UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in vasomotor tone in cardiac failure are related to the severity of the cardiac failure. The causative factors include dysfunction of the baroreceptor reflex, abnormal stimulation of the normal physiological regulators of cardio-circulatory function such as the sympathetic nervous and the renin-angiotensin-aldosterone system, and certain local factors characteristic of cardiac failure such as salt and water retention at vascular wall and interstitial level or changes in the metabolism of certain tissues. These changes are variable according to the region perfused and their interaction results in preferential redistribution of blood flow to the coronary and cerebral circulations at the expense of other regions such as the splanchnic and cutaneous vessels. In addition, they play a key role in the adaptive peripheral mechanisms to left ventricular failure and to the modulation of the vascular effects of drug therapy. An improvement in our understanding of these mechanisms and their consequences is important from the physiopathological, prognostic and therapeutic points of view.
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PMID:[Mechanisms and consequences of changes of the vasomotor activity in cardiac insufficiency]. 205 35

It is not completely clear if the renal sympathetic nerves are essential for normal renal function, however, it has been reasonably well established that the renal nerves can influence renal function under experimental conditions. These influences are manifested as changes in sodium excretion, urine flow, renin release, renal blood flow and glomerular filtration rate. Under conditions of stress the renal nerves can have powerful influences on renal function and, as a result, on systemic hemodynamics. Because renal sympathetic outflow is under central control, the reflex modulation of renal nerve activity is an extremely important factor in the control of salt and water balance. We have shown that cardiac and arterial baroreflex control of renal nerve activity is abnormal in chronic congestive heart failure. The mechanisms for this abnormality can reside in any arm of the reflex arc. The evidence from this and other laboratories has clearly implicated the afferent limb of these reflexes as being abnormal. Experiments done in anesthetized dogs with pacing induced heart failure have indicated that the central component of these reflexes are probably normal. The experiments described above cannot differentiate between abnormal afferent mechanisms and abnormal end organ responses to renal nerve stimulation. Several humoral mechanisms may be operative in heart failure to modulate renal nerve activity. These include bradykinin, prostaglandins and the renin-angiotensin aldosterone axis. Future work should be directed towards a further understanding of the role played by these and other humoral factors in the control of renal sympathetic outflow in heart failure.
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PMID:Reflex control of renal sympathetic nervous activity in heart failure. 206 56

The evolution of our understanding of the pathogenesis and therapy of heart failure can be described in terms of three paradigms that have also proven useful in describing the development of knowledge of cardiovascular regulation and the actions of angiotensin II. Organ physiology, the first paradigm, viewed the variable performance of the heart in terms of length-dependent changes in myocardial contractile function (Starling's Law), and angiotensin II as a pressor factor that elevated blood pressure. This paradigm focused treatment of heart failure on the major circulatory abnormalities: salt and water retention and vasoconstriction. According to the second paradigm, cell biochemistry, regulation of cardiac performance reflected altered calcium fluxes and changing myocardial contractility, and the clinical effects of angiotensin II as arising from altered calcium fluxes involved in the control of smooth muscle tension. Following this second paradigm, treatment of heart failure focused on powerful inotropic agents designed to increase myocardial contractility. The third paradigm, gene expression (molecular biology) describes what is probably the most primitive, and almost certainly the most complex of these regulatory mechanisms. Altered gene expression explains long-term regulation of cardiac performance in terms of adaptive changes in the architecture and composition of the heart, and key effects of angiotensin II as arising from increased protein synthesis and promotion of cell growth. In the case of heart failure, this third paradigm may explain the accelerated deterioration of the hypertrophied, failing heart as being due to altered myocardial cell growth composition. While the useful life of the normal human heart appears to be at least 80-90 years, overload-induced hypertrophy may reduce the heart's life span to about 5 years. This unwelcome consequence of myocardial hypertrophy may arise from the expression of fetal isoforms of key muscle proteins, a hypothesis that is supported by evidence that deterioration of the failing heart can be alleviated by the converting enzyme inhibitors which have important effects to inhibit cellular growth.
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PMID:Is heart failure an abnormality of myocardial cell growth? 207 54

