Ico

■ concentration. Because increased CO2 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in CO2 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 28-6.

Severe, acute respiratory acidosis produces a variety of neurologic abnormalities. Initially these include headache, blurred vision, restlessness, and anxiety. These may progress to tremors, asterixis, somnolence, and/or delirium. If untreated, terminal manifestations include peripheral vasodilation leading to hypotension and cardiac arrhythmias. Chronic respiratory acidosis is typically associated with cor pulmonale and peripheral edema.

Table 28-6 Common Causes of Respiratory Acidosis

Central nervous system disease Brain stern lesions Central sleep apnea Infection

Intracranial hypertension Trauma Tumor Vascular Drugs" Aminoglycosides Anesthetics /3-Blockers Botulism toxin Hypnotics Narcotics

Neuromuscular blocking agents Organophosphates Sedatives Neuromuscular disease Guillain-Barre syndrome

Mubculdi dybliuphy

Myasthenia gravis Polymyositis Pulmonary disease Lower airway obstruction Chronic obstructive pulmonary disease Foreign body Status asthmaticus

Pneumonia Pneumonitis Pulmonary edema Restrictive lung disease Ascites

Chest wall disorder Fibrothorax Kyphoscoliosis Obesity Pleural effusion Pneumoconiosis Pneumothorax Progressive systemic sclerosis

Pulmonary fibrosis Spinal arthritis Smoke inhalation Upper airway obstruction Foreign body Laryngospasm

Obblruclive bleep dpi ie<j

Others Abdominal distention Altered metabolic rate Congestive heart failure Hypokalemia Hypothyroidism Inadequate mechanical ventilation

"Way be observed with therapeutic doses or overdoses

In order to effectively treat respiratory acidosis, the causative process must be identified and treated. If a cause is identified, specific therapy should be started. This may include naloxone for opiate-induced hypoventilation or bronchodilator therapy for acute bronchospasm. Because respiratory acidosis represents ventilatory failure, an increase in alveolar ventilation is required. This can often be achieved by controlling the underlying disease (e.g., bronchodilators and corticosteroids in asthma) and/or physically augmenting ventilation.

Although their precise role and mechanisms of action are unclear, agents such as medroxyprogesterone, theophylline, and doxapram stimulate respiration and have been used to treat mild to moderate respiratory acidosis. Moderate or severe respiratory acidosis requires assisted ventilation. This can be provided to spontaneously breathing patients via bilevel positive airway pressure (BiPAP) delivered via a tight-fitting mask, or by intubation followed by mechanical ventilation. In mechanically ventilated patients, respiratory acidosis is treated by increasing the minute ventilation. This is achieved by increasing the respiratory rate and/or tidal volume.

As with the treatment of metabolic acidosis, the role of NaHCO3 therapy is not well defined for respiratory acidosis. Realize that administration of NaHCC>3 can paradoxically result in increased CO2 generation (HCO3 + H2CO3 —H2O + CO2) and worsened acidemia. Careful monitoring of the pH is required if NaHCO3 therapy is started for this indication. The use of tromethamine in respiratory acidosis (see Metabolic Acidosis, above) has unproven safety and benefit.

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided as they can worsen CO2 retention.

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