Chronic Obstructive Pulmonary Disease - Case Study Example

INTEGRATED CLINICAL CASE (PARAMEDIC) by Student’s Name Code + course name Professor’s Name University Name City, State Date 1. Describe the underlying pathology of COPD and the common pathological characteristics of the condition. Discuss the impact these pathological changes have on normal function, including how alveolar ventilation might be different in Mr Wenham compared to a normal individual. Chronic Obstructive Pulmonary Disease (COPD) consists of pathological alterations within four diverse compartments of the lungs (pulmonary vasculature, peripheral airways, central airways and lung parenchyma), which turn to be changeably present within persons having the disease (Celli, MacNee & Committee Members 2014). Tobacco smoking turn to be COPD’s major risk factor, though other breathed in noxious gases and particles might contribute. That brings about an inflammatory reaction within lungs. The COPD’s pathogenesis comprise of inflammation, a disproportion of antiproteinases and proteinases within lungs together with oxidative stress. The common pathological characteristics of COPD include cilliary dysfunction and mucous hypersecretion, hyperinflation and airflow limitation, systemic effects, pulmonary hypertension and gas exchange anomalies (Siafakas, et al. 2010). As the ailment advances, vital capacity (VC) and forced expiratory volume (FEV1) lessens and residual volume (RV) augments. The decline rate within FEV1 turns to be greater than within normal individuals. Total airway imbalance and resistance within perfusion/ventilation ratio (V’/Q’) goes up. 2. Discuss why you would administer salbutamol and describe how it works at the cellular level. I would administer Salbutamol as it relieves bronchospasm within chronic bronchitis, bronchial asthma, emphysema together with other airway resistance ailments (Warrel 2013). After administering, it would widen (dilate) Mr Wenham’s airways. On the other hand, Salbutamol arouses bronchial β2- adronoceptors, and thus augments the adenylate cyclase activity; that turns to be its effect of pharmacological at the molecular echelon. The adenylate cyclase activity increase contributes to an augment within the intracellular AMP concentration cyclic, a pharmacological outcome at the cellular echelon. The augment within cyclic AMP in some manner changes the bronchial smooth muscle cells’ function and cause an inhibition of the discharge of rabble-rousing mediators from the bronchial mast cells, with upshots of the cell physiology (Warrel 2013). In turn, all this causes bronchodilatation, an upshot on physiology of tissue. Bronchodilatation enhances functioning of the lungs, an upshot upon organ structure. Lastly, the patient becomes capable of breathing more effortlessly, the clinical effect which is required. 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. An arterial blood gas would be taken for measuring the acidity (PH) as well as the carbon dioxide (C02) and oxygen (O2) levels within the blood (Cohn, Smetana & Weed 2015). That test would be utilised in checking how well the patient’s lungs are capable of moving oxygen in the blood together with removing carbon dioxide from blood. On the other hand, a normal PH indicates that the alkalosis or acidosis has been compensated by the body. A lower PH characterises respiratory acidosis whereas an increased PH characterises respiratory alkalosis. Additionally, an increased PaCO2 mirrors alveolar hypoventilation, while a lessened PaCO2 mirrors alveolar hyperventilation. On the other hand, a decreased PaO2 signifies hypoxaemia which might stem from perfusion and ventilation mismatch or hypoventilation. A low partial PaO2 oxygen pressure signifies insufficient oxygen uptake whereas normal range results normally portrays sufficient oxygen uptake. Decreased HCO3- and lower PH characterises metabolic acidosis, while increased HCO3- and elevated PH characterises metabolic acidosis. 4. Discuss the normal control of ventilation and the issues surrounding the use of supplemental oxygen therapy in patients with severe exacerbations of COPD. What problems can it cause and why? Though breathing is capable of being voluntarily altered, it turns to be primarily controlled by the autonic nervous system (Standard Pathophysiology 2011). A huge portion of the regulation turn to be related to sustaining regular blood gas and regular gas exchange levels. Receptors in the body continuously measure hydrogen ions (PH), carbon dioxide (CO2), and oxygen (O2) amounts and notify the brain to regulate the respiration depth and rate. Centres mandated for ventilatory control turn to be lung receptors, chemoreceptors and specific centres within the brainstem. In fact, chemoreceptors turn to be specific receptors which screen the oxygen (O2) and carbon dioxide (CO2) levels and hydrogen ion (PH) numbers within the blood of arteries. On the other hand, the lungs comprise of J-receptors, stretch receptors and irritant receptors. Irritant receptors turn to be sensitive to exasperating particles, aerosols and gases. Stretch receptors prevents over inflation through lessening the ventilation volume and rate when enlarged. J-receptors when activated stimulate shallow rapid respiration. One of the issues in supplemental oxygen therapy is the worsening of hypercapnia within vulnerable patients (Brill and Wedzicha 2014). In this case, high oxygen concentrations administration induces neurological changes, comprising transient augments within intracranial pressure and fatal coma. The other issue within hypercapnic patients administered with supplemental oxygen turn to be the rebound hypoxia phenomenon on withdrawal of the supplemental oxygen. This happens as carbon dioxide and oxygen dislocate one another from the restricted space in the alveoli in accordance to their relative inequitable pressures. 