History

Fact Explanation
Chest pain This is a common presenting complaint. [1] The chest pain is usually described by the patients as a severe tightening type of chest pain with radiation to the left arm and the left side of the jaw and neck. [4] Pain lasts for 20min or more and does not respond to sublingual nitroglycerine.[4] However patients with diabetes related cardiac autonomic neuropathy may not feel the chest pain (“silent infarction”). [2,3,4]
Fatigue [10] or malaise This occurs especially in elderly. [5] Although the exact cause has not been found it is believed to be due to early left ventricular dysfunction. [9]
Light-headedness with or without syncope This also occurs specially in elderly. [5] Syncope may be due to the development arrhythmia, or may occur as a complication of autonomic disturbances. [8]
Nausea with or without vomiting This is due to the sympathetic over activation. This helps to differentiate MI from unstable angina. [7]
Sweating [5] This occurs due to sympathetic over activation. [7]
Cardiogenic shock Especially patients with right ventricular infarct can present with cardiogenic shock. [5]
Clinical triad of hypo tension, clear lung fields, and raised jugular venous pressure [5] This is very common in right ventricular infarction. [5] (Furthermore the inferior leads will have a ST segment elevation as well [6])
Sudden death A possible presentation of MI. This might be due to cardiogenic shock or due to arrhythmia. [7]
References
  1. KRISTIAN THYGESEN, JOSEPH S. ALPERT, HARVEY D. Universal definition of myocardial infarction. Eur Heart J. [online] 2007; 28 (20): 2525-2538. [viewed 22 March 2014]. Available from: doi: 10.1093/eurheartj/ehm355
  2. CHICO A, TOMAS A, NOVIALS A. Silent myocardial ischemia is associated with autonomic neuropathy and other cardiovascular risk factors in type 1 and type 2 diabetic subjects, especially in those with microalbuminuria. Endocrine. [online] 2005;27(3):213–217. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16230776
  3. MANZELLA D, PAOLISSO G. Cardiac autonomic activity and type II diabetes mellitus. Clinical Science. [online] 2005;108:93–99. [viewed 22 March 2014].
  4. VINIK AI, FREEMAN R, ERBAS T. Diabetic autonomic neuropathy. Seminars in Neurology. [online] 2003;23(4):365–372. [viewed 22 March 2014].
  5. Management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. [online] Volume 24, Issue 1. Pp. 28-66. [viewed 22 March 2014]. Available from: doi: 10.1016/S0195-668X(02)00618-8
  6. KINCHJW, RYAN TJ. Right ventricular infarction. N Engl J Med. [online] 1994;330:1211–1217. [viewed 22 March 2014].
  7. S. W. WEBB, A. A. J. ADGEY, AND J. F. PANTRIDGE. Autonomic Disturbance at Onset of Acute Myocardial Infarction. Br Med J. [online] Jul 8, 1972; 3(5818): 89–92. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785615/
  8. ALBERT E. R., KENT A. H., 37-Year-Old Woman With Progressive Fatigue, Syncope, and Chest Pain. Circulation. [online] 1995; 91: 231-235. [viewed 24 March 2014] Available from: doi: 10.1161/​01.CIR.91.1.231
  9. HUGH J.N. B., Fatigue as a Prodromal Symptom of Myocardial Infarct. Circulation. [online] 2004; 109: e311 [viewed 24 March 2014] Available from: doi: 10.1161/​01.CIR.0000129347.00233.8C
  10. NIXON P. G. F., BETHELL H. J. N., Coronary deaths: how unexpected? Br Med J. [online] 1971; 2: 486–487. [viewed 24 March 2014].

