The only EKG book. 9th Ed

Chapter 4. Conduction Blocks

In this chapter you will learn:


what a conduction block is


that there are several types of conduction blocks that can occur between the sinus node and the atrioventricular (AV) node, some that are of little concern and others that can be life threatening


how to recognize each of these AV blocks on the EKG


that conduction blocks can occur in the ventricles as well, and these bundle branch blocks are also easily identified on the EKG


that sometimes conduction along only one fascicle of the left bundle branch can be blocked


how to recognize combined AV blocks and bundle branch blocks on the EKG


what pacemakers are used for, and how to recognize their bursts of electrical activity on an EKG


about the cases of Sally M., Jonathan N., and Ellen O., which will illustrate the importance of knowing when conduction disturbances are truly disturbing

What is a Conduction Block?

Any obstruction or delay of the flow of electricity along the normal pathways of electrical conduction is called a conduction block.

(Technically, not all of what we call conduction blocks are true blocks; whereas some actually do halt the flow of current, in many cases they only slow it down. Nevertheless, the term stands, and we will use it throughout this chapter.)

A conduction block can occur anywhere in the conduction system of the heart. There are three types of conduction blocks, defined by their anatomic location.

1. Sinus node block—This is the sinus exit block that we discussed in the last chapter. In this situation, the sinus node fires normally, but the wave of depolarization is immediately blocked and is not transmitted into the atrial tissue. On the EKG, it looks just like a pause in the normal cardiac cycle. We will not discuss it further.

2. AV block—This term refers to any conduction block between the sinus node and the terminal Purkinje fibers. Note that this includes the AV node and His bundle.

3. Bundle branch block—As the name indicates, bundle branch block refers to a conduction block in one or both of the ventricular bundle branches. Sometimes, only a part of the left bundle branch is blocked; this circumstance is called a fascicular block or a hemiblock.

To a rough approximation, this picture shows typical sites of the three major conduction blocks.

AV Blocks

AV blocks come in three varieties, termed (with a complete lack of imagination) first degree, second degree, and third degree. They are diagnosed by carefully examining the relationship of the P waves to the QRS complexes.

First-Degree AV Block

First-degree AV block is characterized by a delay in conduction at the AV node or His bundle (recall that the His bundle—or bundle of His, depending on your grammatical preference—is the part of the conducting system located just below the AV node. A routine 12-lead EKG cannot distinguish between a block in the AV node and one in the His bundle). The wave of depolarization spreads normally from the sinus node through the atria but upon reaching the AV node is held up for longer than the usual one-tenth of a second. As a result, the PR interval—the time from the start of atrial depolarization to the start of ventricular depolarization, a time period that encompasses the delay at the AV node—is prolonged.

The diagnosis of first-degree AV block requires only that the PR interval be longer than 0.2 seconds.

In first-degree AV block, despite the delay at the AV node or His bundle, every atrial impulse does eventually make it through the AV node to activate the ventricles. Therefore, to be precise, first-degree AV block is not really a “block” at all, but rather a “delay” in conduction. Every QRS complex is preceded by a single P wave.

First-degree AV block. Note the prolonged PR interval.

First-degree AV block is a common finding in normal hearts, but it can also be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity. By itself, it does not require treatment. First-degree AV block is associated with a very slightly increased risk of atrial fibrillation, the need for subsequent pacemaker insertion, and all-cause mortality. The reason for this is not clear but may reflect the possibility that a prolonged PR interval is a precursor to more severe heart block or is a marker for underlying cardiovascular disease.

Second-Degree AV Block

In second-degree AV block, not every atrial impulse is able to pass through the AV node into the ventricles. Because some P waves fail to conduct through to the ventricles, the ratio of P waves to QRS complexes is greater than 1:1.

Just to make things a little more interesting, there are two types of second- degree AV block: Mobitz type I second-degree AV block, more commonly called Wenckebach block, and Mobitz type II second-degree AV block.

Wenckebach Block

Wenckebach block is almost always due to a block within the AV node. The electrical effects of Wenckebach block are unique. The block, or delay, is variable, increasing with each ensuing impulse. Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually every third or fourth) fails to make it through. What you see on the EKG is a progressive lengthening of the PR interval with each beat and then suddenly a P wave that is not followed by a QRS complex (a “dropped beat”). After this dropped beat, during which no QRS complex appears, the sequence repeats itself, over and over, and often with impressive regularity.

The following tracing shows a 4:3 Wenckebach block, in which the PR interval grows longer with each beat until the fourth atrial impulse fails to stimulate the ventricles, producing a ratio of four P waves to every three QRS complexes.

Mobitz type I second-degree AV block (Wenckebach block). The PR intervals become progressively longer until one QRS complex is dropped.

