EKG: Ventricular Dysrhythmias and AV Nodal Blocks

Ventricular Fibrillation

Ventricular fibrillation (VF) can appear as either coarse or fine. This is a chaotic pattern that does not support cardiac output. Impulses from multiple foci in the ventricles create a situation in which no depolarization exists. In this life-threatening dysrhythmia, the patient is unresponsive with no respiratory effort and absent pulses. The quivering heart is in a fibrillatory pattern that has no discernible waves or complexes. There are many etiologies for ventricular fibrillation.

These include (but are not limited to) the following:

  • Ventricular tachycardia
  • Myocardial infarction
  • Electrolyte imbalances
  • Electrocution
  • Heart failure
  • Acid–base imbalances
  • Drug overdoses
  • Hypoxia
  • Medications including some antiarrhythmics

Features that are present on the EKG tracing are as follows (Coarse ventricular fibrillation and Fine ventricular fibrillation):

  • Regularity: Chaotic—irregular
  • Rate: Unable to discern
  • P wave: Not present
  • PR interval: Not present
  • QRS complex: Not present
  • QT interval: Not present
  • T wave: Not present
  • ST segment: Not present

Coarse ventricular fibrillation


Fine ventricular fibrillation


Clinical Alert

Several things can mimic the pattern of ventricular fibrillation on the cardiac monitor. Artifact, electrical interference, loss of patches, and movement of the patient having tremors or seizures can create a pattern similar to that of VF. Be sure to check the patient. Patients who are awake, alert, breathing, and speaking are not in ventricular fibrillation.

Treatment for ventricular fibrillation is included in algorithms taught in cardiac life support classes. Immediate defibrillation is the treatment of choice. Time is very important when dealing with this dysrhythmia. Provide basic cardiopulmonary resuscitation until the defibrillator or automatic external defibrillator (AED) is available. Defibrillation utilizes the same machine as when synchronized cardioversion is provided, however, the sync button is not utilized. The shock provided should cause the heart to stop (asystole), giving it an opportunity to restart with a normal pattern. Place patches or paddles as displayed on the instructions per the machine instructions. It is not necessary to have the patient on the machine monitor for this (as is done with synchronized cardioversion). Be sure to announce “all clear” or accepted phrase before delivering the shock. It is important to protect the health care providers who are assisting in the care of the patient. No one should be touching the patient when the electrical current is delivered.


Asystole is present when the EKG tracing or cardiac monitor shows a flat or nearly flat line. No electrical activity is present and the patient should be unresponsive and apneic. Some of the etiologies that can cause an asystolic rhythm are myocardial infarction, pulmonary embolus, lightening injuries, extended hypoxia, electrolyte imbalances, street drug toxicities, and acid–base disturbances and can also be the immediate transient response to the ending of a tachycardic rhythm that has been treated with medications such as Adenocard (adenosine), synchronized cardioversion, or defibrillation. Refer also to the causes that are listed in pulseless electrical activity.

Clinical Alert

When asystole is suspected on the monitor, it is essential to check the patient and to recheck the rhythm in a second lead. Fine ventricular fibrillation can mimic asystole. The patient may have pulled leads off accidentally or equipment failure may be the cause of the flat line on the monitor.

Asystole can also occur as ventricular standstill (P wave asystole). In this rhythm, P waves are present, but no ventricular activity is present. The following are the features of asystole (Asystole and Ventricular standstill):

  • Regularity: Unable to note—can have regular P waves in ventricular standstill
  • Rate: Not discernible—slow atrial activity may be noted with ventricular standstill
  • P wave: Not present—may be seen with ventricular standstill
  • PR interval: Not present
  • QRS complex: Not present
  • QT interval: Not present
  • T wave: Not present
  • ST segment: Not present



Ventricular standstill


Treat the patient in asystole with immediate cardiopulmonary resuscitation. Follow guidelines from cardiac life support classes regarding medications and treatment of potential causes.

AV Nodal Blocks

When a delay in conduction occurs within the AV node, the bundle of His, or the bundle branches, an AV nodal block is produced. Conducted impulses through this area are slower (the depolarization and repolarization process is lengthened) therefore, making this an area of opportunity for blockage of those impulses to take place. Three incomplete blocks and one complete block are involved in the descriptions of this problem within the cardiac conduction system. Each of these blocks has specific characteristics that make up the EKG features that are seen. The blocks are divided into first degree, second degree, and third degree. Second-degree blocks have two subcategories. Third-degree block is also known as complete heart block. Atrioventricular Blocks lists the types of blocks, the locations of the associated blocked areas, and the conduction that is found with each type. Patients can often tolerate these blocks and the consequences of each block revolve around the degree of the block, the rate of ventricular or junctional response, and the manner in which the patient reacts to the slowed heart rate. At other times the blocks can represent an emergent condition that must be responded to immediately.

