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Stemi or no stemi

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Stemi vs no stemi

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Stemi or no stemi

  1. 1. STEMI or NO STEMI Presented By: Marti Dunn Brian Gerdes Chris Cox
  2. 2. The purpose of this presentation is to review and improve recognition of STEMIs in the field.
  3. 3. Objectives • Review anatomy of the heart • Review rules for interpreting rhythms • Review recognition of STEMI and NO STEMI • Review STEMI Imposters
  4. 4. Anatomy of the Heart • Heart is located to the left side of a patient’s chest • It is about the size of a human fist • The heart is made out of cardiac muscle • Cardiac muscle does not regenerate(when it dies it does not reproduce itself)
  5. 5. • Coronary Arteries are sole suppliers of arterial blood to the heart • They deliver 200 to 250 mL of blood to the myocardium each minute during rest • The left coronary artery carries about 85% percent, of the blood supply • The right coronary artery carries the rest about 15 %
  6. 6. • Left main coronary artery supplies the left ventricle and part of the right ventricle • It has two main branches are the left anterior descending, artery and the circumflex artery
  7. 7. Interpreting a 12 Lead ECG
  8. 8. • Remember that each small box is equal to 0.04 seconds • There should be five small boxes in every big box • One big box equals 0.20 seconds moving horizontal along the ECG • One box vertically equals one mm of elevation • One big box equals five mm of elevation
  9. 9. Rules for Interpreting a Rhythm • Rate – Is the heart rate fast or slow? • 59 and below is bradycardic • 60 to 100 is normal • 101-150 is tachycardia • 150 and above is SVT
  10. 10. Bradycardia Normal Tachycardia SVT
  11. 11. Rhythm • Is the rhythm regular or irregular? Regular Irregular Regular
  12. 12. QRS • Is the QRS narrow or wide Wide QRS Narrow QRS
  13. 13. – P-Wave • Is there a P-wave with every QRS and are they right side up? Without P-Wave With P-Wave
  14. 14. – Is there elevation or no elevation? Elevation Elevation No Elevation
  15. 15. • You can determine the underlying rhythm from a four lead ECG six second strip but definatively a 12 Lead confirms diagnosis of underlying rhythm, the presence of a STEMI and Imposters. • Just because a 4 lead looks normal DO NOT assume that the 12 lead is going to look normal.
  16. 16. Myocardial Infarction
  17. 17. •A sudden and total blockage or near blockage of blood flowing through the affected coronary artery to a area of heart muscle •This blockage results in ischemia, injury and necrosis to the area of the myocardium distal to the occlusion •Acute myocardial infarction most often is associated with atherosclerotic heart disease
  18. 18. STEMI (ST Elevation MI) • The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. It represents the interval between ventricular depolarization and repolarization.
  19. 19. The J-point is the point by which the s wave meets the ST segment. This point is crucial in defining what is a STEMI and what is NOT A STEMI.
  20. 20. Broad, asymmetrically peaked or ‘hyperacute’ T- waves are seen in the early stages of ST- elevation MI (STEMI) and often precede the appearance of ST elevation and Q waves.
  21. 21. The Three I’s Ischemia Injury Infarct
  22. 22. Ischemia Lack of oxygen to the tissue represented by ST depression and/or T Wave inversion
  23. 23. Injury Lack of oxygen to the tissue (ischemia) represented by ST elevation
  24. 24. Infarct Death of tissue may or may not result in Q waves
  25. 25. • “I See All Leads” is a nemonic to help with the location on a 12 lead EKG where the injury to the cardiac muscle is occurring, it is not the only way, but is the most common way. • Inferior – II, III, AvF • Septal – V1, V2 • Anterior – V3, V4 • Lateral – V5, V6, I and AvL
  26. 26. • When determining if a patient is having a STEMI the provider has to use the ST segment to determine if an event is occurring • The ST segment (the isoelectric line that starts at the J-point and goes to the start of the T- wave) will be elevated in relation to the isoelectric line. • Elevation in this segment determines if a STEMI is occurring or not • Not all AMI will show up as an elevation of the ST segment
  27. 27. Normal 12 Lead EKG •Normal Rate •Regular Rhythm •P-Wave with every QRS •Narrow QRS complex •No elevation in any leads NOT A STEMI
  28. 28. Normal 12 Lead EKG •Normal Rate •Regular Rhythm •P-Wave with every QRS •Narrow QRS complex •No elevation in any lead NOT A STEMI
  29. 29. Is this a STEMI? •Regular Rate •Regular Rhythm •P-wave with every QRS complex •Narrow QRS complexes •Elevation in leads II, III, AvF with recipricol changes in V2 and V3
  30. 30. THIS IS A STEMI!!
  31. 31. Remembering your rules. Is this a STEMI? YES ,this is a STEMI!
  32. 32. Remembering your rules. Is this a STEMI? Yes this is a STEMI!
  33. 33. • The numbers at the top left of the print out can be trusted as accurate and are scientific • The interpretation in the upper right hand side of the print out cannot always be trusted • DO NOT BASE YOUR INTERPRETATION ON THIS!!
  34. 34. STEMI Imposters
  35. 35. What are STEMI Imposters? • STEMI Imposters are conditions that mimic a STEMI. They cause a 12 Lead to show elevation but no STEMI is occuring. • Now take that definition with a grain of salt as just because they are having AMI symptoms and showing an imposter does not mean they are not having a cardiac event of some kind. • TREAT YOUR PATIENT AND NOT YOUR MONITOR.
  36. 36. Left Ventricular Hypertrophy (LVH) • LVH is responsible for up to 30% of ST elevation. It’s defined as an increase in mass to the left ventricle, often in response to chronic hypertension. As the heart beats continuously against a higher diastolic afterload, cardiac tissue surrounding the left ventricle grows, stealing space, and thus volume, from its ventricle.
