1. Describe the pathophysiological changes that occur in COPD and lead to the signs and symptoms listed in Table
2. With reference to the relevant pathophysiological changes, explain the reason/s for the patient observations listed in Table 1. (20 marks)
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease that deteriorates over time. The deterioration of disease means the reduction in lung performances which may breathing difficulty, chest tightness and cough that were manifested in this case of the patient named Mr. Wenham. The underlying cause of this reduction in respiratory functions are permanent damage to respiratory airways, peripheral bronchioles and lung parenchyma. One of the main causes of COPD is smoking. Smoking is responsible for cause inflammation in the lung. Inflammation thereafter cause activation of polymorphonuclear leukocytes and macrophases. Both these mediators results in the elastase release which is responsible for decreasing the lung functions (Mosenifar 2017). This is because, inflammation due to smoke increases the number of phagocytes and polymorphonuclear leukocytes particularly because of oxidative stress. Both phagocytes and polymorphonuclear leukocytes cause apoptosis and necrosis of cells present in lung (Feghali-Bostwick et al. 2008; Houben et al. 2009). Furthermore, inflammation is associated with increased secretion of macrophages and metalloproteinase through influx of neutrophil with subsequent development of emphysema (Mosenifar 2017). What is more, structural damage due to apoptosis and necrosis results microalbuminuria to develop hypoxemia (Casanova et al. 2010). In addition, the repair mechanism through growth factor beta is deregulated. Hence, damage and loss of repair capability lead to structural damage with subsequent development of breathing difficulty including shortness of breathing and elevation of respiration rate (Decramer, Janssens & Miravitalles 2012). Also, protease release is responsible for damage to the lung parenchyma as well as higher release of mucus. This is because mucus secreting cells replace the protease inhibitory cells (Stapczynsk et al. 2011). So the patient experience cough with mucus. Besides, presence of mucus in the airway cause narrowing of airways with subsequent difficulty in breathing and reduce inspiratory capacity to cause hyperinflation. Thereafter barrel chest is developed from hyperinflation (Decramer, Janssens & Miravitalles 2012; Mosenifar 2017). Together, narrow airway and presence of mucus results difficulty in breathing with associated tightness in the chest.
2. Discuss why you would administer salbutamol and describe how it works at the cellular level. (10 marks)
The patients with COPD are characterized by breathing difficulties. In such cases, the patients can be symptomatically treated with administration of salbutamol because it is an effective and fast acting bronchodilator. It is a selective beta 2 agonist. Beta 2 adrenoreceptors are present in bronchioles. Therefore, by selective agonism of beta 2 adrenoreceptors by salbutamol allows to relief from bronchospasm by bronchodilation to allow increase in air flow particularly in the patients with COPD (Cazzola et al. 2012; Montuschi 2006). Therefore, I considered to administer salbutamol for quick relief of shortness of breathing.
The mechanism by which salbutamol cause bronchodilatation is through activating cyclic adenosine mono phosphate (cAMP). Primarily adenyl cyclase is activated by salbutamol to produce cAMP before it induces protein kinase activity. Protein kinase thereafter inhibits phosphoinositol hydrolysis and reduction in calcium ions to activate potassium channel. Therefore, hyperpolarization is developed in smooth muscles of the airway for causing relaxation of smooth muscles and subsequent dilatation (Cazzola et al. 2012).