Atrioventricular Blocks


First-Degree AV Block

First-degree AV block represents a delay or pause that occurs as the impulse attempts to cross the AV node. This can occur in some healthy individuals who are athletic (related to an increase in vagal tone) or may occur as a normal deviation during sleep when heart rates reduce. It can also occur when certain medications are taken that can increase the refractory period, such as digoxin, calcium antagonists, and beta-blockers. Other medications that may place the patient at risk for this block are quinidine (Quinaglute), procainamide (Pronestyl), sotalol (Betapace), and amiodarone (Cordarone). It can also be present with deterioration of the conduction system, a myocardial infarction (especially inferior), electrolyte disturbances (hypokalemia or hypomagnesemia), endocarditis, and myocarditis and can be a posttreatment sequelae after catheter
ablation for tachydysrhythmias.

Specific EKG tracing or cardiac monitor changes involve a lengthened or prolonged PR interval. This indicates the delay in conduction. When interpreting this rhythm, the underlying rhythm is recognized first with a notation for the first-degree block—“normal sinus rhythm with first-degree block” (First-degree AV block).

Characteristics of first-degree block are:

  • Regularity: Dependent on underlying rhythm
  • Rate: Dependent on underlying rhythm
  • P wave: Present for each QRS
  • PR interval: Prolonged—greater than 0.20 seconds
  • QRS complex: Present and dependent on underlying rhythm
  • QT interval: Normal
  • T wave: Normal
  • ST segment: Normal

First-degree AV block


Most patients who are experiencing this dysrhythmia are asymptomatic. It does bear watchful observation since it can lead to further degrees of block, especially when it is present in a patient with a myocardial infarction.

Second-Degree AV Block Type I

Second-degree AV block type I is also known as Wenckebach (so named for Dr. Wenckebach, a Dutch internist, who noted changes in the jugular pulse with the two forms of second-degree block before the advent of the electrocardiogram). The term “Mobitz” is also used with second-degree blocks since Dr. Mobitz, a German cardiologist, was able to describe the characteristics of the subclassifications of second-degree AV block on the EKG tracing. The term “Mobitz type I” is used for the changes that occur with “Type I.”

In this dysrhythmia, there is a progressive lengthening of the PR interval until a QRS complex is dropped. The abnormality occurs in the AV node. Just as R-R intervals have been measured in other rhythms, in AV blocks, the P-P intervals now become very important. If the P-P intervals are plotted on either a card or piece of paper or with calipers, it is noted that they fall regularly within the rhythm. This is also important to assist in the evaluation of the rhythm when considering a nonconducted PAC. If it were associated with a nonconducted PAC, the P wave would occur early in the cycle. In second-degree blocks, the P waves look alike as they are all coming from the SA node. The problem occurs as it attempts to conduct through the AV node. After the progressive prolongation of the P wave and the QRS complex is dropped, the series begins again until another beat is dropped. In order to identify this dysrhythmia, a rhythm strip must be explored. This cannot be recognized with only two to three beats on the 12-lead EKG. It can be suspected as the PR interval is seen to lengthen; however, to visualize the dropped beat a longer strip must be investigated. A pattern is usually set so that the dropped beat will occur in a recurring arrangement, that is, every third beat dropped, every fourth beat dropped, etc.

EKG characteristics of this rhythm are (Fig. 9–19):

  • Regularity: Atrial regular, ventricular irregular (due to dropped beat)
  • Rate: Dependent on underlying rhythm—atrial rate is greater
  • P wave: Similar in size and configuration each time
  • PR interval: Gradual prolongation until QRS complex is dropped
  • QRS complex: Not present for each P wave— normal in width
  • QT interval: Normal
  • T wave: Normal
  • ST segment: Normal

Second-degree AV block Mobitz type I/Wenckebach


Clinical Alert

Though patients can be asymptomatic with Wenckebach or Mobitz type I, some may require treatment. Slow rates associated with a drop in blood pressure or lightheadedness may require the use of a pacemaker.

Causes of second-degree AV block, Mobitz type I (Wenckebach) include certain medications, an increase in parasympathetic activity, cardiac tissue ischemia or an inferior myocardial infarction or right ventricular infarct. Be especially observant for the patient who is experiencing this associated with infarctions as they can then elevate the seriousness of the degree of block.

