglycoside antibiotics) acetylcholine release into degree of respiratory muscular effort. A given volume of
synaptic clefts. Synaptic cleft disorders include diseases air may reduce tidal volume to a larger degree than an
that alter the removal of acetylcholine from this site identical volume of fluid in the pleural space. Unlike
(e.g., cholinesterase inhibitors, organophosphates). fluid, air can expand and such expansion during inspira-
Postsynaptic disorders can include forms of myasthenia tion can compromise tidal volume beyond the effect that
gravis as well as administration of depolarizing and non- results from disruption of pleural contact forces alone.
depolarizing muscle relaxants (e.g., succinylcholine). Acute reductions in the compliance of the pulmonary
Myopathies are a potential cause of reduced ventila- parenchyma and interstitium are often seen concurrently
tory capacity as well. Specific myopathies of the respira- with disruption of surface tension forces in inflammatory
tory muscles are rarely diagnosed in veterinary patients and edematous lung diseases. Pulmonary edema, pulmo-
except for traumatic myopathies. Traumatic diaphrag- nary hemorrhage, near‐drowning, pneumonitis, and
matic herniation or avulsion is perhaps the most fre- pneumonia all may lead to reduced pulmonary compli-
quently recognized myopathic process leading to ance both via tissue edema formation and increased sur-
hypercapnia and respiratory failure. Another uncom- face tension due to surfactant dilution and alveolar
mon but well‐recognized myopathy of small animals that collapse. While these effects are important, each of the
may profoundly reduce ventilatory capacity is potassium diseases mentioned in this context is far more likely to
depletion polymyopathy of cats. While hypokalemic cause hypoxemic respiratory failure than the hypercap-
myopathies are more fully characterized in cats than neic form. Acute hypoventilation often occurs only when
dogs, it should be noted that profound hypokalemia also respiratory muscle fatigue develops or the airway becomes
may result in hypoventilation in dogs. Other causes of occluded with exudate, fluid, or foam.
diaphragmatic myopathies reported in humans are rarely Increased airway resistance is another important cause
reported in veterinary species, seldom associated with of hypercapneic respiratory failure due to an excessive