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

Pulmonary edema occurred during and after Cesarean section under general anesthesia in two pregnant women. They had no preoperative complication. After delivery, anesthesia was maintained with 66% N2O in oxygen and intravenous injection of pentazocine and diazepam. At the same time, 0.2 mg of methylergometrin was injected intramuscularly and 2,000 micrograms of prostaglandin F2 alpha was injected to the muscle of the uterus in order to induce uterine contraction. In one case, SpO2 dropped and airway pressure increased immediately after the administration. In another case, chest rale was auscultated on postoperative round at 2 hours after operation. The cases suggest that pulmonary edema was caused by a large quantity of oxytocics, which increased volume load on systemic circulation.
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PMID:[Two cases of pulmonary edema during and after cesarean section]. 194 18

The aims of this randomized study were (1) to determine if isoflurane is effective in controlling blood pressure during thoracic aortic cross-clamping, and (2) to compare its effects on hemodynamics and oxygen transport to those of sodium nitroprusside. Sodium nitroprusside (SNP group, n = 10) or isoflurane (ISO group, n = 10) was started 2 minutes before cross-clamping and was adjusted to maintain systolic arterial pressure as near as possible to preinduction values. The duration of thoracic aortic cross-clamping was 26 +/- 4 minutes in the SNP group and 30 +/- 4 minutes in the ISO group. Administration of isoflurance and sodium nitroprusside was stopped 2 minutes before unclamping. The same anesthetic technique using fentanyl, 6 micrograms/kg, flunitrazepam, 0.02 mg/kg, pancuronium, 0.1 mg/kg, and 50% N2O was used for all patients. At the time of clamping, either isoflurance (maximal expired concentration, 2.5% +/- 0.3%) or sodium nitroprusside (cumulative dose, 11.1 +/- 1.0 mg) was effective in maintaining the systolic blood pressure below 160 mm Hg, whereas the pulmonary capillary wedge pressure did not change. However, only SNP was able to bring the arterial pressure above the cross-clamp back to postinduction levels. During clamping, stroke index values were similar in both groups, but cardiac index increased only in patients receiving SNP. In both groups, at clamping and unclamping, PvO2 was higher than postinduction values, indicating that throughout the study the oxygen needs of the perfused area were adequately met. There was no evidence of acute left ventricular decompensation because pulmonary capillary wedge pressures did not abruptly increase, nor did pulmonary edema occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of isoflurane with sodium nitroprusside for controlling hypertension during thoracic aortic cross-clamping. 213 64

Hepatocellular carcinoma is one of the leading cancers in Taiwan and is responsible for 20% of cancer deaths. Since long-term survival of hepatocellular carcinoma patients cannot be expected with any treatment other than surgery, the therapeutic value of hepatic resection has become more important than ever before. In Keelung Chang Gung Memorial Hospital, twenty-one patients with hepatoma received hepatic resection during the period of August 1985 to July 1989 were reviewed. These patients were induced for anesthesia with thiopental, succinylcholine and fentanyl; maintenance of anesthesia with isoflurane, N2O and O2. Four of them have abnormal coagulopathy preoperatively. Common intraoperative problems were metabolic acidosis and hypotension. Estimated blood loss showed great variety among these patients. Eighteen patients needed respiratory support and intensive care postoperatively. One patient was noted to have pulmonary edema. Otherwise, the overall procedure was smooth and satisfactory. In addition, there is no significantly difference in liver function test after a month of hepatoma resection. All the patients survived except one who died within two months after surgery.
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PMID:[Anesthesia for hepatoma resection]. 216 79

