Chronic Obstructive Pulmonary Disease - Essay Example

Nursing Assignment Explains the role of selected physiological processes in maintaining health – chosen physiological process- gas exchange. Exchange of gases is one of the four components of respiration. The lungs have two main functions of ventilation and providing a surface for diffusion of oxygen into the blood and oxygen out of the blood in what is known as exchange of gases. The alveoli are the functional units of the lungs for the exchange of gases. According to Fick’s law diffusion across the alveolar-capillary membrane is directly proportional to the partial pressure difference of oxygen across the membrane, the area of the membrane, the diffusivity of the gas into the membrane, and inversely proportionate to the thickness of the membrane. Diffusivity of a gas is a physical constant that is derived from calculations based on the solubility of the gas in the membrane and the molecular weight of the gas. The area available for diffusion and the thickness of the membrane is anatomy dependent. Thus the exchange of oxygen from the alveoli to the capillaries is mostly based on the pressure gradient across the alveolar-capillary membrane. The same law applies to the transport of carbon dioxide from the capillaries to the, but carbon dioxide is more soluble than oxygen in the membrane and so diffusion limitation is seldom an issue with carbon dioxide, the elimination of which is dependent heavily on ventilation. (Walley & Russell, 1999). Besides the difference between the partial pressures of the gases in alveoli and the pulmonary capillary bed another important determinant of gas exchange is the relationship between the pulmonary capillary perfusion (Q) and alveolar ventilation (V). A well ventilated alveolus needs to have an equally well perfused capillary, with the ratio V/Q ideally 1. A three compartment model of the lungs helps to understand the perfusion and ventilation relationship. Physiological dead spaces, where exchange of gases does not take place are areas of wasted ventilation, where V/Q is greater than 1. Perfectly matched areas of ventilation and perfusion have V/Q equal to 1. Areas that contribute to venous admixture, which is the mixing of non-oxygenated with oxygenated blood after passing through the lungs, where perfusion has been wasted, in the example of the right to left shunt, V/Q is less than 1. Even in normal lung function, there is a degree of variation in the perfusion and ventilation in different areas of the lung due to gravity, which requires the extra effort in forcing blood supply through the blood vessels above the heart in an erect position. Thus the lower portion of the lobes of the lung is better perfused than the upper lobes of the lung in an erect position. The body compensates for this by preferentially ventilating the better perfused lower portion of the lobes of the lung to maintain the proper V/Q ratio Diseases like chronic obstructive pulmonary disease (COPD) can lead to hypoxemia, which is the right to left shunt in which poorly ventilated areas of the lungs continue to be perfused, leading to a decrease in the ratio of ventilation to perfusion, wherein blood passes through the lung without being oxygenated. Right to left shunt is increased when the alveoli are completely collapsed, or totally consolidated or filled with oedema (Adam & Osborne, 1997). In the case of Mr. Errol two factors in his history stand out as factors affecting the proper functioning of the lung leading to chronic bronchitis and emphysema, which are components of COPD. Smoking one packet a day for one year is a potential risk for chronic bronchitis and emphysema. Errol was smoking nearly two packs a day over a period of fifty years, and even though cessation of smoking occurred eight years back, the negative impact of the history of smoking would still persist, which would include consolidation and filling of the alveoli with oedema. The second factor is the work environment. Mr. Errol worked as a ship fitter and was exposed to asbestos dust, which he would have inhaled. The asbestos dust would have deposited in the airway passages and the alveoli, leading to collapse and consolidation of the alveoli. Finally the immediate infection in the lungs would have exacerbated this condition by adding to the filling of the alveoli and the lungs with oedema. Clinical findings are also suggestive of this. Thus all ingredients for hypoxemia or a right to left shunt are present, leading blood passing through the lungs without proper exchange of gases and the resultant impact on the body (Cole & Mackay, 1990) The exchange of gases within alveoli of the lungs is the way that oxygen from the atmospheres is made available for energy purposes in the human body and the waste gas of carbon dioxide is expelled out of the body. For maintaining good health there should be optimal exchange of gases in the lungs. Factors that have a negative impact on the exchange of gases like poor life habits that include smoking and toxic and dusty work environments need to be avoided for maintaining good health. 