Systematic ECG Interpretation

Systematic ECG Interpretation

1. ECG Interpretation Dr S. A. Medway SCGH ED CME Thursday 12/03/2015 Original Presentation Credit to Dr. James Wheeler

2. Resources Original Presentation – Dr James Wheeler Erics Medical Lectures – YouTube LITFL e min5.com Time on the floor

3. What is an ECG? Graphical representation of the electrical activity of the myocardium over time Standard 12 lead ECG assesses this in various planes (coronal & transverse) to give a roughly 3D view of the heart 3 biploar leads I, II, III 9 unipolar leads aVR , aVL , aVF , V1- V6 Can consider other unipolar lead placements V1-6R – look at RV V7-9 – look at post LV wall

4. Lead placement

5. Anatomical relationship

6. ANATOMICAL RELATIONSHIP OF LEADS

7. Considerations Methodical systematic approach “ More is missed by not looking than by not knowing"[Thomas McCrae, 1870-1935 ] Consider patients clinical condition Obtain previous ECG’s for comparison Limitations of ECG – Electrical activity, not contractility etc… The “ normal” ECG All normal ECG’s do not look the same But they do have features in common

8. ECG helps in detection of: Ischaemic heart disease, acute or chronic Dysrrhythmias Electrolyte disturbances Conduction abnormalities (HB, BBB) CAD (exercise stress test) Cardiac structural abN (LVH, RVH) Cardiac manifestations of non-cardiac disease (PE, metabolic disorders, lung disease… )

9. COMPONENTS OF ECG Rate Rhythm / Regularity Cardiac Axis Waveform (axis, amp, duration) P wave QRS complex T wave U wave Intervals PR interval QT interval RR interval Segments PR segment ST segment

10. ECG systematic evaluation Calibration / Speed N = 10mm/1mV, 25mm/sec Rhythm Regularity / QRS width / Rate Axis N / LAD / RAD P wave ?presence / relationship to QRS Axis Amp: RAA / LAA PR interval Duration / HB / Pre-excitation PR segment Depression QRS duration / amplitude / morphology Q waves R wave ST segment Depression / elevation / morphology T wave Axis / morphology / duration QT interval U wave Other waves (delta, osborne , epsilon, pacing spikes, artifacts) ?other leads (V4R, V7-9, Lewis)

11. Normal ECG

12. ECG Rhythm Rate N / tachy / brady Regularity Regular / reg irreg / irreg irreg QRS morphology Narrow / wide (120ms) P waves Absent Present / morphology / relationship QRS / PR interval

13. ECG Rhythm Is it normal sinus rhythm (NSR)? Can you identify P waves P waves preceding all the QRS complexes QRS complexes after every P wave Normal PR interval Regular P waves most easily seen in II & V1 If not – it’s not Sinus Rhythm. What is it??

14. Arrhythmias - Causes Abnormal impulse generation SA node Outside of the SA node Abnormal impulse conduction Damaged conduction pathways Re-entrant pathways

15. Note: there are many potential pacemaker sites in the heart!

16. AXIS (Coronal Plane) A xis of any ECG depolarisation or repolarisation QRS axis in the coronal (frontal) plane as determined by the limb leads : bipolar (I, II, III) & unipolar ( aVR , aVL , aVF ) Normal axis determined largely by the relative size of both the RV & LV, and the position of the heart may change in various pathological conditions

17. Determining QRS axis Normal QRS coronal axis is (??) -30 to +90 degrees: Both I & aVF + ve = normal Both I & aVF - ve = EAD lead I - ve & aVF + ve = RAD lead I + ve & aVF - ve lead II + ve = normal lead II - ve = LAD N RAD LAD EAD

18. Normal ECG

19. Right axis deviation

20. Causes of RAD RVH (most common) Acute RH strain - Pulmonary embolus Dextrocardia Normal in children and tall thin adults Chronic lung disease even without pulmonary hypertension Left posterior hemiblock Lateral / apical AMI WPW syndrome - left sided accessory pathway Atrial septal defect Ventricular septal defect

21. Left axis deviation

22. Causes of LAD ?LVH Left anterior hemiblock LBBB Q waves of inferior myocardial infarction Artificial cardiac pacing Emphysema WPW syndrome - right sided accessory pathway Tricuspid atresia Ostium primum ASD

