Case Study Congestive Heart Failure

Running head: Congestive Heart Failure: A Comprehensive Study 1

Congestive Heart Failure: A Comprehensive Case Study

Cynthia T. Lee

University of Arizona

Congestive Heart Failure 2

Congestive Heart Failure: A Comprehensive Case Study

The patient is a 65-year-old African-American male with a history of coronary artery

disease, essential hypertension, tobacco-use, abdominal, aortic, and renal artery aneurysms, and

Hepatitis C. His surgical history includes a L4-L5 laminectomy (in 2010) and a coronary artery

bypass graft (in 2007). His chief complaint for his visit to the emergency department (ED) was

back pain. Upon ED assessment, the patient was found to have signs and symptoms of heart

failure: dyspnea, weight gain, abdominal distension, bilateral leg edema, and complaints of

fatigue. Diagnostic tests were performed and confirmed heart failure (see Physician’s Orders and

Diagnostic Tests section). The patient was then transferred to the cardiac floor with the medical

diagnosis of congestive heart failure. The patient’s heart failure is categorized as a New York

Heart Association (NYHA) class III, which means the patient is comfortable at rest usually, but

is limited upon exertion. Less than ordinary physical activity causes dyspnea, angina pain,

palpitations, or fatigue (Lewis et al., 2014)

The patient is a retired veteran who graduated from high school with his diploma. He

states that he is a smoker and smokes two packs of cigarettes per day. The patient mentioned that

he has been doing this for the past thirty years and has not tried quitting in the past. This retired

veteran also drinks two beers on a daily basis. He has a body mass index (BMI) of 34.4, which

places him in the obese category. The patient does not engage in any routine physical activity,

and leads a sedentary lifestyle.

This veteran resides at home with his wife; he is her primary caregiver. They have three

sons, all of which have families of their own. He is currently worried about his wife since she

recently had a stroke. The patient is alert and oriented, and has a friendly disposition. He is

cooperative, and responds appropriately to instruction. The patient is allergic to beta-lactam


antimicrobials, and is currently on two liters of oxygen via nasal cannula. He does not use any

ambulatory aids, nor does he have a history of falls. The patient does not exhibit suicide ideation

and does not have any barriers to learning.

Physiology

The cardiovascular system is made up of the heart and blood vessels. The blood vessels

are arranged into two loops: systemic circulation and pulmonary circulation. While the heart

contracts, it simultaneously pumps blood into both loops (Lewis et al, 2014) The heart is capable

of making adjustments in stroke volume to meet the body’s changing metabolic needs (Fletcher

&Thomas, 2001). The intrinsic elasticity of the myocardium allows optimal ventricular emptying

(cardiac output) without an increase in myocardial oxygen requirement or variation in average

arterial pressure (Fletcher &Thomas, 2001).

The cardiovascular system affects all other body systems as well, especially the

respiratory, renal, and digestive system. The respiratory system is responsible for four main

functions: supplying oxygen to the body for the production of energy, removing carbon dioxide

as a waste products of energy reactions, maintain homeostasis of arterial blood, and maintaining

heat exchange (Lewis et al., 2014). The renal system filters waste from the bloodstream and

produces urine to expel it from the body. The kidneys play an important role in that system; it

prevents the buildup of extra fluid in the body, keeps electrolyte levels stable, and makes

hormones that help regulate blood pressure (Lewis et al., 2014). The digestive system main

functions are to digest and absorb nutrients.

Pathophysiology

It is estimated that 5.1 million people currently have heart failure in the United States

(Lewis et al., 2014). According to the American Heart Association, over 600,000 new cases are


diagnosed each year (Lewis et al., 2014). Nearly 10% of Americans over the age of 65 have

symptomatic heart failure, and approximately 20% of the asymptomatic individuals over the age

of 40 have some evidence of myocardial dysfunction (McCance & Huether, 2014). Hypertension

and coronary artery disease (CAD) are the primary risk factors for heart failure, both of which

are seen in the patient’s medical history. Other predisposing factors are the patient’s advanced

age, use of tobacco, and obesity (Lewis et al., 2014).

Heart failure is a condition that results from an abnormality in myocardial function. This

abnormality causes the heart the inability to deliver enough oxygenated blood to meet the

metabolic needs of the rest of the body (Fletcher & Thomas, 2001). When the right and left

ventricles fail to pump, pulmonary and systemic venous hypertension develops, which results in

the syndrome of CHF. The syndrome of CHF is associated with dyspnea upon rest and exertion,

lower extremity edema, and activity intolerance (Fletcher & Thomas, 2001). The patient

experiences all of these manifestations. He complained about shortness of breath upon exertion,

has +2 pitting edema, and does not engage in much physical activity.

Systolic dysfunction is characterized by an ejection fraction of less than 40%; this results

from the depression of the contractile force of the myocardium which often times results in a thin

and dilated heart muscle that is incapable of maintaining an adequate cardiac output (Fletcher &

Thomas, 2001). Systolic dysfunction is the most common cause of CHF and most often results

from myocardial infarction. Diastolic dysfunction is impairment in the diastolic filing of the left

ventricle and is secondary to the loss of muscle fiber elasticity. Diastolic dysfunction is

associated most often with long standing hypertension. Decreased ventricular compliance

(increased stiffness) and impaired ventricular relaxation are the mechanisms responsible for

diastolic dysfunction (Fletcher & Thomas, 2001). Impairment in the diastolic filling of the left


ventricle can be the result of ischemia, hypertrophy, reduction in beta-adrenergic tone, or

increased myocardial connective tissue. The increased work of the left ventricle eventually

causes hypertrophy of the muscle, which further decreased the contractility of the muscle fiber

and results in impaired relation. The hypertrophied left ventricle is unable to adequately fill,

leading to decreased stroke volume, decreased cardiac output, and symptoms of CHF (Fletcher &

Thomas, 2001). The low cardiac output simulates the compensatory neuro-hormonal systems

that increase circulating blood volume and filling pressures and results in further pulmonary

congestion. The patient’s chest x-ray confirmed the patient’s pulmonary congestion. Crackles are

audible in the lower bases of the patient’s lungs, and he suffers from dyspnea.

Other body organs are affected by CHF: the lungs, kidney, liver, intestines, and

peripheral extremities. The lungs may become congested with fluid thereby increasing activity

intolerance. The reduced function of the kidneys can cause the body to retain more fluid

(McCance & Huether, 2014). Fluid may also accumulate in the liver, which impairs its ability to

produce essential proteins and rid toxins in the body. Intestines may be less efficient in its

absorption of nutrients and medicine. The retained fluid may accumulate in the extremities,

causing peripheral edema.

