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Unformatted text preview: Managing hospitalized CE patients with
What you need to know about the new practice guidelines for evaluation, care, and treatment of heart failure patients in the hospital By Cindy Cunningham, RN, MS, APRN-BC
PETER ROMA, AGE 62, comes to
the emergency department complaining of progressive angina, shortness of breath on exertion, and light-headedness. He reports he is unable to lie flat at night and has a decreased appetite. His medical history reveals tobacco use, hypertension, and a myocardial infarction (MI) 20 years ago. His current medications include 325 mg aspirin taken once daily for the past 15 years. unit with a diagnosis of heart failure (HF). Would you be ready to meet his needs based on the most recent practice guidelines? This article will help prepare you to do just that. These guidelines are the first to address in-hospital medical management of HF patients with acute decompensation. heart failure
The big picture 2.1 contact hours Understanding the basics
In HF, the ventricles fail to fill with or eject blood. Cardiac filling pressures become elevated, causing inadequate tissue oxygenation, which in turn leads to impaired organ function. The most common causes of HF are hypertension, MI, valvular disorders, toxic substances, and a viral syndrome. Prevalence Statistics on the prevalence and cost of HF underscore the scope of this public health problem: Nearly 5 million Americans have HF. About 550,000 new cases are diagnosed annually. HF accounts for 12 to 15 million physician office visits and 6.5 million hospital days each year, at a cost of $28 billion. Demographics HF primarily affects elderly persons; approximately 80% of patients hospitalized with HF are older than age 65. More Medicare dollars are spent for HF diagnosis and treatment than for any other disease. HF is a complex disease--and for many patients, a chronic one. It can necessitate frequent hospitalization and reduce the quality of life. Without appropriate treatment, HF progresses, causing a gradual decline in cardiac LEARNING OBJECTIVES: function and worsening 1. State the role of neurohormonal activation in of symptoms. heart failure (HF). 2. Identify tests used to evaluate HF has many causes patients with HF. 3. Describe nursing care of the and the presenting symppatient hospitalized with HF. 4. Summarize the toms and prognosis vary rationale for drug therapy used to manage patients from patient to patient. with HF. New treatment approaches introduced over the last Physical assessment reveals few years can improve the quality blood pressure of 108/52 mm Hg, of life--but also can make treatpulse of 130 beats/minute, and resment decisions more complicated. pirations of 30 breaths/minute and This article focuses on patients labored. Mr. Roma appears diasuch as Mr. Roma--those with HF phoretic and has jugular venous who are hospitalized to treat acute decompensation, marked by signs distention to 12 cm, an S3 gallop, and symptoms of worsening HF, crackles to the bilateral bases, and such as weight gain, dyspnea on a positive hepatojugular reflux; his exertion, orthopnea, fatigue, and legs show 2+ pitting edema to the decreased appetite. The informaknees bilaterally. He appears anxtion reflects guidelines published ious and expresses feelings of imby the Heart Failure Society of pending doom. Mr. Roma is admitted to your America (HFSA) in February 2006.
