CN II Process Paper

Clinical Nursing II Process Paper: Lower Keys Medical Center Rotation Rachael Crossgrove Clinical Nursing II Professor Sagan November 28, 2011

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TA is a 78 year old Hispanic woman who was admitted to the emergency room with shortness of breath and coughing three days prior to my working with her in the IMC. TAs native language is Spanish and she speaks very little English, but seems to have some understanding of it. It was very fortunate for both TA and myself that a nursing assistant

working on the floor was fluent in Spanish and was able to act as a translator for some of our interactions. This allowed me to discover quite a bit of useful information that probably I otherwise would not have been able to obtain. For example, TA tells the nursing assistant that her pain level is a 7/10 which makes it extremely difficult for her to rest comfortably. TA and I used a means of nonverbal techniques as well by using signs and gestures for her to communicate what she was feeling. For instance, TA demonstrated to me the rapid breathing pattern and used her arms to show me how her chest heaves in and out as she used her accessory muscles to breathe. Then TA sat back in the bed and slumped down while letting out one final sigh in an effort to show me that her breathing pattern makes her exhausted. Both methods of gathering information from TA, as well as reading through her chart helped me put together a good picture of TA. TAs demeanor was pleasant which led me to believe she understood my role as a student nurse. I believe she knew I was interested in listening to her and fostering a healthy nurse-patient relationship to be able to help her as best as I was able. I recognized TA from Key West Health and Rehabilitation. Last semester during clinical rotations I remember her being in a wheelchair, always smiling and very pleasant. TA ate in the cafeteria for her meals, participated in activities and was always dressed up. I learned that TA was a single mother to three children after the death of her husband many years earlier. She came to the United States from Cuba over twenty years ago seeing this country as an opportunity to better her familys life. TA has a close relationship with her daughter who is TAs surrogate

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and translator. Prior to her admission next door TA smoked three packs of cigarettes a day. TA suffers from dementia; therefore it is difficult to obtain accurate surgical and medical histories from her directly so I obtained the necessary information from her medical chart. I made sure to research TAs age related factors; older adults have very high rates of nosocomial infections with urinary tract infections being the most common. Infections in older adults may have atypical presentations showing cognitive and behavioral changes before alterations in laboratory values. Multiple factors lead to respiratory dysfunction in older adults. There is a reduction in ventilatory capacity, diminished elastic recoil and aging of the lungs may lead to alveolar dilation, larger airspaces and loss of surface area. After introducing myself to TA and finding out her psychosocial factors, I began to do my physical assessment of her keeping in mind all body systems are important but wanting to pay extra-special attention to looking at respiratory associated problems. TA is a dark skinned woman so I noted that it could be particularly difficult to tell if cyanosis was present and a good place to look for it would be in the conjunctiva (inside the lower eyelid) or lips. The first thing I had noticed earlier when I entered TAs room was that she was breathing room air and sleeping while sitting up with the head of the bed at about 45 degrees and she also had two pillows behind her back to prop her up even more. Thinking back to this observation, I asked TA if she laid on her back while she slept at night and she vigorously shook her head no and explained to me that she used three pillows, sometimes four to help her breathe. As I took TAs vital signs, I noted that her respirations were shallow, unlabored and 22 breaths per minute; pulse was 82, blood pressure 145/75, temperature 98.4. I noted 30 minutes earlier the respiratory therapist measured her oxygen saturation at 92% before her breathing treatment and 96% afterward. My next step was to auscultate TAs lung fields, so I asked her to breathe slowly and a little bit deeper than

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normal through her mouth. TA told me that she often had trouble breathing through her nez, pointing at her nose. I examined her nose with my penlight and found it to be symmetric with pink nasal mucosa, no edema and no drainage. I then looked inside her mouth, showing the same light pink color and moisture. I asked TA to swallow while I watched and lightly felt her trachea in the midline. I began listening at the apices and right away discovered a high pitched musical sound. I noted these wheezes only on expiration and on both sides. The wheezes decreased as I progressed through the upper, middle and lower fields both in the anterior and posterior of TA all the way to the lung bases. I could not hear these expiratory wheezes without the use of my stethoscope. I did not note any crackles, rhonchi or a friction rub. I watched the movement of TAs chest as she took several breaths and felt with my hands to see if movement (expansion) on both was equal and it was, though my fingers did not separate more than one centimeter at TAs spine signaling a shallow respiratory depth. I did not note an increase in AP diameter. I tried my hand at the percussion techniques to see if my skills at determining any sort of resonance could be useful and noted some low pitch sounds over the top of the lung field and dullness over the organ areas which are normal findings. Continuing my assessment through the various systems TAs eyes were a little reddened (bloodshot), pupils were equal, round and reacted to light and accommodation. No presence of venous neck distention and no bruits in the carotid pulses. I listened to the heart; rate was 82 and regular with normal lub-dub sounds, S1 louder than S2, no murmurs or rubs noted. TAs abdomen was soft, I noted a couple of darkened areas in the upper left quadrant which were bruises left from insulin injections given the previous days because of her sucre eleve (high blood sugar). I performed a blood glucose test on TA and the reading was 122g/dl so no coverage with insulin injection was necessary for the morning. Bowl sounds were present in all

