Ekg interpretation – the basics



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EKG Interpretation – the basics

250 136 94 71



Rate 300 214 150 125 100 88 75 68 60 50 43

187 115 83 65

167 107 79 62

Axis

aixs - 2 001
Right axis deviation Left axis deviation

- left posterior hemiblock - left anterior hemiblock

- right ventricular hypertrophy - LBBB

- acute cor pulmonale (eg PE) - left ventricular hypertrophy

- limb-lead reversal - elevated diaphragm (ascites)

- dextrocardia - inferior infarct (lg Q in aVF)



Intervals
PR < 200ms
1° AV block  PR interval ≥ 200ms

2° AV block  dropped beats (P wave without conduction)

Type I (Wenckebach) – progressive lengthening PR interval

Type II – intermittent loss of AV conduction

3° AV block  complete loss of AV conduction with escape beats
QRS < 120ms
Bundle branch blocks

- RBBB


- QRS > 110ms

- rSR´ in V1 (or, a tall R in V1)

- wide terminal S wave in V6 (and lateral leads)
- LBBB

- QRS > 120ms

- monophasic R wave in V6

- absence of septal q waves in lateral leads


QT < ½ R-R interval that precedes it
↓QT  hypercalcemia

↑QT  hypocalcemia

hypokalemia (actually, ↑QU interval)
Chamber Enlargement
Left ventricular hypertrophy

- deepest S in V1-2 + tallest R in V5-6 > 35mm, or

- R in aVL > 12mm (especially with left axis deviation)
- associated criteria

- strain pattern in lateral leads

- left axis deviation

- then, QRS widening, poor R wave progression, ST elevation


Right ventricular hypertrophy

- tall R wave in V1

- right axis deviation
Right atrial enlargement – “P-pulmonale”

- tall, peaked P waves (> 2.5mm in II, III, or aVF)

- prominent positive initial deflection in V1
Left atrial enlargement – “P-mitrale”

- wide, notched P in I, II, or aVL (> 120ms)

- large, negative terminal deflection in V1

Useful differentials to remember
QRS prolongation – (conduction – poisons – masqueraders)


  1. RBBB (beware other causes of tall R wave in V1 – see below)

  2. LBBB (beware hypothermia and WPW type B)

  3. Severe LVH

  4. Na-channel blocker toxicity (eg TCA)

  5. Hyperkalemia

  6. Wolfe-Parkinson-White

  7. Hypothermia

(also: ventricular rhythms, like AIVR and ventricular paced)
Tall R wave in lead V1 (tall T = T wave > S wave in that complex)

  1. RBBB - wide QRS

  2. RVH - right axis deviation

  3. Old posterior MI - old inferior MI

  4. WPW – type A - delta waves, short PR


ST-segment elevation

  1. STEMI

  2. LBBB

  3. Ventricular paced complex

  4. Severe LVH

  5. Pericarditis

  6. Benign early repolarization

  7. LV aneurysm

(also occasionally: acute PE, hyperK, SAH, HCM, and other case reports)
Impressive T-wave inversion

  1. Ischemia (NSTEMI)

  2. Vasospasm

  3. CNS event (esp SAH)

  4. Wellen’s syndrome

  5. Takotsubo cardiomyopathy

  6. Apical hypertrophic cardiomyopathy

  7. Post-ventricular pacing (“memory T waves”)

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

11a

12.

13. Unknown #1

14. Unknown #2


15. Unknown #3


16. Unknown #4


17.
664 - bipolar vent pacer

18.


19.

19a.

20.

21.

22.

23.
takutobu

24.

25.

26.

27.

28.

29.


30.


31.

31. Unknown #2

32. Unknown #3


34. Unknown #3



35. Unknown #4


36. Unknown #5



EKG Interpretations


  1. Atrial fibrillation with controlled ventricular response of 84/minute, left axis deviation (-50°), QRS slightly prolonged at 100msec, voltage for LVH (with associated changes including left axis, prolongation of the QRS, and repolarization changes of strain pattern laterally, poor R wave progression and ST-elevation V2-3). A good example of the changes of severe LVH.

