Heart Failure in the Elderly
June 1, 2000
Heart Failure in the Elderly
Author: William Franklin Peacock, IV, MD, FACEP, Associate Professor, The Ohio State University, Director of Clinical Operations, Department of Emergency Medicine, The Cleveland Clinic, Cleveland, OH.
Peer Reviewers: Nancy Albert, MSN, RN, CCRN, CNA, Clinical Nurse Specialist in Heart Failure, The Cleveland Clinic, Cleveland, OH; Charles Emerman, MD, FACEP, Chairman, Emergency Medicine, The Cleveland Clinic, Cleveland, OH.
Disproportionally represented in the elderly, heart failure (HF) is the single most economically expensive disease in the United States. Because of the aging of America, and the relative success in treating coronary artery disease, the future impact of HF may be epidemic in proportion. Until recently, there was little improvement in HF outcome, and the diagnosis of HF was a death sentence. Currently, five-year survival for HF is worse than that predicted for most cancers.
Today, therapeutic advances are markedly improving outcomes. To ensure effective treatment, the clinician should have a clear understanding of the divergent pathology in the two main categories of HF and their effects on the aging myocardium. Systolic HF results from pump inadequacy. This is in contradistinction to diastolic HF, where ventricular pumping performance is maintained, but a loss of compliance prevents adequate cardiac filling. The normal aging process increases the overall stiffness of the cardiovascular system, but systolic function is preserved. These distinctions are critical when selecting treatment options.
This article reviews the physiologies of the aging myocardium and the pathologic consequences of the two main types of HF. Clinical diagnostic methods, interventions, and confounders appropriate to care of the elderly HF patient are detailed, and there is a focus on the medical treatment of HF in the aged.
— The Editor
Introduction/Epidemiology
HF is one of the greatest challenges facing the United States health care system. It affects nearly 5 million Americans, and many more with asymptomatic dysfunction who are likely to become symptomatic within the next five years.1,2 (See Table 1.) It is the only cardiovascular disease increasing in both incidence and prevalence, and its death rate has increased sixfold over the last 40 years.2,3
| Table 1. Annual Impact of Heart Failure1,2 | |
| Number of patients | Result |
| 43,000 | HF is principal cause of death4 |
| 250,000 | Deaths in which HF contributes2,38 |
| 500,000 | New cases |
| 3,500,000 | Co-contributor to inpatient hospitalization |
| 11,000,000 | Outpatient visits |
| 20,000,000 | Asymptomatic cardiac dysfunction |
HF disproportionally effects the elderly. Less than 1% of those younger than age 50 are affected, but prevalence doubles each decade, and by age 80 nearly 10% are stricken.4 Of those older than 65 years, HF is the leading cause of hospitalization and accounts for about 700,000 annual admissions.3,5 Furthermore, since HF patients are usually older, management is complicated by high rates of coexisting disease. The expectation that the number of Americans older than age 65 will double in the next 30 years is the impetus to develop more effective therapies.4
HF is the most expensive diagnosis in the Medicare system. As reported at the Heart Failure Society of America 1999 Annual Meeting, current costs are estimated at $23.1 and $14.7 billion for inpatient and outpatient care, respectively. The cost of HF hospitalizations doubles that of all forms of cancer.6
Prognosis. The prognosis of HF is poor. Once symptomatic, two-year mortality is about 35%. Over the next six years, it increases to 80% for men and 65% for women. Symptoms do predict outcome. The yearly risk of death with mild to moderate symptoms is 5-10%, vs. 30-40% with severe symptoms. After pulmonary edema, only 50% survive one year, and following cardiogenic shock, 50-85% die within one week. The New York Heart Association (NYHA) HF class is the most commonly used prognostic scale. (See Table 2.) Despite poor sensitivity and high inter-observer variability, the scale is useful for predicting mortality. Older patients, once rated as class IV, have a one-year mortality of greater than 50%.7
| Table 2. New York Heart Association Classifications for Heart Failure |
| I. No limitation: Asymptomatic during usual daily activities |
| II. Slight limitation: Mild symptoms during ordinary daily activities |
| III. Moderate limitation: Symptoms noted with minimal activities |
| IV. Severe limitation: Symptoms present even at rest |
Pathophysiology. HF can present precipitously following acute myocardial infarction (AMI), and is due to pump failure. As cardiac output (CO) declines, BP and peripheral perfusion decrease. Vasoconstriction may preserve BP at a cost of increased systemic vascular resistance (SVR), which raises myocardial O2 demand and may exacerbate ischemia. As the heart fails, increasing intracardiac pressures develop, pulmonary congestion occurs, and death follows if the pathologic cascade is not interrupted. Symptomatically hypotensive HF patients (i.e., cardiogenic shock) require aggressive circulatory support in an ICU environment. Their care is not covered here.
Less acute presentations, with chronic recidivism, are the more common presentation of HF in the ED environment. When myocardial stress or injury result in a reduction of CO, compensatory mechanisms may partially preserve circulatory function. The responses include neurohormonal activation, which results in increasing levels of norepinephrine (NE), vasopressin, and stimulation of the renin-angiotensin system. The combined effects are sodium and water retention and increased vascular tone. The secondary consequences are elevation of intracardiac pressures. At this stage, patients may be asymptomatic, but the mechanisms initiating cardiac remodeling are established. Interruption and attenuation of cardiac neuroendocrine responses to incipient HF form the theoretical basis for beta-blockade and ACE inhibitor therapies.
HF and the Aging Heart
The consequences of aging include extensive functional and structural myocardial changes. Aging is associated with increases in ventricular wall thickness and myocardial interstitial collagen.7 This significantly impacts diastolic function, resulting in impaired ventricular relaxation and increased LV wall stiffness.7 However, in the absence of concurrent cardiovascular disease, resting systolic function is well preserved and measures of cardiac function are unaffected by age in healthy patients.7,8 The summary effect of age on the cardiovascular system is a loss in the ability to respond to stress.8
Aging results in events that contribute to an increased risk of developing HF. These effects include increased systemic vascular impedance, impaired ventricular relaxation, decreased ventricular compliance, and impaired myocardial metabolism.4,7,8 With aging, a decrease in vascular elasticity and increased impedance to ventricular ejection accentuate systolic hypertension.9
Diminished cardiac relaxation and increased ventricular stiffness predispose to diastolic HF and have consequences in relation to atrial dynamics. Greater ventricular stiffness impairs early diastolic ventricular filling.7 Consequently, atrial contraction becomes more important; as much as 30-40% of end diastolic LV volume is because of atrial contraction.8 Thus, the older patient is more dependent upon atrial kick and will be more symptomatic if atrial fibrillation occurs.8
Aging also diminishes b1 and b2 receptor responsiveness. This decreases maximal heart rate and contractility and impairs peripheral vasodilation. Cellular energy handling is affected by aging; specifically, mitochondrial ATP production is decreased in the elderly.8,9
All these changes impair the ability of the aging heart to respond to cardiovascular stress (e.g., exercise, infection, etc). Older patients are more sensitive to hypertension, atrial fibrillation, and cardiac ischemia; conditions that are all more common in the elderly.
