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- 1. Congestive Heart Failure Madi Capoccia DO 5 Jun 2007 Dewitt Army Hospital
- 17. Classification of Heart Failure: ACC/AHA Stage vs NYHA Class
- 26. Initial and Target Doses of beta-blockers for HF Medication Starting Dose Target Dosage Bisoprolol 1.25mg daily 10mg daily Carvedilol 3.125mg bid 25mg bid Metoprolol CR/XL 12.5-25mg daily 200mg daily
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- 3. Becoming and increasingly common as the US populations ages and survival rates after acute MI increase. 5. Furthermore, heart failure is a progressive condition: once symptoms appear, subsequent morbidity and mortality are high. 5- year survival rates are estimated to be 59% in men and 45% in women.
- Basic pathopysiology makes treatment principles easier to understand The capacity of the heart to adapt to short-term changes in preload or afterload is remarkable, but sudden or sustained changes in the preload (acute mitral regurg, excessive Iv hydration) or afterload (aortic stenosis, severe uncontrolled hypertension) or demand (from severe anemia, or hyperthyroidism) may lead to progressive failure of myocardial function. Asymptomatic dysfunction progresses steadily to overt heart failure. The mechanism by which this occurs are neurohumoral adaptations which are “double-edged swords” great in the acute setting and harmful in the long term setting. Although they are useful because they maintain arterial perfusion pressure in the face of a reduction in cardiac output, they increase the hemodynamic burden and oxygen requirements of the failing ventricle. The signs and symptoms of heart failure (HF) are due in part to compensatory mechanisms utilized by the body in an attempt to adjust for a primary deficit in cardiac output. Neurohumoral adaptations , such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems by the low output state, can contribute to maintenance of perfusion of vital organs in several ways ….
- Neurohumoral adaptations help by maintenance of perfusion of the vital organs by: Maintenance of systemic pressure by vasoconstriction, resulting in redistribution of blood flow to vital organs Restoration of cardiac output by increasing myocardial contractility and heart rate and by expansion of the extracellular fluid volume
- FIRST, the response to a decrease in cardiac output…….is that the Decreased perfusion pressure sensed by carotid sinus and aortic arch receptors results in increased sympathetic and decreased parasympathetic tone, and 2. also enhance release of ADH and stimulation of thirst. Circulating catecholamines are elevated (like norepinephrine), and direct sympathetic outflow to the heart, peripheral vasculature, and muscles is increased. Short-term consequences include 1. increased contractility and heart rate to augment cardiac output, systemic vasoconstriction to increase preload and maintain blood pressure, and redistribution of blood flow away from the skin, muscles, and kidneys to vital organs The long-term cardiovascular effects of sympathetic activation, however, are deleterious.These include myocyte necrosis and apoptosis (cell suicide), and interstitial fibrosis causing further impairment in systolic and diastolic function; cardiac norepinephrine depletion and beta-receptor down-regulation, resulting in inotropic (contractility) and chronotropic (rate or timing) incompetence; calcium overload and proarrhythmia; With this response and the response to decreased cardiac output lead to the activation of the renin-angiotensin-aldosterone system.
- When cardiac output declines the RAAS is activated. Increased concentrations of circulating angiotensin II and albdosterone are both increased, the former contributing to excess vasoconstriction and the latter to the retention of salt and water. The combination of decreased water excretion and increased water intake via thirst often leads to a fall in the plasma sodium concentration. The severity of these defects tends to parallel the severity of the heart failure. As a result, the degree of hyponatremia is an important predictor of survival.
