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STEMI Training

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This is the slide show that was presented at the STEMI training on 07/23/2014.

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STEMI Training

  1. 1. 12 Lead EKG Interpretation and STEMI Management
  2. 2. Who Are These Clowns?  Michael Grzyb  NREMT - Paramedic  17 years EMS Education Experience  ACLS, PALS, BCLS, BTLS Instructor  EMS Management – Clinical Services, Education and Training, and CQI  ZOLL Medical Senior Manager, EMS Clinical Deployment
  3. 3. Who Are These Clowns?  Jeffrey Rupple  NREMT – Paramedic  20 years EMS Education Experience  PALS, BCLS Instructor  EMS Management – Director of Operations, Field Supervisor, Field Training Officer  ZOLL Medical – Clinical Deployment Specialist
  4. 4. Disclaimer Information contained herein is provided for reference only and does not replace local / regional standing orders, protocols, Standard Operating Procedures or equipment manufacturer’s recommendations.
  5. 5. Disclaimer The information and tools presented to you today are outstanding aids to your patient assessment and treatment, and ideally will enable you to provide better patient care. The devices and information provided are designed to AUGMENT your patient assessment NOT REPLACE IT! PLEASE, TREAT THE PATIENT, NOT THE MONITOR!
  6. 6. Benefits of Prehospital 12-Lead ECG  Recognize AMI  Identify Reperfusion Candidates  The Earlier the Better - TIME IS MUSCLE!  Reduce Time to Thrombolysis  Reduce Time to PCI  Prehospital Thrombolytics
  7. 7. Acute Coronary Syndromes Unstable Angina (UA) Non-Q Wave Myocardial Infarction (NQMI) Q Wave Myocardial Infarction (QMI)
  8. 8. Myocardial Infarction Labels For pre-hospital purposes Non- ST- Elevation MI (NSTEMI) = Non-Q-Wave MI (NQMI) ST Elevation MI (STEMI) = Q-Wave MI (QMI)
  9. 9. STEMI
  10. 10. NSTEMI
  11. 11. ACS Risk Factors  Diabetes  Smoking  Hypertension  High Cholesterol  Family History  Obesity  Sedentary Life
  12. 12. The History  Good Assessment • HPI • Nature of Symptoms • OPQRST • Patient History  Traditional Risk Factors • Age • Male Sex • DM • Tobacco • History of CAD • Family History • HTN • Cholesterol  Non-Traditional Risk Factors • DM = CAD • HIV with or without HAART • Cocaine/Meth • CRI • SLE
  13. 13. Chief Complaints in ACS  Chest Pain • Anginal • Atypical  Anginal Equivalents
  14. 14. Chest Pain  Anginal (Ischemic) - Fullness, pressure, crushing may radiate to neck, jaw, back, etc.  Atypical - Unilateral, sharp, changes with position, pleuritic, muscular-skeletal, not in chest but in jaw, neck, back
  15. 15. Anginal Equivalents  Dyspnea  Syncope  Diaphoresis  Weakness, nausea, vomiting  Palpitations, dysrhythmias  Other
  16. 16. Misdiagnosis  Misdiagnosed Chest Pain is the single largest area of litigation against Emergency Room Physicians. MACEP 2005  Patients with ACS may have chest wall tenderness on palpation. MACEP2005  One survey included 600,000 patients diagnosed with M.I. Study included 25% of all hospitals in US. One question asked…  Did you have chest pain at any point?  33% of all patients survey answered “NO”
  17. 17. Misdiagnosis  Although traditionally deemed as low risk: • Pleuritic • Sharp and stabbing pain, • Pain reproducible with palpation or movement • Pain that is either very short or prolonged in duration  A significant number of patients diagnosed with M.I. presented with these symptoms*  One study revealed that 7% of all M.I. patients evaluated had pain that was fully reproducible on palpation*  *Lee TH, Cook EF, Weisberg M, et al Acute chest pain in the ED, Arch Internal Med.
  18. 18. MONA for all ACS patients? Morphine Oxygen? NTG ASA 12 Lead EKG Transport Dx! Beta Blockers?
  19. 19. Therapy: What does it get me?  Aspirin • 21-25% reduction if given during ACS and continued out 35 days (ISIS-2, JACC 1988)  Beta-blocker • Clearly shown to reduce all-cause mortality long term following ACS • Possible 1% reduction in re-infarction and VF is offset by the 1.1% of patients who end up in cardiogenic shock when it is inappropriately given (COMMIT/CCS-2, 2005)
  20. 20. ECG: First Priority Then make a destination decision… …STEMI = PCI Center
  21. 21. Relationship Between DBT and Mortality Deluca G et al. Time delay to treatment and mortality in primary angioplasty for AMI: every minute of delay counts. Circulation 2004; 109(10): 1223-1225 30 minute delay = 7.5% increase in mortality!
  22. 22. Value of an Early ECG  ECG changes from ACS are dynamic  MONA treatment may mask changes  ST elevation = reperfusion indication  EMS is in a privileged position • Early 12-lead • During symptoms • Before medication
  23. 23. Reduce Time to Thrombolysis Many studies have shown significant reductions in hospital-based time to treatment with fibrinolytic therapy in patients with AMI identified before arrival by 12-lead ECG. Time savings ranged from 20-55 minutes. AHA, Guidelines 2000
  24. 24. Bradley EH, et al. N Engl J Med. 2006. November 13. [Epub ahead of print]. Strategies Associated With a Significant Reduction in Door-to-Balloon Time Strategy Mean reduction in door-to-balloon time (min)* Having emergency physicians activate the cath lab 8.2 Having single call to a central page operator activate cath lab 13.8 Having the ED activate the cath lab while patient still en route 15.4 Expecting staff to arrive at cath lab within 20 minutes after page 19.3 Having an attending cardiologist always on site 14.6 Having staff in ED and cath lab use and receive real-time feedback 8.6
  25. 25. Who Are These Clowns?  Jeffrey Rupple  NREMT – Paramedic  20 years EMS Education Experience  PALS, BCLS Instructor  EMS Management – Director of Operations, Field Supervisor, Field Training Officer  ZOLL Medical – Clinical Deployment Specialist
  26. 26. Who Are These Clowns?  Jeffrey Rupple  NREMT – Paramedic  20 years EMS Education Experience  PALS, BCLS Instructor  EMS Management – Director of Operations, Field Supervisor, Field Training Officer  ZOLL Medical – Clinical Deployment Specialist
  27. 27. 12 LEAD ACQUISITION
  28. 28. Obtaining the 12-Lead ECG  Remove the patient’s clothes from waist up • Prevents wire tangle • Permits full chest exam • Allows for rapid defibrillation if needed • Saves time in ER • Use a hospital-type gown  Real World - adjust clothing as appropriate for surroundings
  29. 29. Obtaining the 12-Lead ECG  Clip chest hair • Faster • More comfortable • Prevents infection • Safer (less nicks and cuts)  Shaving is acceptable alternative • Think gross decon • Not Remington close
  30. 30. Obtaining the 12-Lead ECG  Prep the skin • Should be done prior to EVERY 12-Lead ECG • 12 Lead is more sensitive to artifact • Use commercially prepared skin preps if available • 4x4 gauze pads or towel with firm, brisk rub works well • Cardiac Services (Cath Lab, EP Lab) use fine grit sandpaper! • DON’T BE TIMID!