Etiology. HF may arise from numerous sources. (See Table 3.) Decompensation of previously established HF is the final common pathway of cardiac stress from numerous sources. (See Table 4.) Hypertension and coronary artery disease account for more than 70% of HF cases in both the young and elderly. However, in the elderly, the etiology more frequently is multifactorial.8 In the older adult, ischemic heart disease, with a history of MI, is the most common cause of dilated cardiomyopathy.8 Valvular heart disease, specifically calcific aortic stenosis and mitral regurgitation, is increasingly common in the elderly.4 Lastly, hypertensive hypertrophic cardiomyopathy and cardiac amyloidosis more frequently occur in older patients, while alcoholic and dilated idiopathic cardiomyopathies tend to affect younger patients.4,10
| Table 3. Major Etiologies of Heart Failure |
| • Coronary artery disease |
| • MI complications |
| Acute mitral regurgitation, papillary muscle rupture, cardiac free wall rupture |
| • Sustained arrhythmia |
| • Uncontrolled hypertension |
| • Valvular rupture or disease |
| • Myocarditis |
| • Acute pulmonary embolus |
| • Pericardial disease/tamponade |
| Effusion, constrictive pericarditis |
| • Hyperkinetic states |
| Anemia, thyrotoxicosis, A-V Fistula (e.g., dialysis) |
| • Infiltrative disorders |
| Amyloidosis, sarcoidosis, hemochromatosis |
| • Infectious |
| Endocarditis |
| • Toxin |
| Alcoholic cardiomyopathy |
| Table 4. Examples of Common Causes of Heart Failure Decompensation |
| • Exacerbation of comorbidities: |
| Acute MI, emphysema, uncontrolled hypertension, atrial fibrillation, hyperthyroidism, anemia, diabetes |
| • Superimposed infection: |
| Pneumonia, urinary tract infection |
| • Social issues: |
| Medication or dietary non-compliance, excessive alcohol |
| • Iatrogenic causes: |
| Negative inotropic medications (e.g. verapamil, nifedipine, etc.) |
| Non-steroidal anti-inflammatory medication |
Congestive HF
HF commonly presents with fluid overload. However, low CO HF syndromes, that are accompanied by dehydration and intravascular depletion, occur without congestion. Therefore, congestive HF refers only to the fluid overloaded state; it does not reflect myocardial contractility. Fluid status is independent of CO. Both diastolic and systolic HF patients may suffer from congestion.
Systolic vs. Diastolic HF. Ventricular wall tension is a product of afterload (systolic BP) and ventricular radius. Elevated wall tension stimulates cardiac remodeling. Myofibers either hypertrophy or die (apoptosis) and form scar tissue. Why apoptosis occurs is unclear. It is this predominate response (hypertrophy vs apoptosis) that determines HF type. While elements of both systolic and diastolic HF can occur together, this distinction is helpful when designing treatment plans.
Systolic HF. A normal ejection fraction (EF) is 60%; an EF of less than 40% is considered systolic dysfunction. Impaired cardiac contractility is the hallmark of systolic HF. In the normal heart, increasing preload results in improved cardiac contractility (i.e., the Frank Starling mechanism). This is lost in systolic HF. With cardiovascular stress (e.g., walking, volume expansion) the myocardium cannot improve contractility. Increasing venous return results in elevated intra-cardiac pressures that may lead to pulmonary congestion and edema. The process of systolic HF involves impaired contractility, neurohormonal activation, increased intracardiac volume and pressure, and enhanced afterload sensitivity. The most common etiologies of systolic HF are, in descending frequency, coronary artery disease (in two-thirds), hypertension, idiopathic cardiomyopathy, valvular heart disease, other specific cardiomyopathies, and myocarditis.2,11
Diastolic HF. Age-related cardiac changes predispose the older patient to diastolic HF.12 In those younger than age 60, only 6% of HF patients have diastolic dysfunction, as compared to rates of 21% in 61- to 70-year olds, and 41% in those older than 70.13 In diastolic HF, LV systolic function is preserved and the EF is normal or increases. Pathologically, impaired ventricular relaxation and ventricular stiffness result in an abnormal diastolic pressure/volume relationship. Common etiologies of diastolic HF are listed in Table 5.
| Table 5. Diastolic Heart Failure Etiologies87 |
| • Restrictive cardiomyopathy |
| Cardiac amyloidosis |
| • Constrictive pericarditis |
| • Ischemic heart disease |
| Post-infarction scarring/remodeling |
| • Hypertrophic heart disease |
| Hypertrophic cardiomyopathy |
| Chronic hypertension |
| Aortic stenosis |
| Mitral or tricuspid stenosis |
Diastolic HF patients are volume sensitive. Significant preload reduction or afterload increases may cause hypotension. As in systolic HF, circulatory congestion is a common ED presentation. Between 30% and 50% of HF patients have circulatory congestion without LV dysfunction.14 The majority of the elderly will also have underlying hypertension, coronary artery disease, or valvular heart disease.12
HF type is difficult to diagnose at the bedside; consequently, echocardiograms are often obtained.7 In one small study, a diastolic BP of 105 mmHg or greater and absence of jugular venous distention (JVD) was specific (100%) but insensitive (30%) in indicating preserved LV contractility.14
Ultimately, diastolic HF therapy is directed at the underlying etiology. (See Table 5.) Although diastolic dysfunction is a common cause of HF in the aged, treatment is mainly empiric since there are very few large, controlled trials to guide therapy.
Right vs. Left Heart Failure. Left and right HF are sometimes differentiated. Left HF presents with dyspnea, fatigue, weakness, cough, and orthopnea in the absence of peripheral edema, JVD, or hepatojugular reflux (HJR). Right HF results in peripheral edema, JVD, HJR, and ascites, without marked pulmonary symptoms. Since this a closed system, abnormally elevated cardiac pressures/volumes are quickly reflected into the contralateral system. This distinction better describes valvular dysfunction.
Arrhythmia and Sudden Death. Ventricular arrhythmias are common, and HF carries the greatest risk for sudden death. Non-sustained ventricular tachycardia (NSVT) occurs in 30-40% of patients with dilated cardiomyopathy, and premature ventricular contractions (PVCs) are found in 95% of patients with advanced HF. The sudden death risk is proportional to the EF decrease and HF severity.15 Although arrhythmia is common, neither Holter nor electrophysiologic studies predict sudden death.16 Ventricular arrhythmias by Holter monitoring predict all-cause mortality, but are non-specific for sudden death, so therapy is guided by symptoms. Syncope, resuscitation after cardiac arrest, sustained VT, symptomatic NSVT, and ventricular fibrillation (VF), prompt aggressive management.
Atrial fibrillation (AF) is common in the elderly, especially in those with HF.17 Furthermore, the elderly are more symptomatic when this arrhythmia occurs. If AF is acute or is associated with HF exacerbation, attempts at cardioversion are warranted. Chronic antiarrhythmic therapy for AF is less useful.
Half of HF deaths are caused by pump failure. Sudden death occurs in 10-40%, and is due to VF or VT in half.15,16,18 The remaining sudden deaths die from unexplained hypotension or bradycardia progressing to pulseless electrical activity.19 Therapies to decrease sudden death have had little success. Prophylactic antiarrhythmics (e.g., encainide, flecainide) increase mortality by pro-arrhythmic and negative inotropic effects.20 Amiodarone lacks pro-arrhythmic effects but has many non-cardiac side effects. In trials of amiodarone vs. placebo, overall cardiac mortality was unchanged, but there was a 35% reduction in arrhythmic deaths.21 Implantable defibrillators may offer hope, but there is insufficient research to currently recommend them.
Clinical Course
HF frequently follows a pattern of worsening symptoms at home, prompting an ED visit, ED stabilization and diagnosis, then hospitalization. While the average hospitalization for HF patients is 3-7 days, it can be considerably longer in patients older than age 75.10 This cycle repeats, with increasing frequency and worsening disability, until death in five years. Frequent hospitalizations affect the patients’ quality of life and consume significant health care resources.
