Integrated Clinical Case, Case Study Example

Describe the underlying pathology of COPD.

In chronic obstructive pulmonary disease pateints demonstrate volume-dependent airway obstruction(Decramer, Janssens & Miravitlles, 2012). A Spirometry usually shows reduction in the FEV1/FVC ratio as well as a high comparative FEV decline decreasing at a rate of 25% to 75% vital capacity. As airflow obstruction becomes worse the amount of gas usually exhaled is increasingly difficult to maintain influencing a vital capacity decline (Barnes, Buist, Calverley, Fukuchi,2007).

What impacts do these pathological changes have on normal physiology? 

Significantly, abnormalities in gas changes occur. These altered physiologies are manifested in two patterns known as emphysema (pink puffer) and chronic bronchitis (blue bloater). The main symptoms occurring in pink puffer phase is dyspnea while a productive cough is the dominant symptom in blue bloater phase (Currie, 2010).Signs and symptoms in both phases include thin built; hyperinflated quite chest along with stocky build, wheezy right side heart failure in the blue bloater type respectively (Currie, 2010).

In particular, describe alveolar ventilation in a normal individual and discuss how this might be different in Mr. Wenham

Alveolar ventilation relates to the quantity of air reaching the respiratory surface along with the amount of gas available for exchange per blood unit time. Precisely,capillaries laden with deoxygenated blood move from the pulmonary artery across a respiratory surface (alveoli) Alveoli have very thin surfaces. As such, gases must diffuse across a 2 cell thick surface to oxygenate tissues.When Oxygen is inhaled it can be diffused directly into the capillaries from the alveoli. Carbon dioxide emerging as a byproduct from blood synthesis is diffused in the opposite direction into the respiratory surface (alveoli)(Daniels & Orgeig, 2010). Consequently, this facilitates the exhalation of carbon dioxide from the body. An accurate concentration gradient is continuously maintainedthrough capillary blood flow when an individual breaths in and out (Daniels & Orgeig, 2010).

Persons with COPD such as Mr.Wenham experience Ventilation-perfusion imbalance whereby there is uneven distribution of alveolar ventilation as well as pulmonary blood flow. These two physiological features are distinctly described as ventilation-perfusion (V?A/Q?) mismatch. Subsequently, arterial hypoxemia occurs(Rodríguez-Roisin, Drakulovic & Rodríguez, 2009). It can be accompanied by hypercapnia regardless of whether the person is experiencing an exacerbation or is stabled (Rodríguez-Roisin, Drakulovic & Rodríguez, 2009).

Discuss why you would administer salbutamol and describehow it works at the cellular level

Forced expiratory flow rates improved after Nebulised salbutamol (INN) was administered to pateints suffering with chronic obstructive pulmonary disease (COPD)(Aliverti, Rodger & Dellaca, 2010). Studies confirmed this outcome. Pateints with less hyperinflation it reduced the abdominal compartment volume ultimately limiting the exercise capacity induced by airflow obstruction characteristic of this disease. Importantly, this drug is a ?2-adrenergic receptor agonist recommended for best results in treating COPD(Aliverti et.al, 2010). Salbutamol is usually administered orally through inhalation. When used as an inhaled bronchodilator it reaches the lung as a fine mist applying a metered dose inhaler (Aliverti et.al, 2010).

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

Arterial blood gas (ABG) is a test used to measure aspects of blood oxygen/carbon dioxide   capacity includingcarbon dioxide tension (PaCO2);arterial oxygen tension (PaO2); acidity (pH) as well as arterial oxyhemoglobin saturation (SaO2) levels. These value determinations are crucial when managing pateints with COPD because significant alterations occur when air flow is minimized. Primarily, results reveal the extent of breathing difficulty experienced by the patient during that particular episode (Baillie, 2008).

Precisely, low oxygen levels ultimately result in increased carbon dioxide circulating in the blood. Inadequate gas exchange occurring from damaged respiratory surface in COPD is responsible for this altered physiology.  Airway inflammation is more aggressive during exacerbations, with subsequent hyperinflation; limited expiratory airflow influencing gas transfer difficulties demonstrated as low arterial oxygen and increased carbon dioxide blood circulation(Baillie, 2008).

