EKG: Atrial/AV Nodal and Junctional Dysrhythmias

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Patients who present with PSVT are usually symptomatic. They may complain of dizziness, shortness of breath, chest discomfort, palpitations, lightheadedness, near syncope, syncopal episodes, anxiety, heart failure, decreased mentation, nausea, vomiting, and general weakness. The health care provide may be able to see the heart beats in the neck (carotid artery). Hypotension ca also occur and is a good sign that the patient is not tolerating the fast rhythm.

Treatments for PSVT include Vagal maneuvers which include massaging the carotid artery, placing the patient’s face in ice water or using ice to the face, Valsalva’s maneuver, having the patient cough or hold their breath, or producing gagging in the patient by the use of a tongue blade. These vagal maneuvers stimulate the baroreceptors, located in the carotid arteries and aortic arch, which in turn incites the vagus nerve to slow the heart rate. The right-sided vagus nerve is thought to have more filaments in the SA node and atrial tissue and the left-sided vagus nerve contributes more to the AV node and ventricular muscle.

Other treatment options include the use of Adenocard (adenosine), diltiazem (Cardizem), synchronized cardioversion, and catheter ablation. See Treatment Options for Supraventricular Tachycardias for procedures, physiological responses, responsibilities for the health care provider, and special instructions/cautions to be observed for each of these treatment options.

 Clinical Alert

Do not use Adenosine (Adenocard) on patients with Wolff-Parkinson-White (WPW) syndrome. Any medication that slows the conduction through the AV node can actually speed up the use of the accessory pathway and cause an increase in the already high speed rate. Other medications to avoid include digitalis (Digoxin) and diltiazem (Cardizem).

Contents

Atrial/AV Nodal and Junctional Dysrhythmias: Treatment Options for Supraventricular Tachycardias

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias1Atrial/AV Nodal and Junctional Dysrhythmias1Atrial/AV Nodal and Junctional Dysrhythmias11

Atrial/AV Nodal and Junctional Dysrhythmias: Atrial Fibrillation

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial fibrillation, a common dysrhythmia, can be caused by either a reentry problem or the rapid firing of ectopic sites within the atrial tissue (altered automaticity). When this rhythm occurs, there is a loss of atrial kick and stroke volume, and cardiac output can suffer. The atria are not able to produce good quality contractions during this dysrhythmia. They are in a state of quivering or fibrillation and therefore, no discernible P waves are present in this rhythm. A wavy or straight line (fibrillatory waves or f waves) between R waves is seen which is very irregular. These waves may be large (coarse A fib) or small (fine A fib). The AV node protects the heart by blocking the hundreds of chaotic impulses which are rapidly firing at that time. Intermittent impulses are conducted through to the ventricles. The atrial rate can in fact rise as far as 400 to 600 beats per minute. The ventricular rate will vary dependent on the rate of block in the AV node. This rhythm can occur with WPW as well which can then progress to ventricular tachycardia. This is contingent on the refractoriness of the bundle of Kent as the impulses are directed through this passageway.

Clinical Alert

Heart rates can vary with atrial fibrillation. When the heart rate is under 100 beats per minute, it is said to be “controlled.” Over 100 beats per minute constitutes an “uncontrolled” atrial fibrillation. Heart rates over 100 beats per minute are also classified as RVR or rapid ventricular response. Bradycardic rates can also be realized in this rhythm. When counting rates for this type of rhythm the rule of counting R waves in a 6-second strip is usually utilized due to the irregularity. This will provide an average of the rate. The small or large box method can be utilized as well. When this is performed, a range of the pulse rate is obtained. The health care provider will notice that often a wide range will be present with this method. It is not unusual to document “heart rate ranges from mid 70’s to 120” or more specific numbers may be obtained using the box method between two complexes.

