DISCHARGE GOALS
1. Free of life- threatening dysrhythmias and complications of impaired cardiac output and tissue perfusion.
2. Anxiety reduced and managed.
3. Disease pro cess, therapy needs, and prevention of com- plications understood.
4. Plan in place to meet needs after discharge.
NURSING PRIORITIES
1. Prevent or treat life- threatening dysrhythmias.
2. Support client and signifi cant other (SO) in dealing with anxiety and fear of potentially life- threatening situation.
3. Assist in identifi cation of cause or precipitating factors.
4. Review information regarding condition, prognosis, and treatment regimen.
W H Y I T I S D O N E (continued) W H A T I T T E L L S M E (continued)
Can help identify irregularities that can lead to sudden cardiac death in patients at risk, such as those with hypertrophic cardiomyopathy.
• Transthoracic echocardiography (TTE): Employs ultrasound waves to show heart’s size, structure, and motion.
Can rapidly provide visual information about dysrhythmia’s location and effect on cardiac function.
ACTIONS/INTERVENTIONS RATIONALE
Dysrhythmia Management NIC In de pen dent
Palpate radial, carotid, femoral, and dorsalis pedis pulses, 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 and peripheral circulation.
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 client.
Monitor vital signs. Assess adequacy of cardiac output and tissue perfusion, noting significant variations in BP, pulse rate equality, respirations, changes in skin color and temperature, level of consciousness and sensorium, and urine output during episodes of dysrhythmias.
Although not all dysrhythmias are life- threatening, immedi- ate 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 or telemetry monitoring is available:
Useful in determining need and type of intervention required.
Sinus tachycardia Tachycardia can occur in response to stress, pain, fever,
infection, coronary artery blockage, valvular dysfunction, hypovolemia, hypoxia, or because of decreased vagal tone or increased sympathetic ner vous system activity associated with the release of catecholamines. Although it generally does not require treatment, per sis tent tachycar- dia may worsen under lying pathology in clients with ischemic heart disease because of shortened diastolic filling time and increased oxygen demands. These clients may require medi cations.
Sinus bradycardia Bradycardia is common in clients 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.
Clients 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, such as PACs, atrial flutter, AF, and atrial supraventricular tachycardia (SVT) (i.e., paroxys- mal atrial tachycardia [PAT], multifocal atrial tachycar- dia [MAT])
PACs can occur as a response to ischemia and are normally harmless but can precede or precipitate AF. Acute and chronic atrial flutter or fibrillation (the most common dysrhythmia) can occur with coronary artery or valvular disease and may or may not be pathological. Rapid atrial flutter or fibrillation reduces cardiac output because of incomplete ventricular filling (shortened cardiac cycle) and increased oxygen demand.
Ventricular dysrhythmias, such as premature ventricular contractions (PVCs) or ventricular premature beats (VPBs), ventricular tachycardia (VT), and ventricular flutter and fibrillation (VF)
PVCs or VPBs reflect cardiac irritability and are commonly associated with MI, digoxin 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, such as VT or sudden death or cardiac arrest from ventricular flutter or VF. Note: Intractable ventricular dysrhythmias unresponsive to medi cation may reflect ventricular aneurysm. Polymorphic VT (torsades de pointes) is recognized by inconsistent shape of QRS complexes and is often related to use of certain medi cations.
(continues on page 92)
CHAPTER 2 Cardiovascular: Dysrhythmias
ACTIONS/INTERVENTIONS (continued) RATIONALE (continued)
Heart blocks Reflect altered transmission of impulses through normal
conduction channels (slowed, altered) and may be the result of MI or CAD with reduced blood supply to SA or AV nodes, drug toxicity, and sometimes cardiac surgery.
Progressing heart block is associated with slowed ventricular rates, decreased cardiac output, and poten- tially lethal ventricular dysrhythmias or cardiac standstill.
Provide calm and quiet environment. Review reasons for limitation of activities during acute phase.
Reduces stimulation and release of stress- related catechol- amines, which can cause or aggravate dysrhythmias and vasoconstriction, increasing myo car dial workload.
Demonstrate and encourage use of stress management be hav iors such as relaxation techniques; guided imagery;
and slow, deep breathing.
Promotes client participation in exerting some sense of control in a stressful situation.
Investigate reports of chest pain, documenting location, duration, intensity (0 to 10 scale), and relieving or aggra- vating factors. Note nonverbal pain cues, such as facial grimacing, crying, and changes in BP and heart rate.
Reasons for chest pain are variable and depend on under- lying cause. However, chest pain may indicate ischemia due to altered electrical conduction, decreased myo car dial perfusion, or increased oxygen need, such as impending or evolving MI.
Be prepared to initiate cardiopulmonary resuscitation (CPR), as indicated.
Development of life- threatening dysrhythmias requires prompt intervention to prevent ischemic damage or death.
