NUR-635 Topic 6 DQ 1 • Online Nursing Essays

Sample Answer for NUR-635 Topic 6 DQ 1 Included After Question

Albert is 78-year-old male who is being treated with amiodarone 200mg daily for non-valvular atrial fibrillation. His past medical history includes diabetes mellitus and hypertension. He also is prescribed warfarin but is non-compliant due to not understanding why he needs to be on the medication. Use the guidelines and relevant literature in your topic Resources to discuss the following: 

Briefly explain the pathophysiology associated with atrial fibrillation. 
Compare the rhythm control versus rate control pharmacologic strategies when treating atrial fibrillation. 
Based on the mechanism of action, how do the following medications treat atrial fibrillation: metoprolol, diltiazem, digoxin, and amiodarone? 

Briefly explain the various adverse effects associated with amiodarone (e.g., lung, thyroid, eye, liver, and skin). 
Describe the pharmacologic term half-life. What is the half-life of amiodarone? What significance does this have on the drug? 
What are some major considerations when selecting an agent rate or rhythm control to treat atrial fibrillation? 
Explain what the purpose of the CHADS2 score is. How would you apply the CHADS2 to Albert? The patient does not understand the reason for being prescribed warfarin. 
Based on the mode of action, how do the following medications cause anticoagulation: warfarin, dabigatran, rivaroxaban, and apixaban. 
What are the considerations when choosing a DOAC versus warfarin? 
What anticoagulant should Albert be prescribed? What dose/frequency will you write on the prescription? What counseling points would educate the patient regarding the prescribed medication? 

American Association of Colleges of Nursing Core Competencies for Professional Nursing Education 

This assignment aligns to AACN Core Competencies 1.2, 2.2, 2.5. 4.2, 6.4, 9.2 

A Sample Answer For the Assignment: NUR-635 Topic 6 DQ 1

Title: NUR-635 Topic 6 DQ 1

Briefly explain the pathophysiology associated with atrial fibrillation. 

            Atrial fibrillation (AF) is a common cardiac arrhythmia characterized by irregular and rapid electrical impulses in the atria, the upper chambers of the heart. The initiation of AF often involves an ectopic focus, usually located near the pulmonary veins, which triggers abnormal electrical impulses (Nesheiwat et al., 2022). The impulses are irregular, leading to the characteristic irregular rhythm of AF. The irregular heartbeat in AF reduces the heart’s effectiveness in pumping blood, which can result in symptoms like palpitations, shortness of breath, and fatigue. Additionally, the turbulent and abnormal blood flow in the atria during AF increases the risk of blood clot formation, particularly in the left atrial appendage. The blood clots can potentially travel to other parts of the body, such as the brain, causing strokes. 

Compare the rhythm control versus rate control pharmacologic strategies when treating atrial fibrillation. 

            Rhythm control aims to restore and maintain normal sinus rhythm in patients with AF. The strategy often involves the use of cardioversion, AF ablation, or antiarrhythmic medications like amiodarone to prevent AF episodes and potentially improve symptoms (Kelly et al., 2019). On the other hand, rate control focuses on controlling the heart rate in AF patients without necessarily restoring normal sinus rhythm. It involves the use of medications like beta-blockers (e.g., metoprolol), calcium channel blockers (e.g., diltiazem), or digoxin to slow the heart rate in AF. 

Based on the mechanism of action, how do the following medications treat atrial fibrillation: metoprolol, diltiazem, digoxin, and amiodarone? 

Metoprolol is a beta-blocker that reduces heart rate and blood pressure by blocking the effects of adrenaline on the heart. It helps control AF by slowing the heart rate and reducing the risk of rapid ventricular response during AF. On the other hand, diltiazem is a calcium channel blocker that inhibits the influx of calcium ions into cardiac muscle cells, leading to reduced contractility and heart rate (Kapustova et al., 2023). It is used in AF to slow down the heart rate and improve symptoms. Digoxin, however, works by increasing the strength and efficiency of heart contractions while reducing the heart rate (Kapustova et al., 2023). It is used in AF to control the heart rate and manage symptoms, especially in patients with heart failure. Lastly, amiodarone has multiple mechanisms of action, including sodium and potassium channel blockade, calcium channel blockade, and beta-blockade. It is considered a highly effective antiarrhythmic agent used for rhythm control in AF, often when other medications have failed. It can stabilize the heart’s electrical activity and restore normal sinus rhythm. 

Briefly explain the various adverse effects associated with amiodarone (e.g., lung, thyroid, eye, liver, and skin). 

            Amiodarone can lead to pulmonary toxicity, which may manifest as cough, shortness of breath, and lung inflammation. Severe cases can progress to pulmonary fibrosis, a serious and potentially irreversible condition. Amiodarone contains iodine, which can affect thyroid function. It can cause both hypothyroidism (underactive thyroid) and hyperthyroidism (overactive thyroid), making it crucial to monitor thyroid hormone levels regularly (Moroi et al., 2020). Amiodarone can also cause eye-related issues, including corneal microdeposits, which are usually asymptomatic. Amiodarone can cause liver enzyme elevation, hepatitis, or even cirrhosis in rare cases (Moroi et al., 2020). Skin reactions are another potential adverse effect. Patients may experience photosensitivity, making them more prone to sunburn. 

Describe the pharmacologic term half-life. What is the half-life of amiodarone? What significance does this have on the drug? 

            The half-life of a drug is a pharmacokinetic parameter that represents the time it takes for half of the drug to be eliminated from the body. It is a crucial factor in determining dosing frequency and the duration of a drug’s therapeutic effect. In the case of amiodarone, its half-life is quite long of about 100 days due to its extensive tissue distribution (Biancatelli et al., 2019). The long half-life implies that amiodarone stays in the body for an extended period, even after discontinuation. For practical purposes, it means that it takes a significant amount of time for the drug’s effects to wear off completely and for any potential side effects or drug interactions to resolve. 