The cornerstone of characteristics for this rhythm is the irregularly irregular rhythm and the loss of the P wave. The features are as follows (Controlled atrial fibrillation and Uncontrolled atrial fibrillation (RVR)):

  • Regularity: Irregularly irregular
  • Rate: Atrial—400 to 600 beats per minute. Ventricular—varies
  • P wave: Undetectable
  • PR interval: Not measurable
  • QRS complex: Less than 0.10 seconds
  • QT interval: Not measurable
  • T wave: Undetectable
  • ST segment: Can be depressed

 

Atrial/AV Nodal and Junctional Dysrhythmias: Controlled atrial fibrillation

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias: Uncontrolled atrial fibrillation (RVR)

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Atrial fibrillation can occur in short episodes or can become a sustained rhythm. New onset atrial fibrillation is especially concerning. In older patients and those who have underlying cardiac disease, the loss of cardiac output associated with this rhythm, particularly with the faster rhythms, can place these populations of patients at high risk for complications. Causes of Atrial Fibrillation includes several disease processes which can instigate atrial fibrillation.

On occasion normal healthy individuals will develop atrial fibrillation associated with elevated alcohol intake, stress, or increased caffeine intake. In these instances, the rhythm is usually temporary and responds easily to medications or spontaneously converts to a normal sinus rhythm.

Atrial/AV Nodal and Junctional Dysrhythmias: Causes of Atrial Fibrillation

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Symptoms associated with atrial fibrillation can include hypotension, palpitations, syncope or near syncope, lightheadedness, dizziness, shortness of breath, chest discomfort, or fatigue. Apical and radial pulses can vary. Some patients are asymptomatic.

Clinical Alert

Health care providers should be aware that it is important to actually feel radial pulses in their patients even though machines are present to perform the function of pulse rates. An irregular radial pulse can alert the health care professional to an asymptomatic atrial fibrillation or encourage proper questioning of a patient who is unknowingly withholding information regarding symptoms.

Treating atrial fibrillation is dependent on the length of time the dysrhythmia has been present and the manner in which the patient is tolerating the abnormal rhythm. Treatment regimens consist of controlling the rate with medications such as diltiazem (Cardizem), prescribing anticoagulants, and the use of synchronized cardioversion in the face of a seriously symptomatic patient. Cardioversion can also be attempted in patients who are not responding to other treatment options. Best results for the patient are achieved with this option if the rhythm has not been present for long periods of time, especially for those who have experienced it less than 48 hours. Another treatment option may be that of catheter ablation in the electrophysiology setting.

Clinical Alert

Patients who have atrial fibrillation (or flutter) are at risk for the development of thrombi in the atria since they are not fully contracting and emptying their chambers. This is a problematic factor in caring for someone who carries this rhythm normally as well as for the patient who suddenly develops it. Thrombi can break off from the wall of either atria and be propelled into either the systemic or pulmonary system at any time. These patients are at high risk for stroke due to this phenomenon. Long term atrial fibrillation requires the use of anticoagulants to decrease the possibility of this event. If synchronized cardio-version is used after 48 hours of the onset of this dysrhythmia, anticoagulant therapy is recommended if it is possible depending on the patient’s condition. When the patient converts to a normal rhythm, the propulsion of a thrombus can occur at this time as the atria are able to contract in a better form.

Atrial/AV Nodal and Junctional Dysrhythmias: Atrial Flutter

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial flutter, a reentry rhythm, occurs when there is one ectopic focus in the atrium that is sending multiple impulses. Again, the protective AV node only allows so many of these impulses through and there is a variance in the atrial and ventricular rates. The atrial rate typically ranges from 250 to 450 beats per minute and the ventricular rate will depend on the number of impulses allowed through the AV node. When interpreting this rhythm, the “conduction” will be addressed as a ratio of atrial beats to ventricular responses such as “2:1 conduction,” or “4:1 conduction.” At times the conduction will be variable and is recorded as such, that is, “variable conduction.” It is appropriate to use the term “conduction” instead of “block” since the AV node is responding in a physiological manner, not a diseased state. A 1:1 conduction may be caused by the presence of an accessory pathway. In this situation the AV node is bypassed.

The chief identifying characteristic of this rhythm is the sawtooth pattern to the P waves. The isoelectric line is absent as these flutter waves occupy the entire period between QRS complexes. These waves are also known as F waves (capital F as opposed to lower case f for fibrillatory waves). Atrial flutter may be divided into two categories:

  • Type I indicates a reentry problem where the inciting impulse loops around one particular area in the right atrium. This produces atrial rates ranging from 250 to 350 beats per minute.
  • Type II is also known as “atypical.” Patients will have very fast atrial heart rates ranging from 350 to 450 beats per minute and may develop atrial fibrillation. The mechanism of action has not been clearly defined.