23. Causes of extreme axis deviation Emphysema Hyperkalaemia Lead transposition Artificial cardiac pacing Ventricular tachycardia

24. Transverse axis of QRS / Rotation Normal transverse axis is leftward and posterior: Hence usually a progression in R wave height from V1 to V6 Transitional lead (where R = S) usually V3 or V4 Displacement of transition: Right (V1, V2) = counterclockwise rotation Left (V5, V6) = clockwise rotation

25. Normal ECG

26. WAVE MORPHOLOGY Shape Axis Duration Amplitude Progression

27. P wave - Normal Normal P wave Represents atrial depolarisation Axis 0 – 75 deg Upright monophasic I, II , III and AVF Inverted in AVR Biphasic in V1 (RA bf LA ) <2.5mm (0.25mV) in height limb leads <1.5mm in praecordial leads <3mm (120ms sec) in width Lead II

28. Normal ECG

29. P wave - Abnormalities Morphology RAH ( Pulm HTN) increased amplitude LAH (MS, HTN) notched in I & II, deep - ve in V1 A Fib/ Flut no clear P waves / sawtooth Hyperkalaemia reduced amplitude Ectopic atrial rhythm Axis Retrograde Dextrocardia right displacement Pulmonary disease inferior displacement Congenital heart disease left displacement Rhythm Ectopic atrial rhythm A Fib / flutter Multifocal atrial tachycardia SVT (retrograde P waves)

30. P wave – RAE / LAE

31. PR Interval - Normal Start of the P wave - start of the QRS Normal = 120 – 200ms = 3 - 5 small squares Increases with age Is rate dependent Delay at AV node Protect ventricles Allow for ventricular filling

32. PR interval - Abnormal Short Preexcitation of ventricles (WPW) & other SVT’s AV junctional rhythm Exercise induced tachycardia Long AV Block Hyperkalaemia CHD Drugs ( Digoxin , B-Blockers, Quinidine ) Hypothermia Hypothyroidism

33. PR segment Normally isoelectric using the TP (not ST) segment as a baseline Abnormal: Elevation Myocarditis ( aVR , V1) Atrial infarction Depression Myo/pericarditis Atrial infarction Exercise induced tachycardia

34. QRS parameters Q waves ?abnormal Q’s R wave Progression Dominant R wave in aVR / V1 QRS amplitude QRS duration (<100ms)

35. QRS waveform nomenclature R r qR qRs Qrs QS Qr Rs rS qs rSr’ rSR’

36. QRS complex – Q waves Normal Q waves Due to rightward septal depolarisation May occur in I, II,III, aVR , aVF , aVL , V4-V6 Size < 0.4mV (4 squares) or 25% of R wave height Duration < 0.03sec (under 1 square) May be slightly greater in III & aVR (normal variant) No Q waves in V1- V3 Abnormal Q waves >0.4mV (4 squares) or 25% of R wave height >0.03sec ( ie . 1 square or greater) Presence in V1-3 Suggest: evolved AMI / ventricular enlargement / rotation of heart / HOCM / abnormal conduction / lead misplacement

37. Normal ECG

38. QRS – R wave Abnormalities Dominant R wave V1 normal in children / young adults / persistent juvenile pattern RVH / PE / L to R shunt RBBB Post AMI (= Q wave) WPW type A Dextrocardia HOCM Muscular dystrophy Incorrect lead placement Dominant R wave aVR (>3mm, or R/S ratio >0.7) Na channel blockade Dextrocardia RVH Incorrect lead placement Poor R wave progression Prior anteroseptal AMI / LVH / incorrect lead placement / dextrocardia / normal variant

39. QRS abnormal amplitude: Increased LVH ( S in V1 + R in V5 or V6 >35mm sensitive but not specific) BER Hyperthyroidism Normal / athletes Decreased (<5mm limb leads, <10mm precordial ) Pericardial / Pleural effusion Hypothyroidism Pneumothorax Restrictive cardiomyopathy COPD Haemochromatosis Fluctuating / Electrical alternans

