Module 2 interpreting ecg rythm strips-1-converted

ecg

1. MODULE 2 Interpreting ECG rhythm STRIPS

2. Objectives Utilize a systematic process when approaching the interpretation of the ECG. Identify normal and abnormal components on the ECG.

3. ECG interpretation

4. Cardiac Anatomy 2 upper chambers Right and left atria 2 lower chambers Right and left ventricle 2 Atrioventricular valves (Mitral & Tricuspid) Open with ventricular diastole Close with ventricular systole 2 Semilunar Valves (Aortic & Pulmonic) Open with ventricular systole Open with ventricular diastole

5. Anatomy Coronary Arteries

6. 2 major vessels of the coronary circulation Left main coronary artery Left anterior descending and circumflex branches Right main coronary artery Left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia behind the aortic valve leaflets. Anatomy Coronary Arteries

7. Normal Conduction System Sinoatrial node Internodal pathway AV node Bundle of His Bundle Branches Purkinje fibers

8. Pacemakers of the Heart SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute. AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute. Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

9. E C G s ?

10. Basic ECG Interpretation STANDARD CALLIBRATION Speed = 25mm/s Amplitude = 0.1mV/mm 1 large square: 0.2s(200ms) 1 small square: 0.04s (40ms) 1mV: 10mm high 0.1 mV amplitude

11. OBTAIN A N ECG, ACT CONFIDENT, READ THE PT DETAILS

12. OBTAIN A N ECG, ACT CONFIDENT, READ THE PT DETAILS Some ECG machines come with interpretation software. This one says the patient is fine. DO NOT totally trust this software.

13. ECG LIMB LEAD REVERSAL Lead I or aVL is completely inverted (P wave, QRS complex and T wave). Lead aVR often becomes positive. The P-wave is unexpectedly larger in lead I than lead II (it is usually the other way around).

14. The best way to interpret an ECG is to do it step-by-step Step 1: Rate Step 2: Rhythm + Regularity Step 3: P- wave Step 4: PR - interval Step 5: QRS Complex Step 6: ST Segment and T waves Step 7: QT interval (Include T and U wave) Step 8 : Cardiac Axis Step 9: Other ECG signs

15. THE NORMAL SIZE <3 small square <3-5 small square < 2 large square < 2 small square

16. PQRST Configuration One complete cardiac cycle = P, Q, R, S, (QRS complex), and T wave P wave First deflection Rounded and upright in lead II Amplitude: 0.5-2.5mn Duration: 0.10s Atrial depolarization PR Interval Beginning of P wave to beginning of QRS complex Duration: 0.12s-0.2s Atrial depolarization + conduction delay through AV junction (AVN+ Bundle of His) QRS Complex Beginning of Q wave to the end of S wave Duration: 0.06-0.12s Ventricular depolarization ST Segment Between S wave to the beginning of T wave Normal ST segment is flat (isoelectric) Isoelectric, ventricle still depolarized QT Interval Beginning of QRS complex to the end of T wave Duration: ½ of the distance of RR interval Ventricular depolarization + repolarization Mechanical contraction of ventricle T Wave End of ST segment to the end of T wave Rounded and asymmetrical Upright in lead II Amplitude: <5mm Ventricular repolarization

17. 6-STEPS APPROACH FOR ECG RECOGNITION STEP 1 – HEART RATE Bpm calculation= ventricular rate 6s method: count R waves within 6s strip multiply by 10 300 method: 300/no large squares between QRS Normal : 60-100bpm Bradycardia: <60bpm Tachycardia: >100 STEP 2 – HEART RHYTHM Intervals between R waves (measure from R to R) Regular or irregular? Are the rhythm SINUS? Regular: Interval consistent Irregular: Irregular pattern Sinus rhythm: P-QRS-T STEP 3 – P WAVE Look at the P waves Are P waves present? Are P waves occurring regularly? Is there one P wave present for every QRS complex present? Are the P waves smooth, rounded, and upright in appearance, or are they inverted? 5. Do all P waves look similar? Every 1 P for each QRS complex More than 1 P wave indicates AV block None: rhythm is junctional/ventricular STEP 4 – PR INTERVAL Onset of P wave to onset of QRS complex Normal = 0.12–0.20 seconds (3-5 small squares) Are the PR intervals greater than 0.20 seconds? Are the PR intervals less than 0.12 seconds? 3. Are the PR intervals consistent across the ECG strip? PRI shorter: presence of accessory pathways that by passed the AVN PRI longer: AV block STEP 5 – QRS COMPLEX Measured from the start of Q wave to the end of the S wave Normal = 0.06-0.12 seconds (1 ½ to 3 small boxes) Are the QRS complexes greater than 0.12 seconds (in width)? Are the QRS complexes less than 0.06 seconds (in width)? 3. Are the QRS complexes similar in appearance across the ECG strip? Widened QRS: BBB Pre-excitation syndrome Electrolytes imbalance: Hyperkalemia Paced rhythm Impulse originated from the ventricle STEP 6 – EXTRAS or IDENTFYING FEATURES Any ectopic beats? Consider ACS and MI (ST segment and T wave) Identifying features? Prolonged QTI syndrome

