Spalding University
School of Nursing and Health Sciences
Nursing Process Paper
Student Name: _David Morrison______Course #: _Nurs478
Date: 9/23/05, clinical date: 8/25/05 Week #: 1_____
Patient’s initial & room ___DJM, bed #8______Vitals:
Admission date/# of days in hospital: _8/24/05 - 1 day__ Day #1: 2100
BP 118/64 P113 T98.1 R14
Medical diagnosis: _Unstable angina, HT, hyperlipidemia, Day #2: 0800
Diabetes mellitus, degenerative disc disease (L1) BP 126/73 P113 T98.3 R16
(traumatic injury lower back, on disability), tobacco use
Surgical procedure: CABG X4 with SVG and LIMA secondary to cardiac catheterization positive for ostial stenosis Lt main artery (90%). Stenosis also in: Lt anterior descending coronary artery, Rt coronary artery.
Clinical Site: Audubon OHU
Abnormal lab values with rationale and citation (value 0.25):
Porth (2004, p. 298) indicates the importance of differential diagnosis between unstable angina and non-ST segment elevation MI, by stating that unstable angina is characterized by lack of serum markers for MI. The patient had a troponin level of 0.7, which is in the indeterminate range between unstable angina and non-ST segment elevation MI: normal is 0-0.1, indeterminate is 0.1-1.5, (Kee, 2002). A CRP (C-reactive protein) test would also be indicative of extent of inflammatory processes, but unfortunatly I was unable to find this in the chart. Lastly, Porth also states that an elevated WBC count (10K-20K) appearing on the second day and lasting up to a week, is indicative of MI, pt’s WBC count is 16.2K.
There was another issue which was unexpected from ABG’s: uncompensated metabolic acidosis. pH 7.316 (7.35-7.45); pCO2 41.9 (35-45); PO2 128 (80-100); HCO3- 20.8 (22-28); O2 Sat 98.4.
From Henderson-Hasselback equation:
CO2 + H2O ó H2CO3 ó HCO3-
A drop in bicarbonate shifts the equation to the left, and leads to a buildup of the conjugate acid (carbonic acid). Pt. was unabel to compensate with respirations at time of test, due to placement on ventillator (AC mode, FIO2 = 40%, R=14, tidal volume=700, PEEP =5).
Also, at 0700 8/25/05, I = 2359, O=2110 leading to a 24 hour surplus of 249 cc’s of fluid.
This is strange given that pt. was still on a surplus of fluids from drips and lines during the operation, and that the Bumex he was on (2 mg, IV, Q6H, a loop diuretic) has metabolic alkalosis listed as a side effect. Creatinine level = 1.0, BUN = 11, neither of which should indicate excessive HCO3 loss. I cannot explain this finding. Perhaps it is indicative of ketoacidosis, given his diabetes.
Abnormal studies (radiology, EKG, etc.) with rationale and citation (value 0.25):
Stress cardiolite with significant changes on EKG. Subsequent cardiac catheritization was positive for ostial stenosis Lt main artery (90%). Stenosis also in: Lt anterior descending coronary artery, Rt coronary artery. No swan. EF 65%, surprising considering the extent of his CAD.
Pathophysiology:
a. Underlying pathophysiology specific to your client. (value 0.25)
Ignativicius (2002, p. 789-790) states that CAD is caused primarily by atheroscelosis, which occurs as a result of: accumulation of lipids, especially LDL cholesterols, in the connective tissue on the margins between the tunica intima and the tunica media; overgrowth of smooth muscle cells with accumulation of macrophages and T cells, which increase the inflammatory response, further occluding the coronary artery; and, ultimatly, formation of a connective tissue matrix in the vessel intima. These processes lead to narrowing of the lumen; when the obstruction reaches more than 70% blood flow may not be adequate to perfuse the myocardium in response to tissue demands - and pain results. (Porth (2004) states that this occurs with a 75% or more occlusive reduction in cross-sectional area.) An increase in the number and intensity of attacks characterize unstable angina, which may indicate preinfarction angina.