  2. Atrial flutter with 2:1 block (clue – the rate is exactly 150/min), axis -30°, notice how the QRS in some leads (eg, II, III, aVF) appears prolonged by a portion of the flutter wave inscribed behind the QRS.

  3. 2° AV block, Type I (Wenckebach) with rate of 36/minute, with hyperacute T waves inferiorly (II, III, aVF) and ST-segment depression and T wave inversion V1-3 representing acute inferior-posterior infarction.

  4. Sinus at 108/minute, right axis deviation (+120°) and tall R wave in V1 suggest right ventricular hypertrophy in this patient with primary pulmonary HTN.

  5. Sinus at 66/min, axis -30°, PR interval is short (the width of the P wave), widening of the QRS by a delta wave most noticeable in I and aVL – Wolff-Parkinson-White, type B (not LBBB).

  6. Sinus at 84/minute, axis 0°, short PR interval and delta waves – WPW, type A because of the tall R wave in V1.

  7. Sinus at 72/minute, normal axis, PR 200msec (1° AV block), QRS prolonged at 120msec with tall R wave in V1RBBB (also note wide terminal S waves in lateral leads).

  8. Sinus at 78/minute, left axis at -60°, tall R waves in V1-2 with associated Q waves in inferior leads – old inferior-lateral MI.

  9. Sinus at 72/minute, left axis, wide QRS at 160msec with tall monophasic R in lateral leads consistent with LBBB, note expected repolarization changes of ST depression and T inversion laterally, and ST-segment elevation and exuberant T waves in anterior leads (V1-3).

  10. Regular rate at 72/minute, no P waves seen, very wide QRS and peaked T waves (V4) – severe hyperkalemia.

  11. Sinus tachycardia at 105/minute, slight prolongation of both QRS and QT intervals, note prominent R in aVR – all consistent with TCA toxicity. 11a has a noticeably prolonged QRS and an R in aVR > 5mm – a severe TCA overdose in a teenager.

  12. Sinus bradycardia at 48/minute, significant QRS prolongation by an additional wave at the end of each QRS, an Osborne wave – this is hypothermia.

  13. 2° AV block, type II with overall rate of 72/minute, right axis deviation, wide QRS with tall R in V1 – RBBB, the right axis with a RBBB adds the diagnosis of left posterior hemiblock (a bifascicular block). The 9th and 10th complexes are PVCs because P waves march through the rhythm, and thus these beats are dissociated from sinus activity and are necessarily ventricular in origin.

  14. Sinus tachycardia at 126/minute, right axis deviation and tall R in V1 – RVH, negative terminal deflection of biphasic P wave in V1 diagnostic of LA enlargement – this combination is typical of mitral stenosis.

  15. Sinus tachycardia at 144/minute, tall R wave in V1 coupled with tiny but perceptible Q waves inferiorly diagnose a subacute inferior-posterior MI; the very small complexes in the limb leads suggest tamponade – this elderly woman presented in shock three days after severe chest and back pain following rupture of the myocardium resulting in tamponade.

  16. MAT (multifocal atrial tachycardia) at 180/minute, axis +90, although P waves vary because of MAT they are nearly all tall in the inferior leads suggestive of right atrial enlargement (“P-pulmonale”), and the essentially isoelectric complexes in lead I has been called the “lead I sign” suggestive of COPD. This patient had severe COPD and was actually theophylline toxic causing the rapid MAT.

  17. Sinus at 96/min, axis -30, intervals normal, striking ST-segment elevation in V2-6, I, and aVL with reciprocal changes in the inferior leads consistent with an acute anterolateral STEMI.

  18. 100% ventricular paced rhythm at 72/minute, with appropriate “LBBB morphology” of QRS complexes including repolarization changes of ST-segment elevation in V1-3.

  19. Sinus at 90/minute, normal axis and intervals, ST-segment elevation in I, II, V3-6 with PR interval depression in II and PR elevation in aVR – all suggestive of acute pericarditis. 19a additionally has good Spodick’s sign of downsloping T-P segment in lead II rhythm strip.