Examination

Fact Explanation
Pulse Bradycardia, tachycardia and arrhythmias will be detected. [2]
Blood pressure Low blood pressure is associated with high mortality. Narrow pulse pressure may be observed if the systolic pressure is low. [1]
Pulmonary crepitations [2] Due to acute left heart failure. The severity of heart failure can be categorized according to the Killip score. [3]
Signs of Ventricular Septal Defect (VSD) [4] VSD occurs as a complication. Severe clinical deterioration and a loud pan systolic murmur should make the clinician suspicious of a possible VSD due to rupture of the inter-ventricular septum. [1]
Signs of Mitral regurgitation (MR) [2] MR occurs due to rupture or dysfunction of papillary muscles. Sometimes may be due to the dilatation of the mitral annulus as a complication of dilatation of the left ventricle. [2] Pan-systolic murmur at the cardiac apex will be audible. [5]
Signs of Tricuspid Regurgitation [TR] This occurs in right ventricular infarction due to right ventricular and tricuspid annulus dilatation. [2] TR produces a pan-systolic murmur at the lower left sternal edge. [6]
References
  1. LEEKL, WOODLIEF LH, TOPOL EJ, et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation. [online] 1995;91:1659–1668. [viewed 22 March 2014].
  2. Management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. [online] Volume 24, Issue 1. Pp. 28-66. [viewed 22 March 2014]. Available from: doi: 10.1016/S0195-668X(02)00618-8
  3. KILLIPT 3RD, KIMBALL JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol. [online] 1967;20:457–464. [viewed 22 March 2014].
  4. LAVIECJ, GERSH BJ. Mechanical and electrical complications of acute myocardial infarction. Mayo Clin Proc. [online] 1990;65:709–730. [viewed 22 March 2014].
  5. AHMED MI, SANAGALA T, DENNEY T, INUSAH S, MCGIFFIN D, KNOWLAN D, O'ROURKE RA, DELL'ITALIA LJ. Mitral valve prolapse with a late-systolic regurgitant murmur may be associated with significant hemodynamic consequences. Am J Med Sci. [online] 2009 Aug;338(2):113-5. [viewed 22 March 2014]. Available from: doi: 10.1097/MAJ.0b013e31819d5ec6.
  6. J R KELLEY AND W G GUNTHEROTH. Pansystolic murmur in the newborn: tricuspid regurgitation versus ventricular septal defect. Arch Dis Child. [online] Oct 1988; 63(10 Spec No): 1172–1174. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1590213/

Differential Diagnoses

Fact Explanation
Pericarditis or myopericarditis This is the commonest differential diagnosis of ST Elevation Myocardial Infarction (STEMI). [7,8] Myocarditis should be suspected especially in young males with low cardiovascular risk profile. [9]
Hypoglycemia [1] Palpitations, tremor, anxiety and sweating occurs in both conditions. [2]
Pericardial effusion [3] This also presents with pleuritic type of chest pain which is relieved by bending forwards. On auscultation of the precordium a pericardial friction rub is heard over the left lower sternal border. [16]
Non ST elevation MI (Non STEMI) STEMI and Non STEMI have similar clinical presentations.
Angina Pectoris Stable and unstable angina both have similar type of chest pain but autonomic disturbances are not detected in angina pectoris.
Aortic Dissection [3] Patients with acute dissection presents with severe tearing type of chest pain which radiates to the back. [4]
Aortic Stenosis Patients with aortic stenosis can present with recurrent ischemic type chest pain. [5,10]
Musculoskeletal pain The pain typically increases with breathing and movements. [15]
Peptic ulcer disease (PUD) Burning type of epigastric pain occurs in PUD. Inferior MI is a possible differential diagnosis. [6]
Pancreatitis [15] upper abdominal (epigastric or paraumbilical) pain, with associated nausea and vomiting. Abdominal pain radiates to the back typically, but may radiates to the chest, flanks, and lower abdomen as well. [17]
Subarachnoid hemorrhage This is a known reason for ST segment elevation in ECG. [11]
Pneumonia Patients with fever, cough, pleuritic type of chest pain are characteristic. [12,15]
Pneumothorax A medical emergency. The diagnosis is made by clinical examination. Patient with sudden onset shortness of breath, rapid deterioration, tracheal deviation away from the lesion, hyper-resonant percussion note over the affected side and engorged neck veins provide clues to the diagnosis.