Physicians Orders and Diagnostic Tests

The physician’s orders for this patient were a fluid restriction of less than 1500mL per

day, strict measurement of inputs and outputs, a cardiac diet, and daily weights. These are all

common orders for those diagnosed with CHF. These orders were easy to enforce because the

medical staff measured the patient’s intake of liquids after every meal and were aware of how

many times his pitcher was filled a day. The patient also uses a urinal, so his urine output was

measured frequently. When an order is put in for a cardiac diet, a low-sodium food tray is sent up


to the patient’s room for every meal. The diagnostic tests performed on the patient were labs, a

chest x-ray and also an abdominal/ pelvic x-ray. The patient’s hemoglobin levels were low. This

lab measures the gas-carrying ability of red blood cells. When this lab value is low, it indicates

excess fluid volume, which is a common manifestation of CHF. The patient had pitting edema

and a distended abdomen. The patient’s blood urea nitrogen (BUN) values were high. An

increased level of BUN indicates a reduction of the glomerular filtration rate, which means the

kidneys are having problems. If the kidneys are struggling, this supports why there is excess

fluid volume. For a more comprehensive list of lab results, see Appendix B. The purpose of the

chest x-ray was for the patient’s shortness of breath. Crackles were also heard in the lower lobes

of the lungs. The x-ray results showed pulmonary congestion, which is a manifestation of CHF.

The patient had a distended stomach, so an order for an abdominal x-ray was placed. This x-ray

showed an accumulation of fluid in the abdomen. There were no signs of obstruction (Appendix

C).

Medications

The patient’s medical regime is fairly extensive, so only those concerning CHF will be

discussed in this section. For a list of the patient’s full medication regime, please see Appendix A

The medications most commonly used to treat CHF are ACE inhibitors, beta-blockers, and

diuretics (Fletcher & Thomas, 2001). The patient is on the ACE inhib itor lisinopril, which is the

generic of Zestril or Prinivil. He currently gets a 40mg tablet by mouth daily. This drug works by

inhibiting the enzymatic conversion of angiotensin I to angiotensin II, a vasoconstrictor.

Lisinopril decreases both the afterload and preload. This medication also decreases water

retention, by inhibiting the stimulation of adrenal cortex to release aldosterone (Fletcher &

Thomas, 2001). Specifically for the patient, this medication treats his hypertension and his CHF.


The nurse should monitor the patient’s neutrophil levels, blood pressure, and CHF symptoms.

The patient is very cooperative when taking his medications, and his blood pressure (though

high) has stayed stable for the clinical week.

The patient is on the beta-blocker carvedilol, which is the generic for Coreg. The patient

is taking a 3.125 mg tablet by mouth twice a day. This medication is a nonselective vasodilating

beta-blocker with moderate alpha-blocker activity. The therapeutic effects of carvedilol are to

decrease heart rate and blood pressure, improve cardiac output, and slow CHF progression

(Fletcher & Thomas, 2001). Carvedilol also improves renal hemodynamics in patients with CHF.

Nursing implications of this medication are to monitor blood pressure and pulse frequently

during dose adjustment and periodically during therapy. The nurse should also monitor daily

weight and intake and output. Again, the patient is cooperative in taking his medication. His

blood pressure remained steady for the clinical week, and his bilateral lower leg edema lessened

from a +2 to a +1.

The patient is on the diuretic furosemide, which is the generic for Lasix. He is taking

furosemide in two forms: intravenous push (IVP) and by tablet. His dosages are 40mg/4ml IVP

and a 40mg tablet every twelve hours. Diuretics inhibit the reabsorption of sodium and chloride

at the different sites in the renal tubules (Fletcher & Thomas, 2001). This patient abdomen is

distended, and he has pitting edema in his lower extremities. Furosemide was prescribed to the

patient specifically for the excess fluid in his system. Nursing implications for this medication

are to monitor patient’s fluid status: document intake and output, monitor blood pressure, and

check peripheral pulses. The patient’s blood pressure remained steady for the rest of the clinical

week. His radial, dorsal pedis, and post tibialis pulses were palpable bilaterally. The patient’s

bilateral, pitting edema reduced from a +2 to a +1.


The patient is also taking acetylsalicylic acid also known as aspirin. He takes an 81mg

tablet once a day. Aspirin is an antiplatelet agent that has been proven to reduce ischemic events

in patients recovering from a myocardial infarction and patients with angina (Fletcher and

Thomas, 2001). Patients with heart failure secondary to CAD should be prescribed aspirin. The

nurse should assess for pain and monitor for any adverse reactions.

Nursing Diagnoses

Being that the patient was recently diagnosed with congestive heart failure, the nursing

diagnoses are focused on the manifestations from this chronic condition. It was understood that

the patient’s chief complaint was back pain; however, the back pain was a chronic condition that

the patient was aware of. He agreed that his treatment should be focused on CHF and mentioned

that he would like to learn more about his condition. The patient mentioned that his back pain

was a “lost cause.”

The first nursing diagnosis developed for the patient is impaired gas exchange related to

pulmonary congestion secondary to congestive heart failure as evidenced by decreased oxygen

saturations of 83%-90%, shortness of breath upon exertion, headache upon waking, smoking,

and crackles in the bilateral bases. The goal for this diagnosis is to maintain adequate oxygen and

carbon dioxide exchange. The smart, measureable, attainable, realistic, and time-based

(SMART) outcome for this diagnosis is the patient’s oxygen saturation will be at 92% or higher

by the end of the clinical week.

The interventions developed for this diagnosis are: monitor oxygen saturation using pulse

oximetry, work with the patient to determine which strategies help alleviate dyspnea, and

educate the patient on the rationale behind smoking cessation. The rational for the first

intervention is that pulse oximetry is useful in tracking and adjusting supplemental oxygen


therapy (Lewis et al, 2014). The patient was hooked up to the pulse oximeter for the remainder

of the clinical week. If his oxygen saturation level went below 90%, the machine would start

beeping to alert the healthcare staff. Then the staff would adjust the oxygen as needed or tell the

patient to take deeper breaths. The rationale for the second intervention is that self-management

enables patients to use effective methods that manage their illness, which leads to more positive

outcomes (Lewis, et al., 2014). The patient stated that his dyspnea worsens when he is moving

around. The rationale for the third intervention is that by educating the patient on how

interventions are focused on the needs of his personal care and how the illness progresses,

patient’s symptom management is improved (Lewis et al., 2014). The patient verbalized that he

was willing to quit smoking, and that he has not smoked since he was admitted. His only concern

was if he would have resources if he needed them after his hospital stay, in which, I provided

him a handout.

The outcome for this diagnosis was fully met. By the end of my clinical week, the

patient’s oxygen saturation was at a 94% on two liters of oxygen via nasal cannula, and his

headache dissipated. The patient also stated that there was a reduction in his shortness of breath

as he moved from his bed to his chair.

The second nursing diagnosis is excess fluid volume related to the increase of venous

pressure and the decrease of renal perfusion secondary to congestive heart failure as evidenced

by patient’s rapid weight gain of twenty pounds in two months, adventitious breath sounds, and

bilateral edema in the lower extremities. The goal for this diagnosis is to reduce peripheral

edema. The SMART outcome for this diagnosis is that the patient’s bilateral lower leg pitting

edema will reduce from a +2 to a +1 by the end of the clinical week.


The interventions for this patient are: educate the importance of restricting liquid intake

to 1500mL per day, educate the importance of reducing sodium intake to less than 2400mg per

day, and administer diuretic medications in a timely manner. The rational for the first and second

intervention is that decreasing fluid and sodium intake decreases extracellular water, which also

decreases edema, reduces activity intolerance, and enhances quality of life (Ramirez et al, 2004).

