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Learning EKG (for IM residents)

Learning EKG 
  • Even before you look at any EKG, you need to understand the following to make sense of any EKG 
    • First, you should appreciate the cardiac conduction pathway, and review the sequences of normal atrial and ventricular activation. 
(D) Normal sinus rhythm. Am Fam Physician. 2010;82(8):942-952

    • Knowing this : Understand how p wave is formed and its variations. 

      • At this point, appreciate that normal looking p wave can occur in AT if the origin of atrial tachycardia is near SA Node 
      • Short PR segment with Normal QRS (PR is an Isoelectric segment due to AV nodal conduction) 
        • Enhanced AV Nodal conduction (EAVNC) 
        • Pre-excitation pathway that goes to bundle of His (Lown-Ganong-Levine syndrome) 
      • Look for PR and RP relationship 
        • Short PR Tachycardias and Long PR tachycardias are different 
          • Short RP Tachycardia 
          • Long RP Tachycardia
            • Atrial tachycardia
            • Atypical AVNRT
            • ORtw with a slow decremental pathway (PJRT)
    • Look for Isoelectric line to differentiate AT from A flutter . 
      • Atrial flutter has no isolectric line that is representation of atrial depolarization. Where as AT does not isoelectric lines.
        • 2 exception
          • If prior history of cardiac surgery or ablation is present, it is atrial flutter even if isoelectric lines are present
      • Isoelectric lines are absent or decreased if there is ventricular pre excitation. 
    • Now : Understand how does narrow complex and wide complex QRS are formed. 
      • Narrow QRS: Definition: <120 msec
        • When ventricle activates normally (i.e via normal conduction pathway, it gives rise to normal QRS. See above for pictorial example) 
      • Wide QRS Definition: > 120 msec
      • Wide QRS is due to Ventricular activation is slow due to 
        • Site of origin is either at or below his bundle, or in perkinje fibers, or ventricular myocardium OR
        • Site of origin is supra ventricular but there is a preexisting conduction abnormalities in the his-purkinje system, like BBB, or rate related aberrancy
        • Site of origin is supra ventricular but there is a ventricular pre excitation i.e part of ventricle activates through alternate pathway while simultaneously part of the ventricle is activating through his-purkinjee system
    • Knowing this - Locate the possible site of origin of cardiac conduction, and its propagation into the ventricle in the narrow complex tachycardia and in wide complex tachycardia  
N Engl J Med 2012;367:1438-48
  • After this you are ready to look at an EKG 
    • In order to avoid misdiagnosis, few catch points, or not to miss points while reviewing EKG are 
      • Always use caliper or tool in computer. 
      • Always have a same sequence of reviewing EKG. 
      • And, review EKG in its entirety. 
ECG Leads
Normal EKG: 

EKG Abnormalities: 5 main categories

  • 1. Cardiac Enlargement and Hypertrophy
  • 2. BBB and related patterns
    1. The QRS vector usually is oriented in the direction of the myocardial region where depolarization is delayed (Fig. 268-10).Thus, with right bundle branch block, the terminal QRS vector is oriented to the right and anteriorly (rSR′ in V1 and qRS in V6, typically). Left bundle branch block alters both early and later phases of ventricular depolarization. The major QRS vector is directed to the left and posteriorly. 
    2. RBBB
    3. LBBB
      1. Usually a marker of one of the 4 conditions
        1. HTN heart ds, CAD, Aortic Valve Disease, Cardiomyopathy

Coronary Arteries 

    1. Location of the leads: 
      1. I, aVL, V5, V6: Looks at lateral aspect of the heart
      2. II, III, aVF: Looks at inferior part of the heart
      3. Left main infarction findings
        1. V1, V2, V3, I, aVL, aVR STE
        2. V4, V5, V6, II, III, avF ST depression.  

      1. Isolated Right Ventricular Infarction 

STE in II, III, aVF, V1. RV infarction suspected due to STE in V1
Cath: 100 % occlusion of the RCA proximal to the Rt Ventricular Branch (see anatomy of coronary arteries above, and Cath results in full paper) 

45 yo M patient presenting with chest pain, and is found to have the following EKG. Where is the lesion located at? 
Ans: On Cath, patient is found to have RCA lesion causing RV infarct. Since, It is RV infarct, part of the anterior wall is also involved. Hence, anterior leads V1, V2, V3 may also have STElevation, without the involvement of the LAD. 
    1. Evolution of an STEMI (pre-cath era)
      1. 1st:  J point moves upward causing ST elevation (Concave down) 
      2. 2nd: ST segment comes down (still concave down), but T - wave inversion is seen
      3. 3 rd: ST segment is normal, T wave inversion (usually, in a week, but not seen anymore as we intervene immediately, and that changes the course of evolution) 
      4. 4th: Back to normal
      5. (Based on the duration of symptoms, it is important to identify the stage of ischemia patient may be on)
    2. Effect of Blood Supply occlusionL 
      1. Infarction: QRS segment changes 
      2. Injury: ST segment changes 
      3. Ischemia: T wave
    3. Akinesia: Left Main Coronary Artery Thrombosis with AL Akinesia NEJM 2012
    4. Hypokinesia
    5. Asynergia
    6. ST elevation normal varient 
      1. V3, V4 in an symptomatic patient in young patient 
      2. Early Repolarization Pattern: 
        1. What Do We Know About the “Malignant Form” of Early Repolarization? JACC 2013

54 y/o M with Anginal Chest Pain. EKG on presentation is here. 

