PACEMAKERS

The normal pacemaker appearance is:
1. Broad R waves in I and AVL...because the impulse heads towards the left from the paced RV.
2. Broad QS waves in II, III and AVF...because the impulse heads upwards from the paced apex.
3. QS waves in leads V1-V5 with V6 also showing a dominant S wave, but a small r beforehand.

SO, EVERYTHING IS DOWN, EXCEPT FOR AVL AND I.

4. It is normal to have fusion beats and pseudo-fusion beats.
Fusion= spike but the QRS complex is only a little broad (occurs when the sinus rate and pacemaker rate are virtually the same).
Pseudo-fusion= spike but the QRS complex is narrow (occurs when the ventricle is still in its absolute refractory period).



When you see a pacemaker that doesn't look like it's a LBBB, the options are:

1. It's high lead placement - this makes V1 and V2 look like AVR and AVL respectively. You will still see that the limb leads have a superior axis.

2. It's lead reversal, such that leads V4-6 are placed in V1-3 position.

3. It's a BiV pacemaker, because BiV's can be placed in the coronary sinus if the sinus is big enough. You will see 2 ventricular spikes and may have an atrial spike because you want to control the rate and so block the patient's sinus rate with anti-arrhythmics.

4. It's LV pacing from a perforated septum. You know that the LV is being activated first because lead I is isoelectric.

Fused-looking beats

This is an example of a fusion beat from a sinus beat and a junctional ectopic.

When VE's don't lead to a fully compensatory pause

The rule is that VE's lead to a fully compensatory pause (from the R before to the R after is 2x the usual R-R interval) and that SVE's lead to a less-than-compensatory pause.

What leads to a more-than-compensatory pause?
When you have a VE followed by a sinus pause and a junctional escape.

When you have both narrow and wide complexes in the same rhythm strip

This is the one that I hate the most, but it's really not that hard.

The pearl is to look at the coupling interval between two narrow complex beats. And then to look at the coupling interval between a narrow complex beat and a wide complex beat. If it's smaller, then the wide complex is aberrant conduction. If it's larger, then you have an accelerated idioventricular rhythm that is ignoring the sinus or atrial pacemaker that was originally driving the ventricle.

That's it. The only two possibilities.

LVH in the presence of RBBB

The way to diagnose this is to ignore the praecordial leads. Instead, use the limb leads:
AVL>10
RI + SIII >25

Some suggestive findings are:
LAA
LAD (though if have this then the voltage threshhold for AVL is higher).

Poor R wave progression

The differential for old anteroseptal MI is:

1. Emphysema - you see low R wave voltages V1-3 but also an R prime in V1 and V2 (because of the lateral S waves), a vertical axis and RAA.

2. Lead placement

3. LVH/HCM because the tall R waves laterally mean that there will be negative vectors septally..

Not all bigeminy is bigeminy

It may be Wenckebach with 3:2 block.

So, what you see is what appears to be an ectopic supraventricular beat because the P wave is on the T wave. You may also get a wider QRS because the coupling interval is short enough to cause aberrant conduction, and then you get a pause.

It is this pause which is the key.
The pearl is that you must look very hard here to make sure that there is not a P wave in it (easy if the P waves are big, but often they can be very flat).

The other thing to look for is the duration of the pause - if it's:
1. A VE - will block the AV node to the sinus beat but will not reset the sinus cycle - will give a pause that from the R wave of tbeat before the ectopic, to(2) the R wave of the beat after the ectopic, is exactly 2x the sinus cycle. This is called a "fully compensatory cause".
2. An SVE, because it resets the sinus cycle, will give a non-compensatory/LESS THAN COMPENSATORY pause
3. Heart block, will give a compensatory pause because it does not reset the sinus cycle.

So, with a VE, it's easy to tell because you see the VE.
Therefore the usefulness of this rule comes in when you are evaluating whether it is an SVE or a AV block.

Where the P's march through the QRS's

This is either AV dissociation (more Q's than P's) or CHB (more P's than Q's).