Diagnosis/ED Evaluation. The diagnosis of HF may be difficult since no single finding is pathognomonic. In the elderly, HF is both under- and over-diagnosed because routinely used diagnostic elements are neither sensitive nor specific.4,7,22 This is because of a high rate of confounding comorbidities and the fact that the elderly frequently have more advanced disease at diagnosis.17 The greater severity of disease in the older patient at presentation is hypothesized to be caused by a more sedentary lifestyle that does help identify symptoms until physical limitations are severe.17
In primary care, the initial diagnosis of HF may be falsely positive in more than half of patients. Symptoms that mimic HF are often caused by occult cardiac ischemia, obesity, and chronic obstructive pulmonary disease (COPD) exacerbations.23 Gender also may lead to misdiagnosis;23,24 in one study HF was correctly determined in only 18% of women vs. 36% of men.24 Diagnostic criteria for HF may aid the clinician. The Framingham criteria require one major and two minor criteria to be met for diagnosis.25,26 (See Table 6.) Using the Boston criteria, increasing points confer a higher probability of HF.27 (See Table 7.) In the Boston scale, a score of 4 or greater detects a pulmonary artery occlusion pressure (PAOP) of 12 mmHg or higher with a sensitivity of 90% and a specificity of 85%. While validated, these criteria have limited usefulness when patients are asymptomatic.
| Table 6. Framingham Criteria for the Diagnosis of Heart Failure |
| Major Criteria |
| Paroxysmal nocturnal dyspnea |
| Neck vein distention |
| Rales |
| Cardiomegaly |
| Acute pulmonary edema |
| S3 gallop |
| Increased venous pressure (> 16 cm H20) |
| Positive HJR |
| Minor Criteria |
| Extremity edema |
| Night cough |
| Dyspnea on exertion |
| Hepatomegaly |
| Pleural effusion |
| Vital capacity reduce by one-third of normal |
| Tachycardia (>120) |
| Table 7. Boston Criteria for Diagnosing Congestive Heart Failure | |
| History | Score |
| Dyspnea at rest, or orthopnea | 4 |
| Nocturnal dyspnea | 3 |
| Dyspnea while walking | 2 |
| Dyspnea on stair climbing | 1 |
| Chest x-ray | |
| Alveolar pulmonary edema | 4 |
| Interstitial pulmonary edema | 3 |
| Bilateral pleural effusions | 3 |
| Cardiothoracic ratio > 0.5 | 3 |
| Kerley A lines | 2 |
| Physical exam | |
| HR 91-110 bpm | 1 |
| HR > 110 bpm, or JVD > 6 cm H20 | 2 |
| JVD and edema or hepatomegaly | 3 |
| Basilar rales | 1 |
| Rales > basilar | 2 |
| Wheezing or S3 gallop | 3 |
History. The common complaints of HF are shortness of breath, dyspnea on exertion, orthopnea, peripheral edema, weight gain, paroxysmal nocturnal dyspnea, cough, and fatigue. In the elderly, the classic symptoms of HF (i.e., exertional dyspnea, fatigue, orthopnea) are neither sensitive nor specific.4,7 Exertional symptoms may not be reported in older sedentary patients. Thus, non-specific complaints of generalized weakness, anorexia, nausea, fatigue, mental disturbances, altered breathing, and dry cough may be the presenting complaints for HF in the elderly.7,22
When taking the history, search for signs of AMI. AMI should always be considered diagnostically as a cause of HF. The clinician should keep in mind that the elderly have a higher frequency of silent or occult AMI presentation. He or she should ascertain the patients’ CAD risk factors and determine if there are any other events that may worsen or precipitate HF. These include hypertension, anemia, hyperthyroidism, worsening comorbidity, over-the-counter medication use, electrolyte abnormalities, or occult infection. Dietary and medication non-compliance can decompensate HF, so habits are queried. Arrhythmia worsens underlying HF and is suggested by palpitations. Lastly, check for alcohol or drug use, and their withdrawal, since these adversely affect cardiac function.
Non-Compliance. Non-compliance with HF treatment is a pernicious problem for many reasons: Diuretics may cause nocturia, dietary restrictions are onerous, fluid restriction is uncomfortable, medication costs can be exorbitant, and complicated multi-drug regimens can be difficult for the elderly. Therapeutic simplification and education are critical for success; their importance cannot be overemphasized.
Physical Examination. Airway is paramount. Once stability is ensured, further evaluation should proceed. Vital signs should be checked. Note that resting tachycardia is uncommon in the elderly.7 Lung sounds, peripheral edema, JVD, HJR, and extra heart sounds help detect fluid overload. Skin mottling, from poor peripheral perfusion, is associated with markedly increased hospital mortality (odds ratio, 17.5).28 The cardiac point of maximal impulse (PMI) can help estimate HF chronicity; in longstanding HF, cardiac remodeling may shift the PMI laterally.
In the elderly, physical exam limitations are significant. Edema, rales, and the presence of an S3 or S4 are neither sensitive nor specific.4,7 Finding an S4 is of little value; it may simply reflect age-related diastolic dysfunction.4 Ankle edema is common in older patients and probably should not be considered cardiac in origin unless other signs of HF are present.10 Finally, in chronic HF, the physical signs of congestion have a poor predictive value for identifying high PAOP.29
ECG. The ECG is crucial. It is fastest diagnostic test, and screens for arrhythmia, electrolyte imbalance (e.g., hyperkalemia), drug toxicity (e.g., digoxin), and suggests the chronicity and etiology of HF (e.g., LVH). If new ischemic changes are noted, immediate ICU admission is warranted. A diagnosis of systolic HF is unlikely in the presence of a normal 12 lead ECG, which has good sensitivity but poor specificity for detecting systolic dysfunction.30 ECG also has prognostic value; five-year mortality in dilated cardiomyopathy is worse when abnormal Q waves, QRS duration longer than 0.12 s, or left bundle branch block are present.14
Laboratory Tests. Since occult AMI may cause or decompensate HF, cardiac enzymes should be obtained. In the ED setting, cardiac enzymes diagnose but don’t exclude AMI.31 If the enzymes are elevated, ICU admission is needed. Diuresis may cause electrolyte changes, and electrolyte levels are indicated. Serum BUN and creatinine also should be measured, as renal function is commonly affected by HF therapy. A complete blood count (CBC) evaluates for anemia, and if hepatomegaly is present, liver enzymes may differentiate passive congestion from other etiologies.
In the elderly, thyroid function testing is considered, especially if AF is present.1 Toxicology testing (e.g., digoxin) is guided by presentation, with alcohol and drug screening performed when abuse is suspected. Hypomagnesemia is considered with arrhythmia or severe hypokalemia. Arterial blood gas measurements are performed selectively; they should be obtained in those at risk of CO2 retention or those who appear severely ill.
Radiology. All elderly patients with suspected HF need a chest radiograph (CXR). A negative CXR does not exclude abnormal LV function. CXRs can exclude some confounding pathologies (e.g., pneumonia), but physicians should remember that co-morbidities are more likely in the aged. CXR findings of HF are cardiomegaly, Kerley lines, increased pulmonary vascularity, and pleural effusion. Symptoms may precede chest x-ray changes by hours, so treatment should not be withheld while waiting for a CXR or if CXR results are normal.
