My Algo<\/a><\/p>\n ST depression more than 0.1 mV measured 80 milliseconds from the J point<\/p>\n The true Left Ventricular Anatomy (Clinical Anatomy 22:77\u201384 (2009)<\/a>)<\/p>\n Get ekg within 10 minutes.\u00a0 2 sets biomarkers, last at least 8 hours from sx.\u00a0 If presenting in less than 6 hours of symptoms, get myoglobin.<\/p>\n <\/p>\n Most recent article again shows signs and symptoms not helpful (Resus 2010;81:281<\/a>)<\/p>\n <\/p>\n Nature of Sx, History of CAD, Sex, Age, # of traditional risk factors<\/p>\n HTN, increased chol., cigarettes (not so important, only prognostic), Diabetes (true risk)<\/p>\n Inquire about cocaine use in all patients<\/p>\n <\/p>\n Multicenter chest pain study:\u00a0 22% had sharp, stabbing pain, 13% had pleuritic, 7% had reproducible pain (Arch Int Med 1985;145:65-69)<\/p>\n <\/p>\n response to nitroglycerin has no diagnostic role (Am J Card 90:1264, December 1, 2002)<\/p>\n It has a sensitivity of 35% and specificity of 59% (Gibbons RJ\u00a0 Nitroglycerin: Should We Still Ask? Ann Intern Med. 2003;139:1036-1037 and 979 Henrikson)<\/p>\n <\/p>\n Neither does response to antacids (Emerg Med J BETs 20:169, March 2003)<\/p>\n <\/p>\n Spontaneous coronary artery dissection remains an unusual cause of acute coronary syndrome. It should be included in the differential diagnosis of acute myocardial infarction, especially when it affects young, healthy females<\/p>\n <\/p>\n Chest pain of unknown origin:\u00a0 if patient has abnormal ekg, diabetes, or CAD they have a high rate of adverse events (Annals EM 2004;43:1,p.59)<\/p>\n <\/p>\n Goldman Low risk patients have no need of telemetry monitoring (Annals EM 2004;43:1,p.71)<\/p>\n <\/p>\n Retrospective study of confirmed MIs:\u00a0 47% did not present with chest pain, Women and older patients more likely to present without chest pain. (Ann Emerg Med 40(2):180, 2002)<\/p>\n <\/p>\n HIV is an independent risk factor treatment; with protease inhibitors is also an independent risk factor for MI (NEJM 2003 Nov 20; 349)<\/p>\n Lupus accelerates atherosclerosis by about 20 years<\/p>\n 50 x the ACS risk as age matched controls from the Framingham study (Review Am J Emerg Med 2005;23:696)<\/p>\n (1) Mattu A, et al. Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus Am J Emerg Med<\/em> 2005 Sep;23(5):696-703.(2) Karrar A, et al. Coronary artery disease in systemic lupus erythematosus: A review of the literature Semin Arthritis Rheum<\/em> 2001;30(6):436-43.(3) Mehta PK, et al. Acute coronary syndrome as a first presentation of systemic lupus erythematosus in a teenager: revascularization by hybrid coronary artery bypass graft surgery and percutaneous coronary intervention: case report Pediatr Cardiol<\/em> 2008;29(5):957-61.(4) Korkmaz C, et al. Myocardial infarction in young patients (< or =35 years of age) with systemic lupus erythematosus: a case report and clinical analysis of the literature Lupus<\/em> 2007;16(4):289-97.<\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n Conventional Risk Factors:\u00a0 At least one, but not necessarily more than one risk factor was present in ~85% of women and 80% of men.