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

Patients with heart failure should stop smoking, maintain an optimal weight and limit their intake of salt. Alcohol abuse should be avoided. The detection and early treatment of hypertension appears to have had a major impact in preventing heart failure. Diuretics revolutionized the treatment of congestive heart failure and their proper and appropriate use can alleviate peripheral and pulmonary oedema. Diuretics should not be overused and care should be taken to avoid hypokalaemia. Controversy surrounds the use of digoxin in patients in sinus rhythm; the drug should be used in patients in atrial fibrillation. The use of an inotropic drug may be harmful in the presence of coronary artery disease. A reduction in the current use of digoxin might be of benefit to many patients with heart failure. When the drug is prescribed it should be used in a therapeutic and not homeopathic dose. Recent interest has been directed toward the use of vasodilators and the angiotensin-converting enzyme inhibitors in patients with heart failure. In my opinion, these drugs should be used after patients have been treated with thiazide and loop diuretics. Vasodilators are particularly beneficial in acute heart failure or in patients with chronic heart failure when the symptoms are related to fluid overload and volume expansion. The cause of symptoms in patients with chronic heart failure optimally treated with diuretics is controversial. Shortness of breath may not be simply related to the left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing ideas in the treatment of heart failure--an overview. 330 Sep 78

A controlled double-blind trial was carried out to assess the efficacy and safety of a continuous intravenous infusion of diltiazem in preventing perioperative myocardial ischaemia in patients with coronary artery disease. Sixty-six patients undergoing non cardiac surgical procedures (vascular surgery, n = 37; other, n = 29) were randomly chosen to receive either diltiazem (group D, n = 32); or placebo (group P, n = 34); there was no difference between these groups in the number of patients in each NYHA class (I: 13/16; II: 14/14; III: 5/4) or having had a previous myocardial infarct (20/22). ECG leads CM5 and CL5 were recorded continuously with an ICR 7200 Holter monitor. After starting recording, either placebo or a loading dose (0.5 mg.kg-1) of diltiazem was given, followed by an infusion of 5 micrograms.kg-1.min-1. Anaesthesia was induced by thiopentone and suxamethonium, and maintained with nitrous oxide (50%), fentanyl and either halothane or droperidol. The number of myocardial ischaemic episodes was significantly (p less than 0.05) lower in group D (2 ST depressions in two patients) than in group P (8 ST depressions in six patients, 2 myocardial infarcts and 1 pulmonary oedema). No conduction disturbance was observed; the lowest cardiac frequency was found in group P (32 b.min-1). Systolic and diastolic arterial blood pressures were lower in group D than in group P, but no difference was found in heart rate and rate-pressure product.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of per- and postoperative myocardial ischemia in non-cardiac surgery by intravenous diltiazem]. 340 38

In order to evaluate the incidence of myocardial ischaemia in patients who developed acute pulmonary oedema during the immediate post-operative period, continuous monitoring of the electrocardiogram by the Holter method was used in 200 consecutive patients with coronary artery disease. Fourteen of these patients exhibited ST segment depression during the post-operative period and 13 during surgery. Nine patients developed acute pulmonary oedema immediately after the operation and in 7 cases the oedema was preceded by myocardial ischaemia. A continuous nitroglycerin infusion brought about regression of the pulmonary oedema in 8 cases. One patient died despite treatment. These findings underline the part played by myocardial ischaemia in the pathogenesis of acute post-operative pulmonary oedema in patients with coronary artery disease.
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PMID:[Acute postoperative pulmonary edema in the coronary patient: effects of myocardial ischemia]. 622 2

In acute myocardial infarction depression of the ST segment in leads distant from those showing ST elevation has been considered to be "reciprocal" but might reflect local ischaemia. To examine this possibility 103 consecutive patients who underwent exercise testing early after myocardial infarction were reviewed. Treadmill exercise testing was performed a mean of 12 (range 5-30) days after infarction using a limited Naughton protocol. Thirty five (34%) of the patients had had reciprocal change, defined as greater than or equal to 1 mm ST depression in leads remote from the site of the infarct, within 48 hours of infarction. Twenty two (63%) of the 35 patients developed exercise induced ST depression in the leads previously showing reciprocal change. Coronary artery disease was assessed in 10 of these patients by arteriography and in four at necropsy: all but one had stenosis of greater than or equal to 50% in a coronary artery supplying the reciprocal territory in addition to the disease in the vessel to the infarct site. Of patients with reciprocal ST depression, 23.5% experienced nonfatal reinfarction, pulmonary oedema after discharge, or death compared with only 9.5% of patients without reciprocal ST depression. Eight (23.5%) patients with reciprocal depression had ventricular fibrillation while in hospital compared with only two (3%) patients without. Reciprocal ST depression in acute myocardial infarction may reflect ischaemia in territory distant from the site of infarction and is associated with a high risk of fatal arrhythmias and late morbidity.
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PMID:"Reciprocal" depression of the ST segment in acute myocardial infarction. 641 Dec 61