What are some major considerations when selecting an agent rate or rhythm control to treat atrial fibrillation? 

            When selecting an agent for rate or rhythm control in atrial fibrillation (AF), several factors need to be considered. These include the patient’s symptoms, overall health, comorbidities, and individual preferences. 

Explain what the purpose of the CHADS2 score is. How would you apply the CHADS2 to Albert? The patient does not understand the reason for being prescribed warfarin. 

he CHADS2 score is a clinical risk assessment tool used to estimate the risk of stroke in patients with atrial fibrillation. It assigns points based on certain risk factors: Congestive heart failure (1 point), Hypertension (1 point), Age ≥75 (1 point), Diabetes mellitus (1 point), and prior Stroke or transient ischemic attack (2 points) (Wu et al., 2021). The total score helps determine the need for anticoagulation therapy. 

Applying the CHADS2 score to Albert: 

Congestive heart failure: Yes (1 point) 
Hypertension: Yes (1 point) 
Age ≥75: Yes (1 point) 
Diabetes mellitus: Yes (1 point) 
Prior Stroke or transient ischemic attack: No (0 points) 

Albert’s CHADS2 score is 3 points, which indicates a moderate to high risk of stroke. Therefore, he would benefit from anticoagulation therapy like warfarin. Warfarin is an anticoagulant that helps prevent blood clots, and it is prescribed to reduce the risk of stroke in patients with atrial fibrillation. 

Based on the mode of action, how do the following medications cause anticoagulation: warfarin, dabigatran, rivaroxaban, and apixaban. 

            Warfarin is a vitamin K antagonist. It interferes with the production of vitamin K-dependent clotting factors (Factors II, VII, IX, and X) in the liver. By inhibiting these factors, warfarin reduces the blood’s ability to form clots. On the other hand, dabigatran is a direct thrombin inhibitor. It directly inhibits thrombin, an enzyme involved in the blood clotting process, preventing the conversion of fibrinogen to fibrin and ultimately inhibiting clot formation (Heestermans et al., 2022). Lastly, rivaroxaban and apixaban are both factor Xa inhibitors. They target Factor Xa, a key component in the coagulation cascade, and prevent the formation of thrombin, thus inhibiting clot formation. 

What are the considerations when choosing a DOAC versus warfarin? 

            Choosing between a Direct Oral Anticoagulant (DOAC) and warfarin for a patient like Albert requires careful consideration of various factors. DOACs, such as apixaban, dabigatran, edoxaban, and rivaroxaban, have become increasingly popular due to their predictable anticoagulant effects, fewer drug interactions, and no need for frequent monitoring. However, in Albert’s case, his age, comorbidities (diabetes mellitus and hypertension), and non-compliance with warfarin should be taken into account. DOACs have shown efficacy and safety in non-valvular atrial fibrillation and are often preferred in older patients who may struggle with regular monitoring and dose adjustments. Their lower risk of bleeding complications compared to warfarin might also be beneficial for Albert 

What anticoagulant should Albert be prescribed? What dose/frequency will you write on the prescription? What counseling points would educate the patient regarding the prescribed medication? 

            Given Albert’s age and comorbidities, a DOAC like apixaban 5 mg twice daily might be a suitable choice. Dosing decisions should be individualized based on factors such as renal function, bleeding risk, and any potential contraindications. It is crucial to counsel Albert on the importance of medication adherence, the potential risks of bleeding, and the need for regular follow-up visits with his healthcare provider to monitor his response to the medication and adjust the dosage if necessary. Additionally, emphasizing the significance of taking the prescribed anticoagulant consistently can help prevent stroke and other complications associated with atrial fibrillation. 

  

References 

Biancatelli, R. M. C., Congedo, V., Calvosa, L., Ciacciarelli, M., Polidoro, A., & Iuliano, L. (2019). Adverse reactions of Amiodarone. Journal of geriatric cardiology: JGC, 16(7), 552. 

Heestermans, M., Poenou, G., Hamzeh-Cognasse, H., Cognasse, F., & Bertoletti, L. (2022). Anticoagulants: a short history, their mechanism of action, pharmacology, and indications. Cells, 11(20), 3214. 

Kapustova, K., Phan, B., Allison-Aipa, T., & Choi, M. (2023). Acute rate control with metoprolol versus diltiazem in atrial fibrillation with heart failure with reduced ejection fraction. The American Journal of Emergency Medicine, 67, 126-129. 

Kelly, J. P., DeVore, A. D., Wu, J., Hammill, B. G., Sharma, A., Cooper, L. B., … & Hernandez, A. F. (2019). Rhythm control versus rate control in patients with atrial fibrillation and heart failure with preserved ejection fraction: insights from get with the guidelines—heart failure. Journal of the American Heart Association, 8(24), e011560. 

Moroi, M. K., Ruzieh, M., Aboujamous, N. M., Ghahramani, M., Naccarelli, G. V., Mandrola, J., & Foy, A. J. (2020). Dataset for amiodarone adverse events compared to placebo using data from randomized controlled trials. Data in brief, 28, 104835. 

Nesheiwat, Z., Goyal, A., Jagtap, M., & Shammas, A. (2022). Atrial fibrillation (nursing). In StatPearls [Internet]. StatPearls Publishing. 

Wu, Y., Xie, Z., Liang, W., Xue, R., Wu, Z., Wu, D., … & Liu, C. (2021). Usefulness of CHADS2, R2CHADS2, and CHA2DS2‐VASc scores for predicting incident atrial fibrillation in heart failure with preserved ejection fraction patients. ESC Heart Failure, 8(2), 1369-1377.