The Myocardial Infarction Case - Essay Example

 The Myocardial Infarction Case Study Introduction This essay covers a case study of 65-year old woman, Margo McCaffery, who is presented at an emergency department feeling sick. The essay covers mainly, the pieces of assessment data in support of diagnosis of acute myocardial infarction and an explanation of the pathophysiology of each piece of data. Myocardial infarction (MI) is also called heart attack, which occurs due to, the formation of occlusive thrombus after the rapture of an atheromatous plaque in a coronary artery (Davidson, 2008). Pathophysiology is the study of physiological, mechanical and biochemical functions of the body, the abnormal functioning of the body results from a disease or an abnormal syndrome or the disturbances of body functioning caused by a disease (Luis, 2012). Four pieces of assessment data The key pieces of assessment data include: the elevation of serum cardiac troponin levels (cTnT) diagnosed by collecting and testing of the blood; breathlessness, diagnosed by the observation of shortness of breath; appearing pale and tired, diagnosed by observing the patients feeling; patient feeling tired, fatigued, weak and nausea; the detection of heart sound S3 with no adventitious lung sounds or peripheral oedema; and prior history of heart failure as diagnosed by her doctor earlier; and the data of the 12- lead ECG which shows 2mm elevation in anterior leads of V1-V4 with the Q waves in inferior leads 11, 11 and a VF. McCaffery does not complain of chest pain, which is a symptom of acute myocardial infarction the reason for not having chest pain stems from her age and that she is diabetic. Davidson (2008) states that old and diabetic patients experience silent or non-pain myocardial infarction. Pathophysiology of the data pieces of assessment The pathophysiology of the Electrocardiograph (ECG) and the elevation of serum cardiac troponin (TP) piece data. To begin with cardiac troponin is that myocardial infarct causes a rise of plasma concentration of enzymes and proteins within the cardiac cells to rise to a detectable level (Davidson, 2008). The detection of myocardial infarction uses biochemical markers, for example, creatine kinase (CK) and the cardio specific proteins such as troponins (T$ I). The changes in plasma concentration of these markers bring out the diagnostic value; however, confusion may arise for the diagnoses of Angina which when damaged does produce troponins. The difference is that angina with minimal myocardial damage releases troponins to a minor degree. Electrocardiography (ECG) is difficult to interpret unless there exists a previous evidence of myocardial infarction. The first change is the serum troponin elevation followed by diminution of the size of R wave and an occurrence of infarction of a Q wave develops. The Q wave develops because the myocardial infarct acts as an electrical window that transmits the changes from within the ventricular cavity to allow the electrocardiography (ECG) to see the reciprocal R wave from the walls of the ventricle (Hutchison’s, 2007). Therefore, McCaffery’s 12 lead show 2mm segment elevation with leads v1-v4 with the Q wave reciprocal changes of 11, 111, and a VF which leads to no other conclusion but to that of myocardial infarction. Electrocardiography recorded from a 70- year old man who had an acute infarct 2 days ago and had treatment for myocardial infarction 11 months before showed Q waves in the inferior leads (11, 111, and a VF) and serum troponin (ST) elevation on the anterior leads (1 and V2-V6) (Davidson’s, 2008). This diagnosis resembles that of McCaffery so it can rightly be inferred that McCaffery is suffering from myocardial infarction. The other reason from the pathophysiology of the electrocardiography is that one cannot rely on these results unless there is a prior diagnosis of myocardial infarction. This is overcome by the fact that, McCaffery was diagnosed with heart failure by her doctor and drugs prescribed. Therefore, this piece of data leads to the conclusion that McCaffery is suffering from myocardial infarction. Secondly, is the history of nausea experienced by McCaffery, Nausea is a feeling of vomiting which gets initiated, in the brain part called the vomit centre which is a complex array of neurons coordinated by central pattern generator (Armstrong, 2008). The vomit center receives an input from chemoreceptor trigger zone, GI track, and the cerebral cortex. In this case study the chemoreceptor trigger zone, sense chemicals such as increase of toxic substances in the blood and causes nausea to be experienced and initiates a vomit reflex. The brain detects the unusual rise of toxics in the body that constitute a threat to life through two transmitters, such as, dopamine, which acts as D2 receptors and serotonin which acts as 5HT3 receptors (American Heart Association, 2009). Similarly, the gastro intestinal tract (GI) gets involved in inducing a vomit because it is a source of toxin absorption (Wiviott, 2012). Chemoreceptors in the gut meditate the toxic effect of some chemotherapeutic agents like cisplatin. The nausea and vomiting gets triggered through vagal nerve efferent and fibres associated with the sympathetic nervous system. Receptors get stimulated by neurotransmitters such as serotin, histamine and acetylcholine (Wiviott, 2012). Acetylcholine acts as a stimulus of the intestinal tract, so myocardial infarction cause lack of enough blood supply leading to failure to carry away toxics hence the effect of nausea. More so, vestibular apparatus senses the body and then mediate the body motion sickness hence acting sensor of neurotoxins that produce disequilibrium; therefore, the myocardial infarction leads to failure by body organs such as the kidney thus making toxic levels rise causing the vestibular apparatus to detect the toxic thus inducing nausea (Subirana, 2011). Therefore, in this case of McCaffery the myocardial infarction causes lack of enough blood reaching the brain and failure to remove toxic substances from the body. This leads to accumulation of toxic substances in the body such as carbon dioxide then the neurotransmitters convey this message to the brain and so a feeling of nausea is initiated on McCaffery. More so, the dilation of coronary artery causes insufficient blood reaching the brain which lead to the brain triggering the