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. I believe it is a good idea to remove Mr Wenham’s oxygen and have him just breathing air. This is because according to his blood gas analysis, PaO2 does not reveal that Wenham is not receiving sufficient oxygen. Additionally, Wenham’s PH is not very low and there PaO2 is not that high to indicate that he is not taking in sufficient oxygen and removing little carbon dioxide. Through continuing administering oxygen to him might induce neurological changes, thus worsening hypercapnia. Additionally, Wenham might experience rebound hypoxia phenomenon on withdrawal of the supplemental oxygen. In fact, after arterial blood gas examination, it would be possible to diagnose the best treatment for Wenham. 6. What is BiPAP? How might BiPAP help to improve Mr Wenham’s clinical condition? BiPAP means bilevel positive airway pressure (Rice 2014). A BiPAP machine that turns to be more precisely referred as a BPAP machine turns to be an apparatus for breathing which assists its user to obtain additional air in her or his lungs. Importantly, BiPAP turns to be a breathing support method which is frequently used in treating central sleep apnea. In addition, it is also utilised in extra severe obstructive sleep apnea, particularly the moment mixed apnea turns to be present, proposing a central sleep apnea constituent. It might be used in treating people who are incapable of tolerating continuous positive airway pressure (CPAP), particularly persons who protest that is hard for them breathing out against pressure. It might assist in improving compliance. Additionally, it turns to be a non-invasive method of support which can be utilised within hospitalised persons who turns to be within respiratory anguish, but who never wishes being placed upon a ventilator. Importantly, the major unique BiPAP’s feature turns to be that the air that is pressurized turns to be carried at two interchanging levels. The inspiratory upbeat airway pressure turns to be higher and props up a breath when it is inhaled. On the other hand, the expiratory positive upbeat airway pressure turns to be a lower pressure which permits someone to exhale. Those pressures turn to be preset and interchanging akin to a person’s pattern of breathing. BiPAP might assist in improving Wenham’s condition through sustaining a particular air pressure quantity in a mask, like when he would be sleeping. The air pressure would keep his airway open, permitting him to breathe effortlessly when sleeping. The BiPAP machine would permit air which would be carried via the disguise to be put at a single pressure for exhaling and the other for inhaling. 7. What is spirometry? Spirometry turns to be a test that is utilised in assessing how well a person’s lungs function through measuring the amount of air someone inhale, the amount of air someone exhale and how fast someone exhale (Quinn 2006). Spirometry turns to be utilised in diagnosing COPD, asthma, together with other circumstances which possesses an effect on breathing. It is carried out utilising a machine referred as a spirometer. Spirometry turns to be a noninvasive, painless and quick method of seeing whether the lungs have any damages. Later, the spirometer computes the air amount that the lungs are capable of holding and the exhalation and inhalation rates. 8. Discuss the significance of the results by examining the differences between Mr Wenham’s spirometry and that of a normal individual. In fact, the ratio of FEV1/FVC turns to be normally in the middle of 0.7 - 0.8 (Johns & Pierce 2013). Therefore, values that are beneath 0.7 turns to be an indicator of airway obstruction, in exception of aged grown-ups where values between 0.65 and 0.7 might be regarded as normal. In persons older than 70 years, the FEV1/FVC1 ratio might require being decreased to 0.65 being the normal’s lower limit. On the contrary, within persons below 45 years old, utilising the 0.7 ratio might end up in under-diagnosis of the airway impediment. To keep away from such problems, the normal’s lower limit of both ages turn to be recommended by several professionals. Additionally, normal individuals’ spirometry predictions indicate FEV1 and FVC that are beyond 80% and FVC/FEV1 ratio that is above 0.7. The normal individual’s spirometry is different from Mr Wenham’s spirometry in that; Mr Wenham’s spirometry shows that his FEV1/FEV ratio is 0.5, that is; the FEV1 and FVC are 50% which is less than the required 80%. 9. How does the pathology of COPD explain these differences? The pathology of COPD explains that forced vital capacity (FVC) and forced expiratory volume (FEV1) lessens and residual volume (RV) augments. The decline rate within FEV1 turns to be greater than within normal individuals. Thus, total airway imbalance and resistance within perfusion/ventilation ratio (V’/Q’) goes up. The COPD’s stage displayed by Mr Wenham is mild or obstructive since his FEV1/FVC turns to be less than 70% (Wyka, Mathews & Clark 2011). This stage’s symptoms include breath shortness, cough and production of sputum. References Brill, SE Wedzicha, JA 2014, Oxygen Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease, International Journal of Chronic Pulmonary Disease, vol 9, pp. 1241-1252. Celli, BR, MacNee, W & Committee Members 2014, Standards for the Diagnosis and Treatment of Patients with OCPD: A Summary of the ATS/ERS Position Paper, European Respiratory Journal, vol. 23, pp. 932-946. Chin, SL, Smetana, GW, & Weed, HG 2015, Perioperative Medicine: Just the Facts, New York, Maidenhead, McGraw-Hill. Johns, DP & Pierce, R 2013, McGraw-Hill’s Pocket Guide to Spirometry, Washington, McGraw-Hill. Quinn, C 2006, 100 Questions & Answers about Chronic Obstructive Pulmonary Disease (COPD), Sudbury, Mass., Jones and Bartlett Publishers. Rice, D 2014, What is Sleep Apnea, New York, Clinton Gilkie. Siafakas, NM, et al. 2010, Optimal Assessment and Management of Chronic Obstructive Pulmonary Disease (COPD), European Respiratory Journal, 8, 1398-1420. Standard Pathophysiology 2011. Available from < http://catalogue.pearsoned.co.uk/assets/hip/gb/hip_gb_pearsonhighered/samplechapter/0135113512.pdf >. [4 June 2015]. Warrell, DA 2013, Oxford Textbook of Medicine Vol. 2 Sections 11-17, Oxford [u.a.], Oxford Univ. Press. Wyka, KA, Mathews, P & Clark W 2011, Foundations of Respiratory Care, Albany, International Thompson. Read More