\u00a0 Meaning up to 1\/5 had no risk factors. (JAMA 290 (7):891-898, Aug 2003)<\/p>\n <\/p>\n Diabetes should no longer be considered a risk factor but instead an equivalent to known CAD (Heart 2005;91(3):388)<\/p>\n <\/p>\n GERD symptoms should make you rather than less concerned, a suprising number of MIs were probably initiated by reflux attacks (In J Cardiol 2005;99(1):1-8) (In j Cardiol 2005;104(1):67)<\/p>\n <\/p>\n <\/p>\n AMI Odds ratio (CI) <\/strong> ACS Odds ratio (CI) <\/strong> \u00a0 \u00a0 \u00a0 Clinical feature <\/strong>\u00a0 \u00a0 Chest pain radiation \u00a0 \u00a0 Left arm 1.5 (0.6-4.0) 1.7 (0.9-3.1) Right arm 3.2 (0.4-27.4) 2.5 (0.5-11.9) Both left and right arm 7.7 (2.7-21.9) 6.0 (2.8-12.8) Nausea or vomiting 1.8 (0.9-3.6) 1.0 (0.6-1.7) Diaphoresis 1.4 (0.7-2.9) 1.2 (0.8-1.9) Exertional pain 3.1 (1.5-6.4) 2.5 (1.5-4.2) Burning\/indigestion pain 4.0 (0.8-20.1) 1.5 (0.5-4.5) Crushing\/squeezing pain 2.1 (0.4-10.9) 0.9 (0.4-2.9) Relief with nitroglycerin 0.9 (0.1-6.5) 2.0 (0.6-4.9) Pleuritic pain 0.5 (0.1-2.5) 0.5 (0.2-1.3) Tender chest wall 0.2 (0.1-1.0) 0.6 (0.3-1.2) Sharp \/stabbing pain 0.5 (0.1-2.8) 0.8 (0.3-2.1)<\/p>\n Source: Goodacre S, Locker T, Morris F, et al. How useful are clinical features in the diagnosis of acute, undifferentiated chest pain? Acad Emerg Med <\/em>2002 Mar;9(3):203-208.<\/p>\n No historical descriptors were good enough to rule out chest pain (JAMA. 2005 Nov 23;294(20):2623-9.)<\/p>\n <\/p>\n A prospective study of 796 ED patients with suspected cardiac chest pain assessed the value of individual historical and examination findings for diagnosing acute myocardial infarction (AMI) and the occurrence of adverse events (death, AMI or urgent revascularization) within 6 months. AMI was diagnosed in 148 (18.6%) of the 796 patients recruited.The results may surprise some physicians:Sweating observed by the ED physician was the strongest predictor of AMI (adjusted OR 5.18, 95% CI 3.02\u00968.86).Reported vomiting was also a fairly strong predictor of AMI (adjusted OR 3.50, 1.81\u00966.77).Pain located in the left anterior chest was found to be the strongest negative predictor of AMI (adjusted OR 0.25, 0.14\u00960.46). Patients who described the pain as being the same as previous myocardial ischaemia were significantly less likely to be having AMI!Following adjustment for age, sex and ECG changes, the following characteristics made AMI more likely (adjusted odds ratio, 95% confidence intervals):* pain radiating to the right arm (2.23, 1.24-4.00)* pain radiating to both arms (2.69, 1.36-5.36)* vomiting reported (3.50, 1.81-6.77), central chest pain (3.29, 1.94-5.61)* sweating observed by physician (5.18, 3.02-8.86) Pain in the left anterior chest made AMI significantly less likely (0.25, 0.14-0.46)The presence of rest pain (0.67, 0.41-1.10) or pain radiating to the left arm (1.36, 0.89-2.09) did not significantly alter the probability of AMI.Compare these results with the American Heart Association guidelines which state that \u0093chest or left arm pain or discomfort as the chief symptom reproducing prior documented angina\u0094 is associated with a high likelihood of ACS, or the European Society of Cardiology guidelines which state that \u0093the typical clinical presentation of NSTE-ACS is retrosternal pressure or heaviness radiating to the left arm, neck or jaw\u0094, which the authors of this study point out are statements made based on expert opinion for which references are not given.The authors summarise with a powerful message: \u0091Several \u0091atypical\u0092 symptoms actually render AMI more likely, whereas many \u0091typical\u0092 symptoms that are often considered to identify high-risk populations have no diagnostic value.