The diagnosis of Wenckebach block requires the progressive lengthening of each successive PR interval until one P wave fails to conduct through the AV node and is therefore not followed by a QRS complex.

Mobitz Type II Block

Mobitz type II block is usually due to a block below the AV node in the His bundle. It resembles Wenckebach block in that some, but not all, of the atrial impulses are transmitted to the ventricles. However, progressive lengthening of the PR interval does not occur. Instead, conduction is an all-or-nothing phenomenon. The EKG shows two or more normal beats with normal PR intervals and then a P wave that is not followed by a QRS complex (a dropped beat). The cycle is then repeated. The ratio of conducted beats to nonconducted beats is rarely constant, with the ratio of P waves to QRS complexes constantly varying, from 2:1 to 3:2 and so on.

Mobitz type II second-degree AV block. On this EKG, each third P wave is not followed by a QRS complex (dropped beat).

The diagnosis of Mobitz type II block requires the presence of a dropped beat without progressive lengthening of the PR interval.

Is It a Wenckebach Block or a Mobitz Type II Block?

Compare the electrocardiographic manifestations of Wenckebach block and Mobitz type II block on the following EKGs:

(A) Wenckebach block, with progressive lengthening of the PR interval. (B) Mobitz type II block, in which the PR interval is constant.

Now that you are an expert, look at the following EKG. Is this an example of Wenckebach block or Mobitz type II block?

Well, it certainly is an example of second-degree heart block with a P wave- to-QRS complex ratio of 2:1, but you were pretty clever if you realized that it is impossible to tell whether it is due to Wenckebach block or Mobitz type II block. The distinction between these two types of second-degree heart block depends on whether or not there is progressive PR lengthening, but with a 2:1 ratio in which every other QRS complex is dropped, it is impossible to make this determination. It should simply—and most accurately—be called 2:1 AV block.

Here is a bit of technical esoterica that, unless you plan to become a cardiologist, you can probably safely ignore. In cases of 2:1 second- degree AV block, as shown on the previous page, there actually are two ways—one clinical and one invasive—to localize the site of the block and determine how serious the problem may be.

The Bedside Approach: Vagal tone affects the AV node more than the His bundle, so anything that increases vagal tone—for example, a Valsalva maneuver or carotid sinus massage—can increase AV nodal block. However, it will either not effect or may even possibly improve an infranodal block by slowing the heart rate, thereby allowing the infranodal tissue time to recover between beats and conduct more efficiently. Thus, depending on the location of the block, the degree of block will respond differently to vagal stimulation, thus allowing you to distinguish Wenckebach from Mobitz type II heart block.

The Invasive Approach: An electrophysiologic study is the definitive way to make the distinction. A small electrode introduced into the region of the His bundle can identify whether the site of the block is above, within, or below the His bundle.

When circumstances permit an accurate determination, the distinction between Wenckebach block and Mobitz type II second-degree AV block is an important one to make. Wenckebach block is typically transient and benign and rarely progresses to third-degree heart block (see next page), which can be dangerous and even life threatening.

Mobitz type II block is, although less common than Wenckebach block, far more serious, often signifying serious heart disease and capable of progressing suddenly to third-degree heart block.

Whereas pacemaker placement is uncommonly needed for Wenckebach block unless patients are symptomatic (e.g., experiencing syncope), Mobitz type II heart block mandates insertion of a pacemaker.

Third-Degree AV Block

Third-degree heart block is the ultimate in heart blocks. No atrial impulses at all make it through to activate the ventricles. For this reason, it is often called complete heart block. The site of the block can be either at the AV node or lower. The ventricles respond to this dire situation by generating an escape rhythm, usually a barely adequate 30 to 45 beats per minute (idioventricular escape, see page 118). The atria and ventricles continue to contract, but they now do so at their own intrinsic rates—about 60 to 100 beats per minute for the atria and 30 to 45 beats per minute for the ventricles. The atria and ventricles have virtually nothing to do with each other, separated by the absolute barrier of the complete conduction block. We have already described this type of situation in our discussion of ventricular tachycardia: It is called AV dissociation and refers to any circumstance in which the atria and ventricles are being driven by independent pacemakers.

The EKG in third-degree heart block shows P waves marching across the rhythm strip at their usual rate (60 to 100 waves per minute) but bearing no relationship to the QRS complexes that appear at a much slower escape rate. The QRS complexes appear wide and bizarre, just like premature ventricular contractions (PVCs), because they arise from a ventricular source.

Third-degree AV block. The P waves appear at regular intervals, as do the QRS complexes, but they have nothing to do with one another. The QRS complexes are wide, implying a ventricular origin.

