EKG an overview and tutorial for residents teaching medical students

From Ask Dr Wiki

Jump to: navigation, search

EKG Tutorial Blocks, Arrhythmias, Electrolytes and Miscellaneous Michael W. Tempelhof, MD Duke University Medical Center


I. Conduction Abnormalities

1. Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

  1. QRS duration of > 120 milliseconds.
  2. rsR' "bunny ear" pattern in V1.
  3. Terminal wide S waves in leads I, and V6.
  4. INCOMPLETE RBBB: defined as criteria #2-3 are met with QRS duration of 100-119 milliseconds.

Left Bundle Branch Block (LBBB)

  1. QRS duration of > 120 milliseconds.
  2. Absence of Q wave in leads I, V5, and V6.
  3. Monomorphic R wave in I, V5, and V6.
  4. ST and T wave inversion opposite to the deflection of the QRS complex.
  5. Often notched QRS in I and V6.
  6. INCOMPLETE LBBB: defined as criteria #2-4 are met with QRS duration of 100-119 milliseconds.


Intraventricular Conduction Defect (IVCD)

  1. QRS duration > 100 milliseconds.
  2. Criteria for BBB or Fascicular blocks are not met.


  • -Ventricular Hypertrophy (most common)
  • -Class IA and IC antiarrhythmics
  • -Hyperkalemia

Left Anterior Fascicular Block

  1. LEFT axis Deviation: -45 to -90 degrees.
  2. Small Q-wave in I and/or aVL.
  3. QRS < 120millisecs.
  1. rS complexes in II, III, and aVR
  2. Peak of R wave in III occurs earlier then in II.
  3. Peak of R wave in aVL occurs earlier then in aVR.

Most common intraventricular conduction defect.

  Secondary to LAD ischemia

Left Posterior Fascicular Block

  1. RIGHT axis Deviation: 90 to 180 degrees.
  2. QRS< 120millisecs.
  3. The presence of a qR complex in lead III and a rS complex in lead I.
  4. Absence of RAE and RVH.

Posterior block is less common then Anterior fascicular block as the posterior fascicle receives collateral flow from RCA and LAD.

Bifascicular Blocks

  1. Criteria met for RBBB
  2. PLUS LAFB (more commonly) or LPFB

Trifascicular block

  1. Criteria for bifascicular block (RBBB and LAFB or LAPB).
  2. AND criteria for 1st degree AV nodal block.

1st Degree AV Block

  1. PR interval >200 milliseconds (5 small boxes).
  2. 1:1 ratio between P waves and QRS complexes.

1st degree AV block is benign and does not require any treatment. Recommended to avoid AV nodal blocking agents: B-blockers, Ca Channel blockers and Digatalis.

2nd Degree AV Nodal Block AKA: Wenkebach block or Mobitz Type I AV block.

  1. 1:1 P wave to QRS complex ratio NOT maintained.
  2. PR interval becomes progressively longer from beat-to-beat until a P wave is not conducted through the HIS-Purkinje system.
  3. Progressive shortening of the RR interval prior to the missed beat.

2nd Degree type I AV Block

  1. Note progressive prolongation of PR interval with NO P wave QRS complex dissociation.
  2. Note the shortest PR interval is immediately following the non-conducted QRS complex.
  3. AV nodal dysfunction.

2nd degree Type II AV Nodal Block

  1. 1:1 P wave to QRS complex ratio NOT maintained, P waves are conducted more slowly.
  2. PR interval may be normal (120msec-200msecs) or prolonged (>200msec).
  3. Unlike Mobitz Type I (Wenkebach), the PR interval is fixed in length.

An infranodal block: below the AV node. A normal QRS complex width suggests that the block is above the His bundle and not an intra-Hisian block.

Third degree AV Nodal Block (Complete Heart Block)

  1. Complete AV dissociation. No correlation between P waves and QRS complexes.
  2. A Narrow QRS complex at rate of 30-40 BPM characterizes ventricular escape.

Asses if cardiology emergency requiring temporary transcutaneous pacing.

Complete Heart Block

  1. P waves are completely dissociated from QRS complexes.
  2. QRS complexes are narrow, indicating a junctional escape rhythm.
  3. The atrial and ventricular rates are stable, with the atria faster then the ventricles.

