EKG: Ventricular Dysrhythmias and AV Nodal Blocks

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

The ventricles are not effective pacemakers for the heart. The rate is inherently slow (20-40 beats per minute) and the contractions do not provide an efficient cardiac output. Atrial kick is absent which can decrease the cardiac output by as much as 30%. The ventricles may step in to take over the role of pacemaker if the SA node is not functional or if the impulse generated from the SA node is blocked in some way. At times the rate of the impulses is very slow and the ventricles will attempt to protect the heart through escape beats. Another reason for the ventricles to take over is when there is an irritable focus in the ventricles which can occur if an area becomes ischemic or injured.

Ventricular complexes have specific morphologic characteristics. The QRS portion of a ventricular beat is wide due to the longer conduction time. During a normal contraction, the ventricles will beat synchronously. In ventricular rhythms the normal pathway is disrupted and the ventricles can respond at different times. Therefore the QRS complex is larger than normal and carries an unusual or aberrant shape. Repolarization also occurs abnormally and the T wave will occur in the opposite direction of the QRS complex. P waves are not present (Ventricular beat).

Ventricular Dysrhythmias and AV Nodal Blocks: Ventricular beat

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Ventricular dysrhythmias can occur due to reentry problems, enhanced automaticity, or triggered activity. Each of these abnormalities in conduction has been addressed in the previous chapter.

Atrioventricular dysrhythmias will also be discussed. These occur due to blocks at the atrioventricular (AV) junction. Both ventricular dysrhythmias and atrioventricular blocks can create serious outcomes for patients. More discussion on AV blocks will be presented in this chapter.

Ventricular Dysrhythmias and AV Nodal Blocks: Ventricular Dysrhythmias

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

Ventricular Dysrhythmias and AV Nodal Blocks: Premature Ventricular Contraction

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

A premature ventricular contraction (PVC) (or “complex” since they do not always create a true contraction) occurs when there is an ectopic focus in the ventricles that produces a complex. This irritable site produces a beat that occurs earlier than expected in the cardiac cycle on the cardiac monitor or 12-lead EKG. These extra beats normally create a full compensatory pause. To determine this compensatory pause, count the distance between three normal beats on the rhythm strip. Then measure the number of blocks between three beats that includes the PVC. To accomplish this either count the blocks, use calipers or a piece of paper with a mark placed at the first and third complexes. If a full compensatory pause is present, the distances will be the same. This means that the third beat (the normal beat) comes in within the cycle at the same time that it would have if the PVC were not present. Premature atrial complexes will usually have a noncompensatory or incomplete pause (Full and incomplete compensatory pauses). A PVC that occurs within the cycle but does not have a full compensatory pause is called “interpolated.” This means it fits in between two normal complexes but does not interfere with the underlying rhythm (Interpolated PVC).

Ventricular Dysrhythmias and AV Nodal Blocks: Full and incomplete compensatory pauses

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Ventricular Dysrhythmias and AV Nodal Blocks: Interpolated PVC

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Fusion beats can also appear. These beats represent simultaneous firing of both a supraventricular and a ventricular impulse. This complex will not look like a ventricular beat or any of the normal beats that appear on the EKG tracing or cardiac monitor (Fusion beat).

Ventricular Dysrhythmias and AV Nodal Blocks: Fusion beat

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Characteristics of PVCs are:

  • Regularity: Irregular rhythm (underlying rhythm can be regular)
  • Rate: Can be normal, bradycardic, or tachycardic—dependent on underlying rhythm
  • P wave: No P waves are noted with the PVC—may be present in the underlying rhythm
  • PR interval: Not present for PVC
  • QRS complex: Usually greater than 0.12 seconds—wide and bizarre
  • QT interval: Prolonged
  • T wave: Appears as an opposite deflection of the QRS
  • ST segment: Difficult due to the bizarre presentation of the QRS

Ventricular Dysrhythmias and AV Nodal Blocks: Unifocal and multifocal PVCs

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Clinical Alert

PVCs can be unifocal or multifocal. Another term for each of these is “uniform” or “multiform”. Uniform PVCs look alike and arise from the same ectopic site. Multiform means that they have different configurations. It can signify diverse ectopic sites; however, all multiform PVCs do not always have different foci. A single ectopic site can produce multiform PVCs. When identifying rhythm strips the underlying rhythm is classified first with the PVCs mentioned second, that is, “normal sinus rhythm with frequent multifocal PVCs” or “atrial fibrillation with occasional unifocal PVCs” (Unifocal and multifocal PVCs).

Comparable to premature atrial contractions (PACs) and premature junctional contractions (PJCs), PVCs can occur as bigeminy (every other beat), trigeminy (every third beat), and quadrigeminy (every fourth beat). PVCs can also occur as a pairing or couplet—two PVCs together—or as tripling—three PVCs together. When three or more PVCs occur in a row, this is considered to be a short run or burst of ventricular tachycardia. When couplets or tripling occurs, this is considered to be a red flag that the ventricular tissue is very irritable and it may be a precursor to sustained ventricular tachycardia or ventricular fibrillation (Premature ventricular coupling).