The aim of this study was to investigate whether the lagged normal density function is a useful model for the dispersion of intravascular and diffusible indicators in the lungs. In 18 mongrel dogs anesthetized with N2O-piritramide, 221 sets of thermal-indocyanine green dye kinetics were recorded in the pulmonary artery and in the aorta after central venous indicator injection. A model-free deconvolution technique was used to compute the pulmonary transport functions for dye and heart from the measured indicator kinetics (reference method). The lagged normal density function was used to model pulmonary indicator transport. Its parameters were computed by a nonlinear least-squares procedure by iterative convolution. After baseline measurements in nine dogs, pulmonary edema was induced by central venous application of oleic acid. In nine other dogs, measurements were performed before and after postural changes from the horizontal to the vertical position. The mean transit times derived from the lagged normal density function were in good agreement with those obtained after model-free deconvolution. Although the shape (relative dispersion, skewness) of the transport function is less well described by the model, the authors conclude that the lagged normal density function is useful to determine indicator volumes of distribution that require only the correct mean transit times.
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PMID:Validity of the lagged normal density function as a model for pulmonary indicator dispersion. 240 5

The aim of this study was to investigate whether changes in the distribution of pulmonary blood flow and disturbances of the pulmonary microcirculation can be detected by use of inflow-outflow indicator-dilution measurements. In 18 anesthetized (N2O-piritramide) mongrel dogs 221 thermal-indocyanine green dye indicator dilution kinetics were recorded in the pulmonary artery and aorta after central venous indicator injection. The lagged normal density function was used as a model for the pulmonary transport functions for heat and dye. The parameters of the lagged normal density function were computed by a non-linear least squares procedure by iterative convolution. After baseline measurements, in nine dogs, pulmonary edema was induced by central venous application of oleic acid. In nine other dogs, measurements were performed before and after postural changes. Our data show that both the microvascular injury caused by oleic acid edema and the perfusion heterogeneity caused by orthostasis can be detected by the indicator dilution technique since the both relative dispersion and skewness of the transport functions for heat and dye were significantly increased after these interventions.
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PMID:Characteristics of the pulmonary transport functions for heat and dye in pulmonary edema and orthostasis. 265 94

Our aim was to determine whether large central venous doses of ionic diatrizoate, nonionic iopromide, or nonionic iotrolane produce pulmonary edema or pulmonary congestion in dogs. Eighteen dogs (six per group) anesthetized with piritramide and N2O received three sequential doses (1.5 mL/kg body weight) of one contrast medium in less than 20 seconds. Before the first injection, and again 1, 5, 10, 20, and 30 minutes after each contrast injection, extravascular lung water, pulmonary blood volume, and cardiac output were determined by thermal-dye dilution. Neither extravascular lung water nor pulmonary blood volume increased after any contrast medium. Pulmonary blood volume and cardiac output decreased slightly but not significantly after all contrast media during the course of the study. We conclude that diatrizoate, iopromide, or iotrolane do not produce pulmonary edema or congestion in dogs.
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PMID:No pulmonary edema or congestion after central venous injection of conventional and newer contrast media in dogs. 320 83

This study evaluates the routine mathematic approach (monoexponential extrapolation) for analysis of transpulmonary thermal-dye dilution curves and estimates the effects of systemic-indicator recirculation by use of a deconvolution technique. Fifteen dogs anesthetized with N2O-piritramid were studied before and after induction of pulmonary edema by oleic acid. After introduction of central venous indicator (10 ml of a mixture of cold blood and indocyanine green dye), dilution data were recorded from the pulmonary artery and the ascending aorta. The conclusions were: (1) monoexponential extrapolation yields reasonably good estimates of the mean transit times of dye; (2) mean transit times of heat are usually overestimated by monoexponential extrapolation; (3) extravascular lung thermal volume assessed by monoexponential extrapolation is overestimated by 2.03 ml/kg of body mass under baseline conditions; and (4) the prepulmonary volume of distribution of heat exceeds that of dye by 1.4 ml/kg of body mass, thus increasing the overestimation of pulmonary extravascular heat-accessible space by the conventional technique.
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PMID:Evaluation of monoexponential extrapolation of transpulmonary thermal-dye kinetics by use of a new model-free deconvolution algorithm. 328 55

