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

Swan-Ganz hemodynamic monitoring in 49 antepartum patients with severe preeclampsia revealed a variable hemodynamic profile. The majority of patients had normal left ventricular filling pressure (8.4 +/- 0.2 mm Hg), normal to high cardiac index (4.4 +/- 0.1 L.min-1.m2), and upper normal to moderately elevated systemic vascular resistance (1226 +/- 37 dynes.sec.cm-5). Eight patients had pulmonary edema and their findings included high wedge pressure (18 +/- 1 mm Hg), upper normal to high cardiac index (4.9 +/- 0.5 L.min-1.m2), and normal systemic vascular resistance (964 +/- 50 dynes.sec.cm-5). Left ventricular function was hyperdynamic in 73% of the 49 patients. Patients with chronic hypertension and superimposed preeclampsia were hemodynamically indistinguishable from patients with preeclampsia alone. We conclude that, in general, preeclampsia is a high cardiac output state associated with an inappropriately high peripheral resistance. The normal wedge and central venous pressures suggest central redistribution of intravascular volume if the generally accepted reports of decreased plasma volume in preeclampsia are correct.
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PMID:The central hemodynamics of severe preeclampsia. 260 96

A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.
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PMID:Cardiorespiratory collapse and pulmonary oedema due to intravascular absorption of prostaglandin F2 alpha administered extraamniotically for midtrimester termination of pregnancy. 260 61

Cardiomyopathy developed in the peripartum period in two healthy primigravida at 41 and 42 weeks of gestation are presented. In the first case, the patient presented with pulmonary oedema and had cardiac arrest immediately after admission. After resuscitation, a live baby was delivered by Caesarean section. Second cardiac arrest occurred after 12 hours of operation and the patient was resuscitated again. On the 8th post operative day, patient died of D.I.V.C. and renal failure. The second case was a twin pregnancy associated with pregnancy induced hypertension. Caesarean section was performed for foetal distress. She developed pulmonary oedema with left ventricular failure on the second post operative day, was resuscitated and discharged on the 15th day. These are the first two cases to be reported from Hospital University Sains Malaysia. Reference is made to three other cases in which a similar pathological process might have occurred.
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PMID:Cardiomyopathy in pregnancy: 2 case reports. 260 81

We present a rare case of aortitis syndrome associated with dilatation of aorta and coarctation-like effect due to the intraluminal flap formation originated from dissected wall of the aorta. A 31-year-old woman was admitted to our hospital complaining of shortness of breath, palpitation and cough. On admission, her physical status showed congestive heart failure and hypertension of upper extremities and hypotension of lower extremities. Bruits were audible over the neck, the anterior chest and the back. Serological studies showed active inflammation. Chest X-ray film showed upper mediastinal widening, cardiomegaly and pulmonary edema. Aortitis syndrome was strongly suggested by these clinical findings, so that prednisolone therapy was started on 3rd hospital day. Special examinations were performed several days later when inflammatory changes showed a tendency to improve. Chest CT scan, RI angiography and MRI studies showed an aneurysmal dilatation from the ascending aorta to the mid-thoracic aorta. Aortography demonstrated a flap at the terminal portion of this aneurysmal dilatation and grade II (Sellars) aortic regurgitation. There was a pressure difference of 80 mmHg between the parts abutting cranial and caudal sides of the flap. A surgical operation was, then, performed to correct the pressure difference. The dissected wall was extruded toward the aortic lumen creating a flap (2 cm in length). This flap was resected and an artificial graft was inserted. Histologically, the flap consisted of adventitia, media and intima.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of aortitis syndrome which presented coarctation of aorta due to intraluminal flap formation in the middle of the thoracic aorta]. 272 9

To evaluate the early and late results of mitral valve replacement and reconstruction for mitral insufficiency due to ruptured chordae tendineae respectively, 74 consecutive cases were analyzed. Fifty-five (74.3%) of the patients were men, and the mean age was 48 +/- 12 years old (range 16 to 76). The causes of the mitral disease were idiopathic in 50 (67.6%), rheumatic in 7 (9.4%) and infective endocarditis in 11 (14.9%) patients. In idiopathic 50 cases, 24 had mitral valve prolapse and 16 had both mitral valve prolapse and hypertension. Forty-one (55.4%) of the patients were in NYHA functional class III or IV preoperatively. Thirty (40.5%) cases underwent surgery within one year after their initial symptoms of heart failure onsets including six emergency operation cases due to uncontrollable acute lung edema. Chordae to anterior mitral leaflet were ruptured in 31 (a5, m16, p10)[41%] patients, to the posterior mitral leaflet in 45 (a4, m23, p18)[59%], and to both leaflets in one patient. Mitral valve replacement was performed in 68 patients (91.9%) and 6 patients (8.1%) underwent mitral valve repairs. Twenty cases underwent associated procedures that included tricuspid valve annuloplasty in 8, aortic valve replacement in 5 and myocardial revascularization in 4 cases. There were two operative deaths (2.4%); both occurred after replacement, left ventricular rupture in one and DIC in one. Mean follow-up period was 4.5 years (range 1 to 17) in 67 cases. There were four late deaths; all occurred after replacement. However five patients sustained mild mitral insufficiency after mitral valve repair including one that became worse of regurgitation three years after isolated Kay's annuloplasty, there were no cases that had needed reoperation and no late death after reconstruction. Left ventricular function and pulmonary arterial pressure were almost normalized in more than 90% cases postoperatively. Our data indicated that mitral valve reconstruction (McGoon's plus Kay's method as standardized maneuver) was the procedure of choice for selected patients with mitral insufficiency owing to ruptured chordae tendineae to the posterior mitral leaflet, including more limited patients with ruptured chordae to the anterior mitral leaflet.
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PMID:[Mitral insufficiency due to ruptured chordae tendineae--clinical features, early and late results of valve replacement and repair]. 273 33

Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.
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PMID:Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak. 278 46

Hypertension is a well known risk factor of coronary artery disease. The aim of the study was to evaluate a clinical course and prognosis in hypertensive patients with acute myocardial infarction (MI). 100 consecutive patients with acute MI underwent the study. In 38 of them (28 males and 10 females) a history of hypertension and intermittent rises of arterial blood pressure in a course of MI were stated. All patients underwent 2-DE examination and 24 hours Holter ecg monitoring. Clinical characteristics consisted of the heart failure and arrhythmias occurrence as well as the in-hospital mortality. Significantly higher rate of MI in the past and/or angina pectoris as well as a diabetes mellitus was stated in hypertensive patients. In these patients inferior, transmural MI was more often observed, while there was no difference in life-threatening arrhythmias, pulmonary edema and cardiogenic shock between normotensive and hypertensive patients.
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PMID:[Myocardial infarction in patients with hypertension]. 281 Oct 21

The cardiovascular effects of relief of obstruction were examined in 21 patients with painless urinary retention and hydronephrosis and hydroureter associated with hypertension (diastolic blood pressure 95-120 mm Hg, mean 107, 11 patients), severe peripheral oedema (8 patients), raised jugular venous pressure (5 patients), or clinical evidence of pulmonary oedema (5 patients). Before relief of obstruction fractional sodium excretion was appropriate for the reduced rate of glomerular filtration. After urethral catheterisation blood pressure fell (p less than 0.001) and the other cardiovascular abnormalities were rapidly reversed without further therapeutic measures. This improvement was associated with an increase (p less than 0.05) in both absolute and fractional urinary sodium excretion that was greatest at 24 h. 5% of patients undergoing surgery for obstructive disorders of the lower urinary tract have hydronephrosis and hydroureter. Hypertension related to chronic urinary tract obstruction may be the commonest form of surgically correctable renal hypertension.
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PMID:Reversible hypertension associated with unrecognised high pressure chronic retention of urine. 288 94

We confirmed the findings of previous investigators that bilateral anodal lesions of the A1 region were associated with hypertension, bradycardia, pulmonary edema and a high mortality. All these sequelae (except the bradycardia) no longer occurred after cathodal lesions and these were therefore used to investigate the role of the catecholaminergic (CA) neurons of the A1 region in circulatory regulation. Conscious rabbits were studied 2-4 weeks after A1 lesions or sham-operation, when resting mean arterial pressure (MAP) and heart rate (HR) were closely similar in both groups. We tested for differences in MAP and HR responses between lesioned and sham-operated groups: to intracisternal (i.c.) alpha-methyldopa (MD) and to clonidine; and to the acute effects of i.c. 6-hydroxydopamine (6-OHDA) which elicits central CA release. Since these tests depend on the integrity of the central CA neurons, response differences between lesioned and sham-operated groups denote participation by the CA neurons of the A1 region in the central circulatory pathways. The bradycardia responses in the above tests were all smaller in lesioned than sham-operated rabbits, but there were no differences in MAP responses. Electrical stimulation of the region under alfathesin anaesthesia produced depressor responses at low frequencies and pressor responses at high frequencies. From the results in conscious rabbits CA neurons of the A1 region mainly influence the pathways regulating HR, rather than blood pressure. The changes in MAP during electrical stimulation are thus probably mediated through non-CA neurons.
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PMID:Cardiovascular role of A1 catecholaminergic neurons in the rabbit. Effect of chronic lesions on responses to methyldopa, clonidine and 6-OHDA induced transmitter release. 288 85

11 patients with atheromatous renovascular hypertension had a history of multiple episodes of pulmonary oedema. 7 had stenosis of both renal arteries, 2 had stenosis of the artery to a solitary kidney, and 2 had unilateral stenosis with an intact contralateral kidney. Successful revascularisation (by angioplasty in 8, and surgery in 3) improved blood pressure and renal function, and virtually eliminated pulmonary oedema. In a second series of 55 consecutive patients with azotaemia and renovascular hypertension, pulmonary oedema occurred in 13 (23%). Blood pressure and renal function were not significant predictors of pulmonary oedema, but coronary heart disease and bilateral (vs unilateral) renal artery stenosis were. Bilateral renal artery stenosis may be a specific and treatable predisposing factor to pulmonary oedema in azotaemic hypertensive patients.
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PMID:Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. 290 Sep 30


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