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Analysis of Asmatha Case - Assignment Example

Summary
"Analysis of Asmatha Case" paper focuses on the case of BillBill, a 40-year-old, who has had asthma since childhood. He has experienced many hospitalizations and required long-term oral steroids. He presents to the emergency department (ED) with acute exacerbation of his asthma…
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Question 1 Respiration can be described as the conveyance of oxygen from the exterior air to the cells inside tissues. It also involves the movement of carbon dioxide from within the tissues to the peripherals (Moskwa P, 2007, 175). Respiration is facilitated by the action of breathing in and out brought about by the variations of pressure inside the thorax in contrast with the exterior with the lungs being the critical respiration organs (C.Michael Hogan. 2011, 18). Asthma, as in the case of Bill, causes a contraction of the breathing airways of the lungs, which are referred to as bronchioles, which get in the way with the normal movement of air in and out of the lungs. The contractions that arise in asthma are caused by three main factors; these are inflammation, hyperreactivity and bronchospasm. In asthma patients like Bill, there are several effects on the mechanics of breathing. The mechanics of breathing are attained by inspiration and expiration that is accomplished by the contraction and relaxation of striated muscles. The initial and most significant factor that causes contraction of the bronchial tubes is inflammation (C.Michael Hogan. 2011, 24). When inflammation occurs, the bronchial tubes become red, swollen and irritated. These in effect enlarge the thickness of the bronchial walls and thus result in a smaller passageway for air to stream through. The inflamed tissues excrete a surplus quantity of "sticky" mucus into the tubes. The mucus that is produced can bundle together and possibly clog the smaller airways. (Nilsson, Goran E. 2010, 56) During an asthma attack, the muscles of the bronchial tubes tighten further reducing the size of the airways. The constriction of these airways is referred to as bronchospasm (Kevin T. Patton, 2009, 57). Chemical mediators and the nerves in the bronchial tubes lead to tightening of the muscles. This can easily be brought on by the inhalation of cold or dry air. (Campbell, Neil A. 2009, 45) The chronically inflamed and constricted airways become extremely sensitive to asthma triggers such as irritants, allergens and infections. Exposure of an asthmatic to these triggers could easily result in gradually more soreness and contraction of the bronchial tubes. (Campbell, Neil A. 2009, 44) The amalgamation of these three aspects results in difficulty with breathing out, or exhaling. As a consequence, the air in the lungs needs to be vehemently exhaled to triumph over the contraction, which leads to the characteristic "wheezing" sound which is a characteristic indicator of an asthma attack. (Nilsson, Goran E. 2010, 56) Intrapulmonary pressure is the pressure within the alveoli also called the Intra-alveolar pressure. This pressure is subatmospheric during breathing in and larger than the atmospheric pressure during breathing out (Moskwa 2007, 175). Intrapulmonary pressure varies during the breathing process but at all times balances itself with the external atmospheric pressure (Int Panis, L, 2010, 44). Due to the inflammation of the bronchial walls, the intrapulmonary pressure is unable to stabilize itself with the atmospheric pressure. Ventilation can be referred to as the movement of air into and out of the alveoli and lungs. Energy is required for aspiratory muscles to contract and in so doing enlarging the thoracic cavity and to overcome any physical barrier to breathing. (Campbell, Neil A. 2009, 245) There are several factors that may affect Bill’s pulmonary ventilation which also affect breathing; these factors include airway resistance, alveolar surface tension forces and lung compliance. Airway resistance causes friction in the respiratory pathways. This is the foremost source of non elastic resistance to air flow. This is basically determined by the diameters of the bronchioles and bronchi. The smooth muscles that make up the walls of the bronchioles are particularly sensitive to some chemical stimulants. (Nilsson, Goran E. 2010, 156) These are parasympathetic reflexes triggered by breathed in irritants, and elements such as histamine, cause extreme constriction of bronchioles and considerable reduction in the diameter of airways. Another factor that may affect Bill’s pulmonary ventilation is alveolar surface tension forces. The alveoli walls are coated with a slim film of liquid which mainly consists of water and a surfactant. At a gas – liquid interface, the liquid molecules are more powerfully attracted to each other than to the gas which results in surface tension. This tension draws the fluid molecules collectively thus reducing their general contact with the gas molecules. It also opposes any force that is inclined to enlarge the area of the liquid surface. The surfactant in the alveolar film gets in the way of the cohesiveness of water molecules. This reduces the surface tension of the alveolar fluid and results in less energy being required to prevail over the surface tension forces to expand the lungs and discourage the collapse of the alveoli. Lung