General

General EKG physiology

1. INFERIOR("diaphragmatic") LEADS: II, III, aVF
2. ANTEROSEPTAL ("right-sided") LEADS: V1---reciprocal with posterior wall
3. 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 -
4. PRECORDIAL LEADS (V1-6)
   1. Negative electrode corresponds to location of AV node
1. 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 syndrome
      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

2. 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

3. 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.
4. Pre-excitation syndromes (see above)
5. [K] > 7.5 (very wide QRS)
6. Medications: Ia's, tricyclics
7. Ventricular rhythm, inc. paced

2. 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

3. 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

4. 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

2. 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

3. 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. QTc = QT / (square root of RR interval)--all units in seconds (nl = 370-470)
3. 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
4. Prolonged in

1. Type Ia antiarrhythmics (quinidine, procaine, disopyramide); other antiarrhythmics; tricyclics, phenothiazines, organophosphate insecticides, etc.
2. Hypocalcemia
3. Hypokalemia (actually are measuring QT-U)
4. Hypomagnesemia
5. Congenital cardiac defects (Jerwell-Lange-Nielsen and Romano-Ward)
6. Severe CNS events (CVA, seizures, intracranial hemorrhage, etc.)

3. Shortened in

1. Digitalis tx
2. Hypercalcemia

4. QT prolongation is associated with an increased risk of Torsades de Pointes

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

2. ST elevation can indicate:
   1. Myocardial "injury," i.e. ongoing or recentinfarction; usually concave down
   2. Pericarditis
      1. Diffuse ST segment elevation (us. flat or concave up) together with PR segment depression. ST elevation reflects inflammation of the ventricular subepicardial layer and PR segment depression reflects inflammation of the atrial subepicardial layer
      2. TWI can be seen in pericarditis but us. not until the ST elevation has resolved, so TWI accompanying ST elevation is probably not due to pericarditis
   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)

2. 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)

3. Note that LVH and RVH can coexist; suspect if find LVH by voltage criteria but QRS axis close to vertical (+90')

4. Pulmonary Embolus
   1. "S1Q3T3"--Prominent S in I; Q and inverted T in III (highly specific; represents acute RV strain)
   2. Sinus tachycardia
   3. TWI in V1-V4
   4. ST depression in II (often)
   5. Right BBB (often resolves after acute phase)
   6. Low amplitude in general
   7. 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)

5. 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)

4. 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

2. 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

6. Wide-complex tachycardias. 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

7. Right-sided EKG: look in V4R for ST elevation to indicate right ventricular injury; look in all IMI's
8. 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!
9. Low voltage (< 5mm in all limb leads and < 15mm in all precordial leads)
   1. Obesity
   2. Myxedema
   3. COPD
   4. Pericardial effusion
10. 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.

AXIS

You only need to look at leads I and II - this will tell you whether there is a normal axis, LAD,  RAD or a North-West axis ("extreme axis deviation").

The alternative is to use I and aVF - the so-called "axis at a glance...well, 2 glances actually"


Using leads I and aVF the axis can be calculated to within one of the four quadrants at a glance.


If the axis is in the "left" quadrant take your second glance at lead II.

• both I and aVF +ve = normal axis
• both I and aVF -ve = axis in the Northwest Territory
• lead I -ve and aVF +ve = right axis deviation
• lead I +ve and aVF -ve
  • lead II +ve = normal axis
  • lead II -ve = left axis deviation

causes of a Northwest axis (no man's land)

• emphysema
• hyperkalaemia
• lead transposition
• artificial cardiac pacing
• ventricular tachycardia

causes of right axis deviation

• normal finding in children and tall thin adults
• right ventricular hypertrophy
• chronic lung disease even without pulmonary hypertension
• anterolateral myocardial infarction
• left posterior hemiblock
• pulmonary embolus
• Wolff-Parkinson-White syndrome - left sided accessory pathway
• atrial septal defect
• ventricular septal defect

causes of left axis deviation

• left anterior hemiblock
• Q waves of inferior myocardial infarction
• artificial cardiac pacing
• emphysema
• hyperkalaemia
• Wolff-Parkinson-White syndrome - right sided accessory pathway
• tricuspid atresia
• ostium primum ASD
• injection of contrast into left coronary artery

Lead II

This is made by III + I, and by ll*AVF-AVR .
So, it's the 1st and the third storey which are added in the first column, and subtracted in the second column. 



*llAVF stands for "left leg AVF", to remind you where the lead goes.

Lead I

Lead I is made by:
* AVL - AVR ( it is not an actual recording but the signal difference between L and R)
* II - III

So, you take the second storey of the ECG where II and aVL live, and subtract III and avR from that.


What is normal for Lead I:

• If the axis is >60degrees( III, II R waves> I, then the heart is horizontal, and so the septum is in line with "lead" I, so will see small Q's(1 small square and  less then 25%  of the R wave height) in II, III and aVF because the depolarization wave is perpandicular to the lie of the septum.

(correspondingly, if the axis is <60 degrees - III, II R waves

• if you see a high R wave in lead I then there must be either a high R wave in aVL or a deep S in avR. The same goes for leads II and III.
  

Tall R wave in V1

R2-D2-C3PO

RBBB
RVH

Dextrcardia
Duchenne's muscular dystrophy

CounterCloCkwise rotation (?)

Posterior Infarct

Orthodromic reciprocating tachycardia (WPW)