With the onset of third-degree heart block, there may be a delay (or even complete absence) in the appearance of a ventricular escape rhythm. The EKG will then show sinus beats (P waves) activating the atria with no ventricular activity at all for two or more beats before either normal AV conduction resumes or a ventricular escape rhythm finally appears. When there are 4 or more seconds without ventricular activity, the patient usually experiences a near or complete faint. These have been termed Stokes-Adams attacks and almost always require a pacemaker (see Page 208).

This patient was in normal sinus rhythm (see the first complex) when he suddenly went into complete heart block. There is a long pause during which you can see nothing but P waves; no escape beats can be seen for several seconds. Finally, the first ventricular escape beat saves the day, but during the long pause, the patient experienced a Stokes-Adams attack.

Although a ventricular escape rhythm may look like a slow run of PVCs (slow ventricular tachycardia), there is one important difference: PVCs are premature, occurring before the next expected beat, and even the slowest ventricular tachycardia will be faster than the patient’s normal rhythm. A ventricular escape beat occurs after a long pause and is therefore never premature, and a sustained ventricular escape rhythm is always slower than the normal beats. PVCs, being premature intrusions, can be suppressed with little clinical consequence. A ventricular escape rhythm, however, may be lifesaving, and suppression could be fatal.

(A) The third beat is a PVC, occurring before the next anticipated normal be The third ventricular complex occurs late, after a prolonged pause. This is a ventricular escape beat.

AV dissociation can also occur when there is a block high in the AV node, but in this case, there is an accelerated junctional rhythm to drive the ventricles that is faster than the sinus rhythm. This situation rarely requires a pacemaker. It occurs most often in patients undergoing an acute myocardial infarction and in those who have received an overdose of an antiarrhythmic medication.

The diagnosis of third-degree heart block requires the presence of AV dissociation in which the ventricular rate is slower than the sinus or atrial rate.

Degenerative disease of the conduction system is the leading cause of third- degree heart block. Complete heart block can also complicate an acute myocardial infarction. Pacemakers are virtually always required when third- degree heart block develops. It is a true medical emergency.

Most complete heart blocks are permanent. One of the more common causes of reversible complete heart block is Lyme disease, caused by infection with the spirochete, Borrelia burgdorferi. The heart block is caused by inflammation of the myocardium and conducting system, and any level of AV block can occur. Patients with type 1 AV block in which the PR interval is greater than 300 ms can progress rapidly to complete heart block and may require hospitalization. In patients with Lyme disease who develop complete heart block, the block typically occurs within the AV node and is associated with a narrow QRS complex junctional escape rhythm. A stat Lyme titer can avoid the need for a permanent pacemaker, although temporary pacing may be needed. Treatment includes antibiotics and corticosteroids.

Some forms of complete heart block develop prenatally (congenital heart block), and these are often associated with an adequate and stable ventricular escape rhythm. Permanent pacemakers are only implanted in these children if there is clear-cut developmental impairment that can be attributed to an inadequate cardiac output.


AV Blocks

AV block is diagnosed by examining the relationship of the P waves to the QRS complexes.

1. First degree: The PR interval is greater than 0.2 seconds; all beats are conducted through to the ventricles.

2. Second degree: Only some beats are conducted through to the ventricles.

a. Mobitz type I (Wenckebach): Progressive prolongation of the PR interval until a QRS is dropped

b. Mobitz type II: All-or-nothing conduction, in which QRS complexes are periodically dropped without prolongation of the PR interval

3. Third degree: No beats are conducted through to the ventricles. There is complete heart block with AV dissociation. No impulses reach the ventricles from above, and the ventricles are driven by a ventricular escape rhythm.

Note: Different degrees of AV block can coexist in the same patient. Thus, for example, a patient can have both first-degree and Mobitz type II heart blocks. Blocks also can be transient—a patient with Lyme carditis can bounce back and forth between different degrees of AV block within seconds!

Bundle Branch Block

The term bundle branch block refers to a conduction block (or slowing) of current flow in either the left or right bundle branches. The figure below reviews the anatomy of the ventricular bundle branches.

A Quick Review of Ventricular Depolarization

The normal sequence of ventricular activation should be familiar to you by now. The wave of depolarization sweeps out of the AV node and bundle of His into the bundle branch system. The right and left bundle branches deliver the current to the right and left ventricles, respectively. This is the most efficient means of dispersing the electrical current, and the resultant QRS complex, representing ventricular depolarization from start to finish, is narrow—less than 0.10 seconds in duration. Also, because the muscle mass of the left ventricle is so much larger than that of the right ventricle, left ventricular electrical forces dominate those of the right ventricle, and the resultant electrical axis is leftward, lying between 0° and +90°.

The anatomy of the ventricular bundle branches.