If there is a ventricular tachycardia in AV dissociation, then there may be one of the following present as well:
1. Atrial tachycardia
2. Normal atrial rate
2. Atrial bradycardia

Differentiating SVE from VE

There are two pearls to observe:
1. See if there are any non-aberrant ectopics and count the number of big squares between the R waves - this tells you the coupling interval length that will NOT impinge upon the refractory period of the bundle (usually the right bundle).
2. See if the T wave before the ectopic is different to all other T waves (it will usually be HIGHER).

V1-V3 lead misplacement

The way to pick that it is this, rather than a posterior MI, is to look at:

1. P wave - it will be biphasic in V3
2. RSR pattern - R wave in V1, S wave in V3, R wave in V4.

Hypercalcaemia

This teaches the importance of making sure that each ECG has an ST segment.

In hypercalcaemia, there is none, so the J point merges with the T wave and there is no flat bit (ST segment) in between.




This is because phase 2 (aka PLATEAU phase) of the action potential is shortened.



So, 0 is blast-off/depolarization (Sodium channels open)
1 is the notch (sodium channels close)
2 is plateau (calcium channels open, outward potassium channels open)
3 is repolarization (calcium channels close, potassium channels stay open)
4 is rest/electrically neutral

Good pacemaker gone bad

PACEMAKER SYNDROME:
The symptoms of pacemaker syndrome included dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, hypotension, pre-syncope, and even syncope. Heart failure signs include elevated neck veins, rales, and pedal edema. Physical exam can often reveal cannon A-waves. This sign occurs secondary to ventricular-atrial (V-A) conduction and the contraction of the atria against closed A-V valves. Although relatively uncommon, syncope has been attributed to pacemaker syndrome. Syncope is usually associated with systolic blood pressure declines of greater than 20 mm Hg that can occur with the onset of pacing. Additional symptoms attributed to pacemaker syndrome include easy fatigability, malaise, headache, and the sensation of fullness and pulsations in the head and neck. Pacemaker syndrome is most severe when intact V-A conduction is present⁶. The elevated venous pressures associated with the contraction against closed A-V valves causes a vagal afferent response resulting in peripheral vasodilation and hypotension.

So, it occurs if have retorgrade conduction of the paced ventricular signal, or if there is bidirectional block AND both the atrium and ventricle happen to also have the same rate of contraction!

PMT:
This is re-entry using the pacemaker lead.

So, what happens is that each paced beat always, in every pacemaker in the world, creates a retrograde atrial wave. This atrial wave is ignored by virtue of all pacemakers being programmed with a PVARP (postventricular atrial refractory period). But sometimes the VA conduction time is so slow that it outlasts the PVARP, and therefore reentry occurs.
How quick will the pacemaker go? Well, all pacemakers are programmed with an upper rate limit, so it will not exceed that.
The solution for this that companies have come up with and programmed some pacemakers with, is that the pacemaker, when it sees that it is consistently running at the upper rate limit, will intentionally drop a beat/intentionally fail to pace the ventricle for a beat. This ends the tachycardia :)

WHAT TO LOOK AT NEXT WHEN YOU THINK YOU'VE PICKED UP A LIMB LEAD MISPLACEMENT

The key differential is dextrocardia - you can tell it's not that because the R waves in dextrocardia are largest in V1 and smallest in V6.

Bythway, something that is often forgotten is that there is reversal of leads II and III because lead I is inverted.

LVH

The things that happen in LVH are:

- QRS widens and as part of this, the intrinsicoid deflection in V6 ("the downward deflection after the peak of the R wave" aka the downward dog of ECG yoga) increases.

- QRS biggens such that have tall R6 and deep S1.