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four quadrants and normal-active. TA denied any tenderness in the abdominal area, nausea or vomiting. TAs skin was warm and dry with sensation to touch, there was no evidence of breakdown or wounds. TAs skin turgor was fair, capillary refill less than 3 seconds with no clubbing of the nails. TA moved all her extremities; her muscle strength quite weak. Lower extremities showed edema 2+ in the feet and ankle region. Later on I looked at the intake and output records which showed more output (500-1000ml) than input in each of the two days prior. TA had 200ml of urine in the Foley collection bag at 8a.m. and it was pale yellow in color. I made a mental note to pay close attention to how much fluid TA was consuming and voiding as well as her blood pressure, cardiac status, and electrolytes as she was on the diuretic Lasix. Both radial and pedal pulses were palpable, both at a measure of +2. Just about this time the breakfast tray was arriving, so I asked TA if she needed help with anything, she shook her head no, so I placed her call bell within reach. I set the bed alarm and turned the bathroom light on as she had a yellow star above her door meaning fall risk. The Morse Fall Scale was 35 indicating moderate risk with no previous history of falls. TAs past medical history consists of COPD, dementia, depression, hypertension, CHF, adult onset diabetes and anemia. Pertinent lab findings for TA showed a slight increase in CO235(LKMC normal range 22-32) which is characteristic of respiratory alkalosis, an ineffective clearance of carbon dioxide, most likely related to the tenacious mucoid plug obstructing the left main bronchus. Hemoglobin 10.5g/dl (LKMC normal range 12-18) and hematocrit 31.5% (LKMC normal range 35-52) are both below normal range which may reflect the presence of fewer than normal erythrocytes within the circulation which supports TAs history of anemia. Iron 20, which is low (LKMC normal range 28-70) suggests anemia and excessive red blood cell destruction. A chest x-ray is the most common test for assessment of the respiratory system

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(Lewis 2007). A portable chest x-ray was taken to rule out possible interstitial lung disease, which is a general term used to describe pulmonary inflammation and /or fibrosis (Lewis 2007). The report revealed bilateral peripheral infiltrates caused by infection with viruses. Two days later a repeat chest x-ray revealed interval development of complete left lung atelectasis presumably on the basis of an endo-bronchial obstruction of the left main stem bronchus. A bronchoscopy was suggested and showed a decreased function of the right vocal cord and tenacious mucoid plug obstructing the left main bronchus. Blood cultures were performed before any antibiotic treatments were started and results were negative for growth in 5 days. An ECG was performed and results revealed moderate concentric left ventricular hypertrophy at a 70% ejection fraction, impaired left ventricular diastolic reaction, mitral valve stenosis and moderate tricuspid insufficiency with severe pulmonary hypertension. After assessment of history and symptoms the physician made a diagnosis of TAs presenting problem to be pneumonia with acuteon-chronic exacerbation of COPD. Pneumonia is an inflammatory illness of the lung. It is often described as lung parenchyma or alveolar inflammation leading to abnormal alveolar filling with fluid. Pneumonia can result from a variety of causes, including infection with microorganisms like bacteria, viruses, fungi, or parasites. Pneumonia can also result from chemical or physical injury to the lungs. Normally the airway distal to the larynx is sterile because of protective defensive mechanisms. Pneumonia is most likely to result when these defense mechanisms become incompetent or are overpowered by infectious agents. The acute exacerbation of COPD can be caused by a number of factors as the lungs are vulnerable organs to harmful particles in the air. An infection with a virus, bacteria or air pollutant may trigger an event. During exacerbation airway inflammation is increased resulting in hyperinflation, reduced expiratory airflow and decreased gas exchange. Eosinophils