3. Discuss why they would take an arterial blood gas and explain what the results mean and how they relate to the pathophysiology you described. (10 marks)
Arterial blood gas is a test that comprises the measurement of blood pH, partial pressure of oxygen and carbon dioxide. These parameters are thereafter used for assessing a patient’s respiratory disturbances such as COPD (Bonner & Monkhouse 2007). Among healthy people the normal ranges of the arterial blood gas parameters are as below (Belda 2011; Williams 2006) –
• pH: 7.35-7.45
• PaCO2: 35-45 mmHg
• PaO2: 80-100 mmHg
• HCO3-: 22-26 mEq/L
• SaO2: 95-100%
Generally, the arterial blood gas measurements are compared with these above normal ranges (Belda 2011). It was reported that Mr. Wenham’s pH was lowered to 7.12 but PaCO2 level was increased to 110 mmHg. This suggested that the patient may have been experiencing poor perfusion with resulted retention of carbon dioxide in the body. Also, in case of COPD, elastic recoil is lost with reduced alveolar ventilation and hence expiration of carbon dioxide is reduced with subsequent development of hypercapnia manifested with elevated level of PaCO2 (Brill & Wedzicha 2014; Pilcher et al. 2015). Thereafter, retained carbon dioxide produce carbonic acid which dissociates to bicarbonate ions and hydrogen ions to lower blood pH (Ronco, Bellomo & Kellum 2009).
4. Overview the normal physiological control of breathing (not the mechanics of ventilation). Then, explain how carbon dioxide retention might occur when COPD patients are receiving supplemental oxygen. How would you recognise this if it was happening to Mr Wenham? (20 marks)
In the health person, breathing means inhalation of oxygen and expiration of carbon dioxide. However, when a person is suffering from COPD, respiratory functions are altered and affect the ventilation and perfusion which are related to inspiration and expiration. Ventilation is the volume of air that reaches to the alveoli of the lung whereas perfusion is the volume of blood that reaches to the alveoli through capillaries. COPD is associated with mismatch between ventilation and perfusion. Hence the volume of air inheld for exchanging to carbon dioxide and the volume of carbon dioxide that is expelled is altered because of deterioration of gas exchange ability of the lung (Kent, Mitchell & McNicholas 2011). Due to reduced air flow, there is risk of developing hypoxemia and thus supplemental oxygen is given, but in the patients with COPD supplemental oxygen can lead to the retention of carbon dioxide. One reason is that after supplemental oxygen, blood is super oxygenated and hence its capacity to carry carbon di oxide is reduced which is known as the Haldane effect. Ultimately, carbon di oxide is retained in the body. Also, the patient develops hypoventilation due to the dead spaces present in the alveoli of the lung. Therefore, carbon dioxide is not exchanged with oxygen (Kim et al. 2008).
The retention of carbon dioxide is recognized by the results of his arterial blood gas analysis. It has been reported that the PaCO2 of the patient was increased to 110mmHg which was due to retention of carbon dioxide in the body (Bonner & Monkhouse 2007). Also study has reported that oxygen therapy is responsible to increase PaCO2 by 23 mmHg (Kim et al. 2008) which was found in this case. As a secondary effect of carbon dioxide retention, pH of blood is reduced from the dissociation of carbonic acid with increase in bicarbonate ion concentration (Bonner & Monkhouse 2007). Subsequently, hypercapnia and associated decrease in pH are responsible for loss of consciousness due to CNS depression (Brill & Wedzicha 2014; Pilcher et al. 2015).
5. When considering his blood gas analysis, do you think it is a good idea to remove Mr Wenham’s oxygen and have him just breathing air? Provide an argument supporting why it is OR why it is not. (10 marks)
When considering Mr. Wenham’s blood gas analysis, it was indicated that the patient may have developed hypercapnia which was reflected in his low level of pH with higher level of PaCO2. However, his PaO2 was within the normal range although his oxygen saturation level was 82% which was indicative of administering supplemental oxygen to prevent hypoxemia and associated complications (McDonald 2014; Pilcher et al. 2015). However, supplemental oxygen therapy may not be helpful for this patient because his PaO2 was 100mmHg which was over 65mmHg and it was reported that PaO2 over 65mmHg does not get benefit from supplemental oxygen therapy (McDonald 2014). Most importantly, supplemental oxygen may be associated with developing hypercapnia when used for COPD patients mainly because of poor perfusion ability (Brill & Wedzicha 2014; Kim et al. 2008; Pilcher et al. 2015). Thereafter, hypercapnia may lead to unconsciousness as well as respiratory acidosis (Pilcher et al. 2015). Considering these complications and associated risks, it is thus better to remove him from supplemental oxygen and allow him to breath in atmospheric air.
