When teaching a patient about amiodarone the nurse should advise the patient to avoid?

Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delayed electrical impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent. In general, there are three degrees of AV nodal blocks: first degree, second degree (Mobitz type 1 or 2), and third-degree.

At this time, there is no well-characterized large study about the relationship between different types of AV block with age, race, or gender. AV block is sometimes seen in athletes and in patients with congenital heart disorders.

Nursing Diagnosis

  • Ineffective tissue perfusion

  • Impaired cardiac function

Causes

Higher degrees of AV block often suggest some underlying pathology. This is known as a pathophysiologic AV block. About half of such cases are a result of chronic idiopathic fibrosis and sclerosis of the conduction system.

Another common source is ischemic heart disease which is responsible for around 40 percent of cases of AV block . 

AV block is also associated with cardiomyopathies, including hypertrophic obstructive cardiomyopathy and infiltrative conditions such as sarcoidosis and amyloidosis. Infectious causes such as Lyme disease, rheumatic fever, endocarditis, viruses as well as autoimmune disease such as systemic lupus erythematosus should also be explored .

Other potential triggers include cardiac surgery, medications, and inherited conditions .

Risk Factors

First degree AV block can originate from various locations within the conduction system. The levels of conduction delay include the atrium, AV node (most common in first-degree heart block), Bundle of His, bundle branches, fascicles, Purkinje system. Mobitz type I second degree AV block usually occurs within the AV node, while Mobitz type II second degree AV block mainly originates from conduction system disease below the level of the AV node (in the bundle of His and in the bundle branches). In third-degree AV block, no atrial impulses reach the ventricle- it can occur in the AV node or in the infranodal specialized conduction system.  

The following medications can affect different levels of conduction delay: 

1) Increased parasympathetic tone, digoxin (which upgrades vagotonic action), calcium channel blockers (which obstructs the inward calcium current responsible for depolarization) and beta-blockers can affect the AV node 

2) Medications such as procainamide, quinidine, and disopyramide can block sodium channels and delay conduction in the bundle of His

3) Similarly though rarely, medications such as procainamide, quinidine, and disopyramide can also delay infra-Hisian conduction system 

Assessment

History taking for patients with concerns for AV block should include: 

  • History of heart disease, both congenital and acquired

  • Full list of medications and dosing. Particular drugs of interest include beta-blockers, calcium channel blockers, antiarrhythmic drugs, digoxin

  • Signs and symptoms associated with other systemic diseases associated with heart block (amyloidosis, sarcoidosis) 

  • Baseline exercise capacity 

  • Potential exposure to tick bites

 The following symptoms should raise concerns: 

Evaluation

First degree. In first-degree AV block, the P waves always precede the QRS complexes, but there is a prolongation of the PR interval. The PR interval will be greater than 200 milliseconds in duration without any dropped beats. There is a delay, without interruption, in conduction from the atrium to the ventricle. All atrial activation is eventually transmitted to the ventricles. The delay is typically due to a minor AV conduction defect occurring at or below the AV node. 

  • Causes. There are multiple causes of first-degree AV block, including simply being a normal variant. Other causes include inferior myocardial infarction (MI), increased vagal tone (e.g., athletes), status post-cardiac surgery, myocarditis, hyperkalemia, or even medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).

  • Clinical significance. This is benign and does not result in any hemodynamic instability. No specific treatment is required.

Second degree, Mobitz type 1 (Wenckebach). In second-degree Mobitz type 1 AV block, there is a progressive prolongation of the PR interval, which eventually culminates in a non-conducting P wave. The PR interval continues to prolong with each beat of the cycle,  and the subsequent PR lengthening is progressively shorter. The PR interval before the dropped beat is the longest of the cycle, and the PR interval after the dropped beat is the shortest as the cycle starts over.

  • Mechanism. This is usually a result of a reversible conduction block at the level of the AV node. There is typically a functional suppression of AV conduction. The AV nodal cells seem to progressively fatigue until they fail to conduct an impulse to the ventricles and a dropped beat occurs.

  • Causes. There are multiple causes of second-degree Mobitz type 1 (Wenckebach) AV block, including reversible ischemia, myocarditis, increased vagal tone, status post-cardiac surgery, or even medications that slow AV nodal conduction (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).