18. STEP 1: RATE

19. CALCULATING RATE As a general interpretation, look at lead II at the bottom part of the ECG strip This lead is the rhythm strip which shows the rhythm for the whole time the ECG is recorded. Look at the number of square between one R-R interval To calculate rate, use any of the following formulas: OR Rate = 300 the number of BIG SQUARE between R-R interval 1500 the number of SMALL SQUARE between R-R interval R a t e =

20. CALCULATING RATE For example: Rate = 300 3 Rate = 1500 1 5 o r Rate = 100 beats per minute

21. CALCULATING RATE If you think that the rhythm is not regular , count the number of electrical beats in a 6-second strip and multiply that number by 10 .(Note that some ECG strips have 3 seconds and 6 seconds marks) Example below: 1 2 3 4 5 6 7 8 = ( Nu m b e r o f R wa v e s i n 6 -se c o n d s t ri p s ) x 10 = 8 x 10 = 80 bpm R a te There are 8 R waves in this 6-seconds strip.

22. I N T E R P R E T A T ION Interpretation Bpm Causes Normal 60-99 Bradycardia <60 Hypothermia, increased vagal tone (due to vagal stimulation or e.g. drugs), athletes (fit people) hypothyroidism, beta blockade, marked intracranial hypertension, obstructive jaundice, and even in uremia, structural SA node disease, or ischaemia. Tachycardia >100 Any cause of adrenergic stimulation (including pain); thyrotoxicosis; hypovolaemia; vagolytic drugs (e.g. atropine) anaemia, pregnancy; vasodilator drugs, including many hypotensive agents; FEVER, myocarditis

23. Sinus Bradycardia Rate < 60bpm, otherwise normal

24. Sinus Tachycardia Rate >100bpm Rate > 100bpm, otherwise normal

25. STEP 2: RHYTHM

26. RHYTHM If in doubt, use a paper strip to map out consecutive beats and see whether the rate is the same further along the ECG. Measure ventricular rhythm by measuring the R-R interval Is the rhythm regular or irregular?

27. Regular rhythm Sinus rhythm Sinus bradycardia Sinus tachycardia Atrial tachycardia Junctional rhythm SVT (AVNRT, AVRT) Atrial flutter with fixed block Irregular rhythm Atrial fibrillation Atrial flutter with variable block SR with ectopic beats Multifocal Atrial tachycardia (MAT)

28. STEP 3: P- WAVE

29. P -WAVE Normal P- wave 3 small square wide, and 2.5 small square high Always positive in lead I and II in NSR Always negative in lead aVR in NSR Commonly biphasic in lead V1

30. P wave Are P waves present? Is there 1 P for each QRS complex? Are the P waves smooth, rounded and upright in appearance except inverted P waves in lead aVR? Do all P waves look similar?

31. INTERPRETATION Sinus rhythm: Every 1 P for each QRS complex More than 1 P wave indicates AV block None: Rhythm is junctional or ventricular in origin

32. RHYTH M Normal Sinus Rhythm ECG rhythm characterized by a usual rate of anywhere between 60-99 bpm, every P wave must be followed by a QRS . Normal duration of PR interval is 3-5 small squares. The P wave is upright in leads I and II.

33. P -WAVE P pulmonale Tall peaked P wave Generally due to enlarged right atrium - commonly associated with congenital heart disease, tricuspid valve disease, pulmonary hypertension and diffuse lung disease Biphasic P wave It’s terminal negative deflection more than 40 ms wide and more than 1 mm deep is an ECG sign of left atrial enlargement P mitrale Wide P wave, often bifid, may be due to mitral stenosis or left atrial enlargement

34. STEP 4: PR- INTERVAL

35. PR INTERVAL NORMAL PR INTERVAL PR-Interval 3-5 small square (120-200ms) Long PR interval may indicate heart block Short PR interval may disease like Wolf-Parkinson- White

36. PR-INTERVAL Wolff–Parkinson–White Syndrome Wolf Parkinson White Syndrome One beat from a rhythm strip in V2 demonstrating characteristic findings in WPW syndrome Note the characteristic: Delta wave (above the blue bar), the short PR interval (red bar) of 0.08 seconds, and the long QRS complex (green) at 0.12 seconds Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave and short PRI)

37. STEP 5: QRS-COMPLEX

38. QRS complex< 3 small square (0.10 sec) QRS COMPLEX Prolonged indicates hyperkalemia or BBB Q wave amplitude less than 1/3 QRS amplitude(R+S) or < 1 small square