The patient verbalized understanding that his liquid intake should be less than 1.5 of those

hospital pitchers. He also verbalized that to help with thirst, he could suck on ice chips. The

patient also was able discuss which foods were high in sodium, for example, chips, canned

foods, microwaveable foods, and processed foods. He verbalized his understanding that products

that contain high sodium will cause water retention. The rational for the third intervention is that

administering heart failure medications can reduce mortality and morbidity and improve quality

of life and symptoms in heart failure patients (Clark, 2004). The patient was very cooperative in

taking his medications. He only refused heparin occasionally.

The outcome for this diagnosis was fully met. By the end of the clinical week the

patient’s pitting edema reduced from +2 to +1. The patient’s diuretics were administered on

time. The staff was well aware of his fluid restriction, and he had an order for a cardiac diet. The

patient’s legs looked less swollen, and he did not gain weight during the clinical week.

The third nursing diagnosis is activity intolerance related to imbalance of the patient’s

oxygen supply and demand as evidenced by dyspnea, shortness of breath, and weakness. The

goal for this diagnosis is to achieve a program of activity that balances physical exertion with

energy conservation techniques. The SMART outcome for this diagnosis is that the patient will

be able to ambulate to and from the bathroom five times by the end of the nursing shift.


The interventions developed for this intervention are: allow for periods of rest before and

after exertion periods such as baths, treatments, meals, and physical activity, encourage that the

patient ambulates 30 minutes a day three times a week, and help the patient with energy

conservation pertaining to activities of daily living (ADLs). The rational for the first intervention

is that both physical and emotional rest help to lower arterial pressure and reduces the

myocardium workload (Lewis et al., 2014). The patient was told that he might need to take more

breaks than he was used to, and that this was common with heart failure. He verbalized that he

understood. The patient also demonstrated his understanding after he took his shower. He sat in

the shower for ten minutes before getting up to change. The rational for the second intervention

is that aerobic exercise can reduce mortality and morbidity and improve quality of life in patients

with mild to moderate heart failure (Clark et al., 2004). The patient verbalized understanding that

he should try to walk for thirty minutes three times a week. He mentioned that it would be a

challenge, but he would try his best. The patient was observed to be moving around more in his

room. The rational for the third intervention is that by simplifying the workload of ADLs, the

patient will experience less discomfort (Lewis et al., 2014). He would be able to complete his

normal activities without overly exerting himself. The patient was able to verbalize activities in

which he could modify to conserve energy, such as shaving, brushing his teeth, and combing his

hair on a stool rather than standing.

The outcome for this diagnosis was partially met. The patient ambulated to and from the

bathroom three times before the end of the nursing shift. The patient started breathing more

rapidly and complained of shortness of breath. He did take breaks between each ambulation to

and from the bathroom.


Review of Literature

Fayazi, Zarea, Abbasi, and Ahmadi (2012) conducted a study to determine the effect of a

home-based walking program on the performance and quality of life in heart failure patients. The

design of this study was a quasi-experimental trial that compared eight weeks of a home-based

walking exercise program in a training group versus a control group. Assessments of

performance and quality of life were measured in both groups at entry and after eight weeks. The

study was conducted in a hospital that is linked to Iran University of Medical Sciences and also

in the patient’s homes. The design of the study was approved by the local hospital and informed

consent was obtained from the participating patients.

The sample size of this study consisted of sixty New York Heart Association (NYHA)

class II and III heart failure patients. Those included were between the ages of 40-75, had heart

failure for a duration of more than six months, a left ventricular ejection fraction of equal to or

less than forty percent, a documented ejection fraction conducted within the past year by

echocardiogram, stabilization on cardiac medications for at least six months prior to study

enrollment, and stable mild-to-moderate heart failure NYHA class II and III (Fayazi et al., 2012).

Those excluded from the study were those with chronic obstructive pulmonary disease (COPD),

documented ventricular tachycardia, exercise-induced ischemia, uncontrolled hypertension,

uncontrolled diabetes, orthopedic diseases, neurological diseases, renal insufficiency,

psychotropic usage, and psychiatric disorders (Fayazi et al., 2012). The individuals in both

groups matched according to age, sex, body mass index (BMI), heart failure, disease intensity,

disease duration, smoking status, and ejection fraction. The groups were split evenly, 30 in the

training group and 30 in the control group.


The study used the Minnesota Living with Heart Failure Questionnaire (MLHFQ) to

assess quality of life. This questionnaire assessed the patient’s perception of the effects of heart

failure on the socioeconomic, psychological, and physical aspects of their life (Fayazi et al.,

2012). Patients responded to twenty-one questions using a six-point Liker scale, with 0 being the

best and 5 being the worst. Functional performance was measured by distance the patient was

able to reach in a six-minute period. Physical symptoms were observed by the investigator or

reported by the patients themselves.

The thirty individuals allotted to the exercise group were further instructed to keep a daily

activity log reporting heart rate, perceived exertion rating, exercise performed, duration of

exercise, and any symptoms experienced (Fayazi et al., 2012). These logs were collected

biweekly. These individuals walked for thirty minutes daily and participated in other exercises

three days a week for eight weeks. Those in the training group also received daily phone calls to

monitor adherence, progress, answer questions, and provide feedback.

Initial MLHFQ scores did not show any significant differences between the two groups;

however the statistical paired t-tests and Wilcoxon test showed there were significant differences

between mean QOL scores at entry and after eight weeks in the training group, and no significant

difference was seen between the control group at entry and after eight weeks (Fayazi et al.,

2012). The scores of the socioeconomic, physical, and psychological aspects in the training

group decreased from entry to after eight weeks. In the control group, only the psychological

decreased. Results from the six-minute walk test (6MWT) showed that there were not any

significant differences between the training and the control group initially (Fayazi et al., 2012).

Statistical paired t-tests demonstrated that significant differences existed between average

walking distance on the 6MWT at entry and after eight weeks in the training group, while there


were not any significant differences in the pre and post test of the control group. Average

exercise time in the training group from week one to weak eight increased. Repeated measure

tests showed significant differences.

The NYHA class III patients in the training group had the greatest increase in distance

walked on the 6MWT and the most improvement in QOL scores and exercise time. The training

group experienced no adverse events during the 8-week program. This study demonstrates that

CHF patients can perform exercise training safely (Fayazi et al., 2012). Exercise training also

showed improvement in the different QOL aspects: physical, psychological and socioeconomic.

Functional performance improved in the training group significantly compared to the control

group as measured by the 6MWT.

A home-based exercise program can increase exercise capacity, performance, and quality

of life in CHF patients. This applies to the case study patient in that he is a NYHA class III

patient. He currently lives a sedentary lifestyle, and shows symptoms of dyspnea, fatigue, and

peripheral edema. By implementing a walking program for the patient, his CHF symptoms may

reduce and his QOL may improve. ADLs will be less of a challenge.