  31. 31. Obtaining the 12-Lead ECG  Position patient correctly  Supine is ideal  Recline patient as low as they will tolerate  Below 45 degrees is acceptable  Have patient remain still  Watch for muscle tensing (White Knuckle)  Indicate symptoms, treatment, and time
  32. 32. Causes of Poor Tracings  Causes of poor ECG signal • Most common cause is poor electrode contact with skin  Check for • Excessive hair • Loose or dislodged electrodes, especially in diaphoretic (sweaty) patients • Dried conductive gel on disposable electrodes • Poor placement over bony area • Poor quality electrodes
  33. 33. Disclaimer Information contained herein is provided for reference only and does not replace local / regional standing orders, protocols, Standard Operating Procedures or equipment manufacturer’s recommendations.
  34. 34. Electrode Quality  ZOLL recommends the use of a high quality wet gel electrode  Dry gel electrodes do not perform well in the EMS environment  Poor quality electrodes are more likely to provide poor quality tracings
  35. 35. LEAD PLACEMENT
  36. 36. Lead Placement  V1 - Right parasternally, 4th ICS  V2 - Left parasternally, 4th ICS  V3 - Between V2 and V4  V4 - 5th ICS, mid clavicular line  V5 - Between V4 and V6  V6 - Left mid-axillary line, (level with V4)
  37. 37. Indicative Leads  Positive Pole (+)  Acts as point of reference  Imagine the positive pole as a camera lens
  38. 38. 4 Lead Placement for 12 Lead ECG  Contrary to popular belief, the 4 primary monitor leads, often referred to as limb leads, DO NOT need to be placed on the distal extremity (i.e. wrists and ankles)  The primary leads need to be 10 centimeters (approximately 4 inches) from the heart to be diagnostically significant (accurate)  Distal lead placement originates from Dr. Willem Einthoven original EKG experiments in the early 1900s
  39. 39. Ward and Wayne’s First Marketing Project
  40. 40. Distal Lead Placement  If you are still using the machine from the previous slide, then yes, distal lead placement is required
  41. 41. Indicative Lead Groups  Inferior Wall - II, III, and aVF  Septal Wall - V1, V2  Anterior Wall - V3, V4  Lateral Wall - V5, V6, I, and aVL
  42. 42. Disclaimer The information and tools presented to you today are outstanding aids to your patient assessment and treatment, and ideally will enable you to provide better patient care. The devices and information provided are designed to AUGMENT your patient assessment NOT REPLACE IT! PLEASE, TREAT THE PATIENT, NOT THE MONITOR!
  43. 43. Disclaimer The information and tools presented to you today are outstanding aids to your patient assessment and treatment, and ideally will enable you to provide better patient care. The devices and information provided are designed to AUGMENT your patient assessment NOT REPLACE IT! PLEASE, TREAT THE PATIENT, NOT THE MONITOR!
  44. 44. Disclaimer The information and tools presented to you today are outstanding aids to your patient assessment and treatment, and ideally will enable you to provide better patient care. The devices and information provided are designed to AUGMENT your patient assessment NOT REPLACE IT! PLEASE, TREAT THE PATIENT, NOT THE MONITOR!
  45. 45. Presumptive Evidence of an AMI  Presumptive evidence of an AMI • One mm of ST elevation in 2 leads from any group • 2 contiguous chest leads  Contiguous Leads- Anatomic or Numerical  New or “presumably new” Left BBB?  The standard 12-Lead does not have leads facing the posterior left ventricle or the right ventricle. Specialty leads are required to detect these type of MI’s.
  46. 46. Specialty Leads  Posterior Wall - V7-V9  Right Ventricle - V3R-V6R
  47. 47. Survey Says  ST elevation in the inferior leads  II, III and aVF  Acute inferior myocardial infarction
  48. 48. Oh Boy!  ST elevation in the septal, anterior and lateral leads  V1 - V6, I and aVL  Acute anterior-lateral myocardial infarction
  49. 49. Benefits of Prehospital 12-Lead ECG  Recognize AMI  Identify Reperfusion Candidates  The Earlier the Better - TIME IS MUSCLE!  Reduce Time to Thrombolysis  Reduce Time to PCI  Prehospital Thrombolytics
  50. 50. Benefits of Prehospital 12-Lead ECG  Recognize AMI  Identify Reperfusion Candidates  The Earlier the Better - TIME IS MUSCLE!  Reduce Time to Thrombolysis  Reduce Time to PCI  Prehospital Thrombolytics
  51. 51. CORONARY PERFUSION ANATOMICAL REVIEW
  52. 52. Coronary Arteries
  53. 53. Right Coronary Artery  Supplies the inferior wall of the left ventricle and feeds the right ventricle  Branches off into the posterior descending coronary artery which…  Supplies the posterior wall of the left ventricle.  Inferior wall MIs have posterior and/or right ventricular involvement in 50% of the cases.
