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COPD case study

1. Describe the underlying pathology of COPD. What impacts do these pathological changes have on normal physiology? In particular, describe alveolar ventilation in a normal individual and discuss how this might be different in Mr Wenham. (20 marks)

COPD is pathologically distinguished for destruction of lung tissue and characterized by airflow limitation. The cause of COPD is deposition of foreign irritants in the respiratory system (). These irritants can be cigarette smoke, nanoparticles from occupational exposure, and environmental pollution. The major reaction initiating the pathology process is inflammation which due to continued exposure to the irritant compounds turns chronic. The deposition of these irritants causes T-lymphocytes, neutrophils, and other inflammatory cells to accumulate on the airways (Moayedi 2007, p. 308). The immune system of the body does clearance to remove any bodies identified as foreign from the body. With the inflammatory elements deposited on the airways, they trigger an inflammatory response attracting inflammatory mediators to the airways to clear the foreign irritating elements.

Under normal conditions of the body, inflammation response is meant to prompt healing. Actually, as stated by Barnes (2009, p. 837), inflammation is a sign of the body immune system alertness to the health threatening situation and activities to fight it. However, in the case of COPD, due to continued introduction of the foreign irritants, the inflammation mechanism doesn’t shut itself down resulting to structural and physiological damage of the lung tissue and progressively gets worse. With continued inflammation, the airways get constricted and narrower due to swelling. This results to ineffective cilia and excessive mucus production leading to over accumulation due to difficult in clearance of the airways (Beasley 2012, p. 560).

At this stage, the patient develops the hallmark of COPD symptoms like Mr. Wenham. These symptoms include wheezing, dyspnoea, and a chronic productive cough. Additionally, the build up of mucus attracts bacteria. according to Brulotte and Lang (2012, p. 235), the end result is continued inflammation, development of pouch-like sacs, and bacterial lung infection causing COPD exacerbation the situation Mr. Wenham is in.

The effect of the destroyed lungs is evident in the alveoli. COPD patients have permanently enlarged airspaces distal to the bronchioles. The result of this enlargement is decrease of alveoli surface area available for gaseous exchange. In addition, there is limited airflow because of loss of alveolar wall resulting to decrease in elastic recoil and loss of alveolar support structure leading to narrowing of the airway (Moayedi 2007, p. 321). Changes in the alveoli form the basis of emphysema a pathologic diagnosis of the condition.

2. Discuss why you would administer salbutamol and describe how it works at the cellular level. (10 marks)

Salbutamol is one of the “reliever” medications used for COPD and asthma attacks. In the case of COPD, administering the drug has a number of reasons and quick effect; the salbutamol inhaler would be used. Salbutamol is a quick acting drug especially when administered through an inhaler. It is delivered directly where it is needed and acts within 5 to 20 minutes after introduction (Vestbo 2013, p. 40). Salbutamol inhaler reduced whole system side effects because it is delivered to the area of action. Salbutamol administered through inhalation has a large surface area of absorption hence a small dose goes a long way in relieving COPD pathological signs.

Administered salbutamol has a number of functions as stated by Rennard (2013, p. 23). First, it helps to ease breathing through relaxation and widening of the airways. Second, it stops shortness of breath, coughing, chest tightness, and wheezing. Third, it has been shown to enhance the clearance mechanism hence removal of the accumulating mucilage secretion.

To realize these functions, salbutamol works at the cellular level of the respiratory system. The drug is a beta 2 adrenergic agonist therefore it works by stimulating beta 2 adrenergic receptors. Albuterol element in the drug binds to beta 2 receptors in the lungs causing the smooth muscles of the bronchi to relax. According to Bonner et al. (2006, p. 33), salbutamol activates adenylate cylase by increasing cAMP, which also serves to mediate the function of the drug. The increased level of cAMP raises the activity of cAMP-dependent protein kinase A which consequently, reduces intracellular calcium concentration and inhibits phosphorylation of myosin. The effects of reduced calcium concentration are the relations of smooth muscles and widening of the bronchi. According to Vestbo (2013, p. 44), salbutamol also inhibits the production of bronchoconstricting agents from the mast cells leading to stoppage of microvascular leakage and promotes the clearance mechanism.

