QRS INTERVAL IN ECG AND ITS ABNORMALITIES

QRS INTERVAL IN ECG AND ITS ABNORMALITIES

1. QRS INTERVAL Dr.G.VENKATA RAMANA MBBS DNB FAMILY MEDICINE

2. QRS Complex Naming Convention

3. QRS Complex Morphology Main features to consider: Are there any pathological Q waves? Are any R or S waves too big ? Is there a dominant R wave in aVR ? Is there a poor R wave progression? Are the QRS complexes too small? How is the width of QRS complexes? Are any QRS complexes an abnormal shape?

4. ARE ANY R OR S WAVES TOO BIG? The height of the R wave and depth of the S wave vary from lead to lead in the normal ECG As a rule, in the normal ECG : The R wave increases in height from lead V1 to V5 T he R wave is smaller than the S wave in leads V1 and V2 T he R wave is bigger than the S wave in leads V5 and V6 The tallest R wave does not exceed 25 mm in height T he deepest S wave does not exceed 25 mm in depth

5. Always look carefully at the R and S waves in each lead, and check whether they conform to these criteria If not, first of all consider : Incorrect ECG calibration (should be 1 mV = 10 mm). If the calibration is correct, consider whether your patient has one of the following: Left ventricular hypertrophy Right ventricular hypertrophy Posterior myocardial infarction Wolff–Parkinson–White syndrome If the QRS complex is also abnormally wide, think of: B undle branch block

6. Left ventricular hypertrophy LVH causes tall R waves in the leads I,aVL,V5 and V6 and the reciprocal change of deep S waves in leads V1 and V2 Diagnostic criteria for LVH In the limb leads: R wave >11 mm in lead aVL R wave >20 mm in lead aVF S wave >14 mm in lead aVR S um of R wave in lead I and S wave in lead III >25 mm. In the chest leads: R wave of ≥ 25 mm in the left chest leads S wave of ≥ 25 mm in the right chest leads Sum of S wave in lead V1 and R wave in lead V5 or V6 >35 mm ( Sokolow –Lyon criterion ) Sum of tallest R wave and deepest S wave in the chest leads >45 mm

7. The Cornell criteria involve measuring the S wave in lead V3 and the R wave in lead aVL Left ventricular hypertrophy is indicated by a sum of >28 mm in men and >20 mm in women The Romhilt –Estes scoring system allocates points for the presence of certain criteria A score of 5 indicates left ventricular hypertrophy and a score of 4 indicates probable left ventricular hypertrophy 3 points – for (a) R or S wave in limb leads of ≥20 mm, (b) S wave in right chest leads of ≥25 mm, or (c) R wave in left chest leads of ≥25 mm 3 points – for ST segment and T wave changes (‘typical strain’) in a patient not taking digitalis (1 point with digitalis) 3 points – for P-terminal force in V1 >1 mm deep with a duration >0.04 s 2 points – for left axis deviation (beyond –15°) 1 point – for QRS complex duration >0.09 s 1 point – for intrinsicoid deflection (the interval from the start of the QRS complex to the peak of the R wave) in V5 or V6 >0.05 s

8. If there is evidence of left ventricular hypertrophy on the ECG, look also for evidence of ‘strain’: ST segment depression T wave inversion Causes of left ventricular hypertrophy Hypertension Aortic stenosis Coarctation of the aorta Hypertrophic cardiomyopathy

9. Right ventricular hypertrophy Right ventricular hypertrophy causes a ‘dominant’ R wave (i.e. bigger than the S wave) in the leads that ‘look at’ the right ventricle, particularly V1 Right ventricular hypertrophy is also associated with: Right axis deviation D eep S waves in leads V5 and V6 R ight bundle branch block (RBBB ) and, if ‘ strain’ is present: ST segment depression T wave inversion Causes of right ventricular hypertrophy Pulmonary hypertension Pulmonary stenosis Tetralogy of Fallot Arrhythmogenic right ventricular cardiomyopathy

10. Posterior myocardial infarction One of the few causes of ‘dominant’ R wave in lead V1

11. Wolff–Parkinson–White syndrome If you see a dominant R wave in leads V1–V3 in the presence of a short PR interval, think of Wolff–Parkinson–White syndrome Generally, however, a dominant R wave in leads V1–V3 indicates a left-sided accessory pathway, whereas a dominant S wave in leads V1–V3 indicates a right-sided accessory pathway