CXRs also have significant limitations. Cardiomegaly is helpful, and a cardiothoracic (CT) ratio higher than 60% predicts increased five-year mortality.15 But because of intrathoracic cardiac rotation, CXRs are insensitive for its detection.32 In one study of HF with proven cardiomegaly, 22% of patients had CT ratios of less than 50%.32 Likewise, pleural effusion can be missed by CXR. The sensitivity, specificity, and accuracy of the supine CXR for pleural effusion is only 67%, 70%, and 67%, respectively.33
Use of the portable CXR (pCXR) in the ED is common. HF findings on pCXR are, in descending frequency, dilated upper lobe vessels (cephalization), cardiomegaly, interstitial edema, enlarged pulmonary artery, pleural effusion, alveolar edema, prominent superior vena cava, and Kerley lines.34 But, pCXR sensitivity for HF is poor. Only dilated upper lobe vessels are detected in more than 60% of HF patients. Increasing HF severity is associated with more positive pCXR findings. With the exception of Kerley lines (11%) and prominent vena cava (44%), all other pCXR findings occur in at least two-thirds of severe HF cases.34
In chronic HF, CXRs are unreliable. Pulmonary congestion is undetectable by CXR in 39% of patients with mild to moderate PAOP elevation (16-29 mmHg), and in 53% with severe elevation (> 30 mmHg). PAOP is important; survival and quality of life improve when it is normalized.29
The gold standard for thoracic fluid assessment is unclear, although thoracic computed tomography (CT) scan has been proposed. If chest CT scan, PAOP, and CXR are done simultaneously, pulmonary fluid will be seen on the CT scan prior to detection on CXR and before PAOP elevates.35-37 However, in elderly symptomatic ED patients, CT scan is difficult.
Echocardiography. EF is the most important measurement in HF.2 This is especially true in the elderly, for whom a high frequency of diastolic HF exists. There is no correlation between symptoms and EF, but measuring EF is diagnostic and determines HF type.30 Once systolic HF is established, repeat measures are not needed. If systolic HF is not established, or it has been a long time since the last EF measurement, reassessment by echocardiogram can be helpful. Other methods of EF determination are available (e.g., angiogram, cardiac MRI), but are not available or are less useful in the ED setting.
Differential Diagnosis. Many problems mimic acute HF. Breathlessness is common, so conditions causing dyspnea should be included in the differential diagnosis. AMI is also an early consideration. It must always be excluded as the primary cause of presentation, or as the etiology of a HF exacerbation.
An exacerbation of COPD is easily confused with acute HF. Both may present with acute dyspnea and abnormal lung sounds. Worsening of either can precipitate an exacerbation of the other. The history may help differentiate the two diagnoses (e.g., diuretic non-compliance), as well as a careful physical (evaluating for peripheral edema, HJR, S3, etc). Severe hypertension and peripheral vasoconstriction are suggestive of acute HF, even with marked wheezing. The chest x-ray is helpful, but its limitations have been noted.
Pneumonia, or other pulmonary pathologies, may mimic or exacerbate HF. Fever, productive cough, pleuritic chest pain, focal abnormalities on CXR, and leukocytosis suggests this diagnosis. Acute breathlessness also results from pulmonary embolism (PE). Acute onset, pleuritic pain, and a normal ECG, suggest PE. ABGs may demonstrate increases in the alveolar-arterial (A-a) oxygen gradient, because of ventilation perfusion mismatch; however, this is also seen in HF. The CXR can be misleading because chronic HF findings may be unrelated to the presentation. Ventilation perfusion scan or pulmonary angiography may be considered.
Finally, peripheral edema is seen in HF, but is non-specific as it is found in hypoproteinemia, hepatic or renal failure, and vascular stasis.
Supportive Therapy
Oxygen. Supplemental O2 should be provided, with therapy guided by pulse oximetry. Supplemental O2 assists in dyspnea relief and may decrease hypoxic anxiety. Since hypoxia is a greater risk than hypercarbia, O2 is not withheld because of CO2 retention concerns.
Cardiac Monitoring. Cardiac monitoring in the ED is needed. It can diagnose arrhythmia contributing to HF and aid in the detection of electrolyte abnormalities from diuresis or ACEI use.
IV Access. HF may cause ventricular arrhythmia, and prompt therapy may be required. Any delays while attempting peripheral IV placement may have adverse consequences. IV access should be obtained early in ED management.
Medications
Diuretics. While diuretics prompt relief of fluid overload, compared to young patients, the elderly are less responsive.8 Diuretics are used in all patients with congestion, irrespective of HF type, but are not recommended as monotherapy since they do not change mortality rates.2,38 Loop diuretics promote free water and sodium loss, maintaining efficacy until renal function is severely impaired. This is in contrast to distal tubule diuretics (thiazides, potassium sparing agents, etc.) that are not as effective in patients with renal insufficiency.2
Diuretics alter efficacy and toxicity of other HF medications, especially in the older patient.4 Dosing is best guided by daily body weight measurement. Complications include electrolyte depletion (i.e., Na+, K+, Mg++), to which the elderly are more susceptible, as well as hypotension, azotemia, and neurohormonal activation.4,8 Excessive diuresis is avoided in the elderly because of the built-in volume sensitive diastolic dysfunction of aging. Diuretic resistance may be overcome by IV use, combination diuretic therapy, or a brief course of an agent that augments renal blood flow (e.g., dobutamine).1,2
Furosemide is an effective loop diuretic. In ED patients with acute dyspnea and pulmonary congestion, twice the daily oral dose may be given (max: 180 mg) as an IV push, as long as there is adequate BP. If the patient is not on a loop diuretic, 40 mg is a good initial dose. Alternatively, 1 mg bumetadine equals 40 mg furosemide.39 If urinary output is still poor after three hours, double and repeat the dose. Output goals are 500 cc within two hours. If the creatinine exceeds 2.5 mg/dL, halve output goals. If output remains poor, admission is needed. Diuretic response predicts outcome. In acute pulmonary edema, poor diuresis is associated with higher mortality, and net urine output of less than 1 liter is more common in those failing observation unit therapy.28,40
Digoxin. Digoxin improves myocardial contractility at all ages, controls ventricular rate in AF, and is recommended in systolic HF.2,41 It has no effect on mortality, but decreases HF deaths and hospitalizations, even in those older than 80 years.42 Aging changes in lean body mass and renal function lower the therapeutic index in the elderly. If the patient is older than 70 years, appropriate serum levels are 0.5 to 0.9 ng/mL.41,43
Toxicity causes arrhythmias (e.g., heart block, ectopic or re-entrant rhythms), gastrointestinal symptoms (nausea, vomiting), and neurologic complaints (visual disturbances, disorientation, confusion). Toxicity is suggested with elevated serum levels but occurs at lower levels with hypokalemia or hypomagnesemia. The elderly may be more susceptible to the neurologic and cardiac manifestation of digoxin toxicity. Up to 20% of elderly patients on chronic therapy experience toxicity at least once.44 Serum digoxin levels are increased by quinidine, verapamil, spironolactone, flecainide, propafenone, and amiodarone. The dose of digoxin should be decreased if these drugs are added. Digoxin dosing in systolic HF is 0.125 to 0.25 mg qd. For rate control of AF, doses higher than 0.25 mg qd are not recommended.
Vasodilators: Angiotensin-Converting Enzyme Inhibitors (ACEIs). Angiotensin II (AII) may cause or worsen HF. It causes vasoconstriction, aldosterone secretion, sympathetic activation, and contributes to vascular hypertrophy.45 ACEIs prevent the conversion of angiotensin I (AI) to AII, and prevent bradykinin degradation (an anaphylaxis mediator) by ACE.
ACEI use decreases hospitalizations and mortality, improves symptoms, and attenuates cardiac remodeling in systolic HF.19,46,47 They function as balanced vasodilators in that they provide both arterial and venous dilation.48 They lower arterial blood pressure, intracardiac end-diastolic pressures, cardiac work, myocardial oxygen consumption, and decrease neurohormonal activation and sodium and water retention and may reduce complex ventricular arrhythmia.48 All of these effects are beneficial in systolic HF.
