Acute respiratory failure in COPD
Acute respiratory failure in COPD: Excerpt from Handbook of Diseases
In patients with essentially normal lung tissue, acute respiratory failure (ARF) usually means a partial pressure of arterial carbon dioxide (Paco2) greater than 50 mm Hg and a partial pressure of arterial oxygen (Pao2) less than 50 mm Hg. These limits, however, don’t apply to patients with chronic obstructive pulmonary disease (COPD), who commonly have a consistently high Paco2 and low Pao2. In COPD patients, only acute deterioration in arterial blood gas (ABG) levels and corresponding clinical deterioration indicate ARF.
Causes
ARF may develop in COPD patients from any condition that increases the work of breathing and decreases the respiratory drive. Such conditions include respiratory tract infection (such as bronchitis or pneumonia), which is the most common precipitating factor; bronchospasm; or accumulating secretions secondary to cough suppression. Other causes include:
central nervous system (CNS) depression — head trauma or injudicious use of sedatives, narcotics, tranquilizers, or oxygen
cardiovascular disorders — myocardial infarction, heart failure, or pulmonary emboli
airway irritants — smoke or fumes
endocrine and metabolic disorders — myxedema or metabolic alkalosis
thoracic abnormalities — chest trauma, pneumothorax, or thoracic or abdominal surgery.
Signs and symptoms
In COPD patients with ARF, increased ventilation-perfusion mismatching and reduced alveolar ventilation decrease Pao2 (hypoxemia) and increase Paco2 (hypercapnia). This rise in carbon dioxide tension lowers the pH. The resulting hypoxemia and acidemia affect all body organs, especially the central nervous, respiratory, and cardiovascular systems. Specific symptoms vary with the underlying cause of ARF but can include any of the following:
Respiratory symptoms. The respiratory rate may be increased, decreased, or normal, depending on the cause; respirations may be shallow or deep, or they may alternate between the two; and air hunger may occur. Cyanosis may or may not be present, depending on the hemoglobin (Hb) level and arterial oxygenation. Auscultation of the chest may reveal crackles, rhonchi, wheezes, or diminished breath sounds.
CNS symptoms. The patient may show evidence of restlessness, confusion, loss of concentration, irritability, tremulousness, diminished tendon reflexes, and papilledema; he may slip into a coma.
Cardiovascular symptoms. Tachycardia, with increased cardiac output and mildly elevated blood pressure secondary to adrenal release of catecholamines, occurs early in response to a low Pao2.With myocardial hypoxia, arrhythmias may develop. Pulmonary hypertension also occurs.
Diagnosis
Progressive deterioration in ABG levels and pH, when compared with the patient’s baseline values, strongly suggests ARF in COPD patients. (In patients with essentially normal lung tissue, a pH less than 7.35 usually indicates ARF, but COPD patients display an even greater deviation from this normal value, as they do with blood Paco2 and Pao2.) The following findings further support the diagnosis:
Bicarbonate levels are increased, indicating metabolic alkalosis or metabolic compensation for chronic respiratory acidosis.
Hb levels and hematocrit are abnormally low, which may be due to blood loss, indicating decreased oxygen-carrying capacity.
Serum electrolyte levels may indicate hypokalemia, which may result from compensatory hyperventilation — an attempt to correct alkalosis; hypochloremia is common with metabolic alkalosis.
White blood cell count is elevated if ARF is due to bacterial infection; in certain cases of profound septicemia, the leukocyte count may be decreased. Gram stain and sputum culture can identify pathogens.
Chest X-rays reveal pulmonary pathology, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, or effusions.
Electrocardiogram reveals arrhythmias, which commonly suggest cor pulmonale and myocardial hypoxia. Large P waves (“p pulmonale”) may indicate a history of right-sided heart failure.
Treatment
In a COPD patient, ARF is an emergency that requires cautious oxygen therapy (using nasal prongs or a Venturi mask) to raise the patient’s Pao2. If significant respiratory acidosis persists, a bidirectional positive-pressure airway mask over the oronasal region or mechanical ventilation through an endotracheal or a tracheostomy tube may be necessary. High-frequency ventilation may be used if the patient doesn’t respond to conventional mechanical ventilation. Treatment routinely includes an antibiotic for infection, a bronchodilator, an anxiolytic and, possibly, a steroid.
Special considerations
Because most patients with ARF are treated in the intensive care unit (ICU), you’ll want to orient the patient to the environment, procedures, and routines to minimize anxiety.
To reverse hypoxemia, administer oxygen at concentrations to maintain a Pao2 of at least 50 to 60 mm Hg. Patients with COPD usually require only small amounts of supplemental oxygen. Monitor the patient for a positive response, such as improved breathing and color and improved ABG levels.
Maintain a patent airway. If the patient is retaining carbon dioxide, encourage him to cough and to breathe deeply with pursed lips. If the patient is alert, have him use an incentive spirometer; if he’s intubated and lethargic, turn him every 1 to 2 hours.
Use postural drainage and chest physiotherapy to help clear the patient’s secretions.
If the patient is intubated, suction his trachea, as needed, after hyperoxygenation. Observe him for a change in the quantity, consistency, or color of his sputum. Provide humidification to liquefy the secretions.
Observe the patient closely for respiratory arrest. Auscultate for breath sounds. Monitor ABG levels for changes.
Monitor and record serum electrolyte levels carefully, and correct imbalances; monitor fluid balance by recording the patient’s intake and output or daily weight.
Monitor the patient for cardiac arrhythmias.
If the patient requires mechanical ventilation:
Check ventilator settings, cuff pressures, and ABG values often because the fraction of inspired oxygen (Fio2) setting depends on ABG levels. Draw a blood sample for ABG analysis 20 to 30 minutes after every Fio2 change, or check ABG levels with oximetry.
Prevent infection by using sterile technique while suctioning and by changing ventilator circuits every 24 to 48 hours.
CLINICAL TIP:Because stress ulcers are common in intubated ICU patients, check gastric secretions for evidence of bleeding if the patient has a nasogastric tube or complains of epigastric tenderness, nausea, or vomiting. Monitor Hb level and hematocrit, and check all stool for occult blood. Administer an antacid, a histamine-2-receptor antagonist, or sucralfate.
When an artificial airway cuff is overinflated, it compresses the tracheal wall vasculature and can cause tracheal erosion. To prevent this, use the minimal leak technique and a cuffed tube with high residual volume (low-pressure cuff), a foam cuff, or a pressure-regulating valve on the cuff.
To prevent nasal necrosis, keep the nasotracheal tube midline within the nostrils, and provide good hygiene. Loosen tape periodically to prevent skin breakdown. Avoid excessive movement of any tubes, and make sure the ventilator tubing is adequately supported.
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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