Heart Failure - Referat.docx

Heart Failure

1. Definition HF is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Acute Heart Failure can be defined as the new onset or recurrence of symtomps and signs of heart failure requiring urgent or emergent therapy and resulting in seeking unscheduled care or hospitalization. There is no widely accepted nomenclature for HF syndromes requiring hospitalization. Patients are described as having “acute HF,” “acute HF syndromes,” or “acute(ly) decompensated HF”; while the third has gained greatest acceptance, it too has limitations, for it does not make the important distinction between those with a de novo presentation of HF from those with worsening of previously chronic stable HF. Because some patients present without signs or symptoms of volume overload, the term “heart failure” is preferred over “congestive heart failure”. Most patients with HF have symptoms due to impaired left ventricular myocardial function. It should be emphasized that HF is not synonymus with either cardiomyopathy or LV dysfunction; these latter terms describe possible structural or functional reasons for the development of HF; HF may be associated with a wide spectrum of LV functional abnormalities, which may range from patients with normal LV size and preserved EF to those with severe dilatation and/or markedly reduced EF. EF is considered important

in classification of patients with HF because of differing patient demographics, comorbid conditions, prognosis, and response to therapies and because most clinical trials selected patients based on EF, it is preferable to use the terms preserved or reduced EF over preserved (HFpEF) or reduced systolic function (HFrEF). a. HF with Reduced EF (HFrEF) HFrEF is defined as the clinical diagnosis of HF and EF ≤40%. In approximately half of patients with HFrEF, variable degrees of LV enlargement may accompany HFrEF. Those with LV systolic dysfunction commonly have elements of diastolic dysfunction as well. b. HF with Preserved EF (HFpEF) Because some of these patients do not have entirely normal EF but also do not have major reduction in systolic function, the term preserved EF has been used. Patients with an EF in the range of 40% to 50% represent an intermediate group. In the general population, patients with HFpEF are usually older women with a history of hypertension. Obesity, CAD, diabetes mellitus, atrial fibrillation (AF), and hyperlipidemia are also highly prevalent in HFpEF in populationbased studies and registries. Despite these associated cardiovascular risk factors, hypertension remains the most important cause of HFpEF, with a prevalence of 60% to 89% from large controlled trials, epidemiological studies, and HF registries.

2. Classification The ACCF/AHA stages of HF emphasize the development and progression of disease and can be used to describe individuals and populations, whereas the NYHA classes focus on exercise capacity and the symptomatic status of the disease. 3. Epidemiology The lifetime risk of developing HF is 20% for Americans ≥40 years of age. HF incidence increases with age, rising from approximately 20 per 1000 individuals 65 to 69 years of age to >80 per 1000 individuals among those ≥85 years of age. Although survival has improved, the absolute mortality rates for HF remain approximately 50% within 5 years of diagnosis. In the ARIC (Atherosclerosis Risk in Communities) study, the 30-day, 1-year, and 5-year case fatality rates after hospitalization for HF were 10.4%, 22%, and 42.3%, respectively. 4. Patophysiology Heart failure may be viewed as a progressive disorder that is initiated after an index event either damages the heart muscle, with a resultant loss of functioning cardiac myocytes or,

alternatively, disrupts the ability of the myocardium to generate force, thereby preventing the heart from contracting normally. This index event may have an abrupt onset, as in the case of a myocardial infarction; it may have a gradual or insidious onset, as in the case of hemodynamic pressure or volume overloading. Regardless of the nature of the inciting event, the feature that is common to each of these index events is that they all, in some manner, produce a decline in pumping capacity of the heart. In most instances, patients will remain asymptomatic or minimally symptomatic after the initial decline in pumping capacity of the heart, or symptoms develop only after the dysfunction has been present for some time. Although the precise reasons why patients with LV dysfunction remain asymptomatic have not been established with certainty, one potential explanation is that a number of compensatory mechanisms that become activated in the setting of cardiac injury or depressed cardiac output appear to modulate LV function within a physiologic/homeostatic range.

With progression to symptomatic heart failure, however, the sustained activation of neurohormonal and cytokine systems leads to a series of end-organ changes within the myocardium referred to collectively as LV remodeling. As discussed further on, LV remodeling is sufficient to lead to disease progression in heart failure independent of the neurohormonal status of the patient. a. Sympathetic Nervous System The decrease in cardiac output in heart failure activates a series of compensatory adaptations that are intended to maintain cardiovascular homeostasis. One of the most important adaptations is activation of the sympathetic (adrenergic) nervous system, which occurs early in the course of heart failure. Healthy persons display low sympathetic discharge at rest and have a high heart rate variability. In patients with heart failure, however, inhibitory input from baroreceptors and mechanoreceptors decreases and excitatory input increases, with the net result of a generalized increase in sympathetic nerve traffic and blunted parasympathetic nerve traffic, leading to loss of heart rate variability and increased peripheral vascular resistance. Moreover, increasing evidence suggests that apart from the deleterious effects of sympathetic activation, parasympathetic withdrawal also may contribute to the pathogenesis of heart failure. Withdrawal of parasympathetic nerve stimulation has been associated with decreased nitric oxide (NO)

