12-Lead EKG MEPN Level IV

1. 12-Lead EKG MEPN Level IV

2. EISLO’s • Discuss the changes in T wave and ST segment morphology with an MI • List the criteria for identification of right or left bundle branch blocks. • List the anatomically congruent leads associated with an inferior, lateral and anterior wall MI • Describe morphology of Q wave presence

3. Myocardial A&P http://www.healthline.com/vpvideo/how-the-heart-works

4. Heart wall - Three layers • Epicardium (outer) • visceral layer of pericardium • thin, transparent • smooth, slippery • Myocardium (middle) • mass of cardiac muscle • Endocardium(inner) • endothelium over thin connective tissue • smooth lining for the chambers and valves • continuous with blood vessel endothelium

6. Myoglobin Released by all striated muscle Rises fast (2 hours) after myocardial infarction Peaks at 6 - 8 hours Returns to normal in 20 - 36 hours CK Released by all muscles in the body Rises in 4-6 hours after injury Peaks in 24 hours Returns to normal in 3-4 days CK-MB is myocardial “specific” Peaks in 3-4 hours Returns to normal in 2 days Troponin More specific for myocardial injury Rises 2-6 hours after injury Peaks in 12 hours Remains elevated for 5-14 days Cardiac Enzymes

7. Coronary Blood Flow Arteries • first branches off the aorta • blood moves more easily into the myocardium when it is relaxed between beats  during diastole • blood enters coronary capillary beds

8. Collateral Circulation

10. Coronary Circulation

11. Coronary Circulation Pathologies • Compromised coronary circulation due to: • emboli: blood clots, air, amniotic fluid, tumor fragments • fatty atherosclerotic plaques • smooth muscle spasms in coronary arteries • Problems • ischemia (low supply of nutrients) • hypoxia (low supply of O2) • infarct (cell death)

12. Internodal tracts Bundle of His Right Bundle Branch

13. SA Node

14. Intranodal Pathways

15. AV Node Conduction • Normal conduction pathway from atria to ventricles • Limits number of atrial impulses sent to the ventricles

16. Bundle Branches

17. Phase 0 Begins at -70 mV with a slow influx of sodium ions; gradually raising the potential toward threshold When threshold is reached fast sodium channels open; causing the cell to fire Phase 1 Rapid sodium pumps are slowed by influx of potassium Phase 2 Plateau phase Sodium influx slows; calcium begins to enter the cell Calcium stimulates cellular contraction by stimulating the myocyte Phase 3 Reverse pumps open; rapid repolarization Phase 4 Back to the -70 mV resting potential Action Potential

18. Myocardial Action Potential • Depolarization • Phase 1 of the action potential • Stimulation of the cardiac cell by the pacemaker cell causing an influx of Na and Ca, outflow of K. • Repolarization • Phase 2 of the action potential • No impulse entering the cells can cause it to depolarize • Relative refractory period • Phase 3 of the action potential • Impulses entering the cardiac cell now can cause serious, uncontrolled reactions. • Absolute refractory period • Phase 4 of the action potential • The return of the cardiac cells to resting state.

19. EKG Basics • 25 mm per sec • Each small box - horizontally = 0.4 sec • Each small box - vertically = 1 mm

20. EKG Review - Analysis • Rhythm • Regular or irregular • Rate • Too fast, too slow, just right • P waves • Upright, inverted, not there, not related • P-R Interval • 0.12-0.20; >0.20; <0.12 • QRS complex • <0.12 • QT Interval • .34-.44

21. P wave: Represents positive and negative deflections of atrial contraction and relaxation • PR Interval:Distance between the P wave and the Q/R wave .12 -20 • QRS Complex:represents ventricular depolarization • Q wave:First negative deflection • R Wave:First positive deflection • S Wave:second negative deflection • ST Segment:Essentially isoelectric, slopes gently upward • Normal > .08 sec • J point:the point where the S wave meets the isoelectric line • T Wave:Ventricular repolarization • always upright in leads I, II, V2-V6 • aVR is always negative. • Leads III, aVL, aVF, and V1 can be positive or negative • U Wave:unclear etiology, commonly seen in V2-V3 due to proximity to ventricular mass; common in bradycardia, hypokalemia, digitalis

