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

This retrospective study comprises 234 cases of accidental hypothermia (core temperature less than 35 degrees C) hospitalized in 95 Swiss clinics between 1980 and 1987. The most frequent accidents were alpine (n = 78) in origin, followed by cold exposure after injuries (n = 63) and suicide attempts (n = 43). Hypothermia was induced by cold air in 129 cases and by water in 47 cases. Patients were divided evenly between the degree of hypothermia: 75 mild (32-35 degrees C), 79 moderate (28-32 degrees C) and 66 severe (less than 28 degrees C). Among the survivors the coldest patient had a core temperature of 17.5 degrees C and the longest cardiac arrest with a favourable outcome lasted 4.75 hours. Out of the 234 patients 68 died (29%). We assessed all variables relative to outcome, in particular the mechanism of the accident, the mode of cooling, temperature, circulation, age and sex, underlying diseases, rewarming methods, medication and complications during the hospital course. All variables were tested in two multiple regression analysis models (retrospective model n = 181: prospective model n = 128) with regard to significance (p less than 0.05) and survival. Results are expressed with ODD's ratios (OR). The negative survival factors are asphyxia (OR 30), invasive rewarming methods (OR 20), slow rate of cooling (OR 10), asystole on arrival (OR 9), pulmonary edema or ARDS during hospitalization (OR 8), elevated serum potassium (OR 2/mmol/l) and age (OR 1.03/year). The positive survival factors are rapid cooling rate (OR 10), presence of ventricular fibrillation in cardiac arrest patients (OR 9) and presence of narcotics and/or alcohol during hypothermia (OR 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Accidental hypothermia in Switzerland (1980-1987)--case reports and prognostic factors]. 188 13

Sixteen patients (age 13-53 years) with accidental deep hypothermia have been rewarmed in our clinic during the last 10 years, 14 by femoro-femoral cardiopulmonary bypass (CPB) of whom 11 had a cardiopulmonary arrest (asystole in 5 and ventricular fibrillation in 6). On admission, the latter were clinically dead showing wide non-reactive pupils and being supported by ventilation and external heart massage. In the survivors, the mean length of cold exposure was 4.4 h (2-5.5 h) and mean arrest interval until initiation of CPB was 2.5 h (1.4-3.7 h). Rectal temperature on admission ranged from 17.5 degrees C to 26 degrees C (mean 22.5 degrees C). The causes for hypothermia were fall into a crevasse (5), avalanche (1), drowning (2) and cold exposure (3) including 2 suicide attempts. Results are summarized in the following table: [table: see text] Eight of the 11 patients with deep hypothermia and cardiac arrest were rewarmed and resuscitated successfully with CPB. Three patients, including 2 cases of asphyxia (avalanche and drowning), could not be weaned from CPB despite adequate rewarming. The other drowned patient (53 years) died on the 3rd postoperative day (POD) from ARDS. The main complication was pulmonary edema (57%) and transient neurological deficits. All survivors became conscious during the first POD and resumed, their professional activity. We conclude that patients with accidental deep hypothermia and even prolonged cardiopulmonary arrest should be rewarmed and resuscitated rapidly by cardiopulmonary bypass. These measures are very promising particularly if the cause of accident and the circumstances suggest that cardiopulmonary arrest was induced by hypothermia alone without other asphyxiating mechanisms.
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PMID:Accidental deep hypothermia with cardiopulmonary arrest: extracorporeal blood rewarming in 11 patients. 239 32

