University of San Jose-RecoletosCollege of Nursing

Cebu City

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A Case Study on a Patient Diagnosed with Congestive Heart Failure

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Presented to the Faculty

In Partial Fulfillment

Of the Requirements in

Related Learning Experience

(Eversley Childs Sanitarium-Medical Ward)

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Presented by

TANGCALAGAN, Kent C.

TONZO, Hope Glysdi

TUMAMUT, Yvenette Kris

UY, Justin Earl

VILLAMIL, Molly

YBAÑEZ, Ma. Doreen

BSN-III Block 8

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Presented to

Aeda Mae Siao, RN

Clinical Instructor

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April 19-23; 26-30, 2010

I. INTRODUCTION

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a) Definition of the DiseaseHeart Failure often referred to as congestive heart failure

(CHF), is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. However, the term CHF is misleading, because it indicates that patients must experience pulmonary or peripheral congestion to have HF, and it implies that patients with congestion have HF. The Agency for Health Care Policy and Research (AHCPR) HF guidelines panel (1994) defined HF as a clinical syndrome characterized by signs and symptoms of fluid overload or of inadequate tissue perfusion.

These signs and symptoms result when the heart is unable to generate a CO sufficient to meet the body’s demands. The HF guideline panel used the term heart failure because many patients with HF do not manifest pulmonary or systemic congestion. The term HF is preferred and indicates myocardial heart disease in which there is a problem with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) and which may or may not cause pulmonary or systemic congestion.

Some cases of HF are reversible, depending on the cause. Most often, HF is a life-long diagnosis that is managed with lifestyle changes and medications to prevent acute congestive episodes. CHF is usually an acute presentation of HF.

b) Cause or Risk Factors

1. CauseHF may result from a number of causes like cardiac compensatory

mechanisms, other dysfunctions and other disorders of the heart.Cardiac compensatory mechanisms (increases in heart rate,

vasoconstriction, and heart enlargement) occur to assist the struggling heart.These mechanisms are able to compensate for the heart's inability to pump effectively and maintain sufficient blood flow to organs and tissue at rest. Physiologic stressors that increase the workload of the heart (exercise, infection) may cause these mechanisms to fail and precipitate the clinical syndrome associated with a failing heart (elevated ventricular/atrial pressures, sodium and water retention, decreased CO, circulatory and pulmonary congestion). The compensatory mechanisms may hasten the onset of failure because they increase afterload and cardiac work.

Two types of dysfunction may exist with heart failure (see Figure 13-5). Systolic failure: poor contractility of the myocardium resulting in decreased CO and a resulting increase in the systemic vascular resistance. The increased SVR causes an increase in the afterload (the force the left ventricle must overcome in order to eject the volume of blood). Diastolic failure: stiff myocardium, which impairs the ability of the left ventricle to fill up with blood. This causes an increase in pressure in the left atrium and pulmonary vasculature causing the pulmonary signs of heart failure.

It may also be caused by disorders of heart muscle resulting in decreased contractile properties of the heart.

Elevated preload can be caused by incompetent valves, renal failure, volume overload, or a congenital left-to-right shunt. Elevated afterload occurs when the ventricles have to generate higher pressures

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in order to overcome impedance and eject their volume. This disorder may also be referred to as an abnormal pressure load.

An elevation in afterload also may be caused by hypertension, valvular stenosis, or hypertrophic cardiomyopathy. Myocardial dysfunction is most often caused by coronary artery disease, cardiomyopathy, hypertension, or valvular disorders. Atherosclerosis of the coronary arteries is the primary cause of HF.

Coronary artery disease is found in more than 60% of the patients with HF (Braunwald et al., 2001). Ischemia causes myocardial dysfunction because of resulting hypoxia and acidosis from the accumulation of lactic acid. Myocardial infarction causes focal heart muscle necrosis, the death of heart muscle cells, and a loss of contractility; the extent of the infarction correlates with the severity of HF. Revascularization of the coronary artery by a percutaneous coronary intervention or by coronary artery bypass surgery may correct the underlying cause so that HF is resolved.

Cardiomyopathy is a disease of the myocardium. There are three types: dilated, hypertrophic, and restrictive Dilated cardiomyopathy, the most common type of cardiomyopathy, causes diffuse cellular necrosis, leading to decreased contractility (systolic failure). Dilated cardiomyopathy can be idiopathic (unknown cause), or it can result from an inflammatory process, such as myocarditis, from pregnancy, or from a cytotoxic agent, such as alcohol or adriamycin. Hypertrophic cardiomyopathy and restrictive cardiomyopathy lead to decreased

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distensibility and ventricular filling (diastolic failure). Usually, HF due to cardiomyopathy becomes chronic. However, cardiomyopathy and HF may resolve after the end of pregnancy or with the cessationof alcohol ingestion.

Systemic or pulmonary hypertension increases afterload (resistance to ejection), which increases the workload of the heart and leads to hypertrophy of myocardial muscle fibers; this can be considered a compensatory mechanism because it increases contractility. However, the hypertrophy may impair the heart’s ability to fill properly during diastole.

Valvular heart disease is also a cause of HF. The valves ensure that blood flows in one direction. With valvular dysfunction, blood has increasing difficulty moving forward, increasing pressure within the heart and increasing cardiac workload, leading to diastolic HF.

Several systemic conditions contribute to the development and severity of HF, including increased metabolic rate (eg, fever, thyrotoxicosis), iron overload (eg, from hemochromatosis), hypoxia, and anemia (serum hematocrit less than 25%). All of these conditions require an increase in CO to satisfy the systemic oxygen demand. Hypoxia or anemia also may decrease the supply of oxygen to the myocardium. Cardiac dysrhythmias may cause HF, or they may be a result of HF; either way, the altered electrical stimulation impairs the myocardial contraction and decreases the overall efficiency of myocardial function. Other factors, such as acidosis (respiratory or metabolic), electrolyte abnormalities, and antiarrhythmic medications, can worsen the myocardial dysfunction.

Other causes include: pulmonary embolism; chronic lung disease; hemorrhage and anemia; anesthesia and surgery; transfusions or infusions; increased body demands (fever, infection, pregnancy, arteriovenous fistula); drug-induced; physical and emotional stress; and, excessive sodium intake.

2. Risk Factors

GENETIC CONSIDERATIONSHF is a complex disease combining the actions of several genes

with environmental factors. Many HF risk factors have genetic causes or are associated with genetic predispositions. These include hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), coronary artery disease, myocardial infarction, and hypertension. Genetic polymorphisms of the reninangiotensin-aldosterone system (RAAS) and sympathetic system have also been associated with susceptibility to and/or mitigation of HF. Gene variants in the alpha-2c adrenoceptor and the alpha-1 adrenoceptor have been associated with a higher risk of HF among African Americans.

GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONSHF may occur at any age and in both genders as a result of

congenital defects, hypertension, valve disease, coronary artery disease, or autoimmune disorders. Elderly people, however, are much more prone to the condition because of chronic hypertension, coronary artery disease, myocardial infarction, chronic ischemia, or valve disease, all of which occur more frequently in the elderly population. As compared with whites, the incidence and prevalence of HF are higher in African Americans, Hispanic/Latinos, and Native Americans. Compared with the general U.S. population, recent immigrants from

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nonindustrialized nations and the former Soviet republics have a higher prevalence of HF as well. Although men and women have similar rates of HF, women tend to have the condition later in life than men.

OTHER RISK FACTORSOther risk factors include: hypertension; hyperlipidemia.;

diabetes; CAD; family history; smoking; alcohol consumption; and, use of cardiotoxic drugs.

c) Signs and SymptomsThe clinical manifestations produced by the different types of HF

(systolic, diastolic, or both) are similar (Chart 30-2) and therefore do not assist in differentiating the types of HF. The signs and symptoms of HF are most often described in terms of the effect on the ventricles.

Left-sided heart failure (left ventricular failure) causes different manifestations than right-sided heart failure (right ventricular failure). Chronic HF produces signs and symptoms of failure of both ventricles. Although dysrhythmias (especially tachycardias, ventricular ectopic beats, or atrioventricular [AV] and ventricular conduction defects) are common in HF, they may also be a result of treatments used in HF (eg, side effect of digitalis).

LEFT-SIDED HEART FAILURE

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Pulmonary congestion occurs when the left ventricle cannot pump the blood out of the ventricle to the body. The increased left ventricular end-diastolic blood volume increases the left ventricular end-diastolic pressure, which decreases blood flow from the left atrium into the left ventricle during diastole. The blood volume and pressure in the left atrium increases, which decreases blood flow from the pulmonary vessels. Pulmonary venous blood volume and pressure rise, forcing fluid from the pulmonary capillaries into the pulmonary tissues and alveoli, which impairs gas exchange.

These effects of left ventricular failure have been referred to as backward failure. The clinical manifestations of pulmonary venous congestion include dyspnea, cough, pulmonary crackles, and lower-than-normal oxygen saturation levels. An extra heart sound, S3, may be detected on auscultation.

Dyspnea, or shortness of breath, may be precipitated by minimal to moderate activity (dyspnea on exertion [DOE]); dyspnea also can occur at rest. The patient may report orthopnea, difficulty in breathing when lying flat. Patients with orthopnea usually prefer not to lie flat. They may need pillows to prop themselves up in bed, or they may sit in a chair and even sleep sitting up. Some patients have sudden attacks of orthopnea at night, a condition known as paroxysmal nocturnal dyspnea (PND).

Fluid that accumulated in the dependent extremities during the day begins to be reabsorbed into the circulating blood volume when the person lies down. Because the impaired left ventricle cannot eject the increased circulating blood volume, the pressure in the pulmonary circulation increases, causing further shifting of fluid into the alveoli. The fluid filled alveoli cannot exchange oxygen and carbon dioxide. Without sufficient oxygen, the patient experiences dyspnea and has difficulty getting an adequate amount of sleep.

The cough associated with left ventricular failure is initially dry and nonproductive. Most often, patients complain of a dry hacking cough that may be mislabeled as asthma or chronic obstructive pulmonary disease (COPD). The cough may become moist. Large quantities of frothy sputum, which is sometimes pink (blood tinged), may be produced, usually indicating severe pulmonary congestion (pulmonary edema).

Adventitious breath sounds may be heard in various lobes of the lungs. Usually, bi-basilar crackles that do not clear with coughing are detected in the early phase of left ventricular failure. As the failure worsens and pulmonary congestion increases, crackles may be auscultated throughout all lung fields. At this point, a decrease in oxygen saturation may occur.

In addition to increased pulmonary pressures that cause decreased oxygenation, the amount of blood ejected from the left ventricle may decrease, sometimes called forward failure. The dominant feature in HF is inadequate tissue perfusion. The diminished CO has widespread manifestations because not enough blood reaches all the tissues and organs (low perfusion) to provide the necessary oxygen. The decrease in SV can also lead to stimulation of the sympathetic nervous system, which further impedes perfusion to many organs.

Blood flow to the kidneys decreases, causing decreased perfusion and reduced urine output (oliguria). Renal perfusion pressure falls, which results in the release of renin from the kidney. Release of renin leads to aldosterone secretion. Aldosterone secretion causes

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sodium and fluid retention, which further increases intravascular volume. However, when the patient is sleeping, the cardiac workload is decreased, improving renal perfusion, which then leads to frequent urination at night (nocturia).

Decreased CO causes other symptoms. Decreased gastrointestinal perfusion causes altered digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion, restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety increases, so does dyspnea, enhancing anxiety and creating a vicious cycle. Stimulation of the sympathetic system also causes the peripheral blood vessels to constrict, so the skin appears pale or ashen and feels cool and clammy.

The decrease in the ejected ventricular volume causes the sympathetic nervous system to increase the heart rate (tachycardia), often causing the patient to complain of palpitations. The pulses become weak and thready. Without adequate CO, the body cannot respond to increased energy demands, and the patient is easily fatigued and has decreased activity tolerance. Fatigue also results from the increased energy expended in breathing and the insomnia that results from respiratory distress, coughing, and nocturia.

RIGHT-SIDED HEART FAILUREWhen the right ventricle fails, congestion of the viscera and the

peripheral tissues predominates. This occurs because the right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the venous circulation. The increase in venous pressure leads to jugular vein distention (JVD).

The clinical manifestations that ensue include edema of the lower extremities (dependent edema), hepatomegaly (enlargement of the liver), distended jugular veins, ascites (accumulation of fluid in the peritoneal cavity), weakness, anorexia and nausea, and paradoxically, weight gain due to retention of fluid.

Edema usually affects the feet and ankles, worsening when the patient stands or dangles the legs. The swelling decreases when the patient elevates the legs. The edema can gradually progress up the legs and thighs and eventually into the external genitalia and lower trunk. Edema in the abdomen, as evidenced by increased abdominal girth, may be the only edema present. Sacral edema is not uncommon for patients who are on bed rest, because the sacral area is dependent. Pitting edema, in which indentations in the skin remain after even slight compression with the fingertips (Fig. 30-2), is obvious only after retention of at least 4.5 kg (10 lb) of fluid (4.5 liters).

Hepatomegaly and tenderness in the right upper quadrant of the abdomen result from venous engorgement of the liver. The increased pressure may interfere with the liver’s ability to perform (secondary liver dysfunction). As hepatic dysfunction progresses, pressure within the portal vessels may rise enough to force fluid into the abdominal cavity, a condition known as ascites. This collection of fluid in the abdominal cavity may increase pressure on the stomach and intestines and cause gastrointestinal distress. Hepatomegaly may also increase pressure on the diaphragm, causing respiratory distress.

Anorexia (loss of appetite) and nausea or abdominal pain results from the venous engorgement and venous stasis within the abdominal organs. The weakness that accompanies right-sided HF results from reduced CO, impaired circulation, and inadequate removal of catabolic waste products from the tissues.

