1. HEART FAILURE Suggestions for Lecturer -1-hour lecture
-Use GNRS slides alone or to supplement own teaching materials.
-Refer to GNRS for further content and for strength of evidence (SOE) levels.
-Refer to Geriatrics At Your Fingertips for updated information on patient evaluation and management.
-Supplement lecture with handouts.
-The GNRS Teaching Slides reflect care that can be provided to older adults in all settings. The words patient, resident, and older adult have been used interchangeably, as have the words provider, clinician, and primary care provider. Given the continually ongoing changes in health care today, some of the guidelines around reimbursement may have changed since publication.

2. The epidemiology, etiology, and pathophysiology of heart failure (HF)
OBJECTIVES
Know and understand:
The epidemiology, etiology, and pathophysiology of heart failure (HF)
The clinical signs and symptoms of HF as they manifest in older adults
Appropriate management strategies
How to provide end-of-life care with consideration of individual patient prognosis
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3. Etiology and Pathophysiology Clinical Features Diagnosis Management
TOPICS COVERED
Epidemiology
Etiology and Pathophysiology
Clinical Features
Diagnosis
Management
Recurrent Hospitalization
Prognosis
End-of-Life Care
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4. EPIDEMIOLOGY OF HEART FAILURE (HF)
Incidence and prevalence increase with age
Leading cause of hospitalization and rehospitalization in older adults
Median age of patients hospitalized with HF is 75 years, and approximately two thirds of deaths attributable to HF are in patients age 75 years or older
HF is a major cause of chronic disability and impaired quality of life in older adults
Heart failure affects more than 5 million Americans, and >650,000 new cases are diagnosed each year.
Although the incidence of HF is somewhat higher in men, women comprise slightly over half of prevalent HF cases.
The rising prevalence of HF with increasing age reflects the combination of age-related changes in cardiovascular structure and function that serve to diminish cardiovascular reserve, in conjunction with the rising prevalence of cardiovascular diseases with increasing age (especially hypertension and coronary artery disease) that predispose to HF.
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5. ETIOLOGY OF HF HF in older adults is often multifactorial in origin
Hypertension is the most common antecedent cardiovascular condition in both men and women
60%–70% of women, 30%–40% of men
In men, 30%–40% of HF cases are attributable to coronary artery disease (CAD)
Other common causes include valvular heart disease and nonischemic dilated cardiomyopathy
Less common causes of HF include hypertrophic cardiomyopathy, restrictive cardiomyopathy (eg, amyloid), and pericardial disease.
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6. Affects 40% of men and two-thirds of women > 65 years old with HF
DEFINITIONS
HF with reduced left ventricular ejection fraction (LVEF) (HFrEF) – HF with LVEF <40%
Nearly 90% of HF patients < 65 years old have this form of the disease
HF with preserved ejection fraction (HFpEF) — HF with LVEF > 40% - 50%
Affects 40% of men and two-thirds of women > 65 years old with HF
The rising prevalence of HFpEF in older patients is due to age-associated changes in LV diastolic function and increased prevalence of HTN, particularly for women.
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7. SYMPTOMS AND SIGNS OF HF IN OLDER PATIENTS
Often atypical and nonspecific
Most common: exertional shortness of breath, fatigue, orthopnea, and leg edema
Exertional symptoms may be less prominent in older adults because of a more sedentary lifestyle
Prevalence of atypical symptoms increases with age
Decreased mental acuity, confusion, lethargy, irritability, anorexia, abdominal discomfort, or altered bowel function
Classical physical findings of HF in younger patients include tachycardia, narrowed pulse pressure, increased jugular venous pressure, hepatojugular reflux, an S3 gallop, moist pulmonary crackles, diminished breath sounds at the lung bases (due to pleural effusions), and pitting edema of the legs.
However, many or even all of these findings may be absent in older HF patients, especially those with HFpEF, in whom an S3 gallop and signs of right-heart failure are not usually present. In addition, pulmonary crackles in older patients may be due to comorbid chronic lung disease or atelectasis, and peripheral edema may be due to hepatic or renal disease, venous insufficiency, hypoalbuminemia, or medications (especially calcium channel blockers).
The diagnosis of HF can usually be established on clinical grounds in patients who present with a constellation of classical symptoms and signs. Often, however, the diagnosis is uncertain, and additional supporting evidence is required.