A portable heart-lung preservation system was developed to enable distant organ procurement. In 8 dogs, a functioning heart-lung system was isolated, cannulated in situ, removed en bloc, and placed into a Plasmalyte-filled, temperature-controlled (15-38 degrees C) chamber. The perfusion circuit consisted of an adjustable-height, autologous-blood reservoir. The heart ejected through the aortic cannula with venous return (VR) into the superior vena cava. Respiration was maintained with a positive pressure ventilator. Intramyocardial tissue pressure (IMP), tissue pH, right atrial (RAP), aortic pressure (AOP), and cardiac output (CO) were monitored. Autoperfusion at normothermia and CO of 50 mL/min/kg resulted in early (3 h) deterioration of pulmonary function with progressive interstitial lung edema. Pulmonary dysfunction always preceded changes in regional myocardial contractile viability (peak IMP and d(IMP)/dt) and global function (CO, AOP). When tissue pH was regulated ectothermically (as in cold-blooded animals) (delta pH/degrees C = -0.015) the heart maintained a stable pumping mode (greater than 6 h) at myocardial temperatures of 17-28 degrees C, pH = 7.70-7.55, and heart rate of 25-50 bpm, respectively. The results indicate that a viable (greater than 6 h) autoperfused, working heart-lung system can be achieved by reducing the circulating blood flow to 30-50% of normal CO. More significantly, ectothermic alpha-stat modulation of perfusate pH and pCO2 allows a substantial reduction in organ temperature and metabolic demand without endangering induction of fibrillation and ultimate allograft failure.
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PMID:Autoperfusing ectothermic heart-lung preservation system. 248 57

N-Methylthiobenzamide (NMTB) is a pneumotoxin which causes pulmonary edema and hydrothorax in rodents. Reserpine has been shown to attenuate the pneumotoxicity induced by NMTB. Some of that evidence suggests that the protection afforded by reserpine occurs independently of its capacity to reduce peripheral 5-hydroxytryptamine (5-HT). We therefore investigated 2 other pharmacologic properties of reserpine, namely: (1) its capacity to reduce lung norepinephrine (NE); and (2) its capacity to induce hypothermia, in order to more fully understand its mechanism of protection. Pretreatment of mice or rats with 6-hydroxydopamine at a dose which reduced lung NE by approximately 80% did not affect the pneumotoxic response to NMTB. Thus a decrease in lung NE probably does not account for reserpine's protective effect. An investigation of reserpine's effects on core temperature revealed that mice dosed with a combination of reserpine + NMTB presented with core temperatures lower than mice treated with either compound alone. Mice placed in a cold environment (2 degrees C) and dosed with NMTB presented with hypothermia and an attenuated toxic response to NMTB. Thus a reserpine-induced hypothermia could be allowing for a reduction of NMTB metabolism and consequent diminution of toxicity. These observations suggest that reserpine's capacity to protect animals against NMTB-induced pulmonary edema may in part be due to its capacity to induce hypothermia.
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PMID:Effect of reserpine on N-methylthiobenzamide-induced pulmonary edema: role of lung norepinephrine and hypothermia. 249 83

The effect of cold and/or a raised partial pressure of oxygen was examined in eleven people with no demonstrable cardiac abnormality but who had pulmonary oedema when scuba diving or surface swimming, and in ten normal divers. These stimuli induced pathological vasoconstriction in the pulmonary oedema group, nine of whom also showed signs of cardiac decompensation when so stimulated. The pulmonary oedema patients have been followed-up for an average of 8 years. Seven have become hypertensive. Except for the onset of lone atrial fibrillation in one normotensive female diver and development of Raynaud's phenomenon in a normotensive man, there have been no cardiovascular events and no deaths.
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PMID:Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension. 256 80

