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![Unstable angina/NSTEMI
ECG ST-segment depression or prominent T-
wave inversion and/or positive biomarkers
of necrosis in absence of ST-segment
elevation and appropriate clinical setting
(chest discomfort or anginal equivalent)
NSTEMI if elevated biomarkers present
(Troponin T, Troponin I or Creatine Kinase-
MB [CK-MB])
44](https://image.slidesharecdn.com/ecg-part1superfinal-130628062133-phpapp01/85/Ecg-44-320.jpg)
Uploaded byRohan Choudhari
Ecg
The document provides an overview of electrocardiogram (ECG) interpretation. It discusses how ECG is an important diagnostic tool that represents the heart's electrical activity. It then covers the steps for interpreting an ECG, including assessing the rate, rhythm, P waves, PR interval, QRS duration, ST segments, T waves, and changes that can indicate conditions like myocardial infarction. The document emphasizes how analyzing ECG findings can provide clinical insights, such as determining whether a patient may benefit from interventions like thrombolysis.
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Ecg
- 1. Fundamentals of ECG interpretation PartI 1 PART II
- 2. Electrocardiogram (ECG) Providesrepresentation of the electrical activity of the heart Extremely important diagnostic tool for various cardiac dysfunctions Used extensively in healthcare systems 3 2
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- 4. Dr. Nagel developedthe first telemetry unit for transmitting E.C.G.recordings via radio waves from the field to the hospital. 4 4
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- 10. Summary of eventsof cardiac cycle 10 10
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- 13. ECG Reported as: 1.Standardisation9.QRS Complex 2.Voltage 10.QRS Duration 3.Rate 11.ST Segment 4.Rhythm 12.T Wave 5.Axis 13.QT Interval 6.Position 14.U Waves 7.P Waves 15. Conclusion 8.PR Interval 14 13
- 14. Step - Rate Method Countthe number of R waves for a six second interval and multiply by ten 3 sec 3 sec 6 sec (can be used for regular & irregular) 15 14
- 15. Step - Rate Method: Count the number of 5mm squares in R-R interval and divide into 300 300 150 100 75 60 50 43 37 33 30 … slow 16 15
- 16. Step 1 -Rate RATE: Tachycardia exists if the rate is greater than 100 beats/min. Bradycardia exists if the rate is less than 60 beats/min. 17 16
- 17. Step : Rhythm RHYTHM: Determine if the ventricular rhythm is regular or irregular (pattern to irreg.?) R-R intervals should measure the same P-P intervals should also measure the same 18 17
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- 19. STEP - RhythmExample • Irregularly Irregular 20 19
- 20. STEP 3 –Is the P Wave Normal? Relation to QRS? Appearance ? Consistency? Identify and examine P waves: Present? 21 20
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- 23. STEP 3 -Is the P Wave Normal ? Normal P wave with no QRS complex Normal Same Shape Associated with a QRS Complex? 24 23
- 24. STEP 4 –PRInterval/Relationship Consistent PRI of <0.20 secs is normal, lengthened or variant PRIs could indicate an AV block 25 24
- 25. STEP 5 –QRSDURATION • A narrow QRS complex (< 0.12), indicates the impulse has followed the normal conduction pathway • A widened QRS complex (> 0.12), may indicate the impulse was generated somewhere in the ventricles 25
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- 29. STEP 6 –ST segment & T wave • Ventricular repolarization characterized on ECG as ST segment and T wave • Changes in ST segment and T wave often seen in ischemic heart disease ST depression T wave inversion ST elevation 29
- 30. Identifying ST segmentchanges 30
- 31. Regional association withECG Area of infarction Leads associated Vessels involved Inferior Leads II, III, and aVF; ST elevations Right coronary artery, left circumflex Posterior Leads V1, V2, V3 ST depression; large R wave Proximal right coronary artery, left circumflex Anterior Leads V1, V2, V3, V4; ST elevation Left anterior descending Lateral Leads V1, AVL, V5, V6; ST elevation Left circumflex Right ventricular Elevations in leads II, III, aVF, and V1; elevation greater in III than II; large R wave V4 Proximal right coronary artery 31
- 32. ST elevation myocardial infarction(STEMI) ST elevation 1 mm or more in 2 contiguous leads ST elevation in II, III & aVF 32
- 33. Evolving infarction: ECG progression A.Normal ECG prior to MI B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C. Infarction from ongoing ischemia results in marked ST elevation D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves 33
- 34. Sequence of changesseen during evolution of MI 34
- 35. Clinical implications ofECG changes… Peaked T waves ◦ Present only for 5-30 mins after onset of MI ◦ Intervention at this stage may prevent infarction; improved outcomes than initiating therapy at later stages 35
- 36. Clinical implications ofECG changes … ST segment elevation ◦ Injury to myocardium ◦ Patients with largest ST deviation benefit most from fibrinolysis 36
- 37. Clinical implications ofECG changes … Pathological Q waves ◦ May develop within 1-2 hrs of onset of symptoms of acute MI, though often they take 12 hrs to appear ◦ If ST segment elevation and Q waves evident on ECG and chest pain is of recent onset, patient may benefit from thrombolysis or direct intervention ◦ Absence of Q waves post fibrinolysis may serve as favorable prognostic indicator 37
- 38. Clinical implications ofECG changes… T wave inversion ◦ Late sign of evolving MI; occurs in 3/4th patients with completed MI ◦ May persist for months and occasionally remains a permanent sign of infarction 38
- 39. Clinical implications ofECG changes Normalization of ST segment ◦ Last ECG change during MI; occurs when transmural MI progresses to completed infarction ◦ ST elevation with an inferior MI may take up to two weeks to resolve, may persist even longer with anterior MI and may persist indefinitely if left ventricular aneurysm develops ◦ Role of reperfusion therapy limited 39
- 40. Evolving ECG inSTEMI Middle-aged male presents to emergency medical service with chest pain; initial ECG demonstrates nonspecific abnormalities; within 15 minutes during transport, ECG demonstrates significant inferior ST segment elevation, consistent with inferior wall STEMI 40
- 41. Inferior Wall STEMI STelevation in II, III & aVF 41
- 42. Anterior Wall STEMI STelevation in V1-V5 42
- 43. Anterolateral MI This person’sMI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)! 43
- 44. Unstable angina/NSTEMI ECGST-segment depression or prominent T- wave inversion and/or positive biomarkers of necrosis in absence of ST-segment elevation and appropriate clinical setting (chest discomfort or anginal equivalent) NSTEMI if elevated biomarkers present (Troponin T, Troponin I or Creatine Kinase- MB [CK-MB]) 44
- 45. UA vs. NSTEMI Twave inversion in II, III, aVF, V1-V6 If biomarkers normal, Unstable angina If biomarkers elevated, NSTEMI 45
- 46. Angina Patient complained ofchest pain A.ST depression B.5 minutes later, after nitroglycerin, ST segments revert to normal with relief of angina 46
- 47. Prinzmetal’s angina withtransient ST elevation Patient with history of exertional and rest angina A. Baseline resting ECG shows non-specific inferior ST-T changes B. With chest pain, ST elevations in II, III, aVF and reciprocal ST depression in I and aVL C. Return of ST segments to baseline after nitroglycerin 47
- 48. Summary ECG anessential adjunct to clinical history & physical examination in patients with chest pain ECG adds considerable information for risk stratification and clinical decision support for treatment strategies in ACS 48
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