American Nurse Today October 2006 44 Pathophysiology and neurohormonal activation
In HF, myocardial muscle dysfunction (left ventricular hypertrophy, or LVH) causes decreased cardiac output, which in turn activates certain neurohormones. According to the neurohormonal hypothesis, neurohormonal disturbances promote LVH progression and can serve as the basis for medical intervention in HF. Neurohormonal activation has three major components: catecholamine release renin-angiotensin-aldosterone system (RAAS) brain-type natriuretic peptide (BNP). Catecholamine release Release of the catecholamines epinephrine and norepinephrine occurs when the sympathetic nervous system (SNS) is activated. These catecholamines prevent arterial underfilling by increasing cardiac output, which in turn speeds the heart rate, increases myocardial contractility, and causes vasoconstriction. Vasoconstriction leads to increased systemic vascular resistance (SVR)-- the resistance against which the ventricle ejects blood into the aorta and arterial vascular bed. RAAS activity The RAAS regulates blood pressure and cardiac output. An overactive RAAS initially has compensatory effects but eventually contributes to increased vascular resistance and ventricular modeling. Here's how the RAAS works: Increased SNS activity restricts blood flow to the kidneys, which respond by reducing glomerular filtration (GF). GF reduction triggers the release of renin, a renal enzyme. Renin stimulates angiotensin I, which is converted to angiotensin II, a powerful vasoconstrictor. Angiotensin II increases SVR and stimulates secretion of aldos- How neurohormones affect the cardiovascular system
In heart failure, decreased cardiac output is thought to activate a neurohormonal response that promotes progression of left ventricular hypertrophy. Neurohormones involved in this response are shown below. HORMONE Aldosterone ACTION Causes sodium and water retention Induces vasoconstriction Increases preload and afterload Increases preload and afterload Increases hypertrophy of ventricular cells with prolonged secretion Constricts the renal vasculature Stimulates release of aldosterone, endothelin-1, and vasopressin (a potent vasoconstrictor) Increases natriuresis Causes diuresis Increases angiotensin II and norepinephrine release Causes vasoconstriction Increases afterload Increases cardiac contractility Stimulates angiotensin II production Angiotensin II Brain-type natriuretic peptide Endothelin-1 Epinephrine Norepinephrine Renin terone, an adrenal hormone. Increased aldosterone secretion enhances plasma volume by promoting sodium and water reabsorption. As a result, preload increases, causing the heart's workload to increase. Patients with acutely decompensated HF stop responding to aldosterone and consequently experience sodium and water retention and potassium loss. Aldosterone plays a role in ventricular fibrosis; low serum potassium increases the risk of sudden cardiac death in these patients. Brain-type natriuretic peptide Excessive stretch of the ventricular myocardium during pressure or volume overload stimulates BNP. This peptide has several physiologic actions: causes vasodilatation. maintains homeostasis by promoting diuresis and natriuresis (excretion of abnormal amounts of sodium in the urine) decreases levels of vasoconstrictive and sodium-retaining neurohormones. The net effect of these actions is to decrease circulating blood volume and reduce the volume of blood returning to the ventricle, causing blood pressure to drop. (See How neurohormones affect the cardiovascular system.) Left ventricular remodeling Neurohormonal activation leads to remodeling of the left ventricle (LV), characterized by dilatation, hypertrophy, and a more spherical appearance of the chamber. Dilatation, in turn, places hemodynamic stress on the cardiac walls, which
October 2006 American Nurse Today 45 reduces mechanical performance and increases regurgitant flow through the mitral valve. Cardiac remodeling typically precedes symptom development, continues after symptoms emerge, and contributes to worsening of symptoms. Studies show that progressive LV remodeling relates directly to further decline in LV performance and increasing mortality in HF patients. Hemodynamic profiling of heart failure patients
As a quick bedside tool for assessment-- especially in advanced heart failure (HF)--clinicians may place patients into one of four categories based on fluid volume (filling pressures) Warm and dry: and tissue perfusion status. adequate perfusion How the profiles guide treatment without congestion or hypervolemia Warm and wet: normal perfusion with congestion or hypervolemia Assessment
Thorough assessment is crucial to developing a targeted management plan for patients with HF. Assessment includes a complete history and physical examination, checking for typical signs and symptoms. It also may include staging. History and physical examination A thorough patient history and careful physical assessment can help identify underlying causes of HF. Question the patient about past and current medical history, medication use, family history, and lifestyle factors. When obtaining the medical history, stay alert for conditions associated with HF, to help determine if the patient is at risk. Risk factors and common coexisting conditions include hypertension, obesity, diabetes, coronary artery disease, peripheral and cerebrovascular disease, valvular heart disease, family history of cardiomyopathy, history of exposure to cardiotoxins (such as chemotherapy, alcohol, and cocaine), and sleep disorders (such as sleep apnea). Signs and symptoms HF commonly causes: dyspnea and fatigue with rest or exertion nocturnal dyspnea that interrupts sleep fluid retention cough, especially at night when lying flat
