Page 297 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

288 ACID-BASE DISORDERS

extremely responsive as small changes in CO 2 /pH affect
20 38
100
43 breathing dramatically. For example, in resting awake
humans, a 1-mm increase in PCO 2 increases ventilation
Percent
sat. by approximately 20% to 30%. 19
100 The lungs are the only avenue for CO 2 elimination.
Temp
0 Carbon dioxide efficiently diffuses across the alveolar cap-
100
P O 2 illary wall. Thus, under most circumstances, the CO 2 par-
100
80 Percent sat. 20 70 40 tial pressure is essentially the same in the alveoli (PaCO 2 )
and arteries (PaCO 2 ). In the steady state, PaCO 2 is inversely
Percent Hb saturation 60 P Temp↑ DPG↑ 100 0 7.6 P O 2 P CO 2 100 alveolar ventilation equation: VCO 2 ð1Þ
proportional to alveolar ventilation (V A ) based on the
↑ H ↑
PaCO = 0.863
CO 2
2
40
VA
20 Percent sat. 7.4 pH 7.2 where CO 2 is the metabolic production of carbon dioxide
and 0.863 is a constant that equates dissimilar units for
0 CO 2 and A. 83 The A is the fraction of the total minute
100
ventilation (E) that is produced at the gas exchange units
P O 2
0
0 20 40 60 80 100 of the lung. The portion of gas not reaching the gas
P (mm Hg) exchange areas of the lung is termed dead space gas.
O 2
Figure 11-1 Schematic representation of the respiratory control The dead space to tidal volume ratio (VD/VT) refers to
system. Sensors. Chemosensory and mechanosensory information the portion of each tidal volume that ventilates dead space
originates from peripheral (carotid and aortic bodies) and central and is “wasted.” Therefore, the alveolar gas equation can
(brainstem) chemoreceptors. The carotid bodies located at the be rewritten as:
bifurcation of the external and internal carotid arteries are
responsible for the majority of the hypoxemic ventilatory response VCO 2
in mammals, whereas chemosensitive areas found throughout the PaCO = 0.863 VE[1–(VD / VT)] ð2Þ
2
brainstem are the primary receptors mediating the hypercapnic
ventilatory response. Central controller. Information from
peripheral and central receptors is relayed centrally to ventral As determined by equations (1) and (2), measuring the
brainstem structures. Stimulation of the retrotrapezoid nucleus PaCO 2 provides direct information about the adequacy
activates premotor neurons in the ventral respiratory group, which of alveolar ventilation. Many primary respiratory acid-
then activate cranial and spinal motor neurons to initiate respiratory base disorders subsequently result from alveolar
rhythm and modulate pattern of breathing. Effectors. Output from hypoventilation (increased PaCO 2 ) or alveolar hyperventi-
motor neurons reaches the respiratory effector muscles (e.g., lation (decreased PaCO 2 ).
diaphragm, intercostal muscles) producing a breath. Information
from the effectors feeds back to the sensors to modulate breathing. MECHANOREFLEXES
In addition to chemoafferent alterations of ventilatory
control, ventilation is also influenced by sensory inputs
are also present in the CNS, but their contribution to ven- originating from the chest wall, pulmonary and airway
tilatory control remains unclear. 73 receptors*. Many receptors located throughout the
In contrast to O 2 -sensitive receptors, the primary airways are activated in response to changes in pressure,
CO 2 /pH-sensitive receptors are located in the CNS cold, irritation, and stretch. For example, laryngeal
throughout the brainstem (i.e., retrotrapezoid nucleus stimulation by negative pressure or cold results in reflex
[RTN], serotonergic and GABAergic neurons in the activity directed at maintaining upper airway patency
raphe nuclei, noradrenergic neurons in the locus whereas airways below the larynx contain slowly (SAR)
coeruleus, nucleus of the solitary tract [NTS], pre- and rapidly (RAR) adapting stretch receptors and
Bo ¨tzinger complex, and cerebellar fastigial nucleus). 50 bronchopulmonary C fibers which, upon activation,
Although both peripheral and central chemoreceptors result in many reflex events including bronchocon-
contribute to CO 2 -induced ventilatory responses, the striction or bronchodilation, protective reflexes
central receptors appear to be quantitatively more signifi- (i.e., cough), and alterations in respiratory timing. 37
cant for producing changes in ventilation mediated by As discussed, the essential function of the ventilatory
CO 2 ; resection of the peripherally-located carotid bodies control system is to maintain blood gas regulation and
only leads to a small increase in resting PaCO 2 levels (2 to many factors regulate its homeostasis. Although
4 mm Hg) secondary to a decrease in alveolar ventila-
tion. 41,64 The CO 2 -sensitive chemoreceptors are *For review see: Kubin et al., 2006.