|Mean LOS:||3.5 days|
|Description:||MEDICAL: Cardiac Arrhythmias and Conduction Disorders With CC|
Cardiac rhythms that are generated from the area around the atrioventricular (AV) junction node are termed junctional dysrhythmias. For a variety of reasons, the area that surrounds the AV node may generate impulses and become the cardiac pacemaker. Impulses produced in the junction do not necessarily result in an atrial contraction that precedes the ventricular contraction. This lack of coordination leads to a loss of ventricular filling during the last part of diastole; this loss of what is termed the atrial kick may reduce cardiac output by about 20% to 25%.
The inherent rate of the junctional tissue is 40 to 60 beats per minute. When the junctional pacemaker paces at its inherent rate, it produces what is called a passive junctional rhythm or a junctional escape rhythm. When it paces between 60 and 100 beats per minute, the term accelerated junctional rhythm is used. Junctional tachycardia occurs when the junctional pacemaker paces the heart at a rate between 100 and 160 beats per minute. Isolated complexes that arise from the junctional tissue are called premature junctional complexes (PJCs) if they come earlier than the expected sinus beat or junctional escape beats if they come later.
Junctional tissue may take over as the heart’s pacemaker if the sinus node fails to produce an impulse or if that impulse is blocked in its conduction through the AV node. Junctional escape rhythms may be caused by digitalis toxicity, acute infections, oxygen deficiency, inferior wall myocardial infarction, or stimulation of the vagus nerve.
If the junctional tissue becomes irritable or increasingly automatic, it may override the sinus node and pace at a faster rate. Nonparoxysmal junctional tachycardia is often the result of enhanced automaticity, usually called irritability, which can be the result of digitalis toxicity, damage to the AV junction after an inferior myocardial infarction or rheumatic fever, or excessive administration of catecholamines or caffeine. Paroxysmal junctional tachycardia (a rapid rhythm that starts and stops suddenly) is usually the result of a reentry mechanism.
PJCs may be found in healthy individuals or they may be the result of excessive intake of stimulants such as caffeine, tobacco, or sympathomimetic drugs. Digitalis toxicity or use of alcohol may also cause PJCs. Junctional escape beats occur after pauses in the heart’s rhythm. When the sinus node fails to fire, the junctional pacemaker should take over impulse initiation. They may occur normally in people during periods of increased vagal tone (increased activity of the vagus nerve, which slows the firing of the sinoatrial node) such as during sleep.
Studies are ongoing into the inheritable origins of cardiac rhythm. No information specifically targeting the genetics of junctional rhythms is currently available. AV conduction block has been associated with mutations in the sodium channel SCN5A and transcription factors NKX2–5 and TBX5.
Gender, ethnic/racial, and life span considerations
Because of the common causes of junctional dysrhythmias, they occur more often in the elderly patient with cardiac disease. They can occur in any age group and in all races and ethnicities. In adolescent and young adult athletes, junctional escape rhythms may occur during times of increased vagal tone, particularly during sleep.
Global health considerations
No global data are available, but it is reasonable to expect that junctional dysrhythmias exist in all populations around the world.
Many patients with suspected cardiac dysrhythmias describe a history of symptoms that indicate periods of decreased cardiac output. Although some junctional dysrhythmias are asymptomatic, some patients report a history of dizziness, fatigue, activity intolerance, a “fluttering” in their chest, shortness of breath, and chest pain. In particular, question the patient about the onset, duration, and characteristics of the symptoms and the events that precipitated them. Obtain a complete history of all illnesses, dietary restrictions, and activity restrictions and a current medication history.
Symptoms are usually rate dependent and may include palpitations, dizziness, fatigue, activity intolerance, and bradycardia. A passive junctional rhythm (junctional escape rhythm) is a bradycardia. Rates between 40 and 60 beats per minute with a loss of the atrial component to ventricular filling can produce signs of low cardiac output, such as syncope or lightheadedness. A patient who is experiencing accelerated junctional rhythm with a rate between 60 and 100 beats per minute is asymptomatic if his or her cardiac status can accommodate the 20% to 25% reduction in cardiac output from loss of atrial kick.
Isolated PJCs usually produce no symptoms other than some palpitations and the sensation of a “skipped beat.” Junctional tachycardia produces symptoms common to other supraventricular tachycardias. A junctional tachycardia may produce signs of low cardiac output and poor coronary perfusion. Common symptoms include labored breathing, shortness of breath, chest pain, feeling lightheaded, lowered blood pressure, and fainting.
Patient response may vary depending on the origin of the dysrhythmia. Certainly, when the heart is beating unusually fast or slow or when palpitations are noticed, the patient may become distressed. Any disturbance in the brain’s sensory apparatus as produced by low cardiac output can intensify fear or anxiety.
|Test||Normal Result||Abnormality With Condition||Explanation|
|12-lead electrocardiogram||Regular sinus rhythm||Junctional escape: Heart rate of 40–60 beats per min with regular R to R interval; P wave may be inverted and precedes the QRS with a short PR interval||Detects specific conduction defects and monitors the patient’s cardiac response to electrolyte imbalances, drug effects, and toxicities|
|Premature junctional beats: Early beat disrupts rhythm; P wave may be inverted and precedes the QRS with a short PR interval|
|Junctional tachycardia: Ventricular rate is 100–160 beats per min and regular; P wave may be inverted and precedes the QRS with a short PR interval|
Other Tests: Pulse oximetry, ambulatory or Holter monitoring: To provide a 12- to 24-hour continuous recording of myocardial electrical activity as the patient performs normal daily activities. Two-dimensional echocardiography, stress echocardiography.
