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Ecg made easy
The document provides a comprehensive overview of electrocardiograms (ECGs), including their purpose, calibration, electrode placement, and the heart's electrical conduction system. It describes the components of an ECG complex, how to estimate heart rate, and details normal sinus rhythm and various axis deviations. The document also highlights methods for interpreting and reporting ECGs, discussing heart rate classifications and characteristic waveforms in different clinical conditions.
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Ecg made easy
- 3. OBJECTIVES What isan ECG and why it is used? What is the normal calibration of ECG? What is the conductive system of the heart? Where the electrodes are placed? What are the polarities of the 12 leads? What are parts of an ECG complex? How to estimate heart rate from ECG? What are features of normal sinus rhythm? What is axis of heart and axis deviation? What is normal P-QRS-T morphology in different leads? What are changes seen in limb leads reversal?
- 5. WHAT IS ECG? Itis the graphical recording of electrical conduction in the heart over a period of time (usually 10 sec), using electrodes placed over the skin. In conventional 12 lead ECG, a total 10 electrodes are placed: 6 over the chest and one on each limb. The overall magnitude of electrical activity of heart is measured from 12 different angles or “leads”. The graph of voltage versus time produced is called Electrocardiogram.
- 6. USES OF ECG? Itis used to detect: Rate and rhythm disorders Conduction problems Myocardial ischemia Myocardial infarcts Chamber dilation Chamber hypertrophy Inflammation i.e. pericarditis Electrolyte disturbances Drug toxicity Other: pulmonary embolism
- 8. SPEED CALIBRATION X-axis time – 1 small square • 40 ms (0.04 sec) – 1 large square • 200 ms (0.2 sec) Speed: 25 mm/sec
- 9. VOLTAGE CALIBRATION Y axis voltage – 1 large square 0.5 mV – 2 large squares 1.0 mV – Therefore, 1 mV produces deviation of 2 large squares (10 mm)
- 11. CHAMBERS OF HEART Hearthas two electrically functional units: Atria and Ventricles. Electrically divided by the properties of anulous fibrosus cordis.
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- 14. PACEMAKERS Sinoatrial “SA” Node -Dominant pacemaker - Intrinsic rate of 60 - 100 beats/minute. Atrioventricular “AV” Node - Back-up pacemaker - Intrinsic rate of 40 - 60 beats/minute. Ventricular cells - Back-up pacemaker - Intrinsic rate of 20 - 45 beats/minute.
- 15. AXIS OF THEHEART The electrical axis of the heart is the mean direction of the action potentials traveling through the conductive system of the heart.
- 16. WAVEFORMS Contraction of anymuscle is associated with electrical changes called depolarization. This is followed by its relaxation, which is associated with the reversal of these changes called repolarization. These electrical changes will produce waveforms on the ECG. i.e. P-QRS-T waves. No electrical changes will produce an flat isoelectric baseline on the ECG.
- 17. ECG COMPLEX Waveforms –P wave – QRS complex – T wave – U wave Segments – PR segment – ST segment Intervals – PR interval – QT interval – RR interval
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- 19. ELECTROMAGNETICS 1. depolarization towardthe positive electrode produces a positive deflection 2. depolarization away from the positive electrode produces a negative deflection 3. repolarization toward the positive electrode produces a negative deflection 4. repolarization away from the positive electrode produces a positive deflection
- 20. ELECTROMAGNETICS If direction ofconduction is at right angle to the positive electrode it will produce positive deflection (depolarization) and then negative deflection (repolarization).