- axis shifts to left

- J point depresses and there is a convex upwards subtype of downsloping ST depression

There are several criteria:
CORNELL (S3 + RL >20 for women or 24 for men)
SOKOLOW (S1+R5/6>34, RL>10, RI+SIII>25)...and if LAD, then RL>12 AND SIII>14
ESTES

ESTES	Points
Voltage Criteria (any of): R or S in limb leads >20 mm S in V1 or V2 > 30 mm R in V5 or V6 >30 mm	3 points
ST-T Abnormalities: Without digitalis With digitalis	3 points 1 point
Left Atrial Enlargement in V1	3 points
Left axis deviation	2 points
QRS duration 0.09 sec	1 point
Delayed intrinsicoid deflection in V5 or V6 (>0.05 sec)	1 point

Low voltage

Defined as having both precordial <10 and limbs<5 (mnemonic: precordial has 10 letters, limbs has 5).

Anti-arrhythmic drugs

Class I agents affect Phase O.
1c's (flecainide, propafenone) do it most powerfully, so see prolonged QRS and a QT that is prolonged solely by the prolongation of the QRS.

1b's (lignocaine) and 1a's (quinidine, procainamide, disopyramide) don't do it in therapeutic doses, and neither does sotalol.

Amiodarone does.

WPW localization of the accessory pathway

There is a sequence to follow here:

1. Look at V1 - if delta wave is upright, then the pathway is left-sided.

Then...

2. Look at AVL - if delta wave is down, then pathway is left lateral

ECG changes in an ASD

In a septum primum defect, there is hypoplasia of the anterior fascicle, so you see LAHB.

In all ASD, you get enlargement of the RA (therefore see PR prolongation as well as P wave being tall)  and RAD (and a prolonged QRS) from RVH.

Wenckebach

There are a few pearls to determine if the blocked P wave you see is due to Wenckebach:

1. The PR interval after the block is shorter than the one before
2. The P-P interval before is longer than the one before before.

So, the key is to look for 1 thing after, and 1 thing before.

Fast Broad Irregular rhythms

This means WPW with AF.

The thing to remember is that all the stuff you would normally use for any fast rhythm cannot be used in patients with WPW to slow that rhythm down - you can't use A, B or C (adenosine, beta-blockers, or calcium channel blockers) - because they will all convert the AF to 1:1 conduction and therefore VF. So, in WPW patients there is no such thing as rate control, only rhythm control with amiodarone and procainamide.

Regular Atrial Fibrillation

Whenever you see AF that is almost regular, it means that there is a junctional escape, which may be standard or accelerate to a higher speed. This should make you think of digoxin toxicity. The trouble with digoxin toxicity is that the level doesn't necessarily correlate, because if you have low K then you will get toxicity changes even if the level is not that high. So, need to keep people on digoxin, at a normal K level.

Differentiating aberrantly conducted SVT from VT

It's VT if see:
- sinus capture
- fusion
- wiiiide QRS
- V-A conduction (aka AV dissociation)

Also, if the pre-tachycardia QRS complex is narrow then you can use the following criteria, depending upon whether you see a RBBB or LBBB:

RBBB: "ladders"
- LAD
- R>S in V1,
- S>R in V6

...this kind of VT is the one that occurs in structurally normal hearts and is precipitated by exercise.

LBBB: "Q6R1"
- Q6, R1>40msec duration and 70msec from onset of R wave to nadir of S wave (partially because there has to be notching of the downstroke of this S1)


There is also the Brugada way of doing things: "Brugada's absent RS and long RS rule"
1. Is there any praecordial lead that does not have an RS complex?
If they all have RS complexes, go on to:
2. Measuring the distance from the onset of that R to the nadir of the S - if it is >100msec, it's VT.

Torsade de pointes

The problem is not torsade, because torsade is a self-limiting episode of tachycardia...the problem is that it can degenerate to VF.

It is caused by a long-short cycle, the "long" bit occurring because of a VPB that causes a pause.

In the long QT syndrome, patients have slow hearts with a propensity to ectopics from after-depolarizations...therefore get a loooong pause. So, the treatment is to speed up their heart.