12. Dominant R wave in aVR Poisoning with sodium-channel blocking drugs (e.g. TCAs) Dextrocardia Incorrect lead placement (left/right arm leads reversed) V entricular tachycardia (VT)

13. Examples of Dominant R wave in aVR Poisoning with sodium-channel blocking drugs Causes a characteristic dominant terminal R wave in aVR Poisoning with sodium-channel blocking agents is suggested if: R wave height > 3mm R/S ratio > 0.7

14. Dextrocardia P ositive QRS complexes (with upright P and T waves) in aVR Negative QRS complexes (with inverted P and T waves) in lead I Marked right axis deviation Absent R-wave progression in the chest leads (dominant S waves throughout)

15. Left arm/right arm lead reversal

16. Ventricular Tachycardia

17. Poor R wave progression Poor R-wave progression (PRWP) is a common ECG finding that is often inconclusively interpreted as suggestive, but not diagnostic, of anterior myocardial infarction (AMI) Poor R wave progression is described with an R wave ≤ 3 mm in V3 and is caused by: Prior anteroseptal MI Dextrocardia LVH Inaccurate lead placement May be a normal variant

18. Poor R wave progression secondary to prior anteroseptal MI

19. Poor R wave progression due to electrode misplacement (leads V1 and V3 reversed)

20. Dextrocardia The ECG does not show the normal progressive increase in R wave height across the chest leads; instead, the QRS complexes decrease in height across them In addition, the P wave is inverted in lead I and there is right axis deviation Right-sided chest leads will show the pattern normally seen on the left

21. ARE THE QRS COMPLEXES TOO SMALL? Low Voltage QRS Morphology The QRS is said to be  low voltage  when: The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or The amplitudes of all the QRS complexes in the precordial leads are < 10 mm

22. C auses of low voltage include : Incorrect ECG calibration (should be 1 mV = 10 mm) Fluid:   Pericardial effusion ; Pleural effusion Fat:   Obesity Air:   Emphysema ;  Pneumothorax Infiltrative / Connective Tissue Disorders Myxoedema Infiltrative myocardial diseases i.e.  restrictive cardiomyopathy  due to amyloidosis, sarcoidosis , haemochromatosis Constrictive pericarditis Scleroderma Loss of viable myocardium: Previous massive MI End-stage dilated cardiomyopathy

23. Emphysema: Low voltages in the limb leads is classically seen in patients with   emphysema Other assocaited ECG features of emphysema include: Right axis deivation Peaked P waves (P  pulmonale ) Clockwise rotation (persistent S wave in V6)

24. Prior Massive Anterior MI: Low QRS voltage in V1-6. This diffuse loss of R wave height suggests extensive myocardial loss from a prior anterior MI. There is also biphasic anterior T waves ( Wellens syndrome ) indicating new critical occlusion of the LAD artery

25. QRS Width Normal QRS width is 70-100 ms (a duration of 110 ms is sometimes observed in healthy subjects) Us eful in determining the origin of each QRS complex (e.g. sinus, atrial, junctional or ventricular) Narrow complexes  (QRS < 100 ms ) are  supraventricular  in origin Broad complexes  (QRS > 100 ms ) may be either  ventricular  in origin, or due to  aberrant conduction  of supraventricular complexes (e.g. due to bundle branch block, hyperkalaemia or sodium-channel blockade) Sinus rhythm with frequent ventricular ectopic beats  (VEBs) in a pattern of ventricular bigeminy The narrow beats are sinus in origin, the broad complexes are ventricular

26. Narrow QRS Complex Morphology Narrow (supraventricular) complexes arise from three main places: Sino-atrial node (= normal P wave) Atria (= abnormal P wave / flutter wave / fibrillatory wave) AV node / junction (= either no P wave or an abnormal P wave with a PR interval < 120 ms )

