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

The studies on Strophantin effect upon the hemodynamics in the acute stage of cardiac infarction has revealed that it elevates the pressure in pulmonary artery and reduces the cardiac output, in certain cases deteriorating the patient's state. Furanthril and Droperidol reduce the cardiac output but at the same time diminish the pressure in the pulmonary artery and reduce the pulmonary resistance, thus having a favourable effect on the patient's state. Proceeding from the results obtained, a treatment scheme, including Furanthril, Droperidol and Strophantin, is recommended for the cardiac insufficiency treatment in the acute stage of cardiac infarction depending on the disease onset and the degree of cardiac insufficiency manifested.
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PMID:[Treatment of cardiac insufficiency in the acute stage of cardiac infarct]. 47 92

Furosemide was administered intravenously to 11 patients with cardiac failure after acute myocardial infarction. After an initial loading dose furosemide was given four-hourly if the pulmonary capillary wedge pressure (PCW) was not normalized, i.e. less than or equal to 15 mm Hg. The comparison of the hemodynamic results with the results of a previous study with nitrates was as follows: like the nitrates furosemide lowered the PCW early, i.e. within 15 minutes from 22 +/- 3 to 18 +/- 5 mm Hg, but the therapeutic objective (PCW less than or equal to 15 mm Hg) was reached later than with nitrates. During the 24-hour observation period PCW and total peripheral resistance decreased steadily. The decrease of cardiac index to critical low values in some patients after a mean of 7.5 hours of therapy, and of the mean arterial pressure from 100 +/- 13 to 91 +/- 14 mm Hg, may limit the use of furosemide alone in these patients. During nitrate therapy PCW started to rise again after 12 hours in some patients, necessitating higher doses of nitrates with a corresponding decrease of diuresis. A combination of both forms of therapy may be of value and needs further investigation.
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PMID:[Hemodynamic consequences of the furosemide treatment of cardiac insufficiency in recent myocardial infarct]. 53 59

Pulmonary arterial pressure, heart rate and peripheral arterial pressure were followed up by the 15th, 45th and 105th minute post intravenous introduction of 40 mg furanthril in patients with myocardial infarction in acute stage (in 42 cases of 12 patients with left cardiac insufficiency and in 14 cases--of 8 patients without cardiac insufficiency). Furanthril induced clearly manifested pressure decrease in the pulmonary artery in patients with left cardiac insufficiency, developing between the 15th and 45th minute and continuing till the end of the second hour and a negligible elevation of peripheral arterial pressure by the 15th minute, followed by a slight decrease of the latter under the initial value by the 45th and 105th minute. Similar tendency, but less manifested, exists and in patients without cardiac insufficiency. Heart rate is kept unchanged. Furanthril does not induce undesirable hypotonic states when applied in those doses in patients who, as a rule, arenot hyptonics.
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PMID:[Effect of furanthril on several hemodynamic indices during the acute stage of myocardial infarction]. 100 34

Studies were performed to determine whether the intrarenal distribution of cortical blood flow is altered in congestive heart failure. Utilizing the radioactive microsphere method, we studied eight dogs that developed congestive heart failure secondary to the construction of an aortocaval fistula. They had marked reduction in total renal blood flow not accompanied by intracortical redistribution of blood flow. All dogs had developed edema and/or ascites, and gained a mean of 3.4 kg; glomerular filtration rate, hematocrit, and urinary sodium excretion fell significantly. Renal vascular resistance increased; mean blood pressure and filtration fraction were unchanged. Furosemide was administered to a second group of nine fistula dogs. The drug produced a marked natriuresis associated with a decrease in outer cortical blood flow (zone 1) and an increase in midcortical zones 2 and 3; no change was observed in zone 4. We conclude: 1) chronic salt retention occurs in high-output heart failure in the absence of redistribution of renal cortical blood flow, and 2) the effect of furosemide on intrarenal hemodynamics of dogs with heart failure is similar to that seen in normal animals.
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PMID:Distribution of renal blood flow in dogs with congestive heart failure. 125 34

