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NUR-635 Topic 16 DQ 2

Sample Answer for NUR-635 Topic 16 DQ 2 Included After Question

Choose one of the listed symptoms, and then select an antidysrhythmic drug and explain why the medication you selected is appropriate for this condition. Share the mechanism of action of this medication and hints for monitoring, side effects, and drug interactions, including interactions with CAM. What other considerations need to be made when prescribing these medications? Discuss evidence and treatment guidelines to determine appropriate therapeutic options for a patient being prescribed an antidysrhythmic drug. Include the name of the medication in the subject line so that the medications can be followed. Include references using APA format. 

Chest pain 

Dizziness or lightheadedness 

Fainting 

Heart palpitations 

Shortness of breath 

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 16 DQ 2

Title: NUR-635 Topic 16 DQ 2

Cardiac arrhythmias most often occur as atrial fibrillation. The cause of this condition is attributed to atypical electrical activity occurring in the atria of the heart, resulting in fibrillation. The irregularity in the heart’s rhythm leads to turbulent blood flow, increasing the likelihood of thrombus formation (blood clot). This clot might potentially dislodge and result in a stroke. The range of symptoms for this condition spans from being without symptoms to experiencing chest discomfort, palpitations, rapid heart rate, difficulty breathing, nausea, dizziness, excessive perspiration, and overall exhaustion (Nesheiwat, et.al. 2023). β-blockers are essential in the treatment of cardiac arrhythmias. β-blockers are typically safe drugs that successfully control abnormal heartbeats and irregular heart rhythms, and prevent sudden death due to heart problems in a broad range of heart disorders (Al-Khatib et al., 2018). Guidelines state that β-blockers should be used in all patients, except those with AV block, bradycardia, or asthma. They are also recommended for all patients with heart failure, regardless of their baseline rhythm. β-blockers are also utilized to regulate ventricular rates and prevent rapid and irregular ventricular activation caused by rapid and irregular atrial firing during atrial fibrillation (Grandi, E., & Ripplinger, C. M. 2019). Beta-blockers are the preferred first treatment for controlling the ventricular rate in atrial fibrillation (AF). These medications function by reducing the speed of electrical conduction via the atrioventricular (AV) node. They have been shown to be more effective in controlling the heart rate during exercise, particularly in patients with myocardial infarction (MI) or heart failure (HF). They are the preferred choice over digoxin and calcium channel blockers for these patients. Avoid administering β-blockers to individuals with chronic lung illness who are at risk of bronchoconstriction. In cases of acute atrial fibrillation (AF), the intravenous administration of esmolol, propranolol, and metoprolol has been proven to be effective. For chronic AF, oral administration of β-blockers such as atenolol, bisoprolol, metoprolol, nadolol, propranolol, and sotalol (which is a potassium channel blocker) has been found to be effective in controlling the ventricular rate (January, et.al 2014).   
 
 

 Sotalol, the most recently authorized oral antiarrhythmic medication, with a distinctive pharmacologic profile. The electrophysiology of this drug is attributed to its nonselective β-blocking action and class III antiarrhythmic activity. This includes blocking the fast-activating cardiac membrane–delayed rectifier current, resulting in prolonged action potential duration and refractory period in the entire heart. Additionally, it causes an increase in the QT interval on the surface electrocardiogram. The improved hemodynamic tolerance of this β-blocker may be attributed to its greater inotropy, which is linked to its class III action. Sotalol has a comparable capacity to inhibit ventricular ectopy as class I drugs and surpasses that of conventional β-blockers. The primary adverse effects of Sotalol are associated with β-blockade and the potential for torsades de pointes (which may be minimized with proper measures). Unlike many other antiarrhythmics, such as amiodarone, this medication does not have any pharmacokinetic drug-drug interactions, it is not metabolized, and it is completely eliminated from the body via the kidneys. The starting dosage is 80 mg taken twice day, with a progressive increase to a range of 240 to 360 mg per day as required. It is necessary to decrease the daily amount in individuals with renal failure (Anderson, J. L., & Prystowsky, E. N. 1999).  Sotalol is used with caution in patients with renal impairment, since it is mostly eliminated via the kidneys. Consequently, it is necessary to modify the dosage if the estimated glomerular filtration rate (eGFR) falls below 60 ml/min. If the glomerular filtration rate (GFR) is over 60 ml/min, the suggested starting dose of sotalol is 80 mg taken twice daily. The dosage may be gradually raised, with 2 to 3 days between each increment, up to a maximum of 320 mg. The higher amount should be split into 2 or 3 separate doses. If the creatinine clearance is between 40 to 60 ml/min, it is recommended to administer Sotalol once day. Evidence indicates that sotalol should be contraindicated during pregnancy. Sotalol has the potential to cause birth defects, hence it is not often recommended as the first treatment option for pregnant women. Close fetal monitoring is essential, as stated by Mubarik et al. (2022).  
 