3. Discuss why they would take an arterial blood gas and explain how the results relate to the pathophysiology you described. (10 marks)

In COPD cases, arterial blood gas (ABG) is important and it is used to measure blood acidity and the concentration of oxygen and carbon dioxide in the blood. The primary objective of the test, as stated by Herrejón et al. (2006, p. 226) is to determine how well the lungs are functioning in the removal of carbon dioxide and addition of oxygen from the blood. Extraction of the blood sample is done from the artery after leaving the lungs before oxygen is taken up by the cells and carbon dioxide deposited in the blood.

The purpose of ABG is to establish the presence of breathing problems and lung diseases e.g. cystic fibrosis, asthma, and COPD. The test is done on patients under treatment to determine how the treatment is working (Baylis & Till 2009, p. 471). In severe cases, the test is done to establish if extra oxygen or health in breathing is needed. For patient under assistance oxygen supply, the test is done to determine if the patient is receiving sufficient oxygen. Lastly, ABG is done to establish the measure pH level of the blood.

According to Kellum (2007, p. 2633), the tests done in the case of COPD are partial pressure of oxygen (PaO2)and partial pressure of carbon dioxide (PaCO2). Other tests done on ABG are pH level, Bicarbonate (HCO3), and oxygen content (O2CT) and oxygen saturation (O2sat). Oxygen content is the amount of oxygen in the blood while oxygen saturation is the haemoglobin in the red blood cells carrying oxygen.

In a normal person, PaO2 is 80 to 100 mm Hg, PaCO2 is 35-45 mm Hg, HCO3 is 21–28 mEq/L, and pH is 7.35 -7.45. In the case of Mr Wenham, pH is slightly lower indicating acidosis. PaO2 is at the peak level within the bracket of normalcy. This indicates the effects of supplementary oxygen during the transportation to the health centre. PaCO2 is way too high meaning excessive accumulation of CO2 in the blood. Therefore, very little CO2 is removed from the blood and as a result of supplementary oxygen. HCO3 is at 38 higher than the normal level indicating acidosis due to elevated CO2 levels in the blood.

4. Discuss the issues surrounding the use of supplemental oxygen therapy in patients with severe exacerbations of COPD. What problems can it cause and why? (20 marks)

During exacerbations of COPD, supplemental oxygen therapy is used to maintain PaO2 at 60 mmHg or O2sat at w90%. As stated by Stoller et al. (2010, p. 181), the main these levels should be observed when administering oxygen therapy to avoid tissue hypoxia and maintain the right cell oxygenation. The risk of higher levels of oxygen is retention of CO2 due to the oxyhaemoglobin dissociation curve shape, retention of CO2 is high and it leads to acidosis.

In addition to acidosis, continued and increased use of oxygen causes the respiratory system to become dependent on supplemental oxygen supply. In the case of exacerbation COPD, pulmonary rehabilitation is the best alternative. Even though supplemental oxygen is useful in the short term and after exacerbation, as soon as the patient is out of exacerbation supplemental oxygen should be discontinued as much as possible (Hanania 2010, p. 197). Clinical reports have shown that hospitalised patient may over time increase their PaO2 to a sustainable level where they no longer need supplemental oxygen.

Increased supply of oxygen can also lead to atelectasis (Bradley et al. 2007, p. 280). Atmospheric air has 21% oxygen and 79% nitrogen. The alveoli use nitrogen to keep surfactant production and maintain its patency. High levels of oxygen available through supplemental oxygen serve to drive out nitrogen leaving the alveoli susceptible to lack of gas as oxygen diffuses into the blood, and carbon dioxide is breathed out leaving them to collapse. Given the damaged nature of the lungs in COPD patients, this causes leads to rapid-sequence intubation and atelectasis thereafter.

To some level, ABG could cause additional problems because of the fact that it is taken from an artery. According to Lian (2010, p. 27), if the patient has would or blood clotting problems, the puncture into the artery to collect the blood sample cause problems through blood not clotting. In addition to be painful, it causes discomfort to the already suffering patient. In addition to this problem, the results from ABG test can pose challenges in their interpretation. For example, blood acidosis is not only caused by increased CO2 in the blood. Bicarbonate level can be due to dysfunctional kidneys or due to cardiovascular conditions.