compliance is described as the capacity of lungs to stretch (Nilsson, Goran E. 2010, 213). Higher lung compliance means they expand easier at a given transpulmonary pressure. There are a few factors that determine lung compliance; these are elasticity of lung tissue and thoracic cage and the alveoli surface tension. Healthy people have high compliance because the tissue of the lungs and thoracic elasticity are high while the alveolar tension is low. (Campbell, Neil A. 2009, 145) This is due to the surfactant which allows for efficient ventilation. The ventilation/ perfusion ratio or V/Q ratio is the amount of air to the amount of blood that reaches the alveoli which is a determinant of blood oxygen concentration (Culver BH, 2008, 44). In asthma patients like Bill, this V/Q ratio is mismatched characterized by a principal bimodal blood flow model reflecting a distinct decline (increase) of the dispersion of pulmonary blood flow (Peter Raven, 2007, 53). The lungs will receive no ventilation owing to airway blockage and the V/Q ratio will be zero and the area will be designated as shunt. Question 2 Hemodynamic denotes the movement of blood and is referred to as the study of blood flow or blood circulation in the body. The hemodynamic process facilitates aerobic respiration; this is the process through which human cells use oxygen to convert carbon dioxide, proteins and fats into water, carbon dioxide and energy. The circulatory systems role is to transport the blood around the body to deliver oxygen, nutrients and chemicals to cells all over the body to guarantee their health and proper functionality. It also works to eliminate the cellular waste products. The circulatory system consists of a cycle of tubes which include the heart, which pumps the blood, the arteries which carry oxygenated blood, (Homoud, MK Spring 2008, p10) the microcirculation which feeds the tissues and the veins which carry deoxygenated blood back to the heart. In Bill’s case, the hemodynamic process is greatly hampered by the effects of the asthma. This is the case because the bronchial tubes in the lungs are highly inflamed and constricted causing a lot of resistance to the blood flow. This in turn affects the respiration process. (Bernstein, D. P. 2010, p16) In the study of heart physiology, preload is the last part of volumetric pressure also known as the end diastolic volume (EDV) that enlarges the left or right ventricle of the heart to its maximum volumetric dimensions under inconsistent physiologic demand. (Funk DJ, 2009, 894)  Contractility signifies the inherent ability of the heart to contract. It can also be described as the ability of the heart muscle tissue to contract whilst its thick (myosin) and thin (actin) filaments slip past each other. (Homoud, MK Spring 2008, p10) Afterload is the pressure developed in the walls of the left ventricle during the expulsion of blood. In other words, it is the end load or force against which the heart contracts to eject blood. In a patient like Bill, bronchospasm, this refers to the constriction of the airways as a result of tightening of the bronchial tubes. (Klabunde RE, 2007, p35) The effects of asthma prevent the dilation of the bronchial tubes; this in turn affects pressure of blood flow in the passageways. There are three major effects of breathing in asthma patients namely inflammation, bronchospasm and hyperractivity. The amalgamation of these three aspects results in difficulty in the exhalation process. As an effect, the air in the lungs needs to be violently exhaled to overcome the contraction, which leads to the characteristic "wheezing" sound which is a characteristic indicator of an asthma attack. The asthma effects of asthma leads to a larger fraction of blood passing through the lungs that are poorly ventilated which results in an increase in carbon dioxide concentration of the blood exiting the lungs. These effects result in a reduction of oxygen passing into the bloodstream and if severe, carbon dioxide may hazardously accumulate in the blood. (Bernstein, D. P. 2010, p11) The consequence of these increased levels of carbon dioxide displays a reduction in the general level of awareness plus increased respiratory effort. Severe increases in carbon dioxide levels can lead to respiratory arrest. Cardiac output is the volume of blood pumped by the heart per minute (ml blood/min). (Klabunde RE, 2007, p55) This is a role of heart rate i.e. the number of beats per minute and stroke volume i.e. the volume, in millilitres, that each beat pumps out. An increase in heart rate also results in an increase in contractility, and stroke volume. (Funk DJ, 2009, 887) Both the elevated heart rate and compressing action of skeletal muscles on the veins amplify venous return, causing an increased stroke volume. Question 3 Interpret and analyze Bill’s arterial blood gas in your analysis include: -buffering systems -regulatory mechanisms -pressure gradients -solubility of gases Relate the interpretation to the oxygen-hemoglobin dissociation curve. The oxygen hemoglobin curve explains the relationship between oxygen gas and hemoglobin which is the carrier protein for oxygen in the body. Hemoglobin can carry up to four molecules of oxygen at a time. Oxygen hemoglobin n dissociation curve The curve is sigmoid in nature and it represents the partial pressure of oxygen (x axis) against the concentration of oxygen in blood as oxygen