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

Studies conducted by Stroller, Panos and Krashman (2010) regarding oxygen therapy in COPD confirmed that long term use of supplemental oxygen compared to short term improves survival rates of pateints with COPDas well as in serious resting hypoxemia(Stroller, Panos & Krashman, 2010). However, further research revealed that the purpose of oxygen therapy has proven to be very symptomatic. When long term use is compared to short term and moderate there was insufficient evidence supportive of any significant overall benefits in the long term. Short term seemed more effective is relieving exacerbations and increasing survival rates. Besides, other benefits observed included improvement in exercise performance and pulmonary hemodynamics by stabilizing pulmonary pressure (Stroller et.al,2010).

More importantly, these researchers Stroller, Panos and Krashman (2010)discovered that there is inadequacy regarding uniform criteria for defining exertional desaturation and standardized exercise protocols. As such, exertional desaturation seemed to offer a poor prognosis in pateints receiving supplemental oxygen therapy in the long term when administered during exacerbations. Alternatively, pateints normoxemic patients at rest with low desaturated exertion rates tend to have a better survival in the long term. Significantly, supplemental oxygen therapy whether long or short term reduces deoxyhaemoglobin thereby improving cerebral function during exacerbations (Casanova, Cote & Marin, 2008).

However, the real issues surrounding supplemental oxygen therapy include understanding why it is needed; how much to use at a time; the number of hours per day to take the treatment and the expected benefits. These are important issues because Brain Kent; Patrick Micheal and Walter McNicholus (2011) contend that while supplemental oxygen has benefits it is it without serious risks. For example, if administered in supraphysiological doses oxygen could create decrease in the ventricular drive; produce ventilation/percussion mismatch and subsequently hypercapnia.Still research has not been profound in explaining the real side effects of extensive oxygen administration as it pertains the overall quality of life for pateints and the total health care costs (Kent, Micheal & McNicholus, 2011).

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

While it may be true based on the symptoms Mr. Wenham is demonstrating upon arrival to the emergency that decrease in the ventricular drive ventilation/percussion mismatch has occurred and subsequently hypercapnia also the amount of oxygen could be reduced. Alveoli gas evaluations must be conducted and the oxygen levels regulated to meet demands discovered from these tests. Therefore, removing the oxygen entirely could create dangerous desaturation, which can cause heart failure (Selinger, Kennedy, Buescher& Parham, 2007).

In normal physiology when CO2 levelsare elevated respiratory drive is created. Patients inadvanced stages of COPD especially, accompanied by exacerbations do not have the capacity to develop this physiologic prompt. Assuch, they rely on hypoxia for respiratory stimulation. Medical scientists have recommended supportive of this theory that when too much oxygen is administered many pateints tend to develop hypercapnia. In busy emergency settings this condition can take a long time to be detected. However, in cases of acute distress recommendations are to offer appropriate oxygen for maintaining the pulse oximeter at 90% or higher. When changes are observed in patient’s clinical presentation regarded as improvement oxygen concentration ought to be reduced (Agusti, Carrera, Barbe, Munoz & Togores, 2010).

What is BiPAP?  How might BiPAP help to improve Mr. Wenham’s clinical condition?

BiPAP is an abbreviation meaning bi level positive airway pressure (PAP). It is a mechanism administered in pateints who are experiencing cardiac failure or exacerbations in chronic obstructive pulmonary disease (COPD) in type 1 and 2 respiratory failure. A BiPAP machine delivers air via a mask which is regulated to set inhalation and exhalation pressure at two distinct levels. It facilitates breathing by the user’s adaptation to the apparatus. Persons with neuromuscular diseases can sue the devise for breathing in and out without personal muscle effort. Ultimately more air travels in and out of the lungs (Williams, Abramo, Shah & Miller, 2011).

The nature of this apparatus and its purpose could improve Mr.Wenham’s clinical condition. He is experiencing severe breathing difficulties. Obviously, he is manifesting neuromuscular symptoms, which require assistance breathing in and out.BiPAP would help ventilate the lungs and he would not experience the exertion of breathing in and out on his own (Williams et.al, 2011)

What is spirometry?