  54. 54. Left Anterior Descending  The left anterior descending (LAD) coronary artery is a major branch of the LCA  LAD feeds 40% of the left ventricular mass  Because most sudden-death AMI’s result from a proximal occlusion of the LAD, it is known as the “Widow Maker”  LAD feeds the anterior and septal walls of the left ventricle  LAD also supplies the Bundle of His and both branches through the intraventricular septal perforator artery
  55. 55. Adding Insult to Injury  40% involvement of the left ventricle results in irritation that can cause immediate v-fib or v- tach  Patients may develop CHB, BBB’s or hemiblock as another complication of LAD proximal occlusion
  56. 56. Left Circumflex Artery  Is the other major division of the left coronary artery  The LCA feeds the lateral and posterior walls of the left ventricle
  57. 57. ST depression T wave inversion
  58. 58. Evolution of STEMI A. Normal B. Hyper-acute T-waves: Minutes to Hours C. ST-Elevation: 0-12 Hours D. Q-Wave Development: 1-12 Hours E. ST-Elevation with T-wave inversion: 2-5 days F. T-Wave recovery: weeks to months
  59. 59. REVIEW OF EKG COMPLEXES BACK TO BASIC DYSRHYTHMIA INTERPRETATION At least it’s not Acid-Base Balance!
  60. 60. QRS  Q wave: • First negative deflection, usually preceding an R wave  R Wave: • First positive deflection  S Wave: • Negative deflection following an R wave
  61. 61. Acute Coronary Syndromes Unstable Angina (UA) Non-Q Wave Myocardial Infarction (NQMI) Q Wave Myocardial Infarction (QMI)
  62. 62. > 1mm < 1mm Pathological Physiological Q Waves
  63. 63. T Wave  Large wave form following QRS Complex  Represents Ventricular Repolarization  Should be upright in most leads (III and V1)  Look for consistent morphology
  64. 64. UprightUpright InvertedInverted T Waves
  65. 65. T-P Segment  Area between, yup you guessed it, the end of the T-Wave and the beginning of the P-Wave  Indentify this area and use it as your point of reference for ST Segment Deviation  T-P Segment becomes your isoelectric line
  66. 66. T-P SegmentT-P Segment BaselineBaseline T-P Segment
  67. 67. ST Segment  The segment immediately following the QRS complex and ending at the T wave  The J point (junction point) is the exact point where the QRS stops and the ST begins
  68. 68. Isoelectric Elevated Depressed ST Segment
  69. 69. ST Segment  The ST segment is normally level with the T-P segment rather than the PR segment  Examine every lead for ST segment elevation of 1 mm or more. 1998 85
  70. 70. Practice Sample
  71. 71. ST Elevation in Leads II, III, aVF Practice Sample
  72. 72. Myocardial Infarction Labels For pre-hospital purposes Non- ST- Elevation MI (NSTEMI) = Non-Q-Wave MI (NQMI) ST Elevation MI (STEMI) = Q-Wave MI (QMI)
  73. 73. T Wave Inversion Practice Sample
  74. 74. Pathological Q’s in II & III ?? Practice Sample
  75. 75. Indicative Lead Groups  Inferior Wall - II, III, and aVF  Septal Wall - V1, V2  Anterior Wall - V3, V4  Lateral Wall - V5, V6, I, and aVL
  76. 76. EKG PATTERNS OF INFARCTION
  77. 77. ST Segment Elevation  Indicators to look for: • Injury • ST segment elevation >1 mm (>2 mm in septal leads) • Present in two or more related or anatomically contiguous leads • Measure at J point (plus 20 - 40ms) to baseline
  78. 78. ST Segment Elevation - continued  ST elevation means acute transmural injury • Involves three layers of the heart  In an acute MI, the shape is not as diagnostic as • Reciprocal changes • Patient history • Presentation
  79. 79. Injury
  80. 80. ST Depression  The causes of ST depression • Reciprocal changes to ST elevation • Ischemia or subendocardial injury • Certain medications, such as digitalis  If ST segment depression does not appear to be reciprocal • Could be myocardial ischemia or injury to the subendocardial wall • Involves a single layer of the heart muscle.
  81. 81. STEMI
  82. 82. Inverted T Waves  One early sign of an ACS and MI is the T- Wave Inversion  Because at times, the ST changes may disappear as the area is reperfused by NTG, a baseline 12 Lead prior to the administration of NTG can be helpful.
  83. 83. Inverted T Waves - continued  Key points about inverted T Waves • Can represent Ischemia (transient reduction in blood flow) • Symmetrical inverted T waves in two or more related leads • Inverted T waves normal in Leads VI and III
  84. 84. Pathological Q Wave  Signifies infarction, or death of the tissue  Indicators of an Infarct • Pathological Q wave • >40 ms, or 0.04 sec wide, or 1/3 of R wave height • Indicates on-going or permanent damage
  85. 85. COMPONENTS OF THE 12 LEAD EKG What is the box trying to tell us?
  86. 86. Paper SpeedPaper Speed
  87. 87. CalibrationCalibration
  88. 88. Frequency ResponseFrequency Response
  89. 89. Frequency Response  Monitor frequency ranges eliminate artifact at the expense of ST-T accuracy  Do not rely on monitor quality tracings for diagnostic interpretation
  90. 90. Monitor Quality Diagnostic Quality
  91. 91. Lead IdentityLead Identity
  92. 92. One Complete Cardiac CycleOne Complete Cardiac Cycle
  93. 93. Patient AgePatient Age
  94. 94. Patient GenderPatient Gender
  95. 95. Patient Information Patient Information MeasurementsMeasurements Computerized Interpretive Statement Computerized Interpretive Statement
  96. 96. ACUTE INFARCT LOCALIZATION Practice
  97. 97. ST Segment Elevation in Leads? ST Segment Depression in Leads? Interpretation/Localization?
  98. 98. II, III, aVF I, aVL, V2 - V4 I, aVL, V2 - V4 None Acute Inferior Wall MI
  99. 99. ST Segment Elevation in Leads? ST Segment Depression in Leads? Interpretation/Localization?