For indicator-dilution studies, complete thermal recovery after passage of heat through the pulmonary circulation would be desirable. However, the results in the literature obtained by extrapolation techniques are inconsistent. To overcome problems of the extrapolation approach, transport functions of the pulmonary circulation (including the left heart) were computed by deconvolution of pulmonary arterial and aortic pairs of thermodilution curves after central venous indicator injection (10 ml of an ice-cold blood indocyanine green dye mixture). Thermal recovery was determined as the finite integral of the transport function. Thirteen mongrel dogs under piritramid-N2O anesthesia were examined under base-line conditions, in orthostasis to alter the distribution of pulmonary blood flow (9 dogs), and in oleic acid edema (8 dogs). Using the deconvolution approach, thermal recovery was 0.97 +/- 0.04 under base-line conditions, 0.96 +/- 0.03 in orthostasis, and 0.96 +/- 0.05 in pulmonary edema. Thermal recovery determined from extrapolated dilution curves was greater than 100% in all groups, a physically impossible finding. It is concluded that thermal recovery is incomplete but insensitive with respect to the distribution of blood flow and to the size of the extravascular compartment. Monoexponential extrapolation is unsuited for the determination of thermal recovery.
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PMID:Thermal recovery after passage of the pulmonary circulation assessed by deconvolution. 328 69

Cerebral partial pressure of O2 (PO2), relative changes in the ratio of reduced/oxidized cytochrome aa3, blood flow, and the arteriovenous difference in O2 content were measured during seizures with and without pulmonary edema. Seizures were induced with bicuculline (0.2-1.2 mg/kg iv) in rats anesthetized with 70% N2O and paralyzed with curare. Briefer seizures were accompanied by increased cerebral PO2 and increased oxidation of cytochrome aa3. Lung water content and arterial O2 partial pressure (PaO2) remained normal. Longer duration seizures were also accompanied initially by increases in cerebral oxygenation. Within minutes, however, PaO2 fell from a mean of 118 to 51 mmHg, and lung water content increased from 76.2 to 83.6%. Cerebral PO2 fell but most often rose back to or above control levels, while cytochrome aa3 became markedly reduced. Simultaneously, cerebral blood flow increased more than 300% above preseizure values and O2 delivery increased more than O2 consumption. The reductive shift of cytochrome aa3 was greater than that produced by lowering PaO2 to equivalent values in seizure-free rats. The reductive shift of cytochrome aa3, despite increased O2 delivery, may be indicative of derangements in cerebral O2 diffusion or energy metabolism.
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PMID:Seizure-associated pulmonary edema and cerebral oxygenation in the rat. 355 25

A 33-year-old male was scheduled for tonsillectomy and pharyngoplasty due to sleep apnea syndrome. The intubation was uneventful following induction with thiamylal and vecuronium. Anesthesia was maintained with O2-N2O-sevoflurane. No complications were observed during the 90 min operation. After the termination of the anesthesia, a hyperadrenergic state was observed: arterial pressure and heart rate rose to 230/135 mmHg and 135 bpm, respectively. Immediately after extubation, he developed dyspnea with tracheal tag and stridor, and became cyanotic despite the use of a simple oxygen mask and assisted ventilation. Laryngospasm was suspected. The patient was reintubated and suctioned; pink, frothy sputum was not obtained. Arterial blood gases 5 minutes after reintubation revealed a pH of 7.24, Pao2 86 mmHg (FIo2 1.0), and Paco2 54 mmHg. Chest X-ray 30 minutes after reintubation revealed bilateral diffuse alveolar infiltration. The diagnosis was interstitial pulmonary edema. The patient was ventilated mechanically by applying a positive end-expiratory pressure of 5cm H2O, and furosemide and dopamine were administered intravenously. The patient was extubated the next day, and discharged from hospital ten days later. We considered that the lung edema was induced by the severe negative pressure generated by inspirating against a closed upper airway, as well as by the hyperadrenergic state and severe hypoxemia observed during and after extubation.
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PMID:[Pulmonary edema due to acute airway obstruction immediately after tracheal extubation]. 985 97


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