ELECTROCARDIOGRAPHY


See also "Arrhythmias"

I. General EKG physiology

  1. A positive wave of depolarization advancing toward a positive electrode produces a positive deflection on ECG
  2. Leads by region:
    1. LATERAL LEADS: I,L,V4-6
    2. INFERIOR("diaphragmmatic") LEADS: II, III, aVF
    3. ANTEROSEPTAL ("right-sided") LEADS: V1---reciprocal with posterior wall
    4. Limb leads: I, II, III (bipolar); aVR, aVL, aVF (augmented)
      1. I: LA+ RA-
      2. II: LL+ RA-
      3. III: LL+ LA-
      4. aVR, aVL, aVF: Corresponding electrodes +, other 2 combined -
    5. PRECORDIAL LEADS (V1-6)
      1. Negative electrode corresponds to location of AV node
  3. Conductive pathways
    1. 3 main conductive pathways conduct impulses from the SA to the AV node: the Anterior, Middle, and Posterior internodal tracts; there is also Bachmann's Bundle which innervates the left atrium
    2. AV nodal conduction is very s l o w...; the proximal AV node has no automaticity foci but the lower region (the "junction") does
    3. The left Bundle Branch innervates the septum much more than the right, so septal depolarization normally occurs left-to-right
    4. Ventricular depolarization starts at the endocardium and spreads toward the epicardium

II. P waves

  1. Left Atrial Abnormality (e.g. hypertrophy or dilatation) suggested by:
    1. p > 2.5mm wide in any lead ("p mitrale")
    2. M-shaped p in any lead (humps at least 1mm apart)
    3. Negative deflection of terminal portion of p in V1 (at least 1mm x 1mm)--this is the most specific criterion
  2. Right Atrial Abnormality (e.g. hypertrophy or dilatation) suggested by:
    1. p > 2.5mm tall in II, III, or aVF ("p pulmonale")
    2. Biphasic P in V1 with initial portion greater in amplitude
  3. Should be upright in I & II; if not, suspect
    1. Dextrocardia
    2. Ectopic atrial rhythm
    3. Reversed arm electrodes (esp. if QRS and T also predominantly negative)
  4. Widened P waves can be a sign of tx with a Ia antiarrhythmic (quinidine, etc.)
  5. Small or absent P's can be a sign of hyperkalemia
  6. Inverted P's (i.e. opposite the predominant QRS deflection), especially in II, III, and aVF, may indicate retrograde atrial depolarization, e.g. from idiojunctional rhythms.

III. PR interval--normal is 0.12-0.2sec

  1. When depressed, can indicate pericarditis or atrial infarct
  2. Short PR interval:
    1. Pacing
    2. Junctional rhythm with retrograde atrial depolarization
    3. Pre-excitation syndromes
      1. Wolff-Parkinson-White-has "Delta wave" (slurring of R wave)
      2. Lown-Ganong-Levine-no Delta wave
  3. The "sawtooth" pattern of Atrial Flutter is usually best seen in inferior leads

IV. Q waves

  1. May indicate transmural infarct (can start early in MI or in ensuing weeks)
  2. Should be <25ms in duration in II & <30ms duration in lead F; <40ms duration in I, aVL, and precordial leads
  3. Q waves are normal in aVR--if not, consider lead reversal
  4. Small Q waves in I, aVL, V5-6 are normal; reflect depolarization of septum before rest of ventricles ("septal Q's")
  5. Large Q's in I and III can occur in Idiopathic Hypertrophic Cardiomyopathy
  6. Q waves in V1-2 can be due to LVH
  7. Downgoing delta waves in II, III, and aVF can mimic Q waves