46 American Nurse Today October 2006 Each hemodynamic profile Cold and dry: Cold and wet: warrants different therapy. poor perfusion (low poor perfusion with Treatment for warm, dry cardiac output) congestion or patients centers on maintainwithout congestion hypervolemia ing euvolemia (normal fluid or hypervolemia volume) and preventing disease progression. These patients don't need to be admitted to the hospital for symptom management. For warm, wet patients, treatment centers on reversing volume overload; it may take place in either an outpatient or inpatient setting. Diuretics or vasodilators typically are ordered; inotropic drugs should be avoided. Patients with cold, dry HF commonly are stable from a clinical standpoint and don't seem to experience volume overload despite intravascular fullness. Treatment may include inotropic drugs. Cold, wet patients are the sickest and have the highest mortality rate. They should be hospitalized, with treatment focusing on increasing perfusion before diuresis. Treatment may include inotropic drugs and vasodilators. rapid weight gain anorexia decreased daytime urination and increased nighttime urination. However, signs and symptoms vary depending on whether the left or right side of the heart is failing. Left-sided HF presents primarily with pulmonary symptoms, such as shortness of breath, dyspnea on exertion, wheezing, increased blood pressure, and moist cough. Right-sided HF presents with systemic symptoms, such as peripheral edema and swelling, anorexia, weakness, jugular vein distention, and hepatomegaly. Be aware, though, that HF frequently affects both sides of the heart. Hemodynamic profiling Some clinicians use hemodynamic profiling as a clinical tool for evaluating patients, particularly those with advanced HF. This system places the patient into one of four categories according to fluid volume and tissue perfusion status. Hemodynamic profiles also can be used to guide treatment. (See Hemodynamic profiling of heart failure patients.) Signs of fluid congestion include: orthopnea paroxysmal nocturnal dyspnea jugular vein distention ascites edema crackles. Signs of poor tissue perfusion include: narrow pulse pressure sleep obtundation cool extremities hypotension with angiotensinconverting enzyme (ACE) inhibitor therapy renal dysfunction low serum sodium level. Staging Symptoms of Hypoglycemia Signs and heart failure
Several systems exist for staging and classifying patients with heart failure (HF). ACC/AHA classifications
In the 2005 guideline update for diagnosis and management of HF patients, the American College of Cardiology and American Heart Association describe stages A through D, as shown below. Patients in stages A and B are considered to be at risk for HF; those in stages C and D are considered to have HF. STAGE Stage A DESCRIPTION At high risk for HF but without HF symptoms or structural heart disease PATIENT EXAMPLES Patients with hypertension, atherosclerotic disease, diabetes, obesity, or metabolic syndrome Patients using cardiotoxins Patients with a family history of cardiomyopathy Stage B Structural heart disease without HF signs or symptoms Patients with previous myocardial infarction, left ventricular (LV) remodeling (including LV hypertrophy and low ejection fraction) or asymptomatic valvular disease Patients with known structural heart disease and shortness of breath, fatigue, and reduced exercise tolerance Patients with marked symptoms at rest despite maximal medical therapy (such as those who need recurrent hospitalization or who can't be discharged safely without specialized interventions) ment goal is to return the patient to Class II, if possible. (See Staging heart failure.) When should patients be hospitalized? HFSA guidelines recommend hospitalization for patients with evidence of severely decompensated HF, such as hypotension, declining renal function, altered mentation, dyspnea at rest (defined by resting tachypnea and oxygen saturation below 90%), and hemodynamic arrhythmia (ventricular tachycardia, ventricular fibrillation, or atrial fibrillation). The guidelines advise clinicians to consider hospitalization for patients with increased fluid congestion (weight gain of 5 kg [11 lb] or more), signs and symptoms of pulmonary or systemic congestion despite weight gain, pneumonia, pulmonary embolus, diabetic ketoacidosis, transient ischemic attack or stroke, new-onset HF, or repeated firings of an implantable cardioverter-defibrillator. Diagnostic testing On admission, patients with HF typically undergo echocardiography, electrocardiography (ECG), chest Xrays, and various laboratory tests. Echocardiography. Echocardiography evaluates the left ventricle, including size, valvular function, wall thickness, and pumping function, as measured by the ejection fraction (EF). EF indicates the percentage of blood ejected from the ventricle with each heartbeat; normally, it measures between 50% and 65%. In patients with HF, reduced EF indicates systolic dysfunction, whereas normal ("preserved") EF indicates diastolic dysfunction--distinctions that help clinicians make treatment decisions. Patients with either systolic or diastolic dysfunction may experience acute decompensation. ECG. An ECG shows cardiac rhythm and conduction and QRS duration, and can detect myocardial ischemia or previous MI.