Porth (2004), adds that there are two types of atherosclerotic lesions: “fixed or stable plaque, which obstructs blood flow, and the unstable or vulnerable plaque, which can rupture and cause platelet adhesion or thrombus formation”; the unstable plaques are indicated by unstable angina, and put the patient at greater risk of MI.
b. Expected findings compared to your client’s signs & symptoms (Value 0.25)
The patient does, have 2+ generalized edema, indicative of problems with low CO and increased peripheral vascular resistance (PVR). Diminished breath sounds, no JVD, no carotid bruits, no murmurs/gallops, no clubbing/cyanosis.
NURSING DIAGNOSIS Llist 3 appropriate complete 3 part diagnoses & prioritize Value = .6
1) Pain r/t traumatic surgery, postoperative immobility AEB client statements, facial expressions secondary to CABG procedure, degenerative disk disease (L1).
2) Decreased cardiac output (CO) r/t depressed cardiac function, increased systemic vascular resistance (SVR) AEB generalized 2+ pitting edema, peripheral pulses 2/1/1 secondary to CAD.
3) Risk for infection r/t invasive procedure AEB elevated WBC count secondary to CABG procedure.
Diagnosis # 1: Pain r/t traumatic surgery, postoperative immobility AEB client statements, facial expressions secondary to CABG procedure, degenerative disk disease (L1).
Subjective data: =.2pts Objective data: = .2 pts
Pt. rates pain “8” upon assessment HR 100-110’s
Pt. describes pain as “aching” or “intense” HR while awake initially 120’s
Pt. verbalizes “relief” from morphine 6 mg Pt. Frowning/grimicing noted.
Given Q 4 H. Some relief of facial expressions, and client statements, noted subsequent to placement in chair at 12:30.
Goal/Outcome value = .1 pts (What does your patient need to accomplish in your own words?)
Pt needs to learn how to manage pain by asking for pain medicine, before the pain is too intense (to ‘get ahead of the pain’). Pt. must communicate to the RN if pain meds are not providing sufficient relief. Pt. also should use hug pillow to chest while coughing. Pt needs to restart early mobility for pain relief of L1 vertebra. Pt. needs to know S/E of pain medication, including sedation and constipation.
NOC Title and page; date to be met:
Pain Control (p. 419), by 9/1/05.
Indicator #1- Name and present level; projected level and date: v = .1
NOC p. 228.
210001 Physical well-being. Present level 2 (8/25/05), projected level 3 (9/1/05).
Indicator #2- Name and present level; projected level and date: v = .1
210008 Pain control (p. 228).
Present level 2 (8/25/05), projected level 4 (9/1/05).
NIC: Title, Domain, Classification, page: v = .1/each
(See NIC pages 112-115)
Physiologic: basic, domain 1, class E (physical comfort promotion).
(See NIC, p. 529)
Assessment:
1 Perform a comprehensive assessment of pain to include location, characteristics, onset/duration, frequency, quality, intensity or severity, and precipitating factors.
2 Observe for nonverbal cures of discomfort, especially in those pts. Unable to communicate effectively (respirator).
3 Explore the pt’s knowledge and beliefs about pain.
4 Determine the impact of the pain experience on quality of life.
5 Explore with pt factors that relieve/worsen pain.
Therapeutic:
6 Ensure that pt receives attentive analgesic care.
7 Use therapeutic communication strategies to acknowledge the pain experience and convey acceptance of the pt’s response to pain.
8 Evaluate, with the pt and health care team, the effectiveness of past pain control measures that have been used.
Pt Education:
9 Teach principles of pain management.
10. Teach the use of nonpharmacological techniques (e.g., biofeedback, TENS, hypnosis, relaxation, guided imagery, music therapy, distraction, play therapy, activity therapy, acupressure, hot/cold application and massage) before pain occurs or increases, and along with other pain control measures.
11. Explore pt’s current use of pharmocological methods of pain relief.
Evaluation:
Pain Control (p. 419), by 9/1/05.
Indicator #1- Name and present level; projected level and date: v = .1
NOC p. 228.