V. QRS complexes

  1. Differential of wide QRS interval (> 0.12 sec)--note that it's best to measure QRS duration in the limb leads because the high voltages in the precordial leads may exaggerate QRS duration through "needle lag"
  1. Right Bundle Branch Block
    1. RSR' in V1-2
    2. Broad S in I or V6
    3. Broad R in aVR
    4. TWI in V1 or V2; sometimes ST depression there too
    5. "Complete" RBBB--QRS > 0.12 sec
    6. "Incomplete" RBBB (aka "borderline")--QRS 0.09-0.12 sec
  1. Left Bundle Branch Block
    1. QRS duration > 0.12sec (us. widest in I and V6)
    2. RSR' in V5 or V6; may just see flattened peak with small notch between R and R'
    3. Deep S in V1-3
    4. Upright QRS in I or V6 with no Q in either lead
    5. QRS in V1 predominantly negative; may have small R wave
    6. Small R in V1-3
    7. LAD (often)
    8. Absence of the small "septal" Q's in I, aVL, and V5-6
    9. ST depression & TWI's in many leads
    10. May be intermittent, e.g. rate-related
  1. Abberant ventricular conduction of a supraventricular impulse ("Ashmann phenomenon")
    1. This occurs when the impulse is conducted through the AV node after one but not the other bundle branch has repolarized. Conduction to the ventricle corresponding to the refractory bundle branch is delayed resulting in a widened QRS
    2. This occurs occasionally with SVT's and premature supraventricular beats.
  2. Pre-excitation syndromes (see above)
  3. [K] > 7.5 (very wide QRS)
  4. Medications: Ia's, tricyclics
  5. Ventricular rhythm, including paced
  1. Left Anterior Fascicular Block (aka Left Anterior Hemiblock)--much more common than LPFB (see below)
    1. Marked LAD (QRS often > -45 degrees) without other apparent cause
    2. QRS may be slightly widened but rarely > 0.12 sec
    3. qR in I and aVL
    4. rS in II, III, and aVF
    5. Suspect in any patient with RBBB + LAD
  1. Left Posterior Fascicular Block (aka Left Posterior Hemiblock)--much less common than LAFB (see above)
  1. QRS more rightward than previously but often within normal range, i.e. frank RAD is often absent and the diagnosis can often be made only by comparing before & after ECG's. Note that some authorities require more stringent criteria for LPFB, e.g. marked RAD (> 120') w/o other known cause of RAD
  2. QRS may be slightly widened to 0.12 sec
  3. rS in I and aVL
  4. qR in II, III, and aVF
  1. Precordial QRS issues--reflect the QRS vector in the horizontal plane (normally points posteriorly and to the left; hence us. isoelectric in V3 or V4)
  1. Tall R in V1 (> S) can indicate either:
    1. RVH (usually have RAD and TWI in V1)
    2. Posterior MI (often also have some inferior wall involvement and thus, Q waves or TWI in inferior leads and no RAD or TWI in V1)--i.e. the R is the "reciprocal Q" representing posterior transmural MI
    3. Counterclockwise rotation of the heart (looking from the feet up; due to extrinsic anatomic causes; may have TWI in V1 but no RAD or inferior Q's/TWI)
    4. Right Bundle Branch Block
    5. Dextrocardia
    6. WPW type A (LV insertion of the AV bypass tract)
  2. QS in V1
    1. Anterior or anteroseptal MI
    2. Left Bundle Branch Block
    3. WPW type B (RV insertion of the AV bypass tract)
  3. "Poor R wave progression" = no increase in R amplitude from V1 to V3; or R < S in V4; aka "clockwise rotation" (looking up from feet)
    1. Antero-septal MI
    2. COPD (esp. if RVH present)
    3. Incorrect lead placement
  4. RSR' in V1 suggests Right Bundle Branch Block
  5. RSR' in V1 with initial R wave taller than the R' wave in lead V1 suggests posterior MI.

VI. QRS Axis [in the frontal plane]--normal is -30' to +90' (or +100', depending on the reference); may be difficult to determine in the presence of Bundle Branch Block b/c there are actually 2 separate QRS vectors overlapping in time

  1. "No Man's Land," aka "Northwest Axis" (-90 to -180)
    1. Emphysema
    2. Hyperkalemia
    3. Lead transposition
    4. Ventricular pacing
    5. Ventricular arrhythmia
  1. Right Axis Deviation (+90 to +180)
    1. Normal in kids and tall, thin adults
    2. RVH
    3. COPD
    4. Previous anterolateral MI
    5. Left posterior fascicular block
    6. Pulmonary embolus
    7. WPW with left-sided accessory pathway
    8. Atrial or Ventricular Septal Defect
    9. Pectus excavatum
    10. Dextrocardia
    11. Reversed arm leads
  1. Left Axis Deviation (-30 to -90)
    1. Past inferior MI
    2. Left anterior fascicular block
    3. Ventricular pacing
    4. Emphysema
    5. Hyperkalemia
    6. WPW with right-sided accessory pathway
    7. Tricuspid atresia
    8. Ostium primum atrial septal defect