- However, if the neruohumoral response continues maladaptive changes occur. The elevation in diastolic pressures is transmitted to the atria and to the pulmonary and systemic venous circulations; the ensuing elevation in capillary pressures promotes the development of pulmonary congestion and peripheral edema 2. The increase in left ventricular afterload induced by the rise in peripheral resistance can both directly depress cardiac function and enhance the rate of deterioration of myocardial function (show figure 2) [1] 3. Catecholamine-stimulated contractility and increased heart rate can worsen coronary ischemia 4. Catecholamines and angiotensin II may promote the loss of myocytes by apoptosis, the induction of maladaptive fetal isoforms of proteins involved in contraction, and hypertrophy (see below) 5. If chronic, neurohumoral activation may lead to decompensation due to excessive vasoconstriction and volume retention, electrolyte abnormalities, direct myocardial toxicity, and cardiac arrhythmias. The relative importance of these beneficial and detrimental effects is not fully defined. However, the slowing of disease progression and improvement in survival observed with angiotensin converting enzyme (ACE) inhibitors and beta blockers in patients with heart failure due to systolic dysfunction suggest that there is, over time, a net negative effect of the neurohumoral adaptations on ventricular function SUMMARY — In the short term, neurohumoral activation is beneficial in patients with HF since the elevations in cardiac contractility and vascular resistance and renal sodium retention tend to restore the cardiac output and tissue perfusion toward normal. However, the deleterious effects may predominate over the long-term, leading to pulmonary and peripheral edema, increased afterload, pathologic myocardial remodeling, and more rapid progression of myocardial dysfunction. The ability of ACE inhibitors and beta blockers to improve survival and slow the progression of the heart failure is compatible with this hypothesis.
- Systolic and Diastolic Dysfunction Diastolic dysfunction caused by compromise myocardial relaxation in the presence of myocardial contractility and ejection fraction. One third to one half of patients with heart failure have normal ventricular contractile function, and are said to have diastolic heart failure. Abnormal diastolic function may be due to impaired early relaxation, increased stiffness of the ventricle, or both. Diastolic dysfunction results in impairment in ventricular filling. LV end-diastolic pressures are elevated, leading to pulmonary venous congestion. Diastolic dysfunction is most commonly associated with left ventricular hypertrophy (LVH) due to hypertension, and occurs frequently in elderly women. Increased resistance to filling results from the increased LV mass itself, and also from interstitial fibrosis and subendocardial ischemia. Diastolic dysfunction can occur in the absence of LVH due to ischemia, myocardial infiltration (e.g., amyloidosis), or pericardial constriction. Systolic Heart Failure Most commonly, heart failure reflects an abnormality of ventricular contractile function. End-systolic volume, end-diastolic volume, and end-diastolic pressure are increased, and stroke volume falls. Symptoms of reduced cardiac output (e.g., fatigue) develop. In addition, increased LV end-diastolic pressure is transmitted back to the pulmonary veins, resulting in transudation of fluid into the pulmonary interstitium and symptoms of pulmonary congestion. The most common cause of contractile dysfunction is loss of myocytes due to myocardial infarction. Other causes of systolic heart failure include dilated cardiomyopathy, myocarditis, and chronic alcohol use. The most common form of heart failure , that due to coronary artery disease, often reflects a combination of systolic and diastolic dysfunction. Systolic dysfunction is due to prior infarction and ischemia-induced decrease in contractility. Diastolic dysfunction is due to chronic replacement fibrosis and ischemia-induced decrease in distensibility.
- High output Failure- occurs when the demand for blood exceeds the capacity of an otherwise normal heart to meet the demand Low cardiac output- fatigue and loss of lean muscle mass as their most prominent symptoms, may also have dsypnea, impaired renal function or altered mental status Although the symptoms, causes, prevalence and epidemiology of the six different types are somewhat different the is substantial overlap, and type may coexist. Therefore, this review present an approach to diagnosis that is appropriate regardless of the type or cause of heart failure.
- Labs Basic chemistry, CBC, TSH BNP to support dx, assess decompensation, measure response to therapy Other labs as directed by hx (i.e iron studies)
- Rigorous Criteria for identifying heart failure based on clinical history and physical findings were developed for the Framingham study. However, heart failure may not be recognized in up to 40% of patients due to the limited reliability of these findings.