5. Do you think it is a good idea to remove Mr Wenham’s oxygen? Provide an argument supporting why it is OR why it is not.(10 marks)

Yes, supplemental oxygen supply should be removed. Supplemental oxygen helps to sustain the life of COPD patients for longer especially in exacerbated cases, but it should be removed as soon as the PaO2 reaches 60mmHg (Casaburi et al. 2012, p. 8). In the case of Mr. Wenham, supplemental oxygen has been in place for the last 60 minutes during the journey to the hospital and at the hospital, PaO2 measurement showed it to be at 100 mmHg. This is way too high and it can result to tissue hypoxia and destabilize cellular oxygenation.

The high level of oxygen is causing increased accumulation of CO2 in the blood. The ABG reveals PaCO2 to be at 110 mmHg causing acidosis. This can cause organ failure due to increased blood acidity (Bradley et al. 2007, p. 282). Supplemental oxygen should be removed to allow for stop the continued increment of CO2.

Moreover, oxygen is being used to supplementing normal respiration. This should be a mixture of oxygen and nitrogen. The mixture helps to prevent atelectosis of the alveolar when oxygen is diffused into the blood and CO2 exhaled (Wong et al. 2012, p. 915). The presence of nitrogen in the mixture would help to prevent collapsing by occupying the alveolar space.

6. What is BiPAP? How might BiPAP help to improve Mr Wenham’s clinical condition? (10 marks)

BiPAP, Bilevel Positive Airway Pressure, is a non invasive ventilation mechanical method that uses two levels of pressure; Expiratory Positive Airway Pressure (EPAP) and Inspiratory Positive Airway Pressure (Keenan et al. 2011). IPAP has higher pressure and EPAP has low pressure. Therefore, breathing in is a little more difficult causing a decreased amount of air to be inhaled hence a decreased amount of oxygen. On the other hand, due to low EPAP pressure, exhaling is easy and an increased amount of air is exhaled therefore a higher amount of CO2 is exhaled.

Given Mr. Wenham’s condition where the level of PaO2 is very high and the level of PaCO2 also very high, they both need to be reduced to the clinically safe levels of 60 mmHg and 30 mmHg respectively. To achieve this, the amount of inhaled oxygen should be decreased and the more CO2 removed from the body. Through the working mechanism of BiPAP machines, it is possible to achieve this therefore; yes, BiPAP will help to significantly improve Mr. Wenham’s situation.

7. What is spirometry? (5 marks)

Spirometry is a common test on the respiratory system that is done to check how well the lungs are working (Ciprandi & Cirillo 2011, p. 549). It is used for periodic health test and for diagnosis of respiratory related conditions e.g. asthma and COPD. The test measures the volume and air flow of air that can be inhaled or exhaled. The test requires a spirometre, the machine used to make the readings for the parameters used in the test. These parameters used in spirometry are;

  • Forced expiratory volume in one second (FEV1) – the amount of air that can be blown out within a second. With normal lungs and airways, a healthy individual will blow out most of the air in the lungs within one second (Williams et al. 2011, p. 1340).
  • Forced Vital Capacity (FVC) – the total amount of air that can be blown out in one single breath.
  • FEV1/FVC (FEV1 divided by FVC) – the percentage of the total amount of air blown out in one breath that can be blown out within one second.

Spirometry is indicated to establish a number of respiratory concerns among them, diagnosis and management of asthma, detection of respiratory diseases in patients with breathlessness symptoms and distinguish between respiratory and cardiac diseases, determine responsiveness to treatment, diagnose and differentiate between obstructive and constrictive respiratory diseases, establish the history of a diseases, establish the threat of pulmonary barotraumas in events such as scuba diving, for pre-operative risk assessment, and diagnosis of vocal cord dysfunction (Pierce 2005, p. 536).