Primary nursing diagnosis
DiagnosisAltered tissue perfusion (cardiopulmonary, cerebral, renal, peripheral) related to rapid or slow heart rates
OutcomesCirculation status; Cardiac pump effectiveness; Tissue perfusion: Cardiopulmonary, Cerebral, Renal, Peripheral; Vital sign status
InterventionsCirculatory care; Dysrhythmia management; Emergency care; Vital signs monitoring; Cardiac care; Cardiac precautions; Oxygen therapy; Fluid/electrolyte management; Surveillance
Planning and implementation
Treatment of junctional dysrhythmias usually depends on the heart rate. Unless the cardiac output is compromised, treatment may not be initiated. Infrequent PJCs may be tolerated as benign.
PJCs are treated by attempting to alleviate the cause. Stimulants such as caffeine, tobacco, and sympathomimetic drugs may be discontinued. If digitalis toxicity is the cause, digitalis may be withheld. If PJCs are frequent, they may be suppressed by administration of an antidysrhythmic such as quinidine sulfate. Infrequent PJCs may not be treated.
Junctional escape rhythm is a marked bradycardia that may be treated with atropine sulfate intravenously (IV) to increase the rate. In rare circumstances, a temporary cardiac pacemaker is necessary if the bradycardia does not respond to treatment or if it is due to sick sinus syndrome.
An accelerated junctional rhythm, with a rate between 60 and 100 beats per minute, rarely compromises the cardiac output. The rhythm is usually just observed.
Paroxysmal junctional tachycardia is treated the same as any narrow QRS complex tachycardia. If the ventricular rate is faster than 150 beats per minute, cardioversion may be indicated. If the rate is less than 150, vagal maneuvers may be attempted. The drug of choice for emergency treatment is adenosine. The nurse has an important role in the collaborative management of the patient by administering medications as ordered or according to protocol in emergency situations.
|Medication or Drug Class||Dosage||Description||Rationale|
|Atropine sulfate||0.5-1 mg or 0.04 mg/kg IV q 5 min, up to 3 mg total||Anticholinergic||Accelerates heart rate if patient has symptomatic bradycardia|
|Antidysrhythmics||Varies with drug||Quinidine sulfate, phenytoin, lidocaine||Suppress frequent PJCs|
|Calcium channel blockers and beta-adrenergic blockers||Varies with drug||Verapamil, diltiazem, propranolol, esmolol, sotalol||Treat junctional tachycardia|
|Adenosine||6 mg IV over 1–3 sec; may repeat in 1–2 min||Antiarrhythmic||Suppresses paroxysmal junctional tachycardia|
Other Drugs: Other drugs used for continuing significant bradycardias no matter what the origin, particularly when accompanied by hypotension, are dopamine (5 to 20 mcg/kg per minute of IV infusion) and epinephrine (2 to 10 mcg/kg per minute of IV infusion). If the patient is digitalis toxic, digoxin immune FAB (Digibind) may be used to prevent binding of digitalis molecules to tissues.
The nurse’s role is one of monitoring and support. Support the patient who is experiencing symptoms from any rhythm disturbance. Maintain the patient’s airway, breathing, and circulation. To maximize oxygen available to the myocardium, encourage the patient to rest in bed until the symptoms are treated and subside. Remain with the patient to ensure rest and to allay anxiety. Discuss any potential precipitating factors with the patient. For some patients, strategies to reduce stress or lifestyle changes help limit the incidence of dysrhythmias. Teach the patient to reduce the amount of caffeine intake in the diet. If appropriate, encourage the patient to become involved in an exercise program or a smoking-cessation group. Provide emotional support and information about the dysrhythmia, the precipitating factors, and mechanisms to limit the dysrhythmia. If the patient is at risk for electrolyte imbalance, teach the patient any dietary considerations to prevent electrolyte depletion.
Evidence-Based Practice and Health Policy
Grosse-Wortmann, L., Kreitz, S., Grabitz, R.G., Vazquez-Jimenez, J.F., Messmer, B.J., von Bernuth, G., & Seghaye, M.C. (2010). Prevalence of and risk factors for perioperative arrhythmias in neonates and children after cardiopulmonary bypass: Continuous Holter monitoring before and for three days after surgery. Journal of Cardiothoracic Surgery, 5, 85. doi 10.1186/1749-8090-5-85
- A study among 96 neonates and 398 infants and children who underwent cardiopulmonary bypass for corrective surgery of congenital cardiac defects revealed significant risks of dysrhythmias following surgery.
- Infants and children were more likely than neonates to experience dysrhythmias within 24 hours of surgery (79.1% versus 58%; p < 0.0001); however, neonates were more likely than infants and children to experience dysrhythmias 72 hours after surgery (73.4% versus 53.2%; p = 0.0033).
- Premature atrial or junctional contractions occurred in 64% of postsurgical dysrhythmias, and accelerated junctional rhythm occurred in 23%.
- Among children and infants, those with preoperative dysrhythmias were more likely to experience postsurgical dysrhythmias compared to those who did not (68.8% versus 48.9%; p = 0.02). Preoperative dysrhythmias were experienced by 41.2% of infants and children.
- Rhythm strips: Record and analyze according to hospital protocol, note the monitoring lead and document any change in leads
- Patient symptoms and vital signs with any change or new onset of dysrhythmia
- Patient’s response to symptoms
- Patient’s response to management
Discharge and home healthcare guidelines
Make sure the patient understands the role of stimulants in generating dysrhythmias. Explain the importance of taking all medications before discharge. Explain the ordered dosage, route, action, and possible adverse effects. Teach the patient to monitor her or his pulse and to report to the physician any significant changes in rate or regularity.