  20. Sinus at 54/minute, normal axis and intervals, with ST elevation V2-6, notching of J point in same leads, and early transition of R/S – early benign repolarization.

  21. Sinus at 114/minute, ST-segment V1-6 with Q waves in same leads – ventricular aneurysm.

  22. Sinus at 60/minute, PR interval prolonged at 280msec (1° AV block), QT interval prolonged with striking T wave inversion – in this patient with subarachnoid hemorrhage, these changes are consistent with CNS effect.

  23. Sinus at 66/minute, normal axis and intervals, deep T wave inversion in V2-4 – in this patient with prior chest pain, a classic presentation of Wellens’ syndrome.

  24. Sinus at 72/minute, striking T wave inversion and QT intervals – in this middle-aged man it is consistent with Takotsubo cardiomyopathy.

  25. Striking T wave inversion in a young man – Yamaguchi syndrome, or apical hypertrophic cardiomyopathy.

  26. Basic rhythm is atrial fibrillation with two ventricular paced beats, widespread T wave inversion – an example of T-wave inversions due to ventricular pacing or “memory T waves.”

  27. Sinus at 60/min, axis -20°, intervals normal, ST-segment depression in V2-4 consistent with an isolated posterior wall MI.

  28. Sinus at 48/minute, normal axis and intervals, biphasic T waves in V2-3 – in a patient with prior chest pain, consistent with a form of Wellens’ syndrome.

  29. Sinus at 78/minute, normal axis and intervals, persistent hyperacute T waves V2-4 with J point depression and upsloping ST in the same leads – de Winters’ sign of proximal LAD occlusion.

  30. Sinus at 84/minute and PAC, impressive ST-segment depression in 9 of 12 leads, and ST-segment elevation in aVR and aVL – this pattern is predictive of critical left main disease.

  31. Sinus at 96/minute with PVC, wide QRS in a LBBB morphology with concordant ST-segment elevation in I and aVL – positive Sgarbossa criteria for acute MI.

  32. Sinus at 60/minute, normal axis and intervals – ST-seg depression in V2-4, an isolated posterior MI due to total occlusion of the circumflex artery.

  33. Ventricular paced rhythm at 78/minute, with ST-segment in multiple leads and ST-segment elevation in aVR, changes not typical of the expected LBBB morphology, and in fact suggestive of critical left main disease.

  34. Sinus tachycardia at 108/minute, left axis at -60°, intervals normal, voltage criteria for LVH with repolarization changes including T wave inversion laterally and ST-segment elevation V1-2.

  35. Sinus at 54/minute, normal axis and intervals, subtle biphasic T waves V1-2 that were new from prior tracing – a Wellens’ syndrome and the patient went on to have a large anterior MI one week later.

  36. Obvious ST-segment elevation in multiple leads (inferior as well as V1-6) – this is not pericarditis; it is an acute STEMI due to a wrap-around LAD with extension of the distal LAD around the apex to the inferior wall.



References
Armstrong EJ, Kulkarni AR, et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. Am J Cardiol 110:977-983, 2012.
De Winter RJ, et al. A new ECG sign of proximal LAD occlusion. NEJM 359:2071-73, 2008.
Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: classification, differential diagnosis, and caveats. Clev Clin J Med 78: 404-414, 2011.
Hayden GE, Brady WJ, Perron AD, et al. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. Am J Emerg Med 20:252, 2002.
Lawner BJ, Nable JV, Mattu A. Novel patterns of ischemia and STEMI equivalents. Cardiol Clin 20:591-599, 2012.
LeWinter MM. Percarditis – clinical review. NEJM 371:2410-16, 2014.
Pollak P, Brady W. Electrocardiographic patterns mimicking ST segment elevation myocardial infarction. Cardiol Clin 30:601-615, 2012.
Rhinehart J, Brad WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med 20:638-43, 2002.
Smith SW, Dodd KW, et al. Diagnosis of ST-elevation myocardial infarction in the presence of LBBB with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med 60:766-776, 2012.
Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. NEJM 349:2128-35, 2003.


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