Respiratory System

OLEH H. ERRRASMUS SOERASDI

Chronic Obstructive Pulmonary Disease/Emphysema/ Obstructive Disease

Definition
Chronic obstructive pulmonary disease (COPD) is a term used to describe a variety of airway_related disease processes, suchas: emphysema, asthma, chronic bronchitis, bronchiectasis, and cystic fibrosis.
These conditions cause an increase in resistance to flow of gases in the airway that often result in acute and chronic disease states that are reversible or irieersible.

INCIDENCE AND PREVALENCE

In the United States, COPD is most common in males over 50 years of age. It remains the second most common cause of mortality.

ETIOLOGY
The primary predisposing factor is a history of smoking. COPD results from three major pathophysiologic occurrences: chronic infection due to irritation of the bronchi from inhaling smoke or other irritating substances; chronic obstruction of small airways due to excess mucns production, infection, and airway edema; and entrapment of air in alveoli resulting in abnormal enlargement of alveolar airspaces. Exacerbathns may be precipitated by infection, congestive heart failure. oxygen therapy that blunts hypoxic drive, and pulmonary thrornboembclism.

LABORATORY RESULTS
Chest x-rays often show hyperinflation and diaphragmatic flattening, right ventricular hypertrophy, a dilated proximal pulmonary artery, and attenuated pulmonary vasculature in the presence of associated pulmonary vascular disease. Pulmonary function tests will show a decreased FEV1/FVC ratio. Emphysematous patients have increased respiratory volume and total lung capacity but decreased diffusing capacity for carbon monoxide.

The partial pressure of both oxygen (Pa02) and carbon dioxide (PaCO2) are generally not affected until the laser stages of COPD. The ECG may exhibit right ventricular hypertrophy when right-sided heart failure is present. With the chronic respiratory acidosis that often accompanies COPD, PaCO2 is elevated, and pH is low or normal. Acute exacerbations often result in an elevated PaCO2 and an acidic pH. Hematocrit may be elevated in both the acute and chronic disease states.

 Patient History

CLINICAL MANIFESTATIONS

Chronic bronchitis is often manifested by a chronic productive cough, exertional dyspnea, and wheezing. Emphysema is primarily manifested by exertional dyspnea that is progressive in nature with or without a productive cough or wheezing.

Physical Examination
Patients with COPD often have an increased anteroposterior chest diameter (barrel chest), hyperresonance to percussion, and wheezing or rhonchi on auscultation of the chest. Accessory muscles for breathing are used; these patients have a prolonged expiratory phase of respiration and use pursed lip breathing; clubbing of the fingers also may occur.

TREATMENT
Conservative management includes low-flow oxygen via nasal cannula or Venturi mask, bronchodilators, 2-adrenergic agonists, ipratropium bromide, theophylline, and antiinflammatory agents (e.g., cromolyn sodium and adrenocortical steroids). Aggressive therapy includes subcutaneous injection of epinephrine or terbutaline sulfate, inhaled bronchodilators, aminophylline. adienocortical steroids, and intuhation and mechanical ventilation in cases not responsive to other therapies.

ANESTHETIC CONSIDERATIONS Both general and regional anesthesia have been proven acceptable, but these patients are susceptible to postoperative respiratory failure. When sedation is given as during a regional technique, great care should be taken since these patients are extremely sensitive to the respiratory depressant effects of these drugs. Blockade above a sensory level of T-6 may decrease expiratory reserve volume (ERV) so that there is an ineffective cough and thus poor clearance of secretions. With general anesthesia, the clinician should attempt to avoid cold, dry inspired gases.

Volatile agents may produce bronehodilation. Nitrous oxide can cause enlargement and rupture of pulmonary bullae, leading to pneumothorax. Opioids may be used but can be associated with preoperative and postoperative ventilatory depression. Controlled ventilation with high tidal volume (l0 to 15 mL/kg) and slow inspiratory rates optimize Pa02, minimize airflow turbulence, and optimize V/Q matching. During spontaneous ventilation with volatile agents, a greater degree of respiratory depression can be seen in patients with COPD. Perioperative ABGs should be monitored.

PROGNOSIS
The overall long-term prognosis is good for hospitalized patients with acute exacerbations and those with COPD who are stable with therapy. Right ventricular hypertrophy with associated failure is a poor prognostic sign.