II. Sinus Arrhythmias

  1. Sinus Tachycardia
  2. Sinus Bradycardia
  3. Respiratory Sinus Arrhythmia
  4. a. Sinus Block and b. Sinus Arrest
  5. Premature Atrial Contractions
  6. Atrial Tachycardia
  7. Multifocal Atrial Tachycardia
  8. AV Nodal Reentry Tachycardia
  9. Atrial Fibrillation
  10. Atrial Flutter

Sinus Tachycardia/Bradycardia

1. Sinus tachycardia: upright P wave in II preceding every QRS complex with a ventricular rate >100 BPM.

2. Sinus bradycardia upright P wave lead II preceding every QRS complex with a ventricular < 60 BPM.

3. Respiratory Sinus Arrhythmia

  1. Heart rate normally increases with inspiration and decreases with expiration.
  2. Vagal tone changes during the different phases of respiration confers a beat-to-beat variation on the SA node.

4a. Sinus Block SA node action potential IS generated, however not conducted to the atria.

  1. Regular Rhythm.
  2. Pause length IS a multiple of the P-P interval.

4b. Sinus Arrest

 Represents sinus node failure to generate an action potential.  Regular Rhythm.  Pause length is NOT a multiple of the P-P interval.  Pacemaker placement indicated when arrest > 3secs Sick Sinus Syndrome  Sick sinus syndrome is a sinus node dysfunction with an inappropriate atrial rate for physiologic requirements with both components of sinus block and sinus arrest.

5. Premature Atrial Contractions (PACs)  4 Characteristics classify PACs:

 Premature. P wave is earlier than expected if one measures the previous P to P intervals.  Ectopic. The P wave originates outside of the SA node. Therefore the P wave morphology is different than native sinus P wave.  Narrow QRS complexes.  Compensatory pause. The SA node is refractory following a PAC, normal sinus rhythm resumes 1 P to P interval after the PAC. PAC

 Premature P wave  Different Morphology indicates ectopic origin  Narrow QRS complex  A compensatory pause following the PAC 6. Atrial Tachycardia  >3 consecutive Atrial premature beats originating from a SINGLE ectopic atrial focus.  P wave morphology is different from sinus P wave.  P wave often buried in T wave complex.

7. Multifocal Atrial Tachycardia (MAT) Supraventricular rhythm resulting from multiple ectopic foci in the atria.  At least 3 different P wave morphologies in a given lead.  P waves rates of 100-250/min.  P-R intervals are irregular.  Ventricular response is irregularly irregular.

-Most common in patients with chronic or acute exacerbations of chronic obstructive pulmonary disease. -Treatment is to correct the underlying pulmonary pathology. -Wandering Atrial Pacemaker (WAP): criteria for MAT is met with a ventricular rate <100 bpm. Multifocal Atrial Tachycardia  At least 3 different P wave morphologies in 1 lead.  P-R intervals are irregular.  P wave rate of 100-250 per/min.  Irregular Ventricular response.

8. AV Nodal Reentrant Tachycardia (AVNRT)  QRS complex <120millsecs and >100bpm.  P waves visible and often inverted (retrograde) in leads I, II, III and AvF.  P wave may occur AFTER the QRS complex (long RP interval).

-Often diagnostically terminates with AV blocking maneuvers (carotid massage or adenosine).

-AND often preceded by a PAC. AVNRT

 Regular Narrow Complex Tachycardia.  Inverted P waves in I, II, III and aVF.  Possible Long R-P Phenomenon in II.

9. Atrial Fibrillation (Afib)  P waves are absent, or may visualize oscillatory atrial activity.  R-R intervals are irregularly irregular.

 Afib w/a ventricular rate >100bpm is "rapid ventricular response" or "RVR“.  Afib w/a ventricular rate <60bpm is atrial fibrillation with bradycardia.

-With an atrial rate of 400-600 bpm; P waves are not visible. -AV node becomes intermittently refractory and will only allow a certain number of atrial action potentials to reach the ventricles. Therefore, the ventricular rate is NOT 400-600, but rather 100-200 bpm.

AFib w/ RVR and Bradycardia I. Afib w/ RVR -No P waves visible -Irregular Irregular rhytym -Narrow QRS complex w/ >100 bpm.

10. Atrial Flutter  NO discernable P waves are visible.  Biphasic-typical "sawtooth" regular flutter waves (F waves) are present at a typical rate of 300 bpm due to the reentrant nature of the arrhythmia.  Ventricular response is usually one-half the rate of the atrial input (ie, 2:1 AV nodal conduction with a ventricular response of about 150 beats/min).  QRS duration <120millisecs (unless there is underlying conduction abnormality).  Rhythm is regular or variable.  Atypical, defined as without classic sawtooth pattern.