Pulmonary Embolism [13,3] Patients present with dyspnea, pleuritic chest pain and haemoptysis. [14,15]
Radicular pain due to Herpes zoster Herpes zoster in the thoracic dermatomes also produces chest pain, itching, paresthesia and dysesthesia over the affected dermatome. Examination will reveal the vesicles in the affected dermatome. [16]
References
  1. HOLLI A. DEVON, SUE PENCKOFER, KAREN LARIMER. The Association of Diabetes and Older Age With the Absence of Chest Pain During Acute Coronary Syndromes. West J Nurs Res. [online] Feb 2008; 30(1): 130-144. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2247416/#!po=3.57143
  2. BULPITT CJ, PALMER AJ, BATTERSBY C, FLETCHER AE. Association of symptoms of type 2 diabetic patients with severity of disease, obesity, and blood pressure. Diabetes Care. [online] 1998;21(1):111–115. [viewed 22 March 2014].
  3. LENGYEL M. The role of transesophageal echocardiography in the management of patients with acute and chronic pulmonary thromboembolism. Echocardiography. [online] 1995;12:359–366. [viewed 22 March 2014].
  4. ALAN C. BRAVERMAN. Acute Aortic Dissection. Circulation. [online] 2010; 122: 184-188. [viewed 22 March 2014]. Available from: doi: 10.1161/ CIRCULATIONAHA.110.958975.
  5. BARBARA K. JULIUS, MARTIN SPILLMANN, GIUSEPPE VASSALLI, BRUNO VILLARI, FRANZ R. EBERLI, OTTO M. HESS. Angina Pectoris in Patients With Aortic Stenosis and Normal Coronary Arteries. Circulation. 1997; 95: 892-898. [viewed 22 March 2014]. Available from: doi: 10.1161/01.CIR.95.4.892
  6. KURKCIYAN I, SCHIRMAIER E, FROSSARD M, SCHREIBER W, LANGLE F, HUEMER G, STERZ F. Concomitant perforated ulcer and acute myocardial infarct--a diagnostic challenge in emergency medicine. Wien Klin Wochenschr. [online] 1994;106(20):660-3. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7810150
  7. WANG K, ASINGER RW, MARRIOTT HJ. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med. [online] 2003; 349:2128-35. [viewed 22 March 2014].
  8. BERTRAND ME, SIMOONS ML, FOX KA, et al. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. [online] 2002;23:1809-40. [viewed 22 March 2014].
  9. COSTANTINI M,TRITTO C, LICCI E, et al. Myocarditis with ST-Elevation Myocardial Infarction presentation in young man. A case series of 11 patients. Int J Cardiol. [online] 2005;101:157-8. [viewed 22 March 2014].
  10. ANTMAN EM, BRAUNWALD E. ST-elevation myocardial infarction: pathology, pathophysiology, and clinical features. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. [online] Philadelphia, PA: Elsevier Saunders; 2005:1141-65. [viewed 22 March 2014].
  11. WIDIMSKY P, STELLOVA B, GROCH L, et al. Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: experience from the PRAGUE studies. Can J Cardiol. [online] 2006;22:1147-52. [viewed 22 March 2014].
  12. LEE TH, CANNON CP. Approach to the patient with chest pain. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. [online] Philadelphia, PA: Elsevier Saunders; 2005:1129-39. [viewed 22 March 2014].
  13. GU YL, SVILAAS T, ZIJLSTRA F. Conditions mimicking acute ST-segment elevation myocardial infarction in patients referred for primary percutaneous coronary intervention. Neth Heart J. [online] Oct 2008; 16(10): 325-331. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570763/#!po=57.6923
  14. MARTIN RIEDEL. Acute pulmonary embolism 1: pathophysiology, clinical presentation, and diagnosis. Heart. [online] 2001;85:229-240 doi:10.1136/heart.85.2.229. [viewed 22 March 2014].
