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.
Monday, September 28, 2009
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.
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.
Sunday, September 27, 2009
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.
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.
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.
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.
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!).
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!).
Saturday, September 26, 2009
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.
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.
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