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8. DIAGNOSIS OF HF
Standard chest radiograph remains a useful initial test for detecting pulmonary congestion and pleural effusions
Also excludes pneumonia as a cause of shortness of breath
B-type natriuretic peptide (BNP) and its precursor N-terminal pro-BNP (nt-proBNP) are valuable in establishing the diagnosis of volume overload due to HF and, in particular, in distinguishing shortness of breath due to HF from that attributable to noncardiac causes
But specificity decreases with age
Chest radiograph may be difficult to interpret in older adults with chronic lung disease, kyphoscoliosis, or poor inspiratory effort, and absence of pulmonary congestion on chest radiograph does not preclude a diagnosis of HF.
The ECG may show LV hypertrophy, acute ischemia or prior myocardial infarction (MI), left atrial enlargement, or atrial fibrillation—all of which predispose to the development of HF—but the ECG is not usually helpful in establishing a diagnosis of either acute or chronic HF.
It is appropriate to obtain a CBC, routine chemistry panel, thyroid studies, a urinalysis, and, in selected cases, biomarkers of cardiac ischemia (ie, troponin, creatine kinase) in patients with suspected HF, but in most cases these tests are insufficient for confirming or excluding the diagnosis.
BNP and nt-proBNP levels increase with age, especially in women, as well as with decreasing renal function. As a result, the specificity of increased levels of these peptides decreases with age, and the clinical significance of an isolated increased BNP or nt-proBNP level in an older adult may be difficult to interpret. Despite these caveats, a BNP level < 100 pg/mL in an older adult with suspected acute HF makes the diagnosis very unlikely (negative likelihood ratio approximately 0.1), whereas a BNP level  500 pg/mL is consistent with active HF (positive likelihood ratio approximately 6).
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9. OVERVIEW OF HF MANAGEMENT
Goals are to decrease symptoms and improve quality of life, reduce acute exacerbations requiring hospitalization, and increase survival
Hypertension, hyperlipidemia, and diabetes should be treated in accordance with current guidelines
Smoking cessation should be strongly encouraged and supported if indicated, and alcohol intake should be limited to no more than 2 drinks/day in men and 1 drink/day in women
Once a diagnosis of HF has been established, it is important to determine the cause and to assess LV function, because these factors often affect management.
In most patients with recently diagnosed HF, an echocardiogram with Doppler is indicated for the assessment of LV and right ventricular (RV) size, systolic and diastolic function, atrial size, LV and RV wall thicknesses, valve function, and the pericardium.
In patients with suspected CAD who are suitable candidates for revascularization, a stress test should be performed, followed by coronary angiography if the stress test indicates severe CAD, especially in a multivessel distribution.
NSAIDs should be avoided because they promote water and sodium retention and antagonize the effects of diuretics and renin-angiotensin system inhibitors. CAD should be treated with anti-ischemic medications and, if indicated, percutaneous or surgical revascularization.
Valvular lesions should be managed in accordance with established practice guidelines.
Patients should be screened for anemia and thyroid dysfunction, and appropriate therapy should be initiated if indicated.
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10. NONPHARMACOLOGIC THERAPY
HF patients have long been counseled to restrict dietary sodium intake to ≤ 2 g/day
Low-sodium diets have been linked to worse outcomes in several clinical trials and little data exist on optimal sodium intake
Most patients with HF should also engage in regular exercise such as walking, stationary cycling, swimming, or water aerobics
Exercise duration and intensity should be adjusted to the individual patient’s level of conditioning, severity of HF, and comorbidities
Patients should keep an ongoing record of their daily weight
Sodium allowances should likely be individualized, taking into account volume status, serum sodium level, and severity of HF, particularly in older patients predisposed to hyponatremia.
Fluid restriction is not usually necessary except in patients with advanced HF, but patients should be advised to avoid excess fluid intake.
Exercise should be gradually increased over time, if possible, to achieve 30–60 minutes of aerobic exercise most days of the week. These activities should be complemented by stretching and strengthening exercises, as well as by gait and balance exercises if indicated.
Weights should be measured in the morning without clothes after going to the bathroom but before eating. A “dry weight” should be established (based on the home scale, not the office scale), and the patient should be instructed to contact the physician if the weight varies by more than 2–3 pounds above or below the dry weight. Alternatively, selected patients may be provided with detailed instructions for self-adjustment of diuretic dosages based on daily weights.