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d) Epidemiology or Statistics UNITED STATES

As with coronary artery disease, the incidence of HF increases with age. However, the rate of coronary artery disease is decreasing and just the opposite is true for HF. Nearly 5 million people in the United States have HF, with more than one-half million new cases diagnosed each year (American Heart Association, 2001). The prevalence rate of HF among non-Hispanic whites 20 years of age or older is 2.3% for men and 1.5% for women; for non-Hispanic blacks, the rates are 3.5% and 3.1%, respectively (American Heart Association, 2001). HF is the most common reason for hospitalization of people older than age 65 and the second most common reason for visits to a physician’s office. The rate of readmission to the hospital remains staggeringly high. The rise in the incidence of HF reflects the increased number of elderly and improvements in treatment of HF resulting in increased survival rates. However, the economic burden caused by HF is estimated to be more than 23 billion dollars in direct and indirect costs and is expected to increase (American Heart Association, 2001). Many hospitalizations could be prevented by improved and appropriate outpatient care.PHILIPPINES

In the Philippines, HF is the fastest-growing cardiac disorder and it affects 2% of the population. Almost 1 million hospital admissions occur each year for acute decompensated HF, and the rehospitalization rates during the 6 months following discharge are as much as 50%. In spite of recent advances in the treatment of HF, the 5-year estimated mortality rate is almost 50% (Department of Health, 2005).

e) Assessment HighlightsHISTORY

Patients with HF typically have a history of a precipitating factor such as myocardial infarction, recent open heart surgery, dysrhythmias, or hypertension. Symptoms vary based on the type and severity of failure. Ask patients if they have experienced any of the following: anxiety, irritability, fatigue, weakness, lethargy, mild shortness of breath with exertion or at rest, orthopnea that requires two or more pillows to sleep, nocturnal dyspnea, cough with frothy sputum, nocturia, weight gain, anorexia, or nausea and vomiting. Take a complete medication history, and determine if the patient has been on any dietary restrictions. Determine if the patient regularly participates in a planned exercise program.

The New York Heart Association has developed a commonly used classification system that links the relationship between symptoms and the amount of effort required to provoke the symptoms.

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PHYSICAL EXAMINATIONObserve the patient for mental confusion, anxiety, or irritability

caused by hypoxia. Pale or cyanotic, cool, clammy skin is a result of poor perfusion. In rightsided HF, the jugular veins may become engorged and distended. If the pulsations in the jugular veins are visible 4.5 cm or more above the sternal notch with the patient at a 45-degree angle, jugular venous distension is present. The liver may also become engorged, and pressure on the abdomen increases pressure in the jugular veins, causing a rise in the top of the blood column.

This positive finding for HF is known as hepatojugular reflux (HJR). The patient may also have peripheral edema in the ankles and feet, in the sacral area, or throughout the body. Ascites may occur as a result of passive liver congestion.

With auscultation, inspiratory crackles or expiratory wheezes (a result of pulmonary edema in left-sided failure) are heard in the patient’s lungs. The patient’s vital signs may demonstrate tachypnea or tachycardia, which occur in an attempt to compensate for the hypoxia and decreased CO. Gallop rhythms such as an S3 or an S4, while considered a normal finding in children and young adults, are considered pathological in the presence of HF and occur as a result of early rapid ventricular filling and increased resistance to ventricular filling after atrial contraction, respectively. Murmurs may also be present if the origin of the failure is a stenotic or incompetent valve.

PSYCHOSOCIALNote that experts have found that the physiological measures of HF

(such as ejection fraction) do not always predict how active, vigorous, or positive a patient feels about his or her health; rather, a person’s view of health is based on many factors such as social support, level of activity, and outlook on life.

f) Diagnostic Procedures

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g) ManagementThe basic objectives in treating patients with HF are the

following: eliminate or reduce any etiologic contributory factors, especially those that may be reversible, such as atrial fibrillation or excessive alcohol ingestion; and, reduce the workload on the heart by reducing afterload and preload.

MEDICAL MANAGEMENTManaging the patient with HF includes providing general

counseling and education about sodium restriction, monitoring daily weights and other signs of fluid retention, encouraging regular exercise, and recommending avoidance of excessive fluid intake, alcohol, and smoking. Medications are prescribed based on the patient’s type and severity of HF. Oxygen therapy is based on the degree of pulmonary congestion and resulting hypoxia. Some patients may need supplemental oxygen therapy only during activity.

Others may require hospitalization and endotracheal intubation. If the patient has underlying coronary artery disease, coronary artery revascularization with percutaneous transluminal coronary angioplasty (PTCA) or bypass surgery may be considered. If the patient’s condition is unresponsive to advanced aggressive medical therapy, innovative therapies, including mechanical assist devices and transplantation, may be considered.

Cardiac resynchronization, involving the use of left ventricular and biventricular pacing, is a treatment for HF with electrical conduction defects. Left bundle branch block (LBBB) is frequently found in patients with systolic dysfunction. LBBB occurs when the electrical impulse, which normally depolarizes the right and left bundle

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branches at the same time, depolarizes the right bundle branch but not the left bundle branch. The dyssynchronous electrical stimulation of the ventricles causes the right ventricle to contract before the left ventricle, which can lead to further decreased ejection fraction (Gerber et al., 2001). Use of a pacing device (eg, Medtronic InSync), with leads placed on the inner wall of the right atrium and right ventricle and on the outer wall of the left ventricle, provides synchronized electrical stimulation to the heart. In one study, 63% of the patients who had received these devices showed improvement in clinical status, including NYHA functional class and global assessment, compared with 38% of placebo patients (Abraham, 2002).

PHARMACOLOGICAL MANAGEMENTSeveral medications are indicated for systolic HF. Medications for

diastolic failure depend on the underlying condition, such as hypertension (see Chap. 32) or valvular dysfunction (see Chap. 29).

If the patient is in mild systolic failure, an ACE inhibitor usually is prescribed. If the patient is unable to continue an ACE inhibitor (eg, because of development of renal impairment as evidenced by elevated serum creatinine or persistent serum potassium levels of 5.5 mEq/L or above), an angiotensin II receptor blocker (ARB) or hydralazine and isosorbide dinitrate are considered as part of the treatment plan. A diuretic is added if signs of fluid overload develop. Digitalis is added to ACE inhibitors if the symptoms continue. Although previously contraindicated in HF, specific beta-blockers decrease mortality and morbidity if added to the initial medications. Spironolactone, a weak diuretic may also be added for persistent symptoms.

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. ACE inhibitors (ACE-Is) have a pivotal role in the management of HF due to systolic dysfunction. They have been found to relieve the signs and symptoms of HF and significantly decrease mortality and morbidity (when used to treat a symptomatic patient) by inhibiting neurohormonal activation (CONSENSUS Trial Study Group, 1987; SOLVD Investigators, 1992). Available as oral and intravenous medications, ACE-Is promote vasodilation and dieresis by decreasing afterload and preload. By doing so, they decrease the workload of the heart.

Vasodilation reduces resistance to left ventricular ejection of blood, diminishing the heart’s workload and improving ventricular emptying. In promoting diuresis, ACE-Is decrease the secretion of aldosterone, a hormone that causes the kidneys to retain sodium. ACE-Is stimulate the kidneys to excrete sodium and fluid (while retaining potassium), thereby reducing left ventricular filling pressure and decreasing pulmonary congestion.

ACE-Is may be the first medication prescribed for patients in mild failure—patients with fatigue or dyspnea on exertion but without signs of fluid overload and pulmonary congestion. Results from studies (Clement et al., 2000; NETWORK Investigators, 1998) to identify the specific dose to achieve this effect are equivocal, although one large study showed significant reductions in death and hospitalization with higher doses (Packer et al., 1999). However, it is recommended to start at a low dose and increase every 2 weeks until the optimal dose is achieved and the patient is hemodynamically stable. The final maintenance dose depends on the patient’s blood pressure, fluid status, renal status, and degree of cardiac failure.

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Patients receiving ACE-I therapy are monitored for hypotension, hypovolemia, hyponatremia, and alterations in renal function, especially if they are also receiving diuretics. When to observe for these effects and for how long depends on the onset, peak, and duration of the medication. Table 30-3 identifies several types of ACE-Is and their pharmacokinetics. Hypotension is most likely to develop from ACE-I therapy in patients older than age 75 and in those with a systolic blood pressure of 100 mm Hg or less, a serum sodium level of less than 135 mEq/L, or severe cardiac failure.

Adjusting the dose or type of diuretic in response to the patient’s blood pressure and renal function may allow for continued increases in the dosage of ACE-Is. Because ACE-Is cause the kidneys to retain potassium, the patient who is also receiving a diuretic may not need to take oral potassium supplements. However, patients receiving potassiumsparing diuretics (which do not cause potassium loss with diuresis) must be carefully monitored for hyperkalemia, an increased level of potassium in the blood. Before the initiation of the ACE-I, hyperkalemic and hypovolemic states must be corrected. ACE-Is may be discontinued if the potassium remains above 5.0 mEq/L or if the serum creatinine is 3.0 mg/dL and continues to increase. Other side effects of ACE-Is include a dry, persistent cough that may not respond to cough suppressants. However, the cough could also indicate a worsening of ventricular function and failure. Rarely, the cough indicates angioedema. If angioedema affects the oropharyngeal area and impairs breathing, the ACE-I must be stopped immediately.

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS). Although their action is different than that of ACE-Is, ARBs (eg, losartan [Cozaar]) have a similar hemodynamic effect as ACE-Is: lowered blood pressure and lowered systemic vascular resistance. Whereas ACE-Is block the conversion of angiotensin I to angiotensin II, ARBs block the effects of angiotensin II at the angiotensin II receptor. ACE-Is and ARBs also have similar side effects: hyperkalemia, hypotension, and renal dysfunction. ARBs are usually prescribed when patients are not able to tolerate ACE-Is.

HYDRALAZINE AND ISOSORBIDE DINITRATE. A combination of hydralazine (Apresoline) and isosorbide dinitrate (Dilatrate-SR, Isordil, Sorbitrate) may be another alternative for patients who cannot take ACE-Is. Nitrates (eg, isosorbide dinitrate) cause venous dilation, which reduces the amount of blood return to the heart and lowers preload. Hydralazine lowers systemic vascular resistance and left ventricular afterload. It has also been shown to help avoid the development of nitrate tolerance. As with ARBs, this combination of medications is usually used when patients are not able to tolerate ACE-Is.

BETA-BLOCKERS. When used with ACE-Is, beta-blockers, such as carvedilol (Coreg), metoprolol (Lopressor, Toprol), or bisoprolol (Zebeta), have been found to reduce mortality and morbidity in NYHA class II or III HF patients by reducing the cytotoxic effects from the constant stimulation of the sympathetic nervous system (Beta-Blocker Evaluation of Survival Trial [BEST] Investigators, 2001; CIBIS-II Investigators and Committees, 1999; MERIT, 1999; Packer et al., 1996; Packer et al., 2001). These agents have also been recommended for patients with asymptomatic systolic dysfunction, such as after acute

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myocardial infarction or revascularization to prevent the onset of symptoms of HF.

However, beta-blockers may also produce many side effects, including exacerbation of HF. The side effects are most common in the initial few weeks of treatment. The most frequent side effects are dizziness, hypotension, and bradycardia. To minimize these side effects, staggering the administration of the beta-blocker with the ACE-I is recommended. Because of the side effects, betablockers are initiated only after stabilizing the patient and ensuring a euvolemic (normal volume) state. They are titrated slowly (every 2 weeks), with close monitoring at each increase in dose. If the patient develops symptoms during the titration phase, treatment options include increasing the diuretic, reducing the dose of ACE-I, or decreasing the dose of the beta-blocker.

An important nursing role during titration is educating the patient about the potential worsening of symptoms during the early phase of treatment, and that improvement may take several weeks. It is very important that nurses provide support to patients going through this symptom-provoking phase of treatment. Because beta-blockade can cause bronchiole constriction, a beta1-selective beta-blocker (ie, one that primarily blocks the beta-adrenergic receptor sites in the heart), such as metoprolol (Lopressor, Toprol), is recommended for patients with well-controlled, mild to moderate asthma. However, these patients need to be monitored closely for increased asthma symptoms. Any type of beta-blocker is contraindicated in patients with severe or uncontrolled asthma.

DIURETICS. Diuretics are medications used to increase the rate of urine production and the removal of excess extracellular fluid from the body. Of the types of diuretics prescribed for patients with edema from HF, three are most common: thiazide, loop, and potassium-sparing diuretics. These medications are classified according to their site of action in the kidney and their effects on renal electrolyte excretion and reabsorption. Thiazide diuretics, such as metolazone (Mykrox, Zaroxolyn), inhibit sodium and chloride reabsorption mainly in the early distal tubules. They also increase potassium and bicarbonate excretion. Loop diuretics, such as furosemide (Lasix), inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle. Patients with signs and symptoms of fluid overload should be started on a diuretic, a thiazide for those with mild symptoms or a loop diuretic for patients with more severe symptoms or with renal insufficiency

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(Brater, 1998). Both types of diuretics may be used for those in severe HF and unresponsive to a single diuretic. These medications may not be necessary if the patient responds to activity recommendations, avoidance of excessive fluid intake (<2 quarts/day), and a lowsodium diet (eg, <2 g/day).

Spironolactone (Aldactone) is a potassium-sparing diuretic that inhibits sodium reabsorption in the late distal tubule and collecting duct. It has been found to be effective in reducing mortality and morbidity in NYHA class III and IV HF patients when added to ACE-Is, loop diuretics, and digoxin. Serum creatinine and potassium levels are monitored frequently (eg, within the first week and then every 4 weeks) when this medication is first administered. Side effects of diuretics include electrolyte imbalances, symptomatic hypotension (especially with overdiuresis), hyperuricemia (causing gout), and ototoxicity. Dosages depend on the indications, patient age, clinical signs and symptoms, and renal function. Table 30-4 lists commonly used diuretics, dosages, and pharma cokinetic properties. Careful patient monitoring and dose adjustments are necessary to balance the effectiveness with the side effects of therapy. Diuretics greatly improve the patient’s symptoms, but they do not prolong life.