39. I NT E R P R E T A T ON Narrow complexes (QRS <100 ms) are supraventricular in origin. Broad complexes (QRS >100 ms) may be either: Ventricular in origin Due to aberrant conduction e.g. due to bundle branch block Electrolytes imbalance e.g. Hyperkalaemia Ventricular paced rhythm

40. QRS COMPLEX Left Bundle Branch Block (LBBB) indirect activation causes left ventricle contracts later than the right ventricle . QS or rS complex in V1 - W-shaped RsR' wave in V6- M-shaped Right bundle branch block (RBBB) Indirect activation causes right ventricle contracts later than the left ventricle Terminal R wave (rSR’) in V1 - M-shaped Slurred S wave in V6 - W-shaped Mnemonic: W IL L IA M Mnemonic: M AR R O W

41. STEP 6: ST-SEGMENT and T WAVE

42. ST SEGMENT NORMAL ST SEGMENT ST segment < 2-3 small square (80 to 120 ms) ST segment is isoelectric and at the same level as subsequent TP segment

43. ST SEGMENT WE DECIDE THIS BY LOOKING AT THE ST SEGMENT IN ALL LEADS Flat (isoelectric) ± Same level with subsequent TP segment Elevation or depression of ST segment by 1 mm or more, measured at J point is abnormal. J point is the point between QRS and ST segment NORMAL ST SEGMENT OK, WE GONNA TALK ABOUT MYOCARDIAL INFARCTION (MI) THERE ARE 2 TYPES OF MI ST-ELEVATION MI (STEMI) NON ST-ELEVATION MI (NSTEMI) A N D

44. ST-SEGMENT Localizing MI Look at ST changes, Q wave in all leads. Grouping the leads into anatomical location, we Ischemic change can be attributed to different coronary arteries supplying the area. Location of MI Lead with ST changes Affected co r ona ry artery Anterior V1, V2, V3, V4 LAD Septum V1, V2 LAD left lateral I, aVL, V5, V6 Left c i rc u m f l e x inferior II, III, aVF RCA Right atrium aVR, V1 RCA *Posterior Posterior chest leads RCA *Right v en t r i c l e Right sided leads RCA * To help identify MI, right sided and posterior leads can be applied have I. this: II. III. aV R V1 aVL V2 aVF V3 V4 V5 V6 (LAD)

45. ST SEGMENT ST-ELEVATION MI (STEMI) HOUR Pronounced T Wave ST elevation (convex type) 1-24H Depressed R Wave, and Pronounced T Wave Pathological Q waves may appear within hours or may take greater than 24 hr indicating full- thickness MI. Q wave is pathological if it is wider than 40 ms or deeper than a third of the height of the entire QRS complex Day 1-2 Exaggeration of T Wave continues for 24h Days later T Wave inverts as the ST elevation begins to resolve Persistent ST elevation is rare except in the presence of a ventricular aneurysm Weeks later ECG returns to normal T wave, but retains pronounced Q wave An old infarct may look like this

46. I I I I II a V R a V L a V F V1 V2 V3 V4 V5 V6 Inferior MI ST SEGMENT How about this one?

47. ST SEGMENT NON ST-ELEVATION MI (NSTEMI) NSTEMI is also known as subendocardial or non Q-wave MI In a pt with Acute Coronary Syndrome (ACS) in which the ECG does not show ST elevation, NSTEMI (subendocardial MI) is suspected if ST Depression (A) T wave inversion with or without ST depression (B) Q wave and ST elevation will never happen To confirm a NSTEMI, do Troponin test: If positive: NSTEMI If negative : Unstable angina

48. ST SEGMENT NON ST-ELEVATION MI (NSTEMI) N-STEMI: acute coronary syndrome (with troponin increase) Arrows indicate ischemic ST segment changes. Without appropriate treatment in many cases STEMI infarction will occur

49. MYOCARDIAL ISCHEMIA 1mm ST-segment depression Symmetrical Tall T wave Long QT- interval ST depression is more suggestive of myocardial ischemia than infarction ST SEGMENT

50. T wave T wave is the positive deflection after each QRS complex It represents ventricular repolarisation Upright in all leads except aVR and V1 Amplitude < 5mm in limb leads <15mm in precordial leads

51. Step 7: QT- INTERVAL

52. QT- INTERVAL QT interval decreases when heart rate increases As a general guide the QT interval should be 0.35- 0.45 s,(<2 large square) and should not be more than half of the interval between adjacent R waves (R-R interval) < 2 large square

53. T-WAVE Normal T wave Asymmetrical, the first half having more gradual slope than the second half >1/8 and < 2/3 of the amplitude of corresponding R wave Amplitude rarely exceeds 10mm Abnormal T waves are symmetrical, tall, peaked, biphasic, or inverted LONG QT SYNDROME LQT is a rare inborn heart condition in which repolarization of the heart is delayed following a heartbeat Example: Jervell and Lange-Nielsen Syndrome or Romano-Ward Syndrome