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. In recent years, the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in man, it has been found that the nonosmotic release of vasopressin is consistently associated with the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and in the activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context, neither total extracellular-fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade, or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae, and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV). initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.
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PMID:[General physiopathology of chronic left ventricular insufficiency]. 214 35

The cardiovascular reflexes have the key role in the rapid adjustments of the circulatory system in response to daily stresses such as standing and muscular exercise. Arterial and cardiopulmonary mechanoreceptors continuously signal to the cardiovascular centers in the brain the moment to moment pressure changes in the larger arteries, atria and ventricles and exert a tonic restraint on the sympathetic noradrenergic outflow. Depending on the stress, the vasomotor centers adjust this outflow, both qualitatively and quantitatively, to the heart and to the different vascular beds to maintain an appropriate arterial blood pressure. In addition, the sympathetic nerves modulate renin release from the juxtaglomerular cells and receptors at the veno-atrial junctions regulate vasopressin release from the posterior pituitary. Congestive heart failure is characterized by excessive neuro-humoral excitation as evidenced by direct recordings of sympathetic activity and by increased plasma levels of catecholamines, renin, angiotensin II and arginine vasopressin. The evidence indicates that this is a consequence of the reduced ability of the arterial and cardiopulmonary mechanoreceptors to inhibit the vasomotor centers. The cause(s) of this diminished circulatory control requires further studies. The cardiac glycosides, which normally cause vasoconstriction, cause vasodilatation in patients with heart failure. This is attributed to sensitization of the mechanoreceptors. The term atrial natriuretic factor refers to a family of peptide hormones released when the atrial myocytes are stimulated by an increase in transmural pressure. They cause diuresis, natriuresis and vasorelaxation. In severe congestive heart failure, the plasma levels are increased and this helps to compensate for the increased neurohumoral activation by inhibiting the renin-angiotensin system and enhancing sodium and water excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart failure: role of cardiovascular reflexes. 215 12

Many of the electrolyte derangements seen in chronic heart failure are related to activation of the renin-angiotensin system. Activation of the system may cause the retention of both sodium and water; the former is primarily related to the release of aldosterone and the latter is related to an angiotensin-mediated increase in thirst and decrease in the excretion of free water. The interaction of these mechanisms may explain why patients with chronic heart failure have higher values for total body sodium but lower values for serum sodium concentration than hypertensive patients or normal subjects. Activation of the renin-angiotensin system may also cause potassium depletion, which is manifest clinically by a decrease in both total body potassium and serum potassium concentration. These electrolyte disturbances may play a role in the development of ventricular arrhythmias. The renin-angiotensin system may also contribute to the development of magnesium deficits. These hormone-electrolyte interactions have important implications in the treatment of patients with heart failure, especially those in whom the renin-angiotensin system is pharmacologically inhibited.
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PMID:Interrelation of electrolytes and renin-angiotensin system in congestive heart failure. 217 75

