Acute Exacerbations of COPD

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The primary goal of emergency therapy in decompensated chronic airflow obstruction is to correct tissue oxygenation. This requires the restoration of the lungs as gas-exchange organs, assurance of hemodynamic efficiency, repletion of red blood cell mass where deficient, and limitation of excessive oxygen demands and carbon dioxide production. Factors that influence drug therapy in the emergency department include (1) the degree of reversible bronchospasm, (2) prior therapy of the patient, (3) recent drug usage and evidence of potential toxicity, (4) the ability of the patient to cooperate in taking inhaled medications, (5) the presence of contraindications to any drug or class of drugs, and (6) specific causes or complications related to the exacerbation.

OXYGEN The first goal in the treatment of COPD is to correct or prevent life-threatening hypoxemia. The goal of oxygen therapy is correction of hypoxemia to an arterial oxygen pressure (Pao2) of greater than 60 mmHg or an arterial oxygen saturation (Sao2) of more than 90 percent. This can be accomplished in the emergency department through several devices, including the standard dual-prong nasal cannula, simple face mask, a Venturi mask, and finally a non-rebreathing mask with reservoir and one-way valve. The need to increase Pao2 must be balanced against the possibility of producing hypercapnia either by one of two suggested mechanisms: respiratory center depression or, more likely, ventilation-perfusion mismatching. 21 Hypercapnia in the face of insignificant acidosis can be tolerated. Improvement after administration of supplemental oxygen may take 20 to 30 min to achieve a steady state after a change in percent of oxygen administered (Fi o2) in patients with COPD. If adequate oxygenation is unachievable without progressive respiratory acidosis, then assisted ventilation may be required.

b2-ADRENERGIC AGONISTS b2-Adrenergic agonists remain the first-line therapy in the management of acute, severe COPD. Aerosolized forms are preferred because they minimize systemic toxicity. Limited data exist regarding the optimal dose and frequency of administration. According to ATS guidelines, b 2-adrenergic agents may be administered every 30 to 60 min, if tolerated.1 Nebulized aerosols administered every 20 min may result in more rapid improvement of FEV1, but the incidence of side effects is greater.22 The use of subcutaneous epinephrine or terbutaline in patients with COPD should proceed with great caution because many COPD patients suffer from concurrent coronary artery disease.

Side effects of b2-adrenergic agonists include tremor, anxiety, and palpitations, so such agonists should be used with care in elderly patients known to have coexisting heart disease. PaO2 may fall slightly after use of these agents, due to pulmonary vasodilation and resultant ventilation-perfusion mismatch.

ANTICHOLINERGICS Anticholinergics have not yet been adequately assessed as first-step therapy in COPD. However, they are often favored when the history indicates poor responsiveness to b2 agonists. Ipratropium bromide given by metered dose inhaler with a spacer or as an inhalant solution by nebulization (0.5 mg or 2.5 mL of the 0.02% inhalant solution) is the agent of choice.18 Evidence suggests that the combination of a b2-adrenergic agent and an anticholinergic agent may be more effective than albuterol alone in relieving bronchospasm during COPD exacerbation. 23 Repeat doses need not usually be given more often than every 4 to 8 h. Side effects are minimal and appear to be limited to dry mouth and an occasional metallic taste.

CORTICOSTEROIDS There is no firm consensus for the use of systemic steroids in the treatment of COPD exacerbation. -M9 and 10 The use of a short course (7 to 14 days) of systemic steroids appears effective in severe exacerbations of COPD with respiratory failure, but their role in mild-to-moderate exacerbations needs to be further delineated.24 ATS guidelines acknowledge the lack of supporting evidence for the use of steroids in COPD exacerbation, but state that steroids can be useful when an asthmatic component is present.1 A poor bronchodilator response does not preclude a good response to steroid therapy. Current theory holds that steroid responsiveness is on a continuum rather than an all-or-nothing phenomenon. If used, the optimal effective dose ranges between one and three times the maximal physiologic adrenal secretion rate (i.e., the equivalent of 60 to 180 mg prednisone).

ANTIBIOTICS All current guidelines recommend antibiotics for the treatment of COPD exacerbation, especially if there is evidence of infection (e.g., fever, leukocytosis, change in the chest radiograph, abnormal mucus production). -I8,9and 1° Recent meta-analysis demonstrates a small, but statistically significant, benefit for antibiotics.25 Proponents of antibiotic use believe antibiotics have both short-term benefits (i.e., rapid resolution of the symptoms of exacerbation, a rapid return of peak flow rates, avoidance of hospitalization, an early return to work, and prevention of progression of severe airway infection into pneumonia) and long-term benefits (i.e., breaking the vicious cycle of airway infection, inflammation, and loss of lung function; prolonging the time between exacerbations; and preventing secondary infection by resistant organisms). They argue further that differentiating infected from noninfected patients is difficult. Antibiotic choices include macrolides, cephalosporins, trimethoprim-sulfamethoxazole, and the latest-generation fluoroquinolones.