-Narrow complex tachycardia at 150 beats per minute is commonly atrial flutter (manifestation of 2:1 AV block).

Atrial Flutter  Atrial rate of 300 bpm.  Ventricular rate of 150 bpm.  Sawtooth pattern of F waves.  No Discernable P waves.  Narrow QRS complex with regular rhythm.

III. Ventricular Arrhythmias  Premature Ventricular Contractions  Bigemny and Trigemeny  Ventricular Tachycardia

          a. Sustained
          b. Non-Sustained
          c. Monomorphic
          d. Polymorphic

 Idioventricular Rhythm  Ventricular Fibrillation

1. Premature Ventricular Contractions (PVCs)  QRS>120 msec.  Premature in the R-R interval.  Bizarre QRS morphology and axis.  T wave vector is 180 degrees opposite the QRS vector.  Compensatory pause following the PVC. PVC  Premature in the R-R cycle.  Abnormal QRS morphology and axis.  T wave inversion opposite QRS axis.  Compensatory pause before proceeding native beat.

-24-hour holter monitoring has demonstrated up to 80 percent of healthy men or women have PVCs of no significance. 2. Bigeminy and Trigeminy 3. Ventricular Tachycardia  Run of 3 or more PVCs.  QRS>120msec.  St-T vector direction opposite to major QRS deflection.  R-R can be regular or irregular intervals.

Types of V. Tachycardia  Nonsustained: 3 beats to <30secs.  Sustained:>30seconds.  Monomorphic: similar QRS morphology.  Polymorphic: different QRS morphology; more often associated with Ischemia.  Torsade-de-pointes: polymorphic VTach w/ phasic variations in the polarity of the QRS complexes around a wondering baseline. Non Sustained vs. Sustained Monomorphic vs. Polymorphic SupraVentricular Tachycardia vs. Ventricular Tachycardia Four-step Algorithm reported by Brugada:

Step 1: Absence of RS complex in all leads V1-V6?

      Yes: Dx is ventricular tachycardia 

Step 2: No: Is interval from beginning of R wave to nadir of S wave >0.1s in any RS lead?

       Yes: Dx is ventricular tachycardia

Step 3: No: Are AV dissociation, fusions, or captures seen?

       Yes: Dx is ventricular tachycardia

Step 4: No: Are there morphology criteria for VT present both in leads V1 and V6?

       -Bizarre frontal-plane QRS axis (i.e. from +150 to -90 degrees) 
            -QRS morphology similar to previously seen PVCs 
       -All QRS complexes from V1 to V6 are in the same direction 
            -QRS complexes >160msec 
        Yes to any 1 : Dx is ventricular tachycardia 

NO: Diagnosis is supraventricular tachycardia with aberration 4. Idioventricular Rhythm (i.e. ‘Slow VT’)  Ventricular pacemaker driven; appears similar to VTach with BPM<60.  IF BPM 60-100= Accelerated Idioventricular Rhythm.  A benign rhythm; most commonly assoc with reperfusion.  No Treatment necessary.

Idioventricular Rhythm

 V Tach morphology w/ rate <60. No Treatment Req’d; primarily a non-sustained rhythm. 5. Ventricular Fibrillation A pre-terminal event

 Ventricular rate >400BPM.  Wondering baseline.  No discernable QRS complexes.

Ventricular Fibrillation

 Undulating baseline.  No discernable QRS complexes  >400BPM IV. Junctional Rhythms 1. Junctional Escape Beat 2. Junctional Bradycardia/Tachycardia

1. Junctional Escape Beat Protective beats from pacemaker cells in the AV junction.  Classic firing rate is 40-60 bpm.  P waves absent or inverted.  QRS 100-120msecs. 2. Junctional Bradycardia/Tachycardia V. Myocardial Ischemia and Infarcts  Myocardial Ischemia  Anterior Wall MI  Inferior Wall MI  Posterior Wall MI  MI with Bundle Branch Block  Old Infarct: Q-wave Myocardial Ischemia  ST segment depression> 1mm in > 2consectutive leads.  T wave inversion.

