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

The choice of the initial asanguinous fluid--either crystalloid or colloid--used for the resuscitation of the hypovolemic patient remains controversial. Colloid supporters argue for the careful preservation of the plasma colloid osmotic pressure (PCOP) to protect the lung from pulmonary edema. A careful analysis of the Starling microvascular forces operative at the pulmonary capillary makes such an effect unlikely. In fact, the lung is relatively immune to hemodilution and any decrease in PCOP is roughly one fourth as important as increases in hydrostatic pressure in causing increased fluid exchange. A critical review of the experimental and clinical studies comparing crystalloid versus colloid resuscitation essentially shows no physiologic difference in the two solutions. Using the thermal-green dye technique of extra-vascular lung water (EVLW) measurement in twenty crystalloid resuscitated trauma (n = 10) and burn (n = 10) patients, we have specifically evaluated the pulmonary effects of profound depression of PCOP and a negative PCOP - PAWP gradient (a shorthand form of the Starling equation argued to predict the presence of pulmonary edema if + 4 mm Hg or less). Average resuscitative fluid volumes during the first two hospital days were: 31.8 litres of crystalloid and no colloid for each burn patient; and 18.5 liters of crystalloid, 21 units of blood and 1 liter of colloid (as fresh frozen plasma) for each trauma patient. EVLW remained in the normal range of 7.0 +/- 1.0 ml/kg during the first five hospital days for all patients despite profound decrease in PCOP (less than 15 mm Hg) and a low or negative PCOP - PAWP gradient. Crystalloid resuscitation clearly is not harmful to the lung and it is equally as effective as colloid resuscitation. Crystalloid is markedly less expensive than colloid and, given the greater cost of colloid without evident benefit, one wonders how their further use can be justified.
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PMID:Crystalloid versus colloid for fluid resuscitation of hypovolemic patients. 634 5

The pulmonary edema (PE) induced by adrenaline (AD) administration is similar to neurogenic PE. Anisodamine (ADM, 654-2, 30 mg/kg) and tetramethylpyrazine (TMP, 120 mg/kg) have shown significant preventive effects. Electron microscopic observation was carried out to study the changes of microvascular permeability, and the dynamic change of mean pulmonary arterial pressure (PAP, 40 rats), mean pulmonary arterial wedge pressure (PAWP, 20 rats) and mean carotid arterial pressure (CAP) were also measured. The results suggested that both ADM and TMP have significant inhibitory effects on PAWP and CAP increase, as well as on the damage responsible for the increase of microvascular and alveolar permeability.
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PMID:Hemodynamic and nonhemodynamic mechanism of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine--electron microscopic observation and measurement of pulmonary arterial, pulmonary arterial wedge and systemic arterial pressure (Part 2). 790 30

The haemodynamic and gas exchange abnormalities occurring in neurogenic pulmonary oedema (NPO) were examined retrospectively in 20 patients admitted to the Intensive Therapy Unit (ITU) over a 45-month period (February 1992 to November 1995). In 12 patients, where vasoactive therapy with dobutamine was employed, its effect on haemodynamics was examined. Cardiac index (CI median 2.2 l min-1 m-2) and left ventricular stroke work index (LVSWI 20 g.m.m-2) were markedly depressed, while pulmonary artery wedge pressure (PAWP 17 mmHg), mean pulmonary artery pressure (MPAP 30.5 mmHg), systemic vascular resistance index (SVRI 2852 dyne.s.cm-5.m2) and pulmonary vascular resistance index (PVRI 393 dyne.s.cm-5.m2) were substantially elevated above normal values. Mean arterial pressure (MAP 82.5 mmHg) and heart rate (HR 102 bpm) were within normal limits. The poor oxygenation is indicated by a median PaO2/fiO2 ratio of 18.0 kPa. Patients treated with dobutamine showed significant increases in CI and LVSWI and significant falls in SVRI and PAWP at 2 and 6 h after institution of therapy, and there was a significant rise in PaO2/fiO2 ratio to 27.8 kPa at 6 h. NPO was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine.
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PMID:Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. 884 33