Friday, March 29, 2019

Management Of Acute Coronary Syndrome

Management Of Acute Coronary SyndromeAcute coronary thrombosis thrombosis thrombosis syndrome encompasses a collection of three astute processes related to myocardial ischaemia. These complicate unstable angina pectoris, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). Myocardial ischaemia is caused by inadequate perfusion in spite of appearance the myocardial create from raw stuff due to oxygen shoot exceeding oxygen supply.In a healthy person the amount of oxygen required by the myocardium (O2 inquire) is refractory by heart rate, myocardial contractility, myocardial wall stress, and afterload. As explained by Antman, et al (2012), oxygen supply to the myocardium requires a satisfactory level of oxygen-carrying subject of the blood (determined by the inspired level of oxygen, pulmonary function, and hemoglobin parsimony and function) and an adequate level of coronary blood f diminished. The coronary vass have the qualif ication to adjust their level of resistance to adapt to the increase oxygen demand required by the myocardium during certain times (such as during forcible exertion).ischaemic heart disease is typically caused by atherosclerosis, which is a buildup of establishment inner(a) the lumen of the coronary vessels. The emergence of atherosclerosis in the vessels does non proceed everywherenight. Antman, et al. (2012) instal that atherogenesis in humans typically occurs over a purpose of m whatsoever years, usually many decades and that growth of atherosclerotic plaques probably does not occur in a smooth, linear fashion provided discontinuously, with periods of pro muckleal quiescence punctuated by periods of rapid evolution.The process of atherosclerosis begins with an abundance of lipoproteins in the blood stream. These lipoproteins bind to the walls of vessels and argon eventually deposited within the intima of the arteries. To counteract this process, phagocytes are sent in to the vessel to attack these foreign particles (Antman et al., 2012). Once the phagocytes are within the intima, they mature into macrophages and become lipid-laden foam kiosks (Antman et al., 2012). As these plaques advance calcification occurs. This process is scene to be a key step in the unionizeation of atherosclerotic plaques (Antman et al., 2012).Normally this narrowing of the vessel lumen does not cause tit inconvenience or discomfort. Eventually, however, these plaques whitethorn rupture. At this point platelet energizing occurs, which eventually pass ons to clot formation at the sight of the plaque. This clot, or thrombus, whitethorn break off and lodge in a coronary vessel. These ii processes are a usual pathogenic finding with sub sagacious coronary syndrome (Lincoff, Califf, Anderson, Weisman, Aguirre, Kleiman, Harrington Topol, 1997). A partial occlusion of the coronary vessels due to a ruptured plaque/platelet complex causes unstable angina or a NSTEMI. In this case, the oxygen demands of the heart gougenot be met. A complete occlusion causes a STEMI (Anderson, Adams, Antman, Bridges, Califf, Casey Jr, Chavey II Wright, 2011), which eventually leads to myocardial cell death.Discussion/AnalysisThe fatality department providers are oftentimes the first line of defense in the management of uncomplaining roles with titty ache. The ability to quickly assess whether or not the cause of authority pain is potentially fatal is of great importance. sarcastic toilet table pain foot be broken down in to non-cardiac and cardiac causes. Non-cardiac causes include pneumothorax, pulmonary embolism, and Boerhaaves syndrome. Acute coronary syndrome is among several cardiac causes of emergent breast pain.An accurate diagnosis of the cause of chest pain requires several key components. These include patient history (including put on the line factors), physical enquiry, diagnostics, and labs.HistoryHistory is instrumental during the evalu ation of a patient with chest pain. Ischemic chest pain is often described as a fearful pressure or squeezing and is genuinely described as the feeling of an elephant sitting on my chest. Typically this pain is described as substernal chest pain which radiates to the neck, jaw, or down the left arm. excess dilate regarding the onset of chest pain place in addition serve as Copernican clues. For example, pain on exertion that