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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of long-term infusion of fenoterol (a beta 2-sympathomimetic drug) in combination with the calcium antagonist verapamil on water balance, the renin-angiotensin-aldosterone system and antidiuretic hormone during pregnancy were studied. Within two hours of the start of infusion, plasma renin and antidiuretic hormone levels were significantly increased, but plasma aldosterone was strongly decreased. There was a concomitant marked reduction of urinary, sodium, and potassium excretion and a decreased creatinine clearance. The long-lasting reduction of urinary excretion which resulted in an elevated water retention is apparently due to other unknown factors. Results are discussed with special regard to the relationship between water balance disturbances and pulmonary edema.
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PMID:The renin-angiotensin-aldosterone system, antidiuretic hormone levels and water balance under tocolytic therapy with Fenoterol and Verapamil. 610 79

A total of 148 patients presenting within 48 hours of subarachnoid haemorrhage were assigned at random to receive standard management only or standard management and treatment with the adrenergic-blocking agents propranolol and phentolamine (or propranolol alone) for three weeks. One hundred and thirty-four patients completed the study. Assessment at four weeks showed a strong trend for less neurological deficit in the treated group, almost statistically significant (p=0.053) in the women. During the first month the treated group suffered fewer episodes of clinical deterioration consistent with cerebral arterial spasm: thus more treated patients underwent operation and those who did had a better outcome (p=0.030). At one year fewer were dead or disabled (unable to work) in the treated group; a significant difference for women (p=0.030). Possible mechanisms for these actions may include a reduction in pulmonary oedema, prevention of myocardial infarcts, a reduction in plasma renin activity, nd a reduction in cerebral oxygen requirements. It is concluded that early adrenergic blockade benefits patients (particularly women) with subarachnoid haemorrhage for up to one year in terms of lesser neurological deficit. Beta-blocker rather than alpha-blockade appears to be the useful component. A randomised, blind extension of the present study using long-acting propranolol and placebo has shown a significant (p=0.026) decrease in deaths and significantly (p=0.003) fewer poor results in the treatment group.
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PMID:Beneficial effects of adrenergic blockade in patients with subarachnoid haemorrhage. 680 47

With the help of radioimmunoassay method 59 patients, which were operated for the various pulmonary diseases, has been examined. The activity of plasma renin, the level of angiotensin II, aldosterone were determined. Polycardiography with phasic analysis of myocardium contractility of the heart right ventricle, differential rheopulmonography, the zone pulmonography of lungs were done simultaneously, the ABE and coagulation of blood indexes were appraised. The data obtained give evidence of participation of the renin-angiotensin-aldosterone system in patients while postoperative period in forming of the lesser circulation hypertension, which is the basis of the pulmonary edema, cardiac and cardiopulmonary insufficiency appearance.
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PMID:[Effects of the renin-angiotensin-aldosterone system on the indicators of hemodynamics of the lesser blood circulation in patients after lung surgery]. 760 97

At least theoretically, ACE-inhibitors may influence each of the factors involved in the regulation of salt and water metabolism. Angiotensin II exerts an antidiuretic and antinatriuretic action on the kidney through influences on the glomerular filtration coefficient, glomerular filtration rate, mesangial tone, filtration fraction, proximal and distal tubule. Angiotensin II and renin also regulate the input of water and salt through an unequivocal dipsogenic effect. In congestive heart failure angiotensin II participates in the preservation of the glomerular filtration rate through its vasoconstrictor properties on the systemic vessels (maintenance of the perfusion and filtration pressure) as well as on the efferent arteriole (maintenance of the filtration pressure). ACE-inhibition weakens or abolishes these influences. However, two favorable mechanisms may also come into action: rise of cardiac output and improvement in renal blood flow; widening of the filtration surface and increment of the filtration coefficient. The efficacy of these factors depends on renal function, age, functional recovery of the heart, treatment with diuretics, duration of treatment with ACE-inhibitors, duration of action of the ACe-inhibitor used, blockade of the facilitating action on the adrenergic vasoconstriction, formation of vasodilating prostaglandins, reduced degradation of kinins. All these effects may account for the variable and often contradictory clinical results, in particular as concerns the relationship between ACE-inhibition and use of diuretics in congestive heart failure. This also explains the variability of efficacy (from the development of pulmonary edema and requirement of diuretics to diuretic withdrawal and clinical improvement) of the ACE-inhibitors as monotherapy in mild to moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ACE-inhibitors and water metabolism in heart failure]. 763 56

The prevalence of pulmonary oedema during scuba-diving is unknown. In our referral centre for diving accidents we have observed several episodes of pulmonary oedema in four previously healthy persons while scuba-diving or swimming. Four events were documented by physical findings, typical chest radiographic changes, and arterial hypoxaemia. Four additional episodes were identified in one of the individuals by a suggestive history. No technical problems with the diving equipment were detectable and none of the individuals reported aspiration of water. In order to gather information about the incidence of pulmonary oedema, we carried out a survey among 1,250 divers. To elucidate possible underlying mechanisms of this complication we investigated forearm vascular resistance, levels of vasoreactive hormones, and left ventricular function by Doppler echocardiography, at room temperature and during cold exposure, in four patients and in healthy control subjects. We found only one additional person with a history suggestive of pulmonary oedema among 460 responders to the survey. We found no differences in forearm vascular resistance, left ventricular systolic and diastolic function, and plasma levels of epinephrine, norepinephrine, cortisol, aldosterone, renin and atrial natriuretic peptide between the patients with a history of pulmonary oedema and the control subjects. We conclude that the occurrence of pulmonary oedema during scuba-diving or swimming is an extremely rare event in healthy individuals. The mechanisms responsible remain unclear.
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PMID:Pulmonary oedema in healthy persons during scuba-diving and swimming. 765 48