Sometimes patients will move back and forth between atrial fibrillation and atrial flutter.

Clinical Alert

When naming this rhythm it is often hard to distinguish a 2:1 or 1:1 conduction from other tachycardias. Look for the sawtooth pattern. The performance of vagal maneuvers by the physician or licensed practitioner may slow the rhythm enough to visualize the sawtooth design. Also, when vagal maneuvers are used, the rhythm will decelerate but will not convert with atrial flutter.

The following are distinguishing traits for atrial flutter (Atrial flutter with 2:1 AV conduction and Atrial flutter with variable conduction).

  • Regularity: Atrial regular—ventricular dependent on rate of AV conduction— will be regular or irregular with a variable conduction
  • Rate: Atrial—250 to 450 beats per minute. Ventricular—varies
  • P wave: Undetectable—sawtooth flutter waves
  • PR interval: Not measurable
  • QRS complex: Less than 0.10 seconds—buried flutter waves may broaden this
  • QT interval: Not measurable
  • T wave: Undetectable
  • ST segment: Unidentifiable

Atrial/AV Nodal and Junctional Dysrhythmias: Atrial flutter with 2:1 AV conduction

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias: Atrial flutter with variable conduction

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Symptoms associated with atrial flutter are the same as atrial fibrillation. Causes are similar; however, atrial flutter does not usually occur in healthy hearts. It is common with valvular diseases and post cardiac surgery. Alcohol intoxication, pulmonary emboli, and situations which produce ischemia to cardiac tissue are also common etiologies. Treatment options are similar and concern for mural thrombi (atrial chamber clots) are the same.

Atrial/AV Nodal and Junctional Dysrhythmias: Junctional Dysrhythmias

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Junctional dysrhythmias originate in the AV junction. This encompasses the area surrounding the AV node and the beginning portion of the bundle of His before it bifurcates into the two bundle branches. The job of the AV node, itself, is to delay conduction through to the ventricles, creating a situation in which the atria are able to fully contract and fill the ventricles. Optimal cardiac output depends on this and other aspects of the cardiac cycle to perform their required duties in a systematic and efficient manner. When problems occur and the cycle is interrupted, stroke volume can suffer and cardiac output can fall.

The AV node does not initiate impulses. The AV junction, however, does have pacemaker cells present which can take over when the SA node is not functioning optimally. The impulse rate for the junctional area is 40 to 60 beats per minute. When impulses are generated in this area, depolarization will progress in a different manner. One situation which can occur is that in which the stimulus will proceed in a retrograde or backward direction causing the atria to depolarize first, but a P wave that is negative in deflection will be produced in a normally upright P wave lead such as lead II. (Some abnormalities in the atria may create a negative deflection in the P wave. The PR interval that is very short—<0.12 seconds—is the key to proper interpretation that this complex did indeed originate in the AV junction.) The second situation in which the ventricles are depolarized first produces a P wave that occurs after instead of prior to the QRS complex. The last situation which can come about is when both the atria and ventricles are depolarized at the same time generating a P wave that is buried within the QRS complex (P wave formation in junctional tissue).

Atrial/AV Nodal and Junctional Dysrhythmias: P wave formation in junctional tissue

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias: Junctional Rhythm

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Junctional rhythms (also known as junctional escape rhythms) can occur in which the P waves are presented as above. The intrinsic rate of the junctional pacemakers is 40 to 60 beats per minute (can be as high as 50-80 beats per minute in children).

P waves that occur before, after, or buried within the QRS complex and a slow heart rate are the identifying characteristics of a junctional rhythm. Rates below 40 beats per minute are considered to be junctional bradycardia. Junctional rhythms that have heart rates above 60 beats per minute are considered to be accelerated. These rates usually are within the parameters of 60 to 100 beats per minute. In this situation the bundle of His is experiencing enhanced automaticity.