\u0092The value of symptoms and signs in the emergent diagnosis of acute coronary syndromesResuscitation. 2010 Mar;81(3):281-6<\/p>\n Pathophys of ACS is not the large clots, but the small clots that tend to cause MI (Tiong AY, Am Heart J 2005; Hannson GK, NEJM 2005; Libby P Circulation 2005)<\/p>\n systemic inflammation plays a huge role<\/p>\n HS-CRP<\/p>\n lupus is a huge risk factor (<\/p>\n HIV (10 years younger), RA, Chronic Kidney Disease, chronic cocaine use as well<\/p>\n plaque composition is most important fibrous cap, lipid core, and lipid core composition<\/p>\n <\/p>\n <\/p>\n <\/p>\n 58% SOB<\/p>\n weakness<\/p>\n Only 20% had chest pain on presentation<\/p>\n (Circulation 108:2619, Nov 25, 2003)<\/p>\n <\/p>\n <\/p>\n Age>65 Male sex DM Smoking FH HTN High Chol<\/strong><\/p>\n <\/p>\n DM as independent Cocaine\/Meth HIV CRI SLE<\/strong><\/p>\n 3 0r more of seven variables predicts increased risk of death or MI<\/strong>(JAMA 2000; 284, p. 835)<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Age>65<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 3 or more Traditional Risk Factors (HTN, DM, Hyperchol, FH, Smoking)<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Known coronary stenosis of 50% or greater<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 ST-segment deviation on ECG<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 2 or more anginal events in past 24 hours<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 ASA use during past week<\/p>\n \u00b7\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Elevated Cardiac Enzymes<\/p>\n <\/p>\n Can be used for risk stratification (Acad Emerg Med 2006;13(1):13)<\/p>\n <\/p>\n TIMI Score Rate of death, MI, revascularization at 30 days 0 2.1 % (1.4-2.8) 1 5% (3.8-6.2) 2 10% (7.8-12.4)<\/p>\n <\/p>\n of interest, the odds ratio for the 2 or more anginal events in past 24 hrs was 0.95, while all the others were > 1.9<\/p>\n —-<\/p>\n In another study (Ann Emerg Med 2006;48:252)<\/p>\n TIMI Score Rate of death, MI, revascularization at 30 days 0 1.7 % (0.42-2.95) 1 8.2% (5.27-11.04) 2 8.6% (5.02-12.08)<\/p>\n in this study, age>65 fell out.<\/p>\n <\/p>\n meta-analysis shows accuracy, none is sig. lowerer of post-test (CMAJ 2010;182(10):1039)<\/p>\n <\/p>\n timi-risk-index lancet 358-9293-2001-1571<\/p>\n http:\/\/www.heartscore.nl\/en\/<\/a><\/p>\n “A prospective validation of the HEART score for chest pain patients at the emergency department” 2 sets of enzymes, no TIMI critieria, negative ekgs, can send the patient home. 3582 patients, 30 day f\/u. 99.3% sensitivity and 11% specificity.<\/p>\n Actual Study<\/a><\/p>\n 2.5% risk of 30 day events<\/p>\n (Medicine 2009;88(5):307)<\/p>\n <\/p>\n <\/p>\n 53% have chest pain, less and less with age or female sex.\u00a0 SOB in 17%, ABD Pain 2%.<\/p>\n Weak and dizzy is a common presentation for elderly AMI (<\/p>\n Ann Emerg Med 40(2):180, 2002)<\/p>\n <\/p>\n Pts c negative inpatient w\/u for ACS with CP 6 months later 11% risk of adverse events (Academic EM 2002:9, p.896-902)<\/p>\n <\/p>\n JAMA Rational Clinical Exam for MI (JAMA Oct 14, 1998 280:14)<\/p>\n <\/p>\n <\/p>\n Meta-analysis showed little utility to signs & symptoms (British Journal of General Practice, <\/strong> February 2008)<\/em><\/p>\n <\/p>\n Prospective study of 1200 patients.