DIGITALIS. The most commonly prescribed form of digitalis for patients with HF is digoxin (Lanoxin). The medication increases the force of myocardial contraction and slows conduction through the AV node. It improves contractility, increasing left ventricular output. The medication also enhances diuresis, which removes fluid and relieves edema. The effect of a given dose of medication depends on the state of the myocardium, electrolyte and fluid balance, and renal and hepatic function. Although digitalis does not decrease the mortality rate, it is effective in decreasing the symptoms of systolic HF and in increasing the patient’s ability to perform activities of daily living (Digitalis Investigation Group, 1997). It also has been shown to significantly decrease hospitalization rates and emergency room visits for NYHA class II and III HF patients (Uretsky et al., 1993).

A key concern associated with digitalis therapy is digitalis toxicity. Chart 30-3 summarizes the actions and uses of digitalis along with the nursing surveillance required when it is administered. The patient is observed for the effectiveness of digitalis therapy: lessening dyspnea and orthopnea, decrease in pulmonary crackles on auscultation, relief of peripheral edema, weight loss, and increase in activity tolerance. The serum potassium level is measured at intervals because diuresis may have caused hypokalemia. The effect of digitalis is enhanced in the presence of hypokalemia, so digitalis toxicity may occur. Serum digoxin levels are obtained once each year or more frequently if there have been changes in the patient’s medications, renal function, or symptoms.

CALCIUM CHANNEL BLOCKERS. First-generation calcium channel blockers, such as verapamil (Calan, Isoptin, Verelan), nifedipine (Adalat, Procardia), and diltiazem (Cardizem, Dilacor, Tiazac), are contraindicated in patients with systolic dysfunction, although they may be used in patients with diastolic dysfunction. Amlodipine (Norvasc) and felodipine (Plendil), dihydropyridine calcium channel blockers, cause vasodilation, reducing systemic vascular resistance. They may be used to improve symptoms especially in patients with

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nonischemic cardiomyopathy, although they have no effect on mortality.

OTHER MEDICATIONS. Anticoagulants may be prescribed, especially if the patient has a history of an embolic event or atrial fibrillation or mural thrombus is present. Other medications such as antianginal medications may be given to treat the underlying cause of HF. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprophen (Aleve, Advil, Motrin) should be avoided (Page & Henry, 2000). They can increase systemic vascular resistance and decrease renal perfusion, especially in the elderly. For similar reasons, use of decongestants should be avoided.

NUTRITIONAL MANAGEMENT

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A low-sodium (≤2 to 3 g/day) diet and avoidance of excessive amounts of fluid are usually recommended. Although it has not been shown to affect the mortality rate, this recommendation reduces fluid retention and the symptoms of peripheral and pulmonary congestion. The purpose of sodium restriction is to decrease the amount of circulating volume, which would decrease the need for the heart to pump that volume. A balance needs to be achieved between the ability of the patient to alter the diet and the amount of medications that are prescribed. Any change in diet needs to be done with consideration of good nutrition as well as the patient’s likes, dislikes, and cultural food patterns.

SURGICAL MANAGEMENTIf the elevated preload is caused by valvular regurgitation, the

patient may require corrective surgery. Corrective surgery may also be warranted if the elevated afterload is caused by a stenotic valve. Another measure that may be taken to reduce afterload is an intra-aortic balloon pump (IABP). This is generally used as a bridge to surgery or in cardiogenic shock after acute myocardial infarction. It involves a balloon catheter placed in the descending aorta that inflates during diastole and deflates during systole. The balloon augments filling of the coronary arteries during diastole and decreases afterload during systole. IABP is used with caution because there are several possible complications, including dissection of the aortoiliac arteries, ischemic changes in the legs, and migration of the balloon up or down the aorta.

OTHER MEASURESOther measures the physician may use include supplemental

oxygen, thrombolytic therapy, percutaneous transluminal coronary angioplasty, directional coronary atherectomy, placement of a coronary stent, or coronary artery bypass surgery to improve oxygen flow to the myocardium. Finally, a cardiac transplant may be considered if other measures fail, if all other organ systems are viable, if there is no history of other pulmonary diseases, and if the patient does not smoke or use alcohol, is generally under 60 years of age, and is psychologically stable.

h) Nursing Responsibilities and Preventive MeasuresThe nurse is responsible for administering the medications and for

assessing their beneficial and detrimental effects to the patient. It is the balance of these effects that determines the type and dosage of pharmacologic therapy. Nursing actions to evaluate therapeutic effectiveness include the following:

Keeping an intake and output record to identify a negative balance (more output than input)

Weighing the patient daily at the same time and on the same scale, usually in the morning after urination; monitoring for a 2- to 3-lb gain in a day or 5-lb gain in week

Auscultating lung sounds at least daily to detect an increase or decrease in pulmonary crackles

Determining the degree of JVD Identifying and evaluating the severity of dependent edema

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Monitoring pulse rate and blood pressure, as well as monitoring for postural hypotension and making sure that the patient does not become hypotensive from dehydration

Examining skin turgor and mucous membranes for signs of dehydration

Assessing symptoms of fluid overload (eg, orthopnea, paroxysmal nocturnal dyspnea, and dyspnea on exertion) and evaluating changes

MAINTAINING ADEQUATE CARDIAC OUTPUTPlace patient at physical and emotional rest to reduce work of

heart. Provide rest in semi-recumbent position or in armchair in air-conditioned environment that reduces work of heart, increases heart reserve, reduces BP, decreases work of respiratory muscles and oxygen utilization, improves efficiency of heart contraction; recumbency promotes diuresis by improving renal perfusion. Provide bedside commode to reduce work of getting to bathroom and for defecation. Provide for psychological rest since emotional stress produces vasoconstriction, elevates arterial pressure, and speeds the heart. Promote physical comfort. Avoid situations that tend to promote anxiety and agitation. Offer careful explanations and answers to the patient's questions.

Evaluate frequently for progression of left-sided heart failure. Take frequent BP readings. Observe for lowering of systolic pressure. Note narrowing of pulse pressure. Note alternating strong and weak pulsations (pulsus alternans). Auscultate heart sounds frequently and monitor cardiac rhythm. Note presence of S3 or S4 gallop (S3 gallop is a significant indicator of heart failure). Monitor for premature ventricular beats.

Observe for signs and symptoms of reduced peripheral tissue perfusion: cool temperature of skin, facial pallor, and poor capillary refill of nail beds. Monitor clinical response of patient with respect to relief of symptoms (lessening dyspnea and orthopnea, decrease in crackles, relief of peripheral edema). Watch for sudden unexpected hypotension, which can cause myocardial ischemia and decrease perfusion to vital organs.

IMPROVING OXYGENATIONRaise head of bed 8 to 10 inches (20 to 30 cm) reduces venous

return to heart and lungs; alleviates pulmonary congestion. Support lower arms with pillows to eliminate pull of their weight on shoulder muscles. Sit orthopneic patient on side of bed with feet supported by a chair, head and arms resting on an over-the-bed table, and lumbosacral area supported with pillows.

Auscultate lung fields at least every 4 hours for crackles and wheezes in dependent lung fields (fluid accumulates in areas affected by gravity). Mark with ink that does not easily rub off, the level on the patient's back where adventitious breath sounds are heard. Use markings for comparative assessment over time and among different care providers. Observe for increased rate of respirations (could be indicative of falling arterial pH). Observe for Cheyne-Stokes respirations (may occur in elderly patients because of a decrease in cerebral perfusion stimulating a neurogenic response). Position the patient every 2 hours (or encourage the patient to change position frequently) to help prevent atelectasis and pneumonia. Encourage deep-breathing exercises every 1 to 2 hours to avoid atelectasis.

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Offer small, frequent feedings to avoid excessive gastric filling and abdominal distention with subsequent elevation of diaphragm that causes decrease in lung capacity. Administer oxygen as directed.

PROMOTING ACTIVITY TOLERANCEAlthough prolonged bed rest and even short periods of

recumbency promote diuresis by improving renal perfusion, they also promote decreased activity tolerance. Prolonged bed rest, which may be selfimposed, should be avoided because of the deconditioning effects and hazards, such as pressure ulcers (especially in edematous patients), phlebothrombosis, and pulmonary embolism. An acute event that causes severe symptoms or that requires hospitalization indicates the need for initial bed rest. Otherwise, a total of 30 minutes of physical activity three to five times each week should be encouraged (Georgiou et al., 2001). The nurse and patient can collaborate to develop a schedule that promotes pacing and prioritization of activities. The schedule should alternate activities with periods of rest and avoid having two significant energy-consuming activities occur on the same day or in immediate succession. Before undertaking physical activity, the patient should be given the following safety guidelines:

Begin with a few minutes of warm-up activities. Avoid performing physical activities outside in extreme hot,

cold, or humid weather. Ensure that you are able to talk during the physical activity; if

you are unable to do so, decrease the intensity of activity. Wait 2 hours after eating a meal before performing the physical

activity. Stop the activity if severe shortness of breath, pain, or

dizziness develops. End with cool-down activities and a cool-down period.

Because some patients may be severely debilitated, they may need to perform physical activities only 3 to 5 minutes at a time, one to four times per day. The patient then should be advised to increase the duration of the activity, then the frequency, before increasing the intensity of the activity (Meyer, 2001).

Barriers to performing an activity are identified, and methods of adjusting an activity to ensure pacing but still accomplish the task are discussed. For example, objects that need to be taken upstairs can be put in a basket at the bottom of the stairs throughout the day. At the end of the day, the person can carry the objects up the stairs all at once. Likewise, the person can carry cleaning supplies around in a basket or backpack rather than walk back and forth to obtain the items. Vegetables can be chopped or peeled while sitting at the kitchen table rather than standing at the kitchen counter. Small, frequent meals decrease the amount of energy needed for digestion while providing adequate nutrition.

The nurse helps the patient to identify peak and low periods of energy and plan energy-consuming activities for peak periods. For example, the person may prepare the meals for the entire day in the morning. Pacing and prioritizing activities help maintain the patient’s energy to allow participation in regular physical activity.

The patient’s response to activities needs to be monitored. If the patient is hospitalized, vital signs and oxygen saturation level are monitored before, during, and immediately after an activity to identify whether they are within the desired range. Heart rate should return to

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baseline within 3 minutes. If the patient is at home, the degree of fatigue felt after the activity can be used as assessment of the response. If the patient tolerates the activity, short-term and long-term goals can be developed to gradually increase the intensity, duration, and frequency of activity.

Referral to a cardiac rehabilitation program may be needed, especially for HF patients with recent myocardial infarction, recent open-heart surgery, or increased anxiety. A supervised program may also benefit those who need the structured environment, significant educational support, regular encouragement, and interpersonal contact.

MANAGING FLUID VOLUMEPatients with severe HF may receive intravenous diuretic

therapy, but patients with less severe symptoms may receive oral diuretic medication (see Table 30-4 for a summary of common diuretics). Oral diuretics should be administered early in the morning so that diuresis does not interfere with the patient’s nighttime rest. Discussing the timing of medication administration is especially important for patients, such as elderly people, who may have urinary urgency or incontinence. A single dose of a diuretic may cause the patient to excrete a large volume of fluid shortly after administration.

The nurse monitors the patient’s fluid status closely—auscultating the lungs, monitoring daily body weights, and assisting the patient to adhere to a low-sodium diet by reading food labels and avoiding high-sodium foods such as canned, processed, and convenience foods (Chart 30-4). If the diet includes fluid restriction, the nurse can assist the patient to plan the fluid intake throughout the day while respecting the patient’s dietary preferences. If the patient is receiving intravenous fluids, the amount of fluid needs to be monitored closely, and the physician or pharmacist can be consulted about the possibility of maximizing the amount of medication in the same amount of intravenous fluid (eg, double-concentrating to decrease the fluid volume administered).

The nurse positions the patient or teaches the patient how to assume a position that shifts fluid away from the heart. The number of pillows may be increased, the head of the bed may be elevated (20- to 30-cm [8- to 10-inch] blocks may be used), or the patient may sit in a comfortable armchair. In this position, the venous return to the heart (preload) is reduced, pulmonary congestion is alleviated, and impingement of the liver on the diaphragm is minimized. The lower arms are supported with pillows to eliminate the fatigue caused by the constant pull of their weight on the shoulder muscles.

The patient who can breathe only in the upright position may sit on the side of the bed with the feet supported on a chair, the head and arms resting on an overbed table, and the lumbosacral spine supported by a pillow. If pulmonary congestion is present, positioning the patient in an armchair is advantageous, because this position favors the shift of fluid away from the lungs.

Because decreased circulation in edematous areas increases the risk of skin injury, the nurse assesses for skin breakdown and institutes preventive measures. Frequent changes of position, positioning to avoid pressure, the use of elastic compression stockings, and leg exercises may help to prevent skin injury.

CONTROLLING ANXIETY

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Because patients in HF have difficulty maintaining adequate oxygenation, they are likely to be restless and anxious and feel overwhelmed by breathlessness. These symptoms tend to intensify at night. Emotional stress stimulates the sympathetic nervous system, which causes vasoconstriction, elevated arterial pressure, and increased heart rate. This sympathetic response increases the amount of work that the heart has to do. By decreasing anxiety, the patient’s cardiac work also is decreased. Oxygen may be administered during an acute event to diminish the work of breathing and to increase the patient’s comfort.