Spirometry means measuring breath and is one of the most modern test used to estimate lung function as it relates to volume and airflow speed.Importantly, it is generates pneumotachographs, which facilitate assessing air flow and volume in COPD, asthma, cystic fibrosis and pulmonary fibrosis. The diagram below, Figure 11, shows a spirometry application.

Discuss the significance of the results by examining the differences between Mr. Wenham’s spirometry and thatof a normal individual

The above is a diagram showing the normal lung function values. Mr. Wenham’s spirometry results are as follows FEV1 (0.75 liters);FVC (1.5 liters) andFEV1/FVC (50%). These are far below the normal levels meaning that volume as well as flow is diminished.FEV1 represents volume of air that can be forcibly blown out in one second, when a full inspiration is taken. Normal people accomplish this at a rate of 80% – 120%.FEV1/FVC is the calculated ratio between volumes of air that can be forced after inspiration as against the forced expiratory volume in a one second. Normal values are 75%-80%. FVC represents forced vital capacity meaning volume of air which can be forcibly blown out after inspiration measured in litres and is a basic test. Normal values are 4.5 -5.5 litres (Pierce, 2005).

How does the pathology of COPD explain these differences?

When air way is narrowedvolume reduction is produced on inspiration and expiration, respectively. This is directly related to changes in alveoli structure. Anyone with respiratory symptoms and a spirometry of a FEV1/FVC ratio of less than 70% a COPD diagnosis is made. These differences are directly related to the destruction of the respiratory surface(Pierce, 2005).

References

Agusti, A.Carrera, M.  Barbe, F. Munoz, A., & Togores, B. (2010). Oxygen therapy during exacerbations of chronic obstructive pulmonary disease. European Respiratory Journal, 14(4); 934-939

Aliverti, A. Rodger, K., &Dellaca` R. (2010).Effect of salbutamol on lung function and chest wall volumes at rest and during exercise in COPD. Retrieved on May 25^th from http://thorax.bmj.com/content/60/11/916.full.pdf

Baillie, J. (2008). Simple, easily memorized “rules of thumb” for the rapid assessment of physiological compensation for acid-base disorders. Thorax, 63 (3); 289–90

Barnes, P. Buist, S. Calverley, P. Fukuchi, Y. Jenkins, C. Rodriguez-Roisin, R. van Weel, C., & Zielinski, J. (2007). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am. J. Respir. Crit. Care Med. 176 (6); 532–55.

Casanova, C.  Cote, C., & Marin, J. (2008) Distance and oxygen desaturation during the 6-min walk test as predictors of long-term mortality in patients with COPD . Chest, 134 ( 4 ): 746 – 752 .

Currie, P. (2010). ABC of COPD (2nd ed.). Chichester, West Sussex, UK: Wiley-Blackwell, BMJ Books

Decramer, M.Janssens, W. Miravitlles, M. (2012). Chronic obstructive pulmonary disease Lancet 379 (9823): 1341–51.

Daniels, B., & Orgeig, S. (2010). Pulmonary Surfactant: The Key to the Evolution of Air Breathing. News in Physiological Sciences 18 (4): 151–157

Kent, B. Micheal, P., &McNicholus. (2011). Hypoxemia in pateints with COPD: Cause, effects and disease progression. Int J Chron Pulmon Dis,6; 199 -208

Pierce, R. (2010). Spirometry: An essential clinical measurement. Australian family physician 34 (7): 535–539

Rodríguez-Roisin, R. Drakulovic, M., &Rodríguez, A. (2009).Ventilation-perfusion imbalance and chronic obstructive pulmonary disease staging severity.Journal of Applied Physiology Published 106; 1902-190

Selinger, S. Kennedy, T. Buescher, P., & Parham, P.  (2007) Effects of removing oxygen from patients with chronic obstructive pulmonary disease. Am Rev Respir Dis; 136:85–91.

Stroller, J.  Panos R., & Krashman, S. (2010).  Oxygen therapy for patientsCOPD: Current Evidence and the long term oxygen treatment trial. Chest, 138(1); 179 – 187.

Williams, A. Abramo, T. Shah, M., & Miller, R. (2011). Safety and clinical findings of BiPAP utilization in children 20 kg or less for asthma exacerbations.Intensive Care Med 37 (8): 1338–43