210001 Physical well-being. Present level 2 (8/25/05), projected level 3 (9/1/05).
Indicator #2- Name and present level; projected level and date: v = .1
210008 Pain control (p. 228).
Present level 2 (8/25/05), projected level 4 (9/1/05).
Interdisciplinary Team Participation with Rationale: v = .25
1. Dietary consult; it is important for the pt. to understand the nurtitional risk factors leading to atherosclerosis, and the fact that his atherosclerosis is probably systemic, and not specific to his coronary blood vessels. He should know the glycemic index of different foods, the sodium content of processed foods, and the importance of reading content information on saturated fats.
2. Exercise physiologist; this would help the pt with both of his presenting concerns: lower back pain and CAD. I believe CVA associates has an excellent program staffed with nurses and exercise physiologists. It is a minimum of 12 weeks, to encourage lasting lifestyle changes. Given his status post-CABG, it would probably be paid for by his insurance. Exercise is the other key change which can lead to the prevention of both CAD and lower back pain, if properly supervised.
3. Respiratory consult: they could engage in patient education reinforcing the importance of his new commitment to smoking cessation. Also, they would be useful in collaborating on his ABG’s and current acidotic condition. Adequate oxygenation is important for preventing COPD, which the pt is at risk for, given his smoking history, and can lead to a more chronic condition of CHF.
Holistic/Psycho-social/Cultural influences of care: v = .35
Pt. is a 44 year old male who has a smoking Hx of 1 ppd X 22 years, who has recently said he has “smoked his last pack” (yesterday). Pt states that he ‘rarely drinks’. Pt works as a mechanic, for commercial vehicles, and states that many of the parts must be manually lifted out, which has lead to his degenerative disk condition. All of these factors (smoking, alcohol, and chronic pain with resultant stress) place him at further risk for contintued CAD. Pt lives with a 20 year old woman and her young child, but is not spiritually active within an affiliative community of like-minded individuals, and has limited extended peer or familial networks, making his social support network less stable and the role of social support in stress-reduction and overcoming practical obsticles (financial, exercise, maintaining lifestyle changes) potentially problematic.
*Remember to include @ least 2-3 interventions from appropriate research for one of your selected diagnoses. This is worth 1.5 points for seniors (T Nursing process = 6 pts) and 2 points for juniors (T Nursing process = 10 points )
Research Article Interventions:
1) (Patient education) Education on the “back education programme applied in the outpatient clinic of Istanbul Faculty of Medicine, Department of Physical Medicine and Rehabilitation” (Cakmak, et al., 2005, p. 7). Including appropriate “use of body mechanics” and “back protection methods (the structure and function of the spine, main causes of low back pain, importance of relaxation and exercises, appropriate standing, sitting, lying down and getting up, sleeping, weight lifting and weight carrying, etc.)” (Ibid., p. 7).
2) (Therapeutic interventions) Pt should also receive at least 8 weeks of intensive exercise programme three days a week; each lasting 1.5 hours. Pt will be taught relaxation positions (5-10 min duration), stretching exercises (for tissue flexibility and joint mobility), and application of Saal and Saal’s “dynamic lumbar stabilization process” (In Cakmak, et al., 2005, p. 7).
References
Dochterman, J. M. (2004). Nursing Interventions Classification (4th ed.). St. Louis, MO: Mosby.
Filiz, M., Cakmak, A. & Ozcan, E. (2005). The effectiveness of exercise programmes after lumbar disc surgery: a randomized controlled study. Clinical Rehabilitation, 19, 4-11.
Ignatavicius, D. (2002). Medical Surgical Nursing: Critical Thinking for Collaborative Care (4th ed.). Philadelphia, PA: Saunders.
Kee, J. L. (2002). Laboratory and diagnostic tests with nursing implications (6th ed.). Upper Saddle River, NJ: Prentice Hall.
Moorhead, S. (2004). Nursing Outcomes Classification (4th ed.). St. Louis, MO: Mosby.
Porth, C. (2005). Pathophysiology: Concepts of altered health states (7th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
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