Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the beta-agonist, ritodrine HCl, was studied on cardiac output (CO) and pulmonary lymph flow (QL) in sheep. Increased CO is associated with an increase in pulmonary QL in sheep during exercise. Isoproterenol increases CO but has not been shown to increase pulmonary QL. Ritodrine HCl was chosen because of its association with pulmonary edema when used to halt premature labor in pregnant women. Unanesthetized sheep received an intravenous infusion of ritodrine in increasing doses over 4 h up to a maximum of 6.3 micrograms/kg/min. Pulmonary pressure increased 2 mmHg after 1 h and returned to baseline by hours 3 and 4 with no change in left atrial pressure or lymph to plasma protein ratio. Pulmonary QL increased by 61% and CO by 80% at hour 3 of infusion (ritodrine dose 5.4 micrograms/kg/min) and remained at this level. Pulmonary QL and CO (normalized to baseline) correlated, r = 0.72, p less than 0.001, but there was no correlation between pulmonary QL and calculated microvascular pressure. Although an increase in pulmonary microvascular endothelium permeability with concurrent pulmonary vasodilation can not be completely ruled out, it appears from this study that beta-agonist therapy with ritodrine increases pulmonary QL by a CO related recruitment of microvessels.
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PMID:Effects of ritodrine infusion on hemodynamics and lung lymph in awake sheep. 180 92

The development of pulmonary injury in cases of antepartum pyelonephritis is rare but serious. To date, factors that might identify patients at risk have not been determined. We compared 11 patients with pyelonephritis and pulmonary injury with 119 patients with pyelonephritis only. Pulmonary injury was more likely to occur in the more severe cases; however, the presence of a maternal heart rate greater than 110 beats/min and a fever to 103 degrees F 12 to 24 hours before the occurrence of respiratory symptoms in a gestation greater than 20 weeks was highly predictive of pulmonary injury. The most significant predictive factors associated with pulmonary injury were elements of treatment such as fluid overload, use of tocolytic agents, and, to a lesser extent, choice of antibiotic. Therefore, if tocolytic agents are considered at all in the management of acute pyelonephritis in pregnancy, they should be used only in patients with documented cervical change. In addition, urinary output should be monitored very closely. These data also may suggest a cause of the pulmonary edema that is occasionally seen in the management of premature labor with the use of tocolytic agents and fluids in the presence of a possible occult infection.
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PMID:Pulmonary injury associated with antepartum pyelonephritis: can patients at risk be identified? 201 49

The treatment of premature labor with beta-adrenergic substances is complicated by side effects. Although most human control mechanisms are pulsatile, therapy is usually administered continuously. We designed a microprocessor-controlled pump to allow pulsatile tocolytic infusion, hoping to reduce the total dose and thus the side effects. In 33 patients pulsatile bolus tocolysis was compared with continuous tocolysis in a control group of 38 patients. Bolus tocolysis required considerably less beta-sympathomimetic agent for comparable therapeutic success (median dosage 3.0 versus 15.9 mg, p less than 0.001). Duration of therapy under bolus tocolysis was also significantly shorter (p less than 0.05). Birth weight was higher after bolus tocolysis (median 3070 versus 2580 gm, p = 0.05). Additional indicators favored bolus tocolysis but were not statistically significant: a longer gestational period, fewer infants weighing less than 2500 gm, and a lower incidence of respiratory distress syndrome. Pulmonary edema occurred in one patient during continuous tocolysis.
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PMID:Bolus tocolysis: treatment of preterm labor with pulsatile administration of a beta-adrenergic agonist. 256 41

We report a unique case of near fatal acute pulmonary oedema developing with intravenous ritodrine, given in an attempt to suppress premature labour. The novel aspect of the case is that the patient had also been treated in the previous week with high dose nebulized beta-agonists for an episode of acute severe asthma, demonstrating that this idiosyncratic reaction to beta-adrenergic agents only occurs with the intravenous route of administration. The management of acute severe asthma occurring in pregnancy is discussed with a review of previous literature regarding possible mechanisms of beta 2-agonist-induced pulmonary oedema.
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PMID:Asthma in pregnancy complicated by iatrogenic pulmonary oedema. 269 13

We describe a patient who developed acute pulmonary edema while taking oral ritodrine for the treatment of premature labor and recovered after its discontinuation. The mechanism of development of pulmonary edema associated with beta-sympathomimetic agents is still not fully understood. Patients taking oral ritodrine should be observed for cardiopulmonary signs and symptoms.
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PMID:Acute pulmonary edema associated with the use of oral ritodrine for premature labor. 291 9

