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

Frank vectorcardiograms (VCG) and clinical records of 243 patients with right bundle branch block (RBBB) were compared. The patients were classified into three categories on the basis of VCG criteria. The first category included 100 patients with a normal frontal axis, and the second category included 44 patients with concomitant left anterior hemiblock. The third category consisted of 99 patients with RBBB and myocardial infarction. The VCGs were classified into three types accoriding to the QRS configuration in the transverse plane. In type I the initial forces were anterior and counterclockwise and the afferent limb crossed the midline posterior to E point; in type II the initial forces were anterior and counterclockwise and the afferent limb crossed the midline posterior to E point; in type II the initial forces were anterior and counterclockwise and the afferent limb crossed the midline anterior to or through E point; and in type III the entire transverse loop was clockwise and anterior to E point. The patients were further classified according to the presence or absence of cardic failure or severe pulmonary disease. In patients with RBBB and a normal axis, cardiac failure or severe pulmonary disease was found in five of 49 patients wtih type I, 17 of 31 with type II, and 18 of 20 with type III pattern. In patients with RBBB and left anterior hemiblock, significant disease was found in one of 17 with type I, five of 16 with type II, and eight of 11 with type III pattern. These data show that, in patients with RBBB, the position of the afferent limb in the transverse plane can be used to predict cardiac failure or severe pulmonary disease.
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PMID:The vectorcardiogram in right bundle branch block: correlation with cardiac failure and pulmonary disease. 126 27

Congestive heart failure is a syndrome common in the United States, especially in elderly patients. The most common etiology is coronary artery disease. A number of general factors contribute to the heart failure syndrome, including loss of muscle, decreased myocardial contractility, pressure or volume overload, or restricted filling. All of these factors may play a role in a given patient as, for example, with coronary artery disease. Although systolic dysfunction with a reduced ejection fraction is the most common heart failure syndrome, up to 40% of patients may have a relatively preserved ejection fraction with diastolic dysfunction. As the heart begins to fail, a number of compensatory mechanisms are activated. These include increased heart rate, the Frank-Starling mechanism, increased catecholamines, activation of the renin-angiotensin system, and release of atrial natriuretic peptides. Although these mechanisms are initially helpful to the cardiovascular system, they frequently overshoot, initiating a vicious cycle. For example, with a decrease in cardiac output, there is a reflex increase in systemic vascular resistance in order to maintain perfusion pressure. This increase in resistance, however, acts as a load on the left ventricle and further reduces cardiac output. The best evidence for the existence of this vicious cycle is the beneficial change in hemodynamics produced by vasodilator drugs and the ACE inhibitors. Thus, an understanding of pathophysiology allows for the selection of rational therapy. An unresolved problem in heart failure patients is how best to reduce the high incidence of sudden death, which is one of the major challenges for the future.
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PMID:Pathophysiology of congestive heart failure. 139 15

This is a case report of infective endocarditis with idiopathic thrombocytopenic purpura (ITP). Open heart surgery to the patient with ITP has a problem of perioperative hemorrhage. Usually, treatment for ITP is performed before operation, and platelet transfusion is provided for hemorrhage. However, in our patient, we had to perform emergency operation because of progressive heart failure without treatment of ITP. Emergency operation should be performed without treatment of ITP, not to delay operative timing in such a case of progressive heart failure from active infective endocarditis.
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PMID:[Active infective endocarditis with idiopathic thrombocytopenic purpura: a case report]. 143 38

The functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions is discussed, based mainly on animal experiment results (in the dog, pig and rat). The dependence of individual stroke volume on end-diastolic volume can be described adequately using Frank's diagram. This can be illustrated by varying filling pressure (respiratory cycle, vascular tone in the capacitance system, body position, circulating blood volume) and by alterations in the duration of the filling period (heart rate and rhythm, rate of relaxation) and in ventricular compliance (wall thickness, fibrosis; contracture, rigor). The functional importance of the Frank-Starling mechanism lies mainly in adapting left to right ventricular output. During upright physical exercise an increase in end-diastolic volume due to the action of the peripheral muscle pump and increased venous tone can assist in enhancing stroke volume. Reduced contractility leads to a shift of the operating point to the right in the pressure-volume diagram, thus tending to prevent a decrease in stroke volume. However, the consequences of increased circulating blood volume in chronic heart failure are, as a rule, mainly detrimental (congestive symptoms; myocardial component of coronary resistance; cardiac energetics). Reduced contractility results in a flattening of the relation between stroke volume (or stroke work) and end-diastolic volume. Furthermore, the Starling mechanism is prevented from becoming effective if the sarcomere-length reserve is exhausted, or in the presence of inadequate sarcomere extension due to impaired relaxation or reduced distensibility of the ventricular wall. The latter is illustrated using the example of a dilated fibrotic left ventricle from a rat with experimental supravalvular aortic stenosis.
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PMID:Functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions. 147 14