Older patients with moderate or advanced HF, multiple comorbidities, or a recent HF exacerbation requiring hospitalization may benefit from participation in a structured HF disease management program. Such programs offer enhanced education and follow-up, usually by an HF nurse specialist or multidisciplinary team, in some cases supplemented by telemonitoring devices, and have been shown to reduce hospitalizations and inpatient costs, as well as to improve quality of life in older HF patients.
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11. PHARMACOTHERAPY OF HFrEF
Optimal treatment usually requires 3 medications and, in some cases, up to 7
Almost all patients take 1 additional medications for coexisting illnesses
Problems: adherence, high potential for drug interactions and adverse events, cost
Therapy must be individualized: consider the multiple factors that influence QOL and other desirable clinical outcomes in older adults who have multiple chronic illnesses and limited life expectancy
Angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and β-blockers have been shown to improve outcomes and reduce mortality in multiple large prospective trials involving a broad range of HF patients with decreased LV systolic function. These agents are now considered the cornerstone of therapy for HFrEF. Although older patients, especially those with multiple comorbid conditions, have been markedly under-represented in these trials, the available evidence indicates that the beneficial effects of these agents likely extend to older patients.
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12. ACE INHIBITORS FOR HFrEF
In general, start treatment at the lowest dosage and gradually titrate to the maintenance dosage as tolerated
Contraindications include known intolerance to these agents, hyperkalemia, hypotension, and severe renal insufficiency in patients not currently undergoing dialysis
Common adverse events include cough in 5%–10% of patients during long-term treatment, mild worsening of renal function (often transient), hyperkalemia, hypotension, GI distress, and rarely angioedema
ARBs are an option for HF patients unable to tolerate ACE inhibitors because of cough, allergic reactions, or GI disturbances
For a list of ACE inhibitors approved for the treatment of HF, along with recommended initial and maintenance dosages, see GNRS5 Table 50.1.
Renal function and potassium concentrations should be monitored closely during initiation and titration of ACE inhibitor therapy.
Contraindications and adverse events associated with ARBs are similar to those of ACE inhibitors. In particular, the incidence of renal insufficiency, hyperkalemia, and hypotension are comparable with equivalent dosages of ACE inhibitors and ARBs.
Combination therapy with an ACE inhibitor and ARB is not currently recommended because of an increased incidence of adverse events in the absence of a clear clinical benefit.
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13. β-BLOCKERS FOR HFrEF
As with ACE inhibitors and ARBs, treatment should be started at the lowest available dosage and gradually titrated to the maintenance dosage over several weeks
Contraindications include severe decompensated HF, active bronchospastic lung disease, marked bradycardia, relative hypotension, significant atrioventricular nodal block, and known intolerance to β-blockers
β-Blockers counteract the deleterious effects of chronic activation of the adrenergic nervous system in HF patients, and β-blockers have been shown to improve ventricular function and symptoms while reducing the risk of both sudden and nonsudden cardiac death.
See GNRS5 Table 50.1 for starting dosages.
Occasionally, HF symptoms will worsen on initiation or titration of a β-blocker (and patients should be warned about this possibility), but in most cases this is a transient phenomenon. The vast majority of HF patients (>80%) are able to tolerate long-term β-blocker therapy when judiciously initiated and titrated.
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14. An essential component of HF therapy in most patients
DIURETICS FOR HFrEF
An essential component of HF therapy in most patients
Most effective agents for relieving congestion, edema
In general, the diuretic dosage should be adjusted to maintain euvolemia
Manifested by the absence of pulmonary rales, an S3 gallop, increased jugular venous pressure, hepatojugular reflux, and peripheral edema
In patients with equivocal findings, serial measurement of BNP may be useful for tracking volume status.
Some patients with mild HF respond satisfactorily to a thiazide diuretic, but most require maintenance therapy with a loop diuretic, such as furosemide, bumetanide, or torsemide. Patients with advanced HF and/or concomitant renal insufficiency may be resistant to conventional dosages of loop diuretics. In these patients, the addition of metolazone at 2.5–10 mg/day is often effective, but careful monitoring of electrolytes is required. The principal adverse events associated with diuretic therapy are electrolyte disturbances, including hypokalemia, hyponatremia, and hypomagnesemia. Close monitoring of these electrolytes, as well as renal function, is therefore warranted.