  • Clinical significance. Differentiating between second-degree Mobitz type 1 (Wenckebach) and Mobitz type 2 AV blocks is important as the management and treatment are different. Mobitz type 1 is often a benign rhythm. Most patients are asymptomatic, and there tends to be a minimal hemodynamic disturbance. Patients that are asymptomatic do not require treatment and can be monitored on an outpatient basis. Patients that are symptomatic typically respond to atropine and rarely require permanent cardiac pacing. Medication-induced impairment of AV conduction is often reversible after stopping the offending agent.

Second degree, Mobitz type 2. In second-degree Mobitz type 2 AV block, there are intermittent non-conducted P waves without warning. Unlike Mobitz type 1 (Wenckebach), there is no progressive prolongation of the PR interval; instead, the PR interval remains constant, and the P waves occur at a constant rate with unchanged P-P intervals. Because the P waves continue to occur at normal intervals, the R-R interval surrounding the dropped beat is simply a multiple of the preceding R-R interval and remains unchanged.

  • Mechanism. In Mobitz type 2, the block occurs farther along the electrical conduction system below the AV node. 

  • In this case, the cells abruptly and unpredictably fail to conduct an impulse from the atria to the ventricles. This is often the result of structural damage to the conduction system. 

  • Because the defect occurs below the AV node and often times distal to the His Bundle, it produces wide, bizarre-appearing QRS complexes. In the remaining cases, the defect is located within the Bundle of His, resulting in the normal, narrow QRS complexes. There can be a fixed P:QRS relationship (e.g., 2:1, 3:1) or no pattern at all.

  • Causes. Common causes of second-degree Mobitz type 2 AV block include anterior MI, causing septal infarction of the bundle branches. Other causes include idiopathic fibrosis of the conducting system, autoimmune (e.g., systemic sclerosis or systemic lupus erythematosus) or inflammatory (e.g., myocarditis, Lyme disease, or rheumatic fever) conditions, infiltrative myocardial disease (hemochromatosis, sarcoidosis, or amyloidosis), electrolyte imbalance (e.g., hyperkalemia), medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blockers, digitalis, adenosine, or amiodarone), or status post-cardiac surgery (e.g., mitral valve repair).

  • Clinical significance. Mobitz type 2 AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole. Because the onset of dropped beats can occur abruptly and unexpectedly, hemodynamic instability and the consequential syncope and potentially sudden cardiac death can occur at any moment. Thus, patients require a permanent pacemaker. While Mobitz type 1 can improve with atropine, giving atropine in the setting of Mobitz type 2 can worsen the block and increase the risk of complete heart block or asystole.

Third-degree (complete). In third-degree, or complete, heart block there is an absence of AV nodal conduction, and the P waves are never related to the QRS complexes. If ventricular conduction occurs, it is maintained by a junctional or ventricular escape rhythm. There is a complete dissociation between the atria and ventricles and they conduct independently of each other. The P waves (atrial activity) are said to “march through” the QRS complexes at their regular, faster rate. The QRS complexes (ventricular activity) also occur at a regular, but slower rate. There are two independent rhythms occurring simultaneously. 

  • Mechanism. Third-degree heart block is the end result of progressively worsening second-degree AV block. Because a third-degree heart block can occur above or below the AV node, two different rhythms can take over. If it occurs above or at the crest of the AV node, a junctional rhythm will take over and drive the ventricles. The resulting QRS complexes will be narrow and occur at the intrinsic rate of the AV node (40 to 55 beats/minute). Whereas if the block occurs below the AV node, a ventricular pacemaker must take over. In such cases, the QRS complexes will be wide and at the intrinsic rate of the ventricular pacemaker (20 to 40 beats/minute).

  • Causes. Complete heart block is often the result of the same causes as Mobitz type 1 and Mobitz type 2. Other causes include inferior MI, degeneration of the conduction system, and AV-nodal blocking agents such as beta-blockers, non-dihydropyridine calcium channel blockers, adenosine, digitalis, and amiodarone.

  • Clinical significance. Patients with complete heart block are at great risk of developing asystole, ventricular tachycardia, and sudden cardiac death. Insertion of a permanent pacemaker is required.