  15. KRISTIAN THYGESEN, JOSEPH S. ALPERT HARVEY D. Universal definition of myocardial infarction. Eur Heart J. [online] 2007 28 (20): 2525-2538. [viewed 22 March 2014]. Available from: doi: 10.1093/eurheartj/ehm355
  16. NIKLAUS H. MUELLER, DONALD H. GILDEN, MARIA A. NAGEL. Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency. Neurol Clin. [online] Aug 2008; 26(3): 675-viii. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754837/
  17. JENNIFER K. CARROLL, BRIAN HERRICK, TERESA GIPSON, SUZANNE P. LEE. Acute Pancreatitis: Diagnosis, Prognosis, and Treatment. Am Fam Physician. [online] 2007 May 15;75(10):1513-1520. [viewed 22 March 2014]. Available from: http://www.aafp.org/afp/2007/0515/p1513.html

Investigations - for Diagnosis

Fact Explanation
Electrocardiogram (ECG) Persistent ST-segment elevation indicates evolving myocardial infarction. New Q waves indicate established myocardial infarction. [1,2] New onset left bundle-branch block is also an indication to diagnose MI. [1] ST segment elevation in V7and V8 leads indicates a posterior MI. [1] The ST-segment elevation in V4R and or Q waves and ST-segment elevation in V1 are all suggestive of a right ventricular infarction. [1,7] Q wave of any magnitude and or ST segment elevation in lead V2 are suggestive of an anterior MI. [8] ST segment elevation in inferior leads, (lead II,III and aVF) is suggestive of an inferior MI. [9] In ECG prominent symmetrical hyper-acute T-waves, elevation of the ST segment, resolution of the ST segment and the appearance of the Q waves appear in sequence. [10] ECG might be normal during the initial stages of MI. [3,4]
Troponin (I or T) [1,11,12] Troponin (a cardiac enzyme, released after death of cardiac myosites) elevation peaks around 6 to 9 hours after the onset of clinical symptoms and remain elevated for 7 to 14 days.[10,13]These enzymes are more cardio specific than CK-MB and have high specificity. [1,11]
Creatinine Kinase MB (CK-MB) [1,11,12] This is less cardio specific when compared to troponin and it is the next choice of cardiac bio marker when troponin assays are not available. [10] Initial assay at the time of the presentation should be followed by a second assay after 6 to 9 hours of onset of symptoms to demonstrate a rise or fall of CK-MB. [10] CK-MB is valuable in diagnosing re-infarction. [10]
Heart-type fatty acid-binding protein (H-FABP) This is a newer cardiac bio marker with early diagnostic and prognostic value and can be used with in the first 6 hours of onset of symptoms. [14]
2D echocardiogram Regional wall motion abnormalities indicate impending infarction. [5] Absence of regional wall motion abnormalities excludes a major infarction. [1] Complications like mitral regurgitation and ventricular septal defect [6] can also be identified by echo cardiogram. [1]
Coronary angiography Detects the site of the lesion.
Lactate dehydrogenase (LDH) This is not routinely used now due to lack of specificity. [10,11]
Myocardial perfusion scintigraphy Helps to exclude an acute MI. [1]
References
  1. Management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. [online] Volume 24, Issue 1. Pp. 28-66. [viewed 22 March 2014]. Available from: doi: 10.1016/S0195-668X(02)00618-8
  2. LEEKL, WOODLIEF LH, TOPOL EJ, et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation. [online] 1995;91:1659–1668. [viewed 22 March 2014].
  3. ADAMSJ, TRENT R, RAWLES JON. Earliest electrocardiographic evidence of myocardialinfarction: implications for thrombolytic therapy. BMJ. [online]1993;307:409–413. [viewed 22 March 2014].
  4. GRIJSEELSEW, DECKERS JW, HOES AW, et al. Pre-hospital triage of patients with suspected acute myocardial infarction. Evaluation of previously developedalgorithms and new proposals. Eur Heart J. [online] 1995;16:325–332. [viewed 22 March 2014].