With methylprednisolone as a chemical inhibitor of leukocytes, extended preservation was conducted with an isolated rabbit lung model. The heart-lung blocks of 39 New Zealand white rabbits were flushed in situ with 100 ml of Euro-Collins' solution, harvested, inflated (70%), and preserved at 4 degrees C. Lungs immediately reperfused with whole blood (control lungs, group 1) were compared with lungs preserved without methylprednisolone for 5, 12, and 24 hours (groups 2 to 4) and those preserved with methylprednisolone for 12 and 24 hours (groups 5 and 6, respectively). Methylprednisolone (30 mg/kg) was administered before harvest and was used as an additive to the flush and in the blood reperfusate. Hypothermia and Euro-Collins' flush alone provided adequate preservation for up to 5 hours; however, lung edema was evident by 12 hours of cold ischemia and became severe by 24 hours. By all measured parameters, the lungs in group 5 (treated with methylprednisolone) demonstrated values equal to or better than control lungs. By 24 hours of preservation the beneficial effects of the steroid treatment were no longer evident. Histologic evaluation revealed mild to moderate injury after 5 hours of cold ischemia; progressive edema and hemorrhage were found after 12 and 24 hours of preservation. This injury was significantly ameliorated by methylprednisolone treatment at 12 hours but not at 24 hours. This study suggests that static preservation for up to 5 hours is possible with hypothermia and a Euro-Collins' flush and that extended preservation to 12 hours is possible with pharmacologic dosages of methylprednisolone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved static lung preservation with corticosteroids and hypothermia. 319 47

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

The measurement of lung water by the thermal-dye double indicator dilution technique was evaluated in dogs with normal and edematous lungs during a state of reduced cardiac output. The technique used cold indocyanine green dye to measure extravascular thermal volume (EVTV) as an estimate of extravascular lung water (EVLW). Anesthesia was maintained with pentobarbital. In 15 of 21 animals, pulmonary edema was first induced with oleic acid (0.75 to 0.18 ml/kg). Cardiac output (CO) was then decreased by a combination of propranolol and slow exsanguination (mean CO reduction to 36% of baseline). Extravascular lung water produced in this model ranged from 1.4 to 30.2 ml/kg. Predetermination measurements of EVTV correlated closely with EVLW as determined by gravimetric analysis (EVTV = 1.1 EVLW + 4.7 ml/kg, n = 21, r = 0.93, P less than 0.001). Thermodilution cardiac output measured in the abdominal aorta (used in the calculation of the EVTV) correlated well with simultaneous measurements of cardiac output by both indocyanine green dye dilution and pulmonary artery thermodilution (r = 0.86 and r = 0.88, respectively, pretermination). The thermal-dye technique appears to provide an accurate reflection of lung water in normal and edematous lungs, even in the presence of a low cardiac output.
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PMID:The thermal-dye method of lung water measurement is reliable at a low cardiac output. 376 35

It is widely accepted that extravascular lung thermal volume estimated by the double indicator dilution method with heat as a diffusible indicator reliably reflects pulmonary extravascular water volume. Theoretically, as a premise, the indicator should be preserved during its pulmonary circulation. We therefore investigated the thermal conservation during pulmonary circulation; that is, whether there was good agreement in the cardiac outputs "wherever" the thermodilution curves were recorded; for instance, the pulmonary artery trunk (PAT), giving COPAT,heat and the aortic root (Ao), giving COAo,heat. In the present study, we observed a total of 59 pairs of cardiac outputs in dogs (n = 13), including dogs with overt pulmonary edema, produced either by dextran infusion or by alloxan administration. We also studied a total of 23 pairs of cardiac outputs of human subjects (n = 16) with ischemic heart disease or mild mitral stenosis. A mixture of ice-cold 5% glucose solution and indocyanine green was rapidly injected into the right atrium. The thermodilution curve was immediately recorded in the pulmonary artery trunk, and the thermodilution and dye dilution curves were recorded in the aorta using a conventional Swan-Ganz catheter. The cardiac outputs were calculated manually following the Stewart-Hamilton principle. The results were as follows: In dogs, COPAT,heat averaged 2.47 +/- 1.21 L/min (mean +/- SD), COAo,heat averaged 2.44 +/- 1.12 L/min and the difference was not significant (0.3 less than p less than 0.5). The regression equation was COPAT,heat = 1.01 X COAo,heat + 0.02 (n = 59, r = 0.93, p less than 0.001) and the correlation coefficient was excellent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Double indicator dilution method using heat and dye to measure pulmonary extravascular water volume]. 391 10


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