Despite that renin-angiotensin system function declines with age, the beneficial effects ACEIs are preserved in the elderly. These effects are most pronounced in older patients. In post-MI patients with EF less than 40%, captopril decreased mortality by 8% in those 55 years or younger, 13% in those 56-64, and 25% in those 65 years or older.49 Others support these findings.50 All elderly patients with systolic HF, even if asymptomatic, should have a trial of ACEI.2,38,48 With congestive symptoms, ACEIs should be combined with diuretics. In the elderly, ACEIs are at least as effective as in the young, but rates of ACEI prescribing are lower.4,51 Age is not a contraindication for ACEI use.51
ACEIs can cause hypotension or worsening renal insufficiency, especially in the setting of volume depletion. With chronic ACEI use, these complications may be due to over-diuresis or HF progression. If congestion is present, suspect HF progression; in its absence, decrease the diuretic dose. Renal deterioration may also occur following NSAID usage.
ACEIs also may cause hyperkalemia. It may result from deteriorating renal function, ongoing K+ supplementation, or concurrent K+ sparing diuretics.
Idiosyncratic angioedema occurs in less than 1% of ACEI users, even after chronic use. If this occurs, stop the ACEI and assess for critical anaphylaxis. Therapy is routine, but the patient is barred from future ACEI use.
Within months of ACEI use, a non-productive cough occurs in 5-15%. The cough usually resolves within 1-2 weeks after stopping ACEIs and returns on re-introduction. Due to the benefit of ACEIs, tolerating the cough is encouraged. In the ED, cough should prompt a search for other pathology (e.g., early pulmonary edema or pneumonia) as well.
In the elderly, the initial ACEI dose should be low, and then titrated up. Target doses for ACEIs are: captopril, 50mg tid; enalapril or lisinopril, 20 mg qd; or ramipril, 5 mg bid.4 But, if titration fails, even low doses may confer some benefit.4
Vasodilators: Angiotensin II (AII) Receptor Blockers (ARBs). Stopping AII synthesis by ACEI is desirable, but AI is still converted to AII by other chymases. ARBs block the AII receptor, providing AII inhibition while keeping ACE activity intact. Intact ACE degrades bradykinin, therefore decreasing complications from its accumulation (e.g., cough, anaphylaxis).
ARBs are used if ACEIs cause angioedema or intractable cough. They are as likely as ACEIs to cause hypotension, worsen renal function, and induce hyperkalemia. To date, trials are inconclusive as to whether ARBs prolong life and decrease morbidity like ACEIs.52,53 Therefore, ARBs are not ACEI substitutes. They are used after failure of a prior ACEI trial or can be added to an ACEI regimen if symptoms persist.2
ARBs are well tolerated in the elderly and complication rates are comparable to placebo.48,54,55 The rate of hyperkalemia is similar to that found with ACEIs, and is associated with the same risk factors.55 A common ARB is losartan, dosed at 50 mg daily. The initial dose is lowered in those on high-dose diuretics, and potassium and renal function must be monitored.
Vasodilators: Hydralazine and Isosorbide Dinitrate (HISDN). An alternative to ACEI or ARBs, but with less benefit, HISDN is not used unless marked ACEI/ARB intolerance exists.1,2,46,56 There is no use of either agent alone for HF.
Beta-Blockers. Sympathetic activation, mediated by norepinephrine, results in many events contributing to HF.57 (See Table 8.) Beta-blockers interfere with the neurohormonal effects and lead to a decrease in both mortality and hospital admissions.58-63 In a large study of 10,000 patients, beta-blockers decreased mortality by 65%, lowered hospitalizations, and improved symptoms.63 Beta-blockers are recommended in NYHA class II or III systolic HF.2 They are usually combined with diuretics and ACEIs. Data currently are insufficient to indicate use in class IV HF.2
| Table 8. Effects of Norepinephrine Contributing to Heart Failure Development | |
| 1. Increases SVR by vasoconstriction; increases ventricular volume/pressure. | |
| 2. Impairs renal sodium excretion. | |
| 3. Induces cardiac hypertrophy. | |
| 4. Increases myocardial cellular automaticity, may provoke arrhythmia. | |
| 5. Contributes to hypokalemia. | |
| 6. Contributes to apoptosis by stimulating growth and oxidative stress. | |
Contraindications include bronchospastic disease, symptomatic bradycardia, or advanced heart block (without pacemaker protection). They should be used cautiously in asymptomatic bradycardia (heart rate < 60). Diabetes is not a contraindication.62 Beta-blockers should not be initiated in decompensated HF and should be avoided if fluid retention requires IV diuresis, if IV inotropes are anticipated, or if hospitalization is needed. Since ED HF is usually symptomatic, initiating beta-blockers is difficult in this environment.
Carvedilol is the only FDA-approved HF beta-blocker, and should be begun after stabilization of diuretics, ACEI, and digoxin dosing. Starting dose is 3.125 mg bid.64 It is slowly increased, at two-week intervals, based on tolerance. Common complications are bradycardia, hypotension, dizziness, and diarrhea. Metoprolol also is commonly used. The initial dose is 6.25 mg qd, and gradually should be increased to 50 mg bid.
Decompensated HF patients on beta-blockers are a challenging management problem. Beta-blocker termination may cause deterioration, but further dosing can worsen tenuous hemodynamics. A short course of IV inotrope, while giving a lower beta-blocker dose, may allow stabilization by other measures (e.g., IV diuretics, vasodilators).
Spironolactone. Aldosterone has detrimental cardiac effects, independent of AII. Its antagonism by spironolactone can improve HF. The mortality risk and cardiac hospitalizations of NYHA class IV HF decreases by 32% when spironolactone is added to routine therapy.65,66 Thus, NYHA class IV HF may be trialed on low-dose spironolactone therapy, 12.5-25 mg/d.2,65 At this dose, serious hyperkalemia risk is similar to placebo, but gynecomastia is a common adverse event. Spironolactone is not recommend if the creatinine is greater than 2.5 mg/dL or K+ is greater than 5.0 mEq/L. Serum K+ is checked one week after initiation of therapy and after dose changes. There is insufficient evidence for spironolactone in NYHA class I or II HF.
Specifics of Systolic HF Therapy. Standard therapy in systolic HF usually consists of the combination of ACEIs, digoxin, and diuretics for the relief of fluid overload. Beta-blockers are added as appropriate, and in NYHA IV HF, spironolactone is prescribed.
Calcium channel blockers (CCBs) are not recommended.1,2 Short-term use may result in pulmonary edema and cardiogenic shock. Long-term use increases the risk of worsening HF and death.67-70 These adverse effects may be because of the CCBs’ negative inotropicity. Amlodipine, which has not been demonstrated to have a clear adverse mortality effect, may be used for other compelling clinical reasons.
Specifics of Diastolic HF Therapy. Since most large trials focus on the treatment of systolic HF, guidelines for diastolic HF therapy are largely empiric.4 In diastolic HF, diuretics are appropriate if congestion or edema is present, but one should avoid excessive diuresis. Hypotension, confusion, and azotemia may result if intravascular depletion (decreased preload) causes cardiac output to fall.