The R-on-T phenomenon can also come about with a single PVC. When the PVC is initiated so early in the cycle that it falls on the T wave of the preceding complex, the repolarization process occurring at the end of the T wave is unable to complete and ventricular tachycardia or ventricular fibrillation can occur (R-on-T phenomenon).

PVCs can occur as protective measures as well. When the heart rates are slow and the risk is present that the heart is not experiencing sufficient numbers of contractions to supply adequate cardiac output, a ventricular beat can arise to “rescue” the heart. These ventricular beats are late in the cycle rather than early. While they may not provide as good a contraction as a normal beat, it is an attempt to help the heart rate. Do not administer medications to the patient that would destroy these escape beats. The proper treatment for these is to deal with the underlying slow rhythm so that the escape beats are not needed (Escape beat). Another interesting beat that can occur is an aberrantly conducted complex. Impulses that are generated above the ventricles can follow a deviant pathway creating a QRS complex that looks similar to a PVC. These aberrant beats will have a P wave associated with them.

Ventricular Dysrhythmias and AV Nodal Blocks: Premature ventricular coupling

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Ventricular Dysrhythmias and AV Nodal Blocks: R-on-T phenomenon

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Ventricular Dysrhythmias and AV Nodal Blocks: Escape beat

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Clinical Alert

PVCs can occur for a variety of reasons. See Causes of Premature Ventricular Contractions for etiologies. Sometimes individuals have PVCs that are simply “normal” for them. It is not considered necessary to treat all PVCs. The health care provider should talk to the patient to help determine if these extra beats are common for them. Patients are not always great historians or may not understand their past history or reasons for medications. Looking at the list of present medications the patient is taking may help to establish whether the PVCs are part of the patient’s past history or not. Also old records can assist in this process as well as communication with the patient’s primary care physician. Take into consideration symptoms or the lack of symptoms that the patient may be having. Always treat the patient, not the machines! If the patient is in the process of having an acute myocardial infarction and multiple PVCs are present, it may be in the best interests of the patient to treat these. Again, correlate the patient’s presentation with laboratory values and EKG information before deciding if PVCs need to be treated or not.

Also be sure to check the patient’s actual radial pulse with the number seen on the cardiac monitor. PVCs are not always perfusing. Just because they are seen on the screen does not mean that they are actually “working.” This is especially important with the escape beats noted above.

Patients who are symptomatic with premature ventricular contractions will complain with “palpitations” or a feeling that the heart is “flip-flopping in my chest.” They may describe it as “skipping beats” or a feeling that their heart is stopping (due to the long compensatory pause). Patients may have chest pain or discomfort associated with shortness of breath. Basic treatment for premature ventricular contractions is to treat the underlying cause and provide supportive therapy such as oxygen and pain relief. For symptomatic or concerning PVCs, medications that might be used are lidocaine and amiodarone (Cordarone).

Ventricular Dysrhythmias and AV Nodal Blocks: Causes of Premature Ventricular Contractions

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Ventricular Dysrhythmias and AV Nodal Blocks: Idioventricular Rhythm

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

When the heart is attempting to prevent ventricular standstill, escape beats as described above can occur. Three or more ventricular escape beats in a row is considered to be idioventricular rhythm or IVR. Ventricular tissue takes control when the SA and AV nodes are incapable of producing impulses or the impulses are too slow. At times the impulses are present but they are blocked from conduction. Some of the causes of this dysrhythmia are myocardial infarction or ischemia, digitalis toxicity, the use of beta-blocker medication, and metabolic disfunctions. Pacemaker malfunctions can also be an etiologic factor in this rhythm.

The QRS complexes in this rhythm are very wide and bizarre appearing and the rate is 20 to 40 beats per minute. No P waves are present. Patients in this rhythm may be unresponsive or may complain of dizziness, weakness, lightheadedness, confusion, or syncope. The decrease in cardiac output will cause hypotension and weak radial pulses.

Clinical Alert

If the patient does not have pulses, a situation called pulseless electrical activity (PEA) can occur. With this particular problem, any rhythm can be seen on the cardiac monitor or 12-lead EKG, but there is no contraction response. IVR is a common theme with pulseless electrical activity. While providing supportive cardiopulmonary resuscitation, the underlying cause must be determined and corrected to save the patient. Two mnemonics are used to remember treatable causes of PEA. These are: PATCH-4-MD and the 5 H’s and T’s. See Causes of Pulseless Electrical Activity for a listing of these potential etiologies.

