Kansas City University of Medicine & Biosciences
Department of Physiology
Prior to completing this online material, you should review:
- Action potentials in general, cardiac action potentials in specific, including the pre-potentials (pacemaker potentials) and the plateau of the action potential.
- The specialized conduction pathways in the heart
- The normal ECG and how it relates to the conduction of cardiac action potentials Click here to access Dr Karius' ECG tutorial.
After this online activity, you should be able to:
- describe the major changes in the ECG that are associated with conduction blocks in:
- The SA node
- The AV node
- The main bundle branches of the left and right ventricles.
- The fascicles of the left ventricular conduction system.
- identify the block present if given a "typical" ECG tracing of that block, including:
- First Degree AV nodal block
- Second Degree AV nodal block, differentiating between Weckenbach's and Mobitz type II.
- Third Degree AV nodal block
- Right or left bundle branch block
- Fascicular blocks.
This online activity is the equivalent of one hour of lecture. The points for this activity will be derived as follows:
- There will be no questions on the quiz. Rather, a Blackboard quiz (worth one point) has been posted. You must complete this quiz by 11:55 PM Wednesday March 1, 2006.
- There will be two questions on the final examination in the cardiovascular section.
The animations included with this online activity will load in as new pages. Things to remember:
- You may need to set your pop-up blocker in order to accept pop-ups from this page.
- To return to this page, simply close the new window (the red 'x' at the top right of the window)
- These animations are narrated - turn on your volume.
The Conduction Pathways (review)
In order to be able to predict the consequences of a conduction block on the ECG, it is necessary for you to have a thorough understanding of the normal conduction pathway.
The normal path of depolarization through the heart and how the ECG is inscribed at each point is illustrated in the animation.
The SA node (sino-atrial) node contains the cells that initiate the cardiac action potential under normal circumstances. Once the SA node cells reach threshold (due to the pacemaker potential), the action potential travels in two directions simultaneously - it depolarizes the atria and depolarizes the internodal pathway (connecting the SA node and the AV node)
The AV node contains cells with the slowest conduction velocity of the conducting pathways. Therefore, the action potential slows considerably as it goes through the AV node. The PR interval is determined by this delay.
Once the AV node has conducted the depolarization, the action potential spreads through the Bundle of His and invades the Bundle branches. There are two bundle branches - the right bundle branch and the left bundle branch. The left bundle branch then divides into an anterior and posterior fascicle (these aren't shown in this animation, although they can be damaged, leading to a fascicular block). Finally, the conduction system breaks into the Purkinje fibers, which penetrate the endocardial surface of the ventricle. Conduction of the cardiac action potential from the endocardial to epicardial cells occurs relatively slowly via cell-to-cell transmission.
The ventricular action potential spreads no further at this point for two reasons:
- the tissue "behind" the action potential has already been depolarized and is refractory (since it is in the plateau phase).
- The tissue "ahead" of the action potential is incapable of generating an action potential - it is the cartilaginous rings supporting the heart and its valves.
Conduction blocks can occur at any point in the specialized conduction tissue of the heart described above. We will now move onto the discussion the these conduction blocks and the electrocardiographic changes seen in each type of block.
SA Nodal Block
Note: Dr. Karius does not expect you to be able to identify SA nodal block from an ECG tracing on the test. You should be able to recognize it from a written description of its characteristics.
SA nodal block is defined as a failure of the cardiac action potential to emerge from the SA node (paraphrased from Wagner, G.S.; Marriott's Practical Electrocardiography, 10th Edition, 2001, Lippincott Williams & Wilkins, p. 403). Note that it does not say that the SA node pacemaker cells fail (that is commonly referred to as "sick sinus syndrome"). Rather, it appears that the pacemaker cells of the SA node continue to do their job of initiating the cardiac action potential, but the spread of the action potential out of the SA node is blocked. Distinguishing between a failure of the pacemaker tissue itself and a failure of conduction out of the SA node is difficult or impossible from an ECG alone!
Thought Question! Click here (note added: You may get an error message when you click on this links and other animations with embedded questions. Click on "yes" (that you want to run the 'scripts') and continue - the animations/questions work just fine. I am working to fix the "error".)
Luckily, SA nodal block is usually intermittent, meaning that most of the time, the action potential is propagated to the rest of the heart. Because SA block is usually intermittent (lasting only a beat or two), the only effect is a "missed" beat in the heart rate. If it were to become permanent, an alternate pacemaker (the AV node or some other tissue) will have to assume the role of pacemaker for the ventricles.