Subendocardial ischemia Prolonged QT interval and/or increased amplitude T wave. Subepicardial/transmural ischemia In addition to ST segment depression often observe T wave inversion. Localization of Infarct Evolution of AMI 1. Elevated T waves 2. ST Elevation 3. Q waves (>40msec, and >25% R wave amplitude) 4. T wave Inversion 5. ST Normalization

Anterior Wall MI  ST elevation V2-V4.  Reciprocal ST depression in inferior leads II, III aVF.

-Culprit Vessel: LAD

Lateral Wall MI  ST elevation in I, aVL, V6.  Often T wave inversion aVL.

-Culprit Vessel: Left Circumflex Artery

Posterior Wall MI  ST Depression V1-V4  R/S ratio in V1>1.0

-Culprit vessel dependant on Vessel Dominance: 90% population is right dominant, 10% LAD Inferior Wall MI  ST Elevation in II, III, aVF  ST depression in V1-V3

-Culprit Vessel: RCA or Post Descending artery. Right Ventricular Infarct  ST elevation in III>II.  ST elevation in V4R-V6R.  Reciprocal ST depressions are present in I, aVL, V1R, and V2R.

Culprit Vessel: Most Commonly RCA

MI with Bundle Branch Block AMI and RIGHT Bundle Branch Block:

  -Q waves and ST segments are NOT altered by RBBB.

AMI and LEFT Bundle Branch Block:

 - Difficult to dx with late Left ventricular activation.
 - Must follow the preceding diagnostic criteria. 


 ST elevation >1mm concordant with QRS complex (highly sensitive/specific).  ST depression >1mm V1-V3 (specific not sensitive).  ST elevation >5mm discordant with QRS complex. (Suggestive; not confirmatory).

NEJM 1996; 334:481-7. AMI and LBBB  ST elevation >1mm CONCORDANT w/QRS.  ST depression> 1mm V1-V3.  ST elevation >5mm DISCORDANT w/QRS.

‘OLD’ Infarct: Q wave MI Qwave:

         >25% of QRS complex.
         -small ‘septal’ Q wave in I and AvL are NORMAL.

Localization of Qwave MI

 - follows same rules and distribution as acute localization.

Q wave MI Example of Old Inferior MI.

 Note Q waves in inferior distribution: II, III, AvF. VI. Atrial Enlargement 1. Right Atrial Enlargement

   A. The P wave amplitude in lead II greater than 2.5 millimeters
  B. The positive deflection of the P wave in lead V1 greater than 1.5 millimiters.
    P pulmonale: P wave height >2.5 mm in II, III, and aVF. 

2. Left Atrial Enlargement

      A. The P wave width in II > 120 milliseconds.
        B. The negative deflection of the P wave in lead V1 greater than 40 milliseconds in  
            length AND greater than 1 millimeter negative deflection. 
    P mitrale: above criteria meet and associated with Mitral Stenosis.

Right Atrial Enlargement  P wave in lead V1 with positive deflection >1box wide and deep.  P wave height in lead II> 2.5 boxes.

Left Atrial Enlargement

 Pwave in V1 with negative deflection >1box wide and deep.  P wave in lead II notched and > 120 msecs.

VII. Ventricular Hypertrophy

1. Right Ventricular Hypertrophy 2. Left Ventricular Hypertrophy 1. Right Ventricular Hypertrophy

 Right Axis Deviation >+110 degrees.  Dominant R wave in lead V1.

   Additional Supportive Data

ST segment depression and T wave inversion in leads V1 to V4. Deep S waves in leads V5, V6, I, and aVL. Right Ventricular Hypertrophy  R/S ratio in V1>1.  Right axis deviation.  ST segment depression and T wave inversion in leads V1 to V4.

2. Left Ventricular Hypertrophy Common Criteria

 Cornell Criteria: Rwave in AvL plus Swave in V3.

  + LVH if sum > 28 mm in males or > 20 mm  in females.

 Rwave in aVL > 12 mm in amplitude

 Swave in V1 or V2 plus the Rwave in V5 or V6. +LVH if sum>35mm.

LVH: Romhilt-Estes LVH Point Score System If score = 4, then LVH present with 30-54% sensitivity. If score > 5, then LVH is present with 83-97% specificity.