Collaborative
Monitor laboratory studies, such as the following:
Electrolytes Imbalance of electrolytes, such as potassium, magnesium,
and calcium, adversely affects cardiac rhythm and contractility.
Medi cation and drug levels Reveal therapeutic and toxic level of prescription medi- cations or street drugs that may affect or contribute to presence of dysrhythmias.
Administer supplemental oxygen, as indicated. Increases amount of oxygen available for myo car dial uptake, reducing irritability caused by hypoxia.
Prepare for and assist with diagnostic and treatment procedures such as EP studies, radiofrequency ablation (RFA), and cryoablation (CA).
Treatment for several tachycardia dysrhythmias, including SVT, atrial flutter, Wolff- Parkinson- White (WPW) syn- drome, AF, and VT, is often carried out as first- line treatment via heart catheterization or angiographic procedures. After rhythm is confirmed with EP study, the client will then often have either an RFA or a CA to terminate or disrupt the dysfunctional pattern. Medi- cations may be tried first or added after ablation for increased treatment success. Note: Catheter ablation has a success rate of 95% and recurrence rate of less than 5%.
It is the preferred treatment for symptomatic patients with WPW syndrome (Helton, 2015).
Insert and maintain intravenous (IV) access. Patent access line may be required for administration of emergency drugs.
Administer medi cations, as indicated, for example:
Potassium Correction of hypokalemia may be sufficient to terminate
some ventricular dysrhythmias. Note: Potassium imbal- ance is the number one cause of AF.
Antidysrhythmics, such as the following: Antiarrhythmic drugs are used to (1) decrease or increase conduction velocity, (2) alter the excitability of cardiac cells, and (3) suppress abnormal excitability (automatic- ity). (“Antiarrhythmic Agents,” 2000–2017; Levine, 2014;
“Vaughn’s Summaries,” update 2017.)
Class I drugs Class I drugs block sodium (Na+) channels and are
subdivided.
ACTIONS/INTERVENTIONS (continued) RATIONALE (continued)
Class Ia, such as disopyramide (Norpace), procainamide (Procanabid), quinidine (Cardioquin)
These drugs increase action potential, duration, and effective refractory period and decrease membrane responsive- ness, prolonging both QRS complex and QT interval. This also results in decreasing myo car dial conduction velocity and excitability in the atria, ventricles, and accessory pathways. They suppress ec topic focal activity. Useful for treatment of atrial and ventricular premature beats and repetitive dysrhythmias, such as atrial tachycardias and atrial flutter and AF. Note: Class Ia antiarrhythmics are used less often now because of their modest effective- ness and adverse effects (Helton, 2015).
Class Ib, such as lidocaine (Xylocaine), phenytoin (Dilantin, Phenytek), and mexiletine (Mexitil)
These drugs slow conduction by depressing SA node automaticity and decreasing conduction velocity through the atria, ventricles, and Purkinje’s fibers. The result is prolongation of the PR interval and lengthening of the QRS complex. They suppress and prevent all types of ventricular dysrhythmias.
Class Ic, such as flecainide (Tambocor), propafenone (Rhythmol), and moricizine (Ethmozine)
These drugs inhibit the voltage- dependent sodium channels and prolong the depolarization phase, thus increasing conduction velocity, and have little effect on the repolar- ization phase. This makes them useful in the treatment of atrial flutter or fibrillation in clients with structurally normal hearts. Note: Flecainide increases risk of drug- induced dysrhythmias post- MI. Propafenone can worsen or cause new dysrhythmias, a tendency called the
“proarrhythmic effect.”
Class II drugs (most used), such as atenolol (Tenormin), carvedilol (Coreg), propranolol (Inderal), nadolol (Corgard), acebutolol (Sectral), and esmolol (Brevibloc)
Beta blockers have antiadrenergic properties and decrease automaticity. They reduce the rate and force of cardiac contractions, which in turn decrease cardiac output, blood pressure, and peripheral vascular re sis tance.
Therefore, they are useful in the treatment of dysrhyth- mias caused by SA and AV node dysfunction, including SVTs, atrial flutter, and AF. Note: These drugs may exacerbate bradycardia and cause myo car dial depres- sion, especially when combined with drugs that have similar properties.
Class III drugs, such as bretylium tosylate (Bretylol), amiodarone (Pacerone, Cordarone), dofetilide (Tiko- syn), sotalol (Betapace), and ibutilide (Corvert)
These drugs are potassium channel blockers; they prolong the refractory period and action potential duration, consequently prolonging the QT interval. They decrease peripheral re sis tance and increase coronary blood flow.
They have antianginal and antiadrenergic properties. They are used to terminate VF and other life- threatening ventricular dysrhythmias and sustained ventricular tachyarrhythmias, especially when lidocaine and procain- amide are not effective.