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- 24. CHEST ELECTRODES Chest ElectrodePlacement V1 4th ICS, right of sternum V2 4th ICS, left of sternum V3 Between V2 and V4 V4 5th ICS, in left mid clavicular line V5 Same height as V4, in left anterior axillary line V6 Same height as V4, in left mid axillary line
- 25. LEADS 3 limbleads – I - (+LA and -RA) – II - (+LL and -RA) also called ‘sinus lead’ – III - (+LL and -LA) 3 augmented limb leads: – aVR - (+RA and average of LA & LL) – aVL - (+LA and average of RA & LL) – aVF - (+LL and average of RA & LA) 6 Chest leads: – V1, V2, V3, V4, V5, V6 (have +ve electrodes of same name) – Negative electrode is WCT (Wilson’s central terminus), an average of the three limb electrodes (RA, LA, LL) Other Chest leads: • Posterior chest leads: V7, V8, V9 • Right chest leads: V3R, V4R, V5R
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- 27. VECTORS OF LIMBLEADS
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- 34. REPORTING AN ECG Estimatedheart rate Comment on the rhythm Comment on the axis Comment on: – P wave morphology – PR segment – QRS morphology – ST segment – T wave morphology – QT interval Compare with a previous ECG Conclusion
- 35. ESTIMATING HEART RATE Squaremethod – Count large boxes between two adjacent R waves
- 36. ESTIMATING HEART RATE Alt.method – count number of small boxes between two consecutive R waves – divide 1500 by that number to est. HR 3 second method – count number of QRS complexes that fit into 3 seconds (15 large squares) – multiply this number with 20 to est. HR – preferred method in irregularly irregular rhythms
- 37. HEART RATE INTERPRETATION HRof 60-100 beats/min Normal range HR > 100 beats/min Tachycardia Physiologic i.e. exercise Inappropriate i.e. fever, anxiety, tachyarrhythmia HR < 60 beats/min Bradycardia Physiologic i.e. athletes at rest Inappropriate i.e. heart blocks, vaso-vagal reflex Paediatric values New born i.e. 110 - 150 b/m 2 years i.e. 85 - 125 b/m 4 years i.e. 75 - 115 b/m 6 years + i.e. 60 - 100 b/m
- 38. NORMAL SINUS RHYTHM Normalheart rate Regular rhythm P waves should be sinus P wave is round and upward in lead I & II Each QRS is preceded by a P wave The PR interval should remain constant QRS complexes should be narrow
- 39. AXIS DEVIATION (THUMBRULE) QRS IN LEAD I QRS IN LEAD AVF AXIS DEVIATION SEE IN POSITIVE POSITIVE NORMAL POSITIVE NEGATIVE LEFT AXIS DEVIATION • Elevated diaphragm (ascites, pregnancy) • IWMI, hyperkalemia • LVH alone, LVH with LBBB • Occassionally LBBB alone NEGATIVE POSITIVE RIGHT AXIS DEVIATION • Young, thin people • LWMI • RVH alone, RVH with RBBB • Occassionally LBBB alone NEGATIVE NEGATIVE NORTH WEST AXIS • Severe RVH • Severe hyperkalemia
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- 41. P WAVE MORPHOLOGY sinus P wave is round and upward in lead I / II always inverted in aVR can be biphasic or inverted in lead V1 maximal height - 2.5 mm in lead II / III duration is shorter than 0.12 sec (3 small sq)
- 42. PR SEGMENT &PR INTERVAL PR segment – an iso-electric line, due to conduction delay to AV node – from end of P wave to start of QRS complex – diffuse PR segment depression in acute pericarditis PR interval – includes P wave + PR segment – from start of P wave to start of QRS – normally 0.12 to 0.2 sec (3-5 small sq) – short PR interval are seen in pre-excitation: • MAT, WPW, junctional rhythms – prolonged PR interval are seen in: • 1st and 2nd degree AV block • hypokalemia, digitalis toxicity, carditis
- 43. DELTA WAVE In WPWsyndrome, short PR interval manifests as a “delta wave”, a slurred upstroke in the QRS complex
- 44. QRS COMPLEX Normal durationis < 110 ms or < 3 small squares – Q wave – 1st downward deflection after P wave • seen in I, aVL, V5 and V6; usually absent in leads V1-V2 – R wave – 1st upward deflection • short in V1-V2, long in V5-V6 – S wave – 2nd downward deflection • long in V1-V2, short in V5-V6 R wave progression from V1 to V6, R wave height but S wave depth Q S R TZ Normal Transition Zone is at V3-V4, when S wave equals R wave. Represents apex of heart.
