Respiratory acidosis
Respiratory acidosis: Excerpt from Handbook of Diseases
An acid-base disturbance characterized by reduced alveolar ventilation and manifested by hypercapnia (partial pressure of arterial carbon dioxide [Paco2] greater than 45 mm Hg), respiratory acidosis can be acute (from a sudden failure in ventilation) or chronic (as in long-term pulmonary disease). The prognosis depends on the severity of the underlying disturbance and on the patient’s general condition.
Causes
Respiratory acidosis can result from airway obstruction or parenchymal lung disease, which interferes with alveolar ventilation, or from chronic obstructive pulmonary disease (COPD), asthma, severe adult respiratory distress syndrome, chronic bronchitis, large pneumothorax, extensive pneumonia, or pulmonary edema.
Hypoventilation compromises excretion of carbon dioxide produced through metabolism. The retained carbon dioxide then combines with water to form an excess of carbonic acid, decreasing the blood pH. As a result, the concentration of hydrogen ions in body fluids, which directly reflects acidity, increases.
In addition, several factors predispose the patient to respiratory acidosis:
❑ Drugs: Narcotics, anesthetics, hypnotics, and sedatives decrease the sensitivity of the respiratory center.
❑ Central nervous system (CNS) trauma: Medullary injury may impair ventilatory drive.
❑ Chronic metabolic alkalosis: Respiratory compensatory mechanisms attempt to normalize pH by decreasing alveolar ventilation.
❑ Neuromuscular disease (such as myasthenia gravis, Guillain-Barré syndrome, and poliomyelitis): Failure of respiratory muscles to respond properly to respiratory drive reduces alveolar ventilation.
Signs and symptoms
Acute respiratory acidosis produces CNS disturbances that reflect changes in the pH of cerebrospinal fluid rather than increased carbon dioxide levels in cerebral circulation.
Effects range from restlessness, confusion, and apprehension to somnolence, with a fine or flapping tremor (asterixis), or coma. The patient may complain of headaches and exhibit dyspnea and tachypnea with papilledema and depressed reflexes. Unless the patient is receiving oxygen, hypoxemia accompanies respiratory acidosis.
This disorder may also cause cardiovascular abnormalities, such as tachycardia, hypertension, atrial and ventricular arrhythmias and, in severe acidosis, hypotension with vasodilation (bounding pulses and warm periphery).
Diagnosis
❑ The following arterial blood gas (ABG) levels confirm respiratory acidosis: a Paco2 exceeding the normal level of 45 mm Hg, pH usually below the normal range of 7.35 to 7.45, and a bicarbonate level that’s normal in the acute stage but elevated in the chronic stage.
❑ Chest X-ray, computed tomography scan, or pulmonary function test may help diagnose lung disease.
Treatment
Effective treatment of respiratory acidosis is designed to correct the underlying source of alveolar hypoventilation. Significantly reduced alveolar ventilation may require mechanical ventilation until the underlying condition can be treated.
In patients with COPD, treatment includes a bronchodilator, oxygen, a corticosteroid and, commonly, an antibiotic; drug therapy for conditions such as myasthenia gravis; removal of foreign bodies from the airway; an antibiotic for pneumonia; dialysis or charcoal to remove toxic drugs; and correction of metabolic alkalosis. An elevated Paco2 may persist in a patient with COPD despite optimal treatment.
Special considerations
❑ Closely monitor the patient’s blood pH level.
CLINICAL TIP: If the pH level drops below 7.15, profound CNS and cardiovascular deterioration may result, requiring administration of I.V. sodium bicarbonate. However, administration of sodium bicarbonate should be reserved for only the most critical cases because it can cause a paradoxical worsening of CNS effects.
❑ Be alert for critical changes in the patient’s respiratory, CNS, and cardiovascular functions. Also, watch closely for variations in ABG values and electrolyte status. Maintain adequate hydration.
❑ If acidosis requires mechanical ventilation, maintain a patent airway and provide adequate humidification. Perform tracheal suctioning regularly and vigorous chest physiotherapy, if needed. Continuously monitor ventilator settings and respiratory status.
❑ If the patient has COPD and chronic carbon dioxide retention, closely monitor him for signs of respiratory acidosis. Also, administer oxygen at low flow rates, and closely monitor the patient if he is receiving an opioid or a sedative.
❑ Instruct the patient who has received a general anesthetic to turn, cough, and perform deep-breathing exercises frequently to prevent the onset of respiratory acidosis.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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