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Primary and Secondary Surveys of Chris Cardiac - Essay Example

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"Analysis of Heart Attack Case" paper examines the case of Chris Cardiac, a 52-year-old business manager who is rushed into the emergency department complaining of central crushing chest pain following a stressful meeting. His family has a strong history of heart disease…
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Extract of sample "Primary and Secondary Surveys of Chris Cardiac"

Cardiac-Case Study The case Chris Cardiac, a 52 year old business manager is rushed into the emergency department complaining central crushing chest pain following a stressful meeting. His wife is an accountant, has 2 teenage children, lives in a metropolitan suburb, his condition during arrival was, pain for 30 minutes, pale, clammy, short birth. His family has a strong history of heart disease. He has cholesterol, and is under medication for hypertension and mile asthma, with reported allergy to aspirin. He has lots of business dinner outside, stressed and a stressed personality. Primary and Secondary Surveys and the related medical condition The most commonest complaint found in patients arriving in the accident and the emergency department is chest pain. This single symptom may lead to much differential diagnosis, usually it is the clinical history that aids in managing the patient better. The underlying cause of chest pain are varied ,usually may be cardiac, respiratory, gastro intestinal and musculo skeletal system. The conditions are ruled out usually based on the other associated symptoms and based on the severity, site and nature of pain. (1) The crushing chest pain is called as angina, the pain caused by insufficient oxygen reaching the heart muscle due to reduced blood flow. Angina can be described as a feeling of heaviness, tightness or a pain in the middle of the chest that may extend or affect especially the left neck, jaw, back and abdomen. It is usually pound to occur during a phase of exertion, in cold weather after heavy meal or after a stressed condition. The symptoms that the patient produced in the time of admission as crushing chest pain, short breath, paleness, and the clamminess along with the strong family tendency and the condition of hypertension and hyper cholesterolemia added to the unhealthy food pattern and stress life leads us to the diagnosis of heart attack. (2) Heart attack ,medically known as Acute Myocardial Infarction (AMI) can be described as a condition that arises when the arteries that lead to the heart becomes blocked leading to a slow or stopped blood supply. When the heart muscle can’t get enough oxygen and nutrient that it needs, the part of the heart tissue that is affected dies. The symptoms of heart attack are (This could be found to match our patients symptoms that lead to this diagnosis) Chest pain – Often crushing or squeezing or burning pain in the center of the chest that may radiate to arm and jaw. Shortness of breath Cold or clammy skin Gray or very ill or pale appearance Dizziness or faintness Sweating and nausea Rapid or irregular heart beat (3) Most heart attacks are found to be caused by a clot blocking the coronary arteries. The clot usually forms in the arteries that have been already narrowed by atherosclerosis. The plaque, that is built up inside the arterial wall over time burst and this triggers the formation of clot which is also known as thrombus. This clot interrupts the blood flow leading to the eventual death of the heart muscles, the damage heart muscles slowly loosing the capacity to contract, putting stress on the remaining heart muscles to compensate for the weekend area. This overwhelming stress causes sudden attack. (4) The risk factor associates with coronary artery diseases are ( could be seen to match the patient’s case history ) Smoking High blood pressure Intake of diet rich in fat Prevalence of Poor cholesterol level in blood – High LDL and Low HDL level Diabetes Male gender Age Hereditary Stressed life style (5) (6) The Nursing Management for Patient in this initial period The role of nurse in the initial stage of management along with the doctors is very important. When initial examinationis done, usually a rapid pulse is noticed in patients. Blood pressure would be either high or low. While listening through the stereoscope a crackling sound in the lungs or a heart murmur or other abnormal sound may be notice that confirms out doubt of heart attack. (7) Heart attack is a medical emergency and immediate hospitalization and intensive care is necessary to reduce the impending