Other diastolic HF medications are beta-blockers, CCBs, and ACEIs.17 Beta-blockers slow heart rate, which prolongs filling time and improves stroke volume, decreases symptoms, and helps prevent ischemia. In one small study of elderly HF patients (mean age, 81), with an EF 40% or lower, beta-blockers improved survival.71 In contradistinction to systolic HF, CCBs may reduce ischemia and ventricular hypertrophy in diastolic HF. They also have a beneficial effect on diastolic function. Verapamil may improve symptoms and exercise capacity in the elderly diastolic HF patient.72 ACEIs can improve LV compliance by reducing hypertrophy. In 21 elderly patients, enalapril improved exercise capacity, LV mass, and diastolic function.44 However, the mortality-reducing benefits of ACEIs in diastolic HF remains unproven in the aged.10,30
Nitrates and digoxin may be of use in diastolic HF when impaired ventricular relaxation is the primary etiologic factor. But, since they decrease preload, and cause a resultant decline in CO, they should be used with caution. Digoxin, often considered contraindicated in diastolic HF, may have similar benefits to those seen in systolic HF.4 In 988 patients randomized to either placebo or digoxin, digoxin had no overall mortality effect but decreased HF deaths and hospitalizations by 18%.42
Appropriate ACEI use in diastolic HF is unclear. However, since hypertension is a common precipitant of diastolic HF, its use may be of benefit in these patients. Some support the use of ACEIs in diastolic HF.48
A useful approach in diastolic HF is to use beta-blockers if the resting heart rate exceeds 75, or ACEIs if it is less than 75—provided there are no contraindications to their use.4 These drugs can be combined with diuretics and nitrates to relieve congestion or edema. In refractory cases, digoxin is considered.
Measures with Limited Risk/Benefit Analysis
Intermittent Inotropic Therapy. Intuitively, inotropes would seem to be of use to augment contractility and decrease SVR by vasodilation. Short-term use does improve CO, but there is no lasting benefit in symptoms or outcome.2,6 In fact, chronic IV use increases mortality, and so is not recommended.2,6,73,74 Appropriate uses are as a bridge to stabilization in decompensated patients on beta-blockers, or while instituting definitive therapy (e.g., heart transplant).
Anticoagulation. The risk of thromboembolism in stable HF patients is 1-3% annually, and is highest in those with lowest EFs.75,76 Conversely, anticoagulation risk is high in the elderly.11,18 Many use warfarin in HF, but there are few data to support this practice.1,2 Patients with AF should receive warfarin, with dosage adjustments to keep the INR between 2.0 and 3.0.1 Most elderly patients in sinus rhythm who have no history of a past embolic event probably do not need anticoagulation.17
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). NSAIDs inhibit diuretics and ACEIs, worsen both cardiac and renal function, and should be avoided in HF.1,2 With few data for guidance, routine use of aspirin for MI prophylaxis in coronary artery disease, in the setting of concurrent ACEI treatment for HF, is controversial; however, current recommendations are to maintain once daily dosing of aspirin (75-325 mg) to diminish the risk of cardiovascular events in patients with CAD.
Antiarrhythmics. HF patients are sensitive to the pro-arrhythmic and cardiodepressant effects of antiarrhythmics, and antiarrhythmics do not decrease sudden death risk.20,77 Suppression of asymptomatic ventricular arrhythmias is usually unnecessary. However, after resuscitation from sudden death, VF, or sustained VT, electrophysiologic testing and device placement may be considered.2
Class I antiarrhythmics are not used in HF except for immediate treatment of life-threatening ventricular arrhythmias.1,2,77,80 Some class III agents (e.g., amiodarone) do not increase sudden death risk.78,79 Therefore, they are preferred for atrial arrhythmias.2 But, due to toxicity, amiodarone is not routinely recommended to prevent sudden death if the patient has already been treated with mortality-reducing drugs (ACEIs, beta-blockers).2
Disposition
Inpatient Admission Criteria for ED HF Patients. No published criteria exist. Patients with sustained VT, symptomatic arrhythmia, unstable vital signs, unstable airway, ischemic chest pain, new ECG changes, and AMI enzyme elevations, are admitted to an ICU. Severe electrolyte abnormalities may require a monitored bed. If the patient is congested and unable to attain output goals, or if dyspnea is unrelieved after therapy, admission is warranted. A low admission threshold should be used in the very elderly, in the presence of severe comorbidity, or if the home environment precludes successful outpatient management. Hemodynamically stable patients with fluid overload may be considered for observation unit admission.
Discharge Criteria. Patients with a good diuretic response, dyspnea resolution, and edema improvement, are expected to do well. Ambulation prior to discharge is an effective method to evaluate functional reserve and may help determine the ability to perform activities of daily living. In addition, if ACEI therapy is initiated or up-titrated in the ED, ambulation prior to discharge will assure that the revised therapies do not cause orthostatic hypotension.
Discharge Instructions. Patients should receive instruction on the signs and symptoms of worsening HF, and be educated on when to return to the ED. This should specifically include daily weight monitoring, appropriate responses to weight changes, and when to contact their physician. A written list of their medications and doses should be provided, as well as contact phone numbers for future follow-up. They should be encouraged to stop smoking, to reduce alcohol intake, and to exercise.
Dietary and Social Work Evaluation. An important part of HF management is the home environment. Barriers to obtaining medications, attending outpatient appointments, and adhering to dietary constraints (low sodium diet) need to be determined and eliminated. Failure to address these factors often results in minimal improvement and contributes to frequent readmission.80 Since dietary non-compliance is a major contributor to multiple hospitalizations, education is important. Dietary consultation should be arranged, and can be accomplished over the phone.
Readmission. In the elderly, multiple simultaneous disease process are common. This complicates management and contributes to the high re-hospitalization rate. HF 90-day readmit rates are 33-47%, and in Medicare patients older than 65 years, nearly 50% are readmitted within 3-6 months.2,81 Risk factors for re-admission are increasing age, male gender, prior admission within six months, and an initial hospitalization longer than one week.82 Other contributors are a failed social support system (21%), inadequate follow-up (20%), and non-compliance of diet (18%) or medication (15%). Overall, 90-day readmits are possibly preventable in 38%, and probably preventable in 15%.80
A multidisciplinary approach, including physicians, nurses, home care specialists, and pharmacists, decreases 90-day readmission rates, improves quality of life, and lowers costs.4,80,81,83 This is also true for the ED observation unit, where discharge rates increased by 50%, 90-day ED HF re-visits decreased more than 50%, and HF re-hospitalization decreased by two-thirds after instituting a multidisciplinary approach.84,85
Quality Improvement Programs. Like inpatient care, ED management of HF is part of the QI process. Indicators of appropriate levels of care, such as adequate diuretic use and appropriate ACEI treatment, should be documented. Unexpected events, morbidity, and mortality should be reviewed. Patients should be followed for frequency of revisits. Since poor 90-day readmission rates are associated with lower quality inpatient care, this also should be tracked in observation unit HF patients.86
Summary
Treatment for HF in the elderly is similar to that of the younger cohort. However, the underlying pathology is significantly different, the confounders more complex, and the diagnosis more difficult. Although the management challenges are greater, and the ultimate prognosis worse when compared to the younger HF patient, our understanding of HF has increased and new therapies offer hope to our elderly patients with heart failure.
References
1. Guidelines for the evaluation and management of heart failure: Report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee of Evaluation and Management of Heart Failure). Circ 1995;92:2764-2784.
2. Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure. Am J Cardiol 1999;83:2A,1A-38A.
3. Massie BM, Shah NB. Evolving trends in epidemiologic factors of heart failure: Rationale for preventative strategies and comprehensive disease management. Am Heart J 1997;133:703-712.
4. Friesinger GC. Ed. Cardiology Clinics, Cardiovascular Disease in the Elderly. Philadelphia: WB Saunders; 1999.
5. O’Connell JB, Bristow MR. Economic impact of heart failure in the United States: Time for a different approach. J Heart Lung Trans 1994;13:S107-112.
6. Packer M, Carver JR, Rodeheffer RJ, et al for the PROMISE Study Research Group. Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med 1991;325:1468-1475.
7. Tresch DD. The clinical diagnosis of heart failure in older patients. J Am Geriatr Soc 1997;45:1128-1133.
8. Rich MW. Epidemiology, pathophysiology, and etiology of congestive heart failure in older adults. J Am Geriatr Soc 1997;45:968-974.