\u00a0 In the group who had stress tests, MI occurred subsequently in 0.9% while those with no imaging had 2.1% MI rate.\u00a0 Rate of death at 3 months was 0.4% in stress group and 3% in those without imaging. (Am J Card 2003, 91:1410)<\/p>\n <\/p>\n Most recent trial by Cullen et al. used 2 hour high-sensitivity troponin protocol and got many patients out (JACC\u00a02013;62(14):1243)<\/p>\n <\/p>\n and<\/p>\n Emergency Medicine Australasia (2013) 25, 416\u2013421<\/p>\n A 2-Hour Diagnostic Protocol for Possible Cardiac Chest Pain in the Emergency DepartmentA Randomized Clinical Trial ONLINE FIRST M JAMA Intern Med. Published online October 07, 2013. doi:10.1001\/jamainternmed.2013.11362 Text Size: A A A<\/p>\n Negative stress is presumed to clear a patient for 1 1\/2 years, 1 year in diabetics, but no proof in ED pop.<\/p>\n <\/p>\n Conclusion: Among patients presenting with chest pain to the ED and a history of stress testing within the past 2 years, a normal stress test result was associated with a markedly reduced risk of having a major cardiac endpoint. absolute risk of 7% for death within 30 days or MI.<\/p>\n 9 (2.0%, 95% CI 1.1% to 3.8%) had death or MI if normal biomarkers and non-specific ekg<\/p>\n (Annals EM Supplement 44:4 OCTOBER 2004)<\/p>\n Full adult dose, if contraindication give clopidogrel (Plavix, an adp antagonist-300 mg followed by 75 mg per day, contraindication to CABG, so do not give if possibility)<\/p>\n <\/p>\n Caprie and CURE trials prove plavix superior to ASA, in post-MI period (Always use if pt gets a stent)<\/p>\n All patients admitted for r\/o mi without planned intervention should have plavix started<\/p>\n If patient has history of GI bleeding, aspirin plus a PPI is actually safer than Plavix in terms of bleeding side effects in one well-done RCT (NEJM 2005;352:38)<\/p>\n CURE (Circulation. 2002;106:1622)<\/p>\n PCI-CURE (Lancet 2001;358:527)<\/p>\n CREDO (J Am Coll Cardiology 2005;46(5):761)<\/p>\n Review of CURE (Can J Clin Pharmacol Vol 11(1) Spring 2004:e156-e167)<\/p>\n The role of clopidogrel in the emergency department CJEM 2005;7(1)<\/p>\n Building evidence for early initiation of clopidogrel loading in non\u0096ST-segment elevation acute coronary syndromes (Annals of Emergency Medicine\u00a0 2004;43(5):666-668)<\/p>\n <\/p>\n Shortcut Review shows we should give it (Emerg Med J 2006;23:140)<\/p>\n oral then IV, increase dose until relief of sx or BP change.\u00a0 (Not in \u00a024 hrs of Viagra use)<\/p>\n Response to nitro is not sensitive or specific for ACS (Am J Card 90:1264, December 1, 2002)<\/p>\n NTG is contraindicated after use of sildenafil within the previous 24 hours or tadalafil within 48 hours (Circulation, 8\/14\/07, pg. e186)<\/p>\n if still in pain after nitrites, this used to be used. Now, not considered such a great idea. The CRUSADE trial suggest increased mortality, perhaps b\/c it masks recurrent pain (AM Heart J 2005;149:1043)<\/p>\n Consider even in non-cocaine chest pain )Journal of Emergency Medicine Volume 25, Issue 4 , November 2003, Pages 427-437)<\/p>\n Commit trial probably tells us not to use IV b-blocker in the ED, and