October 2006 American Nurse Today 47 Stage C Structural heart disease with current or previous HF symptoms Stage D Refractory HF that warrants specialized interventions NYHA classification system
The New York Heart Association (NYHA) classification system helps clinicians evaluate the severity of heart failure and associated functional limitations. The patient's ability to perform daily activities is graded as below: NYHA Class I: no symptoms (fatigue, dyspnea, palpations) and no physical activity limitation NYHA Class II: slight physical activity limitation; comfortable at rest but symptoms with ordinary physical activity NYHA Class III: marked physical activity limitation; comfortable at rest but symptoms during less than ordinary activity NYHA Class IV: severe limitation; symptoms at rest Heart failure staging The 2005 practice guidelines from the American College of Cardiology and American Heart Association discuss HF on a continuum, ranging from risk for HF through endstage disease. This staging system promotes early HF diagnosis and treatment. To manage patients in daily practice and establish treatment goals, many clinicians use the New York Heart Association (NYHA) classification system, which grades the patient's ability to perform daily activities. A patient with acute decompensation originally may have been categorized as NYHA Class II, but on hospital admission may be at Class IV. In this case, the treat- Chest X-rays. In HF patients, lateral and posterior lateral chest Xrays may indicate cardiomegaly, pleural effusions, and evidence of pulmonary congestion. Blood and urine tests. Laboratory tests for HF patients should include: serum electrolytes, which may reveal below-normal potassium and sodium levels blood urea nitrogen and serum creatinine, which typically increase with HF serum glucose, calcium, and magnesium fasting lipid profile complete blood count serum albumin liver function tests thyroid function tests urinalysis. The physician also may order arterial blood gas studies, which may reveal hypoxemia and hypercapnia in HF patients. Although BNP assays aren't recommended as part of the routine evaluation for structural heart disease, they are recommended for patients with suspected HF when the diagnosis is uncertain. Plasma BNP normally ranges from 0 to 100 pg/ml. However, an elevated BNP level isn't specific to HF. Diuretics are first-line therapy for
acutely decompensated heart failure. Initially, loop diuretics are used.