resolves with rest suggests stable angina, whereas modern onset chest pain or chest pain at rest suggests unstable angina. A good method to differentiate cardiac from non-cardiac chest pain is whether the pain improves after presidentship of nitroglycerin (NTG). If the pain is relieved by NTG it is considered to be likely due to cardiac causes. Additional details suggesting cardiac origin are shortness of breath, nausea +/- vomiting, diaphoresis, and the social movement of syncopal/near-syncopal episodes.It is main(prenominal) to note that a patient wi th chest pain often have a silent or atypical demonstration. This is specially received in elderly men (Woon Lim, 2003) and diabetics (Tabibiazar Edelman, 2003). A patient with an atypical presentation may present with shortness of breath but lack the classical symptom of angina pectoris which radiates to the jaw or left arm. Commonly these patients plain of a feeling of indigestion or epigastric discomfort. Thus it is truly important to consider ACS in these patients.The presence of try factors plays an important use in the evaluation of chest pain, especially in a patient with known disease. The landmark Framingham warmness Study showed that cardiac pretend can be influenced by diet, lifestyle, and familial risk factors (Oppenheimer, 2005). The much than risk factors that a person carries, the greater their risk of developing ischemic heart disease. These risk factors are generally grouped into two categories those that are modifiable and those that are not. Risk fact ors amendable are as followsTobacco smoke (American Heart Association, 2012)High blood cholesterol (AHA, 2012)High blood pressure (AHA, 2012) natural inactivity (AHA, 2012)Obesity and overweight (AHA, 2012)Diabetes mellitus (AHA, 2012)Risk factors that cannot be changed include develop- 82% of people who die of coronary heart disease are 65 (AHA, 2012) masculine sex (AHA, 2012)Heredity- this includes both family history and race (AHA, 2012)Risk is high among Mexican Americans, American Indians, native Hawaiians and some Asian Americans (AHA, 2012)Patients presenting with unstable angina or NSTEMI have variable levels of risk of cardiac death and ischemic cardiac events (Antman, Cohen, Bernink, McCabe, Horacek, Papuchis, Mautner Braunwald, 2000). The trial conducted by Antman et al. (2000) set out to develop a unanalyzable risk build that has broad applicability, is easily calculated at patient presentation, does not require a computer, and identifies patients with different resp onses to treatments for UA/NSTEMI. In doing so, the TIMI risk score was created. The scores are calculated exploitation a score of 1 for each risk factor (7 total categories) assigned to a wedded patient. According to Antman, et al (2000) the score determines the patients risk of death, myocardial infarction, or severe ischemia. Antman, et al. (2000) found 7 prognostic variables that increase a patients risk. These areAge 65 years or olderAt least 3 risk factors for coronary artery disease (male, dyslipidemia, smoking, hypertension, diabetes mellitus, obesity family history)Prior coronary stenosis of 50% or moreST-segment deviation on cardiogram at presentationAt least 2 anginal events in prior 24 hoursUse of aspirin in prior 7 daysElevated serum cardiac markersIn TIMI 11B/ESSENCE, event range increase significantly as the TIMI-score increases (Antman et al., 2000). A score of 0/1 showed a 4.7% event rate 8.3% for 2 13.2% for 3 19.9% for 4 26.2% for 5 and 40.9% for 6/7. This lan dmark pair of trials allows practitioners a quick assessment of a patients risk of suffering a serious cardiac event.Physical interrogationPhysical exam is also a key component in the evaluation of a patient with chest pain, as many clues can suggest acute coronary syndrome. Unstable vital signs can be an important hint that the patient has suffered an MI. A general examination may reveal a patient who is diaphoretic and/or using appurtenance respiratory muscles. The cardiovascular exam could reveal a new murmur, S3/S4 gallop, or JVD. Finally, during the pulmonary exam rales may be heard upon auscultation. diagnosticsDiagnostic testing is an essential part of the evaluation of a patient presenting with chest pain. Several important diagnostic utensils were introduced to the emergency department in the last mentioned half of the 20th century