Thiamine deficiency may occur during long-term treatment with loop diuretics and can contribute to apparent diuretic resistance. Although routine monitoring of thiamine levels is not currently recommended, supplemental thiamine in the form of a multivitamin is reasonable in older patients requiring long-term therapy with a loop diuretic. Older patients are also at increased risk of dehydration during diuretic treatment due to attenuation of the thirst response and diminished oral fluid intake, especially during periods of illness or increased ambient temperatures. Therefore, clinicians should remain vigilant for possible signs of dehydration, including excess weight loss during daily weight monitoring.
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15. ALDOSTERONE ANTAGONISTS FOR HFrEF
The aldosterone antagonist spironolactone has been shown to reduce mortality and hospitalizations in patients with NYHA class III–IV HF and LVEF ≤ 30%
The selective aldosterone antagonist eplerenone has been associated with improved outcomes in patients with recent MI complicated by HF or LVEF < 40%, and in patients with NYHA class II HF and LVEF ≤ 35%
NYHA = New York Heart Association
Spironolactone at 12.5–25 mg/day or eplerenone at mg/day is recommended for patients with NYHA class II–IV HF and an LVEF ≤35%. Benefits are similar in older and younger patients.
Older adults are at increased risk of worsening renal function and hyperkalemia during aldosterone antagonist therapy, and frequent monitoring of electrolytes and creatinine is necessary. Spironolactone and eplerenone are contraindicated in patients with serum creatinine 2.5 mg/dL or serum potassium 5 mEq/L.
Up to 10% of patients develop painful gynecomastia during long-term treatment with spironolactone compared to <1% with eplerenone.
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16. OTHER THERAPIES FOR HFrEF
Digoxin improves symptoms and reduces HF hospitalizations in patients with HFrEF but does not decrease mortality
Adverse events include nausea, visual disturbances, and cardiac arrhythmias
The combination of hydralazinenitrates is recommended for HF patients with contraindications to ACE inhibitors and ARBs and in black patients with advanced HF as an adjunct to ACE-inhibitor and β-blocker therapy
Digoxin remains a reasonable therapeutic option in patients with persistent limiting symptoms or recurrent hospitalizations who have not had a satisfactory response to the measures discussed above. Retrospective analyses based on a large randomized trial suggest that the optimal digoxin concentration for improving clinical outcomes is 0.5–0.9 ng/mL, which is substantially lower than the “therapeutic range” previously reported by most clinical laboratories. Therefore, digoxin should be dosed to maintain the digoxin concentration < 1 ng/mL, and a dosage of mg/day is likely to be sufficient for most older patients with relatively preserved renal function, while a lower dosage might be indicated in patients with renal insufficiency or low lean body mass.
With appropriate monitoring of the serum digoxin concentration, serious digoxin toxicity is infrequent, and there is no convincing evidence that older patients are at increased risk of life-threatening digitalis intoxication. Amiodarone, quinidine, and verapamil, as well as several other medications, are associated with an up to a 2-fold increase in serum digoxin concentrations, and the dosage of digoxin should be reduced by 50% in patients receiving these medications.
Common adverse events associated with hydralazine include palpitations, nausea, and dizziness; rarely, a drug-lupus syndrome may occur during prolonged therapy at high dosage (300 mg/day). The most common adverse event from isosorbide dinitrate is headache; this usually resolves with continued use.
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17. OTHER THERAPIES FOR HFrEF
Current guidelines therefore recommend against routine anticoagulation in HF patients in the absence of atrial fibrillation.
For HF patients with comorbid atrial fibrillation long-term anticoagulation with warfarin or one of the newer oral anticoagulants is indicated in most cases.
Previous guidelines suggested consideration of antiplatelet or anticoagulant therapy for HF patients in normal sinus rhythm, even in the absence of compelling indications for treatment. However, although HFrEF patients are at increased risk of thromboembolic events, the only placebo-controlled trial of antithrombotic therapy in these patients showed no difference in a composite outcome that included stroke. Randomized trials comparing different antithrombotic strategies (aspirin, clopidogrel, warfarin) have also shown no benefit of one strategy over another. Moreover, among HF patients >60 years old, warfarin has been associated with increased bleeding without a corresponding reduction in thromboembolic events.