VII. "J waves"--T wave-like deflection right after QRS; seen in hypothermia

VIII. QT interval

  1. Defined as the interval from start of QRS to end of T
  2. Represents the duration of ventricular (depolarization + repolarization)
  3. Most easily measured in lead II
  4. The upper limit of the QT is 0.40 sec @ 70 bpm. For every 10 bpm above 70, subtract 0.02 sec. Add 0.02 sec for every 10 bpm below 70
  5. Usually measured as "corrected QT" to adjust for heart rate, aka "QTc"
    1. QTc = QT / (square root of RR interval)-all units in seconds
    2. Normal is < 440ms in men or < 460 ms in women
  6. QT prolongation is associated with an increased risk of ventricular tachycardia, Torsades de Pointes, and ventricular fibrillation which may be triggered by physical stress, emotional stress, or being startled; Risk is reduced in pregnancy but increased in postpartum period
  7. Causes of prolonged QT
  1. Congenital long QT syndrome
    1. Medications (not a complete list)
      1. Type Ia antiarrhythmics (quinidine, procaine, disopyramide)
      2. Other antiarrhythmics (sotalol, amiodarone, flecainide, dofetilide)
      3. Some antidepressants (particularly citalopram; risk is lower with escitalopram)
      4. Phenothiazines (particularly haloperidol, chlorpromazine, thioridazine)
      5. Organophosphate insecticides
      6. Fluoroquinolones (particularly moxifloxacin, levofloxacin)
      7. Macrolide antibiotics (risk may be lower with azithromycin than with other macrolides)
      8. Methadone
      9. Chloroquine
      10. Pentamidine
      11. Ondansetron
    2. Hypocalcemia
    3. Hypokalemia (actually are measuring QT-U)
    4. Hypomagnesemia
    5. Hypothyroidism
    6. Cardiomyopathy
    7. HIgh-grade AV block
    8. Severe CNS events (CVA, seizures, intracranial hemorrhage, etc.)
    1. Shortened in
      1. Digitalis therapy
      2. Hypercalcemia

    IX. ST interval--represents the initial, slow phase of ventricular repolarization

    1. ST depression can indicate:
    1. Ischemia (usually flat)
    2. "Reciprocal changes" representing injury in other leads--see Ischemia
    3. Dig effect (concave up;"reverse-checkmark")
    4. LV "strain"--ass'd with LVH--asymmetric ST depression, concave up, with slow downstroke and rapid upstroke, most often in I, aVL, V4-6
    5. RV "strain"--ass'd with RVH--same as #4 but in V1-2
    6. Hypokalemia (usually slight ST depression)
    7. Hypercalcemia
    1. ST elevation can indicate:
      1. Myocardial "injury," i.e. ongoing or recentinfarction; usually concave down
      2. Pericarditis
        1. In acute phase, usually see the following, which may normalize over course of illness:
          1. Diffuse ST segment elevation (us. flat or concave up)-Reflects inflammation of the ventricular subepicardial layer
          2. PR segment depression-Reflects inflammation of the atrial subepicardial layer
        2. Diffuse T-wave inversion can be seen in later stages, usually after resolution of ST elevation
      3. "Reciprocal changes" representing ischemia in other leads--see Ischemia
      4. Hyperkalemia (not necessarily in all leads)
      5. Ventricular aneurysm (suspect if ST elevation persists > 6wks after MI)
      6. Prinzmetal's angina (transient, during chest pain)
      7. "J point" elevation aka "early repolarization" --concave-upward; normal variant; particularly in V1-3
      8. "Proximity effect": V2, sometimes also V1 and V3, thought to reflect an artifact of proximity to heart.

    X. T Wave--represents the rapid phase of ventricular repolarization

    1. Up to 10mm amplitude is nl
      1. Large T waves can indicate hyperkalemia, esp. if "peaked"
      2. Can also be "peaked" in acute myocardial injury in first few hours
    2. TWI may be normal in V1 and aVR
    3. TWI may be normal in III, aVL, and aVF if QRS is predominantly negative
    4. T waves should always be upright in I, II, V3-6
    5. TWI or flattening may indicate:
      1. Ischemia or old MI (us. symmetrical, i.e. downstroke = upstroke)
      2. LVH with "strain" (us. slow downstroke and rapid upstroke, esp. in V5)
      3. RVH (TWI in V1-2)
      4. LBBB (diffuse TWI; should be concordant w/last deflection of QRS)
      5. RBBB (TWI V1-2; should be concordant w/last deflection of QRS)
      6. Pericarditis
      7. Myocarditis
      8. Certain non-cardiac illnesses
      9. Pulmonary embolus (TWI in V1-3)
    6. May be small or absent in hypokalemia

    XI. U Waves: Represents repolarization of Purkinje fibers; prominent in

    1. Best seen in V2-3
    2. Hypokalemia
    3. Tx with Ia antiarrhythmics
    4. May be inverted with ischemia, injury, or HTN