 

β-blockers have been shown to reduce mortality in both acute myocardial infarction and when used for long-term treatment.  Present guidelines for acute myocardial infarction advocate the use of cardioselective oral β-blockers, such as metoprolol or atenolol. When it comes to long-term treatment after a heart attack, it is preferable to choose medications that do not have sympathomimetic effects. The effects of β-blockade include a decrease in the demand for oxygen by the heart muscle and a reduction in the burden of ischemia. This is achieved by lowering the heart rate, myocardial contractility, and blood pressure. Additionally, β-blockade prevents maladaptive ventricular remodeling and failure, and reduces the risk of ventricular fibrillation and sudden cardiac death (Grandi, E., & Ripplinger, C. M. 2019). 

  

The body is full with beta receptors, which have a wide variety of physiological consequences. Beta-blocker drugs that inhibit these receptors may have a variety of negative side effects. Hypotension and bradycardia are two frequent side effects that might happen. Constipation, nausea, fatigue, and dizziness are other often reported symptoms. A few people report experiencing erectile dysfunction and sexual dysfunction.Bronchospasm is less likely in persons using beta-blockers. Patients with asthma are more vulnerable. Individuals who have Raynaud syndrome are also susceptible to aggravation. Beta-blockers have the ability to cause hyperglycemia and conceal hemodynamic symptoms like tachycardia that are often present in hypoglycemic patients. When using beta-blockers, some patients have nightmares, sleeplessness, and altered sleep patterns. When using beta-blockers that penetrate the blood-brain barrier, this impact is more noticeable. Beta blockers may cause weariness or weight gain in some people. Stopping the medicine is one way to manage these side effects. It is more common for certain beta blockers to cause weariness or weight gain. In some cases, carvingilol may exacerbate edema. Sotalol causes QT prolongation by blocking the potassium channels in the heart. Torsades de pointes become more likely as a result. Heart block is a concern associated with all beta-blockers, particularly in people with cardiac risk factors. Glucagon is the antidote for beta-blocker overdose. In cases of beta-blocker-induced cardiotoxicity, it is quite helpful. If glucagon is ineffective, cardiac pacing—which might include transcutaneous or transvenous pacing—is the second line of therapy.  (Jan A. & Farzam K., 2023). 

  

References: 

  

Anderson, J. L., & Prystowsky, E. N. (1999). Sotalol: An important new antiarrhythmic. American heart journal, 137(3), 388–409. https://doi.org/10.1016/s0002-8703(99)70484-9 

  

Farzam K & Jan A. (2023). Beta Blockers. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.https://www.ncbi.nlm.nih.gov/books/NBK532906/ 

  

Grandi, E., & Ripplinger, C. M. (2019). Antiarrhythmic mechanisms of beta blocker therapy. Pharmacological research, 146, 104274. https://doi.org/10.1016/j.phrs.2019.104274 

  

January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr., Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW & Members AATF. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation 130, e199–267.  

  

Markus Meyer, Daniel Lustgarten, Beta-blockers in atrial fibrillation—trying to make sense of unsettling results, EP Europace, Volume 25, Issue 2, February 2023, Pages 260–262, https://doi.org/10.1093/europace/euad010 

  

Mubarik A, Kerndt CC, Cassagnol M. (2022).  Sotalol. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK534832/# 

  

Nesheiwat Z, Goyal A, Jagtap M. (2023). Atrial Fibrillation. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK526072/ 

  

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