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and neutrophils become the major component of the inflammatory response. This increase in inflammation by the causative stimulus leads to increased bronchial tone, increased bronchial wall edema and in increase in mucus production. As these processes worsen the ventilationperfusion mismatch and cause expiratory flow limitation which can cause the patient to manifest clinical symptoms such as dyspnea, cough, wheezing, sputum production and purulence, sensation of chest tightness/restriction, abnormal blood gases and fever. Soluble mediators such as endothelin-1 increase airflow obstruction by inducing bronchospasm and also stimulating mucus production, promoting airway edema and increasing vascular smooth muscle resistance and increasing the production of other cytokines. Infiltration of the airway by these inflammatory cells limits the flow of air and along with vascular protein leakage contributes to edema. (Lewis, 2007). When there is a greater effort required to breathe along with a change in lung volume and shortening of the inspiratory muscles (diaphragm), this can cause functional weakness. The net effect on the patient has to do with their being unable to overcome the increased lung loading and increased resistance to it unloading with weak muscles resulting in hyperventilation and the impending feeling of doom associated with the feeling of not being able to breathe. (Lehne, 2010). TAs current therapeutic drug regimen includes antibiotics; azithrpmycin, a macrolide, 500mg by IV daily and ceftriaxone (Rocephin) 1gm by IV daily, a third generation cyclosporine that treats lower respiratiory tract infections. These medications can be potentially nephrotoxic, which makes it especially important to monitor renal function tests. Protonix, a proton pump inhibitor, 40 mg orally daily increases gastric pH and reduces acid production. Prednisone, an anti-inflammatory adrenal corticosteroid, is administered 40mg orally once a day. Because this medication has many adverse effects patients must be monitored for electrolyte levels,

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fluctuations in blood pressure readings, glucose, infection and a number of other things. Furosemide (Lasix), a loop diuretic, 40mg orally daily which enhances the excretion of sodium and potassium, as well as chloride. Skin turgor, I&O, vital signs (especially blood pressure), and electrolytes should be carefully monitored. Ferrous sulfate 325 mg tab daily, an iron preparation to treat TAs anemia. Aspirin EC an anti-inflammatory, antipyretic and anticoagulant 81mg, is given orally every day. BuSpar HCL, a non-barbiturate antianxiety is given twice daily, a dose of 5mg orally. To treat TAs hypertension Tenormin, a beta blocker is given 25mg orally daily. A sliding scale for regular insulin is used if TAs blood glucose is above 150mg/dl. B12 injections are given subcutaneously, 1000mEq every week to treat her anemia. 600mg of Mucinex ER, an expectorant is given orally with meals. Dulcolax EC, 10mg orally is given daily; it is a GI stimulant, and a laxative that is used to treat constipation. At bedtime TA is given mirtazapine (Remeron), an antidepressant, 30mg orally along with phenytoin sodium ER (Dilantin Kapseal ER) 300mg orally, which is an anticonvulsant, antiarrhythmic (TA has a history of seizures). TAs respiratory treatments include inhalations of the bronchodilators albuterol sulfate, every four hours, formoterol fumarate (Floradil) a beta-2 agonist, twice daily, and tiotropium (Spiriva), an anticholinergic, one time each day. Also included is fluticasone (Flovent), a corticosteroid. (Hodgson, B.B. & Kizior, R.J.,2010). In using the ABCs (airway, breathing, and circulation) of nursing, I have determined the priority nursing diagnosis pertinent for TA is Ineffective Breathing Pattern related to inflammation and pain as evidenced by dyspnea, tachypnea (respiratory rate of 22 breathes per minute) with shallow depth, nasal flaring, expiratory wheezes on auscultation, and patient stating pain 7/10 with shortness of breath.

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My goal for TA: she will have an effective breathing pattern throughout my shift with her at the hospital as evidenced by no episodes of dyspnea, respiratory rate regular and unlabored within the normal limit of 10-20 breaths per minute. I first began with interventions that were used to assess TAs respiratory status to establish a baseline set of data by using the evidence that I gathered from my initial review of systems in the morning. I also looked at her medical chart to compare the data I obtained with information from the previous days to see if I noticed any patterns or trends. For example, I noticed that TAs 8a.m. vital sign measurements of respirations (22-26) tended to be higher than the measurements taken at noon (16-20) over the past week. Could this have been due to respiratory therapy? I made sure to monitor TAs respiratory rate, depth, and ease of respirations every 1-2 hours (a respiratory rate higher than 20 can signal respiratory disease and potential for respiratory distress). I noted the pattern of TAs respirations, if she was breathing too rapidly, slow or deep, and any other abnormal patterns that could signal dyspnea. Patients with COPD often experience a great deal of anxiety in acute exacerbations leading to worsening respiratory distress, so I made sure to monitor TA for any signs of anxiety such as restlessness and agitation, tense muscles, rapid heart rate, headaches, dizziness, tremors, shaking or sweating because dyspnea can be a combination of both physiological and psychological factors. I questioned TA of any pain she had using a pain scale of 0-10, 10 being the worst pain ever felt. I noted if TA used any types of abdominal breathing, use of accessory muscles, nasal flaring, or retractions. I monitored for irritability, confusion and lethargy because both of these physical and mental changes can signal increasing respiratory difficulty and increasing hypoxia. I made sure to observe the color of TAs tongue and oral mucosa especially because of her dark complexion, color changes in these areas could imply central cyanosis, which is very serious. I was also sure