The following are characteristics of idioventricular rhythm (Idioventricular rhythm):

Ventricular Dysrhythmias and AV Nodal Blocks: Idioventricular rhythm

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  • Regularity: Regular rhythm
  • Rate: 20 to 40 beats per minute
  • P wave: No P waves are noted
  • PR interval: Not present
  • QRS complex: Usually greater than 0.12 seconds—wide and bizarre
  • QT interval: Prolonged
  • T wave: Appears as an opposite deflection of the QRS
  • ST segment: Difficult due to the bizarre presentation of the QRS

Ventricular Dysrhythmias and AV Nodal Blocks: Causes of Pulseless Electrical Activity

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This dangerous dysrhythmia is often the precursor to asystole in dying patients. Atropine may be prescribed in an attempt to increase the heart rate. Do not treat this rhythm with lidocaine or other medications that might suppress its activity. A pacemaker is usually necessary for these patients. In this emergency situation, a transcutaneous pacemaker is the first choice until a temporary or permanent transvenous pacemaker can be placed.

Transcutaneous pacing is also known as external pacing. This is a life-saving procedure. If this is necessary, make sure that the patient is receiving appropriate oxygen and has a patent intravenous line. Record the rhythm via a 12-lead EKG and a rhythm strip from the cardiac monitor. The health care provider needs to be familiar with the monitor/defibrillator/pacing machine that is utilized for this process. Provide support to the patient and family. Pacing pads are placed on the patient according to the machine’s provided instructions. Avoid areas that might be open such as cuts, abrasions, sores, wounds, or abscesses. Do not place the pads over pacemaker or implanted intravenous access sites that the patient may already have in place. The pads will then need to be attached to the monitor/pacing unit by the appropriate cable. Turn power on.

The provider will prescribe a particular pacing rate to begin—usually between 60 to 80 beats per minute. At this point the health care provider can start the pacing option on the machine. The mA (milliamperes) will then need to be set. This is the amount of electrical stimulating current that must be utilized to create a pacing spike before each QRS complex. Gradually increase the mA until capture is recognized. This application of electrical current to the skin can cause a considerable amount of pain for the patient. Be sure to provide analgesia for this process if necessary. Watch for facial grimacing, coughing, chest wall movement, or complaints of pain from the patient.

Both electrical and mechanical capture must be assessed. Check the machine for electrical capture. This will be indicated by a pacer spike or blip before each QRS complex. Mechanical capture is measured by palpable pulses and a blood pressure on the patient. Level of consciousness is another good measure of positive mechanical capture. Document patient response and cardiac monitor tracing (Capture and failure to capture with transcutaneous pacemaker).

Ventricular Dysrhythmias and AV Nodal Blocks: Accelerated Idioventricular Rhythm

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

Accelerated idioventricular rhythm is also known by the initials, AIVR. This occurs when the rate of idioventricular rhythm (IVR) is over the rate of 40. This rate can reach as high as 100 to 120. Fusion beats may be seen at the beginning and end of this rhythm which usually lasts for short periods. Causes of this rhythm include acute myocardial infarction, digitalis toxicity, subarachnoid hemorrhage, cardiomyopathy, cocaine ingestion, or heart disease associated with systemic hypertension. This is a very common dysrhythmia when patients are reperfusing after administration of thrombolytics for myocardial infarctions.

Patients may complain of dizziness or lightheadedness or become hemodynamically unstable due to the decrease in cardiac output. When the atria are not participating in the creation of cardiac output, atrial kick is lost. A pacemaker may be necessary for this dysrhythmia if it persists, but it is usually an atrial pacemaker in an attempt to suppress this rhythm and allow the SA node to come back into play. Many times no treatment is necessary and it will spontaneously resolve.

Ventricular Dysrhythmias and AV Nodal Blocks: Accelerated idioventricular rhythm

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Characteristics of AIVR (Accelerated idioventricular rhythm):

  • Regularity: Regular rhythm
  • Rate: 41 to 120 beats per minute
  • P wave: No P waves are noted
  • PR interval: Not present
  • QRS complex: Usually greater than 0.12 seconds—wide and bizarre
  • QT interval: Prolonged
  • T wave: Appears as an opposite deflection of the QRS
  • ST segment: Difficult due to the bizarre presentation of the QRS

Ventricular Dysrhythmias and AV Nodal Blocks: Ventricular Tachycardia

Focus topic: Ventricular Dysrhythmias and AV Nodal Blocks

Ventricular tachycardia (VT) is also known as V-Tach. This is defined as three or more PVCs in a row with an increased rate of over 100 beats per minute. Short bursts of VT can occur or a sustained rhythm lasting greater than 30 seconds can take place. This is a life-threatening dysrhythmia in its own right and often a prodrome for ventricular fibrillation.

