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

In 30 patients operated on under extracorporeal circulation the acid-base, oxygen and electrolytes balance parameters were studied in order to evaluate their potentials as additional diagnostic tests for various clinical forms of acute circulatory disorders in the early post-operative period. Cardiac insufficiency is predominantly characterized by a reduced oxygen saturation of mixed venous blood, an increased oxygen arterio-venous gradient and "lactate excess", hypokalemia and hypernatremia in plasma and erythrocytes. Metabolic and gas parameters of acid-base balance cannot be used for the diagnosis of postoperative cardiac insufficiency. In cases of hypovolemia the changes of the laboratory tests data are determined by the compensatory capacities of the human body in response to circulating blood volume deficit.
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PMID:[Evaluation of the indicators of acid-base equilibrium, oxygen and electrolyte blood levels for early diagnosis of hemodynamic disorders after heart surgery]. 30 21

Glomerular filtration rate and renal plasma flow may be normal, reduced or increased in cirrhosis. The mechanism of departures from normal is not known. Other renal functional changes in cirrhosis include avid sodium reabsorption, impaired concentrating and diluting abilities, and partial renal tubular acidosis. Fluid and electrolyte disorders are common. Sodium retention with edema and ascites should generally be treated conservatively because they tend to disappear as the liver heals and because forced diuresis has hazards. The indications for diuretics are (1) incipient or overt atelectasis; (2) abdominal distress; and (3) possibility of skin breakdown. Hyponatremia is common and its mechanism and treatment must be assessed in each patient. Hypokalemia occurs and requires treatment. Respiratory alkalosis and renal tubular acidosis seldom need therapy. The hepatorenal syndrome is defined as functional renal failure in the absence of other known causes of renal functional impairment. The prognosis is terrible and therapy is unsatisfactory. The best approach is not to equate the occurrence of renal failure in cirrhosis with the hepatorenal syndrome. Rather the physician should first explore all treatable causes of renal failure, eg, dehydration, obstruction, infection, heart failure, potassium depletion, and others.
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PMID:Fluid and electrolyte disturbances in cirrhosis. 96 15

Sixty-three patients (aged from 4 to 75 years) who had suffered severe head injury or cerebrovascular disease were placed on barbiturate regimens in which intravenous administration was given in amounts of 1-4 mg/kg/hr. Dobutamine and dopamine were also administered to prevent cardiac failure and renal failure. Immediate and delayed complications caused by barbiturate therapy were investigated and analyzed. Immediate complications included tachycardia which was seen in 16 cases (25%), and hypotension in 14 cases (22%), respectively. Higher incidence of those complications was noted among the patients who underwent surgery. Delayed complications included hypokalemia (41 cases, 65%), liver dysfunction hypernatremia (24 cases, 38%), infection (21 cases, 33%), cardiac failure (8 cases, 13%) and renal failure (1 case, 2%), respectively. Therefore, in patients treated under barbiturate regimens great care should be taken in order to avoid above mentioned complications.
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PMID:[Problems in general management during barbiturate therapy]. 148 90

Plasma atrial natriuretic peptide levels are increased in heart failure. In rats with experimental heart failure, the elevation in plasma atrial natriuretic peptide bore a close relationship to the size of the myocardial infarct and the degree of ventricular dysfunction. Sodium retention, assessed by changes in exchangeable body sodium, could not be demonstrated in this model of cardiac dysfunction. Even rats receiving a low-sodium diet had increased plasma atrial natriuretic peptide levels following coronary artery ligation despite a significant decrease in exchangeable body sodium. This establishes that the elevated plasma atrial natriuretic peptide levels found in heart failure are a consequence of ventricular dysfunction and increased intracardiac pressures rather than a reflection of the salt and water status. Alternatively, the elevated plasma atrial natriuretic peptide may limit salt and water retention in this model. In these animals with high circulating atrial natriuretic peptide levels, "down-regulation" of renal atrial natriuretic peptide receptors could be demonstrated. This decrease in renal atrial natriuretic peptide receptor numbers may, in part, explain the blunted response to infused atrial natriuretic peptide in heart failure. However, changes in renal atrial natriuretic peptide receptors alone would appear to be insufficient to lead to salt and water retention without the activation of other sodium-retaining mechanisms that occur with the progression of cardiac failure. Nevertheless, this down-regulation of renal atrial natriuretic peptide may then contribute to the salt and water retention that occurs in congestive biventricular heart failure. The close relationship between increases in atrial natriuretic peptide and ventricular dysfunction rather than sodium balance suggests that atrial natriuretic peptide's primary role in the circulation may be to produce venodilation and increase capillary permeability. This may act rapidly to reduce cardiac preload and prevent pulmonary congestion. Vasodilation and natriuresis may then become supplementary actions to maintain cardiac output and remove the excess fluid.
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PMID:Regulation of cardiac preload by atrial natriuretic peptide in congestive cardiac failure. 285 Dec 66

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
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PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

Sodium retention frequently occurs in the critically ill patient. Sodium retention states include cardiac failure, liver failure, nephrotic syndrome, and hypoalbuminemic states. A clear understanding of the pathophysiology and the mechanism of sodium retention are essential for the proper care of these patients.
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PMID:Disordered sodium metabolism: sodium retention states. 333 24