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to be aware for signs of peripheral cyanosis in the nail beds and lips that may not be as serious as central signs. I made sure to listen to TAs breath sounds every 1-2hours, noting if there were decreased or absent sounds, crackles or wheezes because TA has a respiratory pathology (COPD) she may have abnormal lung sounds and a change in the sounds could mean TA has altered breathing. I made sure to monitor TAs oxygenation status via pulse oximeter (an oxygen saturation between 92-100% indicates adequate tissue oxygenation). I followed up with monitoring TAs ABGs, making sure the values were within normal limits (a partial pressure of oxygen of less than 80% indicates significant oxygenation problems). I positioned TA in an upright position, elevating the head of the bed to 45 degrees and providing extra pillows as necessary to accommodate TAs level of comfort (the semi-fowlers position supports lung expansion). I placed the over bed table next to TA because the tripod position can help in the ease of breathing. I encouraged TA to take deep breaths at least every hour and coached her to slow her respirations by breathing at the same rate as me and performing the pursed lip technique. I made sure to administer and titrate oxygen therapy as prescribed (the effectiveness of oxygen therapy is monitored by improvement in clinical signs and symptoms, adequate oxygenation readings or ABG analysis). I administered TAs medications (e.g., bronchodilators) as prescribed to reduce bronchospasm and mobilize secretions. As always, I made sure to explain all procedures to TA and provided her with emotional support to decrease her anxiety. In evaluating as to whether TA had met the priority goal of an effective breathing pattern throughout my shift with her I stated this as being a partially met goal. TA had no episodes, signs or symptoms of shortness of breath (dyspnea), though she did have a respiratory rate of 22bpm on one respiratory assessment at 10a.m. At this time I intervened to elevate the head of

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the bed from 30 degrees to a better position at 45 degrees and assisted in coaching TA to take slower, deeper breaths with pursed-lips to help control her rate. TA was very amendable in listening to and providing return demonstrations of teaching that I was able to provide because there was a nursing assistant there to act as a translator. I provided education on the use of breathing techniques which help reduce anxiety that could be associated with dyspenic episodes allowing TA to feel like she has more control over her breathing. I was able to meet TAs daughter who spoke English so I taught her about TAs medications, their actions, side-effects and how they should be properly used. I explained situations that TA should avoid that could exacerbate an ineffective breathing pattern such as exposure to persons with respiratory infections and air pollutants, especially smoke. TAs daughter identified that she would be vigil in looking out for the potential triggers. Working with TA was a very interesting learning experience for me. It was a challenge to work with someone that spoke a different language, but this did give me a great opportunity to explore and practice the use of other methods of non-verbal communication, like using gestures and reading facial expressions. Being able to be flexible in my work of gathering data from TA allowed me to better plan the use of my time to be able to get information in various ways and at different times than I would have preferred, as I was saving key questions and topics to discuss when the translator was available. I was able to establish a nurse-patient relationship in a circumstance that at first I did not think would be possible, this brought a great feeling of satisfaction in overcoming an obstacle. I could see TA was appreciative for all of the effort spent in helping her in her non-verbal way as she smiled and the translator said TA thanked me many times over for being so dedicated to my duties to her this day. I was grateful to have TA as a

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patient because she helped me to gain knowledge and practice adapting my skills to better meet the needs of each individual patient.

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References Ackley, B.J., and Ladwig, G.B. (2008). Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care. (8th ed.). St. Louis, MO: Mosby Elsevier.

Hodgson, B.B. and Kizior, R.J. (2010). Saunders Nursing Drug Handbook. St. Louis, MO: Saunders Elsevier.

Lehne, R.A. (2010). Pharmacology for Nursing Care. (7th ed.). St. Louis, MO: Saunders Elsevier.

Lewis, S.L., Heitkemper, M.M., Dirksen, S.R., OBrien, P.G., and Bucher, L. (2007). Medical-Surgical Nursing: Assessment and Management of Clinical Problems. (7th ed.). St. Louis, MO: Mosby Elsevier.