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

Diurnal cycles of glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and of excretion rates of sodium, potassium, magnesium, chloride and phosphate were measured in a 22 year old man with moderately severe heart failure under standardized conditions. Cycles of GFR, ERPF and excretion of potassium, chloride, and phosphate were indistinguishable from those of normals. The phases of the sodium and probably the magnesium excretory cycles were reversed from normal. The significance of some of the observations is discussed.
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PMID:Diurnal circadian rhythms of renal function and electrolyte excretion in heart failure. 57 67

d-3-Acetoxy-cis-2,3-dihydro-5-]2-(dimethylamino)ethyl]-2-(p-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one hydrochloride (diltiazem HCl) was orally administered to 9 patients with chronic congestive heart failure (Class IIb to III, NYHA) to examine whether the drug induces sodium retention and aggravates congestive heart failure. Renal hemodynamics and urinary electrolytes excretion were measured for 3 h after the medication in 6 out of 9 patients. Four of the rest of patients had received chronic administration of the drug for about 2 weeks. There was a significant increase in urinary sodium excretion without noticeable change in renal hemodynamics after diltiazem administration, demonstrating the presence of its direct inhibitory action on renal tubules. The increase in urinary sodium excretion was more marked in patients with heart failure than in those without. This difference in the response to diltiazem may be due to the functional constriction of renal cortical vessels in heart failure. This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize. The chronic administration of the drug did not induce sodium retention and edema. There was no deterioration of symptoms due to congestive heart failure such as dyspnea and body weight increase. It may be concluded that diltiazem does not aggravate congestive heart failure through its diuretic action and probably its systemic vasodilating action.
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PMID:The effect of diltiazem hydrochloride upon sodium diuresis and renal function in chronic congestive heart failure. 58 67

The potent vasodilator sodium nitroprusside has been used to treat hypertensive emergencies and to improve the hemodynamics of chronic heart failure and acute myocardial infarction. As the use of this seemingly beneficial agent appears to be increasing, personnel caring for patients should be familiar with nitroprusside in order to use it properly and safely. We have reviewed the pharmacology, mode of mixing and administering, monitoring requirements, and indications of nitroprusside so it may be used with maximal benefit and minimal risk.
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PMID:Clinical application of sodium nitroprusside. 58 2

Eighteen elderly patients (average age 72.3 years) suffering from cardiac failure and from chronic gastric ulcers received carbenoxolone sodium, the risk of surgery being considered too high. The effects of this medical treatment were followed up closely. Side-effects were observed in 12 patients. In 9 patients these effects had to be taken care of (hypokalemia in 5 cases, rise of blood pressure in 3 cases, edema in 3 cases). In 2 cases treatment had to be stopped. The side effects observed in elderly patients with cardiac insufficiency make it mandatory to administer carbenoxolone sodium to this group only during hospitalization, which allows, frequent controls of body weight, blood pressure, serum potassium and transaminases. In most cases side effects can be detected early enough and treated.
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PMID:[Tolerance of carbenoxolone sodium in elderly patients (author's transl)]. 59 29

Severe tachycardia, ventricular ectopy, and sodium retention manifested by hemodynamic deterioration developed with hydralazine hydrochloride therapy in chronic coronary heart disease with congestive failure refractory to digitalis, diuretics, and nitrates. Coronary care unit admission with Swan-Ganz catheterization corrected hemodynamics by sodium nitroprusside treatment after hydralazine withdrawal. Satisfactory cardiac performance with oral long-acting nitrates were unsuccessful. However, the new oral vasocilator, prazosin hydrochloride, achieved considerable hemodynamic benefit by greatly reducing elevated left ventricular filling pressure and increasing severely depressed cardiac index to normal, accompanied by striking symptomatic improvement. Furthermore, long-term enhancement of cardiac dynamics and salutary functional status was maintained by ambulatory oral prazosin therapy for several months. This experience demonstrates the favorable alternative of prazosin nitroprusside-like actions over hydralazine-nitrate therapy in heart failure therapy and emphasizes prazosin's utility when untoward side effects to hydralazine develop.
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PMID:Hydralazine-induced tachycardia and sodium retention in heart failure. Hemodynamic and symptomatic correction by prazosin therapy. 64 47

The action of dopamine was evaluated in 18 patients with cardiogenic shock after myocardial infarction, in 14 patients with heart failure and in 18 patients with low-output syndrome after cardiac surgery. In the patients with shock, dopamine increased significantly systolic arterial blood pressure, myocardial contractility, diuresis and sodium excretion. In patients with heart failure a great increase in diuresis and sodium excretion with decrease of CVP was observed. In patients after cardiac surgery dopamine produced a significant increase of arterial blood pressure and diuresis with decrease of CVP. The clinical application of dopamine and the advantages of the use of dopamine combined with other catecholamines were discussed.
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PMID:[The use of dopamin in shock and heart failure (author's transl)]. 65 65