  37. 37. Left Ventricular Hypertrophy (LVH) • Due to the abnormally thick left ventricular muscle wall • The electrical impulses running through the muscle causing it to contract will have a large amplitude in the height and depth of the QRS complexes
  38. 38. How do we measure for LVH? • We need two pieces of information –The S wave depth in V1 or V2 (Take the largest negative deflection from the isoelectric line) –The R wave height of V5 or V6 (Again take the largest positive deflection) • Now count the boxes of each of the two deflections and add them together. You have LVH if the result is greater than 35mm
  39. 39. • In the normal conduction of the heart, the electrical impulse initiated in the right atrium travels through the internodal pathways to the AV node, down through the bundle of HIS and eventually down to the right and left bundles • In this way, the cardiac muscle contracts sequentially and efficiently Bundle Branch Blocks
  40. 40. • A Bundle Branch Block, however, slows or stops the conduction through one of the bundles. • The block is often caused by death of the specialized conduction cells that transmit the electrical impulse, leaving the affected myocardium primed to contract, but without a signal. • This could be caused by cardiac surgery, LVH or AMI, to name some of the more common problems
  41. 41. • The block that we are most concerned with as an impostor is the Left Bundle Branch Block (LBBB) • Because of its negative deflection and long electrical impulse around the left side of the heart, the EKG strip tracing has a STEMI look to it.
  42. 42. How do we determine if we have a LBBB? First we have to look at the width of the QRS complex to see if it is wide. • We can look at the machine values for the QRS. Which will need to be greater than .12 sec. • We can look the 12 lead ECG and see if the QRS is greater than three small blocks in V1.
  43. 43. • If the QRS width is greater than .12 sec than we have a Bundle branch. • Now we look at the lead V1 to determine if it is a Right Bundle Branch Block (RBBB) or LBBB. • If the QRS complex has a positive deflection than it is a RBBB (think of a turn signal in a car). • If there is a negative deflection to the QRS complex than it is a LBBB.
  44. 44. Early Repolarization • Early Repolariation has historically been thought of as being in good health due to being found in younger athletic persons. • Early repolariztion has the characteristics of a “J wave” or “J point elevation”. This can be seen on the EKG if there is elevation of less than 0.1mV at the J point with a notched look that drops down to the isoelectric line before the raise of the T wave giving the look of hook.
  45. 45. • Due to the history of Early Repolarization being a young/healthy person finding be careful in diagnosing this on a EKG of anyone over the age of 50.
  46. 46. Paced Rhythms • Due to the damage to the heart a patient may have a pacemaker implanted to effect the electrical impulse to cause contraction of either the Atrium or the Ventricles • Depending on the placement location of the pacemaker electrode on he heart the strip tracing may have a normal QRS width with a P wave, or no P wave and a wide QRS complex. • With a paced rhythms the pacemaker sets off an electrical impulse to cause contraction. This impulse may be seen prior to the P wave or QRS complex with a “pacer spike”. This spike will be of low voltage and short duration at the start of the P wave or QRS complex.
  47. 47. Hyperkalemia • Hyperkalemia is a abnormally high level of potassium in the blood. • This condition my be caused by acute or chronic renal failure, burns, crushing injuries and severe infections or other conditions in which large amounts of potassium are released.
  48. 48. • P wave widens and flattens • PR segment lengthens • P waves eventually disappear • Prolonged QRS interval with bizarre QRS morphology • High-grade AV block with slow junctional and ventricular escape rhythms • Any kind of conduction block (bundle branch blocks, fascicular blocks) • Sinus bradycardia or slow AF
  49. 49. Early onset of Hyperkalemia
  50. 50. Severe Onset of Hyperkalemia!!
  51. 51. Treatment for AMI in Pre -Hospital setting
  52. 52. Aspirin Aspirin decrease inflammation, Dilates peripheral vessels and decreases platelet aggregation , The use of aspirin , is strongly recommended for all patients with acute coronary syndrome
  53. 53. Nitroglycerin Is a vasodilation agent that has beneficial hemodynamic effects Dilation arterioles and veins in the periphery ( reducing preload) Dilation of the coronary arteries (reducing the work load )
  54. 54. Oxygen Oxygen is odorless tasteless, colorless gas that is present in room air at a concentration of approximately 21% Oxygen is an important emergency drug used to reverse hypoxemia in doing so it helps oxidize glucose to produce adenosine triphosphate ( aerobic metabolism) Oxygen may help reduce the size of infarcted tissue during an acute myocardial infarction
  55. 55. Morphine • Natural opium alkaloid that has a primary effect of analgesia • Secondary pharmacological effects include depressed responsive of alpha- adrenergic receptors ( producing peripheral vasodilation ) • Morphine decreases preload and after load it may decrease myocardial oxygen demand .
  56. 56. Dilaudid • Analgesic opiate agonist • Onset IN/IM within 15 min • Duration 4-5 hrs • Moderate to severe pain • Analgesia
  57. 57. Conclusion • STEMI recognition is one of the most important things we do as Medics • Remember the five rules for interpreting a 12 lead: – Rate – Regular or Irregular – Wide or Narrow QRS – P-wave with every QRS – Elevation or No Elevation
  58. 58. • Remember your Imposters and how to detect them – Bundle Branch Blocks – LVH – Paced Rhythm – Benign Early Repolarization – Hyperkalemia • Remember the treatment for a AMI – Morphine – ASA – Oxygen – Nitro

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