  100. 100. V1-V4, (aVL?) II, III, aVF, V4, V5 III V1 Acute Anteroseptal MI
  101. 101. NSTEMI
  102. 102. V1 - V5, I, aVL III III V1 - V5, II, III, aVF Acute Extensive Anterior MI & Old Inferior Wall MI
  103. 103. Reciprocal Changes Inferior: II,III,aVF Anterior: V1-V6, aVL, I Septal: V1, V2 Lateral: V5,V6, I, aVL Early Anterior: V1-V3 Posterior: V7-V9
  104. 104. ST Segment Elevation in Leads? Reciprocal ST Segment Depression in Leads? Make Sense?
  105. 105. ST Segment Elevation in Leads: ____________________________ Reciprocal Changes in Leads: ____________________________ ST Segment Elevation in Leads? Reciprocal ST Segment Depression in Leads? Make Sense?
  106. 106. ST Segment Elevation in Leads? Reciprocal ST Segment Depression in Leads? Make Sense?
  107. 107. COMPUTERIZED INTERPRETIVE STATEMENTS The Computer Cardiologist
  108. 108. Computerized Interpretive Statement  In existence for over 50 years  Statistically accurate  Not always correct MUST ALWAYS BE VIEWED IN LIGHT OF THE SURROUNDING CLINICAL CIRCUMSTANCES
  109. 109. 12 Lead ECG Interpretive Algorithms  It is important to note that there are several 12 Lead ECG Interpretive Algorithms used in EMS transport monitors • GE (Marquette) 12SL Interpretive Algorithm • ZOLL M, CCT, and E Series • Physio Control Lifepak 12 • Inovise 12 L Interpretive Algorithm • ZOLL X Series, Propaq MD • Glasgow 12 Lead Analysis Program • Physio Control Lifepak 15 • Philips DXL 12 Lead Algorithm • Philips MRX
  110. 110. Acute Myocardial Infarction Statements ***Acute MI*** ***STEMI*** ***Meets ST Elevation MI Criteria***  98% - 99% specificity  52% - 70% sensitivity Acute MI Statements = STEMI
  111. 111. Sensitivity  Refers to recognition  If the test always recognizes the disorder, sensitivity would be 100%  False negatives are failures of sensitivity  A false negative occurs when the condition exists but the test fails to find it
  112. 112. Specificity  Refers to the number of diagnoses confirmed  If the diagnosis were corroborated every time the test identifies it, it would be 100% specific  False positives are failures in specificity  A false positive occurs when the test indicates the disease is present, when in fact it is not
  113. 113. ACS Risk Factors  Diabetes  Smoking  Hypertension  High Cholesterol  Family History  Obesity  Sedentary Life
  114. 114. ECG Subsets for ACS  Non-Diagnostic  Suspicious for Ischemia  Suspicious for Injury
  115. 115. Non-Diagnostic ECG Normal sinus rhythm Normal ECG ****Unconfirmed**** Normal sinus rhythm Normal ECG ****Unconfirmed****
  116. 116. Interpretive Statement For Non-Diagnostic ECGs  No ST/T abnormality statements  May point out other abnormalities such as chamber hypertrophy, axis deviation, etc.  May point out old Q wave MIs without ST-T abnormalities
  117. 117. Non-Diagnostic ECG  Does not rule out ACS  Look in additional leads if story is strong and or risk factors high  Look for non-cardiac causes of symptoms  Repeat ECG often, it may change
  118. 118. Suspicious for Ischemia ST & T wave abnormality, possible anteriolateral ischemia ST & T wave abnormality, possible inferior ischemia Abnormal ECG ST & T wave abnormality, possible anteriolateral ischemia ST & T wave abnormality, possible inferior ischemia Abnormal ECG
  119. 119. Suspicious for Ischemia  Abnormal ST segment depression and/or T wave inversion  Absence of ST Elevation  May represent UA or NSTEMI
  120. 120. Suspicious for Ischemia  Unstable Angina (UA) or Non-ST Elevation MI (NSTEMI) ?  Cardiac Markers will make the differentiation  Pre-treatment ECG useful  Repeat the ECG often
  121. 121. The History  Good Assessment • HPI • Nature of Symptoms • OPQRST • Patient History  Traditional Risk Factors • Age • Male Sex • DM • Tobacco • History of CAD • Family History • HTN • Cholesterol  Non-Traditional Risk Factors • DM = CAD • HIV with or without HAART • Cocaine/Meth • CRI • SLE
  122. 122. High-Risk Management  Repeat ECG  Heparin  GPIIb/IIIa inhibitors  Integrilin (eptifibatide)  Aggrastat (tirofiban hydrochloride)  Beta blockers or calcium channel blockers  IV Nitrates  Early coronary intervention
  123. 123. Interpretive Statement For Ischemic ECGs  Non-specific ST/T abnormality statements  Suspicious for ischemia  Subendocardial injury pattern  Localized ischemia statements
  124. 124. Special Consideration  ST depression in early V leads • May be anterior ischemia • May be reciprocal changes of posterior MI • Check V7-V9 for ST elevation Move to Acute MI category if ST Elevation present in V7-V9
  125. 125. Sinus rhythm with first degree AV block with occasional supraventricular complexes Possible left atrial enlargement Inferior infarct Marked ST depression consistent with subendocardial injury **Acute MI** Sinus rhythm with first degree AV block with occasional supraventricular complexes Possible left atrial enlargement Inferior infarct Marked ST depression consistent with subendocardial injury **Acute MI** Suspicious for Injury
  126. 126. Suspicious for Injury  ST Elevation  2 or more anatomically contiguous leads  1 mm or more
  127. 127. ECG Subsets Pathological Q Waves  Q waves may appear with acute or old infarcts  Older infarcts will display Q waves without ST-T abnormalities causing computer to note infarct  Do not confuse infarct statement with ***Acute Myocardial Infarction*** statements
  128. 128. Sinus tachycardia Inferior infarct Abnormal ECG Sinus tachycardia Inferior infarct Abnormal ECG Q Waves
  129. 129. RIGHT VENTRICULAR INFARCTION & POSTERIOR WALL INFARCTION
  130. 130. History of RVI  Right Ventricular Infarctions (RVI) were initially described 70 years ago.  It wasn’t until 1974 before the significance of the RVI was truly understood.  Before 1974 cardiologists believed that the right ventricle was not an essential component of adequate circulation.