The following are the basic factors present in a junctional rhythm (Junctional rhythm):

  • Regularity: Regular
  • Rate: 40 to 60 beats per minute (unless bradycardic or accelerated)
  • P wave: Will either be negative deflection (in leads II, III, aVF), after QRS, or embedded in QRS
  • PR interval: Less than 0.12 seconds if seen before QRS—no PR interval if seen after QRS or embedded in QRS
  • QRS complex: Less than 0.10 seconds (unless aberrant conduction)
  • QT interval: Usually normal
  • T wave: Normal—may be distorted if P wave present after QRS
  • ST segment: Normal—may be distorted if P wave present after QRS

Atrial/AV Nodal and Junctional Dysrhythmias: Junctional rhythm

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Junctional rhythms occur when the SA node is not performing its function of impulse generator. This can happen as a response to sick sinus syndrome, hypoxia, digoxin toxicity, hypokalemia, inferior or posterior wall myocardial infarction, rheumatic heart disease, vagal stimulation (increased parasympathetic tone), or use of calcium-channel or beta-blockers. Symptoms of decreased cardiac output can take place. Treatment options for this rhythm include treating the cause and the use of atropine sulfate, dopamine, or epinephrine or the use of a pacemaker.

Atrial/AV Nodal and Junctional Dysrhythmias: Premature Junctional Contraction

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Just as a premature atrial contraction appears early in the context of the underlying rhythm, a premature junctional contraction (PJC) will do the same. The QRS will have similar morphology to the normal QRS complexes. The pause that occurs after the early beat is noncompensatory as described earlier in this chapter with the premature atrial contraction information. At times the QRS may be wide due to aberrant conduction through the ventricles. Most premature junctional beats are of normal width. This abnormality is the presence of one or more extra complexes and therefore the original or underlying rhythm is identified first with the addition of “occasional PJCs” or “multiple PJCs.”

Atrial/AV Nodal and Junctional Dysrhythmias: Normal sinus rhythm with premature junctional complexes

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Characteristics of premature junctional contractions are (Normal sinus rhythm with premature junctional complexes):

  • Regularity: Underlying rhythm may be regular—PJC creates irregularity
  • Rate: Depends on underlying rhythm
  • P wave: Will either be negative deflection (in leads II, III, and aVF), after QRS, or embedded in QRS
  • PR interval: Less than 0.12 seconds if seen before QRS—no PR interval if seen after QRS or embedded in QRS
  • QRS complex: Less than 0.10 seconds (unless aberrant conduction)
  • QT interval: Usually normal
  • T wave: Normal—may be distorted if P wave present after QRS
  • ST segment: Normal—may be distorted if P wave present after QRS

Similarities are present between PJCs and PACs regarding symptomatology and causes. Increased intake of caffeine, nicotine, and alcohol can bring on these extra beats as well as heart failure, fatigue, inferior myocardial infarction, valve diseases, hypoxia, coronary artery disease, post cardiac surgery, and digitalis toxicity. Treating the underlying cause is the most important therapeutic intervention. Watch the patient for signs of decreased cardiac output if the PJCs are extremely frequent.

Atrial/AV Nodal and Junctional Dysrhythmias: Junctional Tachycardia

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

When at least three premature junctional contractions occur in a row with a heart rate that exceeds 100 beats per minute, it is considered to be a junctional tachycardia. In this condition, enhanced automaticity is behind the irritable focus in the AV junction. Both paroxysmal and nonparoxysmal junctional tachycardia can present. Nonparoxysmal rates can range from 100 to 140 beats per minute and are usually triggered by an accelerated junctional rhythm that increasingly speeds up. Paroxysmal rates can exceed 140 beats per minute and are usually unexpectedly started by a premature junctional contraction. Once rates surpass 150 beats per minute, it is often difficult to establish the actual cardiac tissue responsible for the dysrhythmia.

