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Heart Failure. Amanda Ryan, D.O. Cardiology Fellow February 14th, 2008. Learning Objectives. Following this presentation, the participant should be able to: 1. Recognize the magnitude of heart failure epidemic and its public health implications
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Heart Failure Amanda Ryan, D.O. Cardiology Fellow February 14th, 2008
Learning Objectives • Following this presentation, the participant should be able to: • 1. Recognize the magnitude of heart failure epidemic and its public health implications • 2. Distinguish the different classifications and stages of heart failure • 3. Review underlying pathophysiology of heart failure • 4. Discuss signs and symptoms of heart failure exacerbation • 5. Identify current practice guidelines for treatment of acute decompensated heart failure
What is Heart Failure • Heart failure occurs when the heart cannot pump enough blood fast enough to meet the metabolic needs of the body. • No longer use the term “congestive” because all heart failure does not result in clinically apparent volume overload
It is an Epidemic • Estimated that over 5 million Americans have heart failure • Estimated 500,000 new cases per year • Within 5 years, half of those diagnosed will be dead • Over 1 million hospitalizations per year with HF as primary diagnosis • Most common reason for hospitalization in those >65 years old • 85% of HF cases are in adults 65 and older • Heart failure is 4th in a list of quality of care initiatives in vulnerable older adults
Costs of Heart Failure • It is the leading cause of hospitalization in patients older than 65 years of age and is a primary hospital discharge diagnosis in 1.1 million people of all ages each year. • It is one medical condition for which mortality continues to increase. From 1994 to 2004, the overall death rate declined 2.0% in the United States, but deaths from HF increased 28% in the same time period. • According to the National Heart, Lung, and Blood Institute, the estimated direct and indirect costs associated with HF care in the US is $33.2 billion yearly. • The majority of the costs – approximately two-thirds – are attributable to the management of episodes of acute HF decompensation (i.e., hospitalization).
REACH Trial • Researchers at Henry Ford Heart and Vascular Institute found that the annual number of heart failure cases more than doubled for Henry Ford Health System in Detroit from 1989-1997. Over that nine-year period, 26,442 cases were identified. Strikingly, the annual prevalence rose from 9 to 20 cases per 1000 health system patients .
Different Ways to Define HF • Dilated (congestive) cardiomyopathy is a group of heart muscle disorders in which the ventricles enlarge but are not able to pump enough blood for the body's needs, resulting in heart failure. (Example - CAD, myocarditis, EtOH, HIV) • Hypertrophic cardiomyopathy includes a group of heart disorders in which the walls of the ventricles thicken (hypertrophy) and become stiff, even though the workload of the heart is not increased. (Example – congenital HOCM, or acquired) • Restrictive (infiltrative) cardiomyopathy includes a group of heart disorders in which the walls of the ventricles become stiff, but not necessarily thickened, and resist normal filling with blood between heartbeats. (Example – radiation, amyloidosis)
Different Ways to Define HF • Diastolic Versus Systolic Heart Failure A. Systolic cardiac (heart) dysfunction (or systolic heart failure) occurs when the heart muscle doesn't contract with enough force, so there is not enough oxygen-rich blood to be pumped throughout the body. B. Diastolic cardiac dysfunction (or diastolic heart failure) occurs when the heart contracts normally, but the ventricle doesn't relax properly so less blood can enter the heart.
Different Ways to Define HF • Clinically, patients are classified as having HF of ischemic or nonischemic etiology based on a history of myocardial infarction (MI) or based on objective evidence of coronary artery disease (CAD) such as angiography or functional testing.
New York Heart Association • Class I: No obvious symptoms, no limitations on patient physical activity (35 percent). • Class II: Some symptoms during or after normal activity, mild physical activity limitations (35 percent). • Class III: Symptoms with mild exertion, moderate to significant physical activity limitations (25 percent). • Class IV: Significant symptoms at rest, severe to total physical activity limitations (5 percent).
Causes of Heart Failure • Coronary artery disease • Problems with the heart muscle itself [known as cardiomyopathy (myocarditis, etc)] • Hypertension • Problems with any of the heart valves • Abnormal heart rhythms (also called arrhythmias) • Toxic substances (EtOH, cocaine) • Congenital heart disease • Diabetes • Thyroid problems • HIV
Diastolic HF • Diastolic heart failure is defined as a condition caused by increased resistance to the filling of one or both ventricles; this leads to symptoms of congestion from the inappropriate upward shift of the diastolic pressure-volume relation. • 40% of patients • Increasing incidence with age • More common in women • HTN and cardiac ischemia are most common causes • Common precipitating factors include volume overload; tachycardia; exercise; hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection, thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodal block); increased salt intake; and use of nonsteroidal anti-inflammatory drugs.
More About Diastolic Dysfunction • Alterations involve relaxation and/or filling and/or distensibility. • Arterial hypertension associated to LV concentric remodelling is the main determinant of DD but several other cardiac diseases, including myocardial ischemia, and extra-cardiac pathologies also possible.