that greatly improved the diagnosis and explosive charge of acute coronary syndrome.ElectrocardiogramThe introduction of coronary worry un its in the 1960s allows physicians to utilize the cardiogram ( electrocardiogram) to monitor potential fatal arrhythmias in patients with acute myocardial infarction (Julian, 1987). Shortly thereafter the portable electrocardiogram became commonplace within the emergency department to assist in name complications of acute coronary syndrome (Drew, et al, 2004). A patient presenting with myocardial ischemia allow for typically have symmetrically-inverted T waves in leads V2-V6 (Dubin, 2000). As the name suggests, a STEMI is an ST-segment elevation myocardial infarction, though ST-segment elevation can occur with Prinzmetals angina in absence of an infarction (Dubin, 2000). Additionally, the ECG allows us to evaluate chagrin of the heart in the form of the presence of Q-waves. Q-waves are the first downward deflection of the QRS complex (Dubin, 2000). As Dubin (2000) explains, a positive Q-wave MI mustinessLack a preceding spike in the QRS complexBe at least 1 mm wideor make an am plitude of 1/3 the QRS complexAn additional benefit of the ECG is that it allows the practitioner to identify the location of an acute event. Each lead corresponds to a particular location of the heart. For example, leads II, III, and AvF are the inferior leads and reflect the inferior portion of the heart.Due to the relatively high particularity but low sensitivity of the 12 lead ECG in diagnosis of acute coronary syndrome, a group of researchers in Canada recently set out to enhance ischemia detective work by conducted a trial which added a new criteria using a three vessel specific leads derived from the traditional 12 lead ECG (Horacek, Mirmoghisi, Warren, Wagner Wang, 2008). This trial showed a statistically significant improvement in the ability of the vessel specific lead protocol to detect ischemia (Horacek et al., 2008). Horacek et al. (2008) found the following sensitivity and specificity for conventional STEMI criteria versus that of the vessel specific leads (VSL) vasS ensitivitySpecificityLeft Anterior Descending74% conventional, 91% VSL97% conventional, 97% VSLRight Coronary Artery60% conventional, 70% VSL94% conventional, 94% VSLLeft Circumflex Artery36% conventional, 71% VSL deoxycytidine monophosphate% conventional, 100% VSLTotals Set60% conventional, 76% VSL96% conventional, 96% VSLBased on these results, Horacek et al. (2008) concluded that using vessel specific leads can identify acute ischemia better than existing STEMI criteria. While a STEMI criteria using vessel specific leads has yet to become a main cling within the stock emergency room protocol, this probe provides exciting new improvements in the detecting and management of patients with ACS.Serum BiomarkersThe use of biochemical markers to detect cardiac cell death significantly evolved in the 1980s and 1990s. Initially, nonspecific markers such as aspartate transaminase and total creatinine kinase were used to detect myocardial necrosis (Lewandrowski, subgenus Chen Januzzi, 2 002). During the mid-1990s the more cardiac specific enzymes CK-MB became the gold trite for detection of myocardial injury (Lewandrowski et al., 2002). CK-MB, which ordinarily rises 4-9 hours after the onset of angina, was not without its shortcomings. CK-MB may be falsely elevated due to several different causes, including recent backbreaking exercise or skeletal muscle damage, or renal bereavement (Vivekanandan Swaminathan, 2010). In the late 1990s a more predictable biomarker, troponin I, was introduced for more accurate detection of acute coronary syndrome (Heeschen, Goldmann, Moeller Hamm, 1998). According to Heeschen et al. (1998), Troponin I can be evaluated at the bedside in the emergency room and has a higher diagnostic sensitivity for the detection of acute myocardial infarction (60% vs 48%) when compared to CK-MB. The reason for this improvement in accuracy is that troponin I is not found in skeletal muscle tissue or renal distress (Heeschen et al., 1998). As Hees chen et al. (1998) demonstrated in a head to head study that cTnI test systems produced no positive results in patients with end-stage renal failure and acute or chronic skeletal muscle injury, whereas 30% and 71% of the patients, respectively, had increased CK-MB mass