  131. 131. Epidemiology  RVI accompany extensive inferior-posterior wall MIs.  Risk factors include chronic lung disease, and right ventricular hypertrophy.  RVI are difficult to diagnose.  Only 50% of patients will have hemodynamic compromise.
  132. 132. Mortality and Morbidity  Inferior MIs with an associated RVI have mortality rates that range between 30-50%  Inferior MIs without RVI involvement have a 6% mortality rate.  Patients with minimal Left Ventricle (LV) involvement have excellent long term survival
  133. 133. Chief Complaints in ACS  Chest Pain • Anginal • Atypical  Anginal Equivalents
  134. 134. Right Ventricular A & P 150 Right Ventricle Left Ventricle
  135. 135. Right Ventricle A & P  The RV has lower afterload, a lower oxygen demand and a higher oxygen supply  It is relatively resistant to irreversible ischemic damage during right coronary artery occlusion  Normal right ventricular end diastolic pressure is between 2-4 mmHg  Right ventricle has the same CO as the left ventricle 4-6 L/min
  136. 136. Left Dominant vs. Right Dominant  85% of the population is right dominant.  7.5% of the population is left dominant.  7.5% of the population is co-dominant.  Right dominant infers that the RCA supplies circulation to the inferior portion of the interventricular septum.
  137. 137. RVI Causes  There is right ventricle involvement in approximately 33% of Inferior MIs  RVI occurs when there is an occlusion of the RCA proximal to the acute marginal branches in R dominant patients  RVI occurs with an occlusion of the left circumflex artery in patients who are L dominant  RVI can be caused by an occlusion of the LAD but this is rare  Isolated RVI is rare – 2% of autopsies
  138. 138. RVI Causes Right Side Dominant - occlusion above the marginal artery will cause an RVI Left Side Dominant - occlusion of the Circumflex Artery will cause RVI RVI indicates a proximal occlusion and a serious infarction
  139. 139. What Happens  Occlusion to the RCA happens above the marginal branches  The right ventricle now becomes a conduit  It is unable to handle venous return  Resulting in decreased RV compliance, decreased stroke volume, and decreased cardiac output
  140. 140. Signs and Symptoms  Increased jugular venous pressure  Hypotension • Before or after NTG administration  Clear lung fields  Kussmaul sign  Pulsus paradoxus  Cool, clammy skin
  141. 141. Chest Pain  Anginal (Ischemic) - Fullness, pressure, crushing may radiate to neck, jaw, back, etc.  Atypical - Unilateral, sharp, changes with position, pleuritic, muscular-skeletal, not in chest but in jaw, neck, back
  142. 142. 12 Lead ECG Findings  ST segment elevation in inferior leads  Greater ST segment elevation in lead III than lead II in an inferior wall MI  ST segment depression in leads V1-V4 • May be confused with anteroseptal MI.  Right bundle branch blocks and complete heart blocks are the most common conduction disturbances
  143. 143. Right Sided 12 Lead ECG  Complete right side 12 lead is preferable  V4R is the best single view  A 1 mm elevation in the ST segment is 70% sensitive and 100% specific for a RVI  Elevation in this lead is transient and resolves within 10-12 hrs  A right sided EKG should be done as soon as possible on all inferior wall MIs
  144. 144. Ride Sided 12 Lead Placement
  145. 145. Right Sided Lead Placement V3R - Between V1 and V4R V4R - 5th ICS, right mid-clavicular line V5R - Between V4R and V6R V6R - Right mid axillary line, level with V4R
  146. 146. Hemodynamic Consequences of RVI  Compensated • Decreased R ventricular contractility • Decreased blood flow to Left ventricle • Decreased stroke volume • Increased HR to maintain Cardiac Output • Increased systemic vascular resistance • Mildly reduced Cardiac Output  Decompensated • Drastically reduced Cardiac Output • Hypotension • Increased blood volume in Right ventricle • Decreased Right ventricular ejection • Increased pressure in Right atrium and ventricle
  147. 147. Initial 12 Lead
  148. 148. Right Sided 12 Lead
  149. 149. Initial 12 Lead
  150. 150. V4R
  151. 151. Treatment  Early STEMI team activation and reperfusion strategies  Oxygen • Increases oxygen supply to the myocardium. (≥ 94% SpO2)  Aspirin • Decreases platelet aggregation  Fluids • Volume loading with isotonic crystalloid is the initial treatment for hypotensive patients suffering from a RVI • Working on Starling’s Law
  152. 152. Anginal Equivalents  Dyspnea  Syncope  Diaphoresis  Weakness, nausea, vomiting  Palpitations, dysrhythmias  Other
  153. 153. Treatment  The right ventricle is sensitive to beta adrenergic stimulation and blockade  If the response to volume loading is not favorable then a positive inotropic agent should be initiated  Dobutamine is the drug of choice and should be titrated to maintain an adequate cardiac output  Other therapies should include: –TCP initiation for significant heart blocks. –Synchronized cardioversion for hemodynamically unstable atrial fibrillation
  154. 154. Posterior Infarction  Occurs in about 33% of all inferior MI’s  Usually does not create the extraordinary effects that an RVI does.  May present isolated from an inferior MI  Evidenced by ST segment elevation in Leads V7, V8, and V9, with reciprocal depression in Leads VI-V4.
  155. 155. Pure Posterior MI - Note ST depression in early V leads. ST Elevation is present only in direct posterior leads V7-V9.