Stages of Diastole • 1. Isovolumetric relaxation, period occurring between the end of LV systolic ejection (= aortic valve closure) and the opening of the mitral valve, when LV pressure keeps going its rapid fall while LV volume remains constant. • 2. LV rapid filling, which begins when LV pressure falls below left atrial pressure and the mitral valve opens. During this period the blood has an acceleration which achieves a maximal velocity, direct related to the magnitude of atrio-ventricular pressure, and stops when this gradient ends. • 3. diastasis, when left atrial and LV pressures are almost equal and LV filling is essentially maintained by the flow coming from pulmonary veins – with left atrium representing a passive conduit – with an amount depending of LV pressure, function of LV "compliance". • 4. atrial systole, which corresponds to left atrial contraction and ends at the mitral valve closure. This period is mainly influenced by LV compliance, but depends also by the pericardial resistance, by the atrial force and by the atrio-ventricular synchronicity (= ECG PR interval).
Patient Differences • HF is a hemodynamic disorder but there is a poor relationship between measures of cardiac performance and patient symptoms • For example, pts with very low EF may be asymptomatic while someone with preserved EF may be severely disabled with symptoms
Body Compensatory Mechanisms • Epinephrine and norepinephrine release which increases heart rate and contractility which increased myocardial work load • Decrease salt and water excretion from kidneys which helps maintain BP by increasing blood volume, this leads to stretching of heart’s chambers which can impair ability to contract • Hypertrophy and thickening of heart muscle which initially increases contractility but over time leads to stiff chambers and can impair contractility • HF patients have higher levels of epinephrine, norepinephrine, aldosterone, angiotensin II, endothelin, inflammatory cytokines, and vasopressin which contribute to heart remodeling, progression of HF, and higher levels are associated with increased mortality
Potential Reasons • Alternation in ventricular distensibility • Valvular regurgitation • Pericardial restraint • Cardiac rhythm • Conduction abnormalities • RV function • Also several non-cardiac factors including peripheral vascular fxn, reflex autonomic activity, renal sodium handling, etc.
Smoking EtOH use DM HTN Dyslipidemia Thyroid disorder Chemotherapy Radiation Cardiotoxic drugs Fam Hx of sudden death, CAD, conduction problems, HCM HIV status HF Risk Factors - History
Hx of heart failure Angina MI CABG PCI Pacemaker/ICD Embolic events arrhythmias CVA PVD Rheumatic Dx Other valvular hx Congenital Cardiovascular Medical Hx
Dyspnea PND Orthopnea Cough Exercise intolerance Edema Fatigue Nausea Abdominal Fullness Rales S3 Pulmonary edema JVD Tachycardia Cardiomegaly Hepatojugular reflex Peripheral Edema Hepatomegaly Signs and Symptoms of HF
HF Diagnosis and Assessment • Remains primarily a clinical diagnosis but additional information via other diagnostics can be beneficial • Evaluation depends on if this is first presentation, change in clinical symptoms, certainty of diagnosis, etc
Examples • Elevated BNP levels have been associated with reduced LVEF, LVH, elevated LV filling pressures, and acute MI • Evidence supports baseline levels for acute exacerbations at this time • Evaluation with coronary angiography on initial dx or presentation is recommended
ADHERE • The Acute Decompensated Heart Failure National Registry (ADHERE) is the largest clinical database of patients with acute decompensated heart failure (ADHF). It provides a cross-sectional evaluation of the HF population in the United States and provides insights into how patients with ADHF are managed during hospitalization.
ADHERE DATA • The data gathered for this registry include demographic information, medical history, baseline clinical characteristics, initial evaluation, treatment received, procedures performed, hospital course, and patient disposition. • Importantly, registry participation does not require any alteration of treatment or hospital care, and entry of data into the registry is not contingent on the use of any particular therapeutic agent or treatment regimen
Lessons From ADHERE • Prior studies on chronic systolic HF have demonstrated that body mass index (BMI) is inversely associated with mortality, the so-called obesity paradox. ADHERE investigators sought to determine whether BMI influences the mortality risk in ADHF, a subject not previously studied. In the large ADHERE cohort of hospitalized patients with HF, higher BMI was associated with significantly lower in-hospital mortality risk.The authors noted that the relationship between BMI and adverse outcomes in HF appears to be complex and deserving of further study. • Since most ADHF patients present for hospital care via the emergency department (ED), the ADHERE investigators studied the impact of early ED initiation of ADHF-specific therapy, as indicated by nesiritide use, on subsequent outcomes. Nesiritide was started in the ED in 1,613 patients (EDN group) and after admission to an in-patient unit in 2,687 patients (INN group). Nesiritide was initiated a median of 2.8 and 15.5 hours after presentation in EDN and INN patients, respectively (p < 0.001).