22. QT interval • beginning of the QRS complex to the end of the T wave represents ventricular depolarization and repolarization ---- Changes with heart rate • QTc • QT corrected for heart rate QT / R-R = QTc • Evaluates the recovery of the ventricle

23. ECG Leads • 6 limb leads (frontal plane) • 3 bipolar leads • 3 unipolar leads • 6 precordial leads (horizontal plane) • V1 – V6

24. Einthoven’s Triangle Limb Leads BIPOLAR • Lead I • RA (-) to LA (+) • Lead II • RA (-) to LL (+) • Lead III • LA (-) to LL (+)

25. AUGMENTED (UNIPOLAR) LEADS Augmented leads combine 2 leads together (the null point) from the center point of the triangle with one positive pole. aVR (Augmented Voltage Right Arm positive) is a combination of bipolar Leads I and II aVL (Augmented Voltage Left Arm Positive) is a combination of I and III aVF (Augmented Voltage Left Foot positive) is a combination of Bipolar Leads II and III

26. I & AVL II, III & AVF WHAT ARE THE LEADS LOOKING AT? LIMB and AUGMENTED LEADS

27. Precordial Lead Placement • V1 – 4th intercostal space right of sternum • V2 - 4th intercostal space left of sternum • V4 – 5th intercostal space midclavicular line • V3 – midway between V2 and V4 • V6 – 5th intercostal space midaxillary line • V5 – same level as V4 at anterior axillary line between V4 and V6

28. RIGHT SIDED EKG Same lead position as left side – looks directly at the Right ventricle

29. Posterior View Posterior leads: V7 – lateral to V6 at posterior axillary line V8 – level of V7 at the mid-scapular line V9 – level of V8 at the paravertebral line (left posterior thorax midway from spine to V8)

31. V3 & V4 V1 & V2 V5 & V6 PRECORDIAL LEADS

32. calibration marker LIMB LEADS AUGUMENTED LEADS PRECORDIAL LEADS Bottom line is continuous strip

33. R – Wave Progression

34. R – Wave Progression

35. Myocardial ischemia • Various definitions are used. The term commonly refers to diffuse ST segment depression, usually with associated T wave inversion • Myocardial injury • Injury always points outward from the surface that is injured with ST segment elevation • Myocardial infarction • death of heart muscle

36. Ischemia, Injury, Infarction Waveforms

37. ST Segments ST segment should be electrically neutral

38. Visual aid in determining: • Ischemia or injury to myocardium • Normal should be at baseline • Depressed ST segment - >2 mm below baseline

40. EKG 1

41. ST Segment Elevation • ST segment elevation is attributed to impending infarction • but can also be due to pericarditis or vasospastic (variant) angina. • The height of the ST segment is measured at a point 2 boxes after the end of the QRS complex • significant if it exceeds 1 mm in a limb lead or 2 mm in a precordial lead.

42. EKG 2

43. T Waves • T waves are normally positive in leads with a positive QRS • T waves are normally asymmetrical • T waves are normally not more than 5 mm high in limb leads or 10 mm high in precordial leads or 2/3 the height of the R wave

44. T wave Ischemia Ischemia Hyperkalemia Ischemia

45. Hyperkalemia EKG 3

46. ST-T Wave • Combination of infarction and often hyperkalemia • Called Tombstone ‘T’ because of the shape. • Usually a sign of impending cardiac death.

47. Inferior-Anterior-Lateral EKG 4

48. Pathology of an MI

49. Localization of ECG Pathology • Inferior: Abnormalities that appear in leads II, III, and aVF (called the inferior leads) indicate pathology on the inferior or diaphragmatic surface of the heart. • Lateral:Leads I, aVF, and V5-V6 are called lateral leads. Abnormality in these leads indicates pathology on the lateral, upper surface of the heart. • Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I.

50. Overview of Infarcts