Few hours later, patient continues to have chest pain. Repeat EKG is as below. 
Cath shows Mid RCA 99 % stenosis.  

    1. STEMI  Equivalents
      • De Winters T Wave:  deep ST segment depression in leads V2-4 occurs in Proximal LAD lesion
      • Wellens' sign: anterior T-wave inversions with biphasic lateral T waves; seen with LAD disease

      • aVR ST segment elevation with diffuse ST segment depression (aVR STE > V1 STE); Left Main Obstruction is the cause; Associated with extremely high mortality 

      • Sgarbossa Criteria 

      • Right Ventricular Infarct

    1. Pericarditis 
PQ in Lead II depressed (20% sensitive, 80% specific), with STE in I, II, III with no reciprocal changes. Also has mild diffuse STE. Also, notice PR segment elevation in aVR. (Personal Collection) 
    1. Antero-lateral Infarct: Can occur with occlusion of any of the following
      1. LCC
      2. Marginal branch of LCC
      3. Diagnoanl Branch of LAD
    2. Reciprocal Leads: 
      1. Lead II: Reciprocal changes in V1
    3. Apical Dead zone: Q wave in V3 , 4 and inferior leads 
    4. RCC: 
      1. SA Node
      2. AV Node (AV Nodal Artery)
      3. Can have V1 and V2 T wave inversion (if RCA is feeding the posterior wall). V1 and V2 in these situation is representing the reciprocal waves. If Posterior leads are placed, then will show STEMI in posterior leads 
    5. Brugada Syndrome 
    1. Posterior Infarct
      1. If lateral leads are involved, but has ST segment depression in V1,V2, V3 then it is high likely to be posterior intact. In anterolateral infarct, you expect to have STE in all anterior leads. 
      2. Look for Large R in V1. DDx of this includes:
        1. RCA: Look for inferior leads (if inferior leads show injury pattern, then RCA involvement)
        2. LCC: Look for lateral leads (I, aVL, V5, V6) 
      3. Following images have been obtained from link provided below the images. 

  • 4. Metabolic Factors and Drugs Effects
    • Hyperkalemia

    • Hypokalemia
Prolonged QT interval and Prominent U wave 

    • Hypothermia

DDx of Prominent Osborn Waves:
Brugada Syndrome 
Early Repolarization
      • Hypomagenesemia 
      • Hypothermia 
  • 5. Low Voltage EKG and Electrical Alternans 
  • References
    • Harrison's 19 e 
    • As noted above
  • P wave axis and P vector and PR duration: Helps differentiate ST from Atrial Tachycardia.
  • Inspect p wave for atrial pace, aneurysm. Persistent increase in ST elevation could be due to LV aneurysm
  • Negative U - Wave: have strong suspicion for U wave. If present it could be due to CAD and not just LVH
  • I, II, III, aVF : to look for P wave axis. If abnormal suggest of atrial rhythm, and not ST. 
  • Pattern of QRS complex helps differentiate BBB from preexicitation
  • Posteior abnormality
    • aVL: ST elevation . I, V6
    • V1, V2, V3, V4 ST depression. 
      • Q-wave: Infarction
      • Injury: ST Elevation
      • Tall R wave in V1
  • LBBB: no q wave
    • Difficult to say STE 
    • But presence of biphasic T wave increases its likelihood of Acute MI 
  • A Fib with PVC
    • Q wave in V5, V6:  lateral infarct, and high lateral infarct
    • R - wave regression, small Q wave: High lateral or posterior leads
  • Left atrial abnormality
    • LAE
    • Slow left atrial conduction 
  • Biventricular pacing 
    • Atrial Rhythm: Important to look
      • Clinical implication: Anticoagulation
  • Left anterior vascular block
    • Bifascicular block
  • V1: Infarct before the first perforator branch of the LAD
    • Has long term consequences 
  • V2,V3 : Anteroseptal
  • V4: Anterior
  • V5,V6: Anterolateral
  • Mobitz 1 vs 2
    • An entire EKG may help guide that by looking at the conduction pattern
  • Ventricular pacemaker can have normal QRS as well if that rhythm is not paced
  • Concealed conduction:
    • Bifid a wave
    • Slow conduction in the left 
  • Infarction Pattern
    • Q-wave may be present 
    • Acute
    • Age Interdeminate
      • Clinical Hx can guide
  • Atrial escape complex
    • Complex arises after a pause
    • Is different from the sinus complex
  • Ventricular escape complex 
  • Identify rate-related aberrancy