The authors report on the results of treatment of threatening premature labour with clenbuterol. The daily dose was 40 micrograms twice and later 20 micrograms twice with good efficiency. Action of clenbuterol relating to tocolysis, metabolism and cardiovascular system has been compared with fenoterol-perlongettes. 61 pregnant patients were randomized by computer in two groups, 32 ones having clenbuterol tablets and 29 ones having fenoterol perlongettes. No electrocardiographic changes could be demonstrated with clenbuterol, but extrasystolic episodes have to be observed in two following fenoterol-perlongettes. No intravenous treatment is necessary using clenbuterol tablets. Therefore cardiac overload caused by liquid supply may be prevented, simultaneously the peril of pulmonary edema can be diminished. In our opinion tocolysis with clenbuterol tablets is a successful method of treatment of premature labor.
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PMID:[Tocolysis with clenbuterol tablets]. 332 63

The case of a 32-year-old parturient with a quintuplet pregnancy is described. The pregnancy had been complicated by premature labour which was treated with ritodrine tocolysis. Betamethasone was administered to hasten fetal lung maturation. The ritodrine therapy was complicated with fluid overload and pulmonary oedema requiring intravenous diuretic treatment. The patient presented urgently for Caesarean section, with fluid overload and worsening thrombocytopaenia. Life-threatening pulmonary oedema was manifest in the immediate preinduction period, following insertion of a pulmonary artery catheter and surgery was delayed to improve the mother's condition with intravenous diuretic therapy. Induction was carried out with the patient in the sitting position, with cricoid pressure maintained to protect the airway as the patient was lowered to a wedged, supine position. Intravenous nitroglycerin was used to control blood pressure. Low pressure mask-bag ventilation was utilized to maintain oxygen saturation and the patient was intubated and ventilated with positive end-expiratory pressure. Positive pressure ventilation was continued for 24 hours postoperatively. The perioperative course is reviewed and followed by a discussion of the anaesthetic considerations for multiple gestation pregnancies.
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PMID:Anaesthesia for caesarean section in a parturient with quintuplet gestation, pulmonary oedema and thrombocytopaenia. 340 18

A 26 year old previously healthy woman who was treated with fenoterol for premature labor at 30 gestational weeks developed pulmonary edema requiring intubation and mechanical ventilation. Vaginal delivery was accomplished with forceps after tocolytic therapy had been stopped. Right heart catheterization with measurement of pulmonary wedge pressure did not reveal left ventricular failure. Protein determination in lung edema fluid provided evidence of increased pulmonary capillary permeability. Recovery was rapid and ventilatory support was stopped after 36 hours. It is suggested that the infusion of beta-sympathomimetic drugs may alter the permeability of the alveolar-capillary membranes which together with triggering factors such as fluid overload might lead to clinically manifest pulmonary edema.
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PMID:High permeability pulmonary edema (ARDS) during tocolytic therapy--a case report. 340 80

Our hypothesis is that systemic tocolysis of patients in premature labor is associated with a higher incidence of pulmonary edema in the presence of maternal infection. Over a 64-month period, medical records of all patients with a diagnosis at discharge of pulmonary edema or congestive heart failure were reviewed. There were 27 cases of pulmonary edema, 16 of which (59.3%) were associated with treatment of preterm labor. The incidence of pulmonary edema in patients receiving systemic tocolysis for treatment of preterm labor was significantly higher than that in our general obstetric population (3.04% versus 0.05%). Of the 527 patients receiving tocolysis, there was evidence of maternal infection in 52. The incidence of pulmonary edema was higher in the presence of maternal infection than in its absence (11/52 or 21% versus 5/475 or 1%, p = 0.0000). We conclude that there is a very strong association between the development of pulmonary edema and the presence of maternal infection in patients being treated for premature labor with systemic tocolysis.
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PMID:Systemic tocolysis for premature labor is associated with an increased incidence of pulmonary edema in the presence of maternal infection. 342 Dec 69

The effects of intravenous (IV) ritodrine therapy on capillary endothelial damage and colloid osmotic pressure were examined in 15 patients in premature labor. Plasma fibronectin, a marker for capillary endothelial damage, did not change significantly after IV ritodrine therapy. Plasma colloid osmotic pressure was lowered following ritodrine therapy (P less than 0.05). Pretreatment plasma fibronectin levels in the study and control groups were similar. Interestingly, pretreatment colloid osmotic pressure in the study group was significantly lower than that of the control group (P less than 0.05). Our data suggest that there is no evidence of capillary endothelial damage following ritodrine therapy. Lower levels of plasma colloid osmotic pressure in patients with preterm labor, which are further reduced with IV ritodrine therapy, may predispose these patients to pulmonary edema.
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PMID:Does intravenous ritodrine therapy cause capillary endothelial damage? 365 Nov 92


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