Wednesday, September 8, 2010

Nursing Care Plan | NCP Junctional Dysrhythmias

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 re-entry 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.

Nursing care plan assessment and physical examination
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. 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 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.

Nursing care plan primary nursing diagnosis: Altered tissue perfusion (cardiopulmonary, cerebral, renal, peripheral) related to rapid or slow heart rates.

Nursing care plan intervention and treatment plan
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. 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.

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.

Nursing care plan discharge and home health care 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.

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