- 45. QRS ABNORMALITIES Broad QRScomplex (>120 ms) – LBBB, RBBB, hyperkalemia, VT etc Increased QRS height – LVH, RVH Poor R wave progression – AWMI, LVH, LBBB, WPW Dominant R wave in V1 – PWMI, RVH, RBBB, WPW, children Pathologic Q waves – Markers of previous MI – Q wave width > 1 small sq. + Q wave depth > 2 small sq. – Or, Q wave is ≥ 25% of the R wave Pathologic Q
- 46. VENTRICULAR HYPERTROPHY Sokolow Lyonindex for LVH: • S wave depth in V1/V2 + R wave height in V5/V6 ≥ 35 mm • R wave height in aVL ≥ 11 mm Criteria for RVH: • dominant R in V1 + dominant S waves in V5/V6 • deep S waves in leads I, II, III, aVL, V5, V6
- 47. ST SEGMENT Usuallyiso-electric (flat) Measured from J point to beginning of T wave J point is the junction between QRS and ST segment ST elevation in STEMI (convex or obliquely straight upwards) Diffuse ST elevation with PR depression in acute pericarditis ST depression in unstable angina / NSTEMI Sagging ST depression in digoxin effect and hypokalemia ST segment J point P T “sagging” ST depression
- 48. ST SEGMENT ELEVATION “saddleback” patternof diffuse ST elevation & PR depression in Pericarditis obliquely straight ST elevation in STEMI upward convex ST elevation in STEMI notched J point “fish-hook” pat. of ST elevation seen in BER
- 49. T WAVE ANDU WAVE Upwards in most leads Can be inverted in V1, but always inverted in aVR Should be less than 2/3rd the height of R wave Abnormalities of T wave Tall narrow T waves in hyperkalemia Tall broad T waves in acute STEMI (hyperacute) Generalized flat T waves in hypokalemia Flattened or inverted T waves – early sign of ischemia Deep T waves in chest leads – Wellen’s sign Diffuse deep “cerebral” T waves – raised ICP U wave Late repolarization of ventricles Usually seen in V6 after T wave Prominent in hypokalemia
- 50. QT INTERVAL Frombeginning of QRS to the ending of T wave Duration 0.35 - 0.45 sec ( 9 -12 small sq. ) QT duration is inversely proportional to Heart Rate QTc also with HR which can be corrected using Bazzet formula: Short QTc (< 340 ms) • Hypercalcemia • Digoxin effect Long QTc (> 460 ms) • Hypothermia • Hypokalemia • Hypomagnesiumia • Hypocalcemia • Drugs - amiodarone, quinidine, TCAs, erythromycin
- 51. Chamberline’s 10 RULES 1.PR interval should be 0.12-0.2 sec (3-5 small sq.) 2. With of QRS should not exceed 0.11 sec (3 small sq.) 3. QRS should be dominantly upwards in lead I and II 4. QRS and T waves have same direction in limb leads 5. All waves are negative in lead aVR 6. R wave must grow from V1 to V4 while S wave must grow from V1 to at least V3 and disappear in V6 7. ST segment should start iso-electric except in V1 and V2 where it may be elevated 8. P waves should be upright in I, II, and V2 to V6 9. No pathologic Q wave in I, II, and V2 to V6 10. T wave must be upright in I, II, and V2 to V6
- 53. LA / RAREVERSAL Lead I becomes inverted. Leads II and III switch places. Leads aVL and aVR switch places. Lead aVF remains unchanged. What will you see? • Lead I is completely inverted. • Lead aVR often becomes positive. • There may be marked right axis deviation.
- 54. LA / LLREVERSAL Lead III becomes inverted. Leads I and II switch places. Leads aVL and aVF switch places. Lead aVR remains unchanged. What will you see? • Lead III is completely inverted. • P wave is unexpectedly larger in lead I than in lead II.
- 55. RA / LLREVERSAL Lead II becomes inverted. Leads I and III become inverted and switch places. Leads aVR and aVF switch places. Lead aVL remains unchanged. What will you see? • Lead I, II, III and aVF all are completely inverted. • Lead aVR is upright.
- 56. RA / RL(N) REVERSAL Leads I and aVL become inverted. Lead II will be flat. Lead III is unchanged. Lead aVR and aVL become identical. What will you see? • Lead II is a flat line.
- 57. LA / RL(N) REVERSAL Lead I becomes identical to lead II. Lead II is unchanged. Lead III is flat. Lead aVR is an inverted lead II. Lead aVL and aVF become identical. What will you see? • Lead III is a flat line.
- 58. LL / RL(N) REVERSAL Einthoven’s triangle is preserved. What will you see? • ECG is unchanged.
- 59. LA with LL/ RA with RL Bilateral arm-leg electrode reversal. Lead I is flat. Lead II is an inverted lead III. Lead III is inverted. aVR and aVL become identical. aVF looks like negative lead III. What will you see? • Lead I is a flat line.
- 60. QUICK SPOTTING OF LEADREVERSAL Lead I is flat or completely inverted. Lead II is flat or completely inverted. Lead III is flat or completely inverted. Lead aVR is positive. P wave is larger in lead I than in lead II.
- 61. DEXTROCARDIA What will yousee? Right axis deviation. Complete inversion of lead I. All waves in aVR are positive. Absent R wave progression in chest leads - S wave is dominant throughout