Ramirez, Martinez, Tejeda, Gonzalez, David, and Lafuente (2004) conducted a study to

determine the effects of nutritional intervention on the clinical status and quality of life in heart

failure patients. Patients in the intervention group had a diet with decreased intakes of sodium

(less than 2400mg per day) and fluids (less than 1500mL per day). These patients were found to

have a decrease in extracellular fluid, which results in reduced development of edema, an

elevated functional class, and an enhancement in quality of life due to their permitted

engagement of social activities. This study supports two of the interventions developed for the

case study patient: educate the importance of restricting liquid intake to 1500mL per day and


educate the importance of reducing sodium intake to less than 2400mg per day. This study

implies that should the patient follow these restrictions, his edema will reduce and his activity

intolerance will decrease.

Clark, Davidson, Currie, Karimi, Duncan, and Thompson (2010) composed an article

about the importance of understanding and promoting effective self-care to heart failure patients.

This article lists evidence-based practices and categorizes them into sections: pharmacologic

treatment, diet and lifestyle, behavioral and lifestyle management, symptom monitoring, and

emerging therapies. Since this list is very comprehensive, all the interventions developed for the

patient are one of the points listed in this article. This article makes the implication that if the

patient follows the aforementioned interventions, his health status will improve.


References

Clark, A., Davidson, P., Currie, K., Karimi, M., Duncan , A., & Thompson, D. (2010).

Understanding and promoting efective self-care during heart failure. Current Treatment

Options in Cardiovascular Medicine , 1-9.

Fayazi, S., Zarea, K., Abbasi, A., & Ahmadi, F. (2013). Effect of home-based walking on

performance and quality of life in patients with heart failure. Scandinavian Journal of

Caring Sciences , 246-252.

Fletcher, L., & Thomas, D. (2001). Congestive heart failure: understanding the pathophysiology

and management . Journal of the American Academy of Nurse Practitioners , 13 (6), 249-

257.

Lewis, S., Dirksen, S., Heitkemper, M., Bucher, L. (2014). Medical-surgical nursing:

Assessment and management of clinical problems (9th ed.). St. Louis, MO: Elsevier

Mosby.

McCance, K. L., &Huether, S. E. (2014).Pathophysiology: The biologic basis for disease in

adults and children (7th ed.).Brashers, V. L., & Rote, N. S. (eds.) St. Louis, MO:

ElsevierMosby.

Ramirez, C., Martinez , C., Tejeda, O., Gonzalez, R., David, N., & Lafuente, A. (2004). Effects

of a nutritional intervention on body composition, clinical status, and quality of life in

patients with heart failure. Nutrition , 890-895.

Valerand, A., Sanoski, C., & Deglin, J. (2014). Davis’s drug guide for nurses (14th ed.).

Philadelphia, PA: FA Davis Company.

I have reviewed the Code of Academic Integrity and can attest that this document is consistent with the provisions of the code and represents my own original work. Signed: Cynthia Lee


Appendix A:

Drug Name

Generic and

Brand & Time

Due

Classification

and

Mechanism

of action

Actions and

Indications

Patient

dose,

Route,

and

frequency

Most common or

serious side effects

Contraindications &

Major Interactions

Nursing Interventions

and Patient Teaching

Atorvastatin Calcium Tablet

(Lipitor)

0900

Therapeutic: lipid-lowering

agents Pharmacologi

c: HMG-CoA reductase inhibitors

Action:

Inhibits 3-hydroxy-3-methylglutary

l-coenzyme A (HMG-CoA)

reductase, an enzyme which is responsible

for catalyzing an early step

in the synthesis of cholesterol.

Actions: • Lowering of

total and LDL cholesterol and

triglycerides. Slightly increases HDL

cholesterol. • Reduction of

lipids/cholesterol reduces the risk of

myocardial infarction and

stroke sequelae. • Slows the progression of

coronary atherosclerosis

with resultant decrease in coronary heart

disease-related events.

Indication: Lowering

cholesterol

40 mg tab PO daily

Abdominal cramps, constipation, diarrhea,

flatus, heartburn, rashes

Contraindications: • Hypersensitivity;

• Active liver disease or unexplained persistent

elevations in AST and ALT

Drug interations: CYP3A4 enzyme, bile

acid sequestrants (cholestyramine, colestipol), bile acid

sequestrants, cyclosporine,

gemfibrozil, itraconazole, colchicine, erythromycin,

clarithromycin, nelfinavir, ritonavir,/

saquinavir, lopinavir,/ ritonavir, fasamprenavir, digoxin, oral

contraceptives, warfarin

Food: grapefruit juice

Nursing intervention: Obtain a diet history,

especially with regard to fat consumption.

Patient teaching: Instruct patient to notify health

care professional if unexplained muscle pain,

tenderness, or weakness occurs, especially if accompanied by fever or

malaise


Lisinopril Tablet (Zestril or

Prinivil)

0900

Functional class:

Antihypertensive,

angiotensin-converting enzyme 1

(ACE) inhibitor

Chemical class: Enalaprilat

lysine analog

Mechanism of action: Selectively

suppresses renin-

angiotensin-aldosterone system;

inhibits ACE, thereby

preventing conversion of angiotensin I

to angiotensin II

Action: Mild to moderate

hypertension, adjunctive

therapy of systolic CHF, acute MI

Indication:

Heart and blood pressure

40mg tab PO daily

CNS: vertigo, depression, stroke,

insomnia, paresthesias,

headache, fatigue, asthenia, dizziness CV: Chest pain,

hypotension, sinus tachycardia

EENT: blurred vision, nasal congestion,

GI: nausea, vomiting, anorexia,

constipation, flatulence, GI irritation, diarrhea,

hepatic failure, hepatic necrosis

GU: Proteinuria, renal insufficiency, sexual dysfunction,

impotence INTEG: rash,

pruritus MISC: muscle cramps,

hyperkalemia RESP: dry cough,

dyspnea SYST: Angioedema, anaphylaxis, toxic

epidermal necrolysis

Contraindications: Hypersensitivity;

• History of angioedema with previous use of

ACE inhibitors; • Concurrent use with aliskiren in patients with

diabetes or moderate-to-severe renal impairment

(CCr <60 mL/min) Drug interactions:

diuretics, antihypertensive agents,

potassium supplements, potassium-sparing diuretics, or potassium-

containing salt substitutes, angiotensin

II receptor antagonists, aliskien, NSAIDs, COX-2 inhibitors, and lithium

Nursing interventions: Monitor WBC--if

neutrophils <100/mm3, d/c

Baseline renal and hepatic function pre admin

Evaluate response: ↓BP, CHF symptoms

Teach: Taper off med gradually

Rise slowly--orthostatic hypotension

Avoid increasing K+ in diet Report dry cough


Morphine I.R. Tab

(Astramorph PF, AVINza,

Duramorph PF, Embeda, Infumorph,

Kadian, MS Contin)

0500, 1100, 1700, 2300

Classification Therapeutic: opioid

analgesics Pharmacologi

c: opioid agonists

Mechanism of action: Binds

to opiate receptors in the CNS.

Alters the perception of

and response to painful stimuli while

producing generalized

CNS depression.

Action: Decrease in severity of pain.

