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Symptoms of Ischemic Heart Disease Chest discomfort with variable characteristics -pain, pressure, tightness, crushing, squeezing, stabbing, choking sensations.

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Presentation on theme: "Symptoms of Ischemic Heart Disease Chest discomfort with variable characteristics -pain, pressure, tightness, crushing, squeezing, stabbing, choking sensations."— Presentation transcript:

1 Symptoms of Ischemic Heart Disease Chest discomfort with variable characteristics -pain, pressure, tightness, crushing, squeezing, stabbing, choking sensations -substernal origin with variable radiation to arm, neck, or jaw -especially when associated with exertion -duration in minutes (5-30), not seconds or hours Associated symptoms or anginal equivalents (dyspnea, nausea/vomiting, indigestion, diaphoresis, syncope) Patient history is often diagnostic.

2 Physical Findings in Ischemic Heart Disease Diaphoresis or other sign of hypoperfusion Congestive signs: JVD, rales, S3 Abnormal heart sounds: S3, new murmur Hypoxia Arrhythmias, especially ventricular, although must rule out MI with new onset afib Physical exam is most useful to rule out differential diagnoses and often is normal in ischemic heart disease.

3 Etiologies of Ischemia Atherosclerosis Congenital coronary anomalies Coronary arteritis Radiation therapy Cocaine Aortic stenosis Hypertrophic cardiomyopathy

4 Differential Diagnosis of Chest Pain Acute coronary syndromes Other cardiovascular causes Aortic dissection Aortic stenosis Pericarditis Myocarditis Hypertrophic cardiomyopathy Aortic regurgitation Mitral valve prolapse Severe anemia Pulmonary causes Pulmonary embolus Pneumothorax Pleurisy Gastrointestinal causes Esophageal spasm or reflux Esophageal rupture Peptic ulcer disease Biliary or pancreatic disease Musculoskeletal causes Costochondritis Muscle strain Thoracic outlet syndrome Degenerative spine disease Psychogenic causes Anxiety/depression/panic attack Psychosis Secondary gain IT IS IMPERATIVE TO ASSESS FOR POSSIBLE LIFE-THREATENING ALTERNATIVE DIAGNOSES, SUCH AS AORTIC DISSECTION, PE, TENSION PNEUMOTHORAX, OR RUPTURED VISCUS..

5 Patient Education for Early Recognition and Response to Chest Pain Healthcare providers should instruct patients previously prescribed nitroglycerin (NTG) on use for chest discomfort or pain and to call 9-1-1 if symptoms do not improve or worsen 5 minutes after ONE sublingual NTG dose*. (* Nitroglycerin Dose: 0.4 mg sublingually) STEMI: ACC/AHA guidelines at

6 Prehospital Chest Pain Evaluation and Treatment Prehospital EMS providers should administer 162 to 325 mg of aspirin (chewed) to chest pain patients suspected of having STEMI unless contraindicated or already taken by the patient. Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric- coated formulations. It is reasonable for all 9-1-1 dispatchers to advise patients without a history of aspirin allergy who have symptoms of STEMI to chew aspirin (162 to 325 mg) while awaiting arrival of prehospital EMS providers. Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations. STEMI: ACC/AHA guidelines at

7 Options for Transport of Patients With STEMI and Initial Reperfusion Treatment EMS Transport Onset of symptoms of STEMI 9-1-1 EMS Dispatch EMS on-scene Encourage 12-lead ECGs. Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min. GOALS PCI capable Not PCI capable Hospital fibrinolysis: Door-to-Needle within 30 min. EMS Triage Plan Inter- Hospital Transfer PatientEMSPrehospital fibrinolysis EMS-to-needle within 30 min. EMS transport EMS-to-balloon within 90 min. Patient self-transport Hospital door-to-balloon within 90 min. Dispatch 1 min. 5 min. 8 min. STEMI: ACC/AHA guidelines at

8 Emergent Diagnostic Testing 12-lead EKG Cardiac enzymes (CPK, CKMB, Troponin) CBC Basic or comprehensive chemistry panel Coagulation studies D-Dimer PA and lateral CXR

9 Cardiac Biomarkers in ACS CPK (creatine phosphokinase) – enzyme common in skeletal, smooth, and cardiac muscle as well as brain and kidney; three isoenzymes: MB – cardiac and some skeletal muscle MM – primarily in skeletal muscle BB – primarily in brain and kidney Troponin – protein that regulates interaction of actin and myosin Troponin C – common to skeletal and cardiac muscle Troponin T and I – diagnostic & prognostic value in myocardial injury Cardiac biomarkers provide the most accurate diagnosis of acute myocardial injury and are the reference standard for the diagnosis of MI.