- A normal chest radiograph slightly decrease the probability of heart failure and helps identify pulmonary causes of dyspnea. A normal EKG makes heart failure less likely as well. If both ekg and chest x-ray are normal heart failure is unlikely and your differential should broaden. Chest x-ray should look for cardiomegaly, pulmonary vascular congestion. Early radiologic signs of pulmonary venous hypertension and interstitial edema include distension of the pulmonary veins extending upward from the hila, haziness of hilar shadow and thickening of the interlobular septae (Kelye’s B Lines) Therefore, patients with dyspnea and suggestive abnormalities on the ekg and cxr should undergo ECHO Hyponatremia (increased vasopressin levels) in addition to sodium restriction , diuretic therapy and expansion of extracellular volume. It is a negative prognostic indicator at the time of hospital admission, and predicts decreased long-term survival BNP Β NP is a 32-amino acid polypeptide secreted from the cardiac ventricles in response to ventricular volume expansion and pressure overload. The major source of BNP is the cardiac ventricles, and because of its minimal presence in storage granules, its release is directly proportional to ventricular dysfunction. It is a simple and rapid test that reliably predicts the prescience or absence
- Neurohormones-norepi,renin, endothelin
- Slide ID: 7753 The American College of Cardiology/American Heart Association (ACC/AHA) writing committee decided to take a new approach to the classification of heart failure – one that emphasized the evolution and progression of the disease. Only Stages C and D qualify for the traditional clinical diagnosis of heart failure. This classification is intended to complement, but not replace, the New York Heart Association (NYHA) Functional Classification. ACC/AHA Heart Failure Stage Stage A: patients who are at high risk for developing heart failure but have no structural disorder of the heart. Stage B: patients with structural disorders of the heart who have never had symptoms of heart failure. Stage C: patients with past or current symptoms of heart failure associated with underlying structural heart disease. Stage D: patients with end-stage disease who require specialized treatment strategies such as mechanical circulatory support, continuous IV inotrope infusions, cardiac transplantation, or hospice care. NYHA Functional Classification Assigns patients to 1 of 4 functional classes depending on the degree of effort needed to elicit symptoms. Patients with very low LV ejection fractions may be asymptomatic, whereas patients with preserved LV systolic function may have many symptoms. The apparent discordance between severity of systolic dysfunction and the degree of functional impairment is not well understood. Class I: symptoms of heart failure only at levels that would limit normal individuals (asymptomatic). Class II: symptoms of heart failure on ordinary exertion. Class III: symptoms of heart failure on less-than-ordinary exertion. Class IV: symptoms of heart failure at rest. References Hunt SA et al. J Am Coll Cardiol . 2001;38:2101-2113. Farrell MH et al. JAMA . 2002;287:290-297.
- Reduction in combined end points of death and hospitalization by heart failure (numbers needed to treat+11) over 4-5 years regarless of severity but favor more severe cases. Good tolerability with major side effects being cough, angioedema, altered taste, hyperkalemia, and dizziness Hypotension and lightheadedness are common side effects of ACE-I particularly in patients with marked activation of the RAS. Hold diuretic and then start ACE-I and titrate slowly Collaborative Group on ACE inhibitor Trials CONSENSUS Trial Study Group SOLVD Investigators
- Consensus- COOPERATIVE NORTH SCANDINAVIAN ENALAPRIL SURVIVAL STUDY pt were already taking digoxin and diuretics. Subsequent SOLVD- STUDIES OF LEFT VENTRICULAR DYSFUNCTION- Proved consensus at a earlier stage of heart failure even asymptomatic
- ARBs are comparable to ACE-I in reduction all-cause mortality and heart failure-related hospitalizations in patients with NYHA classes II and III heart failure.