When the patient exhibits anxiety, the nurse takes steps to promote physical comfort and psychological support. In many cases, a family member’s presence provides reassurance. To help decrease the patient’s anxiety, the nurse should speak in a slow, calm, and confident manner and maintain eye contact. When necessary, the nurse should also state specific, brief directions for an activity.

After the patient is comfortable, the nurse can begin teaching ways to control anxiety and to avoid anxiety-provoking situations. The nurse explains how to use relaxation techniques and assists the patient to identify factors that contribute to anxiety. Lack of sleep may increase anxiety, which may prevent adequate rest. Other contributing factors may include misinformation, lack of information, or poor nutritional status. Promoting physical comfort, providing accurate information, and teaching the patient to perform relaxation techniques and to avoid anxietytriggering situations may relax the patient.

Cerebral hypoxia with superimposed carbon dioxide retention may be a problem in HF, causing the patient to react to sedative-hypnotic medications with confusion and increased anxiety. Hepatic congestion may slow the liver’s metabolism of medication, leading to toxicity. Sedative-hypnotic medications must be administered with caution.

In cases of confusion and anxiety reactions that affect the patient’s safety, the use of restraints should be avoided. Restraints are likely to be resisted, and resistance inevitably increases the cardiac workload. The patient who insists on getting out of bed at night can be seated comfortably in an armchair. As cerebral and systemic circulation improves, the degree of anxiety decreases, and the quality of sleep improves.

MINIMIZING POWERLESSNESSPatients need to recognize that they are not helpless and that

they can influence the direction of their lives and the outcomes of treatment. The nurse assesses for factors contributing to a sense of powerlessness and intervenes accordingly. Contributing factors may include lack of knowledge and lack of opportunities to make decisions, particularly if health care providers and family members behave in maternalistic or paternalistic ways. If the patient is hospitalized, hospital policies may promote standardization and limit the patient’s ability to make decisions (eg, what time to have meals, take medications, prepare for bed).

Taking time to listen actively to patients often encourages them to express their concerns and ask questions. Other strategies include providing the patient with decision-making opportunities, such as when activities are to occur or where objects are to be placed, and increasing the frequency and significance of those opportunities over time; providing encouragement while identifying the patient’s

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progress; and assisting the patient to differentiate between factors that can be controlled and those that cannot. In some cases, the nurse may want to review hospital policies and standards that tend to promote powerlessness and advocate for their elimination or change (eg, limited visiting hours, prohibition of food from home, required wearing of hospital gowns).

MONITORING AND MANAGING POTENTIAL COMPLICATIONSProfuse and repeated diuresis can lead to hypokalemia (ie,

potassium depletion). Signs are weak pulse, faint heart sounds, hypotension, muscle flabbiness, diminished deep tendon reflexes, and generalized weakness. Hypokalemia poses new problems for the patient with HF because it markedly weakens cardiac contractions. In patients receiving digoxin, hypokalemia can lead to digitalis toxicity. Digitalis toxicity and hypokalemia increase the likelihood of dangerous dysrhythmias (see Chart 30-3). Low levels of potassium may also indicate a low level of magnesium, which can add to the risk for dysrhythmias. Hyperkalemia may also occur, especially with the use of ACE-Is or ARBs and spironolactone.

The sources of sodium should be specified in describing the regimen, rather than simply saying “low-salt” or “saltfree,” and the quantity should be indicated in milligrams. Salt is not 100% sodium; there are 393 mg of sodium in 1 g (1000 mg) of salt.

To reduce the risk for hypokalemia, the nurse advises patients to increase their dietary intake of potassium. Dried apricots, bananas, beets, figs, orange or tomato juice, peaches, and prunes (dried plums), potatoes, raisins, spinach, squash, and watermelon are good dietary sources of potassium. An oral potassium supplement (potassium chloride) may also be prescribed for patients receiving diuretic medications. If the patient is at risk for hyperkalemia, the nurse advises the patient to avoid the above products, including salt substitutes.

Grapefruit (fresh and juice) is a good dietary source of potassium but has serious drug–food interactions. Patients are advised to consult their physician or pharmacist before including grapefruit in their diet.

Periodic assessment of the patient’s electrolyte levels will alert health team members to hypokalemia, hypomagnesemia, and hyponatremia. Serum levels are assessed frequently when the patient starts diuretic therapy and then usually every 3 to 12 months. It is important to remember that serum potassium levels do not always indicate the total amount of potassium within the body.

Prolonged diuretic therapy may also produce hyponatremia (deficiency of sodium in the blood), which results in apprehension, weakness, fatigue, malaise, muscle cramps and twitching, and a rapid, thready pulse.

Other problems associated with diuretic administration are hyperuricemia (excessive uric acid in the blood), volume depletion from excessive urination, and hyperglycemia.

PROMOTING HOME AND COMMUNITY-BASED CAREThe nurse provides patient education and involves the patient in

implementing the therapeutic regimen to promote understanding and adherence to the plan. When the patient understands or believes that the diagnosis of HF can be successfully managed with lifestyle changes and medications, recurrences of acute HF lessen, unnecessary hospitalizations decrease, and life expectancy increases. Patients and

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their families need to be taught to follow the medication regimen as prescribed, maintain a low-sodium diet, perform and record daily weights, engage in routine physical activity, and recognize symptoms that indicate worsening HF.

Although noncompliance is not well understood, interventions that may promote adherence include teaching to ensure accurate understanding. A summary of teaching points for the patient with HF is presented in Chart 30-5.

The patient and family members are supported and encouraged to ask questions so that information can be clarified and understanding enhanced. The nurse should be aware of cultural factors and adapt the teaching plan accordingly. Patients and their families need to be informed that the progression of the disease is influenced in part by choices made about health care and the decisions about following the treatment plan. They also need to be informed that health care providers are there to assist them in reaching their health care goals. Patients and family members need to make the decisions about the treatment plan, but they also need to understand the possible outcomes of those decisions. The treatment plan then will be based on what the patient wants, not just what the physician or other health care team members think is needed. Ultimately, the nurse needs to convey that monitoring symptoms and daily weights, restricting sodium intake, avoiding excess fluids, preventing infection with influenza and pneumococcal immunizations, avoiding noxious agents (eg, alcohol, tobacco), and participating in regular exercise all aid in preventing exacerbations of HF.

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II. OBJECTIVESa) General

After 1-3 hours of case presentation in the medical ward, the students will be able to develop and apply specific knowledge, skills and attitude on the disease process of Congestive Heart Failure generally on the body; anticipate and provide effective nursing care; and, deliver specific interventions needed to treat the disease.

b) Specific1. Nurse-Centered Objectives

Upon completion of this case study, the student nurse should be able to:a) Make a thorough assessment about the patient’s personal history,

family background and lifestyleb) Cite factors that contribute to the patient’s condition.c) Review the anatomy and physiology of the integumentary system.d) Explain the histopathology and pathogenesis of Congestive Heart

Failure.e) Make a comprehensive nursing care plan and its intervention.f) Impart knowledge to the patient regarding on his conditiong) Evaluate patient’s response towards rendered care given by the

student nurse.

2. Patient-Centered Objectives

Upon completion of this case study, the Guest should be able to:a) Establish rapport and trusting relationship with the student nurse.b) Give information about self, family and past experiences.c) Cooperate on management prepared by the student nurse.d) Verbalize feelings and thoughts of his present condition.e) Understand awareness of his disorder.f) Know the possible causes of the disorder.g) Learn and understand why such laboratory examinations are being

done.h) Apply the learned self-care measures to improve well-being.

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III. Health History

a) Client ProfileA case of Patient MR, 33 years old, female, married, Filipino

citizen, a Roman Catholic, housewife and presently living in Paknaan, Mandaue City was assessed last April 23, 2010 by 4:30am at the Evvesley Childs Sanitarium (Female Medical ward). Client was admitted last April 19, 2010 at around 12:00 a.m via Taxi accompanied by her eldest son with admitting complaints of shortness of breath, dizziness and fatigue. Admitting V/S is as follows: T-37.9; PR-92; RR-25; BP-200/160. She's under the care of Dr. Lagora. Patient was transferred to the Female Medical Ward at 4:10 am of the same day. Patient claimed to be hypertensive but not diabetic or asthmatic. Patient is neither a smoker nor an alcoholic beverage drinker. She has no known allergies to drug as well as to foods; but, since she has a heart problem, she ate less on restricted foods high in cholesterol.

b) Past Medical HistoryPatient disclosed that she has received the following

immunizations: BCG 1 and 2, DPT 1, 2 and 3, OPV 1, 2 and 3, Anti Hepa-B 1, 2 and 3, TT1, 2, 3, 4 and 5. Patient is currently having 3

children. Upon her 2nd child, she was admitted to the hospital last year 2001 for 4 days in Eversley Child's Sanitarium under unrecalled doctor and was diagnosed with Pre-eclampsia. She was also unable to recall the specific medications she took that time. Patient MR was then adviced by the doctor not to have another child but then was not

followed since she had her 3rd child in the year 2007 and was confined for 3 consecutive days in Vicente Sotto Memorial Medical Center under the Service of unrecalled Doctor. The patient was diagnosed with Eclampsia with a BP of 180/120mmHg which was her usual BP measurement for her current illness. She was only able to remember Nefidipine as her medication.

c) History of Present IllnessPrior to admission the patient was experiencing dizziness, headache

and fatigue. She then sought for medical assistance in Mandaue District and had a BP of 200/160mmHg. Due to lack of financial support, the patient was unable to comply the necessary medications and decided to stay at home for care. Two days prior to admission, the patient experienced symptoms of shortness of breath. On April 17, 2010, Patient MR manifested symptoms of on and off moderate grade fever, and gradually coughing episodes were noted.

d) Developmental HistoryAccording to Sigmund Freud Psychosexual Stage, Patient MR is in

the Genital phase. This stage represents the major portion of life, and the basic task for the individual is the detachment from the parents. Patient is already living with her own family. In this stage the focus on the genitals, the energy is expressed with adult sexuality. Patient claimed to be sexually active. The ego in the genital stage is well-

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developed, and so uses secondary process thinking, which allows symbolic gratification. Patient MR expressed symbolic gratification that includes the formation of love relationships and families, or acceptance of responsibilities associated with adulthood.

In Erik Erikson's psychosocial Stages of development, Patient MR belongs to Generativity vs. Stagnation wherein it concerns of establishing and guiding the next generation. Socially-valued work and disciplines are expressions of generativity as well as contributing to society and helping future generations. Patient is already raising a family and verbalized her hopes on working towards the betterment of society, a sense of generativity- a sense of productivity and accomplishment.

According to kohlberg's Theory of Moral Development, Patient MR is in the Postconventional Morality wherein people begin to account for the differing values, opinions, and beliefs of other people. Rules of law are important for maintaining a society, but members of the society should agree upon these standards. Patient considers values of honesty, hardwork and nurturing as important values on being a mother and a wife to her family.

In Fowler's stages of faith development, patient belongs to the 4th stage of "Individuative-Reflective" faith (usually mid-twenties to late thirties) a stage of angst and struggle. The patient took personal responsibility for her beliefs and feelings. She expressed her faith to God that despite her situation and that she still believes that God will heal her from her illness.

e) Environmental HistoryPatient MR is currently residing in Paknaan Mandaue City Cebu.

She together with her family with three children are living in a rented house and lot nearby the street side which is made out of mixed materials. They have two bedrooms, a dining area and a living room. Their toilet is a manual flush type, they have electricity and have their own water source. Patient MR disposes their garbage through garbage trucks which collects their trash during Mondays and Thursdays. They use plastic bags and old barrels for garbage containers. They have one dog and a cat as their pet. The patient claimed that there is no difficulty in seeking healthcare because of the distance from the health center is not that far approximately 5km. Patient MR also has no problems with going to Church and to the market which is only 2km away from their house. Patient MR has a quiet type of personality but though such, she can still manage to talk to some friends and mingle with her neighbors from time to time.

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IV. Marjorie Gordon’s Functional Health Patterns

1. Health Perception/ Health ManagementPatient MR defines health as “panglawas”. She scaled her health 6 out

of 10. Her perception of her health was in sync with reality. She was aware of the fact that she was “pretty sick” when she came in to the hospital. She was very independent and did not like to be waited on. Her past medical history was concise as presented previously. She wanted to see a health care provider each time she feels ill but not realized due to financial restraints. She exercised by walking or swimming daily and was very careful about what she ate. She was visibly weak, and was unable to perform all of her ADL’s without assistance. She was not well oriented with knowledgeable and medications of her disease. She once practiced drinking “mangagaw” when she experience fever. She was not well educated about her CHF and the dietary restrictions it imposed.

2. Nutritional/ MetabolicPTA, the patient’s usual diet from breakfast, lunch and dinner is

composed of rice, side dish of fish in varied preparation, vegetables and meat. She can consume 7-9 glasses a day.

During admission, Patient’s current dietary status is DAT. She reported during on her 24-hour diet recall that she had been eating a cup of coffee and bread for breakfast, a cup of rice and fish for lunch, and a cup of rice and a vegetable soup for dinner. She was not aware of the effects of an increase in sodium and fat intake to her CHF. She stated that she did not take vitamin supplements because they are expensive. She reported adequate fluid intake, drinking 1-2 cups of coffee daily and along with two 5-7 glasses of water. She had recently experienced a 5-8 lb weight gain as a result of her CHF. She did not report any changes in appetite or difficulty chewing but have difficulty swallowing. Her diet restrictions were low sodium and low fat because of her CHF and cardiac history. She reported experiencing occasional nausea and loose stools. She was 5’6” and 165 pounds. Her prescribed diet was a cardiac diet. She had no enteral feeding or NG tube, and her IV was 500mL D5W running at 10ggts/min.