Medical Management

In general, patients that present with first-degree or second-degree Mobitz type 1 AV block do not require treatment. Any provoking medications can be removed, and patients can be monitored on an outpatient basis. However, patients with higher degrees of AV block (Mobitz type 2 AV block, 3rd degree) tend to have severe damage to the conduction system. They are at a much greater risk of progressing into asystole, ventricular tachycardia, or sudden cardiac death. Hence, they require urgent admission for cardiac monitoring, backup temporary cardiac pacing, and insertion of a permanent pacemaker.   

Nursing Management

  • Place the patient on a cardiac monitor

  • Check labs to ensure electrolytes are within normal limits

  • Place the patient at bed rest

  • Listen to the heart for murmurs

  • Monitor for fluid retention

  • Hold medications that can disrupt cardiac rhythm (usually beta-blockers and antiarrhythmics)

  • If the patient is to have a pacemaker, educate the patient

  • Call the pacemaker nurse after the pacemaker has been inserted

  • Educate patient about pacemakers, microwaves and TSA security checks which can cause magnetic interference with the pacemaker

  • After surgery, educate the patient to keep the arm still and avoid strenuous activity

  • Ask the patient to wear a medical alert bracelet

  • Tell the patient to inform the cardiologist before undergoing any type of procedure or surgery

Outcome Identification

Prognosis depends on the various factors that include age and other chronic medical conditions such as diabetes mellitus, chronic kidney disease, underlying heart disease, and underlying types of AV block.  

Coordination of Care

The management of heart block is best done with an interprofessional team because if the diagnosis is missed (esp higher degrees of heart block), the condition can have significant morbidity and mortality.

Except for a first-degree heart block, the rest of the patients should be referred to a cardiologist for a more definitive workup. Some of these patients may require a pacemaker which can be life-saving. Following treatment, the cardiology nurse should follow up on the patients to ensure that the heart rate has normalized and the patients have no symptoms.

Anytime patients with a pacemaker undergo surgery, the cardiologist should be consulted first.

Health Teaching and Health Promotion

Patients with first-degree and asymptomatic Mobitz type 1 AV block usually can continue their usual activities but should be advised to avoid medications that can prolong the PR interval. Patients with Mobitz type 2 and third-degree AV block should discuss with their cardiologists about the need for pacemakers. All patients should be educated on alarming symptoms of hypoperfusion such as fatigue, lightheadedness, syncope, presyncope, or angina and seek timely medical treatment 

References

1.

Batra AS, Balaji S. Fetal arrhythmias: Diagnosis and management. Indian Pacing Electrophysiol J. 2019 May-Jun;19(3):104-109. [PMC free article: PMC6531664] [PubMed: 30817991]

2.

Saadi M, Tagliari AP, Danzmann LC, Bartholomay E, Kochi AN, Saadi EK. Update in Heart Rhythm Abnormalities and Indications for Pacemaker After Transcatheter Aortic Valve Implantation. Braz J Cardiovasc Surg. 2018 May-Jun;33(3):286-290. [PMC free article: PMC6089127] [PubMed: 30043922]

3.

Ali H, Furlanello F, Lupo P, Foresti S, De Ambroggi G, Epicoco G, Semprini L, Fundaliotis A, Cappato R. Clinical and electrocardiographic features of complete heart block after blunt cardiac injury: A systematic review of the literature. Heart Rhythm. 2017 Oct;14(10):1561-1569. [PubMed: 28583850]

4.

LENEGRE J. ETIOLOGY AND PATHOLOGY OF BILATERAL BUNDLE BRANCH BLOCK IN RELATION TO COMPLETE HEART BLOCK. Prog Cardiovasc Dis. 1964 Mar;6:409-44. [PubMed: 14153648]

5.

LEV M. ANATOMIC BASIS FOR ATRIOVENTRICULAR BLOCK. Am J Med. 1964 Nov;37:742-8. [PubMed: 14237429]

6.

ZOOB M, SMITH KS. THE AETIOLOGY OF COMPLETE HEART-BLOCK. Br Med J. 1963 Nov 09;2(5366):1149-53. [PMC free article: PMC1874084] [PubMed: 14060910]

7.

