Conduction Blocks

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In this chapter you will learn:

1 | what a conduction block is

2 | 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

3 | how to recognize each of these AV blocks on the EKG

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

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

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

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

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

missing 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.

missing 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 beat. (B) 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.

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May 1, 2020 | Posted by in CARDIOLOGY | Comments Off on Conduction Blocks
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