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

Isoproterenol inhalation increases the pulmonary edema induced in rats by phenylthiourea. Propranolol decreases this response while phenoxybenzamine has no effect upon it. It is proposed that the observed increase in toxicity is related to the beta-adrenergic effects of the isoproterenol and that the specific mechanism responsible might be an increase in pulmonary capillary hydrostatic pressure which is secondary to an increase in pulmonary blood flow.
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PMID:The action of isoproterenol on phenylthiourea induced pulmonary edema. 118 84

A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin B1. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.
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PMID:Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink. 141 37

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

Although catecholamine inotropic drugs are often used to support the circulation of critically ill patients with hypoxemic respiratory failure, their effect on the pulmonary circulation and on gas exchange is incompletely understood. In order to improve our understanding of the effects of these drugs on the pulmonary circulation, we made measurements of total and regional intrapulmonary shunt (Qs/Qt), distribution of pulmonary blood flow, and pulmonary hemodynamics before and after infusions of dopamine (n = 6, 5 micrograms/kg/min), dobutamine (n = 6, 10 micrograms/kg/min), isoproterenol (n = 6, 0.1 micrograms/kg/min), or saline in dogs with unilobar oleic acid-induced pulmonary edema. In addition to permitting determination of the overall hemodynamic and gas exchange effects of these drugs, this preparation allowed measurement of changes in distribution of pulmonary blood flow between normal and edematous lung. In 6 dogs given dobutamine, mean cardiac output (CO) increased by 1 liter/min, while pulmonary arterial pressure (PPA) increased by 2 mm Hg with no change in pulmonary vascular resistance (PVR) or distribution of pulmonary blood flow. There was a 5% increase in mean Qs/Qt which, because of the lack of evidence of pulmonary vasoactivity, was attributed to time or to increased CO. Isoproterenol produced a similar increase in CO, but reduced PPA and PVR indicating pulmonary vasodilator activity. Pulmonary vasodilation was most prominent in edematous lung, resulting in an increase in relative blood flow to the edema lung lobe and a substantial increase in Qs/Qt, exceeding the increase in all other groups. Dopamine, similarly increasing CO, did not change overall PVR but reduced fractional blood flow to the edema lobe by 3.4% of CO. Neither Qs/Qt nor PaO2 changed significantly in this group. The differing effects of these agents on pulmonary hemodynamics, intrapulmonary blood flow distribution, and gas exchange have potentially significant implications affecting the choice of drug used for circulatory support in hypoxemic respiratory failure.
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PMID:The pulmonary vascular effects of dopamine, dobutamine, and isoproterenol in unilobar pulmonary edema in dogs. 333 8

Intravenous isoprenaline was given to 10 patients in septic shock, of which occult myocardial failure was the main indication. Isoprenaline expedited recovery in cases of "benign hypotension," where kidney function paradoxically remained satisfactory at low systolic pressures, and was useful in cases of "cold hypotension" which were complicated by renal failure alone. No significant improvement occurred in cases which were complicated by both massive pulmonary oedema and acute renal failure.
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PMID:Intravenous isoprenaline in treatment of septic shock in man. 544 79

The objective of the present study was to determine whether the ability of the beta-adrenergic agonist isoproterenol to attenuate pulmonary edema occurs via a permeability and/or hemodynamic mechanism. In isolated perfused rabbit lungs, the restrictive property of the vascular barrier to the movement of fluid and protein was assessed by measurements of the capillary filtration coefficient (Kf) and the transvascular clearance of 125I-labeled albumin, respectively. Regression analysis of albumin clearance vs. transvascular fluid flux was performed to estimate the permeability-surface area product (PS) and the reflection coefficient (sigma) by use of the linear or nonlinear flux equation. Arterial, capillary, and venous pressures and resistances, weight gain, and the wet-to-dry weight ratio were also assessed. Isoproterenol (8 ng.ml-1.min-1) attenuated the arachidonic acid (4 mg)-induced increases in fluid flux, wet-to-dry weight ratio, albumin clearance, and PS and the decrease in sigma. Isoproterenol had no effect on the increase in Kf, and there was no correlation between capillary pressure and fluid flux in any of the four groups. Regression analysis revealed that the non-linear flux equation provided estimates of PS and sigma that more accurately described the statistical differences in albumin clearance among the groups studied than the linear flux equation. These findings demonstrate that isoproterenol attenuated the increased transvascular flux of albumin in edematous lungs by modifying the protein permeability of the vascular barrier.
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PMID:Isoproterenol decreases protein permeability in edematous isolated rabbit lungs: estimation of PS and sigma. 796 Dec 54

