3 Cardiac Arrhythmias Nursing Care Plans

Risk for Decreased Cardiac Output

Irregular heart rhythm can impair the heart’s ability to effectively pump blood, resulting in decreased oxygen and nutrient delivery to essential organs and decreased blood flow to the body. Effective management and treatment of cardiac dysrhythmias are essential for lowering the risk of decreased cardiac output and sustaining good cardiovascular health.

Nursing Diagnosis

• Risk for Decreased Cardiac Output

Risk factors may include

• Altered electrical conduction
• Reduced myocardial contractility

Possibly evidenced by

• Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as the problem has not occurred, and nursing interventions are directed at prevention.

Desired Outcomes

• The client will maintain/achieve an adequate cardiac output as evidenced by BP/pulse within normal range, adequate urinary output, palpable pulses of equal quality, and usual level of mentation.
• The client will display reduced frequency/absence of dysrhythmia(s).
• The client will participate in activities that reduce myocardial workload.

Nursing Assessement and Rationales

1. Palpate pulses (radial, carotid, femoral, dorsalis pedis), noting rate, regularity, amplitude (full or thready), and symmetry. Document the presence of pulsus alternans, bigeminal pulse, or pulse deficit.
Differences in pulse equality, rate, and regularity are indicative of the effect on the systemic or peripheral circulation of altered cardiac output.

2. Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, and dropped beats.
Specific dysrhythmias are more clearly detected audibly than by palpation. Hearing extra heartbeats or dropped beats helps identify dysrhythmias in the unmonitored patient.

3. Monitor vital signs. Assess the adequacy of cardiac output and tissue perfusion, noting significant variations in BP/pulse rate equality, respirations, changes in skin color, temperature, level of consciousness, sensorium, and urine output during episodes of dysrhythmias.
Although not all dysrhythmias are life-threatening, immediate treatment may be required to terminate dysrhythmia in the presence of alterations in cardiac output and tissue perfusion.

4. Determine the type of dysrhythmia and document it with a rhythm strip (if cardiac/telemetry monitoring is available):

4.1. Sinus tachycardia
Useful in determining the need for/type of intervention required. Tachycardia can occur in response to stress, pain, fever, infection, coronary artery blockage, valvular dysfunction, hypo­volemia, hypoxia, or as a result of decreased vagal tone or of increased sympathetic nervous system activity associated with the release of catecholamines. Although it generally does not require treatment, persistent tachycardia may worsen underlying pathology in patients with ischemic heart disease because of shortened diastolic filling time and increased oxygen demands. These patients may require medications.

4.2. Sinus bradycardia
Bradycardia is common in patients with acute MI (especially anterior and inferior) and is the result of excessive parasympathetic activity, blocks in conduction to the SA or AV nodes, or loss of automaticity of the heart muscle. Patients with severe heart disease may not be able to compensate for a slow rate by increasing stroke volume. Therefore, decreased cardiac output, HF, and potentially lethal ventricular dysrhythmias may occur.

4.3. Atrial dysrhythmias:

• 4.3.1. Premature Atrial Contractions (PACs)
  PACs can occur as a response to ischemia and are normally harmless but can precede or precipitate atrial fibrillation.

• 4.3.2. Atrial flutter
  Acute and chronic atrial flutter and/or fibrillation (the most common dysrhythmia) can occur with coronary artery or valvular disease and may or may not be pathological.

• 4.3.3. Atrial supraventricular tachycardias (PAT, MAT, SVT)
  Rapid atrial flutter/fibrillation reduces cardiac output as a result of the incomplete ventricular filling (shortened cardiac cycle) and increased oxygen demand.

4.4. Ventricular Dysrythmias

• 4.4.1. Premature ventricular contractions or ventricular premature beats (PVCs/VPBs), ventricular tachycardia (VT), ventricular flutter or fibrillation (VF)
  PVCs or VPBs reflect cardiac irritability and are commonly associated with MI, digitalis toxicity, coronary vasospasm, and misplaced temporary pacemaker leads. Frequent, multiple, or multifocal PVCs result in diminished cardiac output and may lead to potentially lethal dysrhythmias, e.g., VT or sudden death/cardiac arrest from ventricular flutter/fibrillation. Intractable ventricular dysrhythmias unresponsive to medication may reflect ventricular aneurysm. Polymorphic VT (torsades de pointes) is recognized by the inconsistent shape of QRS complexes and is often drug-related, e.g., procainamide (Pronestyl), quinidine (Quinaglute), disopyramide (Norpace), and sotalol (Betapace). Reflect altered transmission of impulses through normal conduction channels (slowed, altered) and may be the result of MI, coronary artery disease with reduced blood supply to sinoatrial (SA) or atrioventricular (AV) nodes, drug toxicity, and sometimes cardiac surgery.

