Page 296 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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CHAPTER • 11



                              Respiratory Acid-Base Disorders






                              Rebecca A. Johnson and Helio Autran de Morais

                              “Life is a struggle, not against sin, not against the Money Power, not against malicious animal magnetism,
                              but against hydrogen ions.”
                                                                                         Henry Louis Mencken (1919)




            Respiratory acid-base disorders are those abnormalities in  many other processes that affect breathing (i.e., cortical
            acid-base equilibrium initiated by a change in arterial  inputs, cardiovascular alterations, etc.). These inputs col-
            carbon dioxide tension (PaCO 2 ). PaCO 2 is regulated by  lectively establish the spatiotemporal efferent signals that
            alveolar ventilation; a primary increase in PaCO 2 acidifies  project to respiratory pump muscles such as the dia-
            body fluids and initiates the acid-base disturbance called  phragm and upper airway muscles involved in airway
                                                                resistance regulation. Altogether, these pathways result
            respiratory acidosis, whereas a decrease in PaCO 2
            alkalinizes body fluids and is known as respiratory alkalo-  in muscular contraction, which subsequently drives
            sis. The neural pathways controlling respiration initiate  alveolar ventilation 50  (Figure 11-1).
            and coordinate respiratory muscle contraction, thereby
            generating adequate alveolar ventilation in the lungs.  CHEMORECEPTORS AND
            The primary responsibility of the mammalian lung is then  CHEMOREFLEXES
            to exchange gases at the alveolar blood-gas interface  Chemoreceptors provide sensory inputs to the respira-
            where carbon dioxide and oxygen move by diffusion   tory control system concerning changes in CO 2 or O 2 .
            from areas of high to low partial pressure. Diffusion of  As a result, alveolar ventilation is altered via negative feed-
            gases is directly proportional to the surface area of the  back mechanisms to minimize variations in normal gas
            interface and inversely proportional to the thickness  levels. 6,19,50,55  The primary stimuli for changes in alveolar
            of the membrane (Fick’s law). With a relatively large  ventilation are hypoxemia (PaO 2 <60 mm Hg) and car-
            surface area and a very thin (<1 micron) blood-gas  bon dioxide-induced changes in intracellular and extra-
            interface, the lungs are well suited for their role in gas  cellular pH, although the magnitude of these changes is
            exchange and thus, greatly influence respiratory acid-base  dependent on the specific chemoreflex. For example,
            regulation.                                         arterial CO 2 levels are tightly regulated under normal
                                                                ventilatory control; increases in arterial CO 2 levels
            CONTROL OF ALVEOLAR                                 (PaCO 2 ) of 1 to 3 mm Hg will double alveolar ventilation.
            VENTILATION                                         In contrast, arterial O 2 pressures (PaO 2 ) can change up to
                                                                20 mm Hg with little alteration in ventilation. 50
            The drive to breathe originates within respiratory centers  In adult mammals, chemoreceptors are located in both
            of the medulla (i.e., ventral respiratory column, VRC),  the peripheral and central nervous systems. The most sig-
            which consist of a network responsible for respiratory  nificant oxygen-sensitive chemoreceptors are primarily
            rhythm generation and respiratory pattern formation.  found within the carotid body at the bifurcation of the
            Although supramedullary brain structures, such as the  internal and external carotid arteries. Although carotid
            pons, cerebellum and forebrain, modulate breathing,  body chemoreceptors sense changes in CO 2 and pH as
            they are not required to breathe. Respiratory rhythm gen-  well, these chemoreceptors dominate the hypoxic ventila-
            eration and pattern formation are altered by homeostatic  toryresponseandareresponsibleforapproximately90%of
            control mechanisms that permit flexibility in the respira-  the increase in minute ventilation seen with hypox-
            tory control system (i.e., plasticity). For example, the  emia. 14,18  Oxygen-sensitive receptors are also found in
            medullary respiratory centers are modified by sensory  the aortic bodies within the aortic arch. However, they
            (i.e., chemoreceptors and mechanoreceptors) and modu-  appear to play a minimal role during normal ventilation. 50
            latory projections (i.e., serotonergic neurons), as well as  In addition to the periphery, O 2 -sensitive chemoreceptors


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