Thus, with normal ventricular depolarization, the QRS complex is narrow, and the electrical axis lies between 0° and 90°. All of this changes -with bundle branch block.

Bundle branch block is diagnosed by looking at the width and configuration of the QRS complexes.

Right Bundle Branch Block

In right bundle branch block, conduction through the right bundle is obstructed. As a result, right ventricular depolarization is delayed; it does not begin until the left ventricle is almost fully depolarized. This causes two things to happen on the EKG:

1. The delay in right ventricular depolarization prolongs the total time for ventricular depolarization. As a result, the QRS complex widens beyond 0.12 seconds.

2. The wide QRS complex assumes a unique, virtually diagnostic shape in those leads overlying the right ventricle: V1 and V2. The normal QRS complex in these leads consists of a small positive R wave and a deep

negative S wave, reflecting the electrical dominance of the left ventricle. With right bundle branch block, you can still see the initial R and S waves as the left ventricle depolarizes, but as the right ventricle then begins its delayed depolarization, unopposed by the now fully depolarized and electrically silent left ventricle, the electrical axis of current flow swings sharply back toward the right. This inscribes a second R wave, called R' (pronounced “R prime”), in leads V1 and V2. The whole complex is called RSR' (“R-S-R prime”), and its appearance has been likened to rabbit ears. Meanwhile, in the left lateral leads overlying the left ventricle (I, aVL, V5, and V6), late right ventricular depolarization causes reciprocal late deep S waves to be inscribed.

Right bundle branch block. The QRS complex in lead V1 shows the classic wide RSR' configuration. Note, too, the S waves in V5 and V6.

In fairness, and in the spirit of full disclosure, you need to know that you will not always see a beautiful pair of rabbit ears with right bundle branch block. Sometimes, as in the tracing below, you will only see tall R waves, but the QRS complexes will certainly be wide.

Right bundle branch block without rabbit ears but with a tall R wave and wide QRS complex.

Left Bundle Branch Block

In left bundle branch block, it is left ventricular depolarization that is delayed. Again, there are two things to look for on the EKG:

1. The delay in left ventricular depolarization causes the QRS complex to widen beyond 0.12 seconds in duration.

2. The QRS complex in the leads overlying the left ventricle (I, aVL, V5, and V6) will show a characteristic change in shape. The QRS complexes in these leads already have tall R waves. Delayed left ventricular depolarization causes a marked prolongation in the rise of those tall R waves, which will either be broad on top or notched. True rabbit ears are less common than in right bundle branch block. Those leads overlying the right ventricle will show reciprocal, broad, deep S waves. The left ventricle is so dominant in left bundle branch block that left axis deviation may also be present, but this is variable.

Left bundle branch block.

Bundle Branch Block and Repolarization

In the previous EKGs, did you notice the depressed ST segments and flipped T waves in V1 through V3 with right bundle branch block and in V5 and V6 with left bundle branch block? These ST segment and T wave changes occur because the repolarization sequence is also affected by the conduction block.

In right bundle branch block, the right precordial leads will show ST-segment depression and T-wave inversion, just like the repolarization abnormalities that occur with ventricular hypertrophy.

Similarly, in left bundle branch block, ST-segment depression and T-wave inversion can be seen in the left lateral leads.

ST-segment depression and T-wave inversion in lead V6 in a patient with left bundle branch block.

Who Gets Bundle Branch Blocks?

Although right bundle branch block can be caused by diseases of the conducting system, it is also a fairly common phenomenon in otherwise normal hearts.

Left bundle branch block, on the other hand, rarely occurs in normal hearts and almost always reflects significant underlying cardiac disease, such as degenerative disease of the conduction system or ischemic coronary artery disease.

Critical Rate

Both right and left bundle branch blocks can be intermittent or fixed. In some individuals, bundle branch block only appears when a particular heart rate, called the critical rate, is achieved. In other words, the ventricles conduct the electrical impulse normally at slow heart rates, but above a certain rate, bundle branch block develops.

The development of a rate-related bundle branch block is directly related to the time it takes a particular bundle branch to repolarize and thus prepare itself for the next electrical impulse to arrive. If the heart rate is so rapid that a particular bundle branch cannot repolarize in time, there will be a temporary block to conduction, resulting in the classic EKG appearance of a rate-related bundle branch block.

An example of critical rate (lead V2). As the heart accelerates, the pattern of right bundle branch block appears.

The occurrence of rate-related bundle branch block depends on the same physiology that accounts for aberrant conduction of supraventricular arrhythmias (see Page 154), in which the aberrantly conducted supraventricular beat results from some portion of the bundle branch system failing to repolarize in a timely fashion.