2. Discuss how selected disease processes or conditions may disrupt physiological mechanisms – selected disease process – COPD. According to Macnee, 2006, “Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs”. These changes are not easy to reverse. The abnormal inflammatory response in the lungs is a reflection of the innate and adaptive immune responses human body to exposure to noxious particles like asbestos particles and gases like cigarette smoke. Exposure to such noxious particle and cigarette smoke causes some inflammation in the lungs, but in the case of COPD the response to inhaling these toxic agents is enhanced and abnormal and results in mucous hyper secretion (chronic bronchitis), tissue destruction emphysema and disruption of normal repair and defence mechanisms causing small airway inflammation and fibrosis (bronchiolitis) (Macnee, 2006). COPD thus is a disease that has one physiological factor and that is the limitation in the expiratory airflow, which normally is slow in progression. There are several anatomical contributions to the airflow limitation, which include loss of lung elastic recoil, fibrosis and narrowing of the airway passages. Airflow limitation is also caused by oedema of the airways, accumulation of secretions and smooth muscle contraction. These contributions to COPD may be variably present in individuals with COPD. The current understanding is that smoking and exposure to toxic agents like asbestos cause an inflammatory response in the lower respiratory tract and can also damage the lung. However, it is generally accepted that mediators released by the inflammatory cells account for most of the alterations seen in the structure of the lung seen in COPD. Cessation of smoking early enough could led to reversal if the inflammatory changes, but cessation after extensive and extended smoking may not prevent the persistence and progress of COPD (Spurzem & Rennard, 2005) The consequences of these anatomical contributions to COPD disrupt the physiological mechanisms involved in respiration. Airway resistance is always abnormal in COPD. There is also an increase in residual volume, functional residual capacity (FRC) and total lung capacity (TLC). The maximum expiratory flow-volume curves show a characteristic convexity in the direction of the volume axis, initially with preservation of peak expiratory flow. The uneven distribution of ventilation in a COPD compromised lung impacts on the ventilated lung volume and through that the carbon monoxide transport factor (TLco). TLco is invariably reduced in COPD. There are characteristic changes in the static/pressure volume (P/V) of the lungs in COPD, which include an increase in the in static compliance and a reduction in static trans-pulmonary pressure at standard lung volume. In COPD the frequent site of fixed airway narrowing is in the peripheral airways of less than 3 mm diameter. There is also the factor of loss of lung elastic recoil pressure. Dynamic expiratory compression is increased as a result of this loss lung recoil and also due to the atrophic changes in the airways and the loss of support from the surrounding alveolar walls. This results in flow limitation at lower driving pressures and flows. The end result of all the changes that occur from COPD is that there is the ventilation-perfusion mismatch, which leads to the impairment in the pulmonary gas exchange, which is the physiological function of the lung. Other factors like alveolar hypoventilation, impaired alveolar-capillary diffusion to oxygen, and increased shunt also contribute to the impairment of pulmonary gas exchange. (Macnee, 2003). In the case of Mr, Errol the symptoms displayed shows that he is suffering from the chronic bronchitis and emphysema, two components of COPD, which has led to disruptions in the physiological mechanisms involved in the functioning of the lung. Two factors have contributed to this status. The first is the smoking of 30-40 cigarettes a day for a period of 50 years. He may have stopped smoking for eight years, but it has come too late. The extended and extensive smoking prior to cessation means COPD has established itself and despite cessation of smoking the disease has persisted and continued to progress. This means the physiological changes like ventilation perfusion mismatch, alveolar hypoventilation, impaired alveolar-capillary diffusion to oxygen and increased have become irreversible. The second factor of working in an environment of toxic asbestos dust has only augmented the physiological changes that have occurred due heavy smoking over a long period of time. These two factors in combination have contributed to the establishment of COPD in Mr. Errol and have ensured that the disease persists and progresses. The current acute stage of the disease in Mr. Errol has come about because of an infection in the lung, which has further exacerbated the situation of impaired respiratory function, due to changes in the physiological mechanisms. 