  156. 156.  Acute Posterior - Lateral myocardial infarction  Hyperacute - The mirror image of acute injury in leads V1 - V3 - Fully Evolved - Tall R wave, tall upright T wave in leads V1 -V3 usually associated with inferior and/or lateral wall MI
  157. 157. Posterior Lead Placement V7 - Post axillary line, level with V4 V8 - Mid scapular line, level with V4 V9 - Left paravertebral area, level with V4
  158. 158. Misdiagnosis  Misdiagnosed Chest Pain is the single largest area of litigation against Emergency Room Physicians. MACEP 2005  Patients with ACS may have chest wall tenderness on palpation. MACEP2005  One survey included 600,000 patients diagnosed with M.I. Study included 25% of all hospitals in US. One question asked…  Did you have chest pain at any point?  33% of all patients survey answered “NO”
  159. 159. Misdiagnosis  Misdiagnosed Chest Pain is the single largest area of litigation against Emergency Room Physicians. MACEP 2005  Patients with ACS may have chest wall tenderness on palpation. MACEP2005  One survey included 600,000 patients diagnosed with M.I. Study included 25% of all hospitals in US. One question asked…  Did you have chest pain at any point?  33% of all patients survey answered “NO”
  160. 160. BUNDLE BRANCH BLOCKS
  161. 161. Introduction  A BBB is an electrical phenomenon characterized by a widening of the QRS of at least 0.12 seconds or greater  The wider the QRS complex, the lower the patient’s Cardiac Output
  162. 162. Anatomy & Physiology  Blood supply for the bundle branches usually comes from the left anterior descending coronary artery, but also can be from the AV nodal branch of the right coronary artery  Usually, depolarization is simultaneous with the right and left ventricle, via the bundle branches
  163. 163. LBB RBB
  164. 164. Ventricular Conduction in LBBB + 1 3 2 V1 120 m/sec 1 2 3
  165. 165. Misdiagnosis  Although traditionally deemed as low risk: • Pleuritic • Sharp and stabbing pain, • Pain reproducible with palpation or movement • Pain that is either very short or prolonged in duration  A significant number of patients diagnosed with M.I. presented with these symptoms*  One study revealed that 7% of all M.I. patients evaluated had pain that was fully reproducible on palpation*  *Lee TH, Cook EF, Weisberg M, et al Acute chest pain in the ED, Arch Internal Med.
  166. 166. Diagnosing BBB’s  V1 is the lead to use to diagnose BBB’s  This lead looks across the ventricles and can see both bundle branches  To diagnose bundle branch blocks, use the turn signal criteria  First – find a supraventricular complex • Associated P wave • Greater 0.12 sec  Next – find the J point, the point in which the QRS turns into the ST segment  Then – look at the direction from which the QRS terminates • If the complex comes from above – then it is a RBBB • If the complex comes from below – then it is a LBBB
  167. 167. LBBB is identified by a wide QRS with the terminal portion of the QRS being negative in V1 LBBB is identified by a wide QRS with the terminal portion of the QRS being negative in V1 Left Bundle Branch Block
  168. 168. RBBB is identified by a wide QRS with the terminal portion of the QRS being positive in lead V1 RBBB is identified by a wide QRS with the terminal portion of the QRS being positive in lead V1 V1 Right Bundle Branch Block
  169. 169. Significance of BBB  In the presence of an AMI, a BBB is a serious complication that usually indicates extensive coronary artery occlusion and anterior wall damage  BBB complication of an MI has a mortality rate 4x greater than those with MI alone  Typically occurs with occlusions to the left anterior descending coronary artery • Septal or anterior wall MI’s • Frequently develop BBB’s or CHB
  170. 170. Significance of BBB - continued  The presence of an LBBB obscures the ST segment, making ECG diagnosis of an AMI very difficult  With RBBB, the ST segment is intact, and MI determination is easier  When a partial LBBB (fasicular) is combined with an RBBB, it is called a bifascicular block  When a bifascicular block exists, antiarrythmics, and morphine can slow the conduction system through the ventricles, resulting in drug-induced CHB, or possibly, ventricular asystole
  171. 171. The Joys of a LBBB  May be new or old  If not proven to be old it is presumptively new  AHA Guidelines state that patients with a new or presumably new BBB are placed in the same category as patients with STEMI  Why?  Because changes that occur with LBBB mask ST Segment changes
  172. 172. AHA MI Consensus Statement 2013  New or presumably new LBBB at presentation occurs infrequently, may interfere with ST- elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation
  173. 173. MONA for all ACS patients? Morphine Oxygen? NTG ASA 12 Lead EKG Transport Dx! Beta Blockers?
  174. 174. MONA for all ACS patients? Morphine Oxygen? NTG ASA 12 Lead EKG Transport Dx! Beta Blockers?
  175. 175. MONA for all ACS patients? Morphine Oxygen? NTG ASA 12 Lead EKG Transport Dx! Beta Blockers?
  176. 176. In LBBB, leads with negative QRS deflection will display ST elevation and an upright T wave In LBBB, leads with negative QRS deflection will display ST elevation and an upright T wave Leads with positively deflected complexes will display ST depression and negative T Waves Leads with positively deflected complexes will display ST depression and negative T Waves ST-T Discordance
  177. 177. Elevation Depression Discordant Concordant Discordant Concordant ST-T Discordance
  178. 178. Normal sinus rhythm with frequent premature ventricular complexes Left axis deviation Left Bundle branch block Normal sinus rhythm with frequent premature ventricular complexes Left axis deviation Left Bundle branch block Note the ST-T discordance—it also occurs with PVCs ST-T Discordance
  179. 179. Sgarbossa’s Criteria  The three criteria Sgarbossa's criteria are: • ST elevation ≥1 mm in a lead with a positive QRS complex (ie: concordance) - 5 points • ST depression ≥1 mm in lead V1, V2, or V3 - 3 points • ST elevation ≥5 mm in a lead with a negative (discordant) QRS complex - 2 points  ≥3 points • 90% specificity of STEMI (sensitivity of 36%)
  180. 180. Other Criteria  ST elevation more than you'd expect from LBBB alone • Must be present in 2 or more contiguous leads - (e.g. > 5 mm in leads V1 - V3)
  181. 181.  Acute myocardial infarction in the presence of Right Bundle Branch Block  Features suggesting acute septal- anterior MI  ST changes not obscured by RBBB
  182. 182. Therapy: What does it get me?  Aspirin • 21-25% reduction if given during ACS and continued out 35 days (ISIS-2, JACC 1988)  Beta-blocker • Clearly shown to reduce all-cause mortality long term following ACS • Possible 1% reduction in re-infarction and VF is offset by the 1.1% of patients who end up in cardiogenic shock when it is inappropriately given (COMMIT/CCS-2, 2005)
  183. 183. Hemodynamic Effects of BBB’s  In some cases, a BBB can have a significant hemodynamic effect  A BBB means a delayed conduction and depolarization time  QRS greater than 0.17 seconds, have an Ejection Fraction (EF) of less than 50% • Normal is 55% - 75%  Contractility is compromised, hence CO is affected
  184. 184. AXIS AND HEMIBLOCKS
  185. 185. Determining Axis and Hemiblock  Axis: defined as the general direction of electrical impulses travel through the heart • As they travel, they are carried in different directions • 90% of the impulses cancel one another out • The remaining 10% travel in one primary direction • Assessing the direction of these impulses provides clues about the severity of a patient’s condition and helps to guide treatment
  186. 186. Hexaxial System  Includes limb Leads I, II, III and the augmented Leads aVL, aVR, and aVF.  The result is like a pie of six equal pieces and lines to which you add in the degrees.