c one timentrations. One disadvantage of troponin I, however, is that it has a refuse sensitivity for the detection of acute myocardial infarction compared to that of CK-MB (Heeschen et al., 1998). This is due to an increased level of cTnI in patients with unstable angina (Heeschen et al., 1998). For this reason, a typical workup for a patient with chest pain in the emergency room includes both cTnI and CK-MB assays, which are draw at presentation and every 3-6 hours thereafter (Ross, Bever, Uddin Hockman, 2000).ImagingA common component of a chest pain protocol is a chest x-ray. This is normally either a standard AP/lateral series or a portable chest x-ray if the patient is unable to go about out of bed. The ches t x-ray is useful to eliminate other feasible causes of chest pain, such as an aortic aneurism or a pneumothorax.Contrast-enhanced computed tomographic angiography, or CTA, has become an integral part of the management of acute coronary syndrome due to its high sensitivity and specificity (Hoffman, Truong, Schoenfeld, Chou, Woodard, Nagurney, Pope Udelson, 2012). According to the ROMICAT-I study performed by Hoffman et al., (2012), CTA is an effective way to rule out myocardial infarction or ischemia as well as major cardiovascular events over the beside 2 years from presentation. The data presented in ROMICAT-I showed that patients undergoing CTA decreased their infirmary stay by 7.6 hours compared to standard therapy (Hoffman et al., 2012). Additionally, 50% of CTA patients were discharged from the hospital within 8.6 hours of presentation versus only 10% of patients undergoing standard therapy (Hoffman et al., 2012). Finally, the mean time to diagnosis was significantly decrea sed with the CT group versus the standard group (Hoffman et al., 2012). Overall, CTA was shown to fasten time spent in the hospital and time to diagnosis when compared to standard therapy for acute coronary syndrome. This is important to note considering the importance of quick coronary reperfusion of STEMI patients (Trost Lange, 2011). An additional observation was that these benefits were achieved without an increase in the cost of care (Hoffman et al., 2012). at that place was no overall difference between the groups in incidence of myocardial infarction 30 days after initial presentation (Hoffman et al., 2012). It is important to note that a patient undergoing a CTA is exposed to increased radiation. Additionally, patients undergoing CTA were more likely to undergo invasive coronary procedures when compared to standard evaluation.Based on this data, a question arises as to whether every patient presenting with possible acute coronary syndrome should undergo a CTA. The populati on studied in ROMICAT-I consisted of low to intermediate risk patients. Overall, CTA was shown to decrease the time to diagnosis and hospital stay for patients with possible ACS. In contrast, CTA increases a patients exposure to radiation and increases the likelihood that these patients go away undergo an increase in invasive coronary procedures. These factors should all be considered when evaluating a patient presenting with chest pain.TreatmentPharmacologicAspirin proto(prenominal) aggressive aspirin (ASA) therapy (162-325mg followed by 81-162mg daily) is currently recommended for all patients with acute coronary syndrome, unless contraindicated (Kirk, Kontos Diercks, 2011).Plavix (Clopidogrel) According to the CURE trial Clopidogrel has been shown to provide a 20% reduction in cardiovascular death, MI, or stroke for NSTEMI patients with positive biomarkers or ischemic ECG changes (Kirk et al., 2011). It is important to note that the significant anti-platelet benefits of Clopid ogrel administration should also be weighed against the increased risk of bleeding events if the patient may be a candidate for coronary artery bypass surgery.Antianginal AgentsNitroglycerin (NTG) NTG is commonly administered by EMS respondents but can also be ordered once the patient arrives in the emergency department, typically sublingually or in the form of Nitro awaye. Nitroglycerin dilates the coronary arteries, which reduces myocardial oxygen demand (Trost Lange, 2011). For this reason, it is important to evaluate the patients baseline blood pressure. If SBP is less than 100, caution should be used.Morphine endovenous morphine may be given in the event that chest