Fourteen patients with refractory ventricular tachyarrhythmias were treated with combined endocardial resection and implantation of the automatic defibrillator. There were 11 men and 3 women with a mean age of 53 years (range, 41 to 58 years). All patients had coronary artery disease; the mean ejection fraction was 26%, and the mean number of cardiac arrests was 2.6. Programmed electrical stimulation induced sustained ventricular tachycardia in 13 patients and nonsustained ventricular tachycardia in 1. Operative endocardial mapping in the 13 patients with sustained ventricular tachycardia demonstrated a septal focus of early activation in 9 patients and a nonseptal site in 4. Following resection, sustained ventricular tachycardia could not be reinduced. There was 1 operative death. Programmed electrical stimulation performed one month after operation induced ventricular tachycardia in 5 patients, but tachycardia could not be induced in the other 8 survivors. The longest follow-up was 32 months; the average was 17 months. There were 2 late deaths. One patient died of myocardial infarction and 1 of pulmonary edema following a routine cholecystectomy. In another patient, late ventricular tachycardia developed but was automatically terminated by the implanted defibrillator. These results suggest that endocardial resection combined with implantation of the automatic defibrillator may offer the greatest protection yet available to patients with malignant ventricular tachyarrhythmias.
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PMID:The treatment of malignant ventricular arrhythmias with combined endocardial resection and implantation of the automatic defibrillator: preliminary report. 669 38

To assess the prognostic importance of resting left ventricular function in survivors of acute myocardial infarction with pulmonary edema, we retrospectively identified 39 consecutive patients who presented with acute pulmonary edema and myocardial infarction. Sixteen patients had radionuclide ejection fractions 10 +/- 2 days postinfarction of greater than 0.45 (group A, mean 0.55 +/- 0.06), and 23 patients had ejection fractions less than or equal to 0.45 (group B, 0.32 +/- 0.06). There were no significant differences between the two groups for age or sex, but group A patients had a significantly greater incidence of first myocardial infarction predominantly inferior in location. The calculated stroke work index during the acute event was significantly greater in group A than in group B (33.4 +/- 2.4 vs 23.4 +/- 2.0) (p less than 0.05). During a follow-up of 9 +/- 3 months, mortality was not significantly different between the two groups: Four (25%) died in group A and seven (30%) died in group B. In addition, eight patients (50%) in group A were hospitalized for recurrent angina, new myocardial infarction or recurrent pulmonary edema, compared with 11 (48%) in group B (NS). Three deaths in group A were preceded by infarction of the anterior wall of the left ventricle, confirmed at autopsy, and two nonfatal infarctions were anterior by electrocardiography. Four patients in group A had coronary arteriography performed during the follow-up period because of unstable angina, and all had significant (greater than or equal to 70% stenosis) three-vessel disease and two had left main coronary artery disease. Therefore, the predischarge ejection fraction did not predict prognosis for this group of patients. Patients with acute pulmonary edema in the course of myocardial infarction form a high-risk group despite good resting left ventricular function at discharge. They have a significant incidence of recurrent myocardial infarction and death and, because they have good residual left ventricular function, are excellent candidates for surgical intervention.
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PMID:Prognosis of patients with acute pulmonary edema and normal ejection fraction after acute myocardial infarction. 684 21

The natural history of acute cardiogenic pulmonary edema was studied in a group of patients who did not have acute myocardial infarction, cardiomyopathy, or valvular heart disease. Most of these patients had coronary artery disease. Cardiac catheterization in selected patients showed depressed contractility in some with segmental abnormalities. In the group older than 70 years, this carried a 70 percent two-year mortality rate. It is important to approach patients with this syndrome vigorously, both diagnostically and therapeutically. Acute, reversible segmental ischemia may be responsible for this syndrome and may respond to measures designed to prevent recurrent ischemia.
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PMID:Acute pulmonary edema due to ischemic heart disease without accompanying myocardial infarction. Natural history and clinical profile. 688 Nov 86