molecules bind to hemoglobin. Initially the uptake of oxygen is low by hemoglobin but as more molecules bind to it the affinity for oxygen increases significantly. . The binding rate increases as more oxygen molecules bind until a saturation point is reached. At this point the curve is flat and the concentration of hemoglobin in blood does not increase even with increased partial pressure of oxygen. In a healthy person at a partial pressure of about 26.6mmHg the hemoglobin is 50% saturated with oxygen. This level is known as P50 and is used to measure the body’s affinity for oxygen. In an ailment there is a shift of the curve either towards right or left with a corresponding change in P50 value. Asthma leads to acute inflammation of the respiratory system and its reaction leads to mechanical obstruction which in turn curtails the flow of air to and from the lungs. Arterial blood gases are a measure of the amount of oxygen, carbon dioxide and acidity in blood. (Healthcare, Arterial Blood Gas Interpretation, 2004) Bill has had had asthma attack from childhood. In a normal person the partial pressure of oxygen (PaO2) ranges from 80-100 mmHg. The CO2 tension averages at 40mmHg.When under attack the oxygen tension fell from about 100mmHg to about 60mmHg while the carbon dioxide tension fell to about 30mmHg in the initial stage of attack. The pH in turn rises from its normal 7.40 to around 7.50. This is referred to as respiratory alkalosis (Parsonage, 2009) .At this time the patient suffers from hyperventilation due to anxiety. The pH level increases to 7.60 and the lungs cannot take in more air or even exhale. Due to lack of oxygen and accumulation of carbon dioxide then the vital organs including the brain can’t function and they are under duress. (Lemanske RF,Busse WW, 2010). Later the condition called acidosis appears due to decreased pH due to other components in blood other than CO2. If the attack does not worsen the body releases the bicarbonate (HCO3) to quench the increased pH. The bicarbonate is the blood buffer that controls acidity or basicity in blood. The regulation is done through the kidneys where more bicarbonate is retained in low pH. The reverse happens in high pH where a lot of bicarbonate is excreted in urine. When the organs are functioning properly an acid to base balance of 1 to 20 is maintained. The diagram below shows the relationship between blood gases .in the diagram, the severity of disease at point B is worse than at point A. this is because PaO2 at point B is lower compared to point B. The exacerbation attack results in hyperventilation due to bronchial inflammation leading to a physiological reaction leading to production of secretions making breathing difficult. A series of muscular reactions are clear with the hyperactivity by coughing sneezing and irregular breathing pattern. The inflammation is triggered by specific stimulants in the environment e.g., smoke, dust, weather conditions or even bacteria. With the obstruction the patient like bill experiences increased heat beat. The amount of blood reaching the tissues is high but with low oxygen concentration. The rate of carbon dioxide accumulation is high as blood flows back to the heart from the organs. The concentration of gases in the alveolar is high and the condition is intrapulmonary pressure. Due to increased heart beat the ventilation/perfusion rate is high which means the amount rate of blood flow though the organs are higher than usual. The unusual cardiac rhythm increases the body pressure of vital organs such as the brain and the kidney. The increased blood pressure resulting from ventilation perfusion mismatch results from bronchoconstriction in the lungs as the heart is triggered to force blood through the lung system. The decreased flow of blood in the body leads to increase malfunctionality of the organs. The pulmonary and hemodynamic changes in the time of exacerbations therefore result in high blood pressure and subsequent organ failure. To assist in the breathing, artificial means breathing is applied together with the other therapeutic techniques to arrest exacerbation. The equipment thus provides artificial ventilation Question 4 Bill was diagnosed with asthma in child age and has thus been using medication for a long time. The drugs for management of asthma are steroids and which Bill has used extensively. In the first place asthma affects the lungs such that it impairs the natural immune capabilities. The inflammation in the bronchial wall leads to damage of the inner linings which protect the inner tissues against infections. The thick secretions on the chest will provide an environment for growth of pathogens and the same time will stress the patient. Hard time during sleep further exposes patients like bill to low immunity. The corticosteroids which bill has used have side effects to the immune system as well. Some of the resulting symptoms include stomach upsets, headache, and liver problems among others. With a depressed immune system the body is exposed to opportunistic infections which only make the health situation worse. As part of the solution asthma patients should remain positive and proactive with the ailment. Take control of upcoming ailments on time by taking medication while being fast to respond to a nagging cough or wheeze. Bill should try and avoid the triggering agents such as the environmental changes or some scents