10 Other Biomarkers Nonspecific serum markers – elevated in MI but non-specific AST (aspartate aminotransferase) LDH (lactate dehyrogenase) Myoglobin – rapid release and return to baseline but elevated with muscle infarct and renal failure Newer biomarkers – predictive of risk in ACS but not commonly used for this purpose BNP (B-type natriuretic peptide) CRP (C-reactive protein)

11 012345678012345678012345678012345678 Cardiac troponin-no reperfusion Days After Onset of STEMI Multiples of the URL Upper reference limit 1 2 5 10 20 50 URL = 99th %tile of Reference Control Group 100 Cardiac troponin-reperfusion CKMB-no reperfusion CKMB-reperfusion Cardiac Biomarkers in ACS Alpert et al. J Am Coll Cardiol 2000;36:959. Wu et al. Clin Chem 1999;45:1104. STEMI: ACC/AHA guidelines at

12 Cardiac Biomarkers in STEMI Troponins- Now the Gold Standard! Rise after 3-6 hours Negative Troponin within 6 hours of onset of S&S rules out the MI Peaks at about 20 hours May be raised for 14 days

13 Cardiac Biomarkers: Troponin T & I Troponin T Levels may help to stratify risk Less specific than Troponin I Increased in angina Increased in chronic renal failure Highly sensitive for detecting myocardial ischemia Troponin I 90% sensitivity for MI 8 hours after onset of S&S and 95% specificity Negative rules out MI Obtain two negative troponin values 4-6-8 hours apart Normally exceedingly low Even a small elevation indicates myocardial damage

14 Troponin I Levels and Mortality in Patients with NSTEMI 0 2 4 6 8 0- <0.4 0.4- <1.0 1.0- <2.0 2.0- <5.0 5.0- <9.0 >9.0 % Mortality at 42 Days Adapted with permission from Antman EA, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med. 1996;335:1342-1349. Copyright © 1996, Massachusetts Medical Society. All rights reserved. Troponin I Level

15 EKG Changes in STEMI ST elevation of 1mm or more in the limb leads or of 2mm or more in precordial leads is significant. The pattern of ST elevation indicates the location of infarct and the involved coronary artery. Dynamic changes in the ST segment or the T wave represent an evolving infarct. A new left bundle branch block is significant.

16 EKG Changes: Ischemia T-wave inversion (flipped T) ST segment depression T wave flattening Biphasic T-waves

17 EKG Changes: Injury ST segment elevation of greater than 1mm in at least 2 contiguous leads Heightened or peaked T waves Directly related to portions of myocardium rendered electrically inactive

18 EKG Changes: Infarct Significant Q-wave where none previously existed Impulse traveling away from the positive lead Necrotic tissue is electrically dead Criteria for Q-wave significance Depth of Q wave should be 25% the height of the R wave Width of Q wave is 0.04 secs Diminished height of the R wave

19 Dynamic EKG Changes 1 Year Baseline Hyperacute T wave ST elevation Inverted T wave Q wave

20 EKG Changes: Anterior/Septal MI ST changes: V 1,V 2, V 3, V 4 Culprit Vessel: LAD

21 EKG Changes: Inferior MI ST Changes: II, III, aVFCulprit Vessel: RCA

22 EKG Changes: Lateral MI ST Changes: I, aVL, V 5, V 6 Culprit Vessel: Circumflex

23 EKG Changes: Posterior MI ST Changes: Reciprocal in V 1, V 2 Culprit Vessels: RCA or Cx

24 Summary of EKG Changes Lat: I, aVL, V5, V6 Ant/Septal: V1, V2, V3, V4 Inf: II, III, aVF Post: Rec V1, V2

25 EKG Changes: Summary

26 Non-invasive Diagnostic Testing Echocardiography Exercise stress testing Pharmacologic stress testing -Adenosine -Persantine Nuclear stress testing Echocardiography CTA Cardiac MRI May be considered only after acute MI or other emergent process has been ruled out.