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18. PHARMACOTHERAPY FOR HF WITH PRESERVED EF (HFpEF)
Optimal therapy remains undefined
Current recommendations:
Aggressively treat hypertension, other risk factors
Manage comorbid CAD
Maintain sinus rhythm or effective rate control in patients with AF
Judiciously use diuretics to maintain euvolemia while avoiding overdiuresis (many of these patients are “volume-sensitive”)
To date no trials have demonstrated a clear reduction in mortality with any pharmacologic intervention in patients with HFpEF
The addition of an ACE inhibitor or ARB, and possibly a β-blocker (especially in patients with CAD), is appropriate to reduce the risk of hospitalization, recognizing that the impact of these agents on other clinically relevant outcomes is unproved.
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19. RECURRENT HOSPITALIZATION
Up to 50% of patients with HF are readmitted within 6 months after the initial hospitalization
Patients who experience recurrent HF hospitalization should be questioned carefully and educated appropriately about:
Adherence to medication regimen; use of OTC medications
Recent changes in weight
Recent dietary choices
Daily fluid intake
Contributors to readmission may include biological factors (severity of heart failure, number and severity of comorbidities), patient behavioral factors (adherence to pharmacotherapy, adherence to diet and lifestyle), and health-care system factors (discharge practices, care transitions, outpatient care resources).
In patients who acknowledge nonadherence to the medication regimen or sodium restriction, reasons for nonadherence should be explored. Reasons for medication nonadherence often include concerns about adverse events, cost, efficacy, and excess number of pills. Nonadherence to sodium restriction often involves lack of knowledge about the salt content of foods, inability to acquire low-sodium foods, frequent eating out, and altered sense of taste. If possible, strategies should be developed to overcome these barriers, and the importance of future adherence as a means to prevent subsequent admissions emphasized. A multidisciplinary team approach, including the physician, an HF nurse specialist (if available), dietitian, social worker, pharmacist (preferably with expertise in geriatric drug prescribing), and home-health representative is most likely to result in significant changes in health behavior, thereby fostering improved adherence, self-efficacy, and decreased risk of early readmission.
When feasible, the patient’s partner and family should be actively engaged in the evaluation and teaching process.
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20. PROGNOSIS Median survival rates of 2–3 years
25%–30% of patients die within 1 year after initial diagnosis
50% survive 1–5 years
20%–25% survive >5 years
Women and patients with HFpEF have somewhat better survival rates than men and patients with HFrEF
Other factors that adversely affect prognosis include older age, more severe symptoms (eg, higher NYHA functional class), lower systolic blood pressure, the presence of CAD (an important factor contributing to worse outcomes in men), diabetes (especially in women), peripheral arterial or cerebrovascular disease, cognitive impairment or dementia, renal insufficiency, anemia, and hyponatremia. Patients with higher BNP also have a worse prognosis, especially if the BNP remains substantially increased despite aggressive therapy.
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21. END-OF-LIFE CARE
Counsel patients to prepare an advance directive, which may include the appointment of a surrogate decision maker and the delineation of interventions desired or to be avoided in the event of clinical worsening and approaching death.
Ask patients with ICDs to indicate under what conditions they would want the ICD turned off to avoid repetitive painful shocks at the end of life
In patients with particularly poor prognosis and remaining life expectancy < 6 months, offer the option of a transition to palliative care and hospice as part of a candid discussion about prognosis and goals of care.
In light of the poor prognosis of older HF patients, which is worse than for most forms of cancer, it is appropriate to initiate discussions about end-of-life care early in the course of treatment, and to readdress these issues as clinical circumstances evolve.
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22. CHOOSING WISELY
Device Therapy, Mechanical Circulatory Support, and Heart Transplantation
Don’t leave an ICD activated when it is inconsistent with the patient/family goals of care.

23. SUMMARY
HF is the leading cause of hospitalization in older adults and a major source of chronic disability
Older patients with HF are more likely to be women and more likely to have preserved LV systolic function
ACE inhibitors, ARBs, β-blockers, aldosterone antagonists, and in selected patients hydralazine/nitrates reduce morbidity and mortality from HFrEF
No pharmacotherapy for HFpEF has been definitively shown to reduce mortality.
Optimal management of HF in older patients often requires a multidisciplinary approach
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24. CASE 1 (1 of 4)
A 92-year-old woman comes to the office because she has increasing shortness of breath that worsens when she walks
History: long-standing hypertension, kyphoscoliosis, and COPD; hypertension and COPD not well controlled over the past decade
Uses inhalers for the COPD; needs 2 pillows for sleeping
40-pack-year history of cigarette smoking
No history of environmental exposure or prior myocardial infarction
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25. CASE 1 (2 of 4)
Examination
Seated blood pressure: 150/85 mmHg (left arm)
Heart rate: 85 bpm
Respiratory rate: 18 bpm
She is overweight. Jugular venous pulse cannot be visualized, because the neck is too thick.