the risks. The first step would be continuous ECG monitoring because unnoticed arrhythmias are leading cause of death during the initial hours. The ECG may be taken several times in the initial period to monitor continuous change. Bloods is drawn and send to laboratory for testing of the cardiac marker enzymes released during the attack. The traetement would be initially aimed to stop the progression of heart attack , thus reducing the demand on the heart so that it can heal preventing any further complication . (8) Direct insertion of medications and fluids into the vain using IV would be next step. Insertion of various monitoring devices and a urinary catheter would be done immediately to closely monitor the fluid status. Oxygen is usually given even if the oxygen level is normal as it makes the oxygen readily available to the body tissues thus reducing the workload of the heart. The following step in the initial medication would be administration of pain control mechanism as intravenous, nitro glycerin medicine that is found to reduce the pain and oxygen requirement of heart. Painkillers as Morphine’s are also sometime used. The patient if is not allergic to Aspirin is given with Aspirin to chew that would prevent further block of artery.(9) If possible the patient or his family members if immediately available are questioned about past family history, past medical history, onset of symptoms,presence of risk factors that along with the ECG patterns leads to proper diagnosis Once the heart attack is diagnosed, the initial treatment would be restoring the blood flow to the heart muscle to minimize the damage and prevent further complication. This is achieved either through administration of blood thinning medication – thromobolytic therapy, aspirin or receptor blocker . (10) Pathophysiology of the patients condition- anterolateral myocardial infarction: Acute Myocardial Infarction is the phase that occurs during the period when the circulation to the region of heart is blocked, causing necrosis that is characterized by severe pain, usually associated with severe pain, pallor, perspiration, dypnea, dizziness and electrocardiograph abnormality that includes Q wave, ST segment and T wave alteration. The Anterolateral MI means infarction occurring in the anterior and lateral position of the heart producing vindictive changes in the pericardium as well as in the Lead 1 and aVL , with the ST segments elevation in V3, V4, V5, V6, I, aVL and depression in II, III, aVF. Thus in nutshell , myocardial infarction can be described as an condition that occurs as the atherosclerotic plaque that slowly builds up in the inner lining of a coronary artery ruptures suddenly , leading to the total occlusion of the artery , thus preventing blood flow downstream. (11) Acute myocardial infarction can be described as a type of acute coronary syndrome, a manifestation of coronary artery disease. The triggering event in is usually the disruption of an atherosclerotic plaque in the coronary artery, that eventually triggers a clotting cascade that sometimes causes a total occlusion of the artery. The gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries slowly over decades, that leads to the narrowing of the arteries is called as Atherosclerosis. ThePlaques are unstable, ruptures, and leads to a thrombus (blood clot) that occludes the artery even in a minutes. Thus when a plaque rupture in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium). As the impaired blood flow to the heart persists over a long time, it triggers a process called the ischemic cascade, wherein usually the heart cells die by necrosis and do not grow back , with the formation of collagen scar in its place. In Recent times yet another form of cell death called apoptosis is also found to play a major role in the tissue damage that subsequently leads to myocardial infarction, leading to the permanentdamage of the heart. This scar tissue, also puts the patient at risk of potentially developing , life threatening arrhythmias. Generally the injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The existence of difference in conduction velocity between injured and uninjured tissue usually trigger the re-entry or a feedback loop that causes lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation, an extremely fast and a chaotic heart rhythm , becoming the leading cause of sudden cardiac death. (12) Other investigations required prior to the commencing of thrombolytic therapy: Before starting the Thrombolytic therapy Physical diagnosis, confirmation of the symptoms and other background details should be collected. Other necessary test and diagnosis should