Acute coronary syndrome free essay sample

Acute coronary syndrome (ACS), also known as unstable angina or myocardial infarction, a fundamental origin of illness as well as untimely death and is also a frequent reason for infirmary admission, is primarily identified to result from sudden fluctuation of blood flow to the heart (Fitchett et al., 2001). The underlying cause of symptoms is owed to myocardial ischemia, which is characterized by a disproportion between supply and demand of myocardial oxygen (Fenton, 2007). It includes an extensive range of coronary artery diseases which includes unstable angina, ST-elevation myocardial infarction (STEMI, which is otherwise called as Q-wave myocardial infarction), and non-STEMI (NSTEMI is often used to denote non-Q-wave myocardial infarction). Primary signs and symptoms as well as the early treatment of unstable angina, STEMI, and NSTEMI are often indistinguishable (Achar et al., 2005), thus it is advised to follow a specific procedure for diagnosis. Acute coronary syndrome is characterized by the clinical condition of acute ischaemic chest pain which involves either rest pain or an upsurge pattern of soreness despite least physical exertion, connected through electrocardiogram (ECG) variations of ischaemia (ST elevation or depression or T inversion) (Gomersall, 2007). Diseases pertaining to chest pain are often alike and similar. Thus, making a distinction between acute coronary syndrome and noncardiac chest pain is a stepwise process which is quite difficult and is considered to be a challenge. In primary evaluation, among the requirements usually looked into are the following: a focused genetic history (which would include risk factor analysis as derived from genetic data), a physical test assessment or examination, an ECG, and oftentimes, the use of biochemical markers is employed such as serum cardiac marker determinations are also essential (Achar et al., 2005). Contributing to the difficulties in the diagnosis of this syndrome is the wide range of symptoms, which at times overlap and thus the need for a specific stepwise process of evaluation, as stated above. Indications of acute coronary syndrome usually consist of chest pain, referred pain, nausea, vomiting, dyspnea, diaphoresis, as well as lightheadedness, and everything correlated to such (Achar et al., 2005). Unstable angina and myocardial infarction are often clinically indistinguishable, usually recognized with a lingering experience of chest pain that starts without aggravation, while myocardial infarction is diagnosed through detection of myocardial damage – identified by the occurrence of unusual degrees of circulating biochemical markers namely creatine kinase (CK) or any of the troponins (Fitchett et al., 2001).   Several patients were noted to be without chest pain, and in previous studies, sudden dyspnea was the only visible characteristic in four to fourteen percent of patients diagnosed with acute myocardial infarction. Areas in the body inflicted with pain associated with the common symptoms were often identified to be in the left or right upper extremities, the jaw, the neck, the back, or in the trunk area, specifically the abdomen. The presence of pain that often sears to the shoulder, left arm, or both arms to some extent elevates the tendency to develop acute coronary syndrome, with further studies noting a likelihood ratio of 1:6 (Achar et al., 2005). Morphological assessment in the form of physical examinations in patients hypothesized to have acute coronary syndrome is usual. Physical findings that may pose a warning to the patient are comprised of new mitral regurgitation noises, visible hypotension, signs correlated with pulmonary rales, a new third heart sound (S3 gallop) in contrast to the usual thubbing sound, and new jugular venous swelling (Achar et al., 2005). The presence of chest-wall tenderness is often considered to decreasingly rule out the probability of having acute coronary syndrome. Acute coronary syndrome usually results from atherosclerotic plaque disturbance and thrombotic occlusion of a coronary artery, whose results depend on the location and degree of plaque rupture, the consequential circulation disturbance, the scope and length of the thrombotic occlusion, as well as the existence or nonexistence of a sufficient collateral coronary movement (Fitchett et al., 2001). The interactions of these factors result to a myriad of effects and visible symptoms and various outcomes, including sudden death. The intensity of the outcome and course of the syndrome will depend on the severity of the original coronary experience and the baseline situation of the patient (factors often associated with age, prior coronary occurrence, left ventricular function and many more) (Fitchett et al., 2001; Rentrop, 2000). Recent clinical findings imply and support important refinement of the previous common notion that this syndrome is only caused by plaque rupture and formation of a platelet thrombus, basing on the subsequent observations: occlusive thrombi causing Q-wave myocardial infarction contains more fibrin than the thrombi found in the other acute coronary syndromes that are characterized by more platelets and less fibrin – factor which explains their greater stability, suggesting furthermore that the coagulation is activated to a greater degree during Q-wave infarction than during non–Q-wave infarction where platelets play a more central part (Rentrop, 2000). Prior to hospital admission, patients with chest pain should at the start be supervised under the supposition that the pain is primarily ischemic, thus pre-hospital interference should be channeled by the nature of the initial symptom, predisposition towards the disease as determined through family history, and additional visibly-linked symptoms such as difficulty in inhalation of air, hemodynamic instability, manifestation of ectopy (Fenton, 2007). Fast evaluation on the airway, breathing as well as circulation should be employed using CPR, ACLS-guided measures, or further procedures as suggested for the unstable patient. Administration of supplemental oxygen should be employed, and it is also advised to give aspirin (about 162-325 mg).   