METHYLXANTHINES The role of aminophylline in the treatment of COPD exacerbation remains controversial. ATS guidelines suggest adding theophylline if aerosol therapy cannot be given or proves inadequate.1 The bronchodilation effect of aminophylline is limited, and its therapeutic range is narrow. A review of the literature reveals a significant effect on spirometry, respiratory muscle strength, resting blood gases, improvement in the sensation of dyspnea, quality of life, cardiac output, and pulmonary vascular resistance, as well as an anti-inflammatory effect.26 Other study data suggest that aminophylline increases the toxicity but not the efficacy when treating patients with b2-adrenergic agonists.27

In most patients, a serum level of 8 to 12 pg/mL is appropriate. The intravenous loading dose usually required to obtain an initial serum concentration of 10 pg/mL (10 mg/L) is 5 to 6 mg/kg ideal body weight in patients not currently receiving the drug. In patients regularly taking theophylline, a miniloading dose may be alternatively selected: (target concentration - currently assayed concentration) * volume of distribution (i.e., 0.5 times ideal body weight in liters). With the miniload method, the target concentration should be between 1o to 15 pg/mL. The intravenous maintenance infusion rate is 0.2 to 0.8 mg/kg ideal body weight per hour. Lower maintenance rates are given to patients with congestive heart failure or hepatic insufficiency with low clearance rates, whereas higher rates are given to smokers with rapid clearance.

Maintenance theophylline infusion in patients on chronic oral therapy is complex (whether or not a miniloading dose has been given), particularly in attempting to account for enteric drug yet to be absorbed. Both loading and maintenance doses may need to be reduced to minimize the risk of "summation toxicity" due to continued enteric absorption. Standard-release preparations may continue to be absorbed for up to 6 h, and sustained-release preparations may require up to 12 h. Therefore, maintenance infusion rates should be reduced for 6 h after ingestion of a standard-release formulation and 12 h after ingestion of a sustained-release preparation (including 24-h-release forms). Theophylline and aminophylline should not be given orally in an emergency setting unless decompensation is not severe, alimentary motility is assured, and forthcoming ambulatory care is imminent.

ASSISTED VENTILATION Mechanical ventilation is indicated in patients with COPD exacerbation if there is evidence of respiratory muscle fatigue, worsening respiratory acidosis, deteriorating mental status, and in those with clinically significant hypoxemia refractory to supplemental oxygen by usual techniques. The main goals of assisted positive-pressure ventilation in acute respiratory failure complicating COPD are the resting of ventilatory muscles and the restoration of gas exchange to a stable baseline.1

Mechanical ventilation is uncomfortable and is associated with a variety of complications including nosocomial pneumonia, sinusitis, pneumothorax, and injury to the trachea and larynx. There are three specific pitfalls in ventilating patients with COPD: (1) overventilation resulting in acute respiratory alkalosis, (2) initiation of complex pulmonary and cardiovascular interactions that may result in systemic hypotension, and (3) creation of intrinsic positive end-expiratory pressure (PEEP), especially if expiratory time is inadequate or if dynamic airflow obstruction exists. 1 The three ventilatory modes most widely used for managing patients with COPD are assist-control ventilation (ACV), intermittent mandatory ventilation (IMV), and pressure support ventilation (PSV). There are some clinical reports that PSV provides increased patient comfort, promotes patient synchrony with the ventilator, and may accelerate weaning, but there is no direct evidence that patient outcome is improved with pressure support modes compared with volume-cycled modes of mechanical ventilation.1

Noninvasive positive-pressure ventilation (NPPV) is a term used to describe delivery of gas under positive pressure to the airways and lungs without insertion of an endotracheal tube. It can be delivered via a nasal mask, full face mask, or mouthpiece. NPPV can provide positive pressure to the airways only during inspiration (inspiratory positive airway or IPAP), or the airway pressure can be maintained continuously at the same level (continuous positive airway pressure or CPAP), or NPPV can be delivered so that the airway pressure is higher during inspiration than during expiration, with end-expiratory pressure maintained above atmospheric (bilevel ventilation or BiPAP).28 NPPV can be delivered using assist-control volume-cycled ventilation, assist-control pressure ventilation, and pressure support ventilation, with or without end-expiratory positive pressure. No particular mode of ventilation or ventilatory device has been shown to be clearly superior. 29 Disadvantages of NPPV include slower correction of gas-exchange abnormalities, risk of aspiration, inability to control airway secretions directly, and possible complications of gastric distension and skin necrosis.29 Contraindications to the use of NPPV include an uncooperative or obtunded patient, inability of the patient to clear airway secretions, hemodynamic instability, and major gastrointestinal bleeding.28 Studies suggest a pooled success rate of 76 percent in patients with acute respiratory failure complicating COPD, but the studies consist of small numbers, and failure rates of up to 40 percent have been reported in some studies. 1

OTHER Tissue oxygen delivery must be maximized by correcting left ventricular failure or arrhythmia to improve cardiac output, replacing red blood cell mass and intravascular fluid to increase arterial oxygen content, and suppressing fever to decrease oxygen consumption.

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