levels, increased inflammation, increased sympathetic activity and worsening LV remodeling. b. Renin-Angiotensin System In contrast with the sympathetic nervous system, the components of the RAS are activated comparatively later in heart failure. The presumptive mechanisms for RAS activation in heart failure include renal hypoperfusion, decreased filtered sodium reaching the macula densa in the distal tubule, and increased sympathetic stimulation of the kidney, leading to increased renin release from jutaglomerular apparatus. Angiotensin II has several important actions that are critical to maintaining short-term circulatory homeostasis. The sustained expression of angiotensin II is maladaptive, however, leading to fibrosis of the heart, kidneys, and other organs. Angiotensin II can also lead to worsening neurohormonal activation by enhancing the release of NE from sympathetic nerve endings, as well as stimulating the zona glomerulosa of the adrenal cortex to produce aldosterone. Analogous to angiotensin II, aldosterone provides shortterm support to the circulation by promoting the reabsorption of sodium in exchange for potassium, in the distal segments of the nephron. However, the sustained expression of aldosterone may exert harmful effects by provoking hypertrophy and fibrosis within the vasculature and the myocardium, contributing to reduced vascular compliance and increased ventricular stiffness.

5. LV Remodeling Although neurohormonal antagonists stabilize and in some cases reverse certain aspects of the disease process in heart failure, in the overwhelming majority of patients, it will progress, albeit at a slower rate. It has been suggested that the process of LV remodeling is directly related to future deterioration in LV performance and a less favorable clinical course in patients with heart failure. The process of LV remodeling also has an important impact on the biology of the cardiac myocyte, on changes in the volume of myocyte and nonmyocyte components of the myocardium, and on the geometry and architecture of the LV chamber. Two basic patterns of cardiac hypertrophy occur in response to hemodyamic overload. In pressure overload hypertrophy (e.g., with aortic stenosis or hypertension), the increase in systolic wall leads to the addition of sarcomeres in parallel, an increase in myocyte cross-sectional area, and increased LV wall thickening. This pattern of remodeling has been referred to as “concentric” hypertrophy. By contrast, in volume overload hypertrophy (e.g., with aortic and mitral regurgitation), increased diastolic wall stress leads an increase in myocyte length with the addition of sarcomeres in series, thereby engendering increased LV ventricular dilation). This pattern of remodeling has been referred to as “eccentric” hypertrophy. Patients with heart failure classically present with a dilated left ventricle

with or without LV wall thinning. The myocytes from these failing ventricles have an elongated appearance that is characteristic of myocytes obtained from hearts subjected to chronic volume overload. 6. Symptoms Worsening dyspnea is a cardinal symptom of HF and typically is related to increases in cardiac filling pressures but also may represent restricted cardiac output.3 The absence of worsening dyspnea, however, does not necessarily exclude the diagnosis of HF, because patients may accommodate symptoms by substantially modifying their lifestyle. Patients may sleep with the head elevated to relieve dyspnea while recumbent (orthopnea); additionally, dyspnea may occur specifically in recumbency on the left side (trepopnea). Paroxysmal nocturnal dyspnea, shortness of breath developing in recumbency, is one of the most highly reliable indicators of HF. These symptoms all typically reflect pulmonary congestion, whereas a history of weight gain, increasing abdominal girth, early satiety, and the onset of edema in dependent organs (extremities or scrotum) indicate right heart congestion; nonspecific, right upper quadrant pain due to congestion of the liver is common in those with significant right-sided HF and may be incorrectly attributed to other conditions. The presence of hypertension, coronary artery disease and/or diabetes is particularly helpful since these conditions account for approximately 90% of the population attributable risk for HF in the United

States. Although most disorders causing HF are cardiac, it is worth remembering that some systemic illnesses (e.g., anemia, hyperthyroidism) can cause this syndrome without direct cardiac involvement.

determine heart size and quality of the point of maximal impulse. In cases of severe HF, a palpable third heard sound may be present.

7. Physical Findings No physical finding in HF is absolutely pathognomonic for HFpEF versus HFrEF. An evaluation for the presence and severity of HF should include consideration of the patient’s general appearance, measurement of vital signs in the seated and standing positions, examination of the heart and pulses, and assessment of other organs for evidence of congestion or hypoperfusion or indications of comorbid conditions. The details of inspection and palpation of the heart are discussed in Chapter 11. By observing or palpating the apical impulse, the examiner can rapidly

Cardiac auscultation (Chapter 11) is a crucial part of HF evaluation. The presence of a third heart sound is a crucially important finding and suggests increased ventricular filling volume; although difficult to identify, a third heart sound is highly specific for HF and carries a substantial prognostic meaning. A fourth heart side usually indicates ventricular stiffening. A key objective of the examination in patients with HF is to detect and quantify the presence of volume retention, with or without pulmonary and/or systemic congestion. The most definitive method for assessing a patient’s volume status by physical examination is by the measurement of jugular venous pressure (JVP), which is discussed in detail in Chapter 11. An elevated JVP has good sensitivity (70%) and specificity (79%) for elevated left-sided filling pressure. Although pulmonary congestion is exceedingly common in HF, physical findings indicating its presence are variable, and many are nonspecific.

