Pathogenesis of Myocardial Infarction - Case Study Example

Running Head: Ischeamic heart disease Ischeamic Heart disease Name Date: Introduction Ischaemic heart disease interferes with the flow of blood through the coronary artery to the heart. It results from the vessels of blood being blocked because of the deposits of cholesterol. Nutrients and oxygen are supplied in inadequate levels and this causes improper functioning of the heart. As a result a section of the heart may die and cause heart failure. The heart then fails to perform its functions of pumping blood to the important organs of the body like the brain hence their eventual death. (Mitchell et al 2007). Some of the risk factors associated with ischemic heart disease include having high levels of cholesterol, being inactive physically, taking foods with a lot of fat and coming from a family that has a back ground of heart problems, diabetes or hypertension. A family line with heart related problems, high blood pressure, diabetes and atherosclerosis may easily pass that condition to the offsprings. (Mitchell et al 2007).Physical activity aids in circulation of blood, break down of fats and reduction of cholesterol levels. When one is inactive physically, there is the possibility of blockage of the blood vessels leading to the heart by fat deposits. Narrowing of the coronary artery reduces the flow of blood to the heart hence ischemic disease is formed. A diet that contains much fat when taken over along time may lead to fats being deposited on the inner walls of the arteries. This in turn reduces the volume of the artery hence hypertension. Reduced rates of blood flow to the heart can lead to ischemic heart disease. Increase in the cholesterol levels in the body can expose one to the risk of ischemic heart disease too. This may happen when the increased levels of cholesterol harden and block the arteries leading to the heart. (Braunwald E. et al 2002). Pathogenesis refers to the origin of a disease, its development and growth and the events that lead to that disease. Myocardial infarction begins when a section of the heart muscle that is not supplied with blood dies. This normally comes from a blockage in the coronary artery or its branch. Myocardial ischemia starts in the internal heart lining (endocardium) as it spreads to the external lining (epicardium). (Braunwald E. et al 2002) In case the artery is blocked for 15-20 minutes it may result in permanent damage. The area under risk experiences maximum permanent damage and also if there is an occlusion of 4-6 hours. The first two or three hours will account for most damage. However if the flow of blood is restored in the first four to five hours then the heart muscle can be rescued, something that can more effected if that restoration is done in the first one to two hours. Myocardial infarction involves in its early stages the destruction of the muscle cells of the heart because of lack of oxygen supply. The muscle that lacks blood flow for a bout 10 to 15 minutes suffers necrosis which does not allow its re growth. Because the heart has to pump blood to the rest of the body its power to do that is greatly lowered. The muscle in the injured part of the heart relays heart beat impulses slowly. In some cases the spread of the impulse becomes so slow that the part of the muscle that is not injured contracts before receiving the impulse. (Loria V. et al 2008). The late impulse moving through the injured part may have a re entry into the muscle that is well and trigger it to beat sooner before the heart relaxes and receives blood from veins. If this process of re-entry sustains heart rates at 200 to 400 beats for every minute (ventricular tachycardia) or (ventricular fibrillation) then this fast pulse rate stops the pumping of the heart. The out put of the heart and blood pressure cause the death of the individual when they fall almost to zero.In the case of Mrs. Gray, her condition may be hereditary since she keeps fit and is on good nutrition. Due to insufficient flow of blood to the heart, her heart muscles may have been damaged due to poor oxygen supply. This death of a part of her heart may have caused it to conduct impulses slowly. The abnormal contraction of the heart may have caused her heart to contract before receiving blood coming through the veins from the body. The presence of atherosclerotic disease and deposits of plaque may have caused the artery to narrow. For a blood clot to occur the plaque might have ruptured causing the blood to clot there due to occlusion. Clotting may also have come from the restricted flow of blood as well as stagnation of the flow of blood at the plaque. (Loria V. et al 2008). Electrocardiogram or ECG recording refers to the measuring of the heart’s electrical activity. When the heart pumps blood in makes electrical impulses that are recorded and displayed on paper. With ECG problems within the heart’s operations can be recorded. In case the heart beat has been affected by any disease the ECG can easily show that. ST elevation refers to a situation where the ST segment in a myocardial infarction is elevated. In this type of myocardial infarction the heart fails to get enough oxygen supply. This happens when the muscle of the heart dies especially when the coronary artery is blocked.The cardiac cycle is a series of events resulting from the beating of the heart. (Loria V. et al 2008). The cycle has systole and diastole phases. The ventricles of the heart relax leading to the filling of the heart with blood in the diastole phase. In systole the heart ventricles contract and blood is pumped to the arteries, is taken to the rest of the body and the cycle is repeated. When the ST is elevated it means the heart will not receive enough blood. The muscles of the heart responsible for pumping blood are therefore starved of nutrients and oxygen which is very necessary for the survival of their cells. Consequently, the muscle dies and blood pumping is interfered with leading to the collapse of the cardiac cycle.The cardiac muscle contains troponin lying inside the groove found between actin filaments in the tissues of the muscle. The filaments contain actin