3. Analyse the pathophysiological changes that may lead to the development of selected signs and symptoms – selected sign and symptom – dark urine. Dark urine is a sign of impaired liver functioning and biliary obstruction is one factor that impairs functioning of the liver (Mann, Lam, Hjelm, So, Yeung, Metreweli & Lau, 2002). According to Bonheur, Ells, and Kamenetz 2006, “Biliary obstruction refers to the blockage of any duct that carries bile from the liver to the gallbladder or from the gallbladder to the small intestine. This can occur at various levels within the biliary system. The major signs and symptoms of biliary obstruction result directly from the failure of bile to reach its proper destination”. Extrahepatic obstruction to the normal flow of bile happens inside the ducts or due compression caused from external reasons. Whatever be the cause the result of the physical obstruction is a predominantly conjugated hyperbilirubinemia. The increased presence of bilirubin in the bloodstream results in a subsequent deposition in the skin leading to the yellowing of the skin typical of jaundice. However, for the skin to turn yellow the serum bilirubin values have to reach 3mg/dl. Darkening of urine is an occurrence even earlier due to the passage of conjugated bilirubin in the urine. Thus the presence of excess urine bilirubin is presenting through darkened urine can be found even before serum bilirubin reaches levels high enough for clinical presentation in biliary obstruction. One of the consequences of biliary obstruction is that bile fails to reach the gastro-intestinal tract. The absence of bile in the gastro-intestinal tract can be made out through from the pale coloured stools passed by the patient. Thus darkening of urine along with the passage of pale coloured urine are clear indications of biliary obstruction. An understanding of the normal structure and function of the biliary tree assists in understanding the pathophysiology involved in biliary obstruction. Bile is an essential and exocrine secretion of the liver, which is continuously produced by the hepatocytes in the liver. Bile consists of cholesterol and waste products including bilirubin and bile salts that assist in the digestion of fats. Nearly half of the bile produced in the moves directly from the liver into the duodenum through a system of ducts that ultimately drains through the common bile duct (CBD). The remainder of the bile is stored in the gall bladder and in response to a meal intake this stored bile is released through the cystic duct, which connects with the ducts from the liver to form the CBD, and from the CBD into the duodenum. Thus any blockage of the CBD means that no bile is available in the duodenum for the digestive system (evinced by pale stools) and disruption in the excretion of waste materials like bilirubin and bile salts, which leads to increasing presence of bilirubin in blood plasma or hyperbilirubinemia (evinced through darkening of urine). (Bonheur, Ells, and Kamenetz 2006). Thus pathophysiological changes occur in the acute critical or complete blockage of the CBD in biliary obstruction. Hepatic secretion of bile continues for some more time. This is due to the capacity of the epithelium to absorb an equal volume of water and also take in all the entering hepatic bile. Once this capacity of the epithelium of the gall bladder has been surpassed and no more hepatic bile can be taken in by the gall bladder, the hepatic secretion of bile decreases, while the pressure in the CBD increases. The pressure in the CBD and the hepatic ducts build up till it equalizes or exceeds the secretory pressure of the hepatocytes. This leads to the cessation of hepatic bile secretion (Krishnamurthy & Krishnamurthy, 2003). This cessation in the secretion of bile results in the increased blood plasma levels of the waste products of bilirubin and bile salts with their normal route of excretion through the gastro-intestinal tract blocked. More bilirubin is seen in the urine, as the kidneys attempt to remove the increasing levels of bilirubin in blood plasma. This darkens the urine as seen in the case of Mrs. Myrtle with a blocked CBD (Bonheur, Ells, and Kamenetz 2006). 4. Discuss the physiological rationale for the use of selected aspects of healthcare – chosen aspect – glyceryl trinitrate (GTN) The heart is in essence a powerful pump, responsible for pumping of blood to the various parts of the body, including its own muscles. The powerful pumping action is the result of the proper functioning of the cardiac muscles. There are two factors to the proper functioning of the cardiac muscles for the heart to fulfil its role of reaching oxygenated blood to every part of the body. The first is the requirement for proper blood supply to the heart muscles itself for the energy requirements of the pumping action of the heart muscles. This role is fulfilled by the coronary arteries which supply blood to the cells of the cardiac muscles. The second is the coordination of the pumping action of all the muscles to ensure proper output volume from the heart to the arteries. This coordination is through an electrical conduction system originating from the SA node to the AV node and then on to every cell in muscles of the heart (Opie, 2004). The coronary arteries thus fulfil the critical role in making oxygen available to the cells of the heart muscles. Any block or narrowing of the lumen in the coronary arteries compromises this function of the coronary arteries and deprives the cells of the heart muscles the much needed oxygen through the blood supply. The