8. Discuss the significance of the results by examining the differences between Mr Wenham’s spirometry and that of a normal individual. (10 marks)

Normal spirometry values are determined through a population-based research for people with normal lung functioning (Pierce 2005, p. 536). Once a spirometry reading is taken, the results are compared to a normal predicted value from a person of the same age, sex, mass, height, and ethnicity. To establish the standard value for each of the parameters for a normal elder man in the age bracket of Mr. Wenham, the predictive formula to be used are; for FEV1, the formula FEV1 {litres} = 4.30*height {metres} – 0.029*age {years} – 2.49 and for FVC, the formula FVC {litres} = 5.76*height {metres} – 0.026*age {years} – 4.34 (Stanojevic et al. 2008, p. 255). Assuming the height of Mr. Wenham to be 2.25 M, the standard predictive spirometric measurements of an individual of the same age of 75 years and height would be a FEV1 is 5.01L, FVC is 6.67L, and FEV1/FVC is 75.11%.

The reading recorded form the spirometry test on Mr. Wenham are significantly low compared to the predictive standards of an normal person with the similar features. This signifies the obstructed nature of the lungs with the volume of air that can be inhaled or exhaled per second as well as the total amount of air that can be inhaled being very low. However, the FEV1/FVC ratio indicates a moderate rating hence the severity of the exacerbated COPD has been lowered through the various COPD management strategies applied in the health centre.

Mr Wenham’s FEV1 is at 0.75 litres with a difference of 4.26 litres from the predictive value. This difference signifies the critical health condition in which Mr Wenham’s lungs are in. the airways are narrowed due to constricted and obstructive swelling and even though they can still allow easy air flow, they are not at the optimum functioning level. Moreover, the amount of air that can be exhaled is limited. Given the reduced surface area of the alveoli and the destruction of alveoli, the amount of CO2 being removed from the lungs is decreased from the normal values. The FVC value indicated a reduced amount of air that can be exhaled within a single breath. This is due to the reduced internal volume of the respiratory system due to inflammation and the development of air sacs in the alveolar.

In general, the significance of the reading made from the spirometric test on Mr Wenham is that, he is suffering from an obstruction of the lungs. So far, his lungs are functioning normally, but due to the damage inflicted by the COPD, the levels are significantly lower than the standard measures for his age group. The evidence of this is in the FEV1/FVC ratio that indicates a moderate case of the COPD. Therefore, the control measures that have been put in place for the last 18 hours have succeeded to put Mr Wenham out of danger. Based on the FEV1/FVC ratio, Mr Wenham is in a stable condition however, he cannot partake in active physiological activities without any support remedies e.g. supplemental oxygen.

9. How does the pathology of COPD explain these differences? (5 marks)

The results from the spirometric reading have a backing on the pathophysiologic nature of the entire respiratory system. In normal cases, these readings are determined by the volume of the chest cavity hence dependent on the age and the height of the individual (Stoller et al. 2010, p. 185). Nevertheless, these values are can be affected by extra physiologic conditions for example, lung diseases which can be constrictive or obstructive.

In the case of Mr. Wenham’s, his lungs have been damaged due to COPD caused by excessive and prolonged smoking. The effects due to this condition include swollen and constricted airway and swollen alveolar due to the air sacs (Qaseem et al. 2012, p. 791). These two aspects serve to decrease the total volume of in the lungs and consequently, the total volume of air that can be contained. The inflammation of the airways caused reduction in FVC and the level of reduction depends on the significance of the inflammation.

Additionally, COPD has caused significant damage of the alveolar. Some of the alveoli have been destroyed reducing their number. A normal person has about 6 million alveoli in 100m3 (Baylis & Till 2009, p, 470). This number has been significantly reduced for Mr Wenham. Moreover, the remaining number has their functioning compromised due to increased surface area due to development of air sacs. Due to these factors, the amount of CO2 being diffused from the blood system and exhaled is very little hence the reduced value of FEV1.




Barnes, P. 2009. Asthma and COPD: basic mechanisms and clinical management (2nd ed.). Amsterdam: Academic. p. 837.

Baylis C, & Till C. 2009, Interpretation of arterial blood gases. Surg.27 (11): 470–4.

Beasley, V., Joshi, P.V., Singanayagam, A., Molyneaux, P.L., Johnston, S.L. & Mallia, P. 2012. Lung microbiology and exacerbations in COPD. International journal of chronic obstructive pulmonary disease 7: 555–69.

