Case Study-Congestive Heart Failure
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University of San Jose-Recoletos College of Nursing Cebu City __________________________________________
A Case Study on a Patient Diagnosed with Congestive Heart Failure
___________________________________________ Presented to the Faculty In Partial Fulfillment Of the Requirements in Related Learning Experience (Eversley Childs Sanitarium-Medical Ward) ___________________________________________ Presented by TANGCALAGAN, Kent C. TONZO, Hope Glysdi TUMAMUT, Yvenette Kris UY, Justin Earl VILLAMIL, Molly YBAÑEZ, Ma. Doreen BSN-III Block 8 __________________________________________ Presented to Aeda Mae Siao, RN Clinical Instructor __________________________________________ April 19-23; 26-30, 2010
INTRODUCTION a) Definition of the Disease Heart 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. Cause HF 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
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
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 cessation of 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.
GENETIC CONSIDERATIONS HF 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 reninangiotensinaldosterone 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 CONSIDERATIONS HF 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
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 FACTORS Other risk factors include: hypertension; hyperlipidemia.; diabetes; CAD; family history; smoking; alcohol consumption; and, use of cardiotoxic drugs. c) Signs and Symptoms The 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
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 lowerthan-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
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 FAILURE When 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.
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 Highlights HISTORY 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.
PHYSICAL EXAMINATION Observe 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 45degree 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. PSYCHOSOCIAL Note 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) Management The 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 MANAGEMENT Managing 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 MANAGEMENT Several 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 (ACEIs) 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. ACEIs 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 ACEIs 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 ACEI 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 (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
NURSING INTERVENTIONS Independent: 1. R: Monitor vital signs and cardiac rhythm I: for baseline data and monitoring 2. R: Auscultate breath sounds, I: notes areas of decreased/adventitious breath sounds 3. R:Note character and effectiveness of cough mechanism I: ability to clear airways of secretions 4. R: Elevate head of bed, provide adjuncts and suction, as indicated I: to maintain airway 5. R: Encourage frequent position changes and deepbreathing/coughing exercises. Use incentive spirometer, chest physiotherapy, as indicated I: promotes chest expansion and drainage of secretions 6. R: Maintain adequate I/O I: for mobilization of secretions 7. R: Encourage adequate rest and
EVALUATION 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 and oxygenation 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 environment helps limit oxygen need/consumption 8. R: Keep environment allergen/pollutant free I: to reduce irritant effect of dust and chemicals on airway 9. R: Provide psychological support, active-listen questions/concerns I: to reduce anxiety Dependent: 1. R: Administer medications, as indicated I: 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 airconditioned 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 anxiety 6. 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 leftsided 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 weight I: provides a comparative baseline 2. R: Auscultate breath sounds I: for presence of crackles and congestion 3. R: Measure abdominal girth for changes that I: may indicate increasing fluid retention/edema
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).
4. R: Assess neuromuscular reflexes I: to evaluate for presence of electrolyte imbalances such as hypernatremia 5. R: Observe skin and mucous membranes I: for presence of decubitus/ulceration 6. R: Elevate edematous extremities, change position frequently I: to reduce tissue pressure and risk for skin breakdown 7. R: Place in semi-Fowler's position, as appropriate I: 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 indicated I: for nutritional therapy Source: Source: Sparks, S and
were partially met. The patient was able to have a normal vital signs of T-37.1 c, P-77 bpm R-19 cpm, BP- 110/70 mmHG
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April 23, 2010
Activity intolerance related to imbalance between oxygen supply and demand Cues and Objectives Subjective: “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 needs. To compensate, blood is
Taylor, C, Nursing Diagnosis Reference Manual 3rd edition; Springhouse Corporation, Pennsylvannia 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 to increased activity.
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. Actual Outcome:
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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
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; Springhouse Corporation,
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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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 making it difficult for the person
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 capabilities. R: To facilitate chest expansion and
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 volume to 3 to 4 liters per day.
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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).
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
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XI. Name of medication or drugs Cefuroxime 750mg IVTT
Drug Study indications/reasons for administrating the drugs
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.
Side effects, adverse reactions a nurse note for CNS: headache, dizziness,letharg y, paresthesias GI: nausea,vomiting , diarrhea,anorexi a, abdominal pain, flatulence, GU: nephrotoxicity Hematologic: bone marrow depression Hypersensitivi ty: 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 postimmunisation 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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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 q6
To relieve bronchospasm associated with acute or
Assessment & Drug Effects Body as a Whole:
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actions: Synthetic sympathomimetic amine and moderately selective beta2adrenergic 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. Aldozide 1 tab BID
chronic asthma, bronchitis, or other reversible obstructive airway diseases. Also used to prevent exercise-induced bronchospasm.
Essential hypertension, edema and ascites of
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.
Gynecoma stia, GI
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.
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 thrombocy topenia, leukopeni a, agranuloc ytosis, cutaneous eruptions, pruritus, mental confusion, paresthesi a, acute pancreatiti s, jaundice, orthostati c hypertensi on, 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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Outcome Identification Nursing Interventions Patients need to understand the purpose, A - Assess patient and SO’s ability to understand regarding home dosage, route, and possible side effects of all medication orders and instructions to be given prescribed medications. 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 Environme nt
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. −
Instruct patient to avoid exercise whenever blood glucose
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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.
A - Assess if the patient is continually sticking to V/S monitoring schedules and treatment regimen.
Stress the importance of close attention to even minor skin injuries.
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
Because of the atherosclerotic changes that occur, encourage patients to stop smoking.
I - Patients need to know when to notify the physician and increase testing during times of illness.
E - Check the response to the interventions and actions performed Health Teaching and
If the patient continues to smoke, provide A - Assess for the patient’s ability to do self-care the name of a smoking cessation program or - Assess patient’s will or degree to decrease/ cease smoking. a support group. You follow the same
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protocol for drinking to avoid other diseases.
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 pregnancy.
A - Assess foods in compliance to given diet -Assess patient’s preference of food I - Instruct patient to watch for timing of food and not to eat more
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than necessary. Encourage patients to avoid alcohol
- 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