AV Node Blocks
AV nodal block (also known as "heart block"), occurs when conduction between the atria and the ventricles is impaired due to damage of the specialized conducting tissue. In a normal person, there is only one electrical connection between the atria and the ventricles - the AV node.
Despite its name, the electrocardiographic characteristics of AV block can be produced by damage to the AV node itself, the Bundle of His, or both the Left and Right bundle branches simultaneously. The latter is sometimes referred to as "infranodal" block. A traditional ECG is unable to distinguish between these possibilities, although we do have techniques that allow a determination to be made. None of Dr. Karius' test questions will hinge on this distinction being made.
Thought Question: Where are you looking? (click for question)
The severity of an AV block can vary from the least severe form (known as 1st degree AV block) in which the impulse is merely slowed down more than normal as it travels through the AV node/Bundle of His to more severe forms (in which the cardiac action potential is not being transmitted to the ventricles some part of the time). Each of these will be discussed individually.
First Degree AV Block
As the name implies, first-degree AV block is the mildest form of AV Block. In first degree AV block, the conduction from the SA node to the AV node is slowed more than normal. However, it is important to note that every impulse generated by the SA node does get through to the ventricles. On the animation, this will be apparent as an increase in the delay between atrial depolarization and ventricular depolarization.
Click here to run animation
Electrocardiographic effects of first-degree AV block: Thinking back to the normal ECG, the AV nodal delay is the primary determinant of the PR interval. Therefore, the effects of first-degree AV block are going to be seen in the PR interval - namely that the PR interval will be longer than normal (just a reminder: the normal PR interval in an adult is 0.12 - 0.20 seconds). Because the AV node is still able to conduct the impulse, an important characteristic of first-degree AV block is that every P wave is followed by a QRS complex. The following is a "typical" ECG tracing illustrating first degree AV block:
|A "typical" tracing of first-degree AV node Block. The ECG looks relatively normal, with the exception that the PR interval is longer than normal, in this case about 0.3 seconds (the normal range is 0.12 - 0.20 seconds).|
To summarize the changes seen in First-Degree AV block:
- waveforms are of normal shape and duration.
- The rate and rhythm of the heart is normal.
- every P wave is followed by a QRS complex.
- The PR interval is prolonged beyond the normal upper limit of 0.21 seconds.
- The QRS and T waves are of normal morphology (shape and duration).
Second-Degree AV Block
As the name implies, a second degree AV block is a more severe form of AV nodal block. In second degree block, the AV node is sufficiently damaged that it remains refractory and unable to conduct an action potential for a much longer time than normal. The result of this is that impulses from the SA node occassionally (but regularly) fail to get through the AV node. Second-degree heart block can occur in a variety of ratios - 3:2 or 4:3 (P waves:QRS complexes) are commonly seen, but 2:1 or even 3:1 can be found. More extreme ratios generally don't occur, as by then the ventricular rate is so slow that a ventricular pacemaker will take over. The following animation illustrates the result of this in the conduction of the cardiac action potential.
Click to run animation
Electrocardiographic appearance of second-degree AV block: The hallmark of second-degree AV block is that not every P wave is followed by a QRS complex. The following illustration shows one example of a second-degree heart block:
|Characteristic ECG of Second-degree heart block: In this example, the waves are of normal shape and duration, but that every third P wave is not followed by a QRS complex (blue asterix). The PR interval of the conducted impulse is also much longer than normal.|
Second-degree AV block can occur in two different forms. The picture (above) is a Mobitz II second degree block. In the Mobitz II block, the refractory period is so prolonged that the AV node is unable to conduct on a consistent basis, so we see a regular pattern of missed QRS complexes (and therefore missed beats). This pattern of missed QRS complexes can occur in many different ratios:
- 3:2 (shown in picture): There are 3 P waves for every 2 QRS complexes.
- 2:1: 2 P waves for every one QRS complex.
- 3:1: 3 P waves for every one QRS complex (this is about as "bad" as second degree AV block can get - at this point, the AV node will often "take" over the ventricles, leaving the SA node to drive the atria).
- other ratios are possible as well.