Yada H, Soejima K. Management of Arrhythmias Associated with Cardiac Sarcoidosis. Korean Circ J. 2019 Feb;49(2):119-133. [PMC free article: PMC6351276] [PubMed: 30693680]

8.

Tselios K, Gladman DD, Harvey P, Su J, Urowitz MB. Severe brady-arrhythmias in systemic lupus erythematosus: prevalence, etiology and associated factors. Lupus. 2018 Aug;27(9):1415-1423. [PubMed: 29665757]

9.

Yeung C, Baranchuk A. Diagnosis and Treatment of Lyme Carditis: JACC Review Topic of the Week. J Am Coll Cardiol. 2019 Feb 19;73(6):717-726. [PubMed: 30765038]

10.

Umapathy S, Saxena A. Acute rheumatic fever presenting as complete heart block: report of an adolescent case and review of literature. BMJ Case Rep. 2018 Feb 11;2018 [PMC free article: PMC5836695] [PubMed: 29440244]

11.

Torres AG. Unexpected Complete Heart Block and Anesthetic Implications. A A Case Rep. 2015 Aug 01;5(3):33-5. [PubMed: 26230304]

12.

Upshaw CB. Comparison of the prevalence of first-degree atrioventricular block in African-American and in Caucasian patients: an electrocardiographic study III. J Natl Med Assoc. 2004 Jun;96(6):756-60. [PMC free article: PMC2568382] [PubMed: 15233485]

13.

Gann D, Samet P. Diagnostic and prognostic value of intracardiac electrophysiological studies. Ten years of experience. Bull Eur Physiopathol Respir. 1979 Sep-Oct;15(5):839-60. [PubMed: 389329]

14.

Hamm W, Rizas KD, Stülpnagel LV, Vdovin N, Massberg S, Kääb S, Bauer A. Implantable cardiac monitors in high-risk post-infarction patients with cardiac autonomic dysfunction and moderately reduced left ventricular ejection fraction: Design and rationale of the SMART-MI trial. Am Heart J. 2017 Aug;190:34-39. [PubMed: 28760211]

15.

Israel CW., European Society of Cardiology (ESC) and the European Heart Rhythm Association (EHRA). [ESC Guidelines on Pacemaker Therapy 2013: what is new and relevant for daily practice?]. Dtsch Med Wochenschr. 2013 Sep;138(39):1968-71. [PubMed: 24046141]

16.

Barold SS, Herweg B. Conventional and biventricular pacing in patients with first-degree atrioventricular block. Europace. 2012 Oct;14(10):1414-9. [PubMed: 22516061]

17.

Epstein AE, Dimarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO., American College of Cardiology/American Heart Association Task Force on Practice. American Association for Thoracic Surgery. Society of Thoracic Surgeons. ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary. Heart Rhythm. 2008 Jun;5(6):934-55. [PubMed: 18534377]

18.

Irwin ME. Cardiac pacing device therapy for atrial dysrhythmias: how does it work? AACN Clin Issues. 2004 Jul-Sep;15(3):377-90. [PubMed: 15475812]

What should be included in teaching your client about amiodarone?

Key teachings for your patient are to monitor pulse daily, avoid grapefruit juice and that side effects can appear up to a year after initiation of therapy. Teach your patient that the effects of amiodarone can persist for months after discontinuation, due to the drugs long half life of up to 100 days.

What should be monitored when taking amiodarone?

Baseline assessment and ongoing monitoring is recommended Before a patient is commenced on amiodarone therapy, prescribers should ensure that the following baseline assessments are completed: pulmonary function assessment (including chest X-ray) ECG and serum potassium levels. liver function tests.

When should you not take amiodarone?

Who should not take Amiodarone HCL?.
thyrotoxicosis..
overactive thyroid gland..
a condition with low thyroid hormone levels..
low amount of magnesium in the blood..
low amount of potassium in the blood..
a painful condition that affects the nerves in the legs and arms called peripheral neuropathy..
deposits on the eye..

What are the most common side effects of amiodarone?

More common.
Cough..
dizziness, lightheadedness, or fainting..
fever (slight).
numbness or tingling in the fingers or toes..
painful breathing..
sensitivity of the skin to sunlight..
trembling or shaking of the hands..
trouble with walking..