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.