Respiratory failure in COPD

The diagnosis of acute respiratory failure in COPD is made on the basis of an acute drop in Pa02 of 10 to 15 mm Hg or any acute increase in PaC02 that decreases the serum pH to 7.3 or less. 

The most common cause of acute respiratory failure in COPD is acute exacerbation of bronchitis with an increase in sputum volume and viscosity. This serves to worsen obstruction and further impair alveolar ventilation, resulting in worsening hypoxemia and hypercapnia. Additional causes are pneumonia, pulmonary embolism, left ventricular failure, pneumothorax, and CNS depressants. 

In advanced COPD, caution should be used since overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. In these patients, mild hypoxemia, rather than carbon dioxide accumulation, triggers their drive to breathe. 

Doxapram is an analeptic that increases the depth of respirations (tidal volume) by stimulating the respiratory center in CNS respiratory rate may increase slightly. It may elevate BP by increasing cardiac output. Respiratory depression from opiates is reversed without affecting pain relief. It is indicated when one requires the stimulation of deep breathing in postoperative patients for reversal of respiratory depression caused by anesthesia (other than muscle relaxants) or drug overdose and as a temporary measure in acute respiratory failure in patients with chronic obstructive pulmonary disease (COPD) who are not undergoing mechanical ventilation. 

From these equations, it follows that VA decreases and so Pacx>2 increases when VE decreases. Likewise, when VE and VD remain unchanged but VT decreases and respiratory frequency (RF) increases (rapid shallow breathing), Pacx)2 increases. Patients adopt a rapid shallow breathing pattern to minimize respiratory work per breath, but this form of compensatory behavior can be deleterious to gas exchange and is a major factor producing chronic hypercapnic respiratory failure in patients with COPD and neuromuscular disorders (6-10). 

Figure 1 The management of respiratory failure in the United States. Many patients are admitted initially to an acute care hospital. If they wean ptomptiy, they may spend time in an LTAC hospital for rehabilitation, and eventually return home. If they fail to wean, they undergo tracheostomy and are transferred to an LTAC when stable. Weaning attempts continue, and a mincnity of patients return home the rest remain at the LTAC or are transferred to a SNF. Patients who deteriorate while at LTACs or at home return to the acute care hospital fOT stabilization. Some patients with chronic respiratory failure do not require acute care but are ventilated noninvasively and remain home. Abbreviations COPD, chronic obstructive pulmonary disease NIV, noninvasive ventilation LTAC, long-term acute care SNF, skilled nursing facility.

Long-term administration of oxygen (greater than 15 hours per day) to patients with chronic respiratory failure has been shown to reduce mortality and improve quality of life.1,2 Oxygen therapy should be initiated in stable patients with very severe COPD (GOLD stage IV) who are optimized on... 

The goals of therapy for patients experiencing exacerbations of COPD are prevention of hospitalization or reduction in length of hospital stay, prevention of acute respiratory failure and death, resolution of symptoms, and a return to baseline clinical status and quality of life. 

Noninvasive positive-pressure ventilation (NPPV) provides ventilatory support with oxygen and pressurized airflow using a face or nasal mask with a tight seal but without endotracheal intubation. In patients with acute respiratory failure due to COPD exacerbations, NPPV was associated with lower mortality, lower intubation rates, shorter hospital stays, and greater improvements in serum pH in 1 hour compared with usual care. Use of NPPV reduces the complications that often arise with invasive mechanical ventilation. NPPV is not appropriate for patients with altered mental status, severe acidosis, respiratory arrest, or cardiovascular instability. 

Acetazolamide should be avoided in patients with severe COPD. These patients may be unable to increase their alveolar ventilation enough to compensate for the acid-base alterations induced by acetazolamide. In some patients, especially those with severe pulmonary disease, increased CO2 gradients or acidosis may lead to acute respiratory failure. Acetazolamide should be used cautiously in such patients, and the practitioner should use the lowest effective dose to reduce lOP... 

The goals of therapy for patieuts experieuciug exacerbatious of COPD are (1) prevention of hospitalization or reduction in hospital stay, (2) prevention of acute respiratory failure and death, and (3) resolution of exacerbation symptoms and a return to baseline clinical status and quality of life. Various therapeutic options are summarized in Table 27-13. Pharmacotherapy consists of intensification of bron-chodilator therapy and a short course of systemic corticosteroids. Antimicrobial therapy is indicated in the presence of selected symptoms. Since the frequency and severity of exacerbations are closely related to each patient s overall health status, all patients should receive optimal chronic treatment, including smoking cessation, appropriate pharmacologic therapy, and preventative therapy such as vaccinations. 