Addition of naltrexone in

Embeda product is designed to prevent abuse

or misuse by altering the

formulation. Naltrexone has no effect unless

the capsule is crushed or

chewed. Indication: Pain

30mg tab PO q6h

Confusion, sedation, hypotension, constipation,

respiratory depression

Contraindications: Hypersensitivity; • Some products contain

tartrazine, bisulfites, or alcohol and should be

avoided in patients with known hypersensitivity; • Acute, mild,

intermittent, or postoperative pain

(extended/sustained-release); • Significant respiratory

depression (extended/sustained-

release); • Acute or severe bronchial asthma

(extended/sustained-release);

• Paralytic ileus (extended/sustained-release);

Drug interactions: MAO

inhibitors, alcohol,sedative/ hypnotics, clomipramine,

barbituates, tricyclic antidepressants,

antihistamines, partial-

Nursing intervention: Assess type, location, and intensity of pain

prior to and 1 hr following PO, subcut,

IM, and 20 min (peak) following IV administration. When

titrating opioid doses, increases of 25-50%

should be administered until there is either a 50% reduction in the

patient's pain rating on a numerical or visual

analogue scale or the patient reports satisfactory pain relief.

When titrating doses of short-acting morphine, a

repeat dose can be safely administered at the time of the peak if previous

dose is ineffective and side effects are minimal.

Assess level of consciousness, BP, pulse, and respirations

before and periodically during administration. If

respiratory rate is


antagonist opioid analgesics,

buprenorphine, nalbuphine, butorphaol,

pentazocine, warfarin, cimetidine

Drug-natural products: kava-kava, valerian, and

chamomile

<10/min, assess level of sedation. Physical

stimulation may be sufficient to prevent

significant hypoventilation. Subsequent doses may

need to be decreased by 25-50%. Initial

drowsiness will diminish with continued use.

Patient Teaching: Instruct patient how and

when to ask for pain medication.

Morphine SR

Tab (Astramorph PF,

AVINza, Duramorph PF, Embeda,

Infumorph, Kadian, MS

Contin) 0900, 2100

Therapeutic:

opioid analgesics

Pharmacologic: opioid agonists

Mechanism of

action: Binds to opiate receptors in

the CNS. Alters the

perception of and response to painful

stimuli while

Action:

Decrease in severity of pain.

Addition of naltrexone in Embeda product

is designed to prevent abuse

or misuse by altering the formulation.

Naltrexone has no effect unless

the capsule is crushed or chewed.

30mg tab

PO bid

Confusion, sedation,

hypotension, constipation,

respiratory depression

Contraindications:

Hypersensitivity; • Some products contain

tartrazine, bisulfites, or alcohol and should be avoided in patients with

known hypersensitivity; • Acute, mild,

intermittent, or postoperative pain (extended/sustained-

release); • Significant respiratory

depression (extended/sustained-release);

• Acute or severe

Nursing intervention:

Assess type, location, and intensity of pain

prior to and 1 hr following PO, subcut, IM, and 20 min (peak)

following IV administration. When

titrating opioid doses, increases of 25-50% should be administered

until there is either a 50% reduction in the

patient's pain rating on a numerical or visual analogue scale or the

patient reports


producing generalized

CNS depression.

Indication: Pain bronchial asthma (extended/sustained-

release); • Paralytic ileus

(extended/sustained-release);

Drug interactions: MAO inhibitors,

alcohol,sedative/ hypnotics, clomipramine, barbituates, tricyclic

antidepressants, antihistamines, partial-

antagonist opioid analgesics, buprenorphine,

nalbuphine, butorphaol, pentazocine, warfarin,

cimetidine Drug-natural products:

kava-kava, valerian, and chamomile

satisfactory pain relief. When titrating doses of

short-acting morphine, a repeat dose can be safely

administered at the time of the peak if previous dose is ineffective and

side effects are minimal. Assess level of

consciousness, BP, pulse, and respirations before and periodically

during administration. If respiratory rate is

<10/min, assess level of sedation. Physical stimulation may be

sufficient to prevent significant

hypoventilation. Subsequent doses may need to be decreased by

25-50%. Initial drowsiness will diminish

with continued use. Patient Teaching:

Instruct patient how and when to ask for pain

medication. Prazosin HCL Cap

(Minipress)

Classification Therapeutic:

antihypertensi

Actions: • Lowering of

BP.

2mg cap PO bid

Dizziness, headache, weakness, first-dose

orthostatic

Contraindication: hypersensitivity

Nursing intervention: Monitor BP and pulse

frequently during initial


0900, 2100

ves Pharmacologi

c: peripherally acting

antiadrenergics

Mechanism of action: •

Dilates both arteries and veins by

blocking postsynaptic

alpha1-adrenergic receptors.

• Decreases contractions

in smooth muscle of prostatic

capsule.

• Decreased cardiac preload

and afterload. • Decreased

symptoms of prostatic hyperplasia

(urinary urgency,

urinary hesitancy, nocturia)

Indication:

PTSD, Blood pressure and prostate higher

dose

hypotension, palpitations

Drug interactions: alcohol,

antihypertensives, nitrates, NSAIDs

dosage adjustment and periodically throughout

therapy. Report significant changes.

Patient teaching: Instruct patient to take

medication at the same time each day. Take

missed doses as soon as remembered. If not remembered until next

day, omit; do not double doses. Instruct patient

and family on proper technique for BP monitoring. Advise them

to check BP at least weekly and to report

significant changes.

Albuterol 0.5%

nebulizer (Accuneb, ProAir HFA,

Proventil HFA, Ventolin HFA,

Ventolin Diskus, VoSpire ER)

0700, 1300,

Therapeutic:

bronchodilators Pharmacologi

c: adrenergics

Mechanism of Action: Binds to beta2-

adrenergic

Action:

Bronchodilation

Indication:

2.5mg/

.5vial, 1 ampule neb RT tid

Nervousness,

restlessness, tremor, paradoxical brochospasm, chest

pain, palpitations, anaphylactic shock

Contraindications:

Hypersensitivity to adrenergic amines Interactions:

Drug-Drug: adrenergic agents,

MAO inhibitors, beta blockers, potassium-losing diuretics

Drug-Natural Products:

Nursing

interventions: Assess lung sounds, BP, and pulse. Monitor

pulmonary function tests before initiating

therapy. Observe for paradoxical bronchospasm.

Patient


1900 receptors in airway

smooth muscle,

leading to activation of adenyl

cyclase and increased

levels of cyclic-3´, 5´-adenosine

monophosphate (cAMP).

Increases in cAMP activate

kinases, which inhibit

the phosphorylation of myosin

and decrease intracellular

calcium. Decreased intracellular

calcium relaxes

smooth muscle airways.

• Relaxation

guarana, tea, coffee

teaching: Instruct patient to take as directed and to

contact health care professional if sob is not

relieved. Educate patient to prime unit with 4 sprays before use.


of airway smooth

muscle with subsequent

bronchodilation. • Relatively

selective for beta2

(pulmonary ) receptors.

Aspirin

Acetylsalicylic acid, Acuprin,

ASA, Aspergum, Aspir-Low, Aspirtab, Bayer,

Easprin, ecotrin, Entophen,

Halfprin, Healthprin, Zorprin

0900

Therapeutic:

antipyretics, nonopioid

analgesics Pharmacologic: salicylates

Mechanism of

Action: Produce analgesia and

reduce inflammation

and fever by inhibiting the production of

prostaglandins.Decreases

platelet aggregation.