Class IV drugs, such as amlodipine (Norvasc), verapamil (Adalat, Calan), and diltiazem (Cardizem, Tiazac)
Calcium channel blockers slow conduction time through the AV node, prolonging PR interval to decrease ventricular response in SVTs, atrial flutter, and AF. Calan and Cardi- zem may be used for bedside conversion of acute AF.
Class V drugs, such as electrolytes (e.g., magnesium, potassium), isoproterenol (Isuprel), adosene (Adeno- card); inotropic agents (digoxin [Lanoxin, Digitek])
Miscellaneous drugs have antiarrhythmic effects using vari ous mechanisms and are chosen for specific circumstances. For example, isoproterenol may be used to treat certain types of heart block, digitalis (may be used alone to improve cardiac pumping force and ejection fraction), or in combination with other antidys- rhythmic drugs to reduce ventricular rate in the presence of uncontrolled or poorly tolerated atrial tachycardias or atrial flutter and AF.
CHAPTER 2 Cardiovascular: Dysrhythmias
ACTIONS/INTERVENTIONS (continued) RATIONALE (continued)
Prepare for and assist with elective cardioversion. May be used in AF after trials of first- line drugs— such as atenolol, metoprolol, diltiazem, and verapamil— have failed to control heart rate or in certain unstable dysrhyth- mias to restore normal heart rate or relieve symptoms of heart failure.
Assist with insertion and maintain pacemaker (external or temporary, internal or permanent) function.
Temporary pacing may be necessary to accelerate impulse formation in bradydysrhythmias, synchronize electrical impulsivity, or override tachydysrhythmias and ec topic activity to maintain cardiovascular function until sponta- neous pacing is restored or permanent pacing is initiated.
These devices may include atrial and ventricular pace- makers and may provide single- chamber or dual- chamber pacing.
Prepare for procedures, such as PCIs, including angiography with pos si ble angioplasty and stent placement; catheter or surgical ablation; or surgery, such as aneurysmectomy or CABG, as indicated.
Treatment may include revascularization procedures such as stenting or CABG, indicated to enhance circulation to myocardium and conduction system. Ablation therapy destroys a small spot of heart tissue and creates an electrical block along the pathway that stops the dys- rhythmia and redirects electrical conduction pathways.
Resection of ventricular aneurysm may be required to correct intractable ventricular dysrhythmias unresponsive to medical therapy.
Prepare for placement of ICD when indicated. This device may be surgically implanted in those clients with recurrent, life- threatening ventricular dysrhythmias (such as might occur with long QT syndrome [LQTS]), or other dysrhythmias unresponsive to tailored drug therapy (NHLB, 2011). The latest generation of devices can provide multilevel or “tiered” therapy, that is, antitachycardia and antibradycardia pacing, cardioversion, or defibrillation, depending on how each device is programmed.
N U R S I N G D I A G N O S I S :
risk for Poisoning [Digitalis toxicity]
Possibly Evidenced By
Inadequate knowledge of pharmacological agents; inadequate knowledge of poisoning prevention Reduced vision, cognitive limitations
[Limited range of therapeutic effectiveness]
Desired Outcomes/Evaluation Criteria— Client Will Knowledge: Medi cation NOC
Verbalize understanding of individual prescription, how it interacts with other drugs or substances, and importance of maintaining prescribed regimen.
Recognize signs of digoxin overdose and developing heart failure, and identify what to report to physician.
Cardiac Pump Effectiveness NOC
Be free of signs of toxicity; display serum drug level within individually acceptable range.
ACTIONS/INTERVENTIONS RATIONALE
Medi cation Management NIC In de pen dent
Evaluate client need for/use of digitalis. Incidence of digitalis toxicity has declined because of reduced digitalis usage, improvement in drug formulation, increased awareness in drug- to- drug interactions, increased availability of other drugs to treat heart failure, and techniques like catheter ablation therapy for supra- ventricular tachycardias. However, digitalis toxicity rates remain relatively stable. Note: One study, which used data from the National Electronic Injury Surveillance System—
Cooperative Adverse Drug Event Surveillance Proj ect, the National Ambulatory Medical Care Survey, and the National Hospital Ambulatory Medical Care Survey, estimated that 1% of emergency department visits for adverse drug events in patients aged 40 years or older resulted from digoxin toxicity, with this figure rising to 3.3% for patients aged 85 years or older (See et al, 2014).
Instruct client not to change dose for any reason, not to omit dose— unless instructed to, based on pulse rate— not to increase dose or take extra doses, and to contact physi- cian if more than one dose is omitted.
Alterations in drug regimen can reduce therapeutic effects, result in toxicity, and cause complications.
Advise client that digoxin may interact with many other drugs and that physician should be informed that digoxin is taken whenever new medi cations are prescribed.