One hundred fourteen patients with ruptured cerebral aneurysms were reviewed in regard to the incidence and etiological factors of preoperative disturbances of water and electrolyte metabolism. Patients with inadequate salt intake, evidence of renal disease, cardiac failure or excessive diuretic therapy were excluded. Twenty-five (21.9%) patients developed water and electrolyte disturbances. Hyponatremia (less than 130 mEq/l) occurred in 18 (15.8%) of 114 patients. The majority of those patients with hyponatremia showed laboratory findings and/or clinical features suggesting the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The mean interval between the last subarachnoid hemorrhage (SAH) and the development of hyponatremia was 13.5 days (range 6 to 26 days). No patients developed hypernatremia (more than 155 mEq/l). Preoperative diabetes insipidus (DI) occurred in 7 (6.1%) of 114 patients. The mean interval between the last SAH and the onset of DI was 26.5 days (range 15 to 35 days). When compared with the onset of hyponatremia following SAH, the development of DI was significantly delayed. The present study showed that the following five types of patients significantly related to the development of preoperative water and electrolyte disturbances after SAH due to cerebral aneurysms. The patients with ruptured aneurysms of anterior communicating, anterior cerebral artery or internal carotid artery. The patients in grade III, IV according to Hunt & Hess. The patients with high density in the basal subarachnoid space on the CT scan. The patients with a small hematoma in the region of the basal frontal interhemispheric fissure in cases with aneurysms of the anterior communicating or anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Etiology of water and electrolyte metabolism imbalance following the rupture of cerebral aneurysms--with special reference to preoperative condition]. 646 63

Chronic heart failure is a complex clinical syndrome characterized by many neuroendocrine manifestations by which the organism responds to the reduced cardiac output--the reduced minute volume. In order to ensure the blood flow to vitally important organs in several regions of the circulation vasoconstriction occurs. The plasma noradrenaline (NA) level rises and this correlates with the stage of chronic heart failure. In chronic heart failure the renin production in the kidney and vascular wall rises and thus also the angiotensin II (AG II) formation is increased. AG II is an affective direct arterial constrictor which facilitates NA release from terminal nerve endings and stimulates aldosterone secretion. AG II conditions also myocardial hypertrophy. Arginine vasopressin (AVP) is usually also elevated in chronic heart failure. In vasoconstriction associated with chronic heart failure participates also endothelin, an effective vasoconstrictor substance which modulates the renin-angiotensin-aldosterone system and has also an antinatriuretic effect. As a compensating response to the increased formation of vasoconstrictor substance during chronic heart failure endogenous vasodilatating and natriuretic substances are formed. Another vasodilatating factor is the atrial natriuretic factor (ANF) which is secreted by atrial myocytes as a result of atrial distension, hypernatremia or tachycardia. ANF inhibits renin, aldosterone and AVP formation. The ANF level correlates closely with the grade of chronic heart failure. With advancing heart failure also down regulation of receptors for ANF occurs. Dopamine, a natural precursor of NA, is also a vasodilatating substance and is secreted during stimulation of the sympathetic nerve. In chronic heart failure the formation of vasoconstrictor substances predominates above vasodilating ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuroendocrine changes in chronic heart failure]. 809 65

The onset and the mechanisms leading to Na+ retention in incipient congestive heart failure (CHF) have not been systematically investigated. To investigate renal Na+ handling in the early or mild stages of CHF, Na+ balance and renal clearances were assessed in 10 asymptomatic patients with idiopathic or ischemic dilated cardiomyopathy and mild heart failure (HF) off treatment (left ventricular ejection fraction, 29.7+/-2%) and in 10 matched normal subjects during a diet containing 100 mmol/d of NaCl and after 8 days of high salt intake (250 mmol/d). Six patients were studied again after 6 weeks of treatment with enalapril (5 mg/d P.O.). At the end of the high salt diet, in patients with mild HF the cumulative Na+ balance exceeded by 110 mmol that of normal subjects (F=3.86, P<.001). During high salt intake, renal plasma flow and glomerular filtration rate were similarly increased in both normal subjects and mild HF patients. In spite of comparable increases of filtered Na+ in the two groups, fractional excretion of Na+, fractional clearance of free water, and fractional excretion of K+ (indexes of distal delivery of Na+) increased in normal subjects and were reduced in patients with mild HF. During enalapril treatment, in the mild HF patients the cumulative Na+ balance was restored to normal; furthermore, enalapril significantly attenuated the abnormalities in the distal delivery of Na+. Our results indicate that a defective adaptation of Na+ reabsorption in the proximal nephron is associated with Na+ retention in response to increased salt intake in the early or mild stages of HF. These abnormalities of renal Na+ handling are largely reversed by enalapril.
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PMID:Intrarenal determinants of sodium retention in mild heart failure: effects of angiotensin-converting enzyme inhibition. 926 Sep 76

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.
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PMID:[Hyponatremia--with comments on hypernatremia]. 1089 27


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