Bonner S, Matta T, Rubin M, Fagan J, Ahern J, Evans D. 2006, Oral β2-Agonist Use by Preschool Children with Asthma in East and Central Harlem, New York. Journal of Asthma, 43: 31-35,

Bradley JM, Lasserson T, Elborn S, Macmahon J, O’Neill B. 2007, A systematic review of randomized controlled trials examining the short-term benefit of ambulatory oxygen in COPD. Chest. 131:278-85.

Brulotte, C.A, Lang, E.S. 2012. Acute exacerbations of chronic obstructive pulmonary disease in the emergency department. Emerg. Med. Clin. North Am. 30 (2): 223–47, vii.

Casaburi R, Porszasz J, Hecht A, Tiep B, Albert RK, Anthonisen NR. 2012, Influence of lightweight ambulatory oxygen on oxygen use and activity patterns of COPD patients receiving long-term oxygen therapy. COPD. Chest; 9:3-11.

Ciprandi, G. & Cirillo, I. 2011. Forced expiratory flow between 25% and 75% of vital capacity may be a marker of bronchial impairment in allergic rhinitis. Journal of Allergy and Clinical Immunology 127 (2): 549–549

Hanania, N. 2010. COPD a Guide to Diagnosis and Clinical Management (1st Ed.). Totowa, NJ: Springer Science and Business Media, LLC. p. 197.

Herrejón A, Inchaurraga I, Palop J, Ponce S, Peris R, Terradez M, 2006. Usefulness of transcutaneous carbon dioxide pressure monitoring to measure blood gases in adults hospitalized for respiratory disease. Arch Bronconeumol.42(5): 225–9.

Keenan SP, Sinuff T, Burns KE, Muscedere J, Kutsogiannis J, Mehta S, Cook DJ, Ayas N, Adhikari NK, Hand L, Scales DC, Pagnotta R, Lazosky L, Rocker G,Dial S, Laupland K, Sanders K, Dodek P. 2011. Clinical practice guidelines for the use of non-invasive positive-pressure ventilation and non-invasive continuous positive airway pressure in the acute care setting. Canadian Medical Association Journal.

Kellum J.A. 2007, Disorders of acid-base balance. Crit Care Med. 35(11):2630-6.

Lian, J.X. 2010. Interpreting and using the arterial blood gas analysis. Nurs Crit Care. 5(3):26–36.

Moayedi, M.S. 2007. Evaluation of the acutely dyspneic elderly patient. Clin. Geriatr. Med. 23 (2): 307–25, vi.

Pierce, R. 2005, Spirometry: An essential clinical measurement. Australian family physician 34 (7): 535–539.

Qaseem A, Wilt TJ, Weinberger SE, Hanania NA, Criner G, van der Molen T, Marciniuk DD, Denberg T, Torres Mackay AJ, Hurst JR. 2012. COPD exacerbations: causes, prevention, and treatment. Med. Clin. North Am. 96 (4): 789–809

Rennard, S. 2013. Clinical management of chronic obstructive pulmonary disease (2nd ed.). New York: Informa Healthcare. p. 23

Stanojevic, S. Wade, A. & Stocks, J. 2008. Reference Ranges for Spirometry Across All Ages: A New Approach. Am. J. Respir. Crit. Care Med. 177 (3): 253–60.

Stoller J.K. 2002, Acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med; 346:988-994.

Stoller JK, Panos R, Krachman S, Doherty D, Make B. 2010, Oxygen therapy for patients with COPD: Evidence for current therapy and the Long-term Oxygen Treatment Trial (LOTT). Chest ; 38:179-187.

Vestbo, J. 2013. Management of Exacerbations. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Global Initiative for Chronic Obstructive Lung Disease. pp. 39–45.

Williams AM, Abramo TJ, Shah MV, Miller RA, Burney-Jones C, Rooks S. 2011. Safety and clinical findings of BiPAP utilization in children 20 kg or less for asthma exacerbations. Intensive Care Med 37 (8): 1338–43.

Wong, D. T., J. Wang and L. Venkatraghavan 2012. Awake bronchoscopic intubation through an air-Q(R) with the application of BIPAP. Can J Anaesth 59(9): 915-916.

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