• 4.4.2. Heart blocks
  Progressing heart block is associated with slowed ventricular rates, decreased cardiac output, and potentially lethal ventricular arrhythmias or cardiac standstill.

5. Monitor laboratory studies:

• 5.1. Electrolytes
  An imbalance of electrolytes, such as potassium, magnesium, and calcium, adversely affects cardiac rhythm and contractility. Electrolyte imbalances can cause changes in the electrical conduction system of the heart, leading to abnormal heart rhythms.

• 5.2. Drug levels
  Reveal therapeutic or toxic levels of prescription medications or street drugs that may affect or contribute to the presence of dysrhythmias.

Nursing Interventions and Rationales

Cardiac arrhythmias are disturbances in the normal heart rhythm. Nursing interventions for managing these conditions involve monitoring and managing symptoms, administering medications and treatments, and providing patient education. The aim is to control the arrhythmia, prevent complications, and improve the patient’s quality of life. Effective nursing care also involves working closely with the healthcare team to develop an individualized care plan and ensure proper communication and coordination of care.

1. Provide a quiet and calm environment. Review reasons for the limitation of activities during the acute phase.
Reduces stimulation and release of stress-related catecholamines, which can cause or aggravate dysrhythmias and vasoconstriction, increasing myocardial workload.

2. Demonstrate and encourage the use of stress management behaviors: relaxation techniques, guided imagery, and slow/deep breathing.
Promotes patient participation in exerting some sense of control in a stressful situation.

3. Investigate reports of chest pain, documenting location, duration, intensity (0–10 scale), and relieving or aggravating factors. Note nonverbal pain cues: facial grimacing, crying, changes in BP/heart rate.
Reasons for chest pain are variable and depend on the underlying cause. However, chest pain may indicate ischemia due to altered electrical conduction, decreased myocardial perfusion, or increased oxygen need.

4. Be prepared to initiate cardiopulmonary resuscitation (CPR) as indicated.
The development of life-threatening dysrhythmias requires prompt intervention to prevent ischemic damage/death.

5. Administer supplemental oxygen as indicated.
Increases the amount of oxygen available for myocardial uptake, which decreases irritability caused by hypoxia.

6. Administer medications for cardiac arrhythmias as indicated:

• 6.1. Potassium
  Dysrhythmias are generally treated symptomatically. Correction of hypokalemia may be sufficient to terminate some ventricular dysrhythmias. Potassium imbalance is the number one cause of atrial fibrillation.
  