The other form of second-degree AV block is know as a Mobitz I second-degree block and is sometimes referred to as the Weckebach phenomenon (pronounced winky-bach). Mobitz I AV blocks are characterized by a series of beats in which the PR interval gets progressively longer, until finally the AV node is refractory when the impulse arrives and a QRS complex is dropped. Click here to run an animation of Mobitz type I heart block. The following picture illustrates this phenomena.
|The Weckebach phenomenon: The red line over each P wave illustrates the PR interval of the first cardiac cycle on the ECG. Note that the PR interval is not constant, but gradually prolongs, until the third P wave has no QRS complex following. The next cycle after that, the PR interval is followed by a QRS complex. The PR interval will then increase in duration until another QRS complex is dropped.|
In general, Mobitz I second-degree AV block is associated with a better prognosis than Mobitz II is. This appears to be the result of the fact that Mobitz I is usually associated with AV node dysfunction (and a generally mild dysfunction, at that), while Mobitz II is usually the result of dysfunction lower in the Bundle of His or even in both the Left and Right Bundle branches (some texts refer to this combination as "infranodal" block). The lower block leaves the victim with the very real possibility that the block will degrade to third-degree or complete heart block (see below).
To summarize the ECG changes seen in second degree AV block:
- waveforms are normal in shape and duration (assuming that there is nothing else wrong - not necessarily a good assumption).
- not every P wave is followed by a QRS complex.
- Second-degree AV block can be divided into two subtypes:
- Mobitz I (Wenckebach): The PR interval gradually lengthens until a QRS complex is dropped (doesn't happen). The cycle resumes on the next beat.
- Mobitz II: There is a consistently prolonged PR interval in the beats that have a QRS complex, but the complex is dropped on a regular basis. This leads to a P:QRS ratio that may range from 4:3 to 3:1.
- Those QRS complexes that occur are the result of the depolarization initiated by the SA node.
- The QRS and T waves are normal in appearance (assuming there is nothing else wrong).
- The pulse of this person will be irregular - there will be pauses in the pulse during those times when the AV node fails to conduction the action potential.
Third-Degree (complete) AV block
In the most severe form of AV block, the AV node has ceased to conduct the depolarization from the atria to the ventricles. The SA node will fire normally leading to atrial depolarization (and therefore contraction). However, the AV node fails to conduct the action potential at all. Therefore, the ventricles are not depolarized and fail to contract. Obviously, this can be a life threatening event. However, the heart has several back-up pacemakers located in the ventricles to take over the job of depolarizing the ventricles. The most reliable of these are located in the conduction pathway of the ventricles, particularly the Bundle of His and the larger bundle branches. Other ventricular sites can become the pacemaker, but they often fire at too slow a rate to drive the heart effectively (these sites won't be receiving any sympathetic influence to make them work faster!) and are not as reliable as the Bundle of His and the bundle branches. Under these conditions, the conduction of impulses occurs as illustrated in the next animation.
|Third-degree AV block with a ventricular pacemaker|
Electrocardiographic appearance of Third-degree AV block: If there is no ventricular pacemaker available to take over the job of depolarizing the ventricles, death rapidly ensues the development of the complete AV block. The ECG seen under these conditions consists only of P waves, with no QRS complexes or T waves.
Third-degree AV block with a ventricular pacemaker is characterized by the complete dissociation of the P waves and the QRS complexes. Under these conditions, there is NO PR interval (since the P wave didn't cause the QRS complex). The atria and the ventricles are functioning entirely independently of each other. However, both P waves and QRS complexes are still identifiable on the ECG. The following ECG (from Dubin, p. 176) illustrates complete AV block.
|Complete AV block: In this figure, you can see the dissociation of the P wave from the QRS complex, although you may confuse this with a second degree AV block. The things that allow you to verify that this is complete AV block are 1) the atrial rate is not a multiple of the ventricular rate (for example, in 3:1 second-degree block, the atrial rate is 3 times that of the ventricular rate - here we have an atrial rate of 120 b/min and a ventricular rate of 45 b/min); 2) there is no consistent PR interval; and 3) the occurrence of P waves virtually on top of the QRS complex (the second labelled QRS complex is immediately preceeded by a P wave - at an interval much shorter than the minimum 0.12 seconds). The QRS complexes are normal in shape and duration, indicating that they arose from the normal conduction pathway - based on the rate, probably the AV node itself.|
Summary of ECG changes in Complete AV block:
- P waves are normal in configuration.