6. What is BiPAP? How might BiPAP help to improve Mr Wenham’s clinical condition? (10 marks)
BiPAP refers to a device that means bilevel positive airway pressure. It has been used for regulating the ventilation of patients who are suffering from respiratory problems. It is a non-invasive procedure to regulate the patient’s breathing (Celli 2008).
In this case, the patient’s PaO2 was normal but his PaCO2 was elevated. In such case, providing oxygen after adjustment of the pressure gradients of the patient. Therefore, it has been considered that use of BiPAP for COPD patients help in expelling more carbon dioxide particularly in case of hypercapnia. Mr. Wenham was developed hypercapnia reflected by his PaCO2 level and thus expiration of retained carbon dioxide is important to reduce the risk of respiratory acidosis and other neurological complications (Celli 2008; Pilcher et al. 2015). Therefore it is believed that recognizing the pressure gradient, BiPAP may help in expiring the accumulated carbon dioxide.
7. What is spirometry? (5 marks)
Spirometry is a test that is used to diagnose any disorder in lung function. It uses forced expiratory volume and forced vital capacity in assessing lung function (Karkhanis & Joshi 2012). It calculates the ratio of FEV1 to FVC in diagnosing the respiratory disorder. Although FEV1/FVC ratio is dependent on variables such as age, height and gender, the alteration in this ratio is suggestive of abnormal lung function (Johns & Pierce 2008).
8. Discuss the significance of the results by examining the differences between Mr Wenham’s spirometry and that of a normal individual. (10 marks)
The normal ratio of FEV1/FVC is 70-75% (Johns & Pierce 2008). In a healthy individual, the FEV1 ranges from 1.57L to 3.97L and the FVC ranges from 2.26L to 5.43L (Johns & Pierce 2008). Here in this case the patient’s FEV1 was 0.75L and his FVC was 1.5L which means the FEV1/FVC was 50%. While comparing with the normal ranges, it is found that both the FEV1 and FVC were reduced but the ratio suggest that only 50% of carbon dioxide was expelling and thus it was indicative of retention of carbon dioxide. This could be a serious risk for Mr. Wenham because of associated respiratory acidosis and CNS effects.
9. How does the pathology of COPD explain these differences? (5 marks)
Poor ventilation is a characteristic of COPD patients because of irreversible damage of the airways. As a result the respiratory load is increased gradually with gradual reduction in FEV1 to 79% (Stapczynsk et al. 2011). Also inflammation induced production of mucus is responsible for airway obstruction. In addition, loss of elasticity reduces the elasticity of the airways. Together these changes reduces the FEV1 and FVC in the COPD patients (Ferguson 2006; Talag & Wilcox 2008). As a result, less amount of air is reaching to the alveoli to deliver to blood and less volume of carbon dioxide is expired and therefore carbon dioxide is accumulated gradually in the body to increase PaCO2 with subsequent reduction in pH.
Belda, FJ 2011, ‘Interpreting arterial blood gas analysis’, European Society of Anaesthesiology, European Society of Anaesthesiology. <https://www.researchgate.net/profile/Francisco_Belda/publication/268270187_-1_-_05RC1_Interpreting_arterial_blood_gas_analysis/links/54e244c20cf296663796498a.pdf>.
Bonner, S & Monkhouse, D 2007, ‘Arterial blood gas interpretation’, Care of the Critically Ill Medical Patient, p. 43.
Brill, SE & Wedzicha, JA 2014, ‘Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease’, International journal of chronic obstructive pulmonary disease, vol. 9, p. 1241.
