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Acute Respiratory Failure In C.O.P.D

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 often 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

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)-the most common precipitating factor - 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, 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 may include the following:

• Respiratory symptoms. Rate may be increased, decreased, or normal, depending on the cause; respirations may be shallow or deep or alternate between the two; and air hunger may occur. Cyanosis mayor 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 shows 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 with 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 < 7.35 usually indicates ARF, but COPD patients display an even greater deviation from this normal value, as they do blood Paco2 and Pao2') The following findings are also supportive:

• Bicarbonate levels are increased, reflecting metabolic alkalosis or metabolic compensation for chronic respiratory acidosis.
• Hematocrit and Hb levels are abnormally low, which may be due to blood loss, indicating decreased oxygen­carrying capacity.
• Serum electrolyte levels may indicate hypokalemia, which may result from compensatory hyperventilation - an attempt to correct alkalosis; hypochloremia often occurs in metabolic alkalosis.
• White blood cell count is elevated if ARF is due to bacterial infection; Gram stain and sputum culture can identify pathogens.
• Chest X-ray findings identify pulmonary pathology, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, and effusions.
• Electrocardiogram reveals arrhythmias, which commonly suggest cor pulmonale and myocardial hypoxia.

Treatment

ARF in COPD patients 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, 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 antibiotics for infection, bronchodilators and, possibly, steroids.

Special considerations

• Because most ARF patients are treated in the intensive care unit (ICU), orient them to the environment, procedures, and routines to minimize their anxiety.
• To reverse hypoxemia, administer oxygen at concentrations to maintain Pao2 of at least 50 to 60 mm Hg. Patients with COPD usually require only small amounts of supplemental oxygen. Watch for a positive response, such as improvement in the patient's breathing and color and in ABG results.
• 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.
• Monitor and record serum electrolyte levels carefully, and correct imbalances; monitor fluid balance by recording intake and output or daily weights.
• Prevent tracheal erosion that can result from artificial airway cuff over inflation, which compresses tracheal wall vasculature. Use 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.