3. EliminationPrior to admission, patient experiences 1-2 bowel movements per day

and usually voids 4-5 times a day with estimates 200ml per urination.During admission, the patient was fully functional in the elimination

pattern. She reported urinating three to four times daily with no difficulty and no recent change in her urinary pattern. She had a bowel movement the day of our interview, and reported moving her bowels daily, sometimes twice. She denied changes in this pattern. Her fluid balance was improving, with an intake total of 200 mL and an output total of 500 mL in the entire shift. Her urine was clear and yellow, and her abdomen was soft with active bowel sounds in all four quadrants. She was fully continent with experience profuse sweating.

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4. Activity/ ExercisePrior to admission, patient complains about her low stamina. She can’t

tolerate strenuous activities. Her ADL includes washing clothes, doing household chores and cleaning the backyard. As a past time she watches television with her children during late afternoon.

During admission, Patient was weak and needs assistive devices. She reported don’t have sufficient energy to perform activities due to fatigue. She reported feeling shortness of breath, fatigue, and palpitations related to her CHF. She reported exercising daily by walking or swimming, and doing her household chores. She needed assistance with her ADL’s and to keep herself well groomed. She had a limited range of motion and her tone and strength were symmetrical in all extremities. She had a steady gait. Her respiratory rate was 28 with normal, symmetrical breaths. O2 was placed through nasal cannula regulated at 4 L. She had fine inspiratory and expiratory crackles posteriorly througout. Her apical pulse was 70 and irregular due to a-fib, and her BP was 119/59. She had +2 strength radial pulses and +1 strength pedal pulses. Her capillary refill was less than 3 seconds and her extremities were warm and pink. Risk for falls is the main nursing diagnosis in this health pattern due to fatigue.

5. Sleep/ RestPTA, patient has an approximately 3-4 hours of sleep. Client usually

wakes at 6am. Client’s problemof the very small number of hours of sleep is due to nocturnal paroxysmal dyspnea. Patient sometimes have short naps in the afternoon.

During admission, she reported sleeping about 4 hours per night and feeling well rested during the day. She reported having occasional difficulty falling asleep for which she sometimes used milk as sleeping aid. She took occasional naps after her walk or during soap operas in the afternoon. She did exhibit lethargy and irritability and during night times due to SOB and nocturnal paroxysmal dyspnea. Her diagnosis in this area is risk for disturbed sleep pattern related to difficulty falling asleep at night.

6. Cognitive/ PerceptualPatient can decode simple instructions such as advising her to change

her position or clothes. She was functional in this health pattern. She had no real visual difficulties other than wearing glasses and no hearing problems. She reported occasional difficulty with her short term memory; things like word and name recall. She said that the easiest way for her to learn things is to do them herself and she did not like being waited on. She did not report any numbness, tingling or pain in her extremities. She was at some risk for impaired short term memory related to her age. Client is not able to read the text of the calendar and writings from chart half a meter away. The client has difficulty to follow the pen placed

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in the six cardinal gazes and sometimes have involuntary movements. Client is unable to hear and comprehend sentences during the test, whispered pectoriloquy. Client can’t hear whispers a foot away and can’t hear distinct conversation 2 meters away. Client has difficulty distinguishing smell (perfume, alcohol). Client can distinguish blunt and sharp areas at the bottom of the pen; hot (rubbed hand) or cold (mineral water bottle) objects and location of touch in the distinct parts of the body. Client is able to taste familiar flavors (sugar, salt, iced tea, vinegar) as verbalized.

She can read and write as verbalized by SO. She can reply appropriately to questions during conversation. Client is dependent in the decision-making process. Client has a clear but weak speech. Client expresses that she can learn better through visual aids and experience.

Client demonstrates nonverbal communication congruent to verbal communication. Client relays messages with consistency and exhibit agreement and disagreement of statements. Her primary language was “Bisaya” and she had a high school degree.

7. Sexuality/ ReproductiveClient has an obstetric history of G3P3. Client has an irregular

menstrual cycle with menses appearing once in two-three months. She was noted menarche at the age of 13. The client speaks of single partner sexual contact to date. Client experienced sexual contact with husband at the age of 22 y.o. with her husband. She stated that her sexual relationship with her husband was satisfying, and that sexual intercourse had been limited for a while due to dypnea during strenuous activity. The client uses contraceptives such as pills from 2005-2008. She verbalizes that sexual activity should be in the context of marriage. Client expresses no concern, abuse or problems regarding illness and sexual patterns. She uses 3-4 napkin pads per day. Thelarche began at 10 years of age. Menarche was experienced during 13 years of age. Client verbalizes no history of sexually related illnesses or problems is currently in UTI. The client is not aware of the importance of self breast examination; and, consents that she never performed it.

8. Self-Perception/ Self-Concept Her recent job is a factory worker. She currently was retired. She described herself as determined and stubborn and said she liked to do things herself and ask for help if she needed it. She stated the feeling of emptiness sometimes. She said that her recent illness had not changed her self image and that it had only motivated her to get better. She said she felt angry/annoyed when she was not in control and experienced occasional heart palpitations when she felt anxious or fearful. Her children and grandchildren had been challenging for her recently, and she reported feeling depressed when she couldn’t help them out with their various issues in life. She said that she sometimes feels weak; she was powerless or had lost hope. She had excellent eye contact and conversational skills.

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9. Role-Relationship PatternShe was fully functional in this pattern. She was married and lived with

her husband, and they had three daughters. She reported that they had no financial concerns. She said that she turns to her older daughter for support. She was very assertive and noticed everything that went on during her hospital stay. She was not afraid to point out when she felt something was not right or could be improved.

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Three Generation Genogram

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10.Coping and Stress ToleranceHer family situation and illness was the major stressor in her life. She

said that she just tries “to get through it.” She reported relieving stress by going for a walk or talking to her daughter and friends. She said that she felt relaxed when she have someone to share to. In this area, her diagnosis is readiness for enhanced family coping related to the situation with her mother and children as evidenced by desire to solve their problems.

11.Values and Belief Patient was fully functional in this health pattern as well. She said that in general, she gets the things she wants from life. She was Catholic and stated that her religion was important to her. She practiced by praying and reading the bible. When I asked her about her beliefs about health and illness, she said, “magkasakit ang tanang taw”. Patient sees respect as the most important value in life. Her source of strength is her family and God. Every time she experiences decision making process, she consults her husband as her second opinion.

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V. Physical Assessment

GENERAL APPEARANCE:Patient seen lying on bed, awake, alert, responsive, coherent, afebrile,

with venoclysis of # 3 D5 Water, infusing well at right hand with the following vital signs: T- 38 C, BP – 180/90, PR – 98 bpm, RR – 28 cpm

HeadHead is rounded with smooth skull contour. Nodules and masses

are absent. Hair is evenly distributed, black in color, and with smooth texture. Facial feature is symmetric, palpebral fissures equal in size and symmetric nasolabial folds. Facial movements are symmetric.

EyesHair in eyebrow is evenly distributed, skin is intact,

symmetrically aligned, moves equally. Eyelashes are equally distributed, curled slightly outward. Skin are intact on eyelids, absence of discharge, and no discoloration. Lids close symmetrically. When lids open, no visible sclera above corneas, and upper and lower borders of cornea are slightly covered. Conjunctiva is transparent, capillaries are evident, and sclera is white. Palpebral conjunctiva is shiny, smooth and pink in color. Lacrimal gland has no edema and no tenderness. Cornea is transparent, shiny and smooth. Patient blinks when the cornea is touched. Pupils are black in color, equal in size, round, and smooth. Iris is flat and round. Patient can see objects in the periphery. Both eyes are coordinated, moves in unison with parallel alignment. Light reflection appears at symmetric spots in both eyes.

EarsColor is the same as the face. Position is symmetric. Auricles are

mobile, firm and not tender. Pinna recoils after it is folded. Tympanic membrane is pearly gray in color and semitransparent. Cerumen is wet and brown in color. Both ears can hear normal voice tones.

NoseSymmetric and straight, no discharge or flaring. No tenderness

noted and lesions are absent. Air moves freely as the patient breath through the nares. The mucosa of the nasal cavities is pink with clear watery discharge. Lesions are absent. Nasal septum is intact and in midline. Facial sinuses are not tender, well outlined, contain air and light up equally.

Mouth and OropharynxLips are uniform in pink color, soft, moist, smooth texture;

contour is symmetrical and has the ability to purse lips. Buccal mucosa is uniform in pink color, moist, smooth, soft, glistening and elastic texture. The patient has 25 teeth with smooth, yellowish and shiny tooth enamel. Gums have no retractions, firm, moist and pink in color. Tongue is centrally located, pink in color, moist, slightly rough and with

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thin whitish coating. Tongue moves freely without tenderness. Bse of the tongue is smooth with prominent veins. Salivary glands has the same color with the buccal mucosa and floor of the mouth. Uvula is light pink and smooth. Hard palate is lighter pink and has more irregular texture. Oropharynx is pink and has a smooth posterior wall. Tonsils are pink and smooth, no discharge.

NeckNeck muscles are equal in size and head is centered. Head

movement is coordinated with smooth motion without discomfort. Nodes are not palpable on the entire neck. Trachea is centrally placed in midline of the neck with space equal on both sides. Thyroid gland is not visible upon inspection. Gland ascends upon telling the patient to swallow but is not visible. Gag reflex is present.

Thorax and Lungs Patient has barrel chest. Spinal alignment is vertical. Posterior

thorax has intact skin and has uniform temperature. Chest wall is intact, no tenderness and masses are absent. Expansion on posterior chest is evident. Crackles and wheezing heard upon auscultation on the chest. Cough is productive. Rapid breathing is noted and use of accessory muscles when breathing.

Heart Pulsations are absent on the aortic and pulmonic areas.

Pulsations are present on the tricuspid area. Upon auscultation of the heart on the aortic, pulmonic, tricuspid and apical, intensity is increased. S3 is present.

Peripheral Vascular SystemPulse volumes on periphery are symmetric. Carotid arteries have

also symmetric pulse volumes. Pulsations are decreased. Jugular veins are absent. When limbs were elevated, veins collapse. Limbs are not tender and symmetric in size. Skin color is pink. Skin temperature is not excessively warm or cold. No edema was noted. Skin texture is resilient and moist.

AbdomenSkin is unblemished on the abdomen, uniform in color, rounded,

and no evidence of enlargement of liver or spleen. The contour of abdomen with reference to the foot is symmetric. Movement of the abdomen while breathing is symmetric. Upon palpation, no tenderness was noted with consistent tension. Liver is not palpable and border feels smooth. Bladder is not palpable.

Musculoskeletal SystemMuscle size is equal on both sides of the body. No contractures

were noted on the tendons and muscles. Upon palpation, muscles at rest are atonic (lacking firm). Patient has slow, coordinated

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movements. Upon palpation of the bone, tenderness or swelling was not noted. Bones have no deformities. Joints have no swelling, no tenderness, swelling or nodules upon palpation.

MENTAL STATUS

Level of ConsciousnessPatient is awake, alert and responds to verbal stimuli. She can

respond to questions simultaneously. Speaks clearly and uses appropriate words. Patient can able to comprehend questions and directions.

AwarenessPatient is oriented to time, place, and person by tactful

questioning. Patient was asked of the time of the day, the date and names of family members.

Thought ProcessPatient can recall three digit numbers that was asked to repeat.

She can still recall the things she has done within the day. Patient can still recall information given earlier such as the name of the student nurse. Patient is able to answer questions that need simple abstract thinking. She can be able to perform simple mathematical calculations and problem solving. Patient has sound judgment and can be able to express her decisions and interests.

Communicating ProcessPatient is able to use verbal and nonverbal communication such

as facial expression and hand gestures. She is able to use appropriate affect and mood and able to use appropriate words when communicating. Patient communicates in a an average page with proper choice of words.

CRANIAL NERVE FUNCTION

Cranial Nerve IPatient is able to identify the smell of alcohol and perfume.

Cranial Nerve IIPatient can see the periphery when one eye is covered. Snellen chart was not used in the assessment.

Cranial Nerve IIIPatient can follow the six ocular movements and pupil reaction when light has been used in testing for PERRLA.

Cranial Nerve IV

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Patient is positive to six ocular movements.

Cranial Nerve VPatient’s blink reflex is positive through the use of cotton in touching the sclera. Alternating blunt and sharp ends over client’s forehead showed positive result.

Cranial Nerve VIEyes equally move, eyeballs move laterally.

Cranial Nerve VIIPatient is able to perform facial expression as assessed. She can also identify sweet and sour taste.

Cranial Nerve VIIIPatient is able to hear words that were spoken to her and can hear audible sounds through the use of alternative device in assessing hearing of the patient.

Cranial Nerve IXSwallowing ability is present and gag reflex. Patient is able to move her tongue freely side to side and up to down.

Cranial Nerve XClient’s speech has no hoarseness. Vibration on vocal chord is felt upon palpation. Swallowing is also present.

Cranial Nerve XIHead can extend to front, back and sides. Patient can shrug shoulder against resistance from hand.

Cranial Nerve XIIPatient can move tongue from side to side and can protrude it.

CEREBELLAR / MOTOR FUNCTIONAssessment on gross motor function is deferred. Patient was able to

squeeze fingers, make fist, able to perform finger to nose test, alternating supine and pronation of hand on lap, finger to nose and to nurse’s fingers, finger to fingers and fingers to thumb.

SENSORY FUNCTIONPatient is able to react on light and touch sensation. Patient is able to

discriminate between sharp and dull sensation. She can able to determine one poin and two point objects being used. Patient can also discriminate between hot and cold temperature. Patient can recognize objects being placed on hands. She can also identify numbers and letters written on palm.

