Page 299 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

290 ACID-BASE DISORDERS

are reached. Within this respiratory zone, alveolar venti- However, at a higher PO 2 (>60 to 70 mm Hg), the curve
lation and gas exchange occur as oxygen moves down its flattens off and little additional hemoglobin loading
concentration gradient and into the red blood cells. The occurs. Unloading of large amounts of oxygen from
partial pressure of oxygen in the red blood cells hemoglobin is facilitated in the tissues where oxygen
approximates that of alveolar gas within the first third pressures are much lower (10 to 60 mm Hg) and the
of the lung capillaries, primarily due to the lung’s consid- curve is very steep. Several factors shift this curve to
erable diffusion capabilities. Oxygen is then carried in the the right and aid in the unloading of oxygen to
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blood to meet the oxygen demand of the tissues in two the tissues, including increased H ion and carbon diox-
forms: dissolved and combined with hemoglobin. Most ide concentrations (as seen in respiratory acidosis),
of the delivered oxygen is bound by hemoglobin with increased temperature, and increased 2,3-diphospho-
only a small contribution from the dissolved oxygen gycerate (2,3-DPG), a compound that competes with
(0.003 mL dissolved O 2 per 100 mL of blood/mm Hg oxygen for its binding site on hemoglobin.
PO 2 ). The maximal amount of oxygen that can be
combined with hemoglobin is called the oxygen capacity. THE ALVEOLAR-ARTERIAL
Approximately 1.36 mL of O 2 can combine with 1 g OXYGEN GRADIENT
of hemoglobin. Assuming 15 g of hemoglobin per
100 mL of blood, approximately 21 mL O 2 per When patients present with hypoxemia associated
100 mL blood is carried to the tissues. As determined with respiratory acid-base disorders, it is important to
by the oxygen-hemoglobin dissociation curve discern between hypoxia from primary lung disease
(Figure 11-3), at low PO 2 , the amount of oxygen carried (e.g., ventilation-perfusion mismatching) and alveolar
by hemoglobin increases rapidly with increases in PO 2 . hypoventilation to manage the patient appropriately.

Neural
controller

RTN
Raphe
VRG

Ventilation
Central network in brainstem
• Rhythm generation
B • Pattern formation

Sensors Effectors

Carotid
body Brainstem
a b
Carotid
sinus
Ventral Intercostal
respiratory muscles
column
SO 7 Diaphragm
Rostral
Retrotrapezoid
nucleus
Aorta
Chemoreceptors Respiratory motor output
Aortic
bodies • Peripheral • Central (CO 2 ) • Diaphragm
· Carotid bodies (O ) · Throughout brainstem • Intercostal muscles
2
· Aortic bodies • Upper airway muscles
A C • Others
Figure 11-3 Rightward shift of the O 2 dissociation curve by increase of H ,PCO 2 , temperature, and
þ
2,3-diphosphogylcerate (DPG). (Adapted from West JB. Respiratory physiology. The essentials, 8th ed.
Philadelphia: Lippincott Williams & Wilkins, 2005: 75–89.)