Conduction Disturbances 20
OVERVIEW/PATHOPHYSIOLOGY
Dysrhythmias are abnormal rhythms of the heart caused by conditions that alter electrical conduction. Dysrhythmias originate in different areas of the conduction system, such as the sinus node, atrium, atrioventricular (A-V) node, His-Purkinje system, bundle branches, and ventricular tissue.
Many conditions and diseases may cause dysrhythmias; the most common are coronary artery disease (CAD) and myocardial infarction (MI). Other causes include fluid and electrolyte imbalance, hormonal imbalance, changes in oxy-genation, medications, and drug toxicity. Cardiac dysrhyth-mias may result from the following mechanisms:
Disturbances in automaticity: May involve an increase
Decreased Cardiac Output
Dysrhythmias and Conduction Disturbances165
Cardiovascular Care Plans
PART I: Medical-Surgical Nursing
Nursing Diagnosis:
Decreased Cardiac Output
related to altered rate, rhythm, or conduction or to negative inotropic changes
Desired Outcome:
Within 1 hr of treatment/intervention, the patient has improved cardiac output as evidenced by BP 90/60 mm Hg or higher, HR 60-100 bpm, and normal sinus rhythm on ECG.
ASSESSMENT/INTERVENTIONS RATIONALES
Assess the patient’s heart rhythm continuously on a monitor. This assessment will reveal whether dysrhythmias occur or increase in occurrence.
Assess BP and symptoms when dysrhythmias occur.
Report significant findings to the health care provider.
Signs of decreased cardiac output include decreased BP and symptoms such as unrelieved and prolonged palpitations, chest pain, shortness of breath, weakened and rapid pulse (more than 150 bpm), sensation of skipped beats, dizziness, and syncope.
Decreased cardiac output should be reported promptly for timely intervention, because it may be life threatening.
If symptoms of decreased cardiac output occur, prepare to transfer the patient to intensive care.
Transfer to a specialized intensive care unit for continual monitoring is essential.
Document dysrhythmias with a rhythm strip, using a 12-lead ECG as necessary.
This assessment will identify dysrhythmias and their general trend.
Monitor the patient’s laboratory data, particularly electrolyte and digoxin levels.
Serum potassium levels less than 3.5 mEq/L or more than 5.0 mEq/L can cause dysrhythmias. Digoxin toxicity may cause heart block or dysrhythmias.
Administer antidysrhythmic agents as prescribed; note patient’s response to therapy based on action of the following classifications:
Class IA: sodium channel blockers: quinidine, procainamide, disopyramide Decrease depolarization moderately and prolong repolarization.
Class IB: sodium channel blockers: phenytoin, mexiletine, tocainide Decrease depolarization and shorten repolarization.
Class IC: sodium channel blockers: encainide, flecainide, propafenone Significantly decrease depolarization with minimal effect on repolarization.
Class II: beta-blockers: propranolol, metoprolol, atenolol, acebutolol Slow sinus automaticity, slow conduction via A-V node, control ventricular response to supraventricular tachycardias, and shorten the action potential of Purkinje fibers.
Class III: potassium channel blockers: amiodarone, sotalol, ibutilide, dofetilide
Increase the action potential and refractory period of Purkinje fibers, increase ventricular fibrillation threshold, restore injured myocardial cell electrophysiology toward normal, and suppress reentrant dysrhythmias.
Class IV: calcium channel blockers: verapamil, diltiazem, nifedipine Depress automaticity in the sinoatrial (S-A) and A-V nodes, block the slow calcium current in the A-V junctional tissue, reduce conduction via the A-V node, and are useful in treating tachydysrhythmias because of A-V junction reentry. This class of drugs also vasodilates.
Monitor corrected QT interval (QTc) when initiating drugs known to cause QT prolongation (e.g., sotalol, propafenone, dofetilide, flecainide).
When QTc is prolonged, it can increase risk of dysrhythmias. QTc equals QT (in seconds) divided by the square root of the R-to-R interval (in seconds).
Provide humidified O2 as prescribed. O2 may be beneficial if dysrhythmias are related to ischemia or are causing hypoxia. Humidity helps prevent oxygen’s drying effects on oral and nasal mucosa.
Maintain a quiet environment, and administer pain medications promptly. Both stress and pain can increase sympathetic tone and cause dysrhythmias.
continued
PART I: Medical-Surgical Nursing
If life-threatening dysrhythmias occur, initiate emergency procedures and cardiopulmonary resuscitation (as indicated by advanced cardiac life support [ACLS] protocol).
This action provides circulation to vital organs and restores the heart to normal or viable rhythm.
When dysrhythmias occur, stay with the patient; provide support and reassurance while performing assessments and administering treatment.
This action reduces stress and provides comfort, which optimally will decrease dysrhythmias.
Nursing Diagnosis:
Deficient Knowledge
related to unfamiliarity with the mechanism by which dysrhythmias occur and lifestyle implications
Desired Outcome:
Within the 24-hr period before hospital discharge, the patient and signifi-cant other verbalize knowledge about causes of dysrhythmias and implications for the patient’s lifestyle modifications.
ASSESSMENT/INTERVENTIONS RATIONALES
Assess the patient’s health care literacy (language, reading, comprehension). Assess culture and culturally specific information needs.
This assessment helps ensure that information is selected and presented in a manner that is culturally and educationally appropriate.
Discuss causal mechanisms for dysrhythmias, including resulting symptoms. Use a heart model or diagrams as necessary.
This information increases the patient’s knowledge about health status. Visual aids augment understanding of verbal information.
A knowledgeable patient is more likely to adhere to the therapeutic regimen.
Teach signs and symptoms of dysrhythmias that necessitate medical attention.
Indicators such as unrelieved and prolonged palpitations, chest pain, shortness of breath, rapid pulse (more than 120 bpm), dizziness, and syncope are serious and should be reported promptly for timely intervention.
Teach the patient and significant other how to check pulse rate for a full minute.
Checking the pulse rate for a full minute ensures a better average of rate and rhythm than if it were measured for 15 seconds and multiplied by 4.
Teach about medications that will be taken after hospital discharge, including drug name, purpose, dosage, schedule, precautions, and potential side effects. Also discuss drug-drug, food-drug, and herb-drug interactions.
See Decreased Cardiac Output, earlier, for a description of these medications and their actions.
The more knowledgeable the patient is, the more likely he or she is to adhere to therapy and report side effects and complications promptly for timely intervention.
Stress that the patient will be taking long-term antidysrhythmic therapy and that it could be life threatening to stop or skip these medications without health care provider involvement.
Stopping or skipping these drugs may decrease blood levels effective for dysrhythmia suppression.
Advise about the availability of support groups and counseling; provide appropriate community referrals. Explain that anxiety and fear, along with periodic feelings of denial, depression, anger, and confusion, are normal following this experience.
Patients who survive sudden cardiac arrest may experience nightmares or other sleep disturbances at home.
Stress the importance of leading a normal and productive life. If the patient is going on vacation, advise taking along sufficient medication and investigating health care facilities in the vacation area.
This concept may be difficult to implement for patients who fear breakthrough of life-threatening dysrhythmias and alter their lives accordingly.
Advise the patient and significant other to take cardiopulmonary resuscitation classes; provide addresses for community programs.
Emergency life-saving procedures may be necessary in the future.