Advise client not to use OTC drugs, such as laxatives, antidiarrheals, antacids, cold remedies, diuretics, and herbals, without first checking with the pharmacist or healthcare provider.
Knowledge may help prevent dangerous drug interactions.
Review importance of dietary and supplemental intake of potassium, calcium, and magnesium.
Maintaining electrolytes at normal ranges may prevent or limit development of toxicity and correct many associated dysrhythmias.
Provide information and have the client and SO verbalize understanding of toxic signs and symptoms to report to the healthcare provider.
Nausea, vomiting, diarrhea, unusual drowsiness, confusion, very slow or very fast irregular pulse, thumping in chest, double or blurred vision, yellow or green tint or halos around objects, flickering color forms or dots, altered color perception, and worsening HF— such as dependent or generalized edema, dyspnea, decreased amount or frequency of voiding— indicate need for prompt evalua- tion and intervention. Note: In severe or refractory heart failure, altered cardiac binding of digoxin may result in toxicity even with previously appropriate drug doses.
Discuss necessity of periodic laboratory evaluations, as indicated:
Drug levels are evaluated in conjunction with clinical mani- festations and ECG to determine individual’s response.
Serum digoxin level Digoxin has a narrow therapeutic serum range (0.6–1.3 to
2.6 ng/mL). Levels associated with toxicity overlap between therapeutic and toxic ranges and are dependent on individual response. Note: Cardiac glycosides (includes digoxin) accounted for 2.6% of toxic plant exposures in the United States in 2008 (Bronstein et al, 2009).
Electrolytes, blood urea nitrogen (BUN), creatinine, and liver function studies
Abnormal levels of potassium, calcium, or magnesium increase the heart’s sensitivity to digoxin. Impaired kidney function can cause digoxin (mainly excreted by the kidney) to accumulate to toxic levels. Digoxin levels (mainly excreted by the bowel) are affected by impaired liver function.
(continues on page 96)
CHAPTER 2 Cardiovascular: Dysrhythmias
ACTIONS/INTERVENTIONS RATIONALE
Teaching: Individual NIC In de pen dent
Assess client and SO level of knowledge and ability and desire to learn.
Necessary for creation of individual instruction plan. Rein- forces expectation that this will be a “learning experience.”
Verbalization identifies misunderstandings and allows for clarification.
Be alert to signs of avoidance, such as changing subject away from information being presented or extremes of
be hav ior (withdrawal or euphoria).
Natu ral defense mechanisms, such as anger or denial of significance of situation, can block learning, affecting client’s response and ability to assimilate information.
Changing to a less formal or structured style may be more effective until client and SO are ready to accept and deal with current situation.
ACTIONS/INTERVENTIONS (continued) RATIONALE (continued)
Collaborative
Review ECG, noting rate and rhythm. Alterations in cardiac rate and rhythm from digitalis toxicity may simulate almost every known type of dysrhythmia (Patel & James, 2017). Effective management relies on early recognition that a dysrhythmia may be related to digitalis intoxication.
Assist in providing supportive therapy, as indicated. Depending on the severity of the toxicity, treatment ranges from simply holding or discontinuing to treatment with IV fluids, oxygenation and support of ventilatory function, and correction of electrolyte imbalances.
Administer medi cations, as appropriate, for example:
Digoxin immune Fab (Digibind) Digibind is currently considered first- line treatment for severe digoxin toxicity accompanied by significant dysrhythmias (e.g., severe bradyarrhythmia, second- or third- degree heart block, ventricular tachycardia or fibrillation) from digitalis. Onset of action ranges from 20 to 90 minutes;
complete response generally occurs within several hours (Patel & James, 2017).
Evaluate serum electrolyte levels (especially potassium, magnesium, and calcium) and renal and hepatic functions periodically during detoxification therapy.
Replace electrolytes as prescribed.
Hypokalemia, hypomagnesemia, or hypercalcemia may make the patient more susceptible to digitalis toxicity.
Prepare client for transfer to critical care unit (CCU), as indicated, such as for dangerous dysrhythmias, exacerba- tion of heart failure.
In the presence of digoxin toxicity, clients frequently require intensive monitoring until therapeutic levels have been restored. Because all digoxin preparations have long serum half- lives, stabilization can take several days.
N U R S I N G D I A G N O S I S :
in effec tive Health Management
May Be Related To
Complexity of/insufficient knowledge of therapeutic regimen Possibly Evidenced By
Reports difficulty with prescribed regimen Failure to take action to reduce risk factors [Unexpected acceleration of disease condition]
Desired Outcomes/Evaluation Criteria— Client Will Self- Management: Dysrhythmias NOC
Verbalize understanding of therapeutic regimen.
List desired action and pos si ble adverse side effects of medi cations.
Demonstrate be hav iors and changes in lifestyle necessary to maintain therapeutic regimen.