                   Criteria                                                       Points

Amplitude of largest R or S in limb leads >20 m 3 Amplitude of S in V1 or V2 > 30 mm 3 Amplitude of R in V5 or V6 > 30 mm 3 ST and T wave changes opposite QRS without digoxin 3 ST and T wave changes opposite QRS with digoxin 1 Left Atrial Enlargement 3 Left Axis Deviation 2 QRS duration > 90 milliseconds 2 Intrinsicoid deflection in V5 or V6 > 50 millisecond 1

Left Ventricular Hypertrophy  Swave in V1 or V2 plus the Rwave in V5 or V6. +LVH if sum>35mm Left Ventricular Hypertrophy  R aVL> 12mm  Romhilt-Estes Score >5  R aVL and S in V3 sum >28mm for male

VIII. Miscellaneous  Low Voltage  Pericarditis  LV Aneurysm  Pericardial Effusion  Pulmonary Embolus  Pneumothorax  WPW  Hypertrophic Cardiomyopathy  Hyperkalemia  Hypokalemia  Hypocalcemia  Hypercalcemia  Hypothermia  Prolonged Qt  Digoxin Effect  Limb Lead Reversal  Neurological Insult 1. Low Voltage  QRS amplitude < 5 mm in the limb leads.  QRS amplitude < 10 mm in the precordial leads.

 Etiology: Pericardial effusion, Infiltrative/restrictive diseases, Severe hypothyroidism, COPD. 2. Pericarditis  Diffuse concave upward ST segment elevation in all leads except AvR.  PR depression in all leads  T waves are usually low amplitude 3. LV Aneurysm  Persistent ST elevation in leads V1-V5 and AvL.  Q waves present in leads V1-V5.

 Often Prevalent >4weeks post AMI 4. Pericardial Effusion/Tompande  Sinus tachycardia.  Low voltage (QRS amplitude < 5 mm in the limb leads and <10 mm in the precordial leads).  Electrical alternans: beat to beat alternation of QRS voltage.

5. Pulmonary Embolus  Most Common Finding is Sinus Tachycardia.  10% experience the classic: "S1Q3T3“.  S wave in I, Q wave in lead III, inverted T wave in III.  Associated findings include RAD, RAE and RVH. 6. Left sided Pneumothorax  Low QRS voltage in the lateral precordial leads and Lead I.  Right axis deviation.

7. Wolff Parkinson White  Short PR interval <120msecs (accessory AV pathway through Bundle of Kent).  Slurring of QRS complex (delta wave) representing early ventricular activation through normal ventricular muscle in region of the accessory pathway.  Prolonged QRS duration >0.10msecs.  Secondary ST-T changes due to the altered ventricular activation sequence . 8. Hypertrophic Cardiomyopathy  Inverted, symmetrical T waves in precordial leads.  Criteria meet for LVH. 9. Hyperkalemia Potassium levels and EKG change 5.5-6.5 Tall peaked T waves 6.5-7.5 Loss of P waves 7.0-8.0 Widening of QRS complexes 8.0-10 Sine wave, ventricular arrhythmias, asystole HyperKalemia  Symmetrical T wave peaks 50%> QRS complex.  Progression of HyperKalemia leading to Sine wave abnormality. 10. Hypokalemia  The classic U wave: most prominent in V3 and V4.  Broad, diffuse flat T waves.  ST depression.  QT interval prolongation.  Ventricular arrhythmias (PVC, ventricular tachycardia, ventricular fibrillation, torsades de pointes).

11. Hypocalcemia  Prolonged QT interval (Qtc > 440msec).  May lead to R on T phenomena and V Tachycardia.

12. Hypercalcemia  Shortened Q-T interval  ST-T complex ‘doming in leads V1-V3. 13. Prolonged Qt  Qt> 50% of R-R interval is considered prolonged.  QTc: corrected for HR is prolonged if >440msec.  QTc = (QT measured) / (R-R interval)½.

 Etiologies: hypocalcemia, hypoKalemia, Romano ward syndrome, Jervell Syndrome, Quinolones, dofetidile, sotalol.

14. Hypothermia  J Wave: "Osborne wave" characterized by a notch in the downward portion of the R wave in the QRS complex.  Low Voltage.  Prolongation of PR, QRS, and QT intervals  Evident with Core Temperatures< 35°C. 15. Digoxin Effect  “Reverse Check” sign of downsloping ST segment.  QT shortening.  Paroxysmal Atrial Tachycardia.  PACs and PVCs.

16. Limb Lead Reversal  Positive P wave and QRS complex in aVR.  Inverted QRS in I and aVL.  NOTE: Dextrocardia has same presentation AND very low voltage in leads V3-V6. 17. Neurological Insult: ICP  Deep symmetric inverted T waves in most leads.  QT prolongation.

Personal tools