resultant imbalance between the myocardial blood supply and the metabolic demand during exercise is characterized by pain below the sternum called angina pectoris. Angina pectoris is a clear sign that the heart is in distress, because of inadequate myocardial blood supply (Trimetazadine: A Well Tolerated and Novel Alternative in Stable Angina Pectoralis). The lack of proper blood supply can also lead to death of cells in the cardiac muscles leading to infarcts. Such infarcts can affect the electrical conduction system that synchronizes the rhythm of the heart leading to a disruption in the rhythm, which adds to the already distressed condition of the heart (Opie, 2004). The shortness of breath and pain in the chest during exercise demonstrated by Mr. George indicates the possibility of ischemic heart disease, as a result of the narrowing of the lumen of the coronary arteries or the loss of elasticity of the coronary arteries. Smoking is one of the many significant factors involved in ischemic heart diseases and the absence of a history of smoking does not rule out ischemic heart disease in the case of Mr. George. The ECG and chest X-ray confirms the Left Ventricular Heart Failure (LVF), brought on by atrial flutter (AF), which has been caused by the disruption of the electrical conducting system. Mr. George has been prescribed a set of medications for LVF and AF, and the use of glyceryl trinitrate (GTN) spray to relieve the chest pain or angina pectoris. GTN is the preferred option in addressing angina pectoris that develops suddenly and from physical activity. There are several significant objectives in the treatment of a compromised heart as a result of reduced coronary blood supply. These goals include the improvement in the force of cardiac contraction; easing the outflow of blood from the ventricles through the reduction in the resistance to the ejection of blood from the ventricles; reducing the end-diastolic ventricular filling volume and the restoration of atrial contribution to the filling of the ventricles. GTN is a vasodilator, which means that it enables the widening of the lumen of the coronary arteries so that more blood can flow through the coronary arteries. When Mr. George uses the GTN spray there is increased flow of blood through the coronary arteries, due to the dilation of the coronary arteries removing the removes the imbalance between the myocardial blood supply and the metabolic demand during exercise which is the cause of the shortness of breath and the pain in the chest. The removal of the imbalance will result in disappearance of the shortness of breath and the pain in chest making Mr. George feel at ease. (Ioannou & Wyncoll, 2004). The GTN spray when directly sprayed under the tongue acts in a quick manner to reduce the work that the heart is doing by making available adequate blood supply as per the demands of the cells in the heart muscle. This is the rationale for advising Mr. George to use the GTN spray, when pain in the chest is felt during exercise (A Patient’s Guide to GTN Spray). Literary References A Patient’s Guide to GTN Spray. (2006). Retrieved February 25, 2008, from, NHS Highland Web Site: http://www2.nhshighland.scot.nhs.uk/Health%20Services/CHD/patient/general/literature/use%20of%20GTN%20spray.pdf Adam, S. K. & Osborne, S. (1997). CRITICAL CARE NURSING: Science & Practice. Oxford: Oxford Medical Publications. Cole, R. B. & Mackay, A. D. (1990). Essentials of Respiratory Disease. Third Edition. Edinburgh: Churchill Livingstone. Ioannou, N. & Wyncoll, L. A. D. (2004). Management of Heart Failure and the Role of the New Inotrope Levosimendan. British Journal of Cardiology, 11(2), AIC 24-AIC 30. Krishnamurthy, G. T. & Krishnamurthy, S. (2003). Pathophysiology of Acute Obstruction of the Common Bile Duct: Role of Quantitative Cholescintigraphy and Ultrasound in the Early Detection and Patient Management. Indian Journal of Nuclear Medicine, 18(3), 66-72. Macnee, W. (2003). “Chronic obstructive pulmonary disease”. In OXFORD TEXTBOOK OF MEDICINE. Fourth Edition. Eds. David A. Warrell, Timothy M. Cox & Joan D. Firth. Oxford, 1377-1396. Macnee, W. (2006). ABC of chronic obstructive pulmonary disease: Pathology, pathogenesis, and pathophysiology. BMJ, 332, 1202-1204. Mann, D. V., Lam, W. W. M., Hjelm, N. M., So, N. M., Yeung, D. K., Metreweli, C. & Lau, W. Y. (2002). Biliary drainage for obstructive jaundice enhances hepatic energy status in humans: a 31-phosphorus magnetic resonance spectroscopy study. Gut, 50, 118-122. Opie, H. Lionel. (2004). Heart Physiology: from Cell to Circulation. Fourth Edition. Philadelphia: Lippincott Williams &Wilkins. Spurzem, J. R. & Rennard, S. I. (2005). Pathogenesis of COPD. Seminars in Respiratory and Critical care Medicine, 26(2), 142-153. Trimetazadine: A Well Tolerated and Novel Alternative in Stable Angina Pectoralis. (2000). Drugs & Therapy Perspectives 16(3), 1-5. Retrieved February 25, 2008, from, Medscape Today Web Site: http://www.medscape.com/viewarticle/406427_1 Walley, K. R. & Russell, J. A. (1999). “Pulmonary Pathophysiology in ARDS”. In Acute Respiratory Distress Syndrome”. Eds. James A. Russell & Keith, R. Walley. Cambridge: Cambridge University Press, pp. 80-106. Read More