The American College of Cardiology, American Heart Association, and Heart Rhythm Society collectively publish guidelines on the management of cardiac arrhythmias. This column will highlight key recommendations from the Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death1  and discuss the clinical implications for nurses. The recommendations contained in this guideline are vast in scope and range from diagnostic testing to pharmacological and device-based treatments. This column will highlight selected class I recommendations (actions that are indicated, beneficial, effective, and should be done) and class III recommendations (actions that are associated with potential harm and should not be performed).

Use of 12-Lead Electrocardiogram in Diagnosis of Wide Complex Tachycardia

A 12-lead electrocardiogram (ECG) should be the first diagnostic test for any patient in a stable wide complex tachycardia. Clinicians use ECG results to determine the etiology of wide complex tachycardia by assessing the cardiac axis and QRS morphology in lead aVR and the precordial leads. Criteria supporting a diagnosis of ventricular tachycardia include right superior axis, monomorphic R wave in aVR, V1 and V6 morphology consistent with ventricular tachycardia rather than supraventricular tachycardia, and negative QRS complexes in all precordial leads (negative concordance). Nurses should observe QRS morphology in leads V1 and V6 during bedside monitoring to differentiate between ventricular tachycardia and supraventricular tachycardia with bundle branch block (aberrancy). Advanced heart disease and antiarrhythmic medications can affect the ECG and thus necessitate exceptions to the rules about using ECG criteria to determine the etiology of a wide complex tachycardia.1  Nurses should consider ventricular tachycardia to be the most likely diagnosis in adult patients with wide complex tachycardia and structural heart disease. The guideline recommends that all cases of wide complex tachycardia be presumed to be ventricular in origin if the diagnosis is not clear.1 

An ECG should also be performed after a wide complex tachycardia has converted to sinus rhythm to shed light on the etiology of the arrhythmia. The 12-lead ECG results could support ventricular etiologies from (1) previous myocardial infarction, (2) chamber enlargement, or (3) inherited disorders such as congenital long QT, Brugada syndrome, or arrhythmogenic right ventricular cardiomyopathy.1  Other findings, such as preexisting bundle branch block or a delta wave indicating the presence of an accessory pathway, would suggest a supraventricular etiology.

Medications for Reducing Sudden Cardiac Death Risk in Heart Failure Patients With Reduced Ejection Fraction

Current evidence-based recommendations for patients with heart failure with reduced ejection fraction focus on using medication to reduce the risk of sudden cardiac death. β-blockers decrease myocardial oxygen demand and block the arrhythmogenic effect of chronic sympathetic nervous system stimulation. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers interfere with the formation of or block the effects of angiotensin II, which results in decreased preload and afterload, decreased myocardial oxygen demand, interrupted ventricular remodeling, and slowed fibrosis progression. Aldosterone antagonists also reduce the formation of myocardial fibrosis.1  In patients with heart failure with reduced ejection fraction, long-term use of β-blockers reduces ventricular arrhythmia and sudden cardiac death.2-4  Angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and combined angiotensin-receptor blockers–neprilysin inhibitors also reduce sudden cardiac death in patients with heart failure with reduced ejection fraction.5-7 

Additional Indications for β-Blockers in Arrhythmia and Prevention of Sudden Cardiac Death

β-Blockers are often the first-line pharmacological treatment in the management of ventricular arrhythmias because of their efficacy and safety profile.8  The antiarrhythmic effect is attributed to the antiadrenergic blockage of beta receptors and slowing of the sinus rate. β-blockers may also play a role in inhibiting excess calcium release.9  β-blockers decrease the risk of death in patients experiencing polymorphic ventricular tachycardia after myocardial infarction10  and suppress ventricular arrhythmias in patients with structurally normal hearts,11  and they can also enhance the efficacy of other antiarrhythmics when used in combination.12 

β-blockers are recommended for patients with long QT syndrome with a resting QTc greater than 470 milliseconds.1  β-blockers are indicated1,13  to reduce the risk of a cardiac event in patients with long QT syndrome types 1 and 2 and in women with long QT syndrome type 3. Table 1 shows the ECG features of long QT syndrome types 1, 2, and 3. There is less evidence1,13  for the efficacy of β-blockers in men with long QT syndrome type 3. Not all β-blockers have the same efficacy in long QT syndrome, and monitoring is required to assess the effect of therapy on QTc over time and to determine the adequacy of β-blocker effect with exertion.13  The guideline recommends that β-blocker therapy for long QT syndrome be continued throughout pregnancy, the postpartum period, and breastfeeding.1  The risk of sudden cardiac arrest or sudden cardiac death is high during the first 9 months of the postpartum period, particularly in women with long QT syndrome type 2; β-blocker therapy decreases this risk.14  Women on β-blocker therapy during pregnancy do not have an increased risk of arrhythmic events.14 