Bundle Branch Block

Bundle branch block is diagnosed by looking at the width and configuration of the QRS complexes.

Criteria for Right Bundle Branch Block

1. QRS complex widened to greater than 0.12 seconds

2. RSR' (rabbit ears) or a tall R wave in V1 and V2 with ST-segment depression and T-wave inversion

3. Reciprocal changes in V5, V6, I, and aVL

Criteria for Left Bundle Branch Block

1. QRS complex widened to greater than 0.12 seconds.

2. Broad or notched R wave with prolonged upstroke in leads V5, V6, I, and aVL, with ST-segment depression and T-wave inversion.

3. Reciprocal changes in V1 and V2.

4. Left axis deviation may be present.

Note: Because bundle branch block affects the size and appearance of R waves, the criteria for ventricular hypertrophy discussed in Chapter 2 cannot be used if bundle branch block is present. Specifically, right bundle branch block precludes the diagnosis of right ventricular hypertrophy, and left bundle branch block precludes the diagnosis of left ventricular hypertrophy. In addition, the diagnosis of a myocardial infarction can be extremely difficult in the presence of left bundle branch block; we will see why in Chapter 6.


Here again is a picture of the ventricular conduction system. The left bundle branch is composed of three separate fascicles—the septal fascicle, the left anterior fascicle, and the left posterior fascicle. The term hemiblock refers to a conduction block of just one of these fascicles. The right bundle branch does not divide into separate fascicles; thus, the concept of hemiblock only applies to the left ventricular conducting system.

Septal blocks need not concern us here. Hemiblocks of the anterior and posterior fascicles, however, are both common and important.

The ventricular conduction system. The right bundle branch remains intact, whereas the left bundle branch divides into three separate fascicles.

Hemiblocks Cause Axis Deviation

The major effect that hemiblocks have on the EKG is axis deviation. Here is why.

As shown on the previous page, the left anterior fascicle lies superiorly and laterally to the left posterior fascicle. With left anterior hemiblock, conduction down the left anterior fascicle is blocked. All the current, therefore, rushes down the left posterior fascicle to the inferior surface of the heart. Left ventricular myocardial depolarization then occurs, progressing in an inferior-to-superior and right-to-left direction.

The axis of ventricular depolarization is therefore redirected upward and slightly leftward, inscribing tall positive R waves in the left lateral leads and deep S waves inferiorly. This results in left axis deviation in which the electrical axis of ventricular depolarization is redirected between -30° and -90°.

Do you remember how to identify left axis deviation? The simplest method is to look at the QRS complex in leads I and aVF. The QRS complex will be positive in lead I and negative in lead aVF. However, this analysis will define a range from 0° to -90°, and the diagnosis of left anterior hemiblock requires left axis deviation of greater than 30°. Therefore, look at lead II, which is angled at +60°; if its QRS complex is negative, then the axis must lie more negative than -30°.

Left anterior hemiblock. Current flow down the left anterior fascicle is blocked; hence, all the current must pass down the posterior fascicle. The resultant axis is redirected upward and leftward (left axis deviation).

There are many causes of left axis deviation. In fact, we’ve just seen one—left bundle branch block. But there are others—can you think of one? How about left ventricular hypertrophy? And there are others which we have yet to explore. You can only diagnose left anterior hemiblock when no other cause of left axis deviation is present.

In left posterior hemiblock, the reverse occurs. All of the current rushes down the left anterior fascicle, and ventricular myocardial depolarization then ensues in a superior-to-inferior and left-to-right direction. The axis of depolarization is therefore directed downward and rightward, writing tall R waves inferiorly and deep S waves in the left lateral leads. The result is right axis deviation (i.e., the electrical axis of ventricular depolarization is between +90° and 180°). The QRS complex will be negative in lead I and positive in lead aVF.

Left posterior hemiblock. Current flow down the left posterior fascicle is blocked; hence, all the current must pass down the right anterior fascicle. The resultant axis is redirected downward and rightward (right axis deviation).

Just as with left anterior hemiblock, there are other causes of right axis deviation. One common cause is chronic lung disease, which we will encounter in Chapter 7. You can only diagnose left posterior hemiblock if no other cause of right axis deviation is present.

Hemiblocks Do Not Prolong the QRS Complex

Whereas the QRS complex is widened in complete left and right bundle branch block, the QRS duration in both left anterior and left posterior hemiblocks is normal. (Actually, there is a very minor prolongation, but not enough to widen the QRS complex appreciably.) There are also no ST-segment and T-wave repolarization changes.

Left anterior hemiblock is far more common than left posterior hemiblock, possibly because the anterior fascicle is longer and thinner and has a more tenuous blood supply than the posterior fascicle. Left anterior hemiblock can be seen in both normal and diseased hearts, whereas left posterior hemiblock is virtually the exclusive province of sick hearts.

