3 Cardiac Arrhythmia (Digitalis Toxicity) Nursing Care Plans

Cardiac arrhythmias, also known as cardiac dysrhythmias, are abnormal electrical conduction or automaticity changes in heart rate and rhythm. Arrhythmias vary in severity, from those that are mild, asymptomatic, and require no treatment to catastrophic ventricular fibrillation, which necessitates immediate resuscitation. It can be the result of a primary cardiac disorder, a response to a systemic condition, the result of electrolyte imbalance or drug toxicity.

Dysrhythmias vary in severity and in their effects on cardiac function, which are partially influenced by the site of origin (ventricular or supraventricular).

Nursing Care Plans

Nursing care planning for patients with cardiac arrhythmia due to digitalis toxicity includes prompt assessment of the patient’s condition, prompt treatment of symptoms, and investigation of the cause.

Below are three (3) Cardiac Arrhythmia (Digitalis Toxicity) Nursing Care Plans (NCP):

  1. Risk for Decreased Cardiac Output
  2. Risk for Poisoning
  3. Deficient Knowledge
  4. Other Possible Nursing Diagnosis
  5. See Also, Further Reading and External Resources

Nursing Priorities

  1. Prevent/treat life-threatening dysrhythmias.
  2. Support patient/SO in dealing with anxiety/fear of potentially life-threatening situation.
  3. Assist in identification of cause/precipitating factors.
  4. Review information regarding condition/prognosis/treatment regimen.

Discharge Goals

  1. Free of life-threatening dysrhythmias and complications of impaired cardiac output/tissue perfusion.
  2. Anxiety reduced/managed.
  3. Disease process, therapy needs, and prevention of complications understood.
  4. Plan in place to meet needs after discharge.

Risk for Decreased Cardiac Output: At risk for inadequate blood pumped by the heart to meet metabolic demands of the body.

Nursing Diagnosis

  • Cardiac Output, risk for decreased

Risk factors may include

  • Altered electrical conduction
  • Reduced myocardial contractility

Desired Outcomes

  • Maintain/achieve adequate cardiac output as evidenced by BP/pulse within normal range, adequate urinary output, palpable pulses of equal quality, usual level of mentation.
  • Display reduced frequency/absence of dysrhythmia(s).
  • Participate in activities that reduce myocardial workload.
Nursing Interventions Rationale
Palpate pulses (radial, carotid, femoral, dorsalis pedis), noting rate, regularity, amplitude (full or thready), and symmetry. Document presence of pulsus alternans, bigeminal pulse, or pulse deficit. Differences in equality, rate, and regularity of pulses are indicative of the effect of altered cardiac output on systemic or peripheral circulation.
Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, 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.
Monitor vital signs. Assess 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.
Determine type of dysrhythmia and document with rhythm strip (if cardiac/telemetry monitoring is available):
  • Sinus tachycardia
Useful in determining 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.
  • 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.
Atrial dysrhythmias: 
  • PACs
PACs can occur as a response to ischemia and are normally harmless but can precede or precipitate atrial fibrillation.
  • 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.
  • Atrial supraventricular tachycardias (PAT, MAT, SVT);
Rapid atrial flutter/fibrillation reduces cardiac output as a result of incomplete ventricular filling (shortened cardiac cycle) and increased oxygen demand.
Ventricular dysrhythmias:
  • 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 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.
  • Heart blocks
Progressing heart block is associated with slowed ventricular rates, decreased cardiac output, and potentially lethal ventricular arrhythmias or cardiac standstill.
Provide quiet and calm environment. Review reasons for limitation of activities during acute phase. Reduces stimulation and release of stress-related catecholamines, which can cause or aggravate dysrhythmias and vasoconstriction, increasing myocardial workload.
Demonstrate and encourage use of stress management behaviors,: relaxation techniques, guided imagery, slow/deep breathing. Promotes patient participation in exerting some sense of control in a stressful situation.
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 underlying cause. However, chest pain may indicate ischemia due to altered electrical conduction, decreased myocardial perfusion, or increased oxygen need.
Be prepared to initiate cardio-pulmonary resuscitation (CPR) as indicated. Development of life-threatening dysrhythmias requires prompt intervention to prevent ischemic damage/death.
Monitor laboratory studies:
Imbalance of electrolytes, such as potassium, magnesium, and calcium, adversely affects cardiac rhythm and contractility.
  • Drug levels
Reveal therapeutic or toxic level of prescription medications or street drugs that may affect or contribute to presence of dysrhythmias.
Administer supplemental oxygen as indicated. Increases amount of oxygen available for myocardial uptake, which decreases irritability caused by hypoxia.
Administer medications as indicated:
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.
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 treatment of atrial and ventricular premature beats, repetitive arrhythmias (atrial tachycardias and atrial flutter or fibrillation). Myocardial depressant effects may be potentiated when class Ia drugs are used in conjunction with any drugs possessing similar properties.
Class Ia: 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, they 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 prolongation of the PR interval and 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 a good result before the drug was removed from the market.
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.
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.
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, atrial flutter/fibrillation. Calan and Cardizem may be used for bedside conversion of acute atrial fibrillation.
Class V drugs:  atropine sulfate, isoproterenol (Isuprel) Miscellaneous drugs useful in treating bradycardia by increasing SA and AV conduction and enhancing automaticity.
cardiac glycosides: digoxin (Lanoxin) Cardiac glycosides may be used alone or in combination with other antiarrhythmic drugs to reduce ventricular rate in presence of uncontrolled or poorly tolerated atrial tachycardias or flutter and fibrillation. First-line treatment for paroxysmal supraventricular tachycardia (PVST).
Adenosine (Adenocard) Slows conduction and interrupts reentry pathways in 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.
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.
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.
Insert and maintain IV access. Patent access line may be required for administration of emergency drugs.
Prepare for invasive diagnostic procedures and surgery as indicated. Differential diagnosis of underlying cause may be required to formulate 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 myocardium and conduction system.
Prepare for implantation of 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, antitachycardia and antibradycardia pacing, cardioversion, or defibrillation, depending on how each device is programmed.