Telemetry, prehospital ECG, as well as the employing of pulse oximetry is advised, and the administration of sublingual or aerosolized nitroglycerin if chest pain is persistent and felt by the patient to be cardiac in origin is also suggested (Fenton, 2007). To have a better understanding on the clinical discourse of ACS, a standard procedure of action is suggested to be administered to patients showing signs and symptoms consistent to what is present in ACS. This is shown through the following diagram in order to understand more effectively the steps needed to be considered prior to treatment. This can also aid in the rapid diagnosis of ACS. Recent techniques suggest the use of the Cardiac Ischemia Time-Insensitive Predictive Instrument, which is a computerized decision-making program incorporated into the ECG machine (Achar et al., 2005). The application of this apparatus in an emergency unit resulted in no alterations in the suitable admittance of patients who had acute coronary syndrome and therefore, an identified advantage of its use was a significant reduction in hospital admissions of patients who did not have acute coronary syndrome, given that the administering physicians are truly educated in the use of the apparatus. Patients who have a large predisposition for ACS (otherwise termed to be at high risk to be diagnosed with ACS) are advised to be admitted to a coronary care unit in order to alleviate as soon as possible the effects of the disease. A precise analysis and inference of the risk of an unfavorable result are prerequisites to selecting the most proper cure. Early selection and ranking (whether at a high, intermediate or low risk) of patients by examination of their family history and electrocardiogram (ECG) findings initiates a clinical notion of ACS; it differentiates ACS patients from those with non-coronary chest pain or stable angina which are mentioned earlier to be very similar (Fitchett et al., 2001), thus accurate treatment may be given. Those at intermediate risk may be supervised in a telemetry bed in an in-patient locale or a chest pain division, wherein it is a specialized unit within an emergency department dedicated to vigilant monitoring and strict execution of diagnostic set of rules (otherwise called clinical guidelines) for the assessment of ACS. Often, low-risk patients may undertake early exercise testing or can be discharged provided that they consistently adhere to careful follow-up by medication elsewhere outside the hospital hence the term outpatient follow-up (Achar et al., 2005). The myriad of indicators of the degree of severity of the acute ischemic occurrence (often characterized by prolonged and recurrent pain at rest, and chest pain associated with dyspnea) as well as the ECG data obtained from the ST-segment shift appropriately recognizes 90% of patients with chest pain who are expected to have undesirable results in the succeeding 30 days. Additional exploration through conducting tests for perceptive biochemical markers of myocardial damage (e.g. test for the levels of creatine kinase) plus a period of observation increases the possibility that roughly all high-risk patients can be identified shortly after consultation given that the apparatus to be used are readily available and the doctors involved are well-trained (Fitchett et al., 2001). In terms of biochemical markers for ACS, previous studies reported that patients with biochemical evidence of myocardial damage (as made visible through several markers that can identify occurrence of serum myoglobin, CK [and MB fraction] and cardiac troponin I and T) have a higher risk (approximately 5-fold) of premature and later reinfarction and mortality as compared to possible ACS patients lacking with biochemical evidence and diagnosis of myocardial damage. Cardiac troponin I and T have recently been introduced as markers of myocardial injury the incidence of cardiac troponin I or T in a patient with a non-ST-elevation ACS is considered indicative of higher risk, with the risk correlated to the peak troponin level that may be observed in the first 8 to 12 hours after subjection to tests (Fitchett et al., 20010, hence,   presence of cardiac troponin is a gauge of a high risk for repeated thrombotic episodes and suggests the necessity for immediate rigid   antithrombotic management. In summary, four common treatment strategies are suggested to repair blood flow and minimize damage to the heart muscle. First, heart-protecting medications that slow the heart and reduce its need for blood should be administered to the patient, and second, these medications should also prevent new clots from forming in the coronary arteries. Thirdly, these medications should be the kind that would dissolve existing clots in the coronary arteries. And lastly, procedures that alleviate the underlying contraction of the artery should be followed these including procedures that rely on a catheter, which is a hollow, elastic tube that can be channeled through an artery (Buller et al., 2002). Catheter-based procedures may be applied to open narrowed or blocked arteries that deprive the heart and muscles of oxygen. A catheter is inserted under the influence of a local painkiller into the femoral artery or into the radial or brachial artery, and is then afterwards guided through the central arteries to the heart. Aside from the two suggested treatments, there are other catheter-based treatments advised. At the end of the procedure all equipment except the stent, which is a tube designed to be inserted into a vessel or passageway to keep it open, is afterwards removed (Buller et al., 2002). REFERENCES: Achar, S.A., S. Kundu and W. A. Norcross. 2005. Diagnosis of Acute Coronary Syndrome. http://www.aafp.org/afp/20050701/119.html.Date Accessed: September 7, 2007. Buller, C. E. and R. G. Carere. 2002. New advances in the management of acute coronary syndromes:The role of catheter-based procedures. CMAJ.166(1):51-61 Fenton, D. E. 2007. Acute Coronary Syndrome.   Ã‚  Ã‚   http://www.emedicine.com/emerg/topic31.htm..Date Accessed: Spetember 7, 2007. Fitchett, D., S. Goodman and A. Langer.   2001. New advances in the management of acute coronary syndromes: Matching treatment to risk. CMAJ. 164 (9): 1309-16 Gomersall, C. 2007. Acute Coronary Syndrome.  Ã‚  Ã‚   http://www.aic.cuhk.edu.hk/web8/coronary%20syn.htm. Date Accessed: September 7, 2007. Rentrop, K. P. 2000. Thrombi in Acute Coronary Syndromes : Revisited and Revised. Circulation.101:1619-1626.