Progressive asymptomatic ventricular dilatation can occur following myocardial infarction and severe ventricular dysfunction is often present by the time clinical congestive heart failure occurs. In a randomized, double-blind trial, the effects of captopril 25 mg tid, frusemide 40 mg daily and placebo were studied in 90 patients with asymptomatic left ventricular dysfunction (ejection fraction less than 45%) 1 week following Q wave myocardial infarction. Left ventricular volumes and function were assessed at intervals during the subsequent year using two-dimensional echocardiography. The frusemide and placebo groups showed significant increases in ventricular volumes with stroke volume index unchanged and ejection fraction slightly reduced, whereas the captopril group showed a significant reduction in left ventricular end-systolic volume index with stroke volume index and ejection fraction increased. At 12 months the difference in the change in ejection fraction from baseline between the captopril and frusemide groups was 10.5% and captopril and placebo groups 9.6% (both P less than 0.0001). There was a significant difference in occurrence of clinical heart failure in the placebo group compared with the other groups (P less than 0.05). Blood pressure increased significantly within the normal range in the placebo and frusemide groups whereas there was essentially no change from baseline in the captopril group. There was no significant correlation between baseline left ventricular volumes and function and subsequent change, and anterior and inferior infarct subgroups showed similar responses within the treatment groups. In conclusion, captopril improves asymptomatic ventricular dysfunction and prevents clinical heart failure during the year following myocardial infarction. Frusemide may also prevent clinical heart failure but not progressive ventricular dilatation.
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PMID:Preventive treatment of asymptomatic left ventricular dysfunction following myocardial infarction. 214 81

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10(-3) M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.
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PMID:Negative inotropic effects of furosemide in the isolated rabbit heart: a prostaglandin-mediated event. 243 13

Of 1894 patients registered in a family medicine clinic, 101 (5.3%) had been taking diuretics for at least 6 months. The sex distribution was equal and the average age was 68.7 years. 60% were taking Kaluril, 30% Aquadon and 10% Frusemide. Most had hypertension or heart failure, or both. 6 patients developed hyperglycemia, 2 hyponatremia, 5 hypokalemia, 2 hyperkalemia and 10 hyperuricemia. In 19 the ECG showed arrhythmias. 5 of 56 patients had hypomagnesemia and another 12 had low borderline levels. In the light of these results and those in the literature, we conclude that diuretics are not as safe as previously thought.
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PMID:[Use of diuretics in family practice]. 273 88

Few studies exist on the interaction of diuretics and angiotensin-converting enzyme inhibitors in patients with chronic heart failure. Twelve subjects with heart failure were studied before and after their usual oral dose of frusemide in random order on consecutive days during fixed sodium, potassium and water intake. Patients then received 10 mg day-1 of enalapril for 5 days and subsequently restudied before and after their usual dose of frusemide. Frusemide was not observed to have an effect on systemic or renal haemodynamics prior to enalapril, but urine volume and sodium content rose as expected. Treatment with enalapril, in the absence of frusemide, was associated with a fall in mean blood pressure from 89 +/- 5 mmHg to 85 +/- 4 mmHg (P less than 0.02) and a rise in renal blood flow from 424 +/- 202 ml min-1 to 494 +/- 225 ml min-1 (P less than 0.02), but cardiac output and glomerular filtration rate were again unchanged. Addition of frusemide to enalapril therapy resulted in a greater fall in mean blood pressure (87 +/- 5 mmHg to 79 +/- 4 mmHg; P less than 0.01) and an increase in cardiac output (3.1 +/- 1.1 l min-1 to 3.6 +/- 1.0 l min-1; P less than 0.02). Renal blood flow increased further than after enalapril alone to 579 +/- 211 ml min-1, but the glomerular filtration rate fell to 63 +/- 26 ml min-1 (P less than 0.01) and the filtration fraction fell to 19 +/- 5% (P less than 0.001). Weight gain occurred and the diuretic response to frusemide was reduced during this early phase of enalapril therapy.
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PMID:The effects of frusemide and angiotensin-converting enzyme inhibitors and their combination on cardiac and renal haemodynamics in heart failure. 283 73

Ten patients in heart failure of various etiologies underwent a placebo-controlled study to determine the effect of indomethacin (150 mg daily by mouth) on urine volume, sodium chloride excretion, glomerular filtration rate, renal prostaglandins, as well as plasma renin and aldosterone concentrations before and after administration of 40 mg frusemide by mouth. None had hyponatremia and plasma renin levels were within normal limits, but prostaglandin synthesis inhibition by indomethacin significantly reduced urine volume (-50%), sodium excretion (-70%) and glomerular filtration rate (-50%), as well as the urinary excretion of prostaglandin E2 (-80%) and 6-keto-prostaglandin F1 alpha (-70%). Frusemide-induced diuresis was halved by indomethacin. The suppression of renal prostaglandin excretion induced by inhibition of cyclooxygenase was not much influenced by frusemide. Plasma renin and aldosterone concentrations after indomethacin administration were not significantly raised by frusemide. The results indicate that renal prostaglandin synthesis is of great importance in the pathophysiology and treatment of mild to moderate heart failure.
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PMID:[Indomethacin and furosemide in patients with cardiac insufficiency. Kidney function, the renin-angiotensin system and renal prostaglandins]. 331 42


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