- Adding an ARB to ACE-inhibitor therapy provides further mortality benfit in slected patients. In this trial of patients with NYHA classes II to IV heart failure, candesartan added to existing ACE-I therapy reduced cardiovasular death (NNT, 28 over 3.5 years) and reduced heart-failure related hospital admission. A second study found no benefit
- POTENTIAL CONCERNS REGARDING INITIATION OF β BLOCKERS BEFORE DISCHARGE The 1999 guidelines of the Heart Failure Society of America suggested that, to maximize safety, there should be a period of clinical stability while on standard therapy before instituting β blockers and that initiation in patients who have HF requires a careful baseline evaluation of clinical status. 26 Because it is based on early, large-scale trials in which patients who had chronic HF were treated with standard therapy consisting of ACE inhibitors, digoxin, and a diuretic for ≥2 months before starting β-blocker therapy, this recommendation led to many HF clinicians postponing β-blocker therapy for ≥2 to 4 weeks until stability had been achieved. This plays into the concern many practitioners have that beginning β blockade in patients who have HF will necessarily worsen HF during the titration period. In the Randomized Evaluation of Strategies for Left Ventricular Dysfunction, there was a significantly larger number of hospitalizations for worsening HF with controlled-release metoprolol than with placebo (p = 0.026). However, there was also a 54% lower risk of death with controlled-release metoprolol (p = 0.057) and a significant increase in LV ejection fraction (p = 0.001). 2 , 27 In the COPERNICUS study, there were significantly fewer patients who used carvedilol and then developed serious adverse events than those who used placebo (p <0.002). 10 This trial showed that the adverse event of utmost concern to clinicians regarding the initiation of β blockers, i.e., worsening HF, occurred less frequently with carvedilol than with placebo. 10 , 28 The COPERNICUS, in effect, indicated that the early initiation of life-saving therapies should be approached with a sense of urgency and provides a mandate for expediting the administration of β-blocker therapy in patients who have HF. After comparing initiation before and after discharge with respect to tolerability and safety in the IMPACT-HF study, it was found that there were no significant differences between groups in the occurrence of serious adverse events (bradycardia, hypotension, and worsening HF) or the occurrence of these events leading to the permanent withdrawal of the β blocker. Fewer patients developed worsening of HF before than after discharge (0.5% vs 1.7%), and there was a lower composite rate of death and rehospitalization. 25 These major trials clearly refute the common practices and perceptions regarding β-blocker therapy for HF that lead to unnecessary delays in treatment and deny patients established benefits of this therapy. Specifically, the results of these studies challenge the beliefs commonly held by many clinicians that initiation of β blockade is characterized by an unfavorable benefit/risk ratio, that survival curves do not diverge in favor of β blockers for many months, and that early initiation necessarily carries the risk of worsening HF or intolerance that leads to withdrawal of treatment. Rather, these studies clearly demonstrate the high degree of tolerability for β blockers and that there is a lower relative rate of discontinuation with β blockers than with placebo. Several β blockers, e.g., atenolol, timolol, and propranolol, have proven efficacy as secondary prevention after myocardial infarction but not as therapy for HF. Among those agents that have established efficacy in HF, e.g., carvedilol, bisoprolol, and metoprolol, there are pharmacologic differences that may alter the clinical responses to these agents in HF 24 and may have an affect on in-hospital initiation of therapy. The β-1–specific blockers may decrease cardiac output, increase vascular resistance, or decrease renal blood flow, all of which can contribute to worsening HF. 30 The β blockers with an α blockade, such as carvedilol, increase cardiac output and decrease vascular resistance. The vasodilatory activity due to α-1 blockade offsets myocardial depression due to β blockade, and the broad-based sympathetic antagonism may protect the patient against worsening HF in the early stages of initiation. 30 In the MERIT-HF trial of patients who had HF of New York Heart Association classes III and IV, a decrease in the mortality rate was observed with the use of metoprolol, a β-1–specific blocker; however, the metoprolol-treated group had a higher rate (8.1%) of withdrawal in the first 90 days than did the placebo-treated group (5.9%). 31 Data from COPERNICUS trial showed that the carvedilol-treated group had a lower rate of worsening HF (5.1%) than did the placebo group (6.4%) during the initiation phase. 25 In the IMPACT-HF study, only 0.5% of patients withdrew due to worsening HF if they had been initiated with carvedilol before discharge versus 1.7% of patients who had been initiated with a β blocker of the physician's choice after discharge. 25 Therefore, these considerations may make carvedilol a better agent for initiating β-blocker therapy in the hospital setting.