Pharmacologic intervention Drug therapy is the cornerstone of treatment for patients with acutely decompensated HF. (See Drug therapy for heart failure.) Various drugs are used during the acute and chronic management stages. Drug selection varies depending on whether the patient has reduced or preserved left ventricular ejection fraction (LVEF). Diuretics are first-line therapy for acutely decompensated HF. Initially, loop diuretics are used. Vasodilators may be ordered for patients in NYHA Class III/IV who need rapid improvement or don't respond to diuretics. Advanced HF with a low output state (marked by decreased urinary output and hypotension) may call for inotropic therapy. Once the patient is stabilized, the physician must determine optimal long-term drug therapy to improve symptoms and quality of life, slow disease progression, and reduce mortality. Drug therapy for reduced LVEF ACE inhibitors are recommended for patients with an EF of 40% or lower. Those who can't tolerate ACE inhibitors typically should receive angiotensin receptor blockers (ARBs). Once long-term efforts to improve LVEF are in place, diuretics commonly can be discontinued or the dosage can be reduced. Betaadrenergic blockers also play a key role and should be initiated once volume overload resolves. Aldosterone inhibitors are beneficial for some patients. Several other drugs may be used as long-term therapy for patients with reduced LVEF. Digoxin may be considered in those who are symptomatic despite ACE inhibitor and beta-blocker therapy. Oral nitrates and antihypertensives may be given to patients who can't receive ACE inhibitors or ARBs because of renal insufficiency or hyperkalemia; in African-Americans, this combination is recommended as standard therapy, in addition to ACE inhibitors and beta blockers. Drug therapy for preserved LVEF ACE inhibitors are used for patients with preserved LVEF. Those who can't tolerate these drugs may receive ARBs. Patients with a history of MI, hypertension, or atrial fibrillation who need rate control may receive beta blockers; if these drugs fail to control the heart rate or the patient has angina or hypertension, calcium channel blockers may be used instead. Nonpharmacologic interventions Education regarding sodium and fluid restrictions is the most important nonpharmacologic intervention for HF patients. Sodium restriction Encourage the patient to limit daily sodium intake to 2,000 to 4,000 mg. (For comparison, the average American consumes 8,000 to 10,000 mg of sodium daily.) Stress the importance of adhering to a dietary plan that features plenty of fresh fruits and vegetables and few or no canned or processed foods (which tend to be high in sodium). As appropriate, advise the patient to count sodium milligrams per portion, such as 600 mg of sodium per meal or 145 mg of sodium per serving. Fluid restriction Fluid restriction typically is reserved for NYHA Class III and Class IV patients, diuretic-resistant patients, and those experiencing hyponatremia Treatment
General treatment goals for patients with HF include: relieving symptoms optimizing volume status identifying the underlying cause of and precipitating factors for HF optimizing long-term oral therapy before discharge determining if the patient might benefit from revascularization educating the patient and family about the disease referring the patient to a disease management program, as appropriate. Medical therapy frequently is based on the hemodynamic profile assessment.
48 American Nurse Today October 2006 Drug therapy for heart failure Signs and Symptoms of Hypoglycemia
This chart, arranged by drug class, summarizes drug therapy recommendations for patients with heart failure (HF). DRUG CLASS/EXAMPLES Aldosterone inhibitors spironolactone (Aldactone) eplerenone (Inspra) ACTIONS NURSING CONSIDERATIONS Block aldosterone and in- Spironolactone is recommended for New York Heart Association Class III and IV patients and post-MI patients with HF symptoms. hibit sodium and water re Spironolactone standard dosage is 25 to 200 mg P.O. given in single or tention divided doses. Withhold dose if serum creatinine level exceeds 2.5 mg/dl, serum potassium level exceeds 5 mmol/L, or creatinine clearance is less than 30 ml/minute. ACE inhibitors are recommended for both symptomatic and asymptoIncrease vasodilation by matic HF in patients with ejection fraction (EF) of 40% or lower. blocking conversion of angiotensin I to angiotensin They are contraindicated in patients with heart block and bilateral renal artery stenosis. II; reduce workload of failing ventricle by reducing blood return and decreasing vasoresistance Angiotensin-converting enzyme (ACE) inhibitors captopril (Capoten) enalapril (Vasotec) lisinopril (Prinivil, Zestril) quinapril (Accupril) ramipril (Altace) trandolapril (Mavik) Angiotensin receptor blockers Block aldosterone and in- ARBs are recommended for patients with either symptomatic or asymptomatic HF, EF of 40% or lower, and ACE inhibitor intolerance. hibit sodium and water re(ARBs) tention candesartan (Atacand) irbesartan (Avapro) losartan (Cozaar) valsartan (Diovan) Beta-adrenergic blockers bisoprolol (Zebeta) carvedilol (Coreg) Increase EF by diminishing Start at low dosage and titrate upward every 2 weeks to target