Page 303 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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294        ACID-BASE DISORDERS


            bring arterial pH back to normal in dogs with          BOX 11-3        Causes of Respiratory
            longstanding (>30 days) respiratory acidosis. Renal com-
            pensation in cats with chronic respiratory acidosis is not             Acidosis
            known. Cats do not increase renal ammoniagenesis dur-
            ing experimental metabolic acidosis. 38  Cats may not be  Large Airway Obstruction
            able to compensate adequately in chronic respiratory   Aspiration (e.g., foreign body, vomitus)
            acidosis because an increase in ammoniagenesis is the  Mass (e.g., neoplasia, abscess)
            most adaptive factor.                                  Tracheal collapse
               Hypochloremia is a common finding in dogs with      Chronic obstructive pulmonary disease
            experimentally induced chronic hypercapnia. 44,62,69,79  Asthma
            During recovery from chronic hypercapnia, chloride     Obstructed endotracheal tube
                                                                   Brachycephalic syndrome

            restriction hinders the return of plasma HCO 3 concen-
                                                                   Laryngeal paralysis/laryngospasm
            tration to normal. Thus the kidney needs chloride to pref-
            erentially resorb chloride with sodium, excrete excess  Respiratory Center Depression
                                                                   Drug induced (e.g., narcotics, barbiturates, inhalant
            HCO 3   in the urine, and reestablish normal SID in
            the plasma.                                               anesthesia)
                                                                   Neurologic disease (e.g., brainstem or high cervical cord
            CAUSES OF RESPIRATORY ACIDOSIS                            lesion)
            Respiratory acidosis and hypercapnia can occur with any  Increased CO 2 Production with Impaired
            disease process involving the neural control of ventilation,  Alveolar Ventilation
            mechanics of ventilation, or alveolar gas exchange,    Cardiopulmonary arrest
            resulting  in  hypoventilation,  ventilation-perfusion  Heatstroke
            mismatches, or both. Acute respiratory acidosis usually  Malignant hyperthermia
            results from sudden and severe primary parenchymal     Neuromuscular Disease
            (e.g., fulminate pulmonary edema), airway, pleural, chest
                                                                   Myasthenia gravis
            wall, neurologic (e.g., spinal cord injury), or neuromus-  Tetanus
            cular (e.g., botulism) disease. 17  Chronic respiratory aci-  Botulism
            dosis results in sustained hypercapnia and has many    Polyradiculoneuritis
            causes, including alveolar hypoventilation, abnormal   Tick paralysis
            respiratory drive, abnormalities of the chest wall and  Electrolyte abnormalities (e.g., hypokalemia)
            respiratory muscles, and increased dead space. 17  In  Drug induced (e.g., neuromuscular blocking agents,
            patients with neuromuscular disease leading to muscular   organophosphates, aminoglycosides with anesthetics)
            weakness, the degree of hypercapnia appears to be out of  Restrictive Extrapulmonary Disorders
            proportion to the severity of muscle disease and may be  Diaphragmatic hernia
            underestimated without blood gas analysis. In these    Pleural space disease (e.g., pneumothorax, pleural
            patients, muscle weakness and elastic load are responsible  effusion)
            for the modulation of central respiratory output. This  Chest wall trauma/flail chest
            results in a rapid shallow or dyspneic breathing pattern  Intrinsic Pulmonary and Small Airway
            that leads to chronic CO 2 retention. 49  A more detailed  Diseases
            list of causes of respiratory acidosis is found in Box 11-3.
                                                                   Acute respiratory distress syndrome
               As determined by the alveolar gas equations (1) and  Chronic obstructive pulmonary disease
            (2) above, hypercapnia can result from a decrease in alve-  Asthma
            olar ventilation (either through a decrease in total minute  Severe pulmonary edema
            ventilation or increase in the dead space to tidal volume  Pulmonary thromboembolism
            ratio), or an increase in metabolic production of carbon  Pneumonia
                                                                   Pulmonary fibrosis
            dioxide. In small animal clinical practice, increased CO 2
            production infrequently results in hypercapnia. In normal  Diffuse metastatic disease
            circumstances (e.g., exercise), an increase in CO 2 produc-  Smoke inhalation
            tion is matched by an increase in CO 2 elimination via the  Ineffective Mechanical Ventilation (e.g.,
            lung. 82  However, if CO 2 production is increased with  Inadequate Minute Ventilation, Improper
            impaired or fixed alveolar ventilation that is unable to  CO 2 Removal)
            effectively remove CO 2 , acute respiratory acidosis may
            develop, as is observed in a few conditions such as heat  Marked Obesity (Pickwickian Syndrome)
            stroke and malignant hyperthermia. 12,74
               Decreased alveolar ventilation produces hypercapnia
            from either a reduction in total minute ventilation (also
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