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

Supplemental albumin added to a standard non-albumin resuscitation regimen has been shown to significantly impair heartwork in seriously injured patients. The role of calcium dynamics in this myocardial depression was analyzed in 94 injured patients who were in shock for an average of 32 minutes, received an average of 14.5 transfusions, 9.2 L crystalloid, 0.9 L plasma, and 20.9 mEq calcium prior to the end of operation. By random selection, 44 patients received an average of 31 gms of albumin during operation, 207 gms during the early postoperative period (mean = 30 hrs) of extravascular fluid sequestration, and 402 gm during the mobilization period. The albumin resuscitated patients had normal total protein and serum albumin levels and higher total calcium (TC) levels, however, they had a significantly lower Ca++ and Ca++/TC. The accumulative slope for heartwork/filling pressure was significantly depressed in albumin patients as was the mean work unit/filling pressure index. The level of Ca++ and the Ca++/TC ratio correlated directly with the calculated work unit index in both the albumin and non-albumin patients. This suggests that a supplemental albumin binds serum Ca++ causing an increase in TC but a reduction in Ca++ and Ca++/TC. The fall in Ca++ and Ca++/TC seems responsible, in part, for heart failure and pulmonary edema in albumin resuscitated patients.
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PMID:The cardiac effect of altered calcium homeostasis after albumin resuscitation. 721 93

Fractional dextran clearances (theta D) were used to ascertain whether the albuminuria accompanying cardiac failure (CF) has a hemodynamic basis. In 17 patients with grade-IV CF in whom GFR and effective renal plasma flow (ERPF) were depressed to 58 +/- 7 and 215 +/- 20 ml/min/1.73 m2, respectively, theta D was elevated relative to normal control subjects over the Stokes-Einstein radius (r) interval of 28 to 46 Angstrom. For dextran of equivalent size to albumin (r = 36 Angstrom), the rate of urinary excretion (UD36V) was not increased because elevated theta D36 was offset by the depressed GFR. In contrast, urinary albumin excretion (UalbV) was increased to 82 +/- 35 microgram/min. Thus, for albuminuria in CF to have the hemodynamic basis suggested by elevation of theta D requires that (I) the fractional clearance for anionic albumin be disproportionately enhanced relative to uncharged dextran by reduced glomerular plasma flow and/or (2) that glomerular electrostatic barrier function be impaired in CF. In seven patients with minimal change nephropathy, UD36V was similar to that in CF, but UalbV was 40 times greater than that in CF. Thus, if glomerular electrostatic barrier function is impaired in CF, such dysfunction is trivial by comparison with minimal change nephropathy.
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PMID:Albuminuria and the permselective properties of the glomerulus in cardiac failure. 739 24

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

Ramipril is a second generation angiotensin converting enzyme (ACE) inhibitor. Like enalapril, it is a prodrug and is hydrolysed in vivo to release the active metabolite, ramiprilat, which has a long elimination half-life, permitting once-daily administration. The antihypertensive efficacy of ramipril has been confirmed in large-scale noncomparative studies conducted in general practice as well as in more rigorously controlled clinical trials. In the former, approximately 85% of patients with mild to moderate essential hypertension have responded successfully to treatment with ramipril 2.5 or 5 mg/day, while comparative trials indicate that the antihypertensive efficacy of the drug is equivalent to that of other established ACE inhibitors and the beta-adrenoceptor antagonist atenolol. As expected, the response rate to ramipril monotherapy is lower in patients with severe hypertension (around 40%), although the blood pressure lowering effect can be enhanced with the addition of a diuretic such as hydrochlorothiazide or piretanide. The antihypertensive efficacy of ramipril is maintained in patients with diabetes mellitus and preliminary data indicate that the drug has the beneficial effect of decreasing urinary albumin excretion in diabetic patients with nephropathy. Ramipril is superior to atenolol in causing regression of left ventricular hypertrophy, although the clinical significance of this effect per se remains to be established. The large-scale Acute Infarction Ramipril Efficacy (AIRE) study demonstrated that ramipril 5 or 10 mg/day significantly decreased the risk of all-cause mortality by 27% in patients with clinical evidence of heart failure after acute myocardial infarction, even if transient. The beneficial effect of ramipril was apparent by 30 days of treatment and appeared to be greatest in patients with more severe ventricular damage after infarction. Ramipril is well tolerated in general practice, with 5% or fewer patients discontinuing therapy because of drug intolerance. The data available suggest that ramipril shares a similar tolerability profile to that of other established ACE inhibitors. Thus, clinical data confirm ramipril as a useful alternative ACE inhibitor for the treatment of patients with mild to moderate hypertension, and indicate a beneficial effect of the drug in patients with clinical evidence of heart failure after acute myocardial infarction. It is also reasonable to assume that ramipril will be of value in the treatment of patients with more established heart failure or asymptomatic left ventricular dysfunction.
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PMID:Ramipril. An updated review of its therapeutic use in essential hypertension and heart failure. 777 15

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in an uremic patient without evidence for a causative (specific) underlying disease. The incidence is not known. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. Rigid fluid control, intensive hemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneatrial pump have all been found ineffective as treatment. Peritoneal dialysis has been shown to resolve ascites, however, the only effective treatment is so far renal transplantation. The development of nephrogenic ascites is associated with a poor prognosis. Thus, one year after the development of nephrogenic ascites 1/3 had died.
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PMID:Nephrogenic ascites. Case report and review of the literature. 781 79