Although the pathophysiology of exercise intolerance in patients with chronic heart failure (CHF) is not fully understood, it appears that the cardiac output response plays an important role in limiting exercise in this disorder. Although previous studies have demonstrated that peak VO2 is not related to left ventricular (LV) ejection fraction, studies have consistently identified peak exercise cardiac output as an important predictor of peak VO2. It is likely that a reduced cardiac output to work rate relationship in CHF causes hypoperfusion of both working skeletal muscle and visceral organs, which leads to early anaerobic metabolism and fatigue. Several factors may influence the cardiac output response in patients with severe systolic LV dysfunction, including heart rate, diastolic LV function, and the mitral regurgitation fraction. Although stroke volume increases through use of the Frank-Starling mechanism in many patients with severe systolic LV dysfunction, some patients with this disorder may not increase stroke volume during exercise due to diastolic LV dysfunction or pericardial constraint. The finding that this latter group has more severe exercise intolerance suggests that diastolic dysfunction may further decrease peak VO2 in this disorder. Variations in the mitral regurgitation fraction also have been found to have an important effect on exercise stroke volume in some patients with CHF. Therefore, the finding that LV ejection fraction at rest or during exercise is not related to peak VO2 in patients with systolic LV dysfunction does not necessarily indicate that central hemodynamics do not play a role in exercise intolerance. Rather, it is likely that variability in the LV ejection fraction with exercise, which does not take variable increases in LV end-diastolic volume or mitral regurgitation into account, plays only a modest role in determining the stroke volume and cardiac output response to exercise in patients with severe systolic dysfunction.
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PMID:Central hemodynamic response to exercise in patients with chronic heart failure. 157 62

Much attention has been paid to the influence of the beta-adrenoceptor system on cardiac function in heart failure. Full agonists and partial agonists acting on cardiac beta 1 receptors have been widely investigated, as has the density of these receptors in the failing heart. However, other cardiac control mechanisms may play important roles in the normal heart as well as in heart failure. The Frank-Starling mechanism of enhanced cardiac contraction produced by mechanical stretching of the ventricular myofibrils is well known. When treating patients with heart failure with diuretics, vasodilators and other drugs that influence preload, it is important to consider their overall effects in relation to the Starling curves. Atrial stretching also produces compensatory responses which are currently being intensively studied. Reflex release of atrial natriuretic factor after stimulation of atrial receptors has important physiologic effects in heart failure. The atria, but not the ventricles, are innervated by the vagus; the influence of the parasympathetic nervous system on the heart and circulation is often overlooked. The initial increase in heart rate during exercise is primarily due to withdrawal of vagal influence. Besides acetylcholine, the parasympathetic transmitter, many other local hormones may affect cardiac function; these include prostaglandins, 5-hydroxytryptamine and histamine. Although the activity of the sympathetic nervous system is mediated primarily through beta 1 adrenoceptors, both beta 2 and alpha receptors are also found in the heart. Myocardial alpha 1 receptors, which mediate a positive inotropic effect, have been identified, and prejunctional alpha 2 receptors may mediate inhibition of norepinephrine release from sympathetic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local cardiac responses--alternative methods of control. 167 88

Based on animal experiments in rats (spontaneous and renal hypertension, experimental aortic stenosis, thyroxine and training-induced hypertrophy, and aorto-caval fistula with and without additional unilateral renal artery coarctation) as well as clinical data and literature, the functional consequences of cardiac hypertrophy and structural ventricular dilatation are analyzed and discussed. A methodological approach, developed on the basis of Frank's diagram and model calculations, permits quantitatively estimating the significance of ventricular geometry (wall thickness and inner dimensions) compared to myocardial alterations (decrease in contractility and distensibility) and hemodynamic load (preload and systolic pressure). As a rule, hypertrophy causes an increase in ventricular working capacity, which allows the heart to cope with an increased hemodynamic load without a decrease in stroke volume and without enhanced systolic stress requirement. Adverse consequences mainly concern ventricular compliance, cardiac energetics, and electrophysiological parameters. Particularly from the example of the aorto-caval fistula, it can be seen that enhanced systolic wall stress does not necessarily lead to heart failure within a few months. However, the length of time for which the additional wall stress, with correspondingly increased energy demand, can be tolerated remains to be determined. In later stages, a multitude of alterations on the cellular, tissue, and organ level occurs, affecting myocardial and ventricular mechanics and energetics, depending on the type, velocity of development, and duration of overload. A distinction should be made between the adverse alterations, which can be related to myocardial growth, and those that are not necessarily related to a certain cell size (receptors, transformation of the contractile proteins) as well as those changes that do not primarily influence the myocardial cell (arteriosclerosis, microangiopathy). Structural dilatation alone could lead to insufficiency only in the case of substantial increase in inner ventricular radius. Reduced contractility, myocardial distensibility, and increased pressure load aggravate the negative effects of dilatation in a predictable manner, as demonstrated on the basis of a representative case of dilative cardiomyopathy. Using the example of spontaneously hypertensive rats, it is shown that ventricular mass and shape are differently influenced by various blood-pressure lowering agents, e.g., atenolol, nifedipine, and dietary interventions. It is concluded from the analysis of chronic cardiac reactions that adaptive processes are, in principle, ambiguous in character, revealing negative components even in the case of regular adaptation. However, it seems unjustified to aim at a regression of hypertrophy without reducing the underlying hemodynamic overload.
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PMID:Functional consequences of cardiac hypertrophy and dilatation. 182 78

Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.
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PMID:Compensatory mechanisms for cardiac dysfunction in myocardial infarction. 183 46

Successive treatment of syndromes of circulatory disorders on the basis of complex evaluation of central hemodynamics was conducted in 73 patients with severe closed chest trauma. Reinfusion reduced the requirements for donor blood by 28%. The volume of the infusion-transfusion therapy was regulated according to the ventricular filling pressure and the Frank-Starling curves. The optimal level of pulmonary capillary pressure blocking was 12-20 mm Hg in patients with cardiac insufficiency and 8-12 mm Hg in the other patients. Spasmolytics, saluretics, and droperidol were prescribed and fluid intake was limited in pulmonary circulation hypertension. Cardiac glycosides, calcium preparations, antiarrhythmic agents, and diuretics were given in cardiac insufficiency.
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PMID:[Principles of the correction of central hemodynamic disorders in severe combined thoracic trauma]. 201 66

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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