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.
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PMID:Susceptibility to high-altitude pulmonary edema in Madison and Hilltop rats. I. Ventilation and fluid balance. 766 30

Severe left ventricular failure, as evidenced by radiographic pulmonary edema or raised left ventricular filling pressure, accompanying acute myocardial infarction, carries a high mortality risk. In this situation, the intravenous loop-diuretic furosemide induces a rapid reduction in the raised left ventricular filling pressure due to an immediate and substantial increase in systemic venous compliance accompanied by increasing diuresis. This diuretic-induced venodilatation is probably due to the release of prostaglandins. The transient systemic arterial constriction and small increase in systemic blood pressure that follows intravenous furosemide probably results from the release of renin and subsequent activation of angiotensin. These diuretic induced hemodynamic changes are accompanied by restoration of the vasodilator reflex, which enables the heart to accommodate an acute volume load. Orally administered loop diuretics achieve slower, but similar, directional hemodynamic changes. There is no information on hemodynamic or neuroendocrine dose-response effects of loop diuretics, and there is no information pertaining to the use of other diuretic groups in this situation. The hemodynamic changes induced by furosemide summate with the changes induced by other anti-heart-failure drugs. In this subset of patients with acute myocardial infarction and severe heart failure, the influence of the diuretics on morbidity incidence and mortality risk remains to be measured.
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PMID:Diuretics in postinfarction heart failure. 801 64

Plasma levels of renin activity, angiotensin II and aldosterone were determined in 16 patients with high altitude pulmonary edema (HAPE) with radioimmunoassay and compared with those in the controls including 9 patients with high altitude acute response (HAAR) and 14 health subjects. All of them arrived recently in Lhasa, a place with an altitude of 3,658 m. The results showed that the concentration of plasma renin activity, angiotensin II, and aldosterone was significantly increased (P < 0.05-0.001) in patients with HAPE and higher than that in the controls. It is suggested that the increase plays a role in the development of pulmonary edema in patients with HAPE.
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PMID:[Clinical significance of changes in plasma renin-angiotensin aldosterone system in patients with high altitude pulmonary edema]. 815 47

In congestive heart failure (CHF), a variety of compensatory mechanisms such as activation of sympathetic nervous system, renin-angiotensin system and vasopressin, facilitate water and sodium retention and increase circulating blood volume, which primarily improve systemic perfusion. However, hypervolemia sometimes induces pulmonary edema and afterload elevation, resulting in a further decrease in cardiac output. Diuretics are administered in patients with CHF to cut this vicious cycle by reducing blood volume. Evaluation of hemodynamic states is important in patients with severe CHF, since an excessive reduction in preload could critically decrease cardiac output. Among conventional diuretics, loop diuretics is the most potent and widely used for management of CHF. Inhibition of such compensatory mechanisms such as angiotensin-converting enzyme inhibitors and atrial natriuretic peptide-related agents is shown to exert natriuretic and desirable hemodynamic effects in CHF and is among candidates for future diuretics.
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PMID:[Progress in management for heart failure: diuretics]. 833 95

Hypertensive crisis is defined as a severe elevation in BP and is classified as either urgency or emergency. In hypertensive urgency there is no end-organ injury and no evidence that acute BP lowering is beneficial. Indeed, rapid uncontrolled pressure reduction may be harmful. Therefore, in hypertensive urgencies BP should be lowered gradually over 24 to 48 hours using oral antihypertensives. When the cause of transient BP elevations is easily identified, appropriate treatment should be given. When the cause is unknown, an oral antihypertensive should be given. The efficacy of available treatments appear similar; however, the underlying pathophysiological and clinical findings, mechanism of action and potential for adverse effects should guide choice. Captopril should be avoided in patients with bilateral renal artery stenosis or unilateral renal artery stenosis in patients with a solitary kidney. Nifedipine and other dihydropyridines increase heart rate whereas clonidine, beta-blockers and labetalol tend to decrease it. This is particularly important in patients with ischaemic heart disease. Labetalol and beta-blockers are contraindicated in patients with bronchospasm and bradycardia or heart blocks. Clonidine should be avoided if mental acuity is desired. In hypertensive emergency there is an immediate threat to the integrity of the cardiovascular system. BP should be immediately reduced to avoid further end organ damage. Sodium nitroprusside is the most popular agent. Nitroglycerin (glyceryl trinitrate) is preferred when there is acute coronary insufficiency. A beta-blocker may be added in some patients. Loop diuretics, nitroglycerin and sodium nitroprusside are effective in patients with concomitant pulmonary oedema. Enalaprilat is also theoretically helpful, especially when the renin system might be activated. Initial treatment of aortic dissection involves rapid, controlled titration of arterial pressure to normal levels using intravenous sodium nitroprusside and a beta-blocker. If beta-blockers are contraindicated, urapidil or trimetaphan camsilate are alternatives. Hydralazine is the drug of choice for patients with eclampsia. Labetalol, urapidil or calcium antagonists are possible alternatives if hydralazine fails or is contraindicated. For patients with catecholamine-induced crises, an alpha-blocker such as phentolamine should be given; labetalol or sodium nitroprusside with beta-blockers are alternatives. There are few, if any, comparative or randomised trials providing definitive conclusions about the efficacy and safety of comparative agents. Some investigators recommend decreasing the diastolic BP to no less than 100 to 110 mm Hg. A reasonable approach for most patients with hypertensive emergencies is to lower the mean arterial pressure by 25% over the initial 2 to 4 hours with the most specific antihypertensive regimen.
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PMID:Comparative tolerability profile of hypertensive crisis treatments. 970 48


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