pain is not relieved by NTG administration. Morphine reduces ventricular preload, thereby decreasing myocardial O2 demand (Trost Lange, 2011).Beta-Andrenergic Blockers Beta-blockers decrease demand on the heart by decreasing heart rate, blood pressure, and myocardial contractility (Trost Lange, 2011). In a patient presenting with ACS, IV Lopressor is typically the agent of choice. These are especially effective agents in patients with elevated blood pressure or tachycardia. It is important to evaluate relevant contraindications to beta-blocker therapy, such as HRCalcium-Channel Blockers Diltiazem and verapamil improve cardiac O2 supply by vasodilation of the coronary vessels, reduce O2 demand by reducing afterload, and reduce heart rate and contractility (Trost Lange, 2011). Calcium-channel blockers are second line treatments for ACS and are typically reserved for patients who are unable to call back a beta-blocker (Trost Lange, 2011). Contraindications include sick sinus syndrome, 2 or 3 AV heart block, hypotension, acute MI with pulmonary congestion, atrial fibrillation or flutter with accessory bypass tract, and ventricular tachycardia, severe left ventricular dysfunction, and cardiogenic shock (Epocrates, 2012).Antithrombotic therapy Antithrombotic therapy is recommended in a patient with suspected ACS, unless contraindicated (Trost Lange, 2011).Unfractionated heparin is unproblematic to administer (IV) and is apace reversible with protamine in the event of bleeding. (Trost Lange, 2011). As with any antithrombotic, there is a risk of bleeding so these patients require blotto monitoring.Low molecular weight heparin is more predictable, has a lower incidence of thrombocytopenia, and does not require monitoring (Trost Lange, 2011). LMWH is the preferred agent for a more conservative, ischemia-guided strategy to prevent in hospital death or myocardial infarction (Trost Lange, 2011).Bivalirudin is an antithrombotic agent that does not cause thrombocytopenia (Trost Lange, 2011). It has been shown to be equally as effective as unfractionated heparin or LMWH but with a significantly lower rate of bleeding (Trost Lange, 2011).Oxygen administration should be administered for patients who are short of breath, showing signs of shock, or O2 saturation nigh Step for NSTEMI or Unstable Angina PatientsIf a patient is considered to be high risk, such as a patient is at risk of future ischemia or infarction, an early invasive strategy is recommended (Trost Lange, 2011). For these patients, cardiac catheterization should be performed within 24-48 hours of admission (Trost Lange, 2011). In a low risk patient, a more conservative treatment is typically recommended. For these patients, catheterization is only recommended if repeated or provocable ischemia occurs (Trost Lange, 2011). TIMI scores are a valuable tool to assess the patients risk and to guide the practitioner on the appropriate next step.Next Step for STEMI PatientsPrompt coronary reperfusion is paramount in patients presenting with STEMI (Trost Lange, 2011). A door-to-balloon time of less than 90 minutes is considered to be the goal (Trost Lange, 2011). If the patient presents to a adeptness without a percutaneous coronary intervention facility the patient should be eitherTreated wi th fibrinolytic therapy if not contraindicated (Trost Lange, 2011)OrTransferred to a nearby PCI facility (Trost Lange, 2011).ConclusionAcute coronary syndrome is spectrum of diseases typically caused by atherosclerotic disease. Emergency department practitioners must be able to rapidly diagnose and manage ACS patients in order to potentially preserve singular heart muscle. While treatments for ACS have improved dramatically over the past 30 years, several recent innovations have brought upon exciting new possibilities for the care of these patients. These include new vessel specific ECG leads, cardiac specific biomarkers, and the use of computed-tomographic angiography to assess patients with possible ACS.One component of the management algorithmic rule that has not changed is the need for a strong history and physical examination to aid in diagnosis. Urgency in obtaining diagnosis cannot be disturbed enough, and patients presenting with STEMI should be rapidly sent for PCI or transferred to a facility with PCI capabilities.

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