Is hemiblock present in the following EKG?

Left axis deviation greater than -30° indicates the presence of left anterior hemiblock.

Remember, before settling on the diagnosis of hemiblock, it is always necessary to make sure that other causes of axis deviation, such as ventricular hypertrophy, are not present. For most individuals, however, if the tracing is normal except for the presence of axis deviation, you can feel reasonably confident that hemiblock is responsible.

Criteria for Hemiblock

Hemiblock is diagnosed by looking for left or right axis deviation.

Left Anterior Hemiblock

1. Normal QRS duration and no ST-segment or T-wave changes.

2. Left axis deviation between -30° and -90°.

3. No other cause of left axis deviation is present.

Left Posterior Hemiblock

1. Normal QRS duration and no ST-segment or T-wave changes.

2. Right axis deviation.

3. No other cause of right axis deviation is present.

Combining Right Bundle Branch Block and Hemiblocks

Right bundle branch block and hemiblocks can occur together. The term bifascicular block refers to the combination of right bundle branch block with either left anterior or left posterior hemiblock. In bifascicular block, only one fascicle of the left bundle branch is supplying electrical current to the bulk of both ventricles. The EKG findings include a combination of features of both hemiblock and right bundle branch block.

Criteria for Bifascicular Block

The features of right bundle branch block combined with left anterior hemiblock are as follows:

Right Bundle Branch Block

Left Anterior Hemiblock

• QRS wider than 0.12 seconds

RSR' in V1 and V2

• Left axis deviation between -30° and -90°

The features of right bundle branch block combined with left posterior hemiblock are as follows:

Right Bundle Branch Block

• QRS wider than 0.12 seconds

• RSR' in V1 and V2

Left Posterior Hemiblock

• Right axis deviation

Can you identify a bifascicular block on this EKG?

This is an example of right bundle branch block combined with left anterior hemiblock. Note the widened QRS complex and rabbit ears in leads V1 and V2, characteristic of right bundle branch block, and the left axis deviation in the limb leads (the QRS complex is predominantly positive in lead I and negative in leads aVF and II) that suggests left anterior hemiblock.

Blocks That Underachieve

Not every conduction block meets all the criteria for a bundle branch block or bifascicular block. These are extremely common and generally fall into two types:

A nonspecific intraventricular conduction delay occurs when there is QRS widening greater than 0.10 seconds without the other criteria for either bundle branch block or bifascicular block.

An incomplete bundle branch block occurs when the EKG tracing shows a left or right bundle branch appearance (e.g., rabbit ears in V1 in right bundle branch block), but the QRS duration is between 0.10 and 0.12 seconds.

These conduction blocks are caused by the same disease processes that cause the other conduction blocks.

Incomplete right bundle branch block; the QRS complex is not widened, but note the classic rabbit ears configuration in V1.

The Ultimate in Playing With Blocks: Combining AV Blocks, Right Bundle Branch Block, and Hemiblocks

Right bundle branch block, hemiblocks, and bifascicular blocks can also occur in combination with AV blocks. (Are you sure you’re ready for this?) Take a look at the following EKG and see if you can identify the different conduction blocks that are present. An orderly approach is essential.

1. Is there an AV block? Look at the relationship between the P waves and QRS complexes.

2. Is there a bundle branch block? Look in the precordial leads for wide QRS complexes with their distinctive configurations; are there any ST-segment and T-wave changes?

3. Is there a hemiblock? Look for axis deviation.

This EKG shows:

1. first-degree AV block (the PR interval exceeds 0.20 seconds)

2. right bundle branch block (there are wide QRS complexes with rabbit ears in leads V1 through V4)

3. left anterior hemiblock (left axis deviation is present)


Many pacemakers, both temporary and permanent, are inserted every year, and in the right circumstances, they can relieve symptoms of inadequate cardiac output and prevent sudden death from complete conduction block or a tachyarrhythmia. Clinical evidence strongly supports their use in patients with

 third-degree (complete) AV block

 a lesser degree of AV block or bradycardia (e.g., sick sinus syndrome) if the patient is symptomatic (especially in atrial fibrillation)

 the sudden development of various combinations of AV block and bundle branch block in patients who are in the throes of an acute myocardial infarction (this situation usually only requires a temporary pacemaker that can be removed after the acute incident has resolved)

 recurrent tachycardias that can be overdriven and thereby terminated by pacemaker activity

 a strong indication for therapy with an AV nodal blocker, for example, a high burden of PVCs, but who are unable to use these drugs without developing a clinically intolerable bradycardia (shortness of breath, dizziness, etc.)

