Signature Assignment:
Chronic Obstructive Pulmonary Disease Case Study

Case Study
R.S. has smoked for many years and has developed chronic bronchitis, a chronic obstructive pulmonary disease (COPD). He also has a history of coronary artery disease and peripheral arterial vascular disease. His arterial blood gas (ABG) values are pH = 7.32, PaCO2 = 60 mm Hg, PaO2= 50 mm Hg, HCO3- = 30 mEq/L. His hematocrit is 52% with normal red cell indices. He is using an inhaled ß2 agonist and Theophylline to manage his respiratory disease. At this clinic visit, it is noted on a chest x-ray that R.S. has an area of consolidation in his right lower lobe that is thought to be consistent with pneumonia

1) What clinical findings are likely in R.S. as a consequence of his COPD? 2) How would the consequences of the COPD of R.S. (identified in question 1) differ from those of emphysematous COPD? 3) Interpret R.S.’s laboratory results. How would his acid-base disorder be classified? What is the most likely cause of his polycythemia? 4) What is the rationale for treating R.S. with Theophylline and a ß2 agonist? 5) What effects would his respiratory disease have on his cardiovascular function?
ANSWERS:

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1. And 2. He is likely to have diminished breath sounds. He may or may not have wheezing depending upon the degree of bronchoconstriction and will almost certainly have crackles and bronchial breath sounds over the RLL. Since he is polycythemic and has hypoxemia, he may have some cyanosis (without a hemoglobin and sat that's hard to say, but folks with polycythemia are more prone to cyanosis simply because they have more hemoglobin. Frank cyanosis is only apparent when 5g/dL of Hb is deoxygenated. With a normal Hb of 15 that is a sat of 66%. With an Hb of 10 that's a sat of 50%. With an Hb of 20 that is a sat of 75%. Suffice it to say, most folks won't desaturate enough to turn blue until it is way too late.)

On inspection, we would expect an increased A-P diameter of the chest (barrel chest). He is in respiratory insufficiency so we would expect tripod positioning and accessory muscle use as well as a prolonged expiratory phase. He is likely to have difficulty completing sentences due to shortness of breath. On palpation and percussion we would expect decreased vocal fremitus over the majority of the lung and increased fremitus over the RLL. We would expect a low, resonant note on percussion over the majority of the lung as well with a more solid note over the RLL. In addition to the lung sounds previously mentioned, we would expect "E-to-A" changes over the lungs except in the RLL (this is a technique wherein you have the patient say a long "EEEEEE" over and over again while listening to the lung fields. In areas where there is significant trapped air, the note sounds like a long "AAAAA" instead of "EEEEEE"). This is much more prominent in emphasematous COPD than bronchitic COPD. In bronchitic COPD we would expect more wheezing and rhonchi/coarse crackles whereas in emphasematous COPD we would expect more diminished breath sounds.

3. He is in a partially compensated respiratory acidosis with moderate hypoxemia and mild polycythemia. The pH is acidotic, which tells you that if there is any compensation present, it is not complete (otherwise the pH would be normal). The PaCO2 is consistent with an acidosis which gives you a clue that it is likely respiratory. The bicarbonate confirms that this is respiratory and not a mixed acidosis. Further, the bicarb is elevated which indicates compensation, but the abnormal pH indicates that the compensation is not complete. Thus it is a partially compensated respiratory acidosis. A PaO2 between 45-60 is considered moderate hypoxemia. Without a hemoglobin you can't calculate the total arterial oxygen content, but given the polycythemia it is likely to be normal or even elevated (you can approximate Hb by Hct/3. So 52/3 = 17.3 which is only slightly elevated. Still, he could tolerate a sat down to 85% and still have a normal CaO2). Polycythemia is a consequence of chronic hypoxemia. The incomplete compensation and polycythemia tells you that this is an acute problem imposed on a chronic problem since the kidneys take several days to fully compensate an acidosis but polycythemia takes months to develop.

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