Action:

Analgesia. Reduction of

inflammation. Reduction of fever.

Decreased incidence of

transient ischemic attacks and MI.

Indication:

prevent MI and strokes

81mg tab

PO daily

Dyspepsia, epigastric

distress, nausea, GI bleeding, allergic

reactions (anaphylaxis and laryngeal edema included)

Contraindication:

Hypersensitivity to aspirin or other

salicylates, bleeding disorders or thrombocytopenia

Drug interactions:

warfarin, heparin, heparin-like agents, thrombolytic agents,

dipyridamole, ticlopidine, clopidogrel,

tirofiban, eptifibatide, ibuprofem, cefoperazone, cefotetan,

valprioc acid, penicillins, phenytoin, methotrexate,

valproic acid, oral hypoglycemic agents, sulfonamides, urinary

acidification, alkalization

Nursing Intervention:

Patients who have asthma, allergies, and

nasal polyps or who are allergic to tartrazine are at an increased risk for

developing hypersensitivity

reactions. Assess pain and limitation of movement; note type,

location, and intensity before and at the peak

(see Time/Action Profile) after administration.

Assess fever and note associated signs

(diaphoresis, tachycardia, malaise, chills).


of the urine, antacids, diuretics, ACE

inhibitors, NSAIDs Drug-natural Products:

arnica, chamomile, clove feverfew, garlic, ginger, ginkgo, panax ginseng,

Food Interactions: foods

capable of acidifying the urine

Patient teaching: Teach patient to avoid

concurrent use of alcohol with this medication to

minimize possible gastric irritation; 3 or more glasses of alcohol per

day may increase risk of GI bleeding. Teach

patient to avoid taking concurrently with acetaminophen or

NSAIDs for more than a few days, unless directed

by health care professional to prevent analgesic nephropathy.

Calcium citrate

tab (Cal-Citrate 250, Citrical, Citrical

Liquitab)

0900, 2100

Classification

Therapeutic: mineral and electrolyte

replacements/supplements

Mechanism of action:

Essential for nervous,

muscular, and skeletal systems.

• Maintain

Action:

Replacement of calcium in deficiency

states. Control of

hyperphosphatemia in end-stage renal

disease without promoting

aluminum absorption.

Indication:

400mg tab

PO bid

Arrhythmias and

constipation

Contraindications:

hypercalcemia, renal calculi, and ventricular fibrillation.

Drug interactions:

digoxin, antacids, tetracyclines, fluoroquinolones,

phenytoin, iron salts, calcium channel

blockers, etidronate, risedronate, atenolol, diuretics (thiazide),

sodium polysterene

Nursing interventions:

Observe patient closely for symptoms of hypocalcemia

(paresthesia, muscle twitching, laryngospasm,

colic, cardiac arrhythmias, Chvostek's or Trousseau's sign).

Notify physician or other health care professional

if these occur. Protect symptomatic patients by elevating and padding

siderails and keeping bed


cell membrane

and capillary permeability.

• Act as an activator in the

transmission of nerve

impulses and contraction of cardiac,

skeletal, and smooth

muscle. • Essential for bone

formation and blood

coagulation. • Treatment of hyperphospha

temia in end-stage renal

disease.

Treatment and prevention of

hypocalcemia.

sulfonate

Drug-food: cereals, spinach, rhubarb

in low position.

Patient teaching: Instruct patients on a regular

schedule to take missed doses as soon as possible, then go back to

regular schedule.

Carvedilol tab

(Coreg, Coreg CR)

0900, 2100

Classification

Therapeutic: antihypertensi

ves Pharmacologic: beta

blockers

Actions: •

Decreased heart rate and BP.

• Improved cardiac output, slowing of the

progression of

3.125mg

tab PO bid

Dizziness, fatigue,

weakness, diarrhea, erectile dysfunction,

hyperglycemia, bradycardia, HF, pulmonary edema,

Stevens-Johnson

Contraindications:

History of serious hypersensitivity reaction

(Stevens-Johnson syndrome, angioedema, anaphylaxis);

• Pulmonary edema;

Nursing interventions: •

Monitor BP and pulse frequently during dose

adjustment period and periodically during therapy. Assess for

orthostatic hypotension


Mechanism of

action: Blocks stimulation of

beta1(myocardial) and beta2 (pulmonary,

vascular, and uterine)-

adrenergic receptor sites. • Also has

alpha1 blocking

activity, which may result in

orthostatic hypotension.

HF and decreased risk

of death.

Indication: Heart failure progression

syndrome, toxic epidermal becrolysis,

anaphylaxis, angioedema

• Cardiogenic shock; • Bradycardia, heart

block or sick sinus syndrome (unless a

pacemaker is in place); • Uncompensated HF requiring IV inotropic

agents (wean before starting carvedilol);

• Severe hepatic impairment; • Asthma or other

bronchospastic disorders.

Drug interactions: general anesthetics, IV phenytoin, diltiazem,

verapamil, digoxin, amiodarone, fluconazole,

antihypertensives, alcohol, nitrates, clonidine, thyroid

preparations, nsulins, oral hypoglycemic

agents, theophylline, dopamine, dobutamine, MAO inhibitor,

cimetidine, NSAIDs, rifampin, digoxin,

cyclosporine.

when assisting patient up from supine position.

• Monitor intake and output ratios and daily

weight. Assess patient routinely for evidence of fluid overload

(peripheral edema, dyspnea, rales/crackles,

fatigue, weight gain, jugular venous distention). Patients may

experience worsening of symptoms during

initiation of therapy for HF.


medication as directed, at the same time each day, even if feeling well. Do

not skip or double up on missed doses. Take

missed doses as soon as possible up to 4 hr before next dose. Abrupt

withdrawal may precipitate life-

threatening arrhythmias, hypertension, or myocardial ischemia.

Teach patient and family


how to check pulse and BP. Instruct them to

check pulse daily and BP biweekly. Advise patient

to hold dose and contact health care professional if pulse is <50 bpm or

BP changes significantly. Folic Acid tab

(folate, Folvite, vitamin B)

0900

Classification

Therapeutic: antianemics, vitamins

Pharmacologic: water

soluble vitamins

Action: Required for

protein synthesis and red blood cell

function. Stimulates the

production of red blood cells, white

blood cells, and platelets.

Action:

Restoration and maintenance of normal

hematopoiesis.

Indication: For vitamin deficiency

1mg tab

PO daily

Derm: rash.

CNS: irritability, difficulty sleeping, malaise, confusion.

Misc: fever.

Contraindication:

Uncorrected pernicious, aplastic, or normocytic anemias (neurologic

damage will progress despite correction of

hematologic abnormalities)

Drug interactions: pyrimethamine,

methotrexate, trimethoprim, triamterene,

sulfonamides, sulfasalazine, antacids,

cholestyramine, estrogens, phenytoin, phenobarbital,

primidone, carbamazepine,

corticosteroids

Nursing intervention:

Assess patient for signs of megaloblastic anemia (fatigue, weakness,

dyspnea) before and periodically throughout

therapy. Patient teaching: Instruct

patient to notify health care professional if rash

occurs, which may indicate hypersensitivity.