9. Wei JY. Age and the cardiovascular system. N Engl J Med 1992;327:1735-1739.
10. Doughty R, Andersen V, Sharpe N. Optimal treatment of heart failure in the elderly. Drugs and Aging 1997;10:435-443.
11. Anonymous. Studies of left ventricular dysfunction (SOLVD) Crationale, design and methods: Two trials that evaluate the effect of enalapril in patients with reduced ejection fraction. Am J Cardiol 1990;66:315-322.
12. Tresch DD, McGough MF. Heart failure with normal systolic function: A common disorder in older people. J Am Geriatr Soc 1995;43:1035-1042.
13. Wong WF, Gold S, Fukuyama O, et al. Diastolic dysfunction in elderly patients with congestive heart failure. Am J Cardiol 1990;66:1257-1259.
14. Ghali JK, Kadakia S, Cooper RS, et al. Bedside diagnosis of preserved versus impaired left ventricular systolic function in heart failure. Am J Cardiol 1991;67:1002-1006.
15. Batsford WP, Mickleborough LL, Elefteriades JA. Ventricular arrhythmias in heart failure. Card Clin 1995;13:87-91.
16. Hobbs RE, Czerska MD. Congestive heart failure. Current and future strategies to decrease mortality. Postgrad Med 1994;96:167-172.
17. Senni M, Redfield MM. Congestive heart failure in elderly patients. Mayo Clin Proc 1997;72:453-460.
18. Stevenson WG, Stevenson LW, Middlekauff HR, et al. Sudden death prevention in patients with advanced ventricular dysfunction. Circ 1993;88:2953-2961.
19. The SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325:293-302.
20. The Cardiac Arrhythmia Suppression Trial (CAST) investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989;321:406-412.
21. Julian DG, Camm AJ, Fangin G, et al. Randomized trial of effect of amiodarone on mortality in patients with left ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet 1997;349:667-674.
22. Wenger NK, Franciosa JA, Weber KT. Heart failure. 18th Bethesda conference. Cardiovascular disease in the elderly. JACC 1987;10:73A-76A.
23. Remes J, Miettinen H, Reunanen A, et al. Validity of clinical diagnosis of heart failure in primary health care. Eur Heart J 1991;12:315-321.
24. Francis CM, Caruana L, Kearney P, et al. Open access echocardiography in management of heart failure in the community. BMJ 1995;310:634-636.
25. McKee PA, Castelli WP, McNamara PM, et al. The natural history of congestive heart failure: The Framingham study. N Engl J Med 1971;285:1441-1446.
26. Ho KKL, Anderson KM, Kannel WB, et al. Congestive heart failure/myocardial responses/valvular heart disease: Survival after the onset of congestive heart failure in Framingham heart study subjects. Circ 1993;88:107-115.
27. Marantz PR, Kaplan MC, Alderman MH. Clinical diagnosis of congestive heart failure in patients with acute dyspnea. Chest 1990;97:776-781.
28. Le Conte P, Coutant V, N’Guyen JM, et al. Prognostic factors in acute cardiogenic pulmonary edema. Am J Emerg Med 1999;17:329-332.
29. Chakko S, Woska D, Marinez H, et al. Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: Conflicting results may lead to inappropriate care. Am J Med 1991;90:353-359.
30. Gillespie ND, Darbar D, Struthers AD, et al. Heart Failure: A diagnostic and therapeutic dilemma in elderly patients. Age Aging 1998;27:539-543.
31. Peacock WF, Emerman CL, McErlean ES, et al. Troponin T: Insensitive for outcome prediction in low risk suspected acute coronary syndrome ED observation unit patients. Acad EM 1998;5:519.
32. Kono T, Suwa M, Hanada H, et al. Clinical significance of normal cardiac silhouette in dilated cardiomyopathy—Evaluation based upon echocardiography and magnetic resonance imaging. Jpn Cir J 1992;56:359-365.
33. Ruskin JA, Gurney JW, Thorsen MK, et al. Detection of pleural effusions on supine chest radiographs. AJR 1987;148:681-683.
34. Chait A, Cohen HE, Meltzer LE, et al. The bedside chest radiograph in the evaluation of incipient heart failure. Radiol 1972;105:563-566.
35. Shiro K, Takaaki N, Mashiko I. Early diagnosis and estimation of pulmonary congestion and edema in patients with left-sided heart disease from histogram of pulmonary CT number. Chest 1996;109:1439-1445.
36. McGredie, M. Measurement of pulmonary edema in valvular heart disease. Circ 1967;36:381-386.
37. Luepker R, Liander B, Korsgren M, et al. Pulmonary extravascular and intravascular fluid volume in resting patients. Am J Cardiol 1971;28:295-302.
38. Clinical Practice Guideline, Number 11. Heart Failure: Evaluation and care of patients with left-ventricular systolic dysfunction. US Department of Health and Human Services. June, 1994. AHCPR publication No. 94-0612.
39. Bumetadine. In: Physician’s Desk Reference, 2441-43. Montvale, NJ: Medical Economics Co.; 1998.
40. Peacock W, Aponte J, Craig M, et al. Predictors of unsuccessful treatment for congestive heart failure in the emergency department observation unit. Acad EM 1997;4:494.
41. Ware JA, Snow E, Luchi JM, et al. Effect of digoxin on ejection fraction in elderly patients with congestive heart failure. J Am Geriatri Soc 1984;32:631-635.
42. The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997;336:525-533.
43. Slatton ML, Irani WN, Hall SA, et al. Does digoxin provide additional hemodynamic and autonomic benefit at higher doses in patients with mild to moderate heart failure and normal sinus rhythm? J Am Coll Cardiol 1997;29:1206-1213.
44. Aronow WS, Kronzon I. Effect of enalapril on congestive heart failure treated with diuretics in elderly patients with prior myocardial infarction and normal left ventricular ejection fraction. Am J Cardiol 1993;71:602-604.
45. Francis G, Cohn J, for the V-HeFT VA Cooperative Studies Group. Plasma norepinephrine, plasma renin activity and congestive heart failure. Circ 1993;87:41-48.
46. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991;325:303-310.
47. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure: Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987;315:1429-1435.
48. Aronow WS. The ELITE study. What are its implications for the drug treatment of heart failure? Evaluation of Losartan in the elderly study. Drugs Aging 1998;12:423-428.
49. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: Results of the survival and ventricular enlargement trial. N Engl J Med 1992;327:669-677.
50. Ambrosioni E, Borghi C, Magnani B. Survival of myocardial infarction long-term evaluation (SMILE) investigators. The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. N Engl J Med 1995;332:80-85.
51. Garg R, Yusef S, for the Collaborative Group on ACE Inhibitor Trials: Overview of randomized trials of Angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. JAMA 1995;273:1450-1456.
52. McKelvie R, Yusuf S, Pericak D, et al. Comparison of candesartan, enalapril, and their combination in congestive heart failure: Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD pilot study). Eur Heart J 1998;19(supp):133.
53. Pitt B, Segal R, Martinez FA, et al. On behalf of Elite Study Investigators. Randomized trail of losartan versus captopril in patients over 65 with heart failure (Evaluation of Losartan in the Elderly Study, ELITE). Lancet 1997;349:747-752.
54. Burrell LM, Johnston CI. Angiotensin II receptor antagonists. Potential in elderly patients with cardiovascular disease. Drugs Aging 1997;10:421-434.
55. Goldberg AI, Dunlay MC, Sweet CS. Safety and tolerability of losartan potassium, an angiotensin II receptor antagonist, compared with hydrochlorothiazide, atenolol, felodipine ER, and angiotensin-converting enzyme inhibitors for the treatment of systemic hypertension. Am J Cardiol 1995;75:793-795.
56. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure: Results of the Veterans Administration Cooperative Study. N Engl J Med 1986;314:1547-1552.
57. Packer M. Adrenergic blockade in chronic heart failure: Principles, progress, and practice. Prog Cardio Dis 1998;41(Supp 1):39-52.
58. Colucci WS, Packer M, Bristow MR, et al. For the US Carvedilol Study Group. Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. Circ 1996;94:2800-2806.
59. Tsuyuki RT, Yusuf S, Rouleau JL, et al. Combination neurohormonal blockade with ACE inhibitors, angiotensin II, antagonists and beta-blockers in patients with congestive heart failure: Design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVED) pilot study (phase II). Eur Heart J 1998;19(Supp):308.
60. The International Steering Committee. Rationale, design, and organization of the Metoprolol CR/XL randomized intervention trial in heart failure (MERIT-HF). Am J Cardiol 1997;80(Supp 9B):54J-58J.
61. CIBIS Investigators and Committees. A randomized trial of b-blockade in heart failure: The Cardiac Insufficiency Bisoprolol Study (CIBIS). Circ 1994;90:1765-1773.
62. Bristow MR, Gilbert EM, Abraham WT, et al. For the MOCHA Investigators. Carvedilol produces dose-related improvements in left ventricular function and survival in subjects with chronic heart failure. Circ 1996;94:2807-2816.
63. Tsuyuki RT, Yusuf S, Rouleau JL, et al. Combination neurohormonal blockade with ACE inhibitors, angiotensin II antagonists and beta-blockers in patients with congestive heart failure: Design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study. Can J Cardiol 1997;13:1166-1174.
64. Prescribing Information: Coreg, 1998. SmithKline Beecham Pharmaceuticals, Philadelphia, PA.
65. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999;341:709-717.
66. The Rales Investigators. Effectiveness of spironolactone added to an angiotensin-converting enzyme inhibitor and a loop diuretic for sever chronic congestive heart failure (The Randomized Aldactone Evaluation Study [RALES]). Am J Cardiol 1996;78:902-907.
67. Elkayam U, Weber L, McKay C, et al. S. Spectrum of acute hemodynamic effects of nifedipine in severe congestive heart failure. Am J Cardiol 1985;56:560-566.
68. Barjon JN, Rouleau JL, Bichet D, et al. Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. J Am Coll Cardiol 1987;9:622-630.
69. Elkayam U, Amin J, Mehra A, et al. A prospective, randomized, double-blind, crossover study to compare the efficacy and safety of chronic nifedipine therapy with that of isosorbide dinitrate and their combination in the treatment of chronic congestive heart failure. Circ 1990;82:1954-1961.
70. Goldstein RE, Boccuzzi SJ, Cruess D, et al. Diltiazem increase late-onset congestive heart failure in post-infarction patients with early reduction in ejection fraction. The Adverse Experience Committee and the Multicenter Diltiazem Post-infarction Research Group. Circ 1991;83:52-60.
71. Aronow WS, Ahn C, Kronzon I. Effect of propranolol versus no propranolol on total mortality plus nonfatal myocardial infarction in older patients with prior myocardial infarction, congestive heart failure, and left ventricular ejection fraction ³ 40% treated with diuretics plus angiotensin-converting enzyme inhibitors. Am J Cardiol 1997;80:207-209.
72. Arrighi JA, Dilsizian V, Perrone-Filardi P, et al. Improvement of the age-related impairment in left ventricular diastolic filling with verapamil in the normal human heart. Circ 1994;90:213-219.
73. Lubsen J, Just H, Hjalmarsson AC, et al. Effect of pimobendan on exercise capacity in patients with heart failure: Main results for the Pimobendan in Congestive Heart Failure (PICO) trial. Heart 1996;76:223-231.
74. Cohn JN, Goldstein SO, Greenberg BH, et al. A dose-dependent increase in mortality with vesnarinone among patients with severe heart failure. N Engl J Med 1998;338:1810-1816.
75. Cioffi G, Pozzoli M, Forni G, et al. Systemic thromboembolism in chronic heart failure. A prospective study in 406 patients. Eur Heart J 1996;17:1381-1389.
76. Baker DW, Wright RF. Management of heart failure. IV. Anticoagulation for patients with heart failure due to left ventricular systolic dysfunction. JAMA 1994;272:1614-1618.
77. The Cardiac Arrhythmia Suppression Trail II Investigators. Effect of antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med 1992;327:227-233.
78. Doval HC, Nul DR, Grancelli HO, et al, for Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA). Randomized trial of low-dose amiodarone in severe congestive heart failure. Lancet 1994;344:493-498.
79. Singh SN, Fletcher RD, Fisher SG, et al for the Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmias. N Engl J Med 1995;333:77-82.
80. Vinson JM, Rich MW, Sperry JC, et al. Early readmission of elderly patients with congestive heart failure. J Am Geriatr Soc 1990;38:1290-1295.
81. Rich MW, Vinson JM, Sperry JC, et al. Prevention of readmission in elderly patients with congestive heart failure. J Gen Int Med 1993;8:585-590.
82. Krumholz HM, Parent EM, Tu N, et al. Readmission after hospitalization for congestive heart failure among Medicare beneficiaries. Arch Intern Med 1997;157:99-104.
83. Rich MW, Beckham V, Wittenberg C, et al. A multidisciplinary intervention to prevent the readmission of elderly patients with congestive heart failure. N Engl J Med 1995;333:1190-1195.
84. Albert NM, Peacock WF. Patient Outcome and Costs after Implementation of an Acute Heart Failure Management Program in an Emergency Department Observation Unit. J Int Soc Heart Lung Trans 1999;18:92.
85. Peacock WF, Albert NM, Kies P, et al. Emergency department observation unit heart failure protocol decreases adverse outcome rates. J Card Fail 1999;5:77.
86. Ashton CM, Kuykendall DH, Johnson ML, et al. The association between the quality of inpatient care and early readmission. Ann Intern Med 1995;122:415-421.
87. Grossman W. Diastolic dysfunction in congestive heart failure. N Engl J Med 1991;325:1557-1564.
Physician CME Questions
33. The consequences of aging on cardiac function include which of the following?
A. Decreased cardiac systolic function
B. Decreased ability to respond to cardiac stress
C. Improved b1 and b2 receptor responsiveness
D. Increased ventricular and systemic vascular compliance
34. Beta-blockers:
A. should not be initiated in HF decompensation.
B. are indicated in all patients with HF.
C. are never indicated in patients with HF.
D. should be up-titrated in HF decompensation.
35. Spironolactone:
A. frequently (> 30%) causes hyperkalemia.
B. is indicated for all patients with HF.
C. does not cause gynecomastia.
D. may be combined with standard HF therapy.
36. Diastolic HF:
A. is more common in the young.
B. is a volume-sensitive condition.
C. is a consequence of pump failure.
D. does not cause congestion.
37. Systolic HF:
A. is the result of a non-compliant ventricle.
B. is treated only with diuretics.
C. patients should receive a trial of ACEIs.
D. patients should receive antiarrhythmics for PVCs.
E. can be accurately differentiated from diastolic HF by exam.
38. HF has:
A. a prognosis better than most cancers.
B. an increasing incidence.
C. greater incidence among the young.
D. similar prognosis for men and women.
39. Diuretics should:
A. only be used in systolic HF patients.
B. only be used in diastolic HF patients.
C. not be used concurrently with beta-blockers.
D. be indicated for most congested HF patients.
40. ACEIs:
A. may be re-started after an allergic reaction.
B. prolong life in systolic HF.
C. should be stopped if cough is noted.
D. cannot be combined with digoxin.