Second-Degree AV Block Type II

Type II second-degree AV block, also known as Mobitz type II, occurs due to a delay in conduction at the level of the bundle of His or the bundle branches. While Mobitz type I is dependent on the progressive lengthening of the PR interval, in Mobitz type II, the PR intervals are constant. Dropped beats occur throughout the rhythm strip. The P waves will again plot out at regular intervals.The ventricular rate is typically slow and irregular and is lower than the atrial rate. When the ratio of atrial beats (P wave) to ventricular beats (QRS complex) is 2:1 (two atrial beats to one ventricular beat), the ventricular rate will be regular. A situation can occur in which there are more than two beats that are dropped in succession. This is indicative of a high grade AV block and is considered more dangerous than the normal pattern of Mobitz type II. This rhythm can be a precursor to third-degree or complete heart block.

Factors that are present for second-degree AV block, Mobitz type II are (Second-degree AV block Mobitz type II):

  • Regularity: Atrial regular, ventricular irregular (due to dropped beat)— may be regular with a 2:1 ratio
  • Rate: Ventricular rate slow—atrial rate is greater
  • P wave: Similar in size and configuration each time
  • PR interval: Normal for each P wave except for the dropped beats—may be prolonged slightly, but will be constant
  • QRS complex: Not present for each P wave—usually wider—greater than 0.10 seconds
  • QT interval: Normal
  • T wave: Normal
  • ST segment: Normal

Second-degree AV block Mobitz type II


Clinical Alert

Mobitz type II can move rapidly into complete heart block. Observe the patient closely and prepare for emergent pacemaker insertion if this occurs. Atropine is not used in this dysrhythmia. This will cause the SA node to fire faster and can trigger more problems for the patient.

This type of second-degree heart block can be caused by an anterior myocardial infarction. Organic cardiac diseases such as myocarditis, endocarditis, and rheumatic fever can also cause this dysrhythmia. Sarcoidosis, Hodgkin’s lymphoma, rheumatoid arthritis, and lupus have also been noted to cause this type of AV block. Medications that may contribute to this dysrhythmia are: digoxin, calcium channel blockers, beta-blockers, and sodium channel blockers. Patients can be stable during episodes of second-degree AV block Mobitz type II. If this is the case, observe closely. If the patient is unstable including hypotension, chest pain, lightheadedness, and syncope, prepare for pacing.

Third-Degree AV Block

In third-degree or complete heart block, the atrial impulses are totally blocked. No conduction is passing through. This can happen at any level within the AV node, the bundle of His, or the bundle branches. The QRS complexes that occur can be generated from either junctional or ventricular tissue. Because of this, the QRS complexes may be narrow or wide. The cause of the block determines the level at which the block is occurring. For instance, an inferior myocardial infarction causing a complete heart block usually happens above the bundle of His. When the ventricles are responsible for the QRS complexes, the rhythm is usually more unstable. The rate is lower and the QRS is wider. An anterior myocardial infarction causing this problem usually recruits the ventricles for assistance in maintaining a pulse rate.

In complete heart block, cardiac output is not at an effective level. This is a serious situation for the patient. Not only is the rate so low that it affects the cardiac output, but atrial kick is also lost. The asynchrony between the atria and the ventricles is seen on the EKG tracing or cardiac monitor as a complete loss of association of the P waves and QRS complexes.

The following are characteristics of third-degree heart block (Complete heart block/third-degree heart block):

  • Regularity: Atrial regular, ventricular regular—independent of each other
  • Rate: Ventricular rate slow—atrial rate is greater
  • P wave: Similar in size and configuration each time
  • PR interval: None present
  • QRS complex: May be narrow wide depending on site of generated impulse
  • QT interval: May be elongated
  • T wave: Normal
  • ST segment: Normal

Complete heart block/third-degree heart block


Clinical Alert

If the rate is extremely slow, there may be “extra beats” that are escape beats. They will look like premature beats but will occur later in the cycle. It is important to not suppress these beats as they are attempting to help with cardiac output.

Patients with complete heart block can be asymptomatic. They may even remain hemodynamically stable. They will still require a pacemaker and should have close monitoring, but the pacemaker can be done on an elective basis rather than emergent. Others who are symptomatic with dizziness, dyspnea, change in mentation, chest pain, lightheadedness, hypotension, pallor, sweating, and syncope should be treated with transcutaneous pacing. A temporary pacer will need to be inserted until it is determined if the patient will require a permanent pacemaker. If it occurs with an anterior myocardial infarction, chances are that a permanent pacemaker will be necessary. Complete heart block associated with an inferior myocardial infarction may resolve and not involve a permanent pacemaker.

Another rhythm that might occur is complete AV dissociation. In this rhythm, the ventricular rate is simply faster and may be very close to the atrial rate. Consider this rhythm if the rate is faster. This can happen due to a problem with the SA node or an increased impulse generation or conduction disruption in the AV node.


