Question

Shirley’s husband died unexpectedly 2 months ago, which is the she entered an assisted living facility. Shirley states she has become depressed form the loss of her husband and the inability to physically do activities she desires due to the COPD. Shirley presents to the ER with difficulty breathing and Shortness of breath at the rest, and increase fatigue. The patient is currently on 2 liters of O2 nasal canula at all times. Shirly smoked cigarettes for 32 years and just recently quit 2 months ago when she was put on full-time oxygen. Hysterectomy at age 48. GERD and Atrial Fibrillation.

The rationale for the priority of patient assessments, the nursing diagnosis, related factor, outcome, and nursing interventions with the patient information NANDA Nursing Diagnosis and related to factor?

Answer 1

Ans.

Herein, GERD was not associated with risk of AF after adjustment for other risk factors. However, acid reflux disease significantly increased the risk of AF only in the presence of oesophagitis (HR 1.94, 95% CI 1.35–2.78). ... In this case–control study, 32 patients with GERD and arrhythmias were included.

Palpitations are irregular heartbeats that can occur sporadically or frequently. Although palpitations have many direct causes, gastroesophageal reflux disease (GERD), the long-term and frequent occurrence of acid reflux, is unlikely to be one of them.

Risk Factors

Certain patients are at risk for GERD. They include those who are/have:

• Obese
• Pregnant
• Smokers
• Dry mouth
• Asthma
• Hiatal hernias (top of stomach goes up into the diaphragm).
• Connective tissue disorders
• Diabetes
• Delayed gastric emptying

An electrical activity disturbance in the heart that causes an irregular and often rapid heartbeat. The atria quiver sending confusing electrical signals to the ventricles, leaving them unsure of when to contract thus beating irregularly. During atrial fibrillation, the heart is a less effective pump because of the quivering as well as not emptying completely. This causes the blood to pool and a clot can form. The clot can venture out of the heart into the lungs (PE), brain (stroke) or extremities (DVT).

Etiology

The specific cause of atrial fibrillation is unknown but there are risk factors that put someone at higher risk of developing afib. Risk factors such as smoking, hypertension, and obesity as well as conditions such as diabetes or heart disease increase the likelihood that a patient may get atrial fibrillation. Post surgical interventions present a major risk for atrial fibrillation as well. Approximately 30%-40% of cardiac surgery patients develop atrial fibrillation.

Desired Outcome

Decreasing risks of clot formation, a heart rate within normal limits and rhythm control. The ultimate outcome is converting back to normal sinus rhythm, however, many people live with atrial fibrillation, especially if rhythm control doesn’t work or isn’t necessary.

Atrial Fibrillation (AFib) Nursing Care Plan

Subjective Data:

Subjective Data:

• Heart Palpitations
• Feeling like the heart is beating out of the chest
• Feeling a fluttering sensation in the chest
• Nausea
• Lightheadedness
• Weakness
• ***Patient may not have any symptoms at all***

Objective Data:

Objective Data:

• Irregular heartbeat
• Tachycardia

Nursing Interventions and Rationales

• Obtain a 12 lead ECG

• Used to diagnose atrial fibrillation
• The waves are more chaotic and random
• The beat is irregular
• You can see the atria quivering between the QRS (ventricles pumping)
• No discernible P waves The ventricular rate is often 110-160 bpm and the QRS complexes is usually less than 120 ms.

• Potential rhythm control: Electrocardioversion, Ablation, Pacemaker

• -Electrocardioversion: AKA cardioversion, is used to “reset” the heart’s electricity.The patient will be shocked on the outside of the chest wall. This treatment is used for patients who have infrequent episodes of atrial fibrillation because if the patient has it frequently, they have a high probability of the afib returning after being cardioverted.***If there is a blood clot in the atria, cardioverting may send the clot out of the heart to the brain, lungs, or extremities. The chance of a blood clot increases the longer the patient is in afib, consider anticoagulation prior to cardioversion***Ablation: used for patient’s that have not been able to control their afib for a long time with medications or cardioversion. A catheter is inserted into the patient’s heart and destroys cardiac muscle cells so they scar, causing the electrical activity to stop in those cells, thus eliminating the passing of chaotic electrical activity.Pacemaker: This is placed under the skin and is a device that sends electrical signals to the heart to help it beat with the right rhythm and pace.

• Heart rate control: Beta Blockers: -Propranolol -Metoprolol -Atenolol Calcium Channel Blockers: -Diltiazem -Verapamil Cardiac Glycosides: -Digoxin

A heart can only sustain rapid beating for so long before it tires out. Using beta blockers, calcium channel blockers and cardiac glycosides will help control the rate of the heart beat.

Beta Blockers: They block beta 1 receptors from being stimulated. Stimulation of Beta 1 causes positive inotropic (force of contraction) and chronotropic (pace of heart beat) effects. If you block beta 1 you will have decreased force of contraction and decreased heart rate.

Calcium Channel Blockers: They block calcium channels… Duh. When calcium enters the cell in causes the cell to contract, thus when the channels are blocked, it decreases the production of electrical activity innately decreasing the heart rate.

Cardiac Glycosides: This medication stimulates the Vagus nerve, which when stimulated slows the heart rate down. The vagus nerve is a CNS nerve that also works with the PNS- specifically the autonomic parasympathetic system… AKA rest and digest… So if this is stimulated your body will rest/slow down, thus decreased heart rate.

It also blocks the Na+/K+ channel in cardiac myocytes. When this channel is open, K+ moves into the cell and Na+ moves out of the cell, called repolarization and is the relaxation part of a heart beat. When it is blocked it causes increased contractility of the heart. If your heart is beating stronger it will inherently slow down.

• Anticoagulant Therapy: Coumadin Aspirin Lovenox Plavix Eliquis

• Thinning the blood helps to disintegrate and break up the clot as well as increasing flow of blood. There are many options for blood thinners each with their own pro’s and con’s. The most common are listed to the left.

• Fall education

• Being on a blood thinner, the patient needs to be informed of their risk of bleeding out especially if they fall and hit their head.
• Make sure to go over environmental hazards such as good lighting and eliminating throw rugs.
• If a patient does fall and hit their head they need to go to the ER immediately, even if they are not experiencing any adverse effects.

• Stroke education Use the FAST Mnemonic: F: Facial drooping A: Arm weakness S: Slurred speech T: Time to call 911

• The risk of a blood clot forming and moving to the brain is fairly high. It is important to teach the patient and their family members the signs and symptoms of stroke.
• Teach the patient that if they feel confused or feel weakness on one side to call for help.

• Cardiac enzyme monitoring: Troponin I Creatine Kinase MB

• Initial measurement of the cardiac enzymes is important because it helps with any trending information, the sooner you get this information the better. Also getting trending results over specific periods of time is helpful.
• Troponin I: Is an enzyme that helps the interaction of myosin and actin in the cardiac muscle. When necrosis of the myocyte happens, the contents of the cell eventually will be released into the bloodstream.
• Troponin can become elevated 2-4 hours after in ischemic cardiac event and can stay elevated for up to 14 days.
• Creatine Kinase MB: This enzyme is found in the cardiac muscle cells and catalyses the conversion of ATP into ADP giving your cells energy to contract. When the cardiac muscle cells are damaged the enzyme is eventually released into the bloodstream.
• CKMB levels should be checked at admission, and then every 8 hours afterwards.