- The atrial rate is generally higher than normal (tachycardia) because the very slow ventricular rate leads to a decrease in systemic blood pressure.
- QRS configuration is dependent on ventricular pacemaker
- if the Bundle of His takes over: The QRS complexes are normal in appearance and have a rate of about 30 - 40/min.
- If lower in the conduction pathway: QRS complexes bizarrely shaped and prolonged. Rate may be 20 - 40 beats/min.
- The P waves and QRS complexes are independent from one another
- no PR interval can be determined.
- QRS complex is initiated by a ventricular pacemaker.
- T wave morphology depends on the nature of the ventricular pacemaker: If the QRS complexes are normal in appearance, the T waves should be as well. If the QRS complexes are bizarre in nature, T wave will not be normal.
- The pulse is regular but slow (ventricular rate in complete AV block is usually 20 - 40 beats/min).
Note: I do not expect you to be able to distinguish between second- and third-degree AV block in an EKG at this point in time. However, you should be able to identify third degree heart block from a written description.
Click here to take a practice quiz on AV blocks.
Bundle Branch Blocks
The ventricles of the heart (either left or right) contain sufficient muscle cell mass that effective depolarization of all the cells requires that there be a specialized conduction pathway within the ventricle. The bundle branches (left and right) are the first division in the ventricular conduction system after the Bundle of His. Conduction blocks can occur in either of the two bundle branches. As noted above, these can occur as the result of infarction of the tissue, although a number of otherwise normal people have a bundle branch block due to the invasion of the conduction pathway with fibrous tissue. In fact, it is quite likely that one of more of your classmates will show a bundle branch block during the ECG labs. Luckily for us, the affected ventricle will continue to depolarize, but via a cell-to-cell interaction which is quite a bit slower than the normal pathway. Being quite the creative folks that we scientists are, these are referred to as "right bundle branch block" (RBBB) and "left bundle branch block" (LBBB).
Right Bundle Branch Block
In right bundle branch block, the right ventricle is activated via cell-to-cell transmission of the action potential. This is illustrated in the following animation:
Notice the delay in the time of right ventricular depolarization. This means that the right ventricle is activated after the left ventricle (which is depolarizing normally) and therefore contracts a "split second" after the left ventricle. Mechanically, this difference doesn't greatly influence the performance of the heart. However, it does produce some characteristic changes in the ECG.
Electrocardiographic changes in RBBB.
As you might be able to guess from the animation, because the depolarization of the ventricle has been altered, the changes show up in the QRS complex and the T wave. The following pictures illustrate right bundle branch block in different leads.
|Appearance of three different leads in RBBB: From top to bottom: Lead I, Lead V1 and Lead V6. Due to the RBBB, the right ventricle is depolarizing after the left ventricle. In all three leads, there is a prolongation of the QRS complex due to the blockade. In leads I and V6 (which "see" the left ventricle best), the delayed depolarization of the right ventricle produces a late, negative going wave (S wave) that is very broad (there is no point to the wave) and prolonged. In lead V1 (which has a good view of the right ventricle, the delay in depolarizing the right ventricle leads to the aptly-named "bunny ears"- the QRS complex is composed of an initial positive wave (the R wave), followed by a negative deflection (the S wave) produced when the left ventricle depolarizes, and then a second positive wave (called R' (spoken "R prime")) as the right ventricle finally depolarizes. Because the normal conduction pathway was not followed for depolarization, the process of repolarization does not occur in the normal sequence leading to abnormalities in the T wave (seen best in V1).|
Summary of electrocardiographic changes in RBBB:
- P wave of normal morphology (shape).
- rate and rhythm normal.
- QRS complex is prolonged (> 0.12 seconds).
- QRS complex is bizarrely shaped in leads with "good" views of the right ventricle, such as V1 and V2.
- The appearance of "bunny ears" is a hallmark of a bundle branch.
- The amplitude of the individual waves in the QRS complex is usually increased because the depolarization in the left and the right ventricles are no longer simultaneous (when they are simultaneous, they cancel each other out to some extent).
- The T wave is abnormal in appearance because of alterations in the repolarization of the heart.
Left Bundle Branch block
Left Bundle branch block (LBBB) is very similar to right bundle branch block, as the following animation illustrates.
As with the RBBB, the major change is that the left ventricle is now depolarized due to the spread of the action potential via cell-to-cell conduction. This results in the left ventricle depolarizes (and therefore contracting) a "split-second" after the right ventricle does. As with RBBB, the mechanical effects of this on the heart are minimal.