Leakage of fluid from pulmonary capillaries into the alveoli can be manifested as rales or rhonchi, and wheezing may occur with reactive bronchoconstriction. Pulmonary rales due to HF usually are fine in nature and extend from the base upwards, whereas those due to other causes (e.g., pulmonary fibrosis) tend to be coarser.

Sinus tachycardia secondary to sympathetic nervous system activation is seen with advanced HF or during episodes of acute decompensation. The presence of increased QRS voltage may suggest left ventricular hypertrophy. Low QRS voltage suggests the presence of an infiltrative disease or pericardial effusion.

Lower-extremity edema is a common finding in volume-overloaded patients with HF but may commonly be the result of venous insufficiency (particularly after saphenous veins have been harvested for coronary artery bypass grafts) or as a side effect of medications (e.g., calcium channel blockers).

The presence of Q waves suggests that HF may be due to ischemic heart disease; new or reversible ST changes identify acute coronary ischemia, which may be present even when chest pain is absent. Indeed, because acute coronary ischemia is a leading cause of acutely decompensated HF, a 12-lead ECG should be immediately obtained in this setting, in order to exclude acute MI.

Assessment for systemic congestion, taken together with evaluation for reduced cardiac output, may be useful to separate patients with HF (Fig. 23-2) into “dry/warm” (uncongested with normal perfusion), “wet/warm” (congested with normal perfusion, the most common combination found in decompensated HF), “dry/cold” (uncongested but hypoperfused), and “wet/cold” (cardiogenic shock) categories. 8. Evaluation a. Chest Radiography The classic chest radiograph appearance in patients with pulmonary edema is a “butterfly” pattern of interstitial and alveolar opacities bilaterally fanning out to the periphery of the lungs. Pleural effusions and/or fluid in the right minor fissure also be seen. b. Electrocardiogram

c. Natriuretic Peptide Assays for BNP (B-type natriuretic peptide) and NT-proBNP (N-terminal pro-B-type natriuretic peptide), which are both natriuretic peptide biomarkers, have been used increasingly to establish the presence and severity of HF. In general, both natriuretic peptide biomarker values track similarly, and either can be used in patient care settings as long as their respective absolute values and cutpoints are not used interchangeably. d. Echocardiography Transthoracic echocardiography is an important part of the evaluation of HF, can be performed without risk to the patient, does not involve radiation exposure, and can be performed at the bedside if necessary. It is particularly well suited for evaluating the structure

and function of both the myocardium and heart valves and providing information about intracardiac pressures and flows. 9. Treatment a. Stage A: Recommendation Recognition and treatment of elevated blood pressure, which is a majorr risk factor for the development of both HfrEF and HfpEF. Treatment of dyslipidemia and vascular risk with know arterosclerotic disease are likely to develop HF. Obesity and Diabetes mellitus have been repeatedly linked to an increase risk of HF. b. Stage B: Recommendation In general, all recommendations for patients with stage A HF also apply to those with stage B HF, particularly with respect to control of blood pressure in the patient with LV hypertrophy and the optimization of lipids with statins. CAD is a major risk factor for the development of HF and a key target for prevention of HF. The 5year risk of developing HF after acute MI is 7% and 12% for men and women, respectively; for men and women between the ages of 40 and 69 and those >70 years of age, the risk is 22% and 25%, respectively. Current evidence supports the use of ACE inhibitors and (to a lower level of evidence) beta-blocker therapy to impede maladaptive LV remodeling in patients with stage B HF and low LVEF to improve mortality and morbidity. ARBs are reasonable alternatives to ACE inhibitors. Elevations in both systolic and diastolic blood pressure are major risk

factors for developing LV hypertrophy, another form of stage B. Although the magnitude of benefit varies with the trial selection criteria, target blood pressure reduction, and HF criteria, effective hypertension treatment invariably reduces HF events. Nevertheless, neither ACE inhibitors nor beta blockers as single therapies are superior to other antihypertensive drug classes, including calcium channel blockers, in the reduction of all cardiovascular outcomes. However, in patients with type 2 diabetes mellitus, ACE inhibitors and ARBs significantly reduced the incidence of HF in patients Diuretic-based antihypertensive therapy has been shown to prevent HF in a wide range of target populations. In refractory hypertensive patients, spironolactone (25 mg) should be considered as an additional agent.

c. Stage C: Recommendation