be performed Certain points and conditions before starting the therapy should be kept in mind. to affirm the presence of heart attack and the extent of heart damage, the following test are carried out: The Electrocardiogram (ECG) is a test to assesss the electrical activity of heart through electrodes attached through the skin, is repeated over several hours– Echocardiography – uses sound wave to produce the image of the heart Coronary angiography –shows whether the arteries are narrowed. Nuclear ventriculography – identify blood flow problem by using radioactive elements. The following tests may show the by-products of heart damage- the cardiac markers The presence of proteins , Troponin I and troponin T , proteins involved in muscle contraction The presence of the heart enzymes CPK and CPK-MB Serum myoglobin The points to be remembered before starting the thrombolytic therapy for the patient is : 1. An ST elevation of at least 1mm in the limb leads or 2mm in the chest leads on the ECG and a new onset of left bundle branch block (LBBB.) 2. in the patients past history no compelling contraindications to thrombolysisis to have occured, that would be difficult to assess when the patient is met for the first time.as thrombolytic drugs are not without risk and careful questioning is requires to ensure proper treatement. It is dangerous to administer the thrombolytic drugs to patients who are having : Intra carnial haemmorrhage , Internal bleeding in their head brain tumors or with blood vessel malformations Stroke occured in the past 3 months or longer Had an Head injury in the past 3 months with an severe blood pressure ,high Underwent a major surgery or major trauma in the past 3 weeks Occurrence of Internal bleeding in the past 2-4 weeks Peptic ulcer disease Pregnant women. The thrombolytic agent acts by dissolving the clots formed in the arteries. The Currently available thrombolytic agents can be listed as Streptokinase, urokinase, Alteplase, Reteplase, Tenecteplase, tissue plasminogen activator etc. (13) (14) (15) Ventricular Tachycardia- the management: Ventricular Tachycardia is the rapid heart beat initiated with in the ventricles that is characterized by three or more consecutive premature ventricular beats. It is an potentially lethal condition of disruption of normal heart beat rendering the heart disabled to pump blood effectively. The rate is as high as 160-240. commonly it is is found to occur as a early or late complication of heart disease as heart attack or cardiomyopathy and myocarditis. It can also occur as an undesired side effect of anti- arrithmic medication or from altered blood chemistries. The causes of ventricular tachycardia could be grouped on the basis morphology of the tachycardia. In the monomorphic form, the impulse is generated from either a single point in the left or right ventricle or is due to a single circuit occuring within the ventricle. mostly this is caused by the scar of dead tissue from a previous myocardial infarction where in ,the scar cannot conduct electrical activity, leaving a a potential circuit around the scar that results in the tachycardia.The Polymorphic ventricular tachycardia, the other form on the other hand is found to arise due to electrolyte abnormalities. The causes of polymorphic ventricular tachycardia is usually the unwanted drug reactions and ischemia of the myocardium . (16) The usual symptoms being the palpitation, dizziness ,apnea, angina and syncope. The diagnosis is through the ECG or echocardigram or coronary angiography As with any other diesease, for the proper treatment of VT the proper diagnosis is necessary. The diagnosis of ventricular tachycardia is usuallydone on the basis of the rhythm seen on a 12 lead EKG or a telemetry rhythm strip. The tricky issue here is to differentiate between occurrence of ventricular tachycardia and supraventricular tachycardia . .Various diagnostic criteria are developed to delineate the condition as either ventricular tachycardia or a more benign rhythm. In addition to these diagnosis, if the individual is known to have a past history of a myocardial infarction, congestive heart failure, or an recent angina, the wide complex tachycardia occures is likely to be ventricular tachycardia.The proper diagnosis is very important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present leads to very worse prognosis. (17) Treatment for Ventricular Tachycardia: Treatment is usually as acute or for long-term. Hypotensive VT requires cardioversion whereas stable VT is treated with drugs and the long term VT doesn’t require any treatement. The primary aim is to avert the death. The long term treatment involves