β-blockers are also indicated for treating catecholaminergic polymorphic ventricular tachycardia15  and ventricular arrhythmia in the setting of arrhythmogenic right ventricular cardiomyopathy.1 

Treatment of Premature Ventricular Contractions

β-blockers or nondihydropyridine calcium channel blockers are recommended for the treatment of premature ventricular contractions (PVCs) in patients who have a structurally normal heart to reduce the arrhythmia burden and improve symptoms.16  In addition to producing symptoms, a high PVC burden can result in a reversible decline in left ventricular function. A decline in left ventricular function is typically seen when PVCs are >15% of total beats and are predominantly of a single morphology.1  Catheter ablation is a potential treatment for these patients when antiarrhythmic medication is not effective or is not tolerated, or if the patient prefers non-pharmacological treatment.17  In one prospective study, 82% of patients treated with catheter ablation for PVC-induced cardiomyopathy demonstrated return of left ventricular function to normal within 6 months.18  PVCs can be a cause of reduced left ventricular function, but reduced left ventricular function can also be a cause of PVCs.1  Although single PVCs are not treated in clinical practice, nurses should assess and report PVC burden because PVCs are a potential etiology of cardiomyopathy.

Treatment of Acquired QT Prolongation and Torsades de Pointes

Intravenous magnesium sulfate is recommended for the suppression of recurrent torsades de pointes in patients with acquired QT prolongation due to medications or electrolyte abnormalities.19,20  Hospitalized patients can acquire torsades de pointes as a result of QT-prolonging medication, potassium and magnesium deficiencies, and risk factors such as advanced age and altered renal function. In acquired torsades de pointes, magnesium replacement is indicated to achieve a normal serum magnesium level and potassium replacement is indicated to achieve a serum potassium level of 4.0 mEq/L or higher.21  If intravenous magnesium is not effective in suppressing recurrent torsades de pointes, increasing the heart rate through atrial or ventricular pacing or through the administration of isoproterenol is indicated.22 

Potentially Harmful Pharmacological Treatments

Lidocaine and high-dose amiodarone are not used for the prevention of ventricular arrhythmias in patients with suspected acute myocardial infarction because they may be harmful.23,24  Prophylactic lidocaine administration can cause bradycardia, and prophylactic high-dose amiodarone post–myocardial infarction has been associated with deaths thought to be a result of hypotension.24  The administration of calcium channel blockers in the setting of a wide complex tachycardia of unknown origin is also potentially harmful because of the risk of severe hypotension or syncope.25  Flecainide and propafenone (class IC antiarrhythmic medications) are not indicated in patients with a history of myocardial infarction because of the increased risk of death from proarrhythmia.26  Additionally, QT-prolonging medications can be harmful in patients with long QT syndrome.1 

Genetic Counseling and Testing

Most inherited disorders that produce cardiac arrhythmias are diagnosed by their clinical features and through family history.1  Genetic testing may verify a diagnosis for which there is clinical suspicion and may also aid in prognostication for the symptomatic patient being tested.1  It is beneficial to offer genetic counseling for patients or family members undergoing genetic testing for risk stratification for sudden cardiac arrest.1  Genotyping may guide clinical decision-making for some, but not all, inherited arrhythmogenic disorders. If genetic testing does not identify a mutation known to cause arrhythmia, that does not exclude the possibility that the disease has a genetic basis; in such cases ongoing monitoring and treatment based on clinical features is indicated.1  Genetic testing and counseling is recommended for first-degree relatives of patients with the following: (1) a causative mutation for long QT syndrome or hypertrophic cardiomyopathy, (2) catechol-aminergic polymorphic ventricular tachycardia, (3) short QT syndrome, or (4) Brugada syndrome.1  Genetic counseling and testing are also recommended in patients with clinically diagnosed long QT syndrome and in first-degree relatives of patients who are 40 years of age or younger who experience sudden cardiac death, sudden cardiac arrest, recurrent exertional syncope, or unexplained near drowning, to rule out an inherited arrhythmia syndrome.27 

