1 / 39

INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY

ECG interpretation for beginners – 2 Axel en Luc De Wolf RZ Tienen UZ Leuven. INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY. 3. 80.

adonis
Download Presentation

INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. ECG interpretation for beginners – 2Axel en Luc De Wolf RZ Tienen UZ Leuven

  2. INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY 3 80 The “golden hour”: 65 lives are saved for every 1,000 patients treated when the treatment is initiated within the first hour of symptom onset! PATHOPHYSIOLOGY + EPIDEMIOLOGY THROMBOLYSIS IN CLINICAL TRIALS AND REGISTRIES NEW TRIALS/ REGISTRIES MANAGEMENT OF ACUTE MI AND THE RATIONALE FOR EARLY REPERFUSION CLINICAL QUESTIONS METALYSE (+ PRESCRIBING INFORMATION) COSTS REFERENCES SYSTEM REQUIREMENTS IMPRESSUM 60 ABSOLUTE BENEFIT PER 1,000TREATED PATIENTS 40 20 0 15 3 6 9 12 18 21 24 0 TREATMENT DELAY IN HOURS Boersma et al. Lancet 1996; 348: 771–775.

  3. A heart • Blood circulates, passing near every cell in the body, driven by this pump • …actually, two pumps… • Atria = turbochargers • Myocardium = muscle • Mechanical systole • Electrical systole

  4. Excitation of the Heart

  5. Excitation of the Heart

  6. Cardiac Electrical Activity

  7. A system • Quality of ECG? • Rate • Rhythm • Axis • P wave • PR interval • QRS duration • QRS morphology • Abnormal Q waves • ST segment • T wave • QT interval

  8. A system • Quality of ECG? • Rate • Rhythm • Axis • P wave • PR interval • QRS duration • QRS morphology • Abnormal Q waves • ST segment • T wave • QT interval

  9. P wave • Are there P waves….? • Pointy = P pulmonale (RA hypertrophy)>2,5mm • Bifid = P mitrale (LA hypertrophy)>2,5mm • Not very accurate or useful….

  10. PR interval • Start of P wave to start of QRS • Normal = 0.12-0.2s • Too short – can mean WPW syndrome (ie. an accessory pathway), or normal! • Too long –means AV block (heart block) - 1st/2nd/3rd degree

  11. A system • Quality of ECG? • Rate • Rhythm • Axis • P wave • PR interval • QRS duration • QRS morphology • Abnormal Q waves • ST segment • T wave • QT interval

  12. QRS complex • Should be <0.12s duration • >0.12s = BBB (either LBBB or RBBB) • ‘Pathological’ Q waves can mean a previous MI (? territory) • >25% size of subsequent complex • Q waves are allowed in V1, aVR and III

  13. BBB Look at V1 and V6 W I LL ia M = LBBB M a RR o W = RBBB

  14. QRS complex • Is there LVH? • Sum of the Q or S wave in V1 and the biggest R wave in V5 or V6 >35mm • (R wave in aVL >11mm) • Not actually very useful….

  15. A system • Quality of ECG? • Rate • Rhythm • Axis • P wave • PR interval • QRS duration • QRS morphology • Abnormal Q waves • ST segment • T wave • QT interval

  16. ST segment • ST depression • Downsloping or horizontal = abnormal • Ischaemia (coronary stenosis) • If lateral (V4-V6), consider LVH with ‘strain’ or digoxin (reverse tick sign) • ST elevation • Infarction (coronary occlusion) • Pericarditis (widespread) • These are usually in ‘territories’ eg. anterior/lateral/inferior etc. and will be present in contiguous leads

  17. T wave • Peaked (hyperkalaemia or normal young man) • Inverted/biphasic (ischaemia, previous infarct) • Small (hypokalaemia) • No pot, no tea!