Casanova, C, de Torres, JP, Navarro, J, Aguirre-Jaíme, A, Toledo, P, Cordoba, E, Baz, R & Celli, BR 2010, ‘Microalbuminuria and hypoxemia in patients with chronic obstructive pulmonary disease’, American journal of respiratory and critical care medicine, vol. 182, no. 8, pp. 1004-1010.
Cazzola, M, Page, CP, Calzetta, L & Matera, MG 2012, ‘Pharmacology and therapeutics of bronchodilators’, Pharmacological reviews, vol. 64, no. 3, pp. 450-504.
Celli, BR 2008, ‘Update on the management of COPD’, CHEST Journal, vol. 133, no. 6, pp. 1451-1462.
Decramer, M, Janssens, W & Miravitalles, M 2012, ‘Chronic obstructive pulmonary disease’, The Lancet, vol. 379, no. 9823, pp. 1341-1351.
Feghali-Bostwick, CA, Gadgil, AS, Otterbein, LE, Pilewski, JM, Stoner, MW, Csizmadia, E, Zhang, Y, Sciurba, FC & Duncan, SR 2008, ‘Autoantibodies in patients with chronic obstructive pulmonary disease’, American journal of respiratory and critical care medicine, vol. 177, no. 2, pp. 156-163.
Ferguson, GT 2006, ‘Why does the lung hyperinflate?’, Proceedings of the American Thoracic Society, vol. 3, no. 2, pp. 176-179.
Houben, JM, Mercken, EM, Ketelslegers, HB, Bast, A, Wouters, EF, Hageman, GJ & Schols, AM 2009, ‘Telomere shortening in chronic obstructive pulmonary disease’, Respiratory medicine, vol. 103, no. 2, pp. 230-236.
Johns, DP & Pierce, R 2008, Spirometry: The Measurement and Interpretation of Ventilatory Function in Clinical Practice 2nd edn, McGraw-Hill, Australia.
Karkhanis, VS & Joshi, J 2012, ‘Spirometry in chronic obstructive lung disease (COPD)’, J Assoc Physicians India, vol. 60, no. Suppl, pp. 22-26.
Kent, BD, Mitchell, PD & McNicholas, WT 2011, ‘Hypoxemia in patients with COPD: cause, effects, and disease progression’, Int J Chron Obstruct Pulmon Dis, vol. 6, no. 1, pp. 199-208.
Kim, V, Benditt, JO, Wise, RA & Sharafkhaneh, A 2008, ‘Oxygen therapy in chronic obstructive pulmonary disease’, Proceedings of the American Thoracic Society, vol. 5, no. 4, pp. 513-518.
McDonald, CF 2014, ‘Oxygen therapy for COPD’, Journal of thoracic disease, vol. 6, no. 11, p. 1632.
Montuschi, P 2006, ‘Pharmacological treatment of chronic obstructive pulmonary disease’, International journal of chronic obstructive pulmonary disease, vol. 1, no. 4, p. 409.
Mosenifar, Z 2017, ‘Chronic Obstructive Pulmonary Disease (COPD)’, Medscape, no. March 2017.
Pilcher, J, Weatherall, M, Perrin, K & Beasley, R 2015, ‘Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease’, Expert review of respiratory medicine, vol. 9, no. 3, pp. 287-293.
Ronco, C, Bellomo, R & Kellum, JA 2009, Critical care nephrology, Elsevier Health Sciences,
Stapczynsk, JS, Cline, Dm, Ma, OJ, Cydulka, RK & Meckler, GD 2011, Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th edn, Mc Graw Hill Medical, New York.
Talag, A & Wilcox, P 2008, ‘Clinical physiology of chronic obstructive pulmonary disease’, British Columbia Medical Journal, vol. 50, no. 2, p. 97.
Williams, C 2006, ‘Interpreting Arterial blood gas analysis’, Nursing, vol. 34, no. 8, pp. 50-53.