NB: "early after depolarizations are depolarizations that interrupt phases 2 and 3. They occur because too many calcium or sodium channels are still open. Delayed AD's are depols that interrupt phase 4 and are due to too much calcium being in the cell cytosol in phase 4.

Bundle Branch Block

The heart is driven by a sergeant-major chanting "left, right, left".
This is why the pattern of depolarization is "left septum, right septum, left ventricle".

The other way to think about it is that the septum is depolarized by the left bundle only. This is why depolarization goes from the left side of the septum to the right side of the septum.

So, with a RBBB, the septal depolarization proceeds normally. Then the left ventricle depolarizes normally. However, after it has finished, the RV is still being depolarized by the slow right bundle. Thus, instead of the usual 2 waves, you will see 3 waves and this third wave will be fat and always be heading towards the right.
So, what you will see is an rSR in V1, though in some people the LV is not very big and so the S wave never makes it below the baseline - in that case you get a notched R wave.

Since the normal QRS is only 100msec (2.5 small squares), an incomplete RBBB is 100-120msec, and a complete RBBB is 120msec.

With LBBB, the first phase of depolarization is reversed as the septum has to depolarize from right to left, and the second phase is prolonged. So, see a totally positive R wave in V6 and a totally negative S wave in V1 (i.e. invert your septal wave and get a prolonged normal second wave). The notching that produces the classic W and M shapes is due to the influence of the RV.

An incomplete LBBB is from 100-120msec.

What can you say if you see an rS pattern in LBBB? It means the septum is still being depolarized from left to right!

You can tell that there has been a septal infarct in the presence of a RBBB if you've lost your septal Q's in I and AVL.

Hypertrophy

The pearl to know about RAE is that after you diagnose it you should go on to look for either pulmonary disease, PE, or for congenital heart disease that will lead to Eisenmengers (ASD, PS/TOF, Ebsteins).

Why not VSD? Because, unlike in ASD where there is continuous flow across the ASD and therefore the left atrium is constantly being decompressed and the right atrium and ventricle constantly loaded, in VSD there is only flow in systole and so the left atrium is loaded all the time and the left ventricle loaded all of diastole, but the right ventricle is never loaded at all because the blood is shunted in systole and straight away ejected through the pulmonary valve...so, in VSD get a big left heart and normal right heart, and in ASD get a big right heart and normal left heart.


The pearl to know about LAE is that see a biphasic wave in V1 because the left atrium is a posterior structure and therefore the depolarization heads posteriorly, therefore see an inverted P wave/P wave heading away from the chest.

The pearl to know about RVH is that what you see is a rR wave in V1 instead of the usual rS wave where the S represents the electricity going to the bigger LV muscle mass. Because there is more muscle mass, depolarization takes longer so you get a partial RBBB too. Finally, repolarization also takes longer, so get TWI in V1 and FLAT (i.e. not necessarily downsloping) ST depression in leads V2-3.
 Therefore, the pearl is that if you see partial RBBB and RAD, think of RVH.

How do you tell if there is only mild RAD or severe RAD? The pearl is that it's all in lead III - if lead III has a taller R wave than lead II, then there is severe RAD.

For LVH, the initial criteria used to be that you had to have abnormal S waves in the right-sided lead (V1) and abnormal R waves in the left-sided leads (V5, V6) [ because V2-4 are on the FRONT of the chest, whereas V5-6 are on the side of the chest). However, people with thin chests kept on being diagnosed with LVH, so the people at the Cornell came up with criteria that were more specific by using the left arm lead.
They still used an S wave on the "relative right" (V3) and an R wave on the lead that was the most left they could get (AVL). The numbers that they came up with were >28mm for men and >20mm for women.

So, the way that you can be the most specific is by looking for:-
- widened QRS
- ST-T changes
- LAE
-LAD

Finally, in vertical hearts, if AVF R>20mm, then suspect LVH.

Horizontal & Vertical hearts

An electrically horizontal heart has tall qR waves in the horizontal leads (I, AVL) and therefore rS waves in II, III, AVF.