probably defer oral until pt stabilizes<\/p>\n <\/p>\n 5 mg IV x 3, then 50 mg PO Q6 shooting for HR<80<\/p>\n Absolute Contraindications:<\/p>\n Marked first-degree AV block (i.e., ECG PR interval [PR] of greater than 0.24 s), any form of second- or third-degree AV block in the absence of a functioning pacemaker, a history of asthma, or severe LV dysfunction with CHF<\/p>\n Relative:<\/p>\n Significant sinus bradycardia (heart rate less than 50 bpm), COPD or hypotension (systolic blood pressure less than 90 mm Hg)<\/p>\n if COPD or another relative contraindication.<\/p>\n 0.1 mg\/kg\/ min with titration in increments of 0.05 mg \u00b7 kg-1 \u00b7 min-1 every 10 to 15 min as tolerated by the patient’s blood pressure until the desired therapeutic response has been obtained, limiting symptoms develop, or a dosage of 0.3 mg \u00b7 kg-1 \u00b7 min-1 is reached. A loading dose of 0.5 mg per kg may be given by slow intravenous administration (2 to 5 min) for a more rapid onset of action.<\/p>\n <\/p>\n B-blockers work by decreasing risk of V. Fib not by controlling heart rate. Give all patients B-blockers except if contraindications<\/p>\n <\/p>\n b-blockers worsen FEV1 and airway hyperresponsiveness in asthma, can also have detrimental effects in COPD (Chest 2005;127(3):818)<\/p>\n <\/p>\n <\/p>\n if beta-blockers contraindicated and no LV dysfunction<\/p>\n in persistent HTN in diabetics, CHF, or LV dysfunction<\/p>\n Give to all ACS pts unless elevated Creatinine<\/p>\n s<\/p>\n All ACS, lipitor if ____ elevated\u00a0 ???, otherwise any statin (ie. Pravachol)<\/p>\n MIRACLE: study-lipid lowering in 24 hrs post-mi<\/p>\n CK\/MB-also from trauma, rhabdomyolysis, hyperthermia.\u00a0 Peak @13, stay 72 hours<\/p>\n Myoglobin 1-4 hours, peaks at 6, stays 24<\/p>\n Troponin seen at 3 hours, peaks at 12-24 hours, stays 1 week<\/p>\n <\/p>\n Troponin levels reflect increased risk death\/MI regardless of renal dysfunction (N Engl J Med<\/em>2002; 346:2047-2052)<\/p>\n Troponin I>0.8 is ischemic in nature<\/p>\n (Acad Emerg Med 2004 11: 979-981)<\/p>\n <\/p>\n (1) Jeremias A, Gibson CM. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. Ann Intern Med 2005;142: 786-91.<\/p>\n <\/p>\n <\/p>\n Myeloperoxidase as new marker (Brennan ML, et al. Prognostic value of myeloperoxidase in patients with chest pain. N Engl J Med<\/em> 2003;349: 1595-1604.)<\/p>\n <\/p>\n CRP as a new Marker?<\/p>\n <\/p>\n One set of markers is not acceptable even if the chest pain has been going on for a while (Can J Emerg Med 4(5):322, September 2002)<\/p>\n <\/p>\n low level troponin I elevations (1-3.0) ARI of 7% compared to Trop<1.0 in patients with suspected ACS HR of 3.4 (Am Heart J 2004;148(5):776)<\/p>\n <\/p>\n PREVALENCE OF ELEVATED TROPONIN I IN END-STAGE RENAL DISEASE PATIENTS RECEIVING HEMODIALYSIS Click here to hear the Reviewer’s comments via MP3.Donnino, M.W., et al, Acad Emerg Med 11:979, September 2004 BACKGROUND: Patients with end-stage renal disease (ESRD) have high rates of atherosclerotic heart disease. In this population, coronary artery disease is the primary cause of death in 45-50%. Some studies have reported false-positive elevation of markers for acute myocardial infarction (AMI) in ESRD patients. Cardiac troponin I (cTnI) has been reported to be specific for cardiac muscle, and is excreted by the