and tropomyosin. Troponin takes part in the contraction of the skeletal and cardiac muscle. Cardiac muscles depend on the calcium concentrations within the cells for their functions. A fall in calcium causes a relaxation in the muscles while a rise causes contraction. To achieve this purposes calcium binds itself to troponin. The smaller units of proponin are TnT, Tnl and TnC. Calcium attaches on certain TnC sites, tropomyosin moves from the way of active sites of actin filament. Myosin normally found in the thick filaments of the muscle, attaches to the thin filaments to create movement. When calcium is lacking, tropomyosin the activity of myosin is hampered making the muscles to remain in a relaxed state. (Braunwald E. et al 2002) When there is a myocardial injury troponin I and T are released to enter the blood stream and they assist in taking away the CK elevations when the skeletal muscle experiences a trauma. They are better at it than CK-MB. The level of Troponinis starts rising within 3-12 hours of a myocardial infarction which is almost the same period of time as CK-KB. Troponins maintain the elevated state more than the time taken by CK which is normally five to ten days in the case of troponin I while troponin T will goes to up to two weeks. Because of this troponins have become an important marker in the diagnosis of myocardial infarction. (Kost et al, 1998)Continued elevation however can make diagnosis of a reinfarction or infarction extension difficult GTN opens blocked blood vessels that transport oxygen to the heart. In the process the workload of the heart is greatly reduced.Organic nitrates are metabolized and bio-activated by enzyme action in the walls of the arteries to produce nitric oxide a compound that is very pharmacologically active. GTN causes the relaxation of the blood vessels concerned. Before this however there is the creation of 1,3 GDN and 1, 2 GDN together with the activation of guanylate cyclase to produce cGMP. cGMP activates the protein kinase which depend on it and brings about effects like myosin light chain phosphorylation, intracellular calcium sequestration and reducing the entry of calcium coming from the extracellular space. It also brings about lowered release of calcium stored in the cells and hinders inositol 1,4,5 triphosphate from being formed. The reduction of preload in the heart is effected through dilation of vessels selectively. (Loria V. et al 2008). For patients with ischaemic disease it lowers the diastolic pressure of the end of the left ventricle. It also lowers the tension of the ventricle walls during systole and also raises cardiac out put. Morphine helps to correct damage resulting from ischemia. The heart possesses opioid receptors called kappa and delta which are activated by morphine to cause certain effects. Morphine contains anti-flammatory properties that tackle inflammation in the heart. Inflammation may result from stress, cholesterol and plaque, heart disease and hypertension. Morphine is normally administered in such cases to stop any more inflammation and serve as an anesthesia in case of surgery. It works through making the center that perceives pain in the brain to become dull. Mrs. Gray may have been given morphine and GTN in order to relieve chest tightness she was experiencing. Angina occurs when oxygen fails to reach the muscle of the heart. Glyceryl trinitrate help to make arteries wide and relax those veins bringing blood to the heart from the body thus making oxygen to reach the muscle. This reduces the pain and the strain in the heart. Coversyl is an ACE inhibitor that hinders the activity of angiotensin in the body that changes (ACE) enzyme. The chemical called angiotensin is produced by ACE. Coversyl lowers the quantity of angiotensin present in the blood. Angiotensin is responsible for making the blood vessels narrow and production of lesser urine by the kidney. When these actions are reversed due to coversyl hindering the production of angiotensin, more urine is produced in the kidneys. This means the blood vessels will have lesser fluid and that the vessels will also open up. (Loria V. et al 2008).Consequently blood pressure and the heart’s work load fall. Betaloc is classed with as a beta blocker. It treats angina and ischaemic heart disease by interfearing with the body system of responding to certain nerve impulses in the heart. It lowers the requirement of the heart for oxygen and blood as well as the work load of the heart. The heart is aided to have regular beats and also the blood vessels are widened. Betaloc also serves the purpose of treating hypertension. Mrs Gray should make sure that she reads the instructions and precautions coming with every drug. Each pack could have instructions about dosage, disposal side effects, and warnings about allergic cases. She needs to open up to her doctor a bout any other medical complications she might be having and also, any other type of medications she may be receiving. (Loria V. et al 2008). The doctor can then give her appropriate instructions in order to help her avoid further health problems. Generally, she needs to understand and adhere to the instructions for every kind of medicine from the manufacturer and consult her physician before taking any of them. Conclusion In conclusion Ischaemic heart disease affects the heart when its muscle fails to pump blood because of death. Death of the muscle comes from lack of blood supply due to blockage of the coronary artery.The case study on Mrs. Gray shows that she may have suffered from this disease because of hereditary factors. The drugs she was given such as morphine and GTN were meant to kill pain and dilate her blood vessels. In order to use the drugs well she needed to follow the instructions on the packs and the doctor’s advice as well. (Mitchell et al 2007). References Braunwald E.(2002) Elevation of myocardial infraction. American Heart Association Task force on practice guidelines. Cambridge Publications Loria V. (2008).Ischemic heart disease and acute coronary syndromes:Amazon Publishers New York City. Mitchell, R(2007). Robbins Basic Pathology 8th edition: Philadelphia Publications. New York city. Read More