An electrically vertical heart has tall qR waves in the vertical leads of II, III, AVF, and therefore there are rS waves in I, AVL.

If I, AVL and II, AVF all show positive complexes, then the heart is in an "intermediate position".

The importance of all this is that the T wave is allowed to be inverted if you are S wave dominant.

The important exceptions to know are:
- you are allowed to have a negative T wave in lead III.
- the T wave is positive in lead II because it is negative in AVR.

R wave progression

In V1 you will see a septal R wave followed by an LV S wave.
In V6 you will see a septal Q wave followed by an LV R wave.

This is amplified in LVH, and dulled in RVH.

Understanding the ECG through its history

Einthoven placed electrodes on the left arm and leg (because the heart is on the left), the right arm, and therefore had to use the right leg as the grounding electrode.

His ECG's therefore consisted of 3 strips:-
- Lead I which was the signal difference between the arms.
- Lead III which was the signal difference on the left
And Lead II was calculated by the machine by adding Lead I to Lead III.

It took another 30 years for the remaining leads to be invented, and this was done by Wilson in Michigan.
He made leads for the right arm, left arm, and left leg.
He then made leads for the chest.
The rule of the limb leads is that if you add all the P's, QRS's and T's then you will get a flat line. If you don't, then there has been lead misplacement.

The only thing to remember about the chest leads is that you start at the 4th interspace, and end at the 5th interspace.

Other rules to follow:-
AVL and I should look the same.
AVR and II should look reversed.
AVF and III should look the same.

Axis

In the frontal plane, AVL is -30, I is 0, II is 60, III is 120.
AVF is 90.
AVR is -150.

In the transverse plane,
V1 is 120
V2 is 90
V3 is 60
V4 is 30
V5 is 0
V6 is -30.

So, another way to think of it is to imagine it on paper in the way the ECG is written:
0 -150 120 30

60 -30 90 0

120 90 60 -30


If there is a superior axis, then you need to decide if it superior and leftward or superior and rightward. You do this by looking at AVL - if it is upright, then the axis is superior and leftward.

Ischaemic ECG changes

The first changes with MI is that the T waves are elevated in the leads looking at the infarcting area. The ST segment then moves the same way - 1/10th of a mV, except 2/10th in leads V1-3.

If there is severe ischaemia then the Purkinje fibres become ischaemic and so you see loss of the S wave praecordially.

The important thing to know about ST elevation is that you will always see it in leads V2 and V3 - so, the way you distinguish abnormal from normal is because in early repolarization you will see a short ST segment (meaning that the T wave takes off almost from the J point!).

PEARLS

The easiest way to count rate is to take a 15cm ruler - that distance will be 6 seconds (because at 25mm/sec, 25mm=2.5cm=1 sec).

Left atrial hypertrophy is best diagnosed in V1 - if have 1 x1mm then it's LAH.

Q waves are no longer physiologic if they are >1/3 of the height of the R wave. However, the most sensitive way of telling if there is an inferior infarct is to see if the Q wave has reached 0.04secs in width. Only the Q wave in III is allowed to exceed these limits of 0.03 and 1/3 of the R wave.

V1- the significance of ST elevation there is RV infarct if no V2 elevation, else septal infarct if there is V2 elevation. You confirm this by doing right chest leads.

Pericarditis - the only leads that fail to show ST elevation are those in which the QRS is predominantly negative - AVR, AVL, III, V1.
However, the specific sign is that the PR segment gets depressed - you can tell it's depressed by comparing it to the TP segment just in front of it. This is said to be due to atrial injury.

The things that tell you it is early repolarization are that the R and T waves tend to be tall, there is early transition, a terminal slur in the QRS praecordially.

One that I'm sure you've stuffed up before is the RBBB. There are two types of RBBB - just RBBB - and RBBB with infarction. You tell the latter by looking at V1-3 to see if there are Q waves, and then looking at the ST segment to see if it is elevated. Neither should be the case!
The ST elevation means that there is either an acute infarct or a large akinetic region.