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VI. Significant Laboratory Findings and Diagnostic Procedures

Diagnostic or Laboratory Procedure

Date Ordered and Date Results

were released

Normal Range

Patient’s Results

Analysis and Interpretation of Results

Male Female

HEMATOLOGY

Hemoglobin 04-20-10

140-180 g/L

120-160 g/L

117 g/L A decrease implies anemia, recent hemorrhage and fluid retention

Hematocrit 04-20-10

0.42-0.52 g/L

0.37-0.47 g/L

0.35 g/L A decrease implies anemia and hemodilution

RBC 04-20-10

4.7-6.1

/L

4.2-5.4

/L

4.4 /L A decreaseimplies anemia and fluid overload of >24 hours

WBC 04-20-10

5-10 x /L 8.8 x /L Within normal range

Differential CountNeutrophils 04-20-

1040-74 % 84 % An increase implies

asthma, hay fever, parasitic infections, chronic myelocytic leukemia, Hodgkin’s disease and metastasis

Lymphocytes

04-20-10

19-48 % 12 % A decrease implies no significant interpretation

Monocyte 04-20-10

3-9 % 2 % A decrease implies no significant interpretation

Eosinophil 04-20-10

0-7 % 2 % Within normal range

Basophil 04-20-10

0-2 % 0 % Withn normal range

URINE CHEMISTRYColor 04-20-

10Straw to dark

yellowDark

YellowNormal Result

Appearance 04-20-10

Clear Cloudy Turbity implies kidney infection

Specific Gravity

04-20-10

Newborns: 1-1.02

Infants: 1.002-

1.030 An increase implies nephritic syndrome

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1.006Adults: 1.016-

1.022pH 04-20-

104.6-6.5 5.0 Within normal range

Protein 04-20-10

None (++) Presence implies proteinuria, renal failure or myeloma

Glucose 04-20-10

Negative Negative Normal result

RBC 04-20-10

0 /hpf 0-2 /hpf

2-4 /hpf Within maximum normal range.

WBC 04-20-10

0-2 /hpf

0-5 /hpf

10-12 /hpf An increase implies trauma or tumors

Casts 04-20-10

Hyaline, coarse.

Fine granular.RBC, WBC.Waxy casts

Coarsely granular.1-2 /hpf

Normal result

Amorphous Materials

04-20-10

Small amounts Few Normal result

Epithelial Cells

04-20-10

Small amounts Few Normal result

Bacteria 04-20-10

None Many Presence implies GUT infection or contamination of external genitalia

Other Procedures:

X-ray 04/20/10Conclusion: Bilateral Pleural Effusion predominantly at the left.

Electrocardiograph 04/20/1010 mm/ mV25 mm/sHF:DF HR=112 bpm

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VII. Summary of Significant Findings

FINDINGS ACTUAL NURSING DIAGNOSES

POTENTIAL/ RISK NURSING DIAGNOSES

a. Marjorie Gordon’s Functional health Patterns

Activity intolerance related to imbalance between oxygen supply and demand

Anxiety related to breathlessness and restlessness from inadequate oxygenation

Powerlessness related to inability to perform role responsibilities secondary to chronic illness and hospitalization.

b. Physical Assessment

Ineffective airway clearance related to presence of tracheobronchial obstruction

Decreased Cardiac Output related to impaired contractility and increased preload and afterload.

Excess fluid volume related to excess fluid or sodium intake and retention of fluid secondary to heart failure and its medical therapy

c. Laboratory and Diagnostic Tests

Impaired gas exchange related to alveolar edema due to elevated ventricular pressure secondary to pleural effusion

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VIII. Anatomy and Physiology

THE HEART

THE HEART WALLS

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THE HEART CHAMBERS AND VALVES

THE CONDUCTION SYSTEM OF THE HEART

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THE CIRCULATORY SYSTEM

The HeartThe heart is located in the thoracic cavity in the mediastinum, between the lungs and deep to the sternum.

Base – broad superior portion of the heart which is the point of attachment for the great vessels

Apex – inferior end that tapers to a blunt point immediately above the diaphragm

The adult heart is about 9 cm wide at the base, 13 cm from base to apex and 6 cm from anterior to posterior at its thickest point – roughly size of one’s fist. Its weight is 300 g.

Pericardium – a double-walled sac that encloses the heart Parts: - Parietal Pericardium – outer wall with thick superficial fibrous layer and thin serous layer.

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- Visceral Pericardium – covers the heart surface.

The Heart Wall Epicardium – serous membrane on the heart surface consisting of

squamous epithelium overlying a thin layer of adipose tissue. It is where the largest branch of coronary blood vessel travel through.

Endocardium – lines the interior of the heart chambers. It is a simple squamous endothelium overlying a thin areolar tissue layer. It covers the valve surfaces and is continuous with the endothelium of the blood vessels.

Myocardium – the layer between the epicardium and the endocardium. It is the thickest and performs the work of the heart.

The Chambers Right and Left Atria – the thin- walled receiving chambers for blood

returning to the heart by way of the great veins. Each atrium has a small earlike extension called auricle that slightly increases its volume.

Right and Left Ventricles – the pumps that eject blood into the arteries And keep it flowing around the body. The right ventricle constitutes most of the anterior aspect of the heart, while the left ventricle forms the apex and inferoposterior aspect.

Sulci (grooves) – boundaries on the surface of the four chambers of the heartNamely:

Coronary Sulcus – encircles the heart near the base and separates the atria above the ventricles below.

Anterior Intraventricular Sulcus – extends obliquely down the heart from the coronary sulcus toward the apex at the front

Posterior Intraventricular Sulcus - extends obliquely down the heart from the coronary sulcus toward the apex at the back

Thin flaccid walls that are exhibited by the atria: Interatrial Septum – separates both atria Intraventricular Septum – much more vesicular

The Valves Atrioventricular (AV) Valves – regulate the openings between the atria

and the ventricles Semilunar Valves – regulate the flow of blood from the ventricles into

the great arteries Pulmonary Valve – controls the opening from the right ventricle into

the pulmonary trunk Aortic Valve - controls the opening from the left ventricle into the

aorta

Blood Flow through the Chambers

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Blood returns to the heart through the two large veins, the superior vena cava draining the head, neck, upper limbs and thoracic cavity, and the inferior vena cava draining the abdominal cavity and lower limbs. Blood in the right atrium flows through the right AV valve and into the right ventricle.

When the right ventricle contracts, the AV valve closes and blood is forced through the pulmonary valve into the pulmonary trunk. This artery ascends from the heart front of the heart and branches into the right and left pulmonary arteries, which lead to the respective lungs. In the lungs, this blood unloads its carbon dioxide and picks up a load of oxygen.

The oxygen-enriched blood returns by way of several veins which converge to form four pulmonary veins by the time they reach heart. These four empty into the left atrium. Blood flows from there past the left valve into the left ventricle. The left ventricle contracts at the same time as the right, and expels blood through the aortic valve into the ascending aorta. Blood in the aorta flows to every organ in the body, unloading some of its O2 from the tissues, and returning to the heart via the vena cavae.

The Conduction System1. Sinoatrial Node – the pacemaker of the heart that initiates each

heartbeat and determines the heart rate.2. Atrioventricular Node – acts as an electrical gateway to the

ventricles;the fibrous skeleton acts as an insulator to prevent currents from getting to the ventricle by another route.

3. Atrioventricular Bundle – forks into the right and left bundle branches, which enter the interventricular septum and descend toward the apex.

4. Purkinje Fibers – distribute the electrical excitation to the myocytes of the ventricles. They form more elaborate networks in the left ventricle than in the right.

Cardiac cycle is the term referring to all or any of the events related to the flow or blood pressure that occurs from the beginning of one heartbeat to the beginning of the next. Heart Rate - the frequency of the cardiac cycle Five Stages of 'beat' of the heart:

1. "Late diastole" which is when the semilunar valves close, the AV Valves open and the whole heart is relaxed. Second,

2. "Atrial systole" when atria is contracting, AV valves open and blood flows from atrium to the ventricle.

3. "Isovolumic ventricular contraction" it is when the ventricles begin to contract, AV valves close, as well as the semilunar valves and there is no change in volume.

4. "ventricular ejection", Ventricles are empty, they are still contracting and the semilunar valves are open.

5. "Isovolumic ventricular relaxation", Pressure decreases, no blood is entering the ventricles, ventricles stop contracting and begin to relax, semilunars are shut because blood in the aorta is pushing them shut.

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Throughout the cardiac cycle, the blood pressure increases and decreases. The cardiac cycle is coordinated by a series of electrical impulses that are produced by specialized heart cells found within the sino-atrial node and the atrioventricular node. The cardiac muscle is composed of myocytes which initiate their own contraction without help of external nerves (with the exception of modifying the heart rate due to metabolic demand). Under normal circumstances, each cycle takes approximately one second.

Myocyte (also known as a muscle cell) is the type of cell found in muscles. They arise from myoblasts. Each myocyte contains myofibrils, which are long chains of sarcomeres, the contractile units of the cell.

Stroke volume (SV) is the volume of blood pumped from one ventricle of the heart with each beat. It is calculated by subtracting the volume of blood in the ventricle at the end of a beat (called end-systolic volume) from the volume of blood just prior to the beat (called end-diastolic volume). This applies equally to both left and right ventricles of the heart. These two stroke volumes are generally equal, both approximately 70 ml in a healthy 70-kg man.

Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.

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IX. Pathophsiology (Left Sided Heart Failure)

HOSTGENES*Genetic predisposition on hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), coronary artery disease, myocardial infarction, and hypertension* Genetic polymorphisms of the reninangiotensin-aldosterone system (RAAS) and sympathetic system have also been associated with susceptibility to and/or mitigation of HF* Gene variants in the alpha-2c adrenoceptor and the alpha-1 adrenoceptorRACE* African Americans* Hispanic/Latinos* Native Americans*Soviet RepublicsAGE*Elderly peopleOTHERS*hypertension*hyperlipidemia* diabetes*CADLIFESTYLE*smoking*alcohol consumption*Use of cardiotoxic drugsENVIRONMENT

Inappropriate methods placed

on the heart

Restricted filling on the heart

Myocyte loss

Decreased myocyte

contractility

Systolic dysfunction

Decreased stroke volume

Decreased cardiac output

hypertrophy Increased catecholamine

release

Increased preload

Increased ventricular

volume

Increased heart rate

Increased contraction of sarcomeres

Increased stroke volume

Increased end-diastolic pressure

Left-sided HF

WHEN SLEEPING

Reduced adrenergic support of ventricular

function

Nocturnal depression of

the respiratory center

Paroxysmal nocturnal breathing

Decreased relaxation

Decreased elastic recoil

Increased stiffness of the

ventricle

Diastolic dysfunction

Increased left ventricular end-

diastolic pressure

Rapid filling in early diastole

S3, apical impulse is displaced laterallyS4

Increased pulmonary capillary pressure

Air in lungs replaced by blood/

interstitial fluid

Pulmonary edema

RalesSmall airway obstruction

wheezing

Stimulates juxta-

capillary I receptors

Reflex shallow and rapid breathing

Reduction in vital capacity Restrictive physiology Air trapping

Work of breathing increases

Respiratory muscle fatigue

Dyspnea

Ventilation/ Perfusion mismatch

Peripheral vascons-triction

Decreased perfusion of

the heart

Underper-fusion of

the cerebrum

Reduced blood pooling in the extremities

and abdomen

Inability of the heart to supply

appropriate amounts of blood to

skeletal muscles

Reduced renal perfusion

during the day

Decreased O2 in

venous blood

Sweating

Skin appears dusky

Ischemia Confusion

Shortness of breath, orthopnea

Fatigue

Normal perfusion at

night

Fluid retention during the day

Nocturia

Right-sided HF

AGENT

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Pathophsiology (Right Sided Heart Failure)

HOSTGENES*Genetic predisposition on hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), coronary artery disease, myocardial infarction, and hypertension* Genetic polymorphisms of the reninangiotensin-aldosterone system (RAAS) and sympathetic system have also been associated with susceptibility to and/or mitigation of HF* Gene variants in the alpha-2c adrenoceptor and the alpha-1 adrenoceptorRACE* African Americans* Hispanic/Latinos* Native Americans*Soviet RepublicsAGE*Elderly peopleOTHERS*hypertension*hyperlipidemia* diabetes*CADLIFESTYLE*smoking*alcohol consumption*Use of cardiotoxic drugsENVIRONMENT

AGENT

Pulmonary HTN Cor Pulmonale

Right Ventricular Pressure > Left Ventricular Pressure

Interventricular septum bows to the left

Prevent efficient filling of the left ventricle

Pulmonary congestion

Partial obstruction of the left ventricular outflow

Left-Sided HF

Increased afterload on the right ventricle

Destruction of pulmonary

capillary bed

Hypoxia-induced vasoconstriction of the

pulmonary arteries

Sequela to pulmonary

disease

Right ventricular ischemia

Systolic dysfunction

Decreased stroke volume

Decreased cardiac output

hypertrophy Increased catecholamine

release

Increased preload

Increased ventricular

volume

Increased heart rate

Increased contraction of sarcomeres

Increased stroke volume

Increased atrial pressure

Increased right-sided pressure

Accumulation of fluid in the

systemic venous

circulation

Venous congestion

Anasarca, ascites, dependent edema

Decreased relaxation

Decreased elastic recoil

Increased stiffness of the

ventricle

Diastolic dysfunction

Decreased ventricular

function

Increased right ventricular end-

diastole pressure

Congestion of hepatic veins

Expansion of the liver

Impinge normal

diaphragm-matic

function

Distention of liver capsule

RUQ pain

dyspnea

Right-Sided HF

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X. Nursing Care Plans

DATE ACTIVE PROBLEM NURSING INTERVENTIONS EVALUATION

April 22, 2010 Impaired gas exchange related to alveolar edema due to elevated ventricular pressures

Subjective cue:“Maglisod jud ko'g ginhawa”,as verbalized by the patient

Objective cue:>restlessness>irritability>diaphoresis>bilateral crackles that do not clear with cough>pale skin color