A 21-year-old woman developed noncardiogenic pulmonary edema within 90 min after the use of buprenorphine, 0.2 mg, sublingually for severe dysmenorrhea. No organic cardiovascular illness was detected. The pulmonary edema resolved spontaneously with conservative treatment. The mechanism of pulmonary edema may be an allergic reaction to buprenorphine.
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PMID:Noncardiogenic pulmonary edema induced by sublingual buprenorphine. 802 Feb 99

A 21-year-old man; complaining of left chest pain and dyspnea, was admitted to our hospital with a diagnosis of spontaneous pneumothorax. Though chest X-ray on admission did not show hemothorax, chest drainage revealed intrapleural bleeding. As chest X-ray on the following day showed evident fluid level, emergency operation was carried out with a diagnosis of spontaneous hemopneumothorax. Bleeding point was a ruptured vessel between parietal pleura and bulla in apex of lung. The bulla was resected following hemostasis. After improvement of complicating postoperative re-expansive pulmonary edema, the patient was discharged on the 18th postoperative day. On treatment of spontaneous hemopneumothorax, existence of such a case as ours should be taken into account.
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PMID:[A case of spontaneous hemopneumothorax occurred after thoracic drainage]. 978 30

A 21-year-old male with bilateral pneumothorax underwent thoracoscopic bullaectomy in the lateral decubitus position. General anesthesia was induced using thiopental 250 mg and suxamethonium 80 mg and maintained using the combination of the thoracic-epidural anesthesia with assisted spontaneous respiration. He was intubated with a tube equipped with mobile bronchial cuff. On the left bullaectomy, two lung ventilation (TLV) was applied and its course was uneventful. On the right, one lung ventilation (OLV) was done. Fifty minutes after the start of OLV of the left lung, percutaneous arterial hemoglobin saturation (SpO2) declined to 60% with PaO2 36 mmHg. Then, under super imposed HFJV (high frequency jet ventilation) added to manual assisted ventilation through the bronchial brocker, SpO2 increased rapidly to 100%. Postoperative chest X-p showed signs of re-expansion pulmonary edema (RPE) in the dependent, left lung. PaO2 after 25 minutes of hypoxic episode increased to 339.2 mmHg. About 2 hours later he was extubated uneventfully. We conclude that superimposed HFJV is very beneficial for treatment of the RPE of the dependent lung during OLV applied for thoracoscopic operation with bilateral pneumothorax.
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PMID:[A case of anesthetic management for re-expansion pulmonary edema of the dependent lung saved by superimposed HFJV during one lung ventilation for the thoracoscopic operation associated with bilateral pneumothorax]. 1088 44

Acute carbon monoxide poisoning is the most common cause of poison-related deaths in the U.S. A 21-year-old white woman was referred to Ruby Memorial Hospital after exposure to carbon monoxide (CO) from a faulty furnace. She developed acute weakness, dyspnea, nausea and vomiting. An electrocardiogram revealed sinus tachycardia, non-specific ST-T wave abnormalities, and a prolonged QTc interval. The chest X-ray revealed pulmonary edema and the 2-D echocardiography revealed decreased left ventricular systolic function with an ejection fraction of 25%. She was treated with high-flow oxygen and supportive medical therapy with complete resolution of the left ventricular dysfunction six weeks later. She has been followed for over one year without medical therapy and without recurrence of her symptoms. This case illustrates that the depressant effect of CO poisoning on the myocardium can be reversed in the short term with supportive medical therapy and recovery sustained in the long term without medical therapy.
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PMID:Carbon monoxide poisoning: a case report of reversible cardiormyopathy. 1577 62


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