    XII. Other issues

    1. Left Ventricular Hypertrophy--all criteria less valid in pts < 35yo; also less valid in the presence of Bundle Branch Blocks which may exaggerate QRS voltages
      1. Most specific criteria:
        1. R in aVL > 11mm (or > 16mm with LAD)
        2. R in I + S in III > 25mm
        3. R in aVL + S in V3 > 28mm in men or > 20mm in women (Circ. 3:565, 1987)
      2. Less specific criteria:
        1. R in II or III > 25mm
        2. R in V6 > 27mm
        3. R in V5 or V6 + S in V1 or V2 > 35mm (Am. Heart J. 37:161, 1949; Circ. 81:815, 1990)
        4. V6 > V5
        5. Loss of R in V1 and V2
        6. R in I > 15mm (or > 18mm with LAD)
      3. ST-T abnormalities (diffuse TWI; ST depression in the "LV Strain" pattern)
      4. Left Atrial Abnormality (often)
      5. LAD (often)
    1. Right Ventricular Hypertrophy
      1. R > S in V1; sometimes RSR' in V1
      2. T wave inversion in V1 & V2; sometimes ST depression in the "RV Strain" pattern
      3. Deep S wave in V4-6
      4. Right atrial abnormality (often)
      5. RAD (often)
    1. Note that LVH and RVH can coexist; suspect if find LVH by voltage criteria but QRS axis close to vertical (+90')
    1. Pulmonary Embolus
      1. "S1Q3T3"--Prominent S in I; Q and inverted T in III (highly specific; represents acute RV strain; present in 50% of patients with acute pulmonary embolus)
      2. Sinus tachycardia and nonspecific ST-T changes (particularly TWI in V1-V4) are the most common findings on ECG in patients with acute pulmonary embolus
      3. ST depression in II (often)
      4. Right BBB (often resolves after acute phase)
      5. Low amplitude in general
      6. In a prospective study of 189 pts with suspected acute PE, the only ECG findings found sig. more frequently in pts who turned out to have PE were incomplete RBBB and tachycardia. S1Q3T3 was not found more often in pts who turned out to have PE (Am. J. Cardiol 86:807, 2000--AFP)
    1. Ischemia & Infarction
      1. ST elevations & "pseudonormalization" of prev. neg. T waves indicate severe, transmural ischemia +/- subepicard. injury
      2. "Electrically silent" ischemia is us. located in POSTERIOR or LAT. walls
      3. "Reciprocal changes"
    1. Precordial leads (particularly V1-3) are reciprocal for posterior & inferior walls (so can get ST depression in these reflecting posterior or inferior infarct & vice-versa)
    2. High Lateral leads (I, aVL) are reciprocal for the inferior wall (so can get ST depression in these reflecting inferior infarct & vice-versa)
    1. Diagnosis of acute MI in LBBB
    1. The following are independent predictors of CK-positive MI in pts with LBBB: 85% of MI pts but only 17% of controls had one or more of these (NEJM 334:481; 1996-JW):
    1. At least 1mm of ST elevation in same direction as QRS complex
    2. At least 1mm of ST depression in V1, V2, or V3
    3. At least 5mm of ST elevation in opposite direction from QRS
    1. From Am. Heart J. 116:23, 1988:
    1. New Q in aVL or new R in V1
    2. Q's in 2 or more of V3-5
    3. Late notching of S in 2 or more of V3-5
    1. Wide [QRS]-Complex Tachycardias (click link for more info)-The main differential is between Supraventricular Tachycardia w/aberrant AV conduction (e.g. LBBB or RBBB) and Ventricular Tachycardia. Also, consider another possibility: WPW with an antidromic reentrant tachycardia (should have an upside-down p wave)
    CHARACTERISTIC VTach SVT w/aberrant conduction
    Ventricular rhythm May be irregular Regular
    Rate >200 Around 150
    QRS width > 0.14s < 0.14s
    Onset Single PVC No PVC
    Axis May be LAD No big change from baseline
    Fusion beats May be present Absent
    Response to carotid sinus massage None Slows ventricular rate
    Morphology of QRS in V1 RRR' with bigger R RSR' with R' bigger or same size
    Q Wave in V6 Usually Rare
    Concordance of precordial QRS complexes May be present Absent
    Beat-to-beat variability of QRS morphology May be present Absent
    Response to adenosine None Usually responds
    AV dissociation May be present Absent
    1. Right-sided EKG: look in V4R for ST elevation to indicate right ventricular injury; look in all IMI's
    2. Fusion beats ("Dressler beats"): In ventr. arrhythmias, when P wave conducts through to ventricles; get a narrow-looking QRS--this won't occur in SVT w/aberrant conduction!
    3. Low voltage (< 5mm in all limb leads and < 15mm in all precordial leads)
      1. Obesity
      2. Myxedema
      3. COPD
      4. Pericardial effusion
    4. Heart transplant
      1. If the native atria with their SA node are left in place so pt will have 2 SA nodes; usually the native atria will depolarize from their SA node but the signal won't pass to the donor atria, so there will be 1 set of dissociated p waves (from the native SA node) and 1 set of p waves each followed by a QRS (from the donor SA node)
      2. If the entire native heart is left in place ("heterotopic" transplant)--ECG shows the equivalent of 2 superimposed ECG's.

    (Sources include Core Content Review of Family Medicine, 2012)