which would trigger respiratory reactions. In Bill’s condition immediate treatment is by supply of oxygen to tackle acute bronchospasm and at the same time improve on hypoxemia. Immediate administration of corticosteroids ids also necessary but the administration depends on the medical condition. In addition to the primary treatment, Bill should be inhaled with iptropium bromide to aid in bronchial dilation which works well with oxygen and helps to reduce the hospitalization time. (Harris, 2009) In some instances, corticosteroids especially in long term use may lead to worsening ventilation in some patients though they work efficiently in most patients. In this case, intubation may be required without delay. The intubation may go hand in hand with mechanical ventilation. However, one has to take adequate care in its use as it can turn fatal. Magnesium sulphate intravenous applied can also be used. This is common to patients with exacerbations which are life threatening. It is also used to those whose exacerbations remain severe even more than an hour of conventional treatment. Magnesium sulphate is seen to inhibit bronchial smooth muscle activity by inhibiting influx of calcium into the cells usually administered at the rate of 2g over 20min in adults. A mixture of oxygen and helium known as heliox can also be used. It decreases turbulent flow of air in the lungs and therefore reduces the work involved in breathing. Common mixes have 80% oxygen and 20% Helium. The more the helium the lower the viscosity and hence it is easier to breathe. However, with more helium there is less oxygen and that increases tendency towards hypoxia. In the emergency unit, intubation then muscle paralysis along with sedation is commonly used. However, the procedure should lie in the hands of an experienced care giver because a minor manipulation of the airway in operation can make bronchospasm more severe. Common sedatives include ketamine and propofol. During sedation a neuromuscular blockade is essential to avoid coughing and allow the respiratory system to have rest. Systemic corticosteroids and oxygen should be applied adequately prior to intubation as part of asthma therapy. This should however continue throughout the period of mechanical ventilation. (Society, 2008)Lation can have serious repercussions which may include hypotension due to increased intra-thoracic pressure. The problems can be controlled by preventing elevation of intrathoracic pressure. Bibliography C.Michael Hogan. 2011. Respiration. Encyclopaedia of Earth. Eds. Mark McGinley and C.J.Cleveland. National Council for Science and the Environment. Washington DC Culver BH. (2008) Gas exchange in the lung. In: Clinical Respiratory Medicine (3rd ed.), edited by Albert RK, Spiro AG, Jett JR. Philadelphia, PA: Mosby Elsevier. Campbell, Neil A. (2009). Biology: Australian Version (8th Ed.). Sydney: Pearson/Benjamin Cummings. p. 334. ISBN 978-1-4425-0221-5. Cordovez JM, Clausen C, Moore LC, Solomon, IC. A mathematical model of pH(i) regulation central CO2 chemoreception. Adv Exp Med Biol. 605:306-11, 2008. Funk DJ, Moretti EW, Gan TJ (March 2009). "Minimally invasive cardiac output monitoring in the perioperative setting". Anesth. Analg. 108 (3): 887–97. Harris, R. (2009). Emergency Management of Acute Asthma. Medical emergencies, 1-4. Healthcare, O. R. (2004). Arterial Blood Gas Interpretation. Interpretation of the Arterial Blood Gas, 1-26. Healthcare, O. R. (2004). Arterial Blood Gas Interpretation. Interpretation of the Arterial Blood Gas, 1-26. Lemanske RF,Busse WW. (2010). Asthma: clinical expression and molecular mechanisms. Journal of Allergy and Clinical immunology, 120-126. Moskwa P, Lorentzen D, Excoffon KJ, et al. (January 2007). "A Novel Host Defense System of Airways Is Defective in Cystic Fibrosis".American Journal of Respiratory and Critical Care Medicine 175 (2): 174–83. doi :10.1164/rccm.200607 1029OC. PMC 2720149.PMID 17082494. Nilsson, Goran E. (2010). Respiratory Physiology of Vertebrates. Cambridge: Cambridge University Press. ISBN 978-0-521-70302-4. Homoud, MK (Spring 2008). "Introduction to Cardiovascular Path physiology".  Tufts Open Courseware. Tufts University. Kevin T. Patton, Gary A. Thibodeau (2009). Anatomy & Physiology (7 edition ed.). Mosby. ISBN 0-323-05532-X.  Int Panis, L (2010). "Exposure to particulate matter in traffic: A comparison of cyclists and car passengers". Atmospheric Environment 44: 2263 2270. doi:10.1016/j.atmosenv.2010.04.028 Klabunde RE (2007-04-05). "Mitral Regurgitation". Cardiovascular Physiology Concepts. Richard E. Klabunde. Archived from the original on 3 January 2010. Klabunde, Richard. "Cardiac Inotropy (Contractility)". Cardiovascular Physiology Concepts. "Pulmonary: heart Failure” http://www.indyrad.iupui.edu/rtf/teaching/medstudents/stf/pul1/pul1.htm. Retrieved 2008-12-21.  "Arteriovenous oxygen difference". Sports Medicine, Sports Science and Kinesiology. Net Industries and its Licensors. 2011. Parsonage, M. (2009). Arterial Blood Gas analysis. Wirral Respiratory Unit Teaching Pack, 1-43. Peter Raven, George Johnson, Kenneth Mason, Jonathan Losos, Susan Singer (2007). "The capture of oxygen: Respiration".Biology (8 ed.). McGraw-Hill Science/Engineering/Math. ISBN 0-07-322739-0. Society, B. T. (2008). Quick Reference guide. British Guideline on the Management of Ashma, 40-100. Read More

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