Scientific Analysis: Dyspnea, or shortness of breath, may be precipitated by minimal to moderate activity (dyspnea on exertion [DOE]); dyspnea also can occur at rest. The patient may report orthopnea, difficulty in breathing when lying flat. Patients with

Independent:1. R: Monitor vital signs and cardiac rhythmI: for baseline data and monitoring2. R: Auscultate breath sounds, I: notes areas of decreased/adventitious breath sounds 3. R:Note character and effectiveness of cough mechanismI: ability to clear airways of secretions4. R: Elevate head of bed, provide adjuncts and suction, as indicatedI: to maintain airway5. R: Encourage frequent position changes and deep-breathing/coughing exercises. Use incentive spirometer, chest physiotherapy, as indicatedI: promotes chest expansion and drainage of secretions6. R: Maintain adequate I/OI: for mobilization of secretions7. R: Encourage adequate rest and

Desired Outcome:After 8 hours of nursing intervention, the patient was able to demonstrate improved ventilation and adequate oxygenation of tissues by ABGs within patient's normal limits and absence of symptoms of respiratory distress

Actual Outcome:After 8 hours of nursing intervention, the objectives were partially met. The patient was able to improved ventilation andoxygenation of tissues as evidenced by patient breathing without using much of the accessory muscle

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orthopnea usually prefer not to lie flat. They may need pillows to prop themselves up in bed, or they may sit in a chair and even sleep sitting up. Some patients have sudden attacks of orthopnea at night, a condition known as paroxysmal nocturnal dyspnea (PND). The cough associated with left ventricular failure is initially dry and nonproductive. Most often, patients complain of a dry hacking cough that may be mislabeled as asthma or chronic obstructive pulmonary disease (COPD). The cough may become moist. Large quantities of frothy sputum, which is sometimes pink (blood tinged), may be produced, usually indicating severe pulmonary congestion (pulmonary edema). Adventitious breath sounds may be heard in various lobes of the lungs. Usually, bi-basilar crackles that do not clear with coughing are detected in the early phase of left ventricular

limit activities to within client tolerance.I: Promote calm/restful environmenthelps limit oxygen need/consumption8. R: Keep environment allergen/pollutant freeI: to reduce irritant effect of dust and chemicals on airway9. R: Provide psychological support, active-listen questions/concernsI: to reduce anxiety

Dependent:1. R: Administer medications, as indicatedI: to treat underlying conditions

Source: Source: Sparks, S and Taylor, C, Nursing Diagnosis Reference Manual 3rd edition; Springhouse Corporation, Pennsylvannia

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failure. As the failure worsens and pulmonary congestion increases, crackles may be auscultated throughout all lung fields. At this point, a decrease in oxygen saturation may occur (Wolkenstein, 2000).

April 22, 2010 Decreased Cardiac Output related to impaired contractility and increased preload and afterload.

Subjective cue:“Sige ra jud kog pangluspad”,as verbalized by the patient

Objective cue:>restlessness>irritability>diaphoresis>pale skin color

Scientific Analysis: In addition to increased pulmonary pressures that cause decreased oxygenation, the amount of blood ejected from the left ventricle may decrease,

Independent:1. R: Place patient at physical and emotional rest I: to reduce work of heart.2. R: Provide rest in semi-recumbent position or in armchair in air-conditioned environment I: that reduces work of heart, increases heart reserve, reduces BP, decreases work of respiratory muscles and oxygen utilization, improves efficiency of heart contraction; recumbency promotes diuresis by improving renal perfusion 3. R:Provide bedside commode I: to reduce work of getting to bathroom and for defecation.4. R: Provide for psychological rest since emotional stress produces vasoconstriction.I:elevates arterial pressure, and

Desired Outcome:After 8 hours of nursing intervention, the patient was able to demonstrate improved cardiac output within normal levels of preload and afterload.

Actual Outcome:After 8 hours of nursing intervention, the objectives were partially met. The patient was able to initiate actions to increase cardiac output but symptoms persisted.

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sometimes called forward failure. The dominant feature in HF is inadequate tissue perfusion. The diminished CO has widespread manifestations because not enough blood reaches all the tissues and organs (low perfusion) to provide the necessary oxygen. The decrease in SV can also lead to stimulation of the sympathetic nervous system, which further impedes perfusion to many organs. Blood flow to the kidneys decreases, causing decreased perfusion and reduced urine output (oliguria). Renal perfusion pressure falls, which results in the release of renin from the kidney. Release of renin leads to aldosterone secretion. Aldosterone secretion causes sodium and fluid retention, which further increases intravascular volume. However, when the patient is sleeping, the cardiac workload is decreased, improving renal perfusion, which then leads to frequent urination at night (nocturia). Decreased CO causes other

speeds the heart.5. R: Promote physical comfort. Avoid situations that tend to promote anxiety and agitation. Offer careful explanations and answers to the patient's questions.I: Decreases anxiety6. R: Take frequent BP readings. Observe for lowering of systolic pressure. Note narrowing of pulse pressure. Note alternating strong and weak pulsations (pulsus alternans). Auscultate heart sounds frequently and monitor cardiac rhythm. Note presence of S3 or S4 gallop (S3 gallop is a significant indicator of heart failure). Monitor for premature ventricular beats. I: Evaluates for progression of left-sided heart failure.

Source: Source: Sparks, S and Taylor, C, Nursing Diagnosis Reference Manual 3rd edition; Springhouse Corporation, Pennsylvannia

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symptoms. Decreased gastrointestinal perfusion causes altered digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion, restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety increases, so does dyspnea, enhancing anxiety and creating a vicious cycle. Stimulation of the sympathetic system also causes the peripheral blood vessels to constrict, so the skin appears pale or ashen and feels cool and clammy.(Wolkenstein, 2000).

April 22, 2010 Excess fluid volume related to excess fluid or NA intake and retention of fluid secondary to Heart failure and its medical therapy

Subjective cue:“puno kaayo akong gibati,”, as verbalized by the patient

Objective cue:>Adventitious breath

Independent:1. R: Compare current weight admission and/or previously stated weightI: provides a comparative baseline 2. R: Auscultate breath soundsI: for presence of crackles and congestion3. R: Measure abdominal girthfor changes that I: may indicate increasing fluid

Desired Outcome:After 8 hours of nursing intervention, the patient was able to stabilize fluid volume as evidenced by balance I/O, vital signs within patient's normal limits, stable weight, and free signs of edema

Actual Outcome:After 8 hours of nursing intervention, the objectives

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sounds(crackles)>changes in respiratory pattern>Dyspnea>Restless>Pulmonary congestion

Scientific Analysis:Fluid that accumulated in the dependent extremities during the day begins to be reabsorbed into the circulating blood volume when the person lies down. Because the impaired left ventricle cannot eject the increased circulating blood volume, the pressure in the pulmonary circulation increases, causing further shifting of fluid into the alveoli. The fluid filled alveoli cannot exchange oxygen and carbon dioxide. Without sufficient oxygen, the patient experiences dyspnea and has difficulty getting an adequate amount of sleep. (Wolkenstein, 2000).

retention/edema4. R: Assess neuromuscular reflexesI: to evaluate for presence of electrolyte imbalances such as hypernatremia5. R: Observe skin and mucous membranesI: for presence of decubitus/ulceration6. R: Elevate edematous extremities, change position frequentlyI: to reduce tissue pressure and risk for skin breakdown7. R: Place in semi-Fowler's position, as appropriateI: to facilitate movement of diaphragm, thus improving respiratory effort

Dependent:1. R: Administer medications (e.g.diuretics)I: To treat underlying conditions

Collaborative:1. R: Restrict sodium and fluid intake, as indicatedI: for nutritional therapy

were partially met. The patient was able to have a normal vital signs of T-37.1 c, P-77 bpmR-19 cpm, BP- 110/70 mmHG

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Source: Source: Sparks, S and Taylor, C, Nursing Diagnosis Reference Manual 3rd edition; Springhouse Corporation, Pennsylvannia

April 23, 2010 Activity intolerance related to imbalance between oxygen supply and demand

Cues and ObjectivesSubjective:“dali ra ko makutasan, dili ko kasugakod ug dugay ug bug-at nga trabaho,” as verbalized by the patient.

Objective:- generalized weakness- limited range of motion- short term performance of an activity

Scientific Analysis:As heart failure becomes more severe, the heart is unable to pump the amount of blood required to meet all of the body’s

Independent:1. I: Discuss with the patient the need for activity.R: Improves physical and psychosocial well-being.2. I: Identify activities the patient considers desirable and meaningful.R: To enhance their positive impact.3. I: Encourage patient to help plan activity progression, being sure to include activities the patient considers essential.R: Participation in planning helps ensure patient compliance.4. I: Instruct and help patient to alternative periods of rest and activity.R: To reduce the body’s organ demand and prevent fatigue.5. I: Identify and minimize factors that decrease the patient’s exercise tolerance.R: To help increase the activity level.6. I: Monitor physiological responses

Desired Outcomes:After 8 hours of nursing interventions,* Patient states desire to increase activity level.* Patient states understanding of the need to increase activity level gradually.* Blood pressure and pulse and respiratory rates remain within prescribed limits during activity.* Patient states satisfaction with each new level of activity attained.* Patient demonstrates skill in conserving energy while carrying out daily activities to tolerance level.* Patient explains illness and connects symptoms of activity intolerance with deficit in oxygen supply or use.

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needs. To compensate, blood is diverted away from less-crucial areas, including the arms and legs, to supply the heart and brain. As a result, people with heart failure often feel weak (especially in their arms and legs), tired and have difficulty performing ordinary activities such as walking, climbing stairs or carrying groceries

to increased activity.R: To ensure return to normal a few minutes after exercising.7. I: Teach patient how to conserve energy while performing activities of daily living.R: These measures reduce cellular metabolism and oxygen demand.8. I: Teach patient exercises for increasing strength and endurance.R: Improves breathing and gradually increase activity level.9. I: Support and encourage activity to patient’s level of tolerance.R: Helps patient develop level of tolerance. 10. I: Before discharge, formulate a plan with the patient and caregivers that will enable the patient either to continue functioning at maximum activity intolerance or to gradually increase the tolerance.R: Participation in planning encourages patient satisfaction and compliance.

Source: Source: Sparks, S and Taylor, C, Nursing Diagnosis Reference Manual 3rd edition;

Actual Outcome:Afer 8 hours of nursing intervenions, the objectives were partially met. The: *Patient stated understanding of the need to perform daily activities.*Patient demonstrated conservation of energy while performing activities.

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Springhouse Corporation, Pennsylvannia

April 23, 2010 Ineffective airway clearance related to presence of tracheobronchial obstruction

Cues and Evidences: Subjective:“maglisod ko ug ginhawa nya huot ako dughan,” as verbalized by the patient.

Objective:- shortness of breath- dyspnea- use of accessory muscles when breathing- tachypnea with RR of 28

Scientific Analysis:Mucus is produced at all times by the membranes lining the air passages. When the membranes are irritated or inflamed, excess mucus is produced and it will retain in tracheobronchial tree. The inflammation and increased in secretions block the airways

Independent: 1. I: Assess respiratory status at least every for hours or according to establishment standards.R: To detect early signs of compromise.2. I: Place patient in Fowler’s position and support upper extremities.R: To aid breathing and chest expansion, and to ventilate basilar lung fields.3. I: Help patient turn, cough, and deep breath every 2 to 4 hours.R: To help prevent pooling of secretions and to maintain airway patency.4. I: Suction as needed. Be alert for progression of airway clearance.R: To stimulate cough and airways.5. I: Encourage fluids (atleast 3,000 mL daily).R: To ensure adequate hydration and loosen secretions, unless contraindicated.6. I: Mobilize patient to full

Desired Outcome: After 8 hours of nursing interventions,* Patient clears airway using controlled coughing techniques.* Patient expectorates sputum.* Patient drinks 3 to 4 liters of fluid daily.*Patient’s arterial blood gas values are within normal limits.*Patient performs chest physiotherapy, especially postural drainage. *Patient understands necessity of adequate hydration

Actual Outcome:After 8 hours of nursing interventions, the objectives were partially met. The:*Patient verbalized understanding on coughing techniques* Patient increased fluid

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making it difficult for the person to maintain a patent airway. In order to expel excessive secretions, cough reflex will be stimulated. An increased in RR will also be expected as a compensatory mechanism of the body due to obstructed airways (Wolkenstein, 2000).

capabilities.R: To facilitate chest expansion and ventilation.7. I: Perform postural drainage, percussion, and vibration every 4 hours or as ordered.R: To enhance mobilization of of secretions that interferes with oxygenation.8. I: Avoid supine position for extended periods. Encourage lateral, sitting, prone, and upright positions as much as possible.R: To enhance lung expansion and ventilation.9. I: Provide tissues and paper bags for hygienic sputum disposal.R: To prevent spreading infection.10. I: Monitor and document sputum characteristics every shift.R: To gauge therapy’s effectiveness.

Source: Sparks, S and Taylor, C, Nursing Diagnosis Reference Manual 3rd edition; Springhouse Corporation, Pennsylvannia

volume to 3 to 4 liters per day.

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XI. Drug Study

Name of medication or

drugs

indications/reasons for administrating the drugs

Side effects, adverse

reactions a nurse note for

Nursing Interventions

Cefuroxime 750mg IVTT It is effective for the treatment

of penicillinase-producing Neisseria gonorrhoea (PPNG). Effectively treats bone and joint infections, bronchitis, meningitis, gonorrhea, otitis media, pharyngitis/tonsillitis, sinusitis, lower respiratory tract infections, skin and soft tissue infections, urinary tract infections, and is used for surgical prophylaxis, reducing or eliminating infection.

CNS: headache, dizziness,lethargy, paresthesias

GI: nausea,vomiting, diarrhea,anorexia, abdominal pain, flatulence,

GU: nephrotoxicity

Hematologic: bone marrow depression

Hypersensitivity: ranging from rash to fever to anaphylaxis, serum sickness reaction

Determine history of hypersensitivity reactions to cephalosporins, penicillins, and history of allergies, particularly to drugs, before therapy is initiated.