  187. 187. Normal Axis  To determine axis – run Leads I, II, III  Normally, electrical impulses start from the SA Node, and travel downward to the lower left side of the heart  Conducted impulses travel toward the positive electrodes in Lead I, II, III, creating an upward QRS deflection.
  188. 188. Left-Axis Deviation  Axis is rotated to the left  Two different categories -  Physiological left-axis deviation (normal variant) • Upward deflection in Lead I, Upward or Isoelectric Deflection in Lead II, and a Negative deflection in Lead III.  Pathological left-axis deviation • Upward deflection in Lead I, Negative deflection in Lead II and III.
  189. 189. Left-Axis Deviation
  190. 190. Right-Axis Deviation  In some patients, the axis may be deviated to the right  In children, this is a normal variant  In adults, a right-axis deviation has • Negative deviation in Lead I • Positive deviation in Lead III • Lead II can be positive, negative, or isoelectric
  191. 191. ECG: First Priority Then make a destination decision… …STEMI = PCI Center
  192. 192. Right-Axis Deviation - continued
  193. 193. Hemiblock  Best defined as a block of one of the two fascicles of the left bundle branch system.  There is a right bundle branch and a left bundle branch that divides into separate fascicles, also known as hemifascicles.  The hemifascicles are known as the left anterior and left posterior, those combined with the right right bundle branch make up a trifascicular system.
  194. 194. Hemiblock - continued  Impulses can travel in three ways to the ventricles: • Right Bundle Branch • Left Posterior Hemifascicle • Left Anterior Hemifascicle  Blocks in this system can be a precursor to heart blocks  Can help determine which patients are at risk for complete heart blocks  In presence of MI, 4 times higher mortality rate than an MI without a hemiblock
  195. 195. Left Anterior Hemiblock  Occurs when the anterior fascicle of the LBB system becomes blocked  A pathological left-axis deviation is indicative of an anterior fasicular block • Other clues: • Small Q wave in Lead I • Small R wave in Lead III • Can have a narrow QRS complex  LAD branch of the left coronary artery provides blood supply for the anterior hemifascicle  4 times higher than an MI without an anterior hemiblock
  196. 196. Left Posterior Hemiblock  Occurs when the posterior fascicle of the LBB system is blocked  A right-axis deviation is indicative of a left posterior hemiblock • Other clues: • Small R wave in Lead I, small Q wave in Lead III  The clinician should also inspect for the presence of: • Right ventricular hypertrophy • JVD, Pedal edema and patient history
  197. 197. Left Posterior Hemiblock - continued  The posterior hemiblock is considered more acute than the anterior hemiblock  The posterior hemifascicle is thicker than the anterior hemifascicle, having more cells and needing a more significant supply of blood  A redundant blood supply is required from two different coronary arteries: • Right coronary artery • Circumflex  If both coronary arteries are blocked, extensive coronary occlusion has occurred
  198. 198. Clinical Significance of Hemiblock  The clinical significance of hemiblock can be summarized as follows: • Four times higher mortality rate for patients having an AMI with a hemiblock than those without hemiblock • Significantly higher risk for complete heart block • In the setting of an AMI, can indicate proximal artery occlusion
  199. 199. RAPID AXIS AND HEMIBLOCK CHART
  200. 200. Relationship Between DBT and Mortality Deluca G et al. Time delay to treatment and mortality in primary angioplasty for AMI: every minute of delay counts. Circulation 2004; 109(10): 1223-1225 30 minute delay = 7.5% increase in mortality!
  201. 201. The Chart and a 3 or 4 Lead ECG  Look at Leads I, II and III  Determine whether the QRS complex is more positively or negatively deflected in each lead.  Compare your findings with the Chart to identify the axis and hemiblock.
  202. 202. Calculated Axis Angle  The number to look for is the R axis or QRS axis  The computerized measurements can be used to identify the axis deviation
  203. 203. CHAMBER ENLARGEMENTS
  204. 204. Right Atrial Abnormality  Right Atrial Enlargement (RAE) will show tall, pointed P waves in the inferior leads, II, III, aVF.  The P wave will be more than 2.5 mm  3-P memory aid • Pointed • Prominent • Pulmonary
  205. 205. Right Atrial Enlargement  Most likely causes • Congenital heart disease • Tricuspid or pulmonary valve disease • Pulmonary hypertension  Clinical implications • Generally not an acute problem • Frequently seen with Right Ventricular Hypertrophy
  206. 206. Left Atrial Abnormalities  Left Atrial Enlargement (LAE)  Most common cause is LVH  ECG criteria • Lead II widened p wave (>120 ms, or 3mm) with a notched or m-shaped appearance • Lead V1 broad terminal negative P deflection of more than 1 mm
  207. 207. Right Ventricular Hypertrophy  Caused by increased pressure, or volume in the right ventricle  Generally occurs in circumstances similar to those for RAE  RVH is characterized by large forces that go away from the lateral leads and towards V1  ECG Criteria for RVH • Right Atrial Enlargement • Narrow QRS • Right axis deviation • R Wave height in V1 greater than 7mm • Asymmetrical down sloping ST segment in inferior leads
  208. 208. Value of an Early ECG  ECG changes from ACS are dynamic  MONA treatment may mask changes  ST elevation = reperfusion indication  EMS is in a privileged position • Early 12-lead • During symptoms • Before medication
  209. 209. Value of an Early ECG  ECG changes from ACS are dynamic  MONA treatment may mask changes  ST elevation = reperfusion indication  EMS is in a privileged position • Early 12-lead • During symptoms • Before medication
  210. 210. Left Ventricular Hypertrophy  Clinical implications • Higher incidence of sudden death or ischemic arrhythmias • Can mimic the ST depression or elevation seen with myocardial ischemia • May be caused by an AMI • In the presence of an LBB, LVH criteria almost impossible to differentiate • May be a useful clue as to hemodynamic condition