Enteral formulas (e.g., Pulmocare, NutriVent, and Respalor) marketed for use specifically by patients with pulmonary disease are also available. In comparison with standard formulas, these products contain a higher percentage of nonprotein calories as fat (>50%). Several studies have evaluated the use of these high-fat/low-carbohydrate products in patients with COPD and acute respiratory failure, and general results have been favorable." These speciahzed pulmonary EN products are calorically dense (1.5 kcal/mL), which may be helpful in feeding patients with severe ARDS or pulmonary edema and in others who may require fluid restriction. 

Long-term oxygen therapy has been shown to improve the client s quality of life and survival. The oxygen must be kept between 1 and 3 L/min to prevent respiratory failure, which occurs when the oxygen level is increased and the client s hypoxic drive is no longer active. Carbon dioxide narcosis occurs in clients with COPD and eliminates that stimulus for breathing. 

Respiratory Possible unwanted effects of carvedilol, metoprolol, and bisoprolol on respiratory function in patients with heart failure and concomitant chronic obstructive pulmonary disease (COPD) have not been clearly defined. In a randomized, open, triple-crossover trial, 51 patients with heart failure, 35 of whom had also COPD, took carvedilol, metoprolol, and bisoprolol, dose-matched, each for 6 weeks before resuming their original beta-blocker. N-terminal brain natriuretic peptide (BNP)... 

Almitrine bismesylate is indicated in patients with respiratory failure with hypoxaemia related to obstructive bronchitis. It was first marketed in France in 1982 for the treatment of chronic obstructive pulmonary disease (COPD), where the airways and air sacks inside the Itmgs become damaged or blocked. Between September 2003 and November 2012, almitrine s safety was xmder increased scrutiny due to increased reports of weight loss and peripheral neuropathy despite France s regulatory actions to minimise the risk of these AR by dose adjustments and increased warnings. 

CRF occurs in tbe very advanced stages of stable COPD when the degree of airflow obstruction becomes severe (26,27). In a report of hospital discharges, respiratory failure accounted for 37% of in-hospital mortality in patients with COPD, as either a primary or a secondary discharge diagnosis (28). Treatment of respiratory failure accounts for a large part of the economic burden of tbe disease. Admission to the hospital for COPD exacerbations, associated with respiratory failure, accounts for approximately two-thirds of the direct costs of COPD (29). The role of HMV in COPD is discussed elsewhere in this text. 

Goldberg A, Leger P, Hill NS, et al. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation-a consensus conference report. Chevy Chase, MD National Association for Medical Direction of Respiratory Care, 1999 521-534. 

In a study of 183 COPD patients with acute respiratory failure, 10.4% remained mechanically ventilated 21 days after intubation (11). In the same ICU, the relative risk of remaining ventilated at day 21 was twice as high in patients intubated for acute lung injury (21 of 107) (42). One explanation for the latter observation is the presence of either critical illness polyneuropathy or ICU-acquired paresis (ICUAP). In a study of 95 patients ventilated for at least seven days, one quarter developed ICUAP, resulting in a longer duration of MV (18 vs. 8 days in patients without ICUAP) (43). 

In healthy volunteers, stimulation of the phrenic nerves elicits twitch pressures of 31 to 39 cmH20, whereas in patients with severe COPD, twitch pressures average 19 to 20 cmH20 (53,60). Twitch pressures in patients recovering from an episode of acute respiratory failure are about half of those recorded in ambulatory patients with severe COPD (Fig. 5) (59,61,62). This decrease is in keeping with respiratory muscle weakness in most of these patients. Respiratory muscle weakness in mechanically ventilated patients can result from preexisting conditions or from new-onset conditions (63). 

Figure 5 Transdiaphragmatic twitch pressure recorded in mechanically ventilated patients recovering from an episode of acute respiratory failure. Box represents range of transdiaphragmatic twitch pressures recorded in ambulatory patients with severe COPD. Most mechanically ventilated patients had evidence of diaphragmatic weakness [data from Ref. 62 (open circles), and from Ref 61 (closed circles)]. Abbreviation COPD, chronic obstructive pulmonary disease. Source From Refs. 44.

Jakobsson P, Jordfelt I, Brundin A. Skeletal musele metabolites and fiber types in patients with advanced COPD with and without chronic respiratory failure. Eur Respir J 1990 3 192—196. 

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