Re: V, newport, and anyone else - respiratory failure

This is what I found so far, trapper. It may not be much, but I'll keep looking:


http://www.wrongdiagnosis.com/c/chronic_bronchitis/book-diseases-7b.htm

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

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.
Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.