Inspect IM and IV injection sites frequently for signs of phlebitis.

Report onset of loose stools or diarrhea. Although pseudomembranous colitis.

Monitor I&O rates and pattern: Especially important in severely ill patients receiving high doses. Report any significant changes.

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Paracetamol 500mg 1 tab q 8h for fever

To relieve mild to moderate pain due to things such as headache, muscle and joint pain, backache and period pains. It is also used to bring down a high temperature. For this reason, paracetamol can be given to children after vaccinations to prevent post-immunisation pyrexia (high temperature). Paracetamol is often included in cough, cold and flu remedies.

Side effects are rare with paracetamol when it is taken at the recommended doses. Skin rashes, blood disorders and acute inflammation of the pancreas have occasionally occurred in people taking the drug on a regular basis for a long time. One advantage of paracetamol over aspirin and NSAIDs is that it doesn't irritate the stomach or causing it to bleed, potential Side effects of aspirin and

Assessment & Drug Effects Monitor for S&S of: hepatotoxicity, even with

moderate acetaminophen doses, especially in individuals with poor nutrition.

Patient & Family Education Do not take other medications (e.g., cold

preparations) containing acetaminophen without medical advice; overdosing and chronic use can cause liver damage and other toxic effects.

Do not self-medicate children for pain more than 5 d without consulting a physician.

Do not use for fever persisting longer than 3 d, fever over 39.5° C (103° F), or recurrent fever.

Do not give children more than 5 doses in 24 h unless prescribed by physician.

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NSAIDs.

Furosemide 80mg IVTT

actions:

Rapid-acting potent sulfonamide "loop" diuretic and antihypertensive with pharmacologic effects and uses almost identical to those of ethacrynic acid. Exact mode of action not clearly defined; decreases renal vascular resistance and may increase renal blood flow

Treatment of edema associated with CHF, cirrhosis of liver, and kidney disease, including nephrotic syndrome. May be used for management of hypertension, alone or in combination with other antihypertensive agents, and for treatment of hypercalcemia. Has been used concomitantly with mannitol for treatment of severe cerebral edema, particularly in meningitis.

CV: Postural hypotension, dizziness with excessive diuresis, acute hypotensive episodes, circulatory collapse. Metabolic: Hypovolemia, dehydration, hyponatremia hypokalemia, hypochloremia metabolic alkalosis, hypomagnesemia, hypocalcemia (tetany), hyperglycemia, glycosuria, elevated BUN, hyperuricemia. GI: Nausea, vomiting, oral and gastric burning, anorexia, diarrhea, constipation,

Assessment & Drug Effects

Observe patients receiving parenteral drug carefully; closely monitor BP and vital signs. Sudden death from cardiac arrest has been reported.

Monitor BP during periods of diuresis and through period of dosage adjustment.

Observe older adults closely during period of brisk diuresis. Sudden alteration in fluid and electrolyte balance may precipitate significant adverse reactions. Report symptoms to physician.

Lab tests: Obtain frequent blood count, serum and urine electrolytes, CO2, BUN, blood sugar, and uric acid values during

first few months of therapy and periodically thereafter. Monitor for S&S of hypokalemia. Monitor I&O ratio and pattern. Report decrease or unusual

increase in output. Excessive diuresis can result in dehydration and hypovolemia, circulatory collapse, and hypotension. Weigh patient daily under standard conditions.

Monitor urine and blood glucose & HbA1C closely in diabetics

and patients with decompensated hepatic cirrhosis. Drug may cause hyperglycemia.

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abdominal cramping, acute pancreatitis, jaundice. Urogenital: Allergic interstitial nephritis, irreversible renal failure, urinary frequency. Hematologic: Anemia, leukopenia, thrombocytopenic purpura; aplastic anemia, agranulocytosis (rare). Special Senses: Tinnitus, vertigo, feeling of fullness in ears, hearing loss (rarely permanent), blurred vision. Skin: Pruritus, urticaria, exfoliative dermatitis, purpura, photosensitivity, porphyria cutanea tarde, necrotizing angiitis (vasculitis). Body as a Whole: Increased perspiration; paresthesias; activation of SLE,

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muscle spasms, weakness; thrombophlebitis, pain at IM injection site.

Salbutamol 1 neb q 6 To relieve bronchospasm

associated with acute or Body as a Whole: Assessment & Drug Effects

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actions:

Synthetic sympathomimetic amine and moderately selective beta2-

adrenergic agonist with comparatively long action. Acts more prominently on beta2

receptors (particularly smooth muscles of bronchi, uterus, and vascular supply to skeletal muscles) than on beta1 (heart)

receptors. Minimal or no effect on alpha-adrenergic receptors. Inhibits histamine release by mast cells.

chronic asthma, bronchitis, or other reversible obstructive airway diseases. Also used to prevent exercise-induced bronchospasm.

Hypersensitivity reaction. CNS: Tremor, anxiety, nervousness, restlessness, convulsions, weakness, headache, hallucinations.CV: Palpitation, hypertension, hypotension, bradycardia, reflex tachycardia. Special Senses: Blurred vision, dilated pupils.GI: Nausea, vomiting. Other: Muscle cramps, hoarseness.

Monitor therapeutic effectiveness which is indicated by significant subjective improvement in pulmonary function within 60–90 min after drug administration.

Monitor for: S&S of fine tremor in fingers, which may interfere with precision handwork; CNS stimulation, particularly in children 2–6 y, (hyperactivity, excitement, nervousness, insomnia), tachycardia, GI symptoms. Report promptly to physician.

Lab tests: Periodic ABGs, pulmonary functions, and pulse oximetry.

Consult physician about giving last albuterol dose several hours before bedtime, if drug-induced insomnia is a problem.

Aldozide 1 tab BID Essential hypertension, edema and ascites of

Gynecomastia, GI

ducate patient to avoid hazardous activity such as driving until response to drug is known.

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Mechanism of Action: : competes with aldosterone for receptor sites in the distal renal tubules, increasing sodium chloride and water excretion while conserving potassium and hydrogen ions, may block the effect of aldosterone on arteriolar smooth muscle as well

CHF, liver cirrhosis, nephritic syndrome, idiopathic edema

symptoms, lethargy, headache and thrombocytopenia, leukopenia, agranulocytosis, cutaneous eruptions, pruritus, mental confusion, paresthesia, acute pancreatitis, jaundice, orthostatic hypertension, muscle spasm, weakness, fever, ataxia

Take with meals or milk; avoid excessive ingestion of food high in potassium or use of salt substitutes

Diuretic effect may be delayed 2-3 days and maximum hypertensive may be delayed 2-3weeks; monitor I and O ratios and daily weight, BP, serum electrolytes (K, Na) and renal function

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XII. Discharge Plan

METHODS Outcome Identification Nursing InterventionsMedication Patients need to understand the purpose,

dosage, route, and possible side effects of all prescribed medications.

A - Assess patient and SO’s ability to understand regarding home medication orders and instructions to be given

I - Remind and instruct the parent on home medication instructions

- Refer to drug instructions for each.

E - Evaluate the patient’s level of understanding on the instructions given about the medications

Exercise and

Environment

Regularly scheduled, moderate exercise performed for at least 30 minutes most days

of the week promotes the utilization of carbohydrates, assists with weight control,

enhances the action of insulin, and improves cardiovascular fitness.

A - Assess patient’s understanding of exercise regimen.

I - Explain the importance of exercise:

Caloric expenditure for energy in exercise Carryover of enhanced metabolic rate and efficient food

utilization- Advise patient to assess blood glucose level before and after strenuous exercise.

- Instruct patient to plan exercises on a regular basis each day.

- Encourage patient to eat a carbohydrate snack before exercising to avoid hypoglycemia.

- Advice patient that prolonged strenuous exercise may require increased food at bedtime to avoid nocturnal hypoglycemia.

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Instruct patient to avoid exercise whenever blood glucose levels exceed 250 mg/day and urine ketones are present. Patient should contact health care provider if levels remain elevated.

Encouraged so to maintain quiet environment

Encouraged so to maintain patient surrounding clean

Encouraged so to provide patient proper hygiene

E - Evaluate patient’s level of understanding on the information given and degree of awareness on the importance of good sanitation and proper exercise.

Treatment Teach patients the appropriate technique for testing blood and urine and how to interpret the results.

Stress the importance of close attention to even minor skin injuries.

Because of the atherosclerotic changes that occur, encourage patients to stop smoking.

A - Assess if the patient is continually sticking to V/S monitoring schedules and treatment regimen.

I - Patients need to know when to notify the physician and increase testing during times of illness.

In addition, teach patients to avoid crossing their legs when sitting and to begin a regular exercise program.

Instructed the patient to right information or advice by the physician

Instructed the patient to follow right time & medication

E - Check the response to the interventions and actions performed

Health Teaching

and

If the patient continues to smoke, provide the name of a smoking cessation program or

a support group. You follow the same

A - Assess for the patient’s ability to do self-care

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Hygiene protocol for drinking to avoid other diseases. - Assess patient’s will or degree to decrease/ cease smoking.

I - Discuss concerns with parent to identify underlying issues

Identify health behaviors/habits that may interfere to improve patient’s health status

Instructed patient to do other way of personal hygiene like proper hand washing, tooth brushing after eating and taking a bath everyday

E - Evaluate responses to wellness plan and action performed

- Evaluate progress of health condition.

Out Patient follow-up

and Observatio

n

Note any referrals to social services. Remind for follow-up schedule. Call if appropriate.

A - Assess for signs and symptoms

- Assess the understanding of the parent as to the possible reason for follow-up visit

I - Instruct patient/ SO to refer immediately to physician if health condition worsens

Instructed the patient to express every time of discomfort

Encourage patient to side to side position

E - Evaluate patient’s level of understanding on the instructions given and information open to her.

Diet Emphasize the importance of adjusting diet during illness, growth periods, stress, and

A - Assess foods in compliance to given diet

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pregnancy.

Encourage patients to avoid alcohol

-Assess patient’s preference of food

I - Instruct patient to watch for timing of food and not to eat more than necessary.

- Teach how to calculate caloric intake.

- Each meal should consist of a balance of carbohydrates, proteins, and fats.

Carbohydrates should be varied to include fruits, starches, and vegetables.

Protein selections that are lean will help reduce fat and cholesterol intake.

Fats should be used sparingly with <10% of total calories derived from saturated fats. High in calories, fats contribute to weight gain in type 2 diabetes mellitus (DM).

- Avoid salt whenever possible.

Do not season foods with salt or salt-containing spices. Limit use of foods with hidden sodium content (eg, crackers,

pickled foods, cheese, processed meats). Use salt-containing condiments sparingly (ketchup, soy sauce,

gravies, bouillon). - Prepare foods to retain vitamins and minerals and reduce fats.

Do not fry foods. Bake, broil, or boil foods and discard fat. Eat raw fruits and vegetables or steam vegetables to retain

fiber. Avoid adding calories with butter or cream sauces, fat back,

and bacon. Trim all visible fat from meat; skim off fat from stews or other

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prepared dishes. - Use alcohol only in moderation.

Do not omit food from meal plan in exchange for alcohol. Limit intake to 1-2 drinks per week (4 oz dry wine, 12 oz beer,

or 1.5 oz distilled liquor = 1 alcohol serving). - Use alternative nonnutritive, noncaloric sweeteners in moderation.

Limit diet: soda intake to 2 L/day. Avoid frequent use of foods and beverages with concentrated

sucrose.E - Evaluate patient’s level of understanding and degree of awareness about strict implementation of the diet.

Spiritual Provide emotional and spiritual support. A - Assess patient’s readiness to be involved in such activities

- Assess for barriers to practice religious beliefs

I - Encourage patient to attend Sunday Masses if Catholic

- Strengthen patient’s relationship with God by letting him participate religious activities: Sunday Mass, Rosary, Prayer Meetings, etc.

E – Evaluate patient’s desire for spiritual growth

- Evaluate emotional, psychosocial and spiritual progress.

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XIII. Bibliography

Amnesi, Sandra M, and et. al. Brunner& Suddarth's Medical-Surgical Nursing 10th Edition. Chicago: Lippincott Williams & Wilkins, 2009.

Doenges, Marilynn, Mary Frances Moorhouse, and Alice Murr. Nurse's Pocket Guide, 11th edition. Pennsylvania: F.A. Davis Company, 2008.

McPhee, Stephen J, Vishwanath R Linggapa, William F Ganong, and Jack D Lange. Pathophysiology of Disease: An Introduction to Clinical Medicine. Stamford, Connecticut: Appleton & Lange, 1997.

Nettina, Sandra M., and Elizabeth Jacqueline Mills. Lippincott Manual of Nursing Practice, 8th Edition. Lippincott Williams & Wilkins, 2006.

PPD's Nursing Drug Guide, 2nd Edition. Pasig: Medicomm Pacific, Inc., 2008.

Sommers, Marilyn S, Susan A Johnson, and Theresa A Beery. Diseases and Disorders: A Nurses; Therapeutic Manual 3rd Edition. Philadelphia: F.A. Davis Company, 2007.

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XIV. Learning Insights

Upon conducting the case study on congestive heart failure, I have learned another aspect in the field of Medical Surgical Nursing. Studying about the disease process itself from factors affecting it, the symptoms, pathophysiology, diagnostic procedures on identifying the disease, its treatment procedures including medical regimen and developing nursing care plans has helped me understood the details and necessary information about the disease.

Through this case study, I was able to learn to identify the problems being encountered by patients and therefore, being able to prioritize them and address then accordingly. Appropriate nursing interventions are needed to be carried on in order to help the patient alleviate symptoms and regain the health status.

* * *