Ventricular dysrhythmias and atrioventricular blocks can present serious issues for the patient experiencing them. Sometimes the patient will have no symptoms; however, the potential for deterioration is always present with these issues. The health care provider must be ready to intervene immediately when these occur. Some of the highlights of these dysrhythmias are:

  • When ventricular rhythms occur, atrial kick is lost which can decrease cardiac output by 30%.
  • The SA node can cease to function or blocks can occur as the impulse attempts to be conducted through the AV node and beyond.
  • At times ventricular rhythms occur due to irritable tissue in the ventricles.
  • Ventricular beats are wide, have aberrant shapes, and no P waves associated with them.
  • PVCs do not always produce a “beat” or participate in perfusion. It is important to check the pulse on these patients.
  • PVCs should have full compensatory pause unless they are considered to be interpolated.
  • A fusion beat can occur that is a combination of a regular beat and a premature ventricular contraction.
  • PVCs can be unifocal or multifocal.
  • PVCs can occur as bigeminal, trigeminal, or quadrigeminal. They may also couple together. Three PVCs together constitutes a short burst of ventricular tachycardia.
  • An escape beat occurs when a PVC attempts to come to the rescue of a slow rate. These beats will be late rather than premature in the cycle.
  • PVCs can be normal for the patient or they can occur due to medications the patient may be taking. An acute myocardial infarction as well as other possible diagnoses can cause these.
  • Three or more escape beats together can create an idioventricular rhythm.
  • Idioventricular rhythms will cause a decrease in cardiac output and the consequences of that as demonstrated by hypotension, weak radial pulses, dizziness, lightheadedness, confusion, or syncope.
  • PEA or pulseless electrical activity can occur with any rhythm, but can commonly occur with idioventricular rhythms.
  • There are several etiologies for PEA. The mnemonic to remember these is PATCH-4-MD or the 5 H’s and 5 T’s. Idioventricular rhythm can be a precursor to asystole for patients.
  • Transcutaneous pacing is a life saving procedure in which the patient receives electrical impulses through the skin.
  • The mA on the transcutaneous pacer is the amount of electricity that must be delivered in order for the patient to attain and maintain “capture.” This can be uncomfortable for the patient.
  • When the rate of an idioventricular rhythm is over 40 beats per minute, it is known as accelerated idioventricular rhythm.
  • Accelerated idioventricular rhythms can occur with several diagnoses such as acute myocardial infarction, subarachnoid hemorrhage, and cocaine ingestion. It is also known to occur transiently with reperfusion after the administration of thrombolytics.
  • Ventricular tachycardia can be monomorphic or polymorphic.
  • Polymorphic ventricular tachycardia can occur due to a prolonged QT interval or it can be present with a normal QT interval. This can be acquired or congenital.
  • Patients in VT can be awake with a pulse or can be unresponsive and pulseless. Treatment depends on how the patient is responding.
  • For those patients who are pulseless, immediate defibrillation is necessary.
  • Torsades de pointes occurs when a long QT interval is the cause of polymorphic ventricular tachycardia.
  • Long QT syndrome can be the cause of syncopal episodes in young people. It can lead to cardiac arrest. This must be diagnosed with an EKG tracing that is performed when the patient is not in VT.
  • Ventricular fibrillation can be either coarse or fine.
  • Fine VF can be misdiagnosed as asystole.
  • Immediate defibrillation must be performed for VF.
  • Asystole occurs when there is no electrical or mechanical activity present. It is represented by a flat line on the EKG tracing.
  • Immediate CPR must be established with asystole.
  • AV nodal blocks occur when there is a delay or block in conduction through the AV node, the bundle of His, or the bundle branches.
  • First-degree AV block is represented by a prolonged PR interval on the EKG tracing or cardiac monitor. This is simply a delay in conduction.
  • Many medications can cause first-degree AV block and other AV blocks.
  • Usually no treatment is necessary for first-degree AV block.
  • Second-degree AV block is divided into Mobitz type I (also known as Wenckebach) and Mobitz type II.
  • Mobitz type I (Wenckebach) is seen on the EKG strip as a progressive prolongation of the PR interval until a beat is dropped.
  • Mobitz type II is seen as dropped beats that occur on the EKG tracing but with consistent PR intervals.
  • Both second-degree AV block, Mobitz type I, and Mobitz type II can require treatment and careful observation of the patient, but the patient may also be asymptomatic.
  • Third-degree or complete heart block is recognized on the EKG tracing or cardiac monitor as a slow rate that has no relationship between the atrial beats and ventricular complexes.
  • Patients with third-degree or complete AV block will require a pacemaker. Some may need it more emergently than others.

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