We experienced two patients with a prosthetic heart valve, who underwent hepatic resection for hepatoma while on anticoagulation therapy. Patients with a prosthetic heart valve have the following characteristics; an increased risk of thromboembolism due to diminished anticoagulation in the perioperative period, a greater risk of endocarditis due to the artificial material in the heart, and impaired cardiopulmonary function including possible arrhythmia and heart failure. Furthermore, when such patients also have liver cirrhosis with a hepatoma, there is an increased risk of perioperative bleeding while on anticoagulation due to coagulopathy and also a risk of infection due to decreased cellular immunity. Patients with a prosthetic heart valve therefore require special care and attention whenever they have to undergo hepatic resection. With respect to anticoagulation, a minimal level is required to prevent bleeding and thromboembolism. Warfarin being administered preoperatively may be switched to heparin while closely monitoring the activated clotting time (biomaterial valve: 130-150 sec, non-biomaterial valve: 150-180 sec); the heparin should then be changed back to warfarin immediately after starting oral intake following operation. For the prevention of infection, a broad spectrum antibiotic should be used prophylactically both intra-operatively and postoperatively. The cardiopulmonary function must also be carefully monitored. For the assessment of postoperative liver function, lecithin: cholesterol acyltransferase, serum bilirubin and albumin are useful because there is no relevance of coagulation parameters such as prothrombin time under anticoagulation.
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PMID:Major hepatic resection in patients with a prosthetic heart valve receiving anticoagulation treatment. 795 57

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.
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PMID:High colloid oncotic therapy for contusional brain edema. 797 45

Wide albumin gradient (transudative) ascites is usually due to liver disease but may also result from many other disorders, including heart failure, hepatic infiltration by tumor, hepatic vein thrombosis, and veno-occlusive disease. It has not been linked with small bowel obstruction. Narrow albumin gradient (exudative) ascites, usually due to peritoneal carcinoma or inflammation, has been noted in cases of necrotic or perforated bowel, but simple small bowel obstruction has not previously been appreciated as a possible cause for ascites. We report a patient who developed wide albumin gradient ascites and secondary bacterial peritonitis in association with small bowel obstruction. The small bowel obstruction, ascites, and peritonitis resolved with lysis of a single abdominal adhesion.
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PMID:Ascites and secondary bacterial peritonitis associated with small bowel obstruction. 805 42

In this study, the acute haemodynamic effects of angiotensin converting enzyme (ACE) inhibition with intravenous enalaprilat alone or in combination with preload restoration were determined in patients with severe heart failure complicating acute myocardial infarction. Ten patients with raised pulmonary arterial wedge pressure (PAWP > or = 18 mmHg) were first studied during constant conventional vasodilation with diuretic and inotropic medication, by monitoring central haemodynamics and arterial blood gases. The same variables were measured before enalaprilat infusion, after preload reduction with enalaprilat (1 mg.h-1, rate doubled every 30 min until PAWP decreased > or = 25% or up to total cumulative dose of 10 mg) and after preload restoration with fluid loading (4% albumin given 15 ml.min-1 to restore PAWP to baseline) during continuous low dose enalaprilat infusion. Enalaprilat alone (median dose 0.9 mg) reduced significantly the PAWP (from 25 to 17 mmHg; P = 0.004), the mean arterial pressure (from 87 to 83 mmHg; P = 0.008), the mean pulmonary arterial pressure and the right atrial pressure. The cardiac index, stroke volume index and systemic vascular resistance index remained unchanged. Preload restoration during continuous enalaprilat infusion (median dose of 4% albumin 230 ml, and enalaprilat 0.2 mg) did not further enhance left ventricular function; rather, there was a nearly significant decrease in myocardial perfusion pressure. Arterial oxygenation remained unchanged throughout the study. In conclusion, adding intravenous enalaprilat to conventional therapy makes it possible to relieve pulmonary congestion while maintaining the cardiac function and arterial oxygenation. Preload restoration during continuous ACE inhibition offers no further advantages, and may have adverse effects, since the myocardial perfusion pressure may fall.
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PMID:Haemodynamic effects of enalaprilat and preload in acute severe heart failure complicating myocardial infarction. 807 Apr 80

This study examined the effects of conventional doses of oral captopril on the renal responses to oral furosemide in ambulant patients with stable chronic heart failure. Twenty-five men (mean age 63 years) were randomized to one of two groups. Group 1 received placebo on days 1 and 2 before furosemide. Group 2 received placebo on day 1 before furosemide and captopril thereafter (i.e., captopril before furosemide on day 2). Urine was collected after either placebo or captopril and after furosemide (taken after placebo or captopril pretreatment). Captopril by itself did not affect renal function. Captopril did, however, significantly affect the renal response to furosemide. The increase in urine flow rate after furosemide in group 2 was decreased from 225% with placebo to 128% with captopril (p < 0.02). The increase in sodium excretion after furosemide was decreased from 623% with placebo to 242% with captopril (p < 0.001). Pretreatment with captopril abolished the increase in creatine clearance after furosemide. The increase in urinary albumin excretion (used as a marker of glomerular function) after furosemide was also significantly blunted by captopril. Conventional doses of captopril acutely inhibit the natriuretic and diuretic responses to furosemide at the glomerular level in ambulant patients with stable chronic heart failure.
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PMID:Acute effects of captopril on the renal actions of furosemide in patients with chronic heart failure. 821 45


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