The syndrome of heart failure results from inappropriate sodium and water retention by the kidneys which results, at least in part, from changes in renal haemodynamics. Renal blood flow at rest in heart failure is reduced in proportion to the reduction in cardiac output and falls dramatically during exercise as the cardiac output is redistributed to the exercising muscles. Both these phenomena are associated with a rise in plasma noradrenaline concentration. Afferent arteriolar tone is partly controlled by alpha-adrenoceptor stimulation while stimulation of beta 2-receptors will stimulate renal release of renin; through the elaboration of angiotensin II, profound effects on extra- and intra-renal vascular tone can occur. Although alpha-adrenoceptor stimulation can result in coronary vasoconstriction and a fall in coronary blood flow in patients with heart failure due to underlying atheromatous coronary heart disease, increased myocardial oxygen demand as the result of beta 1 (and cardiac beta 2) simulation may be more relevant. The control of limb blood flow is of great importance symptomatically. The systemic vasoconstriction that typifies the severe heart failure state has been a target for many vasodilatory interventions including alpha 1-receptor blockade and beta 2-receptor stimulation. Unfortunately, there is little evidence that such treatment leads to any specific increase in muscle blood flow either at rest or during exercise. In severe heart failure, sympathetic activity is increased at rest leading to vasoconstriction in several vascular beds, while in milder heart failure, excessive sympathetic stimulation is evident only during exercise. In either circumstance, however, it is evident that certain advantages may accrue from modulation of this excessive sympathetic activity.
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PMID:Sympathetic activity and regional blood flow in heart failure. 218 37

Treatment for patients with congestive heart failure is primarily directed at reducing symptoms and improving functional capacity. In patients with moderate to severe heart failure, therapeutic interventions incorporating diuretics, digoxin and selected vasodilators, specifically angiotensin-converting enzyme (ACE) inhibitors, are designed to correct pathophysiological mechanisms such as left ventricular dysfunction, excessive vasoconstriction and renal reabsorption of sodium and water. Physician-investigators are turning their attention to identifying and treating patients early in the course of their disease. Vasodilator therapy in patients with mild symptoms of heart failure may not only improve exercise performance, but also reduce mortality. In addition, recent studies have suggested that ACE inhibitors may prevent progression of disease in patients with asymptomatic left ventricular dysfunction. It is hoped that ongoing research will demonstrate that early identification and treatment of these patients may prevent development of symptoms and improve survival.
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PMID:Early intervention in heart failure. 219 53

Ventricular dysfunction due to an abnormality of the heart which is associated with typical hemodynamic, renal and hormonal reactions, characterizes the clinical syndrome heart failure. The traditional definition of heart failure as the inability to pump an amount of blood sufficient to cover the metabolic needs of the body in the presence of adequate venous return, emphasizes mainly the reduction in cardiac output but not the increase in intracardiac pressures. Pressure or volume overload, decreased contractility, loss of muscle mass or restricted filling represent the most important pathological processes leading to heart failure. The disturbance of systolic ventricular function due to pressure or volume overload or diminished contractility is characterized by a decrease in the ejection fraction, the disturbance in diastolic ventricular function associated with restricted filling is characterized by elevated chamber stiffness. Decreased contractility is most commonly responsible for the development of heart failure. Impairment of diastolic ventricular function can only be regarded as the dominant mechanism leading to heart failure in the presence of a small noncompliant ventricle. Impairment of diastolic ventricular function in an enlarged heart is always associated with an impairment of systolic ventricular function and is, then, relegated to a subordinate role. Common causes of heart failure are coronary artery disease, hypertension, cardiomyopathies, valvular heart diseases and congenital heart diseases, for the incidence of which coronary artery disease is most frequently responsible. Most of these diseases lead to heart failure not via a single, but rather several of the specified pathophysiological processes. Possible mechanisms for loss of contractility include structural changes as well as alterations in excitation-contraction coupling. Possible mechanisms responsible for impaired diastolic ventricular function encompass, in addition to altered calcium flux, structural changes such as fibrosis and hypertrophy and factors such as asynchrony and abnormal loading conditions. With increasing derangement of cardiac function, there is recruitment of the compensatory mechanisms: hypertrophy of the cardiac muscle, Frank-Starling mechanism, activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system and the arginine-vasopressin system. The goal is maintenance of adequate blood pressure and cardiac output whereby blood flow is redistributed in favor of the heart and brain and away from the skin, musculature and visceral organs. Activation of the neurohumoral system can lead to excessive vasoconstriction as well as sodium and water retention resulting in an undesired elevation of preload and afterload which, in turn, leads to further worsening of the heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiologic and diagnostic aspects of heart failure]. 219 15

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