kidneys. Although studies have reported false-positive elevation of cTnI in up to 21% of patients with ESRD, several of these studies included patients with acute illnesses that might be associated with cTnI elevation. METHODS: The authors, from Henry Ford Hospital in Detroit, measured pre- and post- dialysis cTnI in 113 ESRD patients aged 26-92 with no symptoms of acute coronary syndrome who presented for maintenance dialysis. A cTnI above 0.8ng\/dL was considered to be elevated. RESULTS: Nearly all of the patients (94.5%) had hypertension and just over half (53.2%) were diabetic. No patient had a cTnI level positive for AMI either before or after dialysis. Predialysis levels ranged between 0-0.7ng\/dL (mean, 0.13ng\/dL), and postdialysis levels ranged between 0-0.5ng\/dL (mean, 0.11ng\/dL). CONCLUSIONS: These findings suggest that cardiac troponin I is a reliable marker of myocardial injury in patients with ESRD on chronic dialysis. 11 references (mdonnino@aol.com<\/a>)<\/p>\n <\/p>\n Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.Emerg Med Australas. 2011 Apr;23(2):181-5<\/a><\/p>\n <\/p>\n <\/p>\n Acute Coronary Syndrome vs Nonspecific Troponin Elevation (Arch Intern Med. 2007;167:276-281. )<\/p>\n <\/p>\n Heterophile antibodies Human anti-mouse antibodies Autoantibodies Fibrin clots Rheumatoid factor Microparticles in specimen Interference by endogenous components in blood (bilirubin, hemoglobin, lipemia) High concentration of alkaline phosphatase Immunocomplex formation Analyzer malfunction<\/p>\n <\/p>\n <\/p><\/blockquote>\n an elevation of either in the absence of the other was associated with a higher risk of ACS<\/p>\n (Ann Emerg Med 2006;48(6):660)<\/p>\n http:\/\/www.acc.org\/clinical\/guidelines\/unstable\/unstable.pdf<\/p>\n Feature<\/p>\n High Likelihood<\/p>\n (At least 1)<\/p>\n Intermediate Likelihood<\/p>\n (No High, and at least 1)<\/p>\n Low Likelihood<\/p>\n (No High or inter. Risk)<\/p>\n History<\/p>\n Chest or left arm pain or discomfort as chief symptom reproducing prior documented angina<\/p>\n <\/p>\n Known history of CAD, including MI<\/p>\n Chest or left arm pain or discomfort as chief symptom<\/p>\n Age>70<\/p>\n Male sex<\/p>\n DM<\/p>\n <\/p>\n Probable ischemic symptoms in absence of any of the intermediate likelihood characteristics<\/p>\n <\/p>\n Recent Cocaine Use<\/p>\n Exam<\/p>\n Pulmonary Edema<\/p>\n Transient MR murmur<\/p>\n Rales<\/p>\n Hypotension<\/p>\n Diaphoresis<\/p>\n Extracardiac Vascular Disease<\/p>\n Chest Discomfort reproduced by palpation<\/p>\n EKG<\/p>\n New or presumably new ST seg changes >.05 mV<\/p>\n or<\/p>\n T wave inversions >.2 mV<\/p>\n with symptoms<\/p>\n Fixed Qs<\/p>\n Old abnormal st segments or T waves<\/p>\n T-wave flattening or inversion in leads with dominant R waves<\/p>\n Normal EKG<\/p>\n Cardiac Markers<\/p>\n Elevated Troponin<\/p>\n Normal<\/p>\n Normal<\/p>\n <\/p>\n <\/p>\n Feature<\/p>\n High Risk<\/p>\n (At least 1)<\/p>\n Intermediate Risk<\/p>\n (No High, and at least 1)<\/p>\n Low Risk<\/p>\n (No High or inter. Risk)<\/p>\n History<\/p>\n Accelerating Tempo of Ischemic Sx<\/p>\n Prior MI or CAD, CVA, PVD<\/p>\n <\/p>\n Pain<\/p>\n Prolonged (>20 min), ongoing rest pain<\/p>\n Prolonged rest pain, now resolved<\/p>\n Anginal Sx in past 2 weeks, s rest pain>20 min<\/p>\n Clinical Findings<\/p>\n