Pacemakers are nothing more than a power source controlled by a microchip and connected to electrodes. The power source is usually placed subcutaneously, and the electrodes are threaded into the right atrium and right ventricle through veins that drain to the heart. Pacemakers provide an alternate source of electrical stimulation for a heart whose own intrinsic source of electricity (the sinus node) or whose ability to conduct electrical current is impaired.

Whereas early pacemakers were capable of firing only at a single predetermined rate (fixed rate pacemakers) no matter what the heart itself was doing, today’s pacemakers are responsive to the moment-to-moment needs of the heart. They are programmable in terms of sensitivity, rate of firing, refractory period, and so on. The present generation of pacemakers can also increase the heart rate in response to motion or increased respirations for those patients who cannot increase their own heart rate appropriately during activity, either because of disease of the sinus node or the effects of medications.

The most popular pacemaker is a demand pacemaker. A demand pacemaker fires only when the patient’s own intrinsic heart rate falls below a threshold level. For example, a demand pacemaker set at 60 beats per minute will remain silent as long as the patient’s heart rate remains above 60 beats per minute. As soon as there is a pause between beats that would translate into a rate below 60, the pacemaker will fire.

Pacemaker electrodes can be placed in the atrium or ventricle alone (singlechamber pacemakers) or, more commonly, in both chambers (dual-chamber pacemakers). Dual-chamber pacemakers are also called A-V sequential pacemakers.

(A) Site of atrial pacemaker implantation. (B) Ventricular pacemaker. (C) Sequential pacemaker with atrial and ventricular leads.

When a pacemaker fires, a small spike can be seen on the EKG. With a ventricular pacemaker, the ensuing QRS complex will be wide and bizarre, just like a PVC. Because the electrodes are located in the right ventricle, the right ventricle will contract first and then the left ventricle. This generates a pattern identical to left bundle branch block, with delayed left ventricular activation. A retrograde P wave may or may not be seen.

EKG from a patient with a ventricular pacemaker.

An atrial pacemaker will generate a spike followed by a P wave, a normal PR interval, and a normal QRS complex.

EKG from a patient with an atrial pacemaker.

With a sequential pacemaker, two spikes will be seen, one preceding a P wave and one preceding a wide, bizarre QRS complex.

EKG from a patient with an AV sequential pacemaker.

When used appropriately, pacemakers save lives. They do, however, have risks. First, there is a small chance of infection. Second, the pacemaker spike itself always has the potential to induce a serious arrhythmia. For example, if a ventricular pacemaker should happen to fire mistakenly during the vulnerable period of ventricular repolarization (remember the R-on-T phenomenon? see page 152), ventricular tachycardia or ventricular fibrillation can be induced. Fortunately, this is an extremely rare occurrence with modern advances in pacemaker technology.

Patients with impaired left ventricular function or congestive heart failure may not always benefit from a pacemaker inserted in the right ventricle (depicted in figures B and C on Page 209). Indeed, such a pacemaker may actually precipitate an episode of heart failure by overriding effective intrinsic electrical conduction and worsening ventricular contractile function. This happens because the pacemaker may create a situation mimicking left bundle branch block by pacing the right ventricle first. The resulting ventricular dyssynchrony (i.e., the ventricles are no longer contracting at the same time) can reduce the pumping function of the heart. Thus, a newer pacing option has been introduced for such patients in which a third electrode is threaded into the coronary sinus from the right atrium and passed into the lateral veins of the left ventricle to allow for ventricular epicardial pacing. Pacing from both the right and left ventricular electrodes resynchronizes the heart and can improve left ventricular function and reduce the symptoms of heart failure.

Patients with significantly reduced left ventricular function and a native left bundle branch block may also benefit from implantation of a pacing device with both right and left ventricular electrodes. This is called cardiac resynchronization therapy (CRT), and it has been shown to reduce rates of hospitalization and death in patients with class II and class III (i.e., symptomatic but not severe) heart failure. CRT mainly benefits patients whose heart failure is associated with a wide QRS complex (>0.15 ms) and left ventricular systolic dysfunction.

Among the latest developments in pacemaker technology is the leadless pacemaker, a self-contained pacemaker placed through the femoral vein into the right ventricle. This type of pacemaker eliminates the need for any leads and for any incisions. So far it can only be used for ventricular pacing, but technology to allow for dual-chamber pacing is being developed.

In some patients, pacemaker spikes can be difficult to see on a standard EKG because their amplitude may be less than 1 mV. If you are examining an EKG from a patient unknown to you that demonstrates wide QRS complexes and left axis deviation, you must always suspect the presence of a pacemaker even if the tiny pacemaker spikes cannot be seen. Obviously, examination of the patient or—if the patient is lucid—a simple question or two will reveal the presence or absence of an electrical pacemaker.