• 6.2. Antidysrhythmics. Antidysrhythmics are medications used to regulate heart rhythm and treat various types of arrhythmias. These include:
  • 6.2.1. Class I drugs.
    Class I drugs depress depolarization and alter repolarization, stabilizing the cell. These drugs are divided into groups a, b, and c, based on their unique effects. These drugs increase action potential, duration, and effective refractory period and decrease membrane responsiveness, prolonging both QRS complex and QT interval. Useful for the treatment of atrial and ventricular premature beats, and repetitive arrhythmias (atrial tachycardias and atrial flutter or fibrillation). Myocardial depressant effects may be potentiated when class Ia drugs are used in conjunction with medications possessing similar properties.
    • Class Ia drugs: disopyramide (Norpace), procainamide (Pronestyl, Procan SR), quinidine (Quinaglute, Cardioquin)
      These drugs shorten the duration of the refractory period (QT interval), and their action depends on the tissue affected and the level of extracellular potassium.
    • Class Ib: lidocaine (Xylocaine), phenytoin (Dilantin), tocainide (Tonocard), mexiletine (Mexitil); moricizine (Ethmozine)
      Drugs of choice for ventricular dysrhythmias are also effective for automatic and reentrant arrhythmias and digitalis-induced dysrhythmias. These drugs may aggravate myocardial depression.
    • Class Ic: flecainide (Tambocor), propafenone (Rythmol), encainide (Enkaid)
      These drugs slow conduction by depressing SA node automaticity and decreasing conduction velocity through the atria, ventricles, and Purkinje fibers. The result is a prolongation of the PR interval and a lengthening of the QRS complex. They suppress and prevent all types of ventricular dysrhythmias. Flecainide increases the risk of drug-induced dysrhythmias post-MI. Propafenone can worsen or cause new dysrhythmias, a tendency called the “proarrhythmic effect.” Encainide is available only for patients who demonstrated good results before the drug was removed from the market.
  • 6.2.2. Class II drugs: atenolol (Tenormin), propranolol (Inderal), nadolol (Corgard), acebutolol (Sectral), esmolol (Brevibloc), sotalol (Betapace); bisoprolol (Zebeta)
    Beta-adrenergic blockers have antiadrenergic properties and decrease automaticity. Therefore, they are useful in the treatment of dysrhythmias caused by SA and AV node dysfunction (SVTs, atrial flutter, or fibrillation). These drugs may exacerbate bradycardia and cause myocardial depression, especially when combined with drugs that have similar properties.
  • 6.2.3. Class III drugs:  bretylium tosylate (Bretylol), amiodarone (Cordarone), sotalol (Betapace), ibutilide (Corvert)
    These drugs prolong the refractory period and action potential duration, consequently prolonging the QT interval. They are used to terminate ventricular fibrillation and other life-threatening ventricular dysrhythmias or sustained ventricular tachyarrhythmias, especially when lidocaine and procainamide are not effective. Sotalol is a nonselective beta-blocker with characteristics of both class II and class III.
  • 6.2.4. Class IV drugs: verapamil (Calan), nifedipine (Procardia), diltiazem (Cardizem)
    Calcium antagonists (also called calcium channel blockers) slow conduction time through the AV node (prolonging PR interval) to decrease ventricular response in SVTs, and atrial flutter/fibrillation. Calan and Cardizem may be used for bedside conversion of acute atrial fibrillation.
  • 6.2.5. Class V drugs:  atropine sulfate, isoproterenol (Isuprel)
    Miscellaneous drugs are useful in treating bradycardia by increasing SA and AV conduction and enhancing automaticity.
    
• 6.3. Cardiac glycosides: digoxin (Lanoxin)
  Cardiac glycosides may be used alone or in combination with other antiarrhythmic drugs to reduce ventricular rate in the presence of uncontrolled or poorly tolerated atrial tachycardias or flutter and fibrillation. First-line treatment for paroxysmal supraventricular tachycardia (PVST).
  
• 6.4. Adenosine (Adenocard)
  Slows conduction and interrupts reentry pathways in the AV node. Note: Contraindicated in patients with second or third-degree heart block or those with sick sinus syndrome who do not have a functioning pacemaker.

7. Prepare and assist with elective cardioversion.
May be used in atrial fibrillation or certain unstable dysrhythmias to restore normal heart rate and relieve symptoms of heart failure.

8. Assist with insertion and maintenance of pacemaker function.
Temporary pacing may be necessary to accelerate impulse formation or override tachydysrhythmias and ectopic activity, to maintain cardiovascular function until spontaneous pacing is restored or permanent pacing is initiated.

9. Insert and maintain IV access.
Patent access line may be required for the administration of emergency drugs.

10. Prepare for invasive diagnostic procedures and surgery as indicated.
A differential diagnosis of the underlying cause may be required to formulate an appropriate treatment plan. Resection of ventricular aneurysm may be required to correct intractable ventricular dysrhythmias unresponsive to medical therapy. Surgery: CABG, may be indicated to enhance circulation to the myocardium and conduction system.

11. Prepare for implantation of a cardioverter or defibrillator (ICD) when indicated.
This device may be surgically implanted in those patients with recurrent, life-threatening ventricular dysrhythmias unresponsive to tailored drug therapy. The latest generation of devices can provide multilevel (“tiered”) therapy, that is, anti-tachycardia and anti-bradycardia pacing, cardioversion, or defibrillation, depending on how each device is programmed.