Pulmonary Edema<\/p>\n Worsening MR murmur<\/p>\n S3<\/p>\n Hypotension, tachycardia, bradycardia<\/p>\n Age>75 y\/o<\/p>\n Age>70<\/p>\n <\/p>\n EKG<\/p>\n Angina at Rest with transient ST seg changes >.05 mV<\/p>\n BBB, new or presumed new<\/p>\n Sustained VT<\/p>\n T wave inversions >.2 mV<\/p>\n Pathological Qs<\/p>\n Normal EKG during chest discomfort<\/p>\n Cardiac Markers<\/p>\n Elevated Troponin (>.1)<\/p>\n Gray Zone Troponin<\/p>\n Normal<\/p>\n <\/p>\n <\/p>\n in derivation, right now (Annals Emerg Med 2006;47(1):1)<\/p>\n All intermediate and high risk ACS<\/p>\n UFH:\u00a0 60 U\/kg loading and then 12 U\/kg\/hr<\/p>\n Use lovenox unless CABG planned in 24 hours or elevated Creatinine<\/p>\n Lovenox:\u00a0 1 mg\/kg q 12 (Bolus 30 mg IV if STEMI)<\/p>\n 2002 guidelines specifically recommend lovenox, heparinization is now Ia<\/p>\n LMH-preferentially bind Xa with decreased effect on platelets<\/p>\n ESSENCE trial supports lovenox over UFH<\/p>\n Not for anticoagulation of mech. Valves (not approved)<\/p>\n Can use during PCI (Am Heart J 144:615 2002)<\/p>\n Same cost as UFH (West J Med 173:138, August 2000)<\/p>\n <\/p>\n safe in PCI<\/p>\n Enoxaparin versus Unfractionated Heparin in Elective Percutaneous Coronary Intervention<\/p>\n Conclusions In elective PCI, a single intravenous bolus of 0.5 mg of enoxaparin per kilogram is associated with reduced rates of bleeding, and a dose of 0.75 mg per kilogram yields rates similar to those for unfractionated heparin, with more predictable anticoagulation levels. Target anticoagulation levels were reached in significantly more patients who received enoxaparin (0.5-mg-per-kilogram dose, 79%; 0.75-mg-per-kilogram dose, 92%) than who received unfractionated heparin (20%, P<0.001). (NEJM 2006;355(10):1006-1017<\/p>\n <\/p>\n <\/p>\n LOW MOLECULAR WEIGHT HEPARINS VERSUS UNFRACTIONATED HEPARIN FOR ACUTE CORONARY SYNDROMES Background This review aimed to identify randomized controlled clinical trials to determine the relative safety and efficacy of subcutaneous low-molecular-weight heparins (LMWH) versus intravenous unfractionated heparin (UFH) for people with acute coronary syndromes (ACS; unstable angina or non-ST segment elevation myocardial infarction). Results Seven studies (n = 11 092) were included. No difference was found in overall mortality between the groups treated with LMWH and UFH (RR 1.0, 95% CI: 0.69 to 1.44). LMWH reduced the occurrence of myocardial infarction (RR 0.83, 95% CI 0.70 to 0.99) and the need for revascularization procedures (RR = 0.88, 95% CI 0.82 to 0.95). A decrease in the incidence of thrombocytopenia (RR 0.64, 95% CI 0.44 to 0.94) was noted in patients who were given LMWH. No evidence was found for difference in occurrence of recurrent angina, or major or minor bleeds. SOCRATES says LMWH should be used rather than UFH in ACS. Insufficient data exist to recommend a single form of LMWH. Magee KD, Sevcik W, Moher D, et al. Low molecular weight heparins versus unfractionated heparin for acute coronary syndromes. In: Cochrane Library, Issue 2. Oxford: Update Software, 2006 .<\/p>\n <\/p>\n <\/p>\n Most recent study shows lovenox is superior to UFH (BMJ 2012;344:e553)<\/p>\n All going to cath:<\/p>\n Reopro-.25 mg\/kg bolus followed by .125 mg\/kg\/min<\/p>\n All elevated troponin:<\/p>\n <\/p>\n (UA\/NSTEMI guidelines, ACC.\u00a0 2002\u00a0 Ia if going to cath, IIa if high risk s cath, IIb if not)<\/p>\n Integrilin Drip Chart<\/p>\n Transfuse elderly with hematocrit <30 (NEJM 345:17)<\/p>\n Associated with worse outcomes in patients with ischemic disease\u00a0 (JAMA Vol. 292 No. 13, October 6, 2004)<\/p>\n<\/span>Initial Approach<\/span><\/h2>\n