You've messed this one up before - before you say there is Wenckebach, have a look between the QRS and T wave for P waves. If they're there then this is CHB, and there is a junctional escape.

If you see a bifascicular block then look for the anterior MI that is causing it.

If see ST depression in V1 think of acute posterior MI.

Excluding RVH as the cause of a prominent R in V1 - should see a deep S wave laterally if there is RVH. So, what you see is in v4-6 there is never a situation of R dominance - it's a VERY late transition!

The other thing to do in whatever lead you see your P wave best is to look for a second P wave on the other side of the QRS. If you see one then there is 2:1 block. But it has to occur every time - if you only see it once then this is just a blocked PAC. The differential for when you see this is typical atrial flutter that has been slowed by anti-arrhythmics - the way you tell this is to then look at the inferior leads- if you see three negative defelections with no flat bits in between in AVF, then this is flutter.

-A mistake you've already made is not looking for the RAE in II once you've seen the LAE in V1.

- PR depression in association with LAE is due to depolarization of a large atrium.

- The last thing you do on your examination is check for hypoelectrolytaemia (ca, mg, k) and hypothyroidism or hypothermia - this causes long QT (little - long). You have to look for the END of the T wave, not its highest point. You can actually differentiate between these- low K produces a long T wave (and a U wave to give the impression that it's even longer), and low Ca produces a long ST segment.

Along with looking at the QT you therefore cast a glance at one of the T waves to make sure that it is not sharp and symmetrical, because that means HIGH potassium.

The rule for >1/2 of the R-R interval only works when the heart rate is >80bpm.

- what to do when you get a paced rhythm?
Some basic rules are:
- a big spike means an old (unipolar) system.
- two spikes means "an AV sequential pacemaker"
- spikes should never be seen anywhere but in front of a complex - if they are seen elsewhere then this is undersensing, and undersensing is lead fracture till proven otherwise.
- spikes should always be completed by a complex - if they are not then this is failure of capture - and this complex should always be the same - if it is not then there is fusion.

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)

AVNRT

The funniest thing about this is that it takes 30 years to show up!

Typical symptoms include a pounding in the neck, chest heaviness, dizziness and polyuria.

Fast and regular rhythm strip without P waves

This is simply called an SVT.

You can conceptualize the types by visualizing the area around the AV node.

Thus, the types are:

- AV node dependent

• AVNRT, this being a nodal reentry
  

• Accessory Pathway (aka AVRT/AV reciprocating tachycardia)

- AV node independent = Atrial tachycardia, this being either automatic or atrial reentry/AF/AFlutter

- Sinus tachycardia

• physiologic
• sinus node reentry/inappropriate sinus tachycardia

So, you can summarize it as Reentry, Accessory, Automatic, Physiologic, Flutter...like the 5 fingers.

If you're a betting man then you'd put your money on Nodal Reentry, followed by Accessory pathway.

Only some paced beats on the rhythm strip

The best way to express this is to say "underlying SR with intermittent pacing".
Remember that if the PR interval is short enough, you will see fusion beats.

Just wide complexes on the rhythm strip

Slow and wide...call it Idioventricular
Fast and wide...call it SVT with aberrancy or VT

The rhythm strip that is irregular but you see sinus beats

This could either be sinus arrhythmia or NSR with ectopics.
Some of these ectopics will be so early that they will be blocked - this creates the longer intervals seen on the ECG.
The surprising thing about atrial ectopics is that they can occur even before the qrst is finished! Thus, you can see them in the ST segment and superimposed on the T wave!

The rhythm strip in which you only see 1 or 2 P waves

The options for this are:

1. It's AF

2. It's NSR with a LOT of atrial ectopics (aka "runs of atrial tachycardia")

Tall R wave in V1

The differnetial is pretty easy to break down:

1. It aint RVH unless there is also RAD

2.