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Reduced elastins due to emphysema causing airway collapse. Reduced elasticity of the lung which increases lung volume. Patient has severe reduction of FEV1 as his observed value is below 40% of the predicted value. Unable to expire adequate amount of air in the first second when compared to the FVC.
Reduced elastins due to emphysema causing airway collapse. Reduced elasticity of the lung which increases lung volume. Patient has severe reduction of FEV1 as his observed value is below 40% of the predicted value. Unable to expire adequate amount of air in the first second when compared to the FVC.
Reduced elastins due to emphysema causing airway collapse. Reduced elasticity of the lung which increases lung volume. Patient has severe reduction of FEV1 as his observed value is below 40% of the predicted value. Unable to expire adequate amount of air in the first second when compared to the FVC.
1) Reduced elastins due to emphysema causing airway collapse which leads to air
trapping then to hyperinflation (Ferguson. 2006). Another reason could be due to
reduced elasticity of the lung which increases lung volume (Ferguson. 2006).
2) The patient has a very severe reduction of FEV1 as his observed value is below 40% of the predicted value (White. 2014). This suggests that the patient has a severe obstructive disease.
The patients has a 64% reduction of FVC, therefore he has a moderate reduction in FVC (White. 2014). This suggests that the volume of the lungs is decreased possibly due to a restrictive disease.
The patients FEV1/FVC % ratio is below predicted which suggests that he may have an obstructive or mixed disease (obstructive and restrictive) (Pellegrino et al. 2005). He is unable to expire adequate amount of air in the first second when compared to the FVC.
FEF25 is reduced and it represents the mid portion of the airways (small airways) and this is consistent with an obstructive pattern.
3) The peak expiratory flow (PEF) is reduced due to airway obstruction (Llwellin et al. 2002). The area under curve B is significantly lower than curve A, indicating that the volume of the lungs is decreased and this could be due to a restrictive disease. There is also a dip in the curve which represents FEF 25%-75% which is seen in obstructive diseases (Pellegrino et al. 2005).
4) The spirometry results show that the FEV1, FVC, FEV1/FVC and FEF 25%-75% are all below the predicted values. The reduced FEV1/FVC indicated that the patient may be suffering from an obstructive disease (Pellegrino et al. 2005). However, the FVC was significantly lower than predicted value and the flow volume loop showed a TLC that was lower than normal, which should not be the case with a solely obstructive disease. The lower than predicted FVC and lower than normal TLC strongly suggested a mixed disease (Pellegrino et al. 2005). Due to the patients long history of smoking he is likely suffering from interstitial lung disease (ILD) (which is the restrictive component) and Chronic Obstructive Pulmonary Disease (COPD) with characteristics of emphysema (which is the obstructive component).
The wheezing of the patient is possibly due to the obstructive nature of emphysema. The hyperinflation seen in the chest x-ray is possibly due to emphysema which is causing elastin breakdown and reduces alveolar wall integrity. This causes the alveoli to collapse in expiration causing gas trapping which increases residual volume. Inspiring ontop of the increased residual volume causes the hyperinflation seen in the x-ray.
The low TLC value observed may possibly be due to pulmonary fibrosis associated with ILD. The decreased intensity of breath sounds are commonly seen in patients with emphysema, this is because there is reduced ventilation due to alveolar destruction.
Relationship between lower than predicted PO 2 and CO 2 and patients shortness of breath symptoms
The arterial blood gas results showed a lower than predicted PO 2 and higher than predicted PCO 2 which indicated hypoxemia and hypercapnia respectively. The hypoxemia and hypercapnia could possibly be related to emphysema. The reduction of elastin in the alveolar walls in emphysema leads to airspace enlargement in the alveoli which reduces alveolar capillary exchange area (Stoller & Juvelekian. 2012). These structural changes lead to the decreased ability of the alveoli to exchange oxygen and extract CO 2 from the capillaries which causes elevated arterial CO 2 leading to hypercapnia and lowered arterial O 2 leading to hypoxemia (Stoller & Juvelekian. 2012). Furthermore, the gas trapping associated with emphysema causes CO 2 retention and can lead to hypercapnia. Airflow obstruction indicated by the patients severely low FEV1 also makes expiration very difficult which can also lead to hypercapnia and shortness of breath symptoms. The patient felt out of breath on minimal exertion. This is likely because the metabolic demand for O 2 and CO 2 extraction on exertion cannot be met effectively because there are less functional alveoli and less surface area for gas exchange. The progressive shortness of breath over the last 3 years is possibly due to the progressive narrowing of the patients airways. Studies have shown that in patients with COPD, terminal bronchiole narrowing precedes the emphysemic destruction of the alveoli (McDonough et al. 2011). This suggests that the patients alveolar ventilation may have become progressively worse over time due to the increasing severity of obstruction in his terminal bronchioles. This interpretation is consistent with the patients increasing intensity of shortness of breath in the last 3 years.
References
-Ferguson, G.T. 2006, "Why does the lung hyperinflate?", Proceedings of the American Thoracic Society, vol. 3, no. 2, pp. 176-179.
- White, A 2014, '3014BPS Advanced Physiology Week 10 Lecture: Introduction to Respiratory Function Testing', Retrieved from Griffith University, School of Natural Sciences, Learning@Griffith web site: https://bblearn.griffith.edu.au/bbcswebdav/pid- 1120011-dt-content-rid- 3173540_1/courses/3014BPS_3145_NA/Lecture%205%20respiratory%20full%20colour %20slides.pdf
- Pellegrino, R., Viegi, G., Brusasco, V., Crapo, R.O., Burgos, F., Casaburi, R., Coates, A., van der Grinten,C P M., Gustafsson, P., Hankinson, J., Jensen, R., Johnson, D.C., MacIntyre, N., McKay, R., Miller, M.R., Navajas, D., Pedersen, O.F., Wanger, J., Sahlgrenska akademin, Institutionen fr kvinnors och barns hlsa, Sahlgrenska Academy, University of Gothenburg, Institute for the Health of Women and Children & Gteborgs universitet 2005, "Interpretative strategies for lung function tests", The European respiratory journal, vol. 26, no. 5, pp. 948-968.
- Llewellin, P., Sawyer, G., Lewis, S., Cheng, S., Weatherall, M., Fitzharris, P. & Beasley, R. 2002, "The relationship between FEV1 and PEF in the assessment of the severity of airways obstruction", Respirology (Carlton, Vic.), vol. 7, no. 4, pp. 333-337.
-Stoller, JK., Juvelekian, G. 2012, Chronic Obstructive Pulmonary Disease, viewed 16 October 2014, <http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/pulmonary/ch ronic-obstructive-pulmonary-disease/#bib13>
-McDonough, J.E., Yuan, R., Suzuki, M., Seyednejad, N., Elliott, W.M., Sanchez, P.G., Wright, A.C., Gefter, W.B., Litzky, L., Coxson, H.O., Par, P.D., Sin, D.D., Pierce, R.A., Woods, J.C., McWilliams, A.M., Mayo, J.R., Lam, S.C., Cooper, J.D. & Hogg, J.C. 2011, "Small-Airway Obstruction and Emphysema in Chronic Obstructive Pulmonary Disease", The New England journal of medicine, vol. 365, no. 17, pp. 1567-1575.