VT is divided into monomorphic and polymorphic types. Monomorphic VT carries QRS complexes which have the same shape and height. This uniformity is the identifying characteristic for the monomorphic type. In the polymorphic classification, two categories are present. These are separated dependent on the length of the QT interval. Normal QT interval is the first type of polymorphic VT. The second subtype is recognized by the prolonged QT interval. A further subclassification can be distinguished by whether the prolonged QT was congenital or acquired. Another term for congenital is idiopathic and the term associated with acquired is iatrogenic. (Classification of Ventricular Tachycardia). Idiopathic reasons for this dysrhythmia are imperfections within the sodium and potassium channels which cause abnormalities of the electrical conduction system.

Ventricular Dysrhythmias and AV Nodal Blocks: Classification of Ventricular Tachycardia

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Mechanically, the heart is normal, but genetic problems cause disruption in the functionality of the electrical system. These genetic mutations can occur when an individual inherits a variant gene from one parent or when they inherit variations from both parents. Some research has been done in determining if there is a correlation between this congenital problem and sudden infant death syndrome (SIDS). Iatrogenic causes are those involved with medications that can prolong the QT interval. There are over 50 medications that can cause a prolonged QT including some of those used to treat infections, diabetes, psychiatric problems, anxiety, high cholesterol, allergies, and cardiac problems.

When polymorphic ventricular tachycardia occurs with a prolonged QT interval, it is known as torsades de pointes (TdP). In this situation, the QRS complexes that are present are of varying shapes, widths, and amplitude. The name of this special VT stands for “twisting of the points.” This classification of polymorphic VT is also known as long QT syndrome (LQTS).

Factors that are present with ventricular tachycardia are listed as follows (Monomorphic ventricular tachycardia and Polymorphic ventricular tachycardia):

  • Regularity: Regular rhythm with monomorphic/or can be irregular with polymorphic
  • Rate: 101 to 250 beats per minute (monomorphic), 150 to 300 beats per minute (polymorphic)
  • P wave: No P waves are noted
  • PR interval: Not present
  • QRS complex: Greater than 0.12 seconds—wide and bizarre (variations in size, height, shape with polymorphic)
  • QT interval: Unmeasurable
  • T wave: Appears as an opposite deflection of the QRS
  • ST segment: Difficult due to the bizarre presentation of the QRS

Ventricular Dysrhythmias and AV Nodal Blocks: Monomorphic ventricular tachycardia

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Ventricular Dysrhythmias and AV Nodal Blocks: Polymorphic ventricular tachycardia

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Clinical Alert

Treatment for VT is dependent on whether monomorphic or polymorphic VT is present, the length of the QT interval, and the patient’s response. Patients who have ventricular tachycardia can be pulseless and apneic or may maintain a pulse and respiratory effort. If patients are hemodynamically stable, alert, and oriented during monomorphic VT, apply oxygen, obtain a patent intravenous line, and prepare for the administration of antiarrhythmics such as amiodarone (Cordarone), procainamide (Pronestyl), or sotalol (Betapace). If they become unstable, synchronized cardioversion is the treatment of choice. Patients can be considered to be unstable when they have symptoms such as chest pain, shortness of breath, mental status changes, and hypotension. Those who are pulseless and apneic, require immediate defibrillation. Patients with polymorphic VT should receive defibrillation.

Patients who are in ventricular tachycardia can have chest pain, dizziness, altered mentation, shortness of breath, and hypotension. They can also have rapid onset of syncope and sudden death. It is important to determine whether the patient has a prolonged QT interval or not when treating these patients. If possible, an EKG or cardiac monitor tracing before the onset of the VT can help in assessing this. This is important when medications are prescribed post treatment. For those patients who are in torsades de pointes, magnesium is the drug of choice. Potassium chloride can also be used in this circumstance. Amiodarone, which might be used for VT, is inappropriate for torsades de pointes. This drug can actually prolong the QT interval and create a decline in the treatment of the VT rhythm. Search for electrolyte disturbances and correct these as well as remove medications which the patient may have been taking, that can prolong the QT interval. Overdrive pacing can also be performed which will help to eliminate or stop the triggering cause. The patient may also require the implantation of a cardioverter-defibrillator.

Some causes of VT include the following:

  • Myocardial infarction
  • Cardiomyopathy
  • Overdoses of medications such as tricyclics or digitalis
  • Street drugs such as cocaine
  • Valve diseases
  • Blunt cardiac injury
  • Electrolyte imbalances
  • Acid–base imbalances

LQTS should be suspected in young people who have syncopal episodes, especially if it occurs during activities, outbreaks of anger, loud noises, and tense situations. Family histories should be explored for instances of sudden death. LQTS should be suspected in children who present in cardiac arrest with no other explainable cause.

Clinical Alert

Wide QRS tachycardia should be assumed to be VT until proven otherwise. It is often difficult to distinguish between VT and supraventricular tachycardia that has an intraventricular conduction defect.

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