dosage. catecholamine effects, de- Carvedilol standard dosage is 3.125 mg P.O. twice daily, not to exceed 50 mg P.O. twice daily. creasing heart rate and contractility, and reducing During initiation, beta blockers may cause HF symptoms to worsen; however, symptoms usually improve with continued use. workload of failing ventricle Increase force of myocardial contractions Consider digoxin for patients who experience HF symptoms while receiving ACE inhibitors and beta blockers. Most patients should receive 0.125 mg daily or less often. Serum digoxin level should be below 1 ng/ml. Diuretics are first-line therapy in acute decompensated HF. Loop diuretics may need to be given I.V. in decompensated HF (abdominal-wall edema decreases their bioavailability). Dosage varies with specific diuretic and underlying cause of HF. Adverse effects include hypokalemia, hypotension, and dizziness. Monitor vital signs, breath sounds, SpO2, urine output, weight, potassium level, and uric acid levels for indications of fluid status changes. Thiazide and thiazide-like diuretics are used in patients who don't respond to loop diuretics; they shouldn't be given long-term because resistance may occur. Cardiac glycosides digoxin (Lanoxin) Diuretics Loop diuretics: bumetanide (Bumex) ethacrynic acid (Edecrin) furosemide (Lasix) torsemide (Demadex) Thiazide and thiazide-like diuretics: hydrochlorothiazide (HydroDIURIL) metolazone (Zaroxolyn) Inotropic drugs dobutamine (Dobutrex) milrinone (Primacor) Inhibit sodium, potassium, and chloride reabsorption in kidneys, which increases sodium and water excretion and reduces preload Decrease rate of sodium and chloride reabsorption by distal renal tubule and increase water excretion Improve end-organ func- Careful patient selection is required; inotropics may benefit patients with hypotension, low to normal systemic vascular resistance, and vation in patients with disodilator intolerance. minished peripheral perfu Milrinone initially is given as 50 mcg/kg I.V. bolus slowly over 10 minutes, sion (systolic pressure followed by continuous I.V. infusion of 0.375 to 0.75 mcg/kg/minute. below 90 mm Hg) Dobutamine standard dosage is 2.5 to 10 mcg/kg/minute by continuous I.V. infusion, adjusted to hemodynamic response. Dilate coronary arteries and reduce pulmonary pressure Some patients receiving nitroglycerin may need drug-free intervals to prevent drug resistance. Patients requiring nitroglycerin dosages above 200 mcg/minute are considered nonresponders and should be monitored closely. Nesiritide standard dosage is 2 mcg/kg I.V. bolus, followed by continuous infusion of 0.01 mcg/kg/minute. Nitroprusside standard dosage is 0.3 to 10 mcg/kg/minute I.V., titrated to response. Vasodilators nesiritide (Natrecor) nitroglycerin nitroprusside (Nipride) October 2006 American Nurse Today 49 Nursing research on heart failure
Nursing research on heart failure (HF) has examined various aspects of the disease, including caregiver burden and the value of transitional care. Mr. Roma's outcome
So what happened to Mr. Roma? He received diuretics and vasodilators until he was stabilized. An echocardiogram showed an EF of 30%. He was started on an ACE inhibitor, a beta blocker, and an aldosterone inhibitor. Also, he was referred to the outpatient HF program, where he received education regarding smoking cessation, dietary sodium control, and exercise--plus a referral for cardiac rehabilitation. Eventually, he was weaned off diuretics and continues to do well at home. B Selected references
Adams KF, Lindenfeld J, Arnold JMO, et al. HFSA 2006 Comprehensive heart failure practice guideline. J Card Fail. 2006;12:e1e119. Available at: www.heartfailureguideline .com/index.cfm?id=73. Accessed August 11, 2006. American Heart Association. Heart Disease and Stroke Statistics: 2005 Update. Dallas, Tex: American Heart Association; 2005. Bryson CL, Mukamal KJ, Mittleman MA, et al. The association of alcohol consumption and incident HF: the cardiovascular health study. J Am Coll Cardiol. 2006;48(2):305-311. Available at: www.sciencedirect.com. Accessed August 3, 2006. Hunt SA, Abraham WT, Chin MH, et al. 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2005;112:1-82. McBride BF, White CM. Acute decompensated heart failure: a contemporary approach to pharmacotherapeutic management. Pharmacotherapy. 2003;23(8):997-1020. O'Connell JB, Bristow MR. Economic impact of heart failure in the United States: time for a different approach. J Heart Lung Transplant. 1994;13(4):S107-112. The Vasodilation in the Management of Acute Congestive Heart Failure (VMAC) Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated heart failure. JAMA. 2002;287:1531-1540. Caregiver burden
In this study, researchers asked 50 caregivers of patients with HF to self-administer a 13question questionnaire to determine their concerns about such issues as breathing, diet, falls, medications, and family dynamics. The measuring tool, the Zarit scale, has been used with caregivers of dementia patients. The study found the level of burden among these caregivers was similar to that reported among caregivers of dementia patients. The researchers recommend that this tool be tested in a larger caregiver sample, and suggest that support groups for caregivers might be helpful.