  211. 211. ELECTROLYTE, DRUG AND OTHER ECG CHANGES
  212. 212. Potassium - Hypokalemia  Hypokalemia • Serum levels below 3.5 mEq/L • Most commonly caused by vomiting, diarrhea, diuretics, and gastric suctioning • Muscle weakness and polyuria are common signs and symptoms • Digitalis resulting from hypokalemia, causing serious dysrthythmias, ie: torsades • A-flutter, heart blocks, and bradycardia
  213. 213. Potassium - Hypokalemia  ECG Changes • ST segment depression • T waves flattened or joined with U waves • U waves getting larger than the T waves as the potassium level falls • QT interval appearing to lengthen as T combines with U • PR interval increases
  214. 214. Potassium - Hyperkalemia  ECG Changes • Mild cases – less than 6.5 mEq/L • Tall, tented, peaked T waves with a narrow bases • Best seen in Leads II, III, V2, and V4 • Normal P waves • Moderate cases – less than 8 mEq/L • QRS widens • Broad S wave in V leads • Left-axis deviation • ST segment is gone, contiguous with peaked T wave • P wave starts to flatten and diminish
  215. 215. Potassium - Hyperkalemia  Severe Cases  Greater than 8 mEq/L • P wave disappear • Sine waves
  216. 216. Hyperkalemia
  217. 217. Hyperkalemia
  218. 218. Calcium  Hypercalcemia is suggested by a shortened QT interval  Hypocalcemia is suggested by a prolonged QT interval
  219. 219. Hypocalcemia
  220. 220. Hypercalcemia
  221. 221. QT Interval  Represents the time from the start of depolarization of the ventricles to the end of repolarization  QT interval is measured from the start of the QRS to the end of the T wave  QTc is represents the corrected QT interval for the current heart rate
  222. 222. Reduce Time to Thrombolysis Many studies have shown significant reductions in hospital-based time to treatment with fibrinolytic therapy in patients with AMI identified before arrival by 12-lead ECG. Time savings ranged from 20-55 minutes. AHA, Guidelines 2000
  223. 223. Reduce Time to Thrombolysis Many studies have shown significant reductions in hospital-based time to treatment with fibrinolytic therapy in patients with AMI identified before arrival by 12-lead ECG. Time savings ranged from 20-55 minutes. AHA, Guidelines 2000
  224. 224. Digitalis Effect
  225. 225. Digitalis Effect
  226. 226. Pericarditis  ECG clues • ST Segment elevation • Concave in almost all leads, except aVR and V1 • T wave elevation starting above the isolectric line • ST segment depression, or T wave inversion
  227. 227. Pericarditis
  228. 228. Pericarditis
  229. 229. Pericarditis
  230. 230. Wolf-Parkinson-White (WPW)  Caused by accessory pathway between Atria and Ventricles.  Pathway known as the Bundle of Kent  Classic signs • Delta Wave • Short P-R Interval
  231. 231. Wolf-Parkinson-White (WPW)
  232. 232. Wolf-Parkinson-White (WPW)
  233. 233. Bradley EH, et al. N Engl J Med. 2006. November 13. [Epub ahead of print]. Strategies Associated With a Significant Reduction in Door-to-Balloon Time Strategy Mean reduction in door-to-balloon time (min)* Having emergency physicians activate the cath lab 8.2 Having single call to a central page operator activate cath lab 13.8 Having the ED activate the cath lab while patient still en route 15.4 Expecting staff to arrive at cath lab within 20 minutes after page 19.3 Having an attending cardiologist always on site 14.6 Having staff in ED and cath lab use and receive real-time feedback 8.6
  234. 234. Lown-Ganong-Levine Syndrome
  235. 235. Takotsubo Cardiomyopathy  Also known as: • Transient apical ballooning syndrome • Stress-induced cardiomyopathy • Gebrochenes-Herz Syndrom • Broken heart syndrome  Can be triggered by: • Emotional stress • Death of a loved one • Divorce or break up • Constant anxiety • Physical Stressor • Asthma attack • Sudden illness
  236. 236. Takotsubo Presentation  EMS and E.D. presentation • Chest pain with or without dypsnea • ECG changes mimicking anterior AMI (V2-V5) • Sudden onset of congestive heart failure • Moderate cardiac enzyme elevation  Invasive evaluation and enhanced imaging • Bulging of the left ventricular apex • Hypercontracile base of the left ventricle • No significant coronary artery blockages on angiogram  Takotsubo Cardiomyopathy is found in 1.7% – 2.2% of all ACS patients
  237. 237. Takotsubo vs. Normal Takotsubo – Japanese octopus pot
  238. 238. Takotsubo Cardiomyopathy
  239. 239. Takotsubo Cardiomyopathy
  240. 240. Treatment and Prognosis  Treatment includes • ASA • NTG for Chest Pain • Fluids • Negative inotropes • Calcium Channel Blockers, Beta Blockers, ACE Inhibitors • Intra-aortic balloon pump support • Cautious use of positive inotropic agents  Symptom resolution • LV function improvement in first few days • Normalization in first few months  Mortality rate 0 - 8%
  241. 241. Brugada Syndrome  Caused by a genetic disorder  Characterized by ECG changes and an increase risk of Sudden Cardiac Arrest (SCA)  ECG changes • Typically V1 - V3 • ST segment elevation • RBBB like appearance  Most common cause of SCA in young men without underlying cardiac disease in Thailand and Laos
  242. 242. Brugada Syndrome
  243. 243. Brugada Syndrome
  244. 244. PRACTICE EKG’S
  245. 245. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  246. 246. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  247. 247. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  248. 248. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  249. 249. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  250. 250. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  251. 251. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  252. 252. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  253. 253. ST Segment Elevation in Leads: ____________________________ ST Segment Depression in Leads: ____________________________ Interpretation/Localization: ____________________________
  254. 254. QUESTIONS?
  255. 255. Acknowledgements  David Lacaillade  Eric Kessler Thanks!

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