In a normal lung at an altitude of 2000 meters the pO2 in the alveolar air is 77 mm Hg. At 3800 meters it drops to 57 mm Hg. In the healthy individual increasing hypoxia leads to hypoxemia, tachycardia at low levels of exercise, increased sympathetic tone, pulmonary hypertension and, in some instances, retention of water. Under these circumstances acute mountain sickness or high altitude pulmonary edema may occur. In patients with marginal cardiocirculatory function these effects of hypoxia are potentially dangerous and may lead to cardiac decompensation. Patients with coronary artery disease, congestive heart failure, arrhythmias, pulmonary hypertension and valvular heart disease can tolerate altitude and air travel only if, with adequate therapy, they are either asymptomatic or only slightly symptomatic at rest, or if they show some functional reserve during exercise testing.
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PMID:[Staying at high altitudes and plane travel for heart patients]. 724 86

Percutaneous balloon mitral valvulotomy (PBMV) with the Inoue-balloon is a proven therapy in young patients with mitral stenosis. In this study, we investigated primary results in PBMV of elderly patients. In 383 patients with mitral stenosis PBMV was done with the Inoue-balloon. We compared primary success rates and short-term follow-up of 287 (74.9%) < 65-year-old patients and 96 (26.1%) > or = 65-year-old patients. Elderly patients were more likely to have atrial fibrillation (58% vs. 45%; p < 0.05), tricuspid regurgitation < or = II degrees (58% vs. 45%; p < 0.05), coronary artery disease (16% vs. 6%; p < 0.01), and previous pulmonary edema (42% vs. 30%; p < 0.05). PBMV was successful in 73.9% of the elderly and 84.7% of the younger patients (p < 0.05). Mitral valve gradients could be reduced from 12.5 +/- 11.6 mm Hg to 6.2 +/- 6.8 mmHg (p < 0.001) in elderly patients and from 15.5 +/- 6.9 mm Hg to 7.0 +/- 3.2 mm Hg (p < 0.001) in younger patients. Mitral valve areas increased from 1.0 +/- 0.3 cm2 to 1.6 +/- 0.5 cm2 (p < 0.001) in elderly patients and from 1.0 +/- 0.3 cm2 to 1.7 +/- 0.4 cm2 (p < 0.001) in younger patients. No patient died during the procedure. Two younger patients had emergency surgery because of pericardial tamponade following transseptal puncture. After PBMV elderly patients had more often an increase of mitral regurgitation (47% vs. 35%; p < 0.05) without need of an emergency mitral valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Percutaneous mitral valvulotomy with the Inoue balloon in over 65-year-old patients--acute results and short-term follow-up in comparison with younger patients]. 778 96

The majority of hemodialysis patients die from cardiovascular disease. However, the contribution of myocardial infarction to mortality is relatively minor, despite the fact that coronary artery disease is common in uremic patients. Hypertension seems to be the major risk factor for the development of atherosclerosis in hemodialysis patients, although abnormalities of the lipid spectrum, characterized by an increase in triglycerides and very low density lipoprotein levels and a decrease in high-density lipoprotein levels, are frequent in hemodialysis patients. The existence of left ventricular (LV) hypertrophy is a serious risk factor for morbidity and mortality in hemodialysis patients. LV hypertrophy can present as a dilated cardiomyopathy or as concentric or asymmetric septal hypertrophy. Loss of myocardial contractility by coronary artery disease or carnitine deficiency can lead to systolic LV dysfunction with a compensatory dilated cardiomyopathy. Furthermore, the presence of a hypercirculation in uremic patients, resulting from anemia, the arteriovenous fistula, or fluid overload, can also lead to a dilated cardiomyopathy. Systolic LV dysfunction occurs when the increase in LV wall thickness is inadequate for the increase in LV radius, which might be caused by increased levels of parathyroid hormone. LV diastolic dysfunction, resulting from an increase in LV mass due to the effects of hypertension or to uremic interstitial fibrosis, can both lead to pulmonary edema and hypotensive periods during hemodialysis and is a severe risk factor for mortality in hemodialysis patients. Therefore, in uremic patients, anemia should be corrected and hypertension adequately treated early in the development of renal failure. Chronic fluid overload should be prevented by adequate estimation of optimal dry weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular aspects in renal disease. 792 20


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