  5. HAUSERAM, GANGADHARAN V, RAMOS RG, et al. Sequence of mechanical, electrocardiographic and clinical effects of repeated coronary arterial occlusion in human beings: echocardiographic observation during coronary angioplasty. J Am Coll Cardiol. [online] 1985;5:193–197. [viewed 22 March 2014].
  6. LAVIECJ, GERSH BJ. Mechanical and electrical complications of acute myocardial infarction. Mayo Clin Proc. [online] 1990;65:709–730. [viewed 22 March 2014].
  7. DELL'ITALIALJ, STARLING MR, O'ROURKE RA. Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med. [online] 1983;99:608–611. [viewed 22 March 2014].
  8. ROBERT A. WARNER, MARK REGER, NORMA E. HILL, SAKTI MOOKHERJEE, HAROLD SMULYAN. Electrocardiographs criteria for the diagnosis of anterior myocardial infarction: Importance of the duration of precordial R waves. The American Journal of Cardiology. [online] Volume 52, Issue 7, 1 October 1983, Pages 690–692. [viewed 22 March 2014]. Available from: http://dx.doi.org/10.1016/0002-9149(83)90399-5
  9. PAHLM O, CASE D, HOWARD G, POPE J, HAISTY WK. Decision rules for the ECG diagnosis of inferior myocardial infarction. Comput Biomed Res. [online] 1990 Aug;23(4):332-45. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2394092
  10. KRISTIAN THYGESEN, JOSEPH S. ALPERT, HARVEY D. Universal definition of myocardial infarction. Eur Heart J [online] (2007) 28 (20): 2525-2538. [viewed 22 March 2014]. Available from: doi: 10.1093/eurheartj/ehm355
  11. JAFFE AS, RAVKILDE J, ROBERTS R, NASLUND U, APPLE FS, GALVANI M, KATUS H. It's time for a change to a troponin standard. Circulation. [online] 2000;102:1216-1220. [viewed 22 March 2014].
  12. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined. Eur Heart J. [online] 2000;21:1502-1513. [viewed 22 March 2014].
  13. MACRAE AR, KAVSAK PA, LUSTIG V, BHARGAVA R, VANDERSLUIS R, PALOMAKI GE,YERNA M-J, JAFFE AS. Assessing the requirement for the six-hour interval between specimens in the American Heart Association classification of myocardial infarction in epidemiology and clinical research studies. Clin Chem. [online] 2006;52:812-818. [viewed 22 March 2014].
  14. NAKATA T, HASHIMOTO A, HASE M, TSUCHIHASHI K, SHIMAMOTO K. Human heart-type fatty acid-binding protein as an early diagnostic and prognostic marker in acute coronary syndrome. Cardiology. [online] 2003;99(2):96-104. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12711885

Investigations - Followup

Fact Explanation
Pulse oxymetry Measures oxygen saturation. [3]
Electrocardiogram (ECG) Complications like atrial fibrillation ventricular tachycardia and ventricular fibrillation can be detected. [3] Holter monitoring should be done during the first 24hours. [8]
Stress ECG [3] This should be done within six weeks of MI to detect exertion induced ischemia. [3]
Echo cardiogram Detects left ventricular mural thrombi [8] and other complications associated with MI. (Eg: ventricular septal defects, mitral regugitation)
Myocardial perfusion scintigraphy This investigation provides the actual size of myocardial necrosis and ischemia. Although not routinely practiced if done prior to the thrombolysis and after the thrombolysis it reflects the success of reperfusion, as the zone of ischemia reduces after successful reperfusion. [4,5] Also detects myocardial stunning (re-perfused myocardium but with delayed contractile recovery) and myocardial hibernation. In the presence of these reversible conditions, coronary intervention should be planned to achieve reperfusion. [3,9]
Coronary angiography [3] Demonstrates the anatomy of the coronary circulation and estimate the degree of narrowing so enable further planning of the treatment. [3,9] Patients with more risk factors like old age, multiple infarcts and multiple cardiovascular risk factors should have an early coronary angiography. [10]
Cardiac catheterization right heart catheterization detects the right atrial pressure and enable early detection of cardiogenic shock. [3] Detects the pulmonary artery and wedge pressure which is useful in the management of left heart failure. [3]
MRI Detects the thickness of resting myocardium. [11]
Chest X-ray (CXR) [3] CXR aids in diagnosing heart failure.