40. QRS prolonged duration: Causes BBB (may be rate related) Ventricular origin / Ventricular pacing Hyperkalaemia Na channel blockade Pre-excitation Hypothermia

41. ST Segment - Normal Represents period between depolarisation & repolarisation (J point to T wave) Normally isoelectric with respect to TP & PR segment Abnormal if : Elevated Depressed

42. Normal ECG

43. ST segment - Elevation Morphology Concave - some non-AMI causes Convex - suggestive of AMI Distribution Widespread - ?non- AMI Localised to anatomically contiguous leads - suggestive of AMI Magnitude Larger suggestive of AMI QRS morphology Large amplitude - consider LVH Widening - consider BBB or vent. paced rhythm

44. ST segment elevation causes: Acute Coronary Syndrome Acute pericarditis Benign early repolarisation (BER) LV aneurysm LVH BBB Left - R to mid precordial leads Right - lateral leads Cardiomyopathy Acute myocarditis Hypothermia Hyperkalaemia Myocardial contusion CNS injury Brugarda Syn Paced vent. Rhythms Post-electrical cardioversion

45. BER Prominent, assymetrical , concordant (with QRS) T waves Widespread concave ST segments V2-5 J point elevation (notching / slurring) <25% T wave height in V6 (usually <2mm precordial ) No reciprocal ST depression Stable over time

46. ST Segment - Depression Morphology Flat or downsloping with ACS Distribution QRS morphology Large amplitude - consider LVH Wide complex - BBB, vent. Pacing, LVH

47. ST segment depression causes: ACS (>1mm depression at J point, diffuse, horizontal or downsloping , not localising ) AMI (NSTEMI, Post MI, reciprocal) BBB LVH Ventricular pacing Digoxin effect Rate related Myocardial contusion Metabolic Post-electrical cardioversion

48. T wave - Normal Magnitude No clearly defined range (<5mm limb, <15mm precordial ) General rule - 1 /2 the height of preceding QRS Axis Largely dependent on QRS (concordant) Positive in I, II, V3-V6 Negative in aVR , V1 Variable in III, aVF , aVL , & V2

49. Normal ECG

50. T wave - Abnormalities Prominent AMI ( hyperacute ), Hyperkalaemia , BER, Myopericarditis ( concave STE & PR depression ) , BBB ( esp. LBBB in V1-V3 ) , LVH (similar to LBBB) Inverted ACS (all stages) NB may be flattened Wellen’s Syn. (critical prox LAD stenosis without MI) NB may be biphasic Past MI Pericarditis Children / Persisting juvenile pattern (V1-V3) CNS injury/ICH BBB PE, RVH, LVH, HOCM, Digoxin , toxic, metabolic

51. U wave Positive deflection that occasionally occurs after T wave Most visible at slow HR’s in V1-V4 The origin is uncertain ( repol of the IVS) Presence or absence does not signify pathology Abnormal if : >1/3 preceding T wave height (N 1-2mm) Disconcordant with T wave

52. U wave - Abnormalities Increased amplitude Athletes Bradycardia HypoK + / HypoCa2+ / HypoMg2+ CNS event Hypertension Hypothermia Medications ( digoxin , quinidine ) Inversion Ischaemia LV overload RV overload PE

53. QT interval - Normal Measured from the start of the QRS to the end of the T wave Measure in II, V 5-6 use slope include U waves if continuous with T wave Represents the time required for ventricular activation & recovery Range 330 - 440ms (460ms women) Rule of thumb < half RR interval QT interval corrected to the heart rate

54. QT c calculation Multiple formulas Bazett’s QTc = measured QT interval  R-R interval Hence QTc = QT at HR of 60bpm

55. QTc - Abnormal Duration Short Hypercalcaemia / Digoxin / Congenital Long lengthened repolarisation time ventricle more susceptible to early after depolarisation which can precipitate a variety of potentially fatal arrhythmias (VF, VT, torsades de pointes) Congenital long QT syndromes CNS disease Metabolic syndromes (HYPO: K+, Ca++, T4) Hypothermia Drugs: erythromycin, cisapride , amiodarone , haloperidol, quinidine …

56. Overview Rate & rhythm Axis Wave morphology Intervals Segments In the context of: Look at the patient (hear the story) Compare to old ECG’s Get a second opinion