Sally M. works at your hospital as a volunteer. One day, she is instructed to take some intravenous solutions from the pharmacy in the hospital basement to the intensive care unit (ICU) on the third floor. At the same time, you just happen to be standing at the third floor elevator, waiting impatiently for a ride down to the cafeteria. When the elevator door opens, you find Sally collapsed on the floor. A quick purview of her vital signs reveals that she is breathing adequately, has a strong pulse, and is slightly tachycardic. You grab a gurney that is conveniently parked nearby and rush her into the ICU.

On the way to the unit, you try talking to her. She is confused and disoriented, and you notice that she has been incontinent. In the ICU, this rhythm strip is obtained.

Does this rhythm strip tell you what happened to Sally on the elevator?

In a word, no. The rhythm strip reveals a modest sinus tachycardia, first-degree AV block, and the rabbit ears of right bundle branch block. Nothing here can account for her collapse. Had you found significant bradycardia, a ventricular arrhythmia, or an advanced degree of heart block, you would certainly have cause to suspect the presence of Stokes-Adams syncope, that is, a sudden faint from inadequate cardiac output. The prolonged period of disorientation following her collapse is also not typical of Stokes-Adams syncope but is typical of the postictal state seen after a seizure.

About 15 minutes after her collapse, Sally’s mental state has returned to normal, and she is anxious to return to work. You are able to persuade her that a short stay in the ICU for observation would be a good idea. Continual cardiac monitoring reveals no significant arrhythmias or conduction blocks, but a magnetic resonance imaging (MRI) of her head does reveal a meningioma. It is likely, therefore, that Sally did suffer a seizure caused by an expanding (but fortunately not malignant) brain lesion. The meningioma is excised without complication, and several months later, you see Sally happily plying her trade once again, a joyful reminder to all that performing a service for others is the surest way to achieve true satisfaction in life.


Jonathan N., dressed in a magnificent three-piece bespoke suit and wearing hand-sewn shoes whose cost could fund an overseas medical clinic for a month, is the chief executive officer of a large investment firm, a position he describes as “more stressful than anything you, my friend, could ever imagine.” He is new to your practice and tells you that he has recently been suffering from some exertional shortness of breath but doesn’t have time for “all the nonsense of a history and physical.” He insists that you simply run an EKG and tell him if he is having a heart attack. Taking a deep breath and trying not to roll your eyes too obviously, you hook him up to your EKG machine. The 12- lead EKG does not show any acute ischemia, but lead V1 does show this:

What do you see, what do you infer, and what do you do?

The most striking finding is the procession of pacemaker spikes marching across the EKG bearing no relation whatsoever to the P waves and QRS complexes. The pacemaker is failing to capture the heart. You can infer a heart history that required the pacemaker in the first place. Because the rate and rhythm appear to be otherwise well maintained, it is not at all clear that this consummate executive’s shortness of breath is related to the failure of the pacemaker to adequately capture and drive the heart. What you do, of course, is now insist on a careful history and physical examination to guide your next move (you are not surprised when you discover that he has a history of high degrees of AV block that necessitated placement of the pacemaker, and a prior myocardial infarction, items he neglected to mention in your initial conversation).


Ellen O. is a 60-year-old biochemist who presents to your office with fever, chills, and dysuria. Her history is notable for a prior aortic valve replacement several years ago for a congenital bicuspid valve. You suspect urosepsis—soon confirmed—but you also hear a loud systolic murmur and a prominent diastolic murmur on cardiac auscultation, consistent with aortic valve stenosis and insufficiency. Her EKG is shown below—what do you see?

Her EKG shows a normal PR interval (look closely; the P waves are tiny but they are there) and the classic rabbit ears of right bundle branch block. Fortunately, you have an old EKG taken a year ago, and it appears identical.

Suspecting bacterial endocarditis (fever, chills, and new heart murmurs in someone with a valve replacement), you draw blood cultures and send her to the hospital. A echocardiogram reveals an aortic valve vegetation, and the blood cultures grow out Enterococcus faecium, a common culprit in this setting. Antibiotics are begun, and an EKG taken 24 hours later looks like this—now what do you see?

Her PR interval is now increased—she has first-degree AV block. Although in most settings this is a benign finding, in a patient with bacterial endocarditis it is not, and may indicate extension of the infection. Anatomy fans, please note: The aortic valve lies right adjacent to the bundle of His. The infection has extended and is now disrupting electrical conduction. This is a poor prognostic sign and mandates aggressive intervention, in Ellen’s case, the need for urgent surgical aortic valve replacement.

Because of your careful attention to her EKG and recognition of the relatively subtle progression to first-degree AV block, you have helped save her life!

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