Unique traits of this dysrhythmia are (Junctional tachycardia):

  • Regularity: Regular
  • Rate: 100 to 180 beats per minute
  • P wave: Will either be negative deflection (in leads II, III, and aVF ), after QRS, or embedded in QRS
  • PR interval: Less than 0.12 seconds if seen before QRS—no PR interval if seen after QRS or embedded in QRS
  • QRS complex: Less than 0.10 seconds (unless aberrant conduction)
  • QT interval: Usually normal
  • T wave: Normal—may be distorted if P wave present after QRS or the rate is too fast
  • ST segment: Normal—may be distorted if P wave present after QRS or the rate is too fast

Atrial/AV Nodal and Junctional Dysrhythmias: Junctional tachycardia

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Atrial/AV Nodal and Junctional Dysrhythmias

Etiologies for junctional tachycardia consist of digoxin toxicity, inferior or posterior myocardial infarctions, heart failure, congenital heart disease processes, administration of theophylline based medications, or cardiac surgery (may cause AV junctional swelling). The patient may complain of lightheadedness, palpitations, anxiety, or chest pain/discomfort and may have changes associated with a decreased cardiac output such as hypotension. This can cause increased strain on a heart that is already in a stressed situation when accompanied by a myocardial infarction and can extend the size of the initial infarction. Treatments presented to treat tachycardias previously can be attempted with this tachycardia as well.

Clinical Alert

When dysrhythmias occur due to digitalis toxicity, medications such as Digibind or DigiFab (digoxin immune fab) can be used to treat the process. Be aware that if the patient is showing signs of heart failure, these medications can precipitate an increase in the symptoms.

[sociallocker]

Atrial/AV Nodal and Junctional Dysrhythmias: Conclusion

Focus topic: Atrial/AV Nodal and Junctional Dysrhythmias

Dysrhythmias can occur from several different foci in the atrium and the AV nodal area. These can occur for a variety of reasons within the tissue and arise from many disease processes. Some of the key points of this chapter are:

