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Chapter 8: Respiratory System
CASE STUDY: CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Read the case study and answer the questions that follow. Most of the terms are included in this chapter. Refer to the glossary or to your medical dictionary for the other terms. Helga is a 57-year-old who came to the urgent-care clinic today complaining of SOB. On admission, respirations were labored, at a rate of 32 breaths per minute. SpO 2 was just 84%, and VC was decreased. Helga appeared anxious and stated, “I can’t get enough air.” The lungs had bilateral expiratory wheezes throughout, scattered rhonchi, and bibasilar crackles. There was a frequent cough, productive of thick green sputum. Stat ABGs were drawn. Helga was put on O 2 at 2 liters per minute (lpm) per nasal cannula (NC) and given a nebulizer Tx. A sputum specimen was collected and sent for culture and sensitivity (C&S). IV doses of a broad-spectrum antibiotic and a steroid drug were given. Upon review of ABGs, it was determined that Helga was in a state of mild respiratory acidosis. A short time later, Helga reported breathing “much better” and demonstrated a decreased respiratory rate to 20 breaths per minute, and an increased O 2 saturation to 91%. Helga was then transferred to the hospital for further monitoring and continued therapy. COPD is a chronic disease with several different causes. The most common cause is smoking, because the lungs are subjected to chronic irritation by an inhaled substance 20 to 40 times each day for years on end. As a result, the lung tissue becomes inflamed. Under normal circumstances, body tissue can repair itself; however, in the case of smoking, chronic, repeated exposure to the irritants prevents healing and results in chronic inflammation. Over time, permanent damage occurs. The walls of the delicate alveoli lose their elasticity and become permanently distended, like balloons that have been inflated too many times. The walls of the alveoli also erode and thicken and, as a result, function less effectively. They begin to trap air rather than allowing it to escape during expiration. This decreases the amount of oxygen-rich air that can be inhaled in each breath. When chronic air-trapping occurs, the chest changes dimension, becoming more barrel- like. The lungs also flatten on the bottom, robbing the diaphragm (an important respiratory muscle) of its effectiveness. Cilia in the airway normally move debris upward to be coughed out, but, in COPD, cilia become clogged with tar and thus lose their effectiveness. As a result of these physical changes, the COPD patient may begin to experience some or all of the following symptoms: Orthopnea: The need to remain upright to breathe effectively. Physicians often quantify the severity of orthopnea by referring to the number of pillows the patient must recline against while sleeping (e.g., three-pillow orthopnea). Hypercapnia: The chronic retention of CO 2 . In some cases, this changes the way the person’s body determines when to breathe. The person may begin to function according to the “hypoxic drive” and feel the urge to breathe when the O 2 level gets too low instead of when the CO 2 level gets too high. This becomes a problem when the person requires supplemental O 2 . Too much O 2 can, in some circumstances, actually knock out the urge to breathe, leading to respiratory arrest. Furthermore, hypercapnia can lead to symptoms of mental cloudiness and lethargy. Chronic hypoxia: A chronic lack of oxygen. While gas exchange becomes less effective, breathing becomes increasingly difficult. Eventually, the person becomes dependent on oxygen. Yet, in the last stages of the disease, supplemental O 2 is of little help. The person feels chronically short of breath and becomes severely dyspneic with the slightest exertion.
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