27. Examples of Narrow Complex Rhythms : Sinus rhythm: Each narrow complex is preceded by a normal P wave

28. Atrial flutter : Narrow QRS complexes are associated with regular flutter waves

29. Junctional tachycardia : Narrow QRS complexes with no visible P waves

30. Broad QRS Complex Morphology A QRS duration > 100 ms is abnormal A QRS duration > 120 ms is required for the diagnosis of bundle branch block or ventricular rhythm Broad complexes may be ventricular in origin or due to aberrant conduction secondary to: Bundle branch block (RBBB or LBBB) Hyperkalaemia Hypothermia Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants) Pre-excitation (i.e. Wolff-Parkinson-White syndrome) Ventricular pacing Intermittent aberrancy (e.g. rate-related aberrancy)

31. Example of a Broad Complex Rhythm: Ventricular tachycardia: Broad QRS complexes with no visible P waves

32. Ventricular vs supraventricular rhythms Differentiation between  ventricular  complexes and  aberrantly conducted  supraventricular complexes may be difficult In general, aberrant conduction of sinus rhythm and atrial rhythms (tachycardia, flutter, fibrillation) can usually be identified by the presence of preceding atrial activity (P waves, flutter waves, fibrillatory waves) However, aberrantly conducted junctional (AV nodal) complexes may appear identical to ventricular complexes as both produce broad QRS  without  any preceding atrial activity In the case of ectopic beats, this distinction is not really important (as occasional ectopic beats do not usually require treatment) However, in the case of sustained tachyarrhythmias , the distinction between ventricular tachycardia and SVT with aberrancy becomes more important

33. Fortunately, many causes of broad QRS can be identified by pattern recognition: Right bundle branch block  produces an RSR’ pattern in V1 and deep slurred S waves in the lateral leads Left bundle branch block  produces a dominant S wave in V1 with broad, notched R waves and absent Q waves in the lateral leads Hyperkalaemia  is associated with a range of abnormalities including peaked T waves Tricyclic poisoning  is associated with sinus tachycardia and tall R’ wave in aVR Wolff-Parkinson White syndrome  is characterised by a short PR interval and delta waves Ventricular pacing  will usually have visible pacing spikes Hypothermia  is associated with bradycardia , long QT, Osborn waves and shivering artefact

34. RBBB: Right Bundle Branch Block V1: RSR’ pattern in V1, with (appropriate) discordant T wave changes V6: Widened, slurred S wave in V6

35. LBBB: Left Bundle Branch Block V1: Dominant S wave V6: broad, notched (‘M’-shaped) R wave

36. Hyperkalemia Prolonged PR interval Broad , bizarre QRS complexes - these merge with both the preceding P wave and subsequent T wave Peaked T waves

37. Shivering artefact in a patient with hypothermia (note also the Osborn waves, bradycardia , prolonged QT )

38. Ventricular paced rhythm: Ventricular pacing spikes precede each QRS complex (except perhaps complex #2 — although the QRS morphology in this complex is identical to the rest of the ECG, suggesting that this beat is also paced) No atrial pacing spikes are seen The underlying native rhythm is probably coarse atrial fibrillation — there are several possible P waves visible in V1 but otherwise the atrial activity is chaotic

39. ARE ANY QRS COMPLEXES AN ABNORMAL SHAPE? Spot Diagnoses These cardiac diseases produce  distinctive QRS morphologies  that are important not to miss: Brugada syndrome  (partial RBBB with ST elevation in V1-2) Wolff-Parkinson White Syndrome  (delta wave) Tricyclic poisoning  (wide QRS with dominant R wave in aVR )

40.   Brugada Syndrome

41. Sinus Rhythm – Type A Pattern Sinus rhythm with a very short PR interval (< 120 ms ) Broad QRS complexes with a slurred upstroke to the QRS complex — the  delta wave Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred to as “Type A” WPW Tall R waves and inverted T waves in V1-3 mimicking  right ventricular hypertrophy  (RVH) Negative delta wave in aVL simulating the Q waves of  lateral infarction  — this is referred to as the “pseudo-infarction” pattern

42. Sinus rhythm – Type B Pattern Sinus rhythm with very short PR interval (< 120 ms ) Broad QRS complexes with a slurred upstroke to the QRS complexes - delta wave Dominant S wave in V1 indicates a right-sided AP — sometimes referred to as “Type B” WPW Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of  left ventricular hypertrophy  (LVH)

43. TCA Toxicity:  Sinus tachycardia, widened QRS, dominant terminal R wave in aVR