  • Atrial and AV nodal rhythms are also known as supraventricular.
  • Atrial rhythms will have different foci in the atria than the SA node.
  • End cardiac output is usually affected due to the loss of atrial kick with these rhythms.
  • Atrial dysrhythmias arise from one of three causes: enhanced automaticity, reentry rhythms, and triggered activity.
  • A premature atrial contraction (PAC) comes early in the rhythm cycle and looks like the other atrial beats.
  • Premature contractions are also called premature complexes since not all of them always cause a contraction.
  • A PAC may be a forerunner of another rhythm such as atrial fibrillation or atrial flutter.
  • Causes of PACs include: atrial enlargement, valvular disease, medication toxicities, electrolyte imbalances, and hyperthyroidism as well as increased intake of caffeine or nicotine.
  • Sometimes healthy individuals will have PACs without adverse effects.
  • Patients will have the feeling of a skipped beat or palpitations with premature beats.
  • A noncompensatory pause occurs after a PAC.
  • When an extra or premature beat occurs after each regular beat, it is known as bigeminy.
  • WAP is wandering atrial pacemaker and means that the origination of the impulse is changing from one place to the other.
  • The morphology of the P waves changes in wandering atrial pacemaker depending on the impulse generating site.
  • Wandering atrial pacemaker can be a normal variant for athletes or can occur during the sleep cycle.
  • At least three distinct P waves are seen with WAP.
  • Wandering atrial pacemaker at a rate greater than 100 beats per minute constitutes multifocal atrial tachycardia.
  • Chronic obstructive pulmonary disease is one of the major causes of multifocal atrial tachycardia.
  • Treatment for multifocal atrial tachycardia is to control the rate and resolve the underlying problem.
  • Atrial tachycardia occurs at rates of 150 to 250 beats per minute.
  • Atrial tachycardia has a regular rhythm.
  • It may be difficult to see the P wave in atrial tachycardia due to it being lost or buried in the T wave.
  • Paroxysmal atrial tachycardia (PAT) can occur with a sudden beginning and ending of the fast rhythm.
  • PAT will not respond as well to vagal maneuvers as paroxysmal supraventricular tachycardia (PSVT).
  • Atrial tachycardia with block occurs when the AV node protects the heart by blocking some of the fast impulses coming from the atria.
  • Fast rhythms are often difficult to analyze and can therefore cause differences of opinion.
  • P waves are not present in a supraventricular tachycardia.
  • Two types of PSVT are AV nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT).
  • In AVNRT two pathways are present—one that is fast and one that is slow.
  • The two factors present in AVNRT are the speed of the impulse and the refractory time of each pathway.
  • A loop is formed in AVNRT.
  • AVRT is a type of pre-excitation passageway.
  • Wolff-Parkinson-White (WPW) syndrome is a form of AVRT.
  • The impulse for Wolff-Parkinson-White (WPW) syndrome travels through the bundle of Kent.
  • Important factors with Wolff-Parkinson-White (WPW) syndrome are short PR interval, presence of a delta wave, and a wide QRS.
  • PSVT usually has rates of 150 to 250 beats per minute.
  • Patients with PSVT are usually symptomatic.
  • Hypotension can occur with PSVT.
  • Treatments for PSVT can include vagal maneuvers, the use of Adenocard (adenosine), synchronized cardioversion, and catheter ablation.
  • Do not use Adenocard (adenosine) on patients with Wolff-Parkinson- White (WPW) syndrome. This can speed up the heart rate.
  • Carotid massage is a physician procedure.
  • Bradycardia or asystole can occur with vagal maneuvers.
  • Carotid massage should be used with great caution in the older patient.
  • Adenocard (adenosine) must be given rapidly followed by the administration of a 20 to 30 mL bolus of normal saline (NS) and NS drip at a wide open rate.
  • A short episode of asystole will precede the return of a normal sinus rhythm with Adenocard (adenosine).
  • Always be sure to prepare the patient who is receiving administration of Adenocard (adenosine).
  • With synchronized cardioversion the paddles must be held on to the chest and both buttons pushed until the energy load has been delivered.
  • The “sync” button must be pushed prior to charging the paddles for the delivery of a synchronized shock.
  • The machine being used to deliver the synchronized cardioversion energy must be recognizing each R wave prior to delivery of the shock.
  • It is best to sedate patients who are receiving synchronized cardioversion.
  • There are different amounts of joules delivered to different types of rhythms with synchronized cardioversion.
  • In atrial fibrillation, the atria are firing so fast that the atria are quivering rather than actually contracting.
  • The ventricular rate in atrial fibrillation is much lower than the atrial rate.
  • The rhythm in atrial fibrillation is irregularly irregular.
  • If a patient is displaying atrial fibrillation at ventricular rates greater than 100 beats per minute, they are said to be “uncontrolled.”
  • No P waves are discernible with atrial fibrillation.
  • Mural thrombi can develop in patients who are experiencing sustained atrial fibrillation.
  • Mural thrombi can be expelled into the pulmonary or systemic circulation and cause disease processes such as strokes.
  • In atrial flutter, the P waves take on a distinct sawtooth pattern.
  • Conduction through the AV node in atrial flutter will cause a 2:1, 3:1, or 4:1 conduction. This conduction can also be variable.
  • The P waves in atrial flutter are called flutter waves.
  • Two types of atrial flutter are: Type I—rates of 250 to 350 and Type II— rates of 350 to 450 beats per minute.
  • Vagal maneuvers will not convert atrial flutter but may slow it down enough to visualize the sawtooth pattern.
  • Junctional dysrhythmias originate in the AV junction.
  • The AV node itself does not have pacemaker cells. The AV junction area does have pacemaker cells.
  • In a junctional rhythm, the P wave will come either before the QRS, but will be very short and negative, come after the QRS, or be buried within the QRS.
  • The intrinsic rate of the junctional tissue is 40 to 60 beats per minute in the adult patient.
  • Junctional pacemaker cells come into play when the SA node is not functioning correctly.
  • Premature junctional contractions come early in the cycle of the underlying rhythm—just like a premature atrial contraction.
  • Many different disease processes can cause premature junctional contractions as well as intake of caffeine, nicotine, or alcohol.
  • Three premature junctional contractions in a row can constitute junctional tachycardia.
  • With junctional tachycardia rates can surpass 150 beats per minute.
  • The use of Digibind or DigFab, used to treat digitalis toxicity, can precipitate an exacerbation of heart failure.
[/sociallocker]

FURTHER READING /STUDY:

Resources:

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.