Furosemide inj. Solution

(Lasix)

Classificatio

n: loop

diuretics

Action: Diuresis

and subsequent

40mg/4ml IVP q12h

Erythema multiforme, stevens-johnson

syndrome, toxic

Contraindications:

hypersensitivity, cross-

sensitivity with thiazides

Nursing Interventions:

Assess fluid

status: document and


0900, 2100

Action:

inhibits reabsorption

of sodium and chloride, increases

renal excretion of

water, sodium, chloride,

magnesium, potassium,

and calcium.

mobilization of excess fluid,

decreased BP

Indication: Excess fluid

epidermal necrolysis dehydration,

hypocalcemia, hypochloremia,

hypokalemia, hypomagnesemia, hyponatremia,

hypovolemia, metabolic alkalosis

and sulfonamides, hepatic coma or anuria,

alcohol intolerance Interactions:

antihypertensives, nitrates, or alcohol, other diuretics, amphotericin

B, stimulant laxatives, corticosteroids, lithium,

cisplatin, NSAIDs, methotrexate, sucralfate, cholestyramine,

colestipol, salicylate, cyclosporine.

monitor fluids (I/O). Monitor BP and

pulse. Assess patient for allergy to sulfonamides,

tinnitus and hearing loss, and skin rash. monitor electrolytes, renal and

hepatic function, serum glucose, and uric acid

levels. Patient

teaching: Instruct

patient to change positions slowly to

minimize orthostatic hypotension, teach patient S/S to report to

the health care provider such as rash, muscle

weakness, cramps, nausea, dizziness, numbness, or tingling of

extremities occurs. Teach patients to

continue taking medication even if feeling better and teach

patient about additional therapies for

hypertension.

Furosemide tab

(Lasix)

Classificatio

n: loop

Action: Diuresis

and subsequent

40mg tab

PO q12h

Erythema multiforme,

stevens-johnson

Contraindications:

hypersensitivity, cross-


Assess fluid


0900, 2100

diuretics

Action:

inhibits

reabsorption of sodium and chloride,

increases renal

excretion of water, sodium,

chloride, magnesium,

potassium, and calcium.

mobilization of excess fluid,

decreased BP

Indication: Excess fluid

syndrome, toxic epidermal necrolysis

dehydration, hypocalcemia,

hypochloremia, hypokalemia, hypomagnesemia,

hyponatremia, hypovolemia,

metabolic alkalosis

sensitivity with thiazides and sulfonamides,

hepatic coma or anuria, alcohol intolerance

Interactions:

antihypertensives, nitrates, or alcohol, other

diuretics, amphotericin B, stimulant laxatives,

corticosteroids, lithium, cisplatin, NSAIDs, methotrexate, sucralfate,

cholestyramine, colestipol, salicylate,

cyclosporine.

status: document and monitor fluids

(I/O). Monitor BP and pulse. Assess patient for

allergy to sulfonamides, tinnitus and hearing loss, and skin rash. monitor

electrolytes, renal and hepatic function, serum

glucose, and uric acid levels. Patient

teaching: Instruct patient to change

positions slowly to minimize orthostatic hypotension, teach

patient S/S to report to the health care provider

such as rash, muscle weakness, cramps, nausea, dizziness,

numbness, or tingling of extremities

occurs. Teach patients to continue taking medication even if

feeling better and teach patient about additional

therapies for hypertension.


Heparin inj

0700, 1500, 2300

Classificatio

n: anticoagul

ant, antithromboti

cs Action: prevention of

thrombus formation and

extension of existing thrombi.

Indication: Blood thinning

5,000 units/ml

SQ tid

Bleeding, Heparin-induced

thrombocytopenia (with or without

thrombosis), anemia

Contraindications:

hypersensitivity,

uncontrolled bleeding, severe

thrombocytopenia, open wounds, benzyl alcohol products in premature

infants Interactions:

Drug-drug: drugs that affect platelet functions including NSAIDs,

aspirin. Drugs that cause hypoprothrombinemia,

concurrent use of thrombolytics, warfarin Drug-natural products:

arnica, anise, chamomile, clove, dong quai, fever

few, garlic, ginger, and panax ginseng


Assess for signs of

bleeding and hemorrhage, assess

patient for evidence of additional or increased thrombosis, observe

injection sites for hematomas, ecchymosis,

or inflammation. Monitor aPTT and hematocrit,

platelet count Patient teaching: Teach

patient to report symptoms of unusal bleeding or

burising. Instruct patient not to take medications

containing aspirin or NSAIDs. Teach patient to use a soft toothbrush

and electric razor.

Isosorbide dinitrate tab (Dilatrate-SR,

Isordil)

0900, 1500, 2100

Classification Therapeutic: antianginals

Pharmacologic: nitrates


Produce

Action: Relief and prevention of anginal

attacks.

Indication: Chest pain

20mg tab PO tid

Dizziness, hypotension, tachycardia

Contraindications: • Hypersensitivity; • Concurrent use of

sildenafil, vardenafil, or tadalafil.

Drug interactions: sildenafil, tadalafil,

vardenafil alcohol, beta

Nursing Interventions: Assess location, duration, intensity, and

precipitating factors of anginal pain.

• Monitor BP and pulse routinely during period of dosage adjustment.


vasodilation (venous

greater than arterial).

• Decrease left ventricular end-diastolic

pressure and left

ventricular end-diastolic volume

(preload). Net effect is

reduced myocardial oxygen

consumption. • Increase

coronary blood flow by dilating

coronary arteries and

improving collateral flow to ischemic

regions.

blockers, calcium channel blockers, and

phenothiazines


medication as directed, even if feeling better.

Take missed doses as soon as remembered; doses of isosorbide

dinitrate should be taken at least 2 hr apart (6 hr

with extended-release preparations); daily doses of isosorbide

mononitrate should be taken 7 hr apart. Do not

double doses. Do not discontinue abruptly.

Thiamine tab

(Vitamin B1) 0900

Classification

Therapeutic: vitamins Pharmacologi

c: water

Action:

Replacement in deficiency states.

100mg tab

PO daily

Vascular collapse and

agioedema

Contraindication: •

Hypersensitivity; • Known alcohol intolerance or bisulfite

hypersensitivity (elixir

Nursing Intervention:

Assess for signs and symptoms of thiamine deficiency (anorexia, GI

distress, irritability,


soluble vitamins

Mechanism of

action: Required for carbohydrate

metabolism.

Indication: vitamin

deficiency

only). Drug intervention: None

signficant

palpitations, tachycardia, edema, paresthesia,

muscle weakness and pain, depression,

memory loss, confusion, psychosis, visual disturbances, elevated

serum pyruvic acid levels).

• Assess patient's nutritional status (diet, weight) prior to and

throughout therapy.

Patient teaching: Teach patient that foods high in thiamine include cereals

(whole grain and enriched), meats

(especially pork), and fresh vegetables; loss is variable during cooking.