  18. QT interval • Don’t worry about too much… • Start of QRS to end of T wave • Needs to be corrected for HR • Various formulae • eg. Bazett’s: • Computer calculated often wrong • Long QT can be genetic (long QT sy.) or secondary eg. drugs (amiodarone, sotalol) • Associated with risk of sudden death due to Torsades de Pointes

  19. Morfologische afwijkingen Hypertrofie Voorkamer en Kamer

  20. K51 – Rechter voorkamerhypertrofie Dilatatie van de rechter voorkamer Hoge spitse P toppen in afl. II & aVF ( 0,25 mV) Toename initiële P voltage in afl. II, III, aVF & V1 Normale duur P golf Vaak in combinatie met tekenen van rechter kamerhypertrofie P pulmonale

  21. Dilatatie van de linker voorkamer P golf > 120 ms GehaakteP top door toenameamplitude terminaaldeel van P golf in afl. I, II, aVL & V6 BifasischeP golfin afl. V1 met terminaalnegatiefdeel ( 0,1 mV,  40 ms) K52 - Linker voorkamerhypertrofie Risico op atriale fibrillatie

  22. (R in V5 of V6) + (S in V1 of V2) > 3,5 mV (35 mm) ST elevatie concaaf naar boven met hoge positieve T top in rechtszijdige afleidingen ST depressie convex naar boven met asymmetrisch negatieve T top in linkszijdige afleidingen Normale as K53 - Linker kamerhypertrofie

  23. As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage. Increased QRS voltage Left Ventricular Hypertrophy Why is left ventricular hypertrophy characterized by tall QRS complexes? LVH ECHOcardiogram For more presentations www.medicalppt.blogspot.com

  24. Left Ventricular Hypertrophy • Criteria exists to diagnose LVH using a 12-lead ECG. • For example: • The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm. • However, for now, all you need to know is that the QRS voltage increases with LVH. For more presentations www.medicalppt.blogspot.com

  25. Hoge R in V1 (> 0,7 mV) met R/S ratio > 1 Vlakke R progressie Diepe S in V5-V6 ( > 0,7 mV) met R/S ratio < 1 qR of rSR’ in V1 met hoge spitse R’ (diff. diagnose RBTB) Hoge, terminale R in aVR Rechter asdeviatie (komt overeen met diepe S in I en aVL) K55 – Rechter kamerhypertrofie Kliniek van longlijden

  26. Ischemie en Infarkt

  27. K56 - Ischemie Wanneer een elektrode geplaatst wordt tegenover een zone van ischemie betekent - ST segment depressie: subendocardiale ischemie - ST segment elevatie: transmurale (subepicardiale) ischemie

  28. Characteristic changes in AMI • ST segment elevation over area of damage • ST depression in leads opposite infarction • Pathological Q waves • Reduced R waves • Inverted T waves

  29. R ST P Q ST elevation • Occurs in the early stages • Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2

  30. R ST P T Q Deep Q wave • Only diagnostic change of myocardial infarction • At least 0.04 seconds in duration • Depth of more than 25% of ensuing R wave

  31. R ST P T Q T wave changes • Late change • Occurs as ST elevation is returning to normal • Apparent in many leads

  32. Bundle branch block Anterior wall MI Left bundle branch block aVR aVL aVF V1 V2 V3 V4 V5 V6 aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III I II III

  33. Sequence of changes in evolving AMI R R R ST ST T P P P T Q Q S Q 1 minute after onset 1 hour or so after onset A few hours after onset R ST T ST P P P T T Q Q Q A few months after AMI A day or so after onset Later changes

  34. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Anterior infarction Anterior infarction Left coronary artery

  35. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Inferior infarction Inferior infarction Right coronary artery

  36. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Lateral infarction Lateral infarction Left circumflex coronary artery

  37. Location of infarct combinations I aVR V1 V4 ANT POST LATERAL ANT SEPTAL aVL II V2 V5 ANT LAT V3 V6 aVF III INFERIOR

  38. Diagnostic criteria for AMI • Q wave duration of more than 0.04 seconds • Q wave depth of more than 25% of ensuing r wave • ST elevation in leads facing infarct (or depression in opposite leads) • Deep T wave inversion overlying and adjacent to infarct • Cardiac arrhythmias

More Related