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Acute Respiratory Failure in COPD

When the lungs can't adequately maintain arterial oxygenation or eliminate carbon dioxide (C02.), acute respiratory failure results. If not checked and treated, the condition leads to tissue hypoxia. In patients with essentially normal lung tissue, acute respiratory failure usually produces a partial pressure of arterial CO2 (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). These patients consistently have high Paco2 (hypercapnia) and low Pao2 (hypoxemia) levels. For patients with COPD, only acute deterioration in arterial blood gas (ABG) values and corresponding clinical deterioration signal acute respiratory failure.


Acute respiratory failure may develop in COPD patients from any condition that increases the work of breathing and decreases the respiratory drive. These conditions may result from respiratory tract infection (such as bronchitis or pneumonia), bronchospasm, or accumulated secretions secondary to cough suppression. Other common causes are related to ventilatory failure, in which the brain fails to direct respiration, and gas exchange failure, in which respiratory structures fail to function properly.

Other causes of acute respiratory failure include:

  • central neryous system depression due to head trauma or injudicious use of sedatives, narcotics, tranquilizers, or oxygen
  • cardiovascular disorders (myocardial infarction, heart failure, or pulmonary emboli)
  • airway irritants, such as smoke or fumes
  • endocrine or metabolic disorders, such as myxedema or metabolic acidosis
  • thoracic abnormalities, such as chest trauma, pneumothorax, or thoracic or abdominal surgery.

Signs and Symptoms

Diagnostic tests

ABG analysis is the key to diagnosis (and subsequent treatment) of acute respiratory failure in patients with COPD. Progressively deteriorating ABG values and pH compared with the patient's normal values strongly suggest acute respiratory failure. In patients with essentially normal lung tissue, a pH less than 7.35 usually indicates acute respiratory failure. In patients with COPD, the pH deviation from the normal value is even lower.

Chest X-rays are used to identify underlying pulmonary diseases or conditions, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, and effusions.

Electrocardiography (ECG) can demonstrate arrhythmias. Common ECG patterns point to cor pulmonale and myocardial hypoxia

Pulse oximetry reveals a decreasing arterial oxygen saturation.

Blood tests such as a white blood cell count are used to detect underlying causes. Abnormally low hematocrit and decreased hemoglobin levels signal blood loss, which indicates decreased oxygen- carrying capacity.

Serum electrolyte findings vary. Hypokalemia may result from compensatory hyperventilation, the body's attempt to correct alkalosis; hypochloremia usually occurs in metabolic alkalosis.

Pulmonary artery catheterization helps to distinguish pulmonary and cardiovascular causes of acute respiratory failure and is used to monitor hemodynamic pressures.

Additional tests, such as a blood culture. Gram stain, and sputum culture, may be used to identify the pathogen.


Acute respiratory failure in patients with COPD is an emergency. The patient needs cautious oxygen therapy (nasal prongs or a Venturi mask) to increase his Pao2. If significant respiratory acidosis persists, mechanical ventilation with an endotracheal or a tracheostomy tube may be necessary. High-frequency ventilation may be initiated if the patient doesn't respond to conventional mechanical ventilation. Treatment routinely includes antibiotics (for infection), bronchodilators and, possibly, corticosteroids.

If the patient also has cor pulmonale and decreased cardiac output, fluid restrictions and administration of positive enotropic agents, vasopressors, and diuretics may be ordered.

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