Electrocardiographic changes in LBBB:
The following pictures illustrate left bundle branch block as seen in three different leads:
|The appearance of LBBB in three different leads: As with right bundle branch block, the major change is in the shape and duration of the QRS complex (since it is ventricular depolarization that has been altered). All of the leads show a prolonged QRS complex due to the time it takes the left ventricle to depolarize. Leads I and V6 record long R waves (lead I shows a small initial R wave (you might be mistaking it for a P wave) and a larger R' leading to a somewhat odd pair of "bunny ears") because the depolarization is heading "at" the lead for a prolonged period of time as the ventricle depolarizes. Lead V1 (on the right side of the sternum sees an initial very small positive wave as the faster right ventricle depolarizes, followed by a prolonged S wave produced by the left ventricular depolarization (note that the S wave also has two peaks - an inverted pair of "bunny ears").|
Summary of electrocardiographic changes in LBBB:
- P wave of normal morphology (Note: like a lot of things in this world, the ECG tracing shown above for LBBB has more than one thing wrong with it - no P waves are visible because this person is in atrial fibrillation).
- Normal rate and rhythm.
- Normal PR interval
- QRS complex is prolonged and bizarrely shaped.
- Bunny ears
- other leads may show QRS complexes that aren't "pointy", instead they are rounded at the top/bottom.
- The amplitude of the QRS complex peaks are often increased, due to the failure of the left and right ventricle to depolarize simultaneously.
- The T wave is abnormal in morphology because repolarization cannot occur normally if depolarization did not.
Thought Question #3
The left bundle branch branches into a left anterior fascicle and a left posterior fascicle that help spread the action potential across the larger left ventricle. These fascicles were not shown in the original animation, but the next animation illustrates the posterior fascicle in place with the other parts of the conduction pathway. The fascicles can also be damaged, leading to what is called fascicular block (usually specified as left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB). The effects of this on the conduction of the action potential are illustrated in the next animation.
One important thing to notice as the animation proceeds is that the entire process of ventricular depolarization is not prolonged by the fascicular block. There is ventricular tissue that takes longer to depolarize than it normally would have (all the tissue affected by the loss of the fascicle), but the bulk of the ventricle continues to depolarize as normal. These facts determine the some aspects of electrocardiographic appearance of fascicular blocks.
Electrocardiographic appearance of fascicular blocks: Because the overall duration of ventricular depolarization is not prolonged, the duration of the QRS complex in either anterior or posterior fascicular blocks is usually normal (i.e. < 0.10 seconds). This leaves you with other more subtle changes in the ECG to identify fascicular blocks.
A left anterior fascicular block is identified when:
- there is left axis deviation (usually > - 60 degrees).
- small Q waves appear in leads I and aVL.
- small R waves appear in leads II, III, and aVF.
- aVL has a small shoulder late in the deflection (this isn't actually a second peak, but a subtle "flattening" of the downward deflection).
- the limb lead voltages are larger than normal.
If you use these leads (above, aVF and Lead I) to plot the mean electrical axis, a clear left axis deviation is present.
Another sign of a left anterior fascicular block is the presence of Q waves in lead I (see above) and lead aVL (left). Since these leads are "positioned" to the left of the heart, most current should flow straight at them. With the loss of the anterior fascicle, current flow to the left is initially decreased, leading to the right ventricle's depolarization being "seen" in the ECG.
Leads II, III (immediately above) and aVF (second figure) show smaller R waves than normal in the presence of anterior fascicular block. In addition, the limb leads (I, II and III) show larger voltages than normal in the overall QRS complex.
Like the anterior fascicular block, left posterior fascicular block produces very subtle changes in the ECG. Depolarization of the posterior wall of the left ventricle lags slightly behind the rest of the heart, leading to a depolarizing wave heading towards the right as the posterior wall is depolarized by conduction around the free wall, rather than via the fascicle. On the ECG, left posterior fascicular block is indicated when:
- there is right axis deviation (> + 120 degrees).
- no evidence of right ventricular hypertrophy (right ventricular hypertrophy also produces right axis deviation).
- aVF has the small shoulder late in the deflection.
- The limb lead voltages are larger than normal.
The bold red text highlight the points that distinguish between anterior and posterior fascicular blocks.
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