BNP Level in ADHERE • BNP levels within 24 hours of presentation were obtained in 48,629 (63%) out of 77,467 hospitalization episodes entered into the ADHERE registry. • BNP levels were <100 pg/ml in only 3.3% of hospitalization episodes in ADHERE. (The normal plasma level of BNP is currently accepted as <100 pg/ml.) • In-hospital mortality risk for the overall patient population was 3.6%. When stratified by BNP level, there was a near linear relationship between BNP quartiles and in-hospital mortality. • Overall, mortality risk varied more than three- to four-fold on the basis of the patient’s initial BNP.
More Implications • BNP quartile remained highly predictive of mortality even after adjusting for age, gender, systolic blood pressure, blood urea nitrogen, creatinine, sodium, pulse, and dyspnea at rest • BNP quartiles independently predicted mortality in patients with reduced and preserved systolic function. BNP quartile groups also predicted other clinical outcomes including need for mechanical ventilation, length of stay, time in the intensive care unit, and percent hospitalization in the intensive care unit
Signs and Symptoms Sign or Symptom +Why It Happens +People with Heart Failure May Experience... 1. Shortness of breath or dyspnea A. Blood "backs up" in the pulmonary veins because the heart can't keep up with the supply. This causes fluid to leak into the lungs a. Breathlessness during activity (most commonly), at rest, or while sleeping, which may come on suddenly and wake them up. They often have difficulty breathing while lying flat and may need to prop up the upper body and head on two pillows. They often complain of waking up tired or feeling anxious and restless.
More Signs and Symptoms 2. Persistent coughing or wheezing A. Fluid builds up in the lungs a. coughing that produces white or pink blood-tinged mucus. 3. Lack of appetite of nausea A. Digestive system receives less blood causing problems with digestion a. Full feeling, early satiety, nausea
Additional Signs 4. Confusion, impaired thinking A. Changing levels of certain substances in the blood, such as sodium, can cause confusion.. a. memory loss and feelings of disorientation. A caregiver or relative may notice this first.
More Signs & Symptoms 5. Increased heart rate A. To "make up for" the loss in pumping capacity, the heart beats faster.. . . a. heart palpitations, which feel like the heart is racing or throbbing. 6. More symptoms – weight gain, frequent urination, cough, decreased physical activity
Physical Examination • Signs that suggest heart failure include: • Tachycardia • Third heart sound (S3) (LISTEN LL RECUMBANT) • Increased jugular venous pressure • Positive hepatojugular reflux • Bilateral rales (not always present) • Peripheral edema not due to venous insufficiency • Laterally displaced apical impulse • Weight gain
Limitation of ADL’s • Adults, particularly geriatric aged persons, are much more likely to have difficulties with ADL’s. • 55% of pts with heart disease over the age of 70 are limited in their ADL’s versus 26% of those who do not have heart disease
What We Should Know about the Individual Patient’s HF • Identify the patient’s with HF • Assess for S/S and risk factors for HF • Initial work up should have been included work up for reversible causes if appropriate (TSH, HIV, etc.) • Echocardiogram to determine systolic and diastolic LV performance, cardiac output (ejection fraction), and pulmonary artery and ventricular filling pressures
Individual Patient’s HF • Chest X-ray to help identify vascular congestion, infiltrates, effusions • Evaluation and classification of severity of heart failure • Nuclear imaging for assessment of ejection fraction or areas of ischemia (as appropriate)
Management/Treatment Pharmacotherapy A. Loop diuretics [furosemide (THRESHOLD DRUG), bumentanide, torsemide] to treat volume overload – may add metolazone to any NO EFFECT ON MORTALITY B. Management of systolic dysfunction with an ACE inhibitor like captopril, lisinopril 1. Main side effects cough, hyperkalemia, angioedema, orthostasis
Management/Treatment • B-blocker such as carvedilol (coreg), metoprolol XL (toprol), ***GOAL DOSES • Addition of ARB may be substituted for ACE-I • Spironolactone – for patients with Stage III or IV heart failure, the RALES trial ** Watch for hyperkalemia • Digoxin – helps with morbidity not mortality **10-18% of nursing home pts develop toxicity Side effects include arrhythmias, visual changes, GI complaints, altered mental status • Nitrates and Hydralazine – particularly in African Americans
Basic Pharmacotherapy for HF patients • All patients with systolic heart failure should be on ACE-I and ß-blockers unless contraindications are present (ARBs can substitute if there is intolerance to these drug classes, i.e.: ARBs can be used in combination with ACE-I or with ß blockers). • Concerns about blood pressure may occur as these drugs are titrated upwards – limitations should relate to symptoms of low BP rather than actual BP values (for systolic BP above 80 mm Hg) so persistence with the titration should occur unless such symptoms occur. Concerns about renal function may occur as these drugs are titrated upwards.
Electrolytes • Please remember that many of these medications have severe impacts on patient’s electrolyte panels. • Check electrolytes on a regular basis in patients with heart failure • Have open communication with your physician’s regarding medications/plans of care for your HF patients.