54. STEP 8: CARDIAC AXIS

55. CARDIAC AXIS To determine cardiac axis look at QRS complexes of lead I , II, III. Axis Lead I Lead II Lead III Normal Positive Positive Positive/Negative Right axis. deviation Negative Positive Positive Left axis dev i a ti on Positive Negative Negative Remember, positive(upgoing) QRS complex means the impulse travels towards the lead. Negative means moving away

56. Positive Positive Positive Normal Axis Deviation CARDIAC AXIS

57. Negative Po si t ive Po si t ive Right Axis Deviation CARDIAC AXIS

58. P o s i t i ve Negative N e g a ti v e Left Axis Deviation CARDIAC AXIS

59. I (0º) I I aVF aVF (+90º) ( 18 º) NORMAL AXIS LEFT AXIS D EV I A TION RIGHT AXIS DEVIATION EXTREME RIGHT AXIS DEVIATION I a VF I a VF

60. Cardiac Axis Causes Left axis deviation Normal variation in pregnancy, obesity; Ascites, abdominal distention, tumour; left anterior hemiblock, left ventricular hypertrophy, Q Wolff- Parkinson-White syndrome, Inferior MI Right axis deviation Normal finding in children and tall thin adults, chronic lung disease(COPD), left posterior hemiblock, Wolff-Parkinson-White syndrome, anterolateral MI North West Emphysema, hyperkalaemia. lead transposition, artificial cardiac pacing, ventricular tachycardia CARDIAC AXIS

61. S T EP 9 : O T H E R E C G SIGNS

62. LEFT VENTRICULAR H Y PE R T R O P HY RIGHT VENTRICULAR H Y P E R T R O P H Y A ND So, we have to start looking at the S waves and R waves

63. Left ventricular hypertrophy (LVH) C ri t e r i a : E x a m pl e: To determine LVH, use one of the following: Sokolow & Lyon Criteria : S (V1) + R(V5 or V6) > 35mm Cornell Criteria : S (V3) + R (aVL) > 28 mm (men) or > 20 mm (women) Others : R (aVL) > 13mm S (V1) + R(V5) = 15 + 25 = 40mm S(V3) + R (aVL)= 15 + 14 = 29mm R(aVL) = 14 mm L V H!

64. Tall R waves in V4 and V5 with down sloping ST segment depression and T wave inversion are suggestive of left ventricular hypertrophy ( LVH) with strain pattern LVH with strain pattern usually occurs in pressure overload of the left ventricle as in systemic hypertension or aortic stenosis Let’s see another example of LVH LVH strain pattern

65. Right ventricular hypertrophy (RVH) E x a mp l e: Right axis deviation (QRS axis >100 o ) V1(R>S), V6 (S>R) Right ventricular strain T wave inversion So, it’s RVH!

66. Common Causes of LVH and RVH LVH RVH Hypertension (most common cause) Aortic stenosis Aortic regurgitation Mitral regurgitation Coarctation of the aorta Hypertrophic cardiomyopathy Pulmonary hypertension Tetralogy of Fallot Pulmonary valve stenosis Ventricular septal defect (VSD) High altitude Cardiac fibrosis COPD Athletic heart syndrome

67. Narrow and tall peaked T wave (A) is an early sign PR interval becomes longer P wave loses its amplitude and may disappear QRS complex widens (B) When hyperkalemia is very severe, the widened QRS complexes merge with their corresponding T waves and the resultant ECG looks like a series of sine waves (C) If untreated, the heart arrests in asystole HYPOKALAEMIA T wave becomes flattened together with appearance of a prominent U wave The ST segment may become depressed and the T wave inverted These additional changes are not related to the degree of hypokalemia HYPERKALAEMIA

68. ECG RULES Professor Chamberlains 10 rules of a normal ECG, a foundation to ECG interpretation used all over the world to this date

69. 1 RULES OF A NORMAL ECG Rule 1 PRI should be 120 to 200ms (3 to 5 small squares) Rule 2 QRS complex width should not exceed 120ms (<3 small squares) Rule 3 QRS complex should be Rule 4 QRS and T waves tend to have dominantly upright in lead 1 and the same direction in the limb II leads Rule 5 All waves are negative in lead Rule 6 R wave must grow from V1 to v4 AVR and S wave must grow from V1 to V3 and disappear in V6 Rule 7 ST segment should start Rule 8 P waves should be upright in I,II isoelectric except V1 and V2 and V2 to V6 (maybe elevated) Rule 9 No Q wave or only a small q wave (<0.04 in width) in I,II,V2 to V6 Rule 10 T wave must be upright in 1,II, V2- V6

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