Acute respiratory failure in COPD
Acute respiratory failure in COPD: Excerpt from Professional Guide to Diseases (Eighth Edition)
In patients with essentially normal lung tissue, acute respiratory failure (ARF) usually means partial pressure of arterial carbon dioxide (PaCO2)above 50 mm Hg and partial pressure of arterial oxygen (PaO2) below 50 mm Hg. These limits, however, don’t apply to patients with chronic obstructive pulmonary disease (COPD), who usually have a consistently high PaCO2 and low PaO2. In patients with COPD, only acute deterioration in arterial blood gas (ABG) values, with corresponding clinical deterioration, indicates ARF.
Causes and incidence
ARF may develop in patients with COPD as a result of any condition that increases the work of breathing and decreases the respiratory drive. Such conditions include respiratory tract infection (such as bronchitis or pneumonia). The most common precipitating factor is bronchospasm, or accumulating secretions secondary to cough suppression. Other causes of ARF in COPD include:
❑ central nervous system (CNS) depression — head trauma or injudicious use of sedatives, opioids, tranquilizers, or oxygen (O2)
❑ 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.
The incidence of ARF increases markedly with age and is especially high among people age 65 and older.
Signs and symptoms
In patients who have COPD with ARF, increased ventilation-perfusion mismatch and reduced alveolar ventilation decrease PaO2 (hypoxemia) and increase Paco2 (hypercapnia). This rise in carbon dioxide (CO2) lowers the pH. The resulting hypoxemia and acidemia affect all body organs, especially the CNS and the respiratory and cardiovascular systems.
Specific symptoms vary with the underlying cause of ARF but may include these systems:
❑ Respiratory — Rate may be increased, decreased, or normal depending on the cause; respirations may be shallow, deep, or 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, wheezing, or diminished breath sounds.
❑ CNS — When hypoxemia and hypercapnia occur, 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 — Tachycardia, with increased cardiac output and mildly elevated blood pressure secondary to adrenal release of catecholamine, occurs early in response to low PaO2. With myocardial hypoxia, arrhythmias may develop. Pulmonary hypertension, secondary to pulmonary capillary vasoconstriction, may cause increased pressures on the right side of the heart, elevated jugular veins, an enlarged liver, and peripheral edema. Stresses on the heart may precipitate cardiac failure.
Diagnosis
Progressive deterioration in ABG levels and pH, when compared with the patient’s “normal” values, strongly suggests ARF in COPD. (In patients with essentially normal lung tissue, pH below 7.35 usually indicates ARF, but patients with COPD display an even greater deviation from this normal value, as they do with PaCO2 and PaO2.)
Other supporting findings include:
❑ Bicarbonate — Increased levels indicate metabolic alkalosis or reflect metabolic compensation for chronic respiratory acidosis.
❑ Hematocrit (HCT) and Hb — Abnormally low levels may be due to blood loss, indicating decreased oxygen-carrying capacity. Elevated levels may occur with chronic hypoxemia.
❑ Serum electrolytes — Hypokalemia and hypochloremia may result from diuretic and corticosteroid therapies used to treat ARF.
❑ White blood cell count — Count is elevated if ARF is due to bacterial infection; Gram stain and sputum culture can identify pathogens.
❑ Chest X-ray — findings identify pulmonary pathologic conditions, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, or effusions.
❑ Electrocardiogram — Arrhythmias commonly suggest cor pulmonale and myocardial hypoxia.
Treatment
ARF in patients with COPD is an emergency that requires cautious O2 therapy (using nasal prongs or Venturi mask) to raise the PaO2. In patients with chronic hypercapnia, O2 therapy can cause hypoventilation by increasing Paco2 and decreasing the respiratory drive, necessitating mechanical ventilation. The minimum fraction of inspired air (FIO2) required to maintain ventilation or O2 saturation greater than 85% to 90% should be used. If significant uncompensated respiratory acidosis or unrefractory hypoxemia exists, mechanical ventilation (through an endotracheal [ET] or a tracheostomy tube) or noninvasive ventilation (with a face or nose mask) may be necessary. Treatment routinely includes antibiotics for infection, bronchodilators, and possibly steroids.
Special considerations
❑ Because most patients with ARF are treated in an intensive care unit, orient them to the environment, procedures, and routines to minimize their anxiety.
❑ To reverse hypoxemia, administer O2 at appropriate concentrations to maintain PaO2 at a minimum of 50 to 60 mm Hg. Patients with COPD usually require only small amounts of supplemental O2. Watch for a positive response — such as improvement in the patient’s breathing, color, and ABG levels.
❑ Maintain a patent airway. If the patient is retaining CO2, encourage him to cough and to breathe deeply. Teach him to use pursed-lip and diaphragmatic breathing to control dyspnea. 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 secretions.
❑ In an intubated patient, suction the trachea as needed after hyperoxygenation. Observe for a change in quantity, consistency, and color of sputum. Provide humidification to liquefy secretions.
❑ Observe the patient closely for respiratory arrest. Auscultate for chest sounds. Monitor ABG levels and report any changes immediately.
❑ Check the cardiac monitor for arrhythmias.
If the patient requires mechanical ventilation:
❑ Check ventilator settings, cuff pressures, and ABG values often because the FIO2 setting depends on ABG levels. Draw specimens for ABG analysis 20 to 30 minutes after every FIO2 change or oximetry check.
❑ Prevent infection by using sterile technique while suctioning.
❑ Stress ulcers are common in the intubated patient. Check gastric secretions for evidence of bleeding if the patient has a nasogastric tube or if he complains of epigastric tenderness, nausea, or vomiting. Monitor Hb level and HCT; check all stools for occult blood. Administer antacids, histamine-2 receptor antagonists, or sucralfate, as ordered.
❑ Prevent tracheal erosion, which can result from artificial airway cuff overinflation. 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 oral or vocal cord trauma, make sure that the ET tube is positioned midline or moved carefully from side to side every 8 hours.
❑ To prevent nasal necrosis, keep the nasotracheal tube midline within the nostrils and provide good hygiene. Loosen the tape periodically to prevent skin breakdown. Avoid excessive movement of any tubes; make sure the ventilator tubing is adequately supported.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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