Some wheezing and crackles at both lower lung fields.
Cardiac examination is difficult; S1 and S2 heart sounds present (but no S3 or S4) and infrequent extra systoles
There is pitting pedal edema.
She uses a rolling walker, and she gets dyspneic at about 40 feet.
Laboratory orders include measurement of serum brain-type natriuretic peptide (BNP) to determine whether symptoms are due to heart failure or to COPD.
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26. CASE 1 (3 of 4)
Which one of the following should be considered when interpreting her BNP results?
Her kyphoscoliosis
Her obesity
Her recent exertion
Her inhaler use
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27. CASE 1 (4 of 4)
Which one of the following should be considered when interpreting her BNP results?
Her kyphoscoliosis
Her obesity
Her recent exertion
Her inhaler use
ANSWER: B
Serum BNP levels are excellent at discriminating between a pulmonary and cardiac cause of dyspnea. Although originally discovered in the brain, BNP is released by the distended ventricle as proBNP. The proBNP is cleaved into an inactive 76 amino acid N-terminal peptide, NT-proBNP, and a C-terminal 32 amino acid active hormone, BNP. BNP may increase in patients with renal failure, pulmonary hypertension, arterial hypertension, or liver cirrhosis, and appears to be decreased in obese persons. The cutoff value for identifying heart failure is at least doubled in 75-year-old compared with 55-year-old adults. Increase in BNP with age is consistent with increases in filling pressure and diastolic dysfunction. However, the increases may also reflect known age-related reduction in renal clearance of the peptide. The patient’s kyphoscoliosis, use of inhalers, or recent physical exertion will not affect the interpretation of the BNP results.
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28. CASE 2 (1 of 4)
An 82-year-old woman goes to the emergency department because she fell on her knees. The fall was clearly accidental and not caused by arrhythmias or syncope. Radiography shows no fracture, and she is prescribed treatment for her pain.
One week later, she comes to the office because of fatigue, increased pedal edema, and weight gain. Documentation from the emergency department visit is unavailable.
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29. CASE 2 (2 of 4)
History: heart failure, which has been stable for 18 months.
Medications: metoprolol, furosemide, and an ACE inhibitor.
Physical examination: neck veins are distended. There are crackles in both lower lung fields.
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30. CASE 2 (3 of 4)
Which one of the following is most likely the treatment prescribed in the emergency department for the knee pain that exacerbated her CHF?
Acetaminophen 500 mg every 6 hours
Naproxen sodium 220 mg every 12 hours
Diclofenac patch to knee twice daily
Tramadol 50 mg every 8 hours
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31. CASE 2 (4 of 4)
Which one of the following is most likely the treatment prescribed in the emergency department for the knee pain?
Acetaminophen 500 mg every 6 hours
Naproxen sodium 220 mg every 12 hours
Diclofenac patch to knee twice daily
Tramadol 50 mg every 8 hours
ANSWER: B
Nonsteroidal anti-inflammatory drugs (NSAIDs) can precipitate increased salt and water retention. In the setting of compensated heart failure, treatment with NSAIDs can lead to decompensated heart failure. In a more severe situation, NSAIDs can precipitate renal failure and worsen heart failure.
In contrast, acetaminophen and tramadol are not considered important precipitants of heart failure and are safe for use in older adults with this condition. Tramadol should perhaps be used at a reduced dosage or increased interval. The volume of distribution and conjugation of acetaminophen are both decreased in younger patients with heart failure compared with age-matched controls, leading to higher concentrations of the drug but without evidence of worsening heart failure.
Topical diclofenac is effective for local injury. Because systemic absorption is typically <10% of the dose, topical NSAIDs have lower rates of such adverse effects as gastrointestinal bleeding, dyspepsia, and fluid retention and are less likely than oral NSAIDs to exacerbate heart failure.
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32. GNRS5 Teaching Slides Editor: Barbara Resnick, PhD, CRNP, FAAN, FAANP, AGSF GNRS5 Teaching Slides modified from GRS9 Teaching Slides based on chapter by Justin Vader, MD and Michael W. Rich, MD, AGSF and questions by George E. Taffet, MD, FACP Managing Editor: Andrea N. Sherman, MS Copyright © 2016 American Geriatrics Society
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