Arterial blood gas analysis [3] Arterial hypoxemia is a common occurrence within the first 24hours of myocardial infarction. [6] It is worsened by the respiratory depression caused by the opioid analgesics.
Serum electrolytes [3] Electronic disturbances can occur due to autonomic disturbance [12] and it is an easily correctable condition. Persistent electrolyte imbalance might lead to the development of arrhythmia. [3]
Lipid profile Total cholesterol, LDL and HDL cholesterol levels and fasting triglyceride levels should be measured. [3]
Fasting blood sugar Diabetes increases the risk of cardiac mortality by two to five times in women and three times in men, compared to the age and sex matched normal population. [1,2,7]
References
  1. BLENDEA MC, MCFARLANE SI, ISENOVIC ER, GICK G, SOWERS JR. Heart disease in diabetic patients. Current Diabetes Reports. [online] 2003;3:223–229. [viewed 22 March 2014].
  2. NORRISRM, CAUGHEY DE, MERCER CJ, et al. Prognosis after myocardial infarction. Six-year follow-up. Br Heart J. [online] 1974;36:786–790. [viewed 22 March 2014].
  3. Management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. [online] Volume 24, Issue 1. Pp. 28-66. [viewed 22 March 2014]. Available from: doi: 10.1016/S0195-668X(02)00618-8
  4. SCHOMIGA, KASTRATI A, DIRSCHINGER J, et al. Coronary stenting plus platelet glycoprotein Ilb/IIIa blockade compared with tissue plasminogen activator in acute myocardialinfarction. Stent versus Thrombolysis for Occluded Coronary Arteries in Patients with Acute Myocardial Infarction Study Investigators. N Engl J Med. [online] 2000;343:385–391. [viewed 22 March 2014].
  5. GIBBONSRJ, MILLER TD, CHRISTIAN TF. Infarct size measured by single photon emission computed tomographic imaging with (99m)Tc-sestamibi: a measure of the efficacy of therapy in acute myocardial infarction. Circulation. [online] 2000;101:101–108. [viewed 22 March 2014].
  6. WILSON AT, CHANNER KS. Hypoxaemia and supplemental oxygen therapy in the first 24 hours after myocardial infarction: the role of pulse oximetry. J Roy Coll Phys Lond. [online] 1997;31:657–661. [viewed 22 March 2014].
  7. STONE P, MULLER J, HARTWELL T, et al. The effect of diabetes mellitus on prognosis and serial left ventricular dysfunction after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the ADVERSE PROGNOSIS. J AM COLL CARDIOL. [online] 1989;14:49–57. [viewed 22 March 2014].
  8. THOMAS J. RYAN, JEFFREY L. ANDERSON, ELLIOTT M. ANTMAN, BLAINE A. BRANIFF, NEIL H. BROOKS ROBERT, M. CALIFF, L. DAVID HILLIS, LOREN F. HIRATZKA, ELLIOT RAPAPORT, BARBARA J. RIEGEL, RICHARD O. RUSSELL, EARL E. SMITH III, W. DOUGLAS WEAVER. ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction:Executive Summary. Circulation. [online] 1996; 94: 2341-2350. [viewed 22 March 2014]. Available from: doi: 10.1161/01.CIR.94.9.2341
  9. MAHMARIANJJ, MAHMARIAN AC, MARKS GF, et al. Role of adenosine thallium-201 tomography for defining long-term risk in patients after acute myocardial infarction. J Am Coll Cardiol. [online] 1995;25:1333–1340. [viewed 22 March 2014].
  10. DE FEYTERP, VAN EENIGE MJ, DIGHTON DH, et al. Prognostic value of exercise testing, coronary angiography, and left ventriculography 6–8 weeks after myocardial infarction. Circulation. [online] 1982;66:527–536. [viewed 22 March 2014].