Thirteen patients with severe cardiac failure underwent a single crossover study of dopamine and dobutamine in order to compare the systemic and regional hemodynamic effects of the two drugs. The dose-response data demonstrated that dobutamine (2.5--10 microgram/kg/min) progressively and predictably increases cardiac output by increasing stroke volume, while simultaneously decreasing systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure. There was no change in heart rate or premature ventricular contractions (PVCs)/min at this dose range. Dopamine (2--8 microgram/kg/min) increased the stroke volume and cardiac output at 4 microgram/kg/min. Dopamine at less than 4 microgram/kg/min provided little additional increase in cardiac output and increased the pulmonary wedge pressure and the number of PVCs/min. At greater than 6 microgram/kg/min, dopamine increased heart rate. During the 24-hour maintenance-dose infusion of each drug (dopamine 3.7--4, dobutamine 7.3--7.7 microgram/kg/min), only dobutamine maintained a significant increase of stroke volume, cardiac output, urine flow, urine sodium concentration, creatinine clearance and peripheral blood flow. Renal and hepatic blood flow were not signfiicantly altered by the maintenance dose of either drug. Systemic and regional hemodynamic data suggest that dobutamine has many advantages over dopamine when infused in patients with cardiac failure.
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PMID:Comparative systemic and regional hemodynamic effects of dopamine and dobutamine in patients with cardiomyopathic heart failure. 67 37

We determined alterations in plasma and red-cell electrolyte concentrations associated with digoxin administration in 11 children in heart failure, 24 nontoxic patients receiving maintenance digoxin and 11 children in whom digoxin toxicity developed. Twenty normal children served as controls. Digoxin therapy was associated with a mean (+/- S.E.M.) increase in red-cell sodium from a pretreatment level of 6.2 +/- 0.7 meq per liter to 11.9 +/- 1.2 meq per liter and a decrease in red-cell potassium from 105.4 +/- 1.4 to 99.5 +/- 1.9 meq per liter (P less than 0.001). The red-cell sodium levels of toxic patients exceeded those of nontoxic patients whereas the potassium concentrations were lower (P less than 0.001). Toxic patients manifested significantly higher ratios of red-cell sodium to red-cell potassium (0.213 +/- 0.003) than nontoxic patients (0.085 +/- 0.008; P less than 0.001). Changes in red-cell electrolytes are sensitive indicators of digoxin affects.
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PMID:Relation between plasma and red-cell electrolyte concentrations and digoxin levels in children. 68 6

Dietary potassium depletion plus high sodium intake has been reported to elevate resting heart rate and cardiac output and to cause heart failure during exercise. We implanted aortic root electromagnetic flowmeters and aortic and pulmonary artery catheters in five splenectomized dogs condition-trained to run at 9 km/h on an 11% grade for 20 min. Postoperatively, the dogs ate a potassium-enriched diet until completion of control studies; then potassium was withdrawn. During 4 wk of depletion, skeletal muscle potassium fell from 380 +/- 22 to 311 +/- 8 meq/kg, and muscle sodium rose from 142 +/- 14 to 207 +/- 27 meq/kg (mean +/- SE). Cardiac output, aortic blood pressure, heart rate, acceleration of aortic blood flow at rest or during exercise, and the oxygen cost of exercise remained at control levels. Serum creatine phosphokinase at rest, an indicator of rhabdomyolysis, was never elevated. A 24% dietary depletion of muscle potassium in the dog did not change resting and exercise hemodynamics and exercise performance from control.
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PMID:Exercise performance and hemodynamics during dietary potassium depletion in dogs. 73 May 69

A study of the alterations in the intracellular electrolytes in the left failing heart due to induced mitral insufficiency was made in dogs. The extracellular space increased significantly. There was no significant change in the plasma Na+ and Ca++. However, there was a significant decrease in the plasma K+. The ratio of wet weight to dry weight increased during mitral insufficiency, although not significantly. There were no significant changes in the tissue Na+, K+ and Ca++. However, there were significant decreases in the intracellular Na+ and Ca++, and tendency for an increase in the intracellular K+ during mitral insufficiency. These results suggest that the decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++ and associated changes in Na+ and K+ as a result of increased sarcolemmal ATPase.
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PMID:Cardiac intracellular and blood electrolytes in chronic mitral insufficiency. 74 36


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