vomiting effect (Park, 2012). Therefore, the data on the symptoms of vomiting lead to the conclusion of myocardial infarction. Question # (2) rationale for the initial interventions The oxygen via face mask gets given because McCaffery is in a respiratory distress; this is observed from the breathlessness, feeling tired and the paleness of the skin which signifies lack of enough oxygen supply to body tissues. McCaffery has tarchypnea; this is observed in the increased respiratory rate of 24 instead of the normal 18 respiratory rate (Park, 2012). Therefore, the oxygen face mask is for rectifying the respiratory rate. The sublingual glyceryl trinitrate gets given as a first aid for threatened infarction and is useful in treatment of left ventricular heart failure and can also relieve persistent ischemic pain, this is because McCaffery is experiencing this pain and application of this medication helps to relieve the pain and restore proper functioning of the heart (Liyori, 2009). Similarly, the reason for administering the aspirin 330g orally is that aspirin is an anti platelets agent so the aspirin gets administered to help dissolve the thrombus, therefore, enhancing the blood flow to the heart and easing of the pain. Aspirin reduces the effect of blood clotting (Panzini, 2007). The morphine applied is analgesia used to relieve pain, severe distress and also to lower adrenergic drive, thereby reducing pulmonary antisystemic vascular resistance and ventricular arrhythmias (Kumar, 2009). This helps in reducing the pain and lowering the distress. Lastly the application of percutaneous transluminal coronary angioplasty (PTCA) is to help dilate coronary arterial reperfusion; this is because the occasioned myocardial interaction is characterized by either a blockage of a coronary artery thus impairing the supply of blood to the heart (Panzini, 2007). Question # (3) Management of Heart attack The first management is to sit-up the patient in bed at 45 degrees, this helps in reducing pulmonary congestion (Somme, 2008). The patient is sat up in half sitting position to make him comfortable and ease the pain of the heart the recommended posture requires that the head and shoulders be well supported, and the knees bent (Hutchison, 2007). The pulmonary congestion is evidenced by full neck veins this is a clear indicator that blood is not returning to the heart, which is the reason of the patients restlessness and shortness of breath. The half sitting posture helps the flow of the fluids down to the heart. This condition needs to be treated as a matter of priority, so McCaffery should be given high flow oxygen to improve the breathing of the patient and ensure enough oxygen supply to body tissue. A positive ventilation pressure by a tight fitting face mask can also be administered to the patient. This can help improve the clinical state rapidly, because the patient’s respiratory rate has gone up to thirty (30) per minute, oxygen helps restore the respiration rate to about eighteen rates per minute. The second intervention is to administer a loop diuretic such as furosemide which helps reduce the accumulation of the fluid in the lungs (Maurits, 2011). Furosemide inhibits sodium reabsorb ion by blocking the action of apical membrane, sodium, potassium, chloride co transporter (Maclure, 2012). This acts in the thickly ascending limb of the loop of henle a significant fraction of the filtered sodium is reabsorbed by this segment. Sodium causes salt and water retention increasing the blood pressure, so reabsorbing of sodium by henle helps in lowering the blood pressure. Similarly, it leads to excreting the fluid through urinating (Rogers, 2008). Then proceed to administer digoxin which helps in strengthening the cardiac contraction and prolonging the duration of cardiac contraction (Arnold, 2007). This results to an increase in cardiac output and improvement of tissue perfusion, hence, promoting the recovery of ailing heart (Maurits, 2011). The provision of blood supply to the kidney improves the ability to excrete water and salt. The diuretic effect gets enhanced by a reduction of the compensatory mechanism that favors water and sodium retention by reducing blood volume (National Heart and Blood Institute, 2009). The dieresis reduces peripheral resistance further improving cardiac output. Digoxin helps improve coronary circulation, by inhibiting the responsitivity to atrophic stimuli within the heart. Perfusion enhancement reduces stress level so improving the functions of other body organs impaired by congestion. It ensures adequate control of ventricular rate with positive inotropic effect. Then we proceed to administer a vasodilate such as ACE inhibitor to lower the blood pressure which inhibits the conversion of angiotensin I to II. Angiotensin II is a vasoconstrictor that stimulates the production of aldosterone, with less angiotensin and aldosterone vasodilation and decreased blood pressure occurs (Jaffe, 2007). Question # 4 the evaluation criteria The patient will be assessed physically by examining the sitting position, when the neck veins get full or reduce, and the level of paleness, also, by monitoring vital signs such as respiratory rate pulse and blood pressure. Laboratory assessment includes: biochemistry examination of urea electrolytes and creatinines to check on any improvement on the functioning of body organs associated with the heart. Imaging, done by taking an X-ray of the chest to access pulmonary oedema, pleural effusion and cardiomegaly, this is to check for improvement or deterioration. Lastly, monitor the improvement of the heart by performing an electrocardiograph to check for signs of heart failure. Conclusion The case study involves the diagnosis of myocardial infarction in an aged woman, Mrs. McCaffery, which later leads to heart failure. The patient is diabetic so some symptoms of myocardial infarction, such as acute chest pain, do not manifest in the elderly. The pathophysiology of the data is used to conclude that she is suffering from myocardial infarction; it is achieved by differential diagnosis, evaluation and investigation as one piece of data can lead to different conclusions. The management of heart failure is by easing the pains and treating the symptoms which arise, the treatment ranges from comfortable sitting positions to administering of drugs. 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