- 6 RCT’s that included more than 9,000 patients already taking ACE-I showed a significant reduction in total mortality and sudden dearth (NNT 24, and #% over 1-2 years) Carvedilol or Metoprolol European Trial 2003 In a recent trial , patient with NYHA classes II to IV heart failure who were treated with carvedilol had greater reductions in mortality (NNT, 18 over 5 years) and cardiovascular mortality (NNT, 16 over five years) than those treated with metoprolol but, hypotension was more common among the carvedilol group (14 versus 11 percent) Bisoprolol and metoprolol are b1-selective with no vasodilating properties Coreg- is alpha 1 beta 1 and beta 2 with vasoldilating properties
- Add aldactone in moderate to severe heart failure, favorable effects on LV remodeling Randomized Aldactone RALES-survival benefit of spironolactone in patient with severe heart failure and favorable effexts on LV remodeling Most common risk is hyperkalemia and 10 % of men will experinece breast pain an gynecomastia Eplerenone-newer more selective aldosterone inhibitor has been shown to reduce all-cause mortality following myocardial infraction with Left ventricular dysfunction (NNT, 43 for 16 months) Has not yet been studied in patient with CHF who have not yet had a MI
- Some studies report a decease in all cause morality of 28% and a more recent trial with enlaptirl showed no difference but over 30% dropped out due to side effects. Side effects are flushing, headaches, gi upset, less frequently can cause positive ANA titers and lupus-like syndrome
- Vasodilator combination that improves endothelial function by increasing NO levels A-HeFT (Taylor AI et al. N Engl J Med 2004;351:2049-57): 1050 African American patients with primarily NYHA Class III sx Randomized to standard therapy vs. standard therapy plus hydralazine and isosorbide dinitrate Significant decrease in morbidity and mortality with additional treatment Most frequent adverse effects: HA, dizziness
- Patients taking digoxin are less lekely to be hospitalized for worseing heart failrue (NNT, 27 to 115 over three years) and their heart failure symptoms may worsen if digoxin is withdrawn Positive inotrope with autonomic effects: increased parasympathetic tone DIG Trial (Garg R et al. N Engl J Med 1997;336:525-33.) : 6,800 pts w/ EF < 45% randomized to digoxin vs. placebo (Background tx: ACEI, diuretic) No difference in mortality between two groups 25% reduction in CV death or hospitalization for HF (p<0.001) 28% reduction in hospitalization for HF (p<0.001) Toxicity: renal dysfunction, elderly
- Help symptoms regardless of NYHA classification
- Aspirin may mitigate the beneficial effects of ACE-I
- $530/dy Decreased 30 days survival Side effect of hypotension No benefit as an outpatient basis
- Restriction of sodium-can aid in control of fluid and symptoms but no dec in morbidity or mortality Exercise-moderate exercise 2-3 hours per week improves quaility of life, decreased motality (nnt 4 for 14 months) A multidisciplinary, disease-management approach to heart failure includes intensive patient education about the condition and its treatment, dietary assessment and instruction, medication analysis, and follow-up by telephone and home visits. Usually it also includes aggressive management of comorbidities and risk factors, including control of blood glucose levels in patients with diabetes, treatment of hypertension to a target measurement of 140/90 mm Hg (130/80 mm Hg in patients with diabetes and those with chronic renal insufficiency), and lipid management to a target low-density lipoprotein level of less than 100 mg per dL (1 g per L) in high-risk patients and less than 70 mg per dL for very high-risk patients.38 This approach results in fewer hospitalizations (NNT, five for three months) and reduced cost of care.39 It also decreases the frequency of unplanned and repeat hospitalizations, and increases functional status and quality of life.40 WE do poorly at starting and keeping the correct dose of medicaion, these programs help!
- SCD (sudden cardiac death)
- Pt more mobile, less depressed and less symptomatic Use as a bridge to transplant as well REMATCH said can use it as therapy instead of just a bridge to transplant REMATCH (Rose EA et al. N Engl J Med 2001;345:1345-43) 129 patients with end-stage HF Randomized to standard therapy vs. standard therapy plus LVAD 48% decrease in mortality with LVAD