  11. PIERARDLA, DE LANDSHEERE CM, BERTHE C, RIGO P, KULBERTUS HE. Identification of viable myocardium by echocardiography during dobutamine infusion in patients with myocardial infarction after thrombolytic therapy: comparison with positron emission tomography. J Am Coll Cardiol. [online] 1990;15:1021–1031. [viewed 22 March 2014].
  12. S. W. WEBB, A. A. J. ADGEY, J. F. PANTRIDGE. Autonomic Disturbance at Onset of Acute Myocardial Infarction. Br Med J. [online] Jul 8, 1972; 3(5818): 89–92. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785615/

Management - General Measures

Fact Explanation
Basic life support [6,7] In an unconscious patient management of airway, breathing and circulation (ABC) should be given the priority. Rapid administration of intravenous fluids (200ml in 10 minutes) will help to improve the blood pressure. Blood pressure and volume status should be monitored through out to prevent fluid overload. [1] Infusion of intravenous inotropes should be administered to maintain a systolic blood pressure more than 90mmHg. [1]
Analgesics [1,2,9] Narcotic analgesics are the first choice. [2] Respiratory depression is a possible side effect. [2] Diamorphine and methadone acts more quickly. [3] Initial dose of morphine is 4 to 8 mg and thereafter 2 mg dose titrations are given every 5 minutes till the pain is relieved. [1] Opioids should be combined with an anti emetic to reduce the side effect of vomiting. [9] Morphine will also cause a fall in blood pressure [3,4] Nitrous oxide is also an effective analgesic. [5] Intravenous nitrates [11] or intravenous beta-blockers can be used if pain does not respond to opioids. [1,10] Nitrates or opioids do not show any survival benefit. [12,13]
Oxygen Given in a rate of 2–4l/min. [1] The effectiveness of the reperfusion therapy depends on the arterial oxygen concentration as well. [9]
Endotracheal intubation and mechanical ventilation[1] If the oxygen tension drops (less than 60 mmHg) despite giving 100% oxygen (8-10 L/min) via the face mask or nasal prongs, intubation and mechanical ventilation is lifesaving. [1]
Pharmacological management of heart failure [8] In the presence of mild heart failure slow intravenous infusion of furosemide 20–40mg can be given and repeated 1 to 4 hourly. [1] However severe heart failure may need higher doses. Titrating doses of intravenous nitroglycerine (0.25μg/kg/min titrate the dose every 5minutes) or oral nitrates can be administered if there is no response to diuretics. Hypotension is a possible complication and blood pressure should be monitored. [1]
Inotropic agents [1] If hypotension or renal hypo perfusion develops intravenous dopamine (0.5–5.0μg.kg/min) is recommended. [1] In the presence of pulmonary edema dobutamine (2.5μg/kg/min increased every 5–10min intervals. Maximum dose-10μg/kg/min) is preferred. [1]
Correction of electrolyte disturbances Electrolyte disturbances especially hypokalemia can induce arrhythmias. [1]
Correction of acid base disturbances [1] Due to respiratory depression, renal hypo perfusion and anaerobic metabolism acid base disturbances can occur.
Management of arrhythmias [1] Ventricular tachycardia can be treated with beta-blockers, unless contraindicated. [1] Lidocaine is preferred if there is impending ventricular fibrillation. [1] Defibrillation is indicated if ventricular fibrillation develops. [6,7] Supraventricular tachycardia is treated with carotid sinus massage and if it fails with beta blockers or intravenous adenosine. [1] Sinus bradycardia is treated with intravenous atropine (0.3–0.5mg, repeated maximum total dose is 1.5–2.0mg). [1]
References
  1. Management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal. [online] Volume 24, Issue 1. Pp. 28-66. [viewed 22 March 2014]. Available from: doi: 10.1016/S0195-668X(02)00618-8
  2. REMETZ MS, Analgesic therapy in acute myocardial infarction. Cabin HS. Cardiol Clin. [online] 1988 Feb;6(1):29-36. [viewed 22 March 2014]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2901910
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  4. TOMAS WOLFF, SUNE LEWARD,ANDERS HAGMAN, MATS ANDERSSON,LEONARD LARSSON, KJELL ELGEN. Analgesic Treatment in Acute Myocardial Infarction: A Double-blind Comparison of Ketobemidone + the Spasmolytic A29 (Ketogan®) and Morphine. Acta Medica Scandinavica. [online] Volume 223,(5), pages 423–430. [viewed 22 March 2014]. Available from: DOI: 10.1111/j.0954-6820.1988.tb15893.x
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  10. Gruppo Italiano per lo Studio della Sopravvivenza nell-infarcto Miocardio. GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Lancet. [online] 1994;343:1115–1122. [viewed 22 March 2014].