Clinical screening and genetic testing and counseling are recommended for first-degree relatives of patients with arrhythmogenic right ventricular cardiomyopathy in whom a disease-causing mutation has been identified28 ; clinical screening results in the diagnosis of arrhythmogenic right ventricular cardiomyopathy in 35% to 45% of first-degree relatives.29  Clinical testing with an ECG and echocardiogram is also indicated in first-degree relatives of patients with hypertrophic cardiomyopathy.30  Genetic testing is not recommended for patients with early repolarization on an ECG.1 

Conditions Requiring Only Initial Observation

There are several asymptomatic conditions for which the guideline recommends only observation, including (1) asymptomatic early repolarization, (2) asymptomatic short QT interval, and (3) asymptomatic inducible type 1 Brugada ECG pattern.1  The prevalence of early repolarization in the inferior or lateral leads is as high as 5.8% in adult patients.31  The early repolarization pattern is more common in men than in women and can disappear over time.32  In patients presenting for medical care who have early repolarization, ischemia should be ruled out as a reversible cause. Early repolarization becomes a syndrome when patients present with syncope or an arrhythmia.1 

In patients with a medication-induced Brugada type 1 pattern without spontaneous type 1 ECG changes and who are asymptomatic the risk of major adverse cardiac events is low.33  The Brugada type 1 pattern involves coved ST-segment elevation in more than 1 of the right precordial leads V1 to V3. The ST segment gradually descends into an inverted T wave.34  A family history of sudden cardiac arrest or Brugada syndrome does not predict adverse events in patients with Brugada syndrome.35  Asymptomatic short QT is often an incidental finding and does not require treatment, but ongoing monitoring and follow-up may be indicated.1 

Implantable Cardioverter/Defibrillators

Clinical Indications for Implantable Cardioverter/Defibrillator Placement

Table 2 outlines the clinical criteria for implantable cardioverter/defibrillator (ICD) placement for both primary and secondary prevention. Regardless of the clinical criteria placing the patient at risk for sudden cardiac arrest or sudden cardiac death, patients must have an expected meaningful survival of greater than 1 year to be a candidate for an ICD.

Indications for a Subcutaneous Implantable Cardioverter/Defibrillator

A subcutaneous ICD is suitable for patients who meet all general criteria for an ICD but have a relative contraindication for a transvenous implant such as inadequate vascular access or high risk for infection. The subcutaneous ICD does not provide pacing for ventricular tachycardia termination or bradycardia, except for limited postshock bradycardia pacing; patients with these needs are not candidates for subcutaneous ICD placement.36-38  In a subcutaneous ICD, the pulse generator is placed between the fifth and sixth intercostal spaces at the midaxillary line, and a lead with 2 sensing electrodes and shocking coil are placed near the sternum.1  A subcutaneous ICD may not be able to adequately sense arrhythmias in all patients, thus ECG screening to assess sensing must be done prior to implantation.39  Patients receiving a subcutaneous ICD must meet other requirements for trans-venous ICD implants including recommended waiting periods.

Implantable Cardioverter/Defibrillator Deactivation

Patients should receive counseling regarding the option to deactivate their ICD shock therapy at the time of implantation and during any discussions about advance care planning. Deactivation may be requested by patients at any time it is consistent with the goals of their care. A clinician-initiated discussion about ICD deactivation should occur in patients with refractory heart failure, refractory ventricular arrhythmias, or when approaching end-of-life for any other reason.1  In a study by Kinch Westerdahl et al40  of deceased patients with ICDs, 25 of 125 patients had detection turned off 24 hours before death. Of the remaining 100 patients, 31 experienced 1 or more shocks in the final 24 hours of life.

Summary

The Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death1  provides comprehensive recommendations for adult patients with ventricular arrhythmias who are at risk for sudden cardiac death on topics including diagnosis, prognostication, pharmacological treatment, device therapy, population-specific issues, and genetic testing and counseling. Guideline-based care for this vulnerable group of patients improves safety and clinical outcomes. This column highlights a sample of these recommendations and provides nurses with information that can be used in clinical practice and in patient and family education.

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Footnotes

The author declares no conflicts of interest.