Reference: Barry MB, Fortinsky RH, Kearney L, et al. Heart failure caregivers: an assessment of burden and concern. Heart Failure Society of America, 10th Annual Scientific Meeting. September 10-13, 2006. Abstract available at: www.abstracts2view.com/hfsa/sessionindex. Value of transitional care by advanced practice nurses
This randomized, controlled trial examined the effectiveness of a transitional care intervention delivered by advanced practice nurses to 118 patients age 65 or older who had been hospitalized for HF. One year after hospital discharge, patients in the transitional care group had fewer rehospitalizations, hospital days, and deaths and a lower total cost of care than the 121 patients in the control group.
Reference: Naylor MD, Brooten DA, Campbell RL, et al. Transitional care of older adults hospitalized with heart failure: a randomized, controlled trial. J Am Geriatr Soc. 2004;52(7):1228. To learn more about HF, consider joining the American Association of Heart Failure Nurses (http://aahfn.org). (serum sodium level below 130 mEq). These patients should restrict fluids to 1 or 2 L daily. Nursing interventions
For all patients, assess cardiovascular and respiratory status, vital signs, and hemodynamic variables. For patients in acute decompensation, closely monitor vital signs and response to medication. Other nursing interventions include measuring and recording fluid intake and output and measuring daily weight and abdominal girth. Screen patients for adherence to the prescribed medication and dietary regimen, presence of social supports, risk for depression, and appropriateness of cardiac rehabilitation referral. (For information on transitional care interventions by advance practice nurses, see Nursing research on heart failure.) Patient education Advise patients to watch for signs and symptoms of decompensation
50 American Nurse Today October 2006 (weight gain, dyspnea on exertion, orthopnea, fatigue, and decreased appetite). Decompensation typically results from dietary or medication nonadherence, so be sure to emphasize the importance of adherence. (The Joint Commission on Accreditation of Healthcare Organizations requires that patients with HF receive discharge instructions on diet, activities, drugs, and signs of potential problems.) Other important patient teaching points include the following: Encourage patients to carry a list of their medications at all times. Teach patients to weigh themselves each morning after urinating. If they gain more than 3 lb within 2 days, advise them to call their healthcare provider. Urge patients to stop smoking. Advise them to limit alcohol intake. Instruct them to avoid herbal therapies and nonsteroidal antiinflammatory drugs because these could interfere with drugs prescribed to treat HF. Cindy Cunningham, RN, MS, APRN-BC, is Coordinator of the Heart Failure Program at Baystate Medical Center in Springfield, Mass. The author does not have any financial arrangements or affiliations with any corporations offering financial support or educational grants for continuing nursing education activities. Take the Test ...
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This note was uploaded on 12/10/2011 for the course ACCT Accountanc taught by Professor Jenkins during the Spring '11 term at Sacread Heart University.
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