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Management - Specific Treatments

Fact Explanation
Aspirin [4,14] Loading dose of 160 to 325 mg orally should be given to the patient to chew as the MI is suspected. This should be followed up by low dose aspirin daily for thrombo-prophylaxis. (75mg at night). [14,15,40]
Clopidogrel This is a glycoprotein IIb/IIIa inhibitor and belongs to antiplatelet group. Clopidogrel is used when aspirin is contraindicated and there is no evidence for routine long term use of clopidogrel in addition to aspirin. [41]
Percutaneous coronary interventions (PCI) [12,13,8,9,10] Door to balloon time for primary PCI is 90 minutes. [50] After failed medical thrombolysis rescue PCI can be done. [11,22] Primary PCI is the preferred treatment for patients in shock and for patients with contraindications for pharmacological thrombolysis. [2] When facilities are available within the effective time period, primary PCI is considered better than the pharmacological thrombolysis. [20,21] Especially in right ventricular infarcts primary PCI is preferred over the pharmacological thrombolysis. [37]
Tissue plasminogen activator (t-PA)[6,7] This is considered a superior method of thrombolysis when compared to streptokinase(SK). [17,18] Also the left ventricular function preservation is higher with t-PA. [19]
Streptokinase [16] Risk of stroke is lower with streptokinase when compared to t-PA or anistreplase. [4,6] Reperfusion therapy [2,3,4,5,]limits the infarct size. Timely reperfusion is effective in preventing heart failure, shock and severe life-threatening arrhythmias. [2] If the infarction is established for more than 12hours fibrinolytic therapy should not be given, unless there is ECG evidence of ongoing ischaemia. [2]
Emergency coronary artery bypass graft (CABG) [25,38] A surgical method of establishing reperfusion.
Angiotensin Converting Enzyme Inhibitors (ACEI) [42,43,44] Should be started within first 48h of MI provided there is no hypotension, hypovolaemia or renal failure. [2,32] If given within the first 24 hours ACEIs significantly reduce the cardiovascular mortality. [29,30,31]
Beta blockers [26,27] Beta blockers reduces the blood pressure and heart rate. They also have anti-arrhythmic properties. [23,24]
Intravenous magnesium [33,34] Reduces the peripheral vascular resistance, increases the cardiac output and reduces the risk of arrhythmias. [14]
Calcium channel blockes Reduces the vasospasm. [1] The use of CCB in the management of MI remains contravertial. [28] However some studies have failed to prove the beneficial effects of magnesium in the management of MI. [30,35]
Glucose-insulin-potassium This combination is used in the treatment based on the fact that this favorably influence the metabolism of ischemic myocardium. [2] Although some studies have proven a significant reduction in mortality [36] this is not routinely practiced. [2]
n-3 polyunsaturated fatty acids (1g/day) This is proven to reduce the cardiovascular mortality and risk of re-infarction. [39]
Lipid-lowering agents Lipid lowering therapy reduces the serum lipid levels and significantly reduces the risk of re-infarction. [46,47,48] Statins is the preferred lipid lowering drug which should be prescribed in addition to dietary guidelines to reduce the serum lipid levels. [48] Statins should be continued despite normal serum lipid levels. [49,48]
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