Hydralazine tab (Hydralazine)

0900, 1500, 2100

Classification Therapeutic:

antihypertensives Pharmacologi

c: vasodilators

Mechanism of action: Direct-acting

peripheral

Action: Lowering of BP

in hypertensive patients and decreased

afterload in patients with

HF. Indication:

Blood pressure

50mg tab PO tid

Tachycardia, drug-induced lupus

syndrome, sodium retention

Contraindication: Hypersensitivity;

• Some products contain tartrazine and should be avoided in patients with

known intolerance.

Drug interactions: alcohol, antihypertensives,

nitrates, MAO inhibitors,

Nursing interventions: Monitor BP and pulse

frequently during initial dose adjustment and periodically during

therapy. About 50-65% of Caucasians,

Black, South Indians, and Mexicans are slow

acetylators at risk for toxicity, while 80-90%


arteriolar vasodilator.

epinephrine, NSAIDs, beta blockers,

metoprolol, propranolol

of Eskimos, Japanese, and Chinese are rapid

acetylators at risk for decreased levels and

treatment failure. Patient teaching: nstruct

patient to take medication at the same

time each day; last dose of the day should be taken at bedtime. Take

missed doses as soon as remembered; do not

double doses. If more than 2 doses in a row are missed, consult health

care professional. Must be discontinued

gradually to avoid sudden increase in BP. Hydralazine controls but

does not cure hypertension.

Magnesium Sulfate inj (Magnesium

Sulfate)

1000 (one time)

Classification Therapeutic: mineral and

electrolyte replacements/

supplements Pharmacologic:

minerals/elect

Action: Replacement in deficiency

states.

Indication: Magnesium Deficiency

2gm/50ml IVPB one infusion

over 120 minutes

diarrhea Contraindications: Hypermagnesemia; • Hypocalcemia;

• Anuria; • Heart block;

Drug interactions: calcium channel blockers

and neuromuscular

Nursing intervention: Monitor pulse, BP, respirations, and ECG

frequently throughout administration of

parenteral magnesium sulfate. Respirations should be at least 16/min

before each dose.


rolytes


Essential for the activity of many

enzymes. • Plays an

important role in neurotransmis

sion and muscular

excitability.

blocking agents Patient teaching: Teach

purpose of medication to patient and family

Congestive Heart Failure

36

Appendix B

Lab Data

(per Level) Description of Lab Test Normal

Value

Admissi

on

Result

10/16/14

Recent

Result

10/21/14

Recent

Result

10/22/14

Pathophysiology explanation of

abnormal lab value, including trends

and correlation with disease process

WBC

--Measurement of total number of leukocytes;

--Provide clues to etiology; --WBC differential – determination of whether each

kind of WBC is present in proper proportion

4000-

11,000 /µL (4.0-11.0 x

10^3/µL)

4.3 4.1 Not Accessed

Neutrophils

(ANC)

Primary phagocytic cells

involved in acute inflammation

50-70% of WBC differenti

al (0.5-0.7 SI

units)

56.9 51.9 Not

Assessed

Lymphocyte

Form the basis of cellular and

humoral immune responses (B and T cells); transiently circulate in blood & reside in lymphoid

tissues

20-40% of WBC

differential (0.2 –

0.4 SI units)

18.2 17.8 Not Assessed

<20% -- corticosteroid therapy; whole body irradiation

Monocytes

Potent phagocytic cells; only present in blood for short amount of time before migrating

to tissues to become macrophages

4-8% of

WBC differenti

al (0.04-0.08 SI units)

19 22.9 Not

Assessed

>8% -- chronic inflammatory disorders;

acute infections

Hemoglobin

(Hgb)

Measurement of gas-carrying

ability of RBC

Females: 11.7-16.0

g/dL Males:

12.2 11.1 Not

Assessed

Hemodilation (excess fluid volume;


37

13.2-17.3 g/dL

Hematocrit (Hct)

Measurement of packed cell

volume of RBCs expressed as percentage of total blood

volume

Females:

35-47% Males:

39-50%

37.8 36.8 Not Assessed

Increase and decreases are the results of the same conditions that increase/decrease hemoglobin (Hgb)

Platelets

# of platelets available to maintain platelet clotting

function (not a measure of quality)

150,000 –

400,000/ µL

116,000 101,000 Not

Assessed

<100,000/ µL (thrombocytopenia) – bleeding, spontaneous hemorrhaging

may occur

Serum Na Main extracellular electrolyte

determining blood volume

135-145

mEq/L 138 139 139

Serum K

Major intracellular electrolyte;

found in most body fluids; total K content is about 4000 mEq – serum K indicates ECF

concentration

3.5-5.0 mEq/L

4.4 4 4

Serum Cl

Anion that works as an

electrolyte to maintain body fluid and acid/base balances

96-106

mEq/L 92 95 94

<96 –respiratory acidosis

Serum CO2 Measure of the bicarbonate level 23-29 mEq/L

30 30 30

>29 – compensated respiratory acidosis,

breathing disorders

BUN

Blood urea nitrogen Used to detect renal problems Concentration of urea in blood is

regulated by rate which kidney excretes urea – reflects GFR and urine-concentrating capacity

6-20

mg/dL 25 20 23

Increases as GFR (glomerular filtration rate) decreases; rises in states of dehydration and acute and chronic renal

failure; varies as a result of altered protein intake and protein catabolism

Creatinine

More reliable than BUN as a determinant of renal function

Creatinine is end product of muscle and protein metabolism and is released at a constant rate

0.6-

1.1mg/dL 1.9 1.3 1.4

>1.1 - impaired renal function,

congestive heart failure


38

Glucose

Fasting glucose test is the measurement of the level of sugar in the blood after not

eating or drinking for at least 8 hours

Fasting: 70-99

mg/dL

84 99 91

Ca Necessary ion for many fundamental metabolic processes

8.6-10.2 mg/dL

Not assessed

Not Assessed

10.1

Mg Major intracellular cation; Small amount is in serum (1%).

1.5-2.5 mg/dL

Not assessed

Not Assessed

1.3 <1.5 –severe malabsorption; low levels cause renal conservation of Mg; renal

tubular dysfunction, uses of diuretics

Prothrombin Time (PT)

---Determination of prothrombin activity

---Generally ordered in relation to a bleeding problem to

determine the effects of anticoagulant such as warfarin

11-16 sec.

16.2 Not Assessed

Not Assessed

>16 sec – Warfarin therapy; deficiency of factors I, II, V, VII, & X; vitamin K deficiency; liver disease

International Normalized Ratio (INR)

---Standardized system of

reporting PT based on a reference calibration model and

calculated by comparing the patient’s PT with a control value ---Generally ordered in relation

to a bleeding problem to determine the effects of

anticoagulant such as warfarin

2-3 1.3 Not Assessed

Not Assessed

High levels indicate an issue in clotting factors seen in PT test;

Troponin

To assist in evaluating

myocardial muscle damage related to disorders such as myocardial infarction.

<0.5 ng/mL

(Negative)

<.01 Not Assessed

Not Assessed


39

Appendix C

Tests

Purpose of Test

(For THIS patient)

Date of

Test

Test Results

Abdomen 3 or more views Abdominal distention 10/16/2014 Fluid in the abdomen, no obstruction observed Chest 2 views PA & LAT Pt shortness of breath 10/16/2014 Found pulmonary vascular congestion


40

Case Study Congestive Heart Failure

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