27 Acute Pharmacologic Interventions in STEMI Oxygen Nitroglycerin Analgesia (Morphine) Aspirin Beta Blockers MONAMONAB

28 Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO 2 < 90%). It is reasonable to administer supplemental oxygen to all patients with uncomplicated STEMI during the first 6 hours. Oxygen STEMI: ACC/AHA guidelines at

29 Patients with ongoing ischemic discomfort should receive sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous NTG. Intravenous NTG is indicated for relief of ongoing ischemic discomfort that responds to nitrate therapy, control of hypertension, or management of pulmonary congestion. Nitroglycerin STEMI: ACC/AHA guidelines at

30 Nitrates should not be administered to patients with: Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil/Cialis©). systolic pressure < 90 mm Hg or to 30 mm Hg below baseline severe bradycardia (< 50 bpm) tachycardia (> 100 bpm) or suspected RV infarction. Nitroglycerin STEMI: ACC/AHA guidelines at

31 Analgesia Morphine sulfate (2 to 4 mg intravenously with increments of 2 to 8 mg intravenously repeated at 5 to 15 minute intervals) is the analgesic of choice for management of pain associated with STEMI. STEMI: ACC/AHA guidelines at

32 Aspirin Aspirin should be chewed by patients who have not taken aspirin before presentation with STEMI. The initial dose should be 162 mg (Level of Evidence: A) to 325 mg (Level of Evidence: C) Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations. STEMI: ACC/AHA guidelines at

33 NSAIDs NSAIDS (except ASA) should not be given during the acute hospitalization due to increased risk of mortality, reinfarction, HTN, heart failure, and myocardial rupture. This restriction includes both nonselective as well as COX-II forms of NSAIDs. STEMI: ACC/AHA guidelines at

34 Oral beta-blocker therapy should be administered promptly to those patients without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI. It is reasonable to administer intravenous beta- blockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present. Beta-Blockers STEMI: ACC/AHA guidelines at

35 Primary PCI for STEMI: General Considerations Patient with STEMI (including posterior MI) or MI with new or presumably new LBBB PCI of infarct artery within 12 hours of symptom onset Balloon inflation within 90 minutes of presentation Skilled personnel available (individual performs > 75 procedures per year) Appropriate lab environment (lab performs > 200 PCIs/year of which at least 36 are primary PCI for STEMI) Cardiac surgical backup available STEMI: ACC/AHA guidelines at

36 Primary PCI for STEMI: Specific Considerations Medical contact–to-balloon or door-to-balloon should be within 90 minutes. PCI preferred if > 3 hours from symptom onset. Primary PCI should be performed in patients with severe congestive heart failure (CHF) and/or pulmonary edema (Killip class 3) and onset of symptoms within 12 hours. STEMI: ACC/AHA guidelines at

37 Times to remember 10 minutes time for ED eval 30 minutes door to needle 90 minutes door to balloon 3 hours (symptom onset) Fibrinolytic vs. PCI therapy 12 hours (symptom onset) Time limit for revascularization therapies as supported by data

38 Given the current literature, it is not possible to say definitively that a particular reperfusion approach is superior for all pts, in all clinical settings, at all times of day. The main point is that some type of reperfusion therapy should be selected for all appropriate pts with suspected STEMI. The appropriate & timely use of some reperfusion therapy is likely more important than the choice of therapy. Caveat on Reperfusion STEMI: ACC/AHA guidelines at

39 Caveat on Reperfusion The medical system goal is rapid recognition and treatment of patients with STEMI such that either: 1. Door-to-needle time for initiation of fibinolytic therapy can be achieved within 30 miutes OR 2. Door-to-balloon time for PCI can be kept within 90 minutes. STEMI: ACC/AHA guidelines at

40 Maintenance Management of the Patient after MI Aspirin Plavix Beta Blocker ACE inhibitor/ARB Statin therapy

41 Aspirin A daily dose of aspirin (initial dose of 162 to 325 mg orally; maintenance dose of 75 to 162 mg) should be given indefinitely after STEMI to all patients without a true aspirin allergy. STEMI: ACC/AHA guidelines at

42 Thienopyridines (Plavix) In patients for whom PCI is planned, clopidogrel (Plavix) should be started and continued: 1 month after bare-metal stent 3 months after sirolimus-eluting stent 6 months after paclitaxel-eluting stent Up to 12 months in absence of high risk for bleeding. STEMI: ACC/AHA guidelines Duration of Plavix use varies among interventional cardiologists. Use of generic Plavix was strongly discouraged, but the generic form is no longer available.

43 Thienopyridines (Plavix) 2007 STEMI guidelines now include long- term use of Plavix regardless of reperfusion therapy (ie-fibrinolysis, PCI, or neither): Plavix 75mg po daily (LOE A) for at least 14 days (LOE B) or one year if patients under 75 years of age (LOE C). Plavix should be held for 5-7 days prior to to CABG. STEMI: ACC/AHA guidelines

44 Maintenance Management Beta blockers should be continued indefinitely in all patients who have no known contra- indications. ACE inhibitor (or ARB) if necessary should be continued indefinitely in all patients post MI. Aggressive lipid management with a statin should be initiated promptly and continued.

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