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<\/a><\/p>\n<\/span>History<\/span><\/h3>\n
<\/span>Systemic Lupus<\/span><\/h3>\n
<\/span>from Cliff at resus.me<\/span><\/h3>\n
<\/span>Pathophys<\/span><\/h3>\n
<\/span>Women c MI at presentation<\/span><\/h3>\n
<\/span>traditional risk factors<\/span><\/h3>\n
<\/span>New risk factors<\/span><\/h3>\n
<\/span>relief with antacids (Emerg Med J 2003;20:170)<\/span><\/h3>\n
<\/span>TIMI Risk Score<\/span><\/h3>\n
<\/span>TIMI Risk Index<\/span><\/h2>\n
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<\/p>\n<\/h2>\n
<\/span>HEART Risk Score<\/span><\/h2>\n
\nhttp:\/\/www.ncbi.nlm.nih.gov\/pubmed\/23465250<\/a><\/p>\n<\/span>Aspect Trial<\/span><\/h2>\n
<\/span>Long Term Outcomes using AHCPR Criteria<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part3\/lowcardrisk_small.gif\")
<\/a><\/p>\n<\/span>Presentation c AMI<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/pathophys_small.jpg\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/jama%20study%20for%20cp_small.png\")
<\/a><\/p>\n<\/span>Pathophysiology<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part1\/acs%20path_small.jpg\")
<\/a><\/p>\n<\/span>Patients Discharged without Stress Testing<\/span><\/h2>\n
<\/span>Patients Returning after Negative Stress Testing<\/span><\/h2>\n
<\/span>Empiric Treatment<\/span><\/h2>\n
<\/span>O2<\/span><\/h3>\n
<\/span>Aspirin<\/span><\/h3>\n
<\/span>Clopidogrel<\/span><\/h3>\n
<\/span>Nitroglycerin<\/span><\/h3>\n
<\/span>Morphine<\/span><\/h3>\n
<\/span>Benzodiazepines<\/span><\/h3>\n
<\/span>B-Blockers<\/span><\/h3>\n
Contraindications:<\/h4>\n
\n
\n
Lopressor<\/h4>\n
Esmolol<\/h4>\n
<\/span>Diltiazem<\/span><\/h3>\n
<\/span>ACEI<\/span><\/h3>\n
<\/span>Statin<\/span><\/h3>\n
<\/span>Risk Stratify Based on EKG and History<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part1\/stsegmentevaldiagram_small.jpg\")
<\/a><\/h3>\n<\/span>EKG In ACS:<\/span><\/h3>\n
<\/span>Cardiac Markers<\/span><\/h2>\n
Ultra-senstitive Troponins<\/h4>\n
![\"\"](\"\/wp-content\/images\/part1\/wu%20of%20elevated%20troponin.gif\")
<\/p>\nCauses of False-Positive Troponin Results<\/h4>\n
Discordant MB and Troponin<\/h4>\n
<\/span>Likelihood that presentation represents ACS secondary to CAD (ACC Guidelines 2002)<\/span><\/h2>\n
<\/span>Short-term risk of Death or Nonfatal MI in Patients with UA\/NSTEMI (ACC Guidelines 2002)<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/rxforacs_small.jpg\")
<\/a><\/p>\n<\/span>Vancouver Very Low Risk Patient Identification<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/vancouver%20chest%20pain%20rule_small.gif\")
<\/a><\/p>\n<\/span>Treatment of UA\/NSTEMI<\/span><\/h2>\n
<\/span>Heparin<\/span><\/h3>\n
<\/span>IIb\/IIIa<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/2b3achart_small.jpg\")
<\/a><\/p>\n<\/span>Transfusions<\/span><\/h3>\n
<\/span>Treatment of STEMI<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part1\/lysiscontraind_small_small.gif\")
<\/a><\/p>\n