the other method described below. Of the different modalities of treatement, the therapies are generally aimed at either terminating the episode of the arrhythmia or at suppressing the occurrence of future episode . Generally the treatment varies with the symptoms, the situation, and the underlying cardiac disorder . At times no treatment would be required in some cases.Thus the treatment is usually tailored made for specific patient, keeping in mind the individual’s tolerance of ventricular tachycardia, and on the frequency of occurence. (18) the treatement regime usually includes antiarrhythmic agents as lidocaine, procainamide, bretylium, or sotalol or a Implantable cardioverter-defibrillators (ICDs)and an electrical cardioversion ( electric shock) that uses an external defibrillator in a very acute setting Generally it is used only when the patient is unconscious and in cases of Generally the Anti-arrhythmic medication are found to have many severe side effects, and their use is currently decreasing in favor of other treatments. As a Recent invention , the Radiofrequency catheter ablation method is used as a curative treatment for selected tachycardias. thus the recent for chronic VT in recent years is implanting of a device called implantable cardioverter defibrillator (ICD). The ICD is implanted usually in the chest, like a pacemaker, and it is connected to the heart with wires. The ICD is programmed by the doctor to sense ventricular tachycardia during its occurrence , with administration of a shock to abort it. The ICD may also be programmed to send a rapid burst of paced beats to interrupt the ventricular tachycardia. In some cases the ventricular tachycardia may require also the use of concomitant anti-arrhythmic agents to prevent repeated firing of the ICD. It is important to understand the underlying causes in providing the effective treatment. (19) Bibliography: 1. What is Angina , 2005, http://www.bhf.org.uk/questions/index.asp?secondlevel=1162&thirdlevel=1316 2. Medical Encyclopedia: Heart attack URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/000195.htm 3. Anterolateral myocardial infarction,2000 http://www.cnn.com/HEALTH/library/DS/00094.html 4. Prescriber Guide – Summary of NICE guidelines for the early treatment of acute myocardial infarction 5. P A J Krijnen et al, 2002 ,Apoptosis in myocardial ischaemia and infarction. Journal of Clinical Pathology ;55:801-811. PMID 12401816 6. Jensen G, Nyboe J, Appleyard M, Schnohr P. (1991). "Risk factors for acute myocardial infarction in Copenhagen, II: Smoking, alcohol intake, physical activity, obesity, oral contraception, diabetes, lipids, and blood pressure.". Eur Heart J 12 (3): 298-308. PMID 2040311.  7. Myocardial infarction: diagnosis and investigations - GPnotebook, retrieved November 27, 2006. 8. DE Fenton et al., 2006 . Myocardial infarction - eMedicine, 9. HEART SCAN - Patient information from University College London. Retrieved November 27, 2006. 10. Gillum RF, Fortmann SP, Prineas RJ, Kottke TE, 1984. International diagnostic criteria for acute myocardial infarction and acute stroke. Am Heart J ;108:150-8. PMID 6731265 11. S. Garas et al.. Myocardial Infarction. eMedicine. Retrieved November 22, 2006. 12. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. Harrison's Principles of Internal Medicine, 2005 . p. 1444. New York: McGraw-Hill, ISBN 0-07-139140-1. 13. Boland A, Dundar Y, Bagust A, Haycox A. Hill R, Mujica Mota R, Walley T, Dickson R, 2003. Early thrombolysis for the treatment of acute myocardial infarction: a systematic review and economic evaluation. Health Technology Assessment ; Vol.7: No.15 14. Comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group. N Engl J Med. 1993;328:673-679. 15. GISSI Investigators. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano por lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet. 1986;1:397-402. 16. Wellens HJ, Bar FW, Lie KI. (1978). "The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex.". Am J Med 64 (1): 27-33. PMID 623134.  17. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. (1991). "A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.". Circulation 83 (5): 1649-59. PMID 2022022.  18. Baerman JM, Morady F, DiCarlo LA Jr, de Buitleir M. (1987). "Differentiation of ventricular tachycardia from supraventricular tachycardia with aberration: value of the clinical history.". Ann Emerg Med 16 (1): 40-3. PMID 3800075.  19. Stewart RB, Bardy GH, Greene HL. (1986). "Wide complex tachycardia: misdiagnosis and outcome after emergent therapy.". Ann Intern Med 104 (6): 766-71. PMID 3706928.  Read More
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