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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 frequently accompanies acute myocardial infarction (MI). We measured pulmonary arterial (PAP), left atrial (LAP), and aortic pressures (AP),lung lymph flow (QL), and clearance of total serum protein and each of eight protein fractions in five anesthetized sheep before and after coronary artery ligation. After a stable base line of 1 h, ligation produced significant increases in LAP, QL, and clearance of total protein and four protein fractions, but no significant changes in PAP, AP, or lymph-to-plasma total protein concentration ratio (CSL/CSP). Variables returned to pre-MI levels within 2 h after occlusion. The ratio of wet to dry lung weight measured 2 h after ligation was within normal limits. Two sheep in which the time course of postligation LAP was duplicated by left atrial balloon inflation showed no change in QL. The QL changes seen cannot be caused by LAP increase alone without substantial decrease in CSL/CSP. Increased QL with high CSL/CSP is typical of increased lung vascular permeability, which is a plausible explanation of our results.
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PMID:Increased lung lymph transport without heart failure after coronary ligation in sheep. 51 87

The goal of fluid therapy in the PACU setting is the restoration of blood volume and tissue perfusion. Choosing the type of fluid infusion depends on the preoperative, intraoperative, and postoperative condition of the patient. An understanding of the functional fluid compartments, the composition of body fluids and commercially available fluids, and the steps to evaluate fluid depletion allow one to determine the fluid needs of the patient. The orderly and expedient evaluation of fluid status of the postoperative patient involves the assessment of volume status, concentration status, composition status, and signs and symptoms of inadequate tissue perfusion. Recovery after surgery is a dynamic process, and fluid reassessment should be conducted periodically. Fluid challenges may be necessary in the hypovolemic patient or in patients with clear signs and symptoms of end-organ hypoperfusion. Weil and Rackow and Shoemaker provide useful approaches to fluid challenge guided by CVP and PAP monitoring. The decision of whether to use crystalloids or colloids for fluid resuscitation is complex, controversial, often determined by personal preference and concern over expense, and may be inconsequential as long as fluids are infused appropriate to the needs of the patient. There are disadvantages and advantages to both crystalloid and colloid fluid administration. As with any therapeutic intervention, there are complications with fluid administration, congestive heart failure and pulmonary edema being of more immediate concern. Finally, blood components are colloid-type solutions that should be reserved for specific patient problems. Red blood cells are indicated to increase oxygen-carrying capacity in patients with anemia. Platelets are used to treat bleeding associated with deficiencies in platelet number or function. Fresh frozen plasma is transfused to increase clotting factor levels in patients with demonstrated deficiency. A good understanding of fluid types available, of a systematic approach to evaluating fluid depletion, and of the indications for blood component therapy will allow one to make appropriate decisions when implementing fluid therapy in the PACU.
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PMID:Fluid therapy in the PACU. 204 19

Acute pulmonary edema can be induced by phorbol myristate acetate (PMA). Oxygen radicals released from the neutrophils have been considered to play an important role in the pathogenesis of PMA-induced pulmonary edema. In the present experiment, we studied the effect of dimethylthiourea (DMTU) on PMA-induced pulmonary injuries in isolated perfused lungs of rats. DMTU is a potent scavenger of the hydroxyl radical and hydrogen peroxide. PMA infusion into the isolated lung increased pulmonary arterial pressure (delta PAP) by 37.8 +/- 3.9 mmHg. The lung weight gain (LWG) and lavage albumin concentration (LAC) amounted to 6.2 +/- 1.2 g and 102.0 +/- 22.9 mg/dl, respectively. DMTU (100 mM) pretreatment significantly reduced the PAP increase (delta PAP = 4.6 +/- 0.8 mmHg, p less than 0.001), LWG (0.3 +/- 0.1 g, p less than 0.01) and LAC (25.3 +/- 1.7 mg/dl, p less than 0.01). Additional in vitro experiments demonstrated that DMTU depressed the chemiluminescence released from neutrophils activated by PMA (17.9 +/- 2.6 mV.min to 2.6 +/- 0.5 mV.min, p less than 0.01). The results suggest that DMTU, a scavenger of toxic radicals, decreases the lung edema through both attenuation of pulmonary hypertension and protection of vascular permeability from PMA injury.
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PMID:Dimethylthiourea decreases acute pulmonary edema induced by phorbol myristate acetate in isolated blood-perfused lung of the rat. 211 32

Ethanol is a pulmonary vasoconstrictor in rat lungs perfused in situ with Krebs-Henseleit salt solution. Pentobarbital-anesthetized rats were tracheotomized, and an in situ recirculating isolated lung perfusion was instituted using a Krebs-Henseleit buffer with 3% bovine albumin at 37 degrees C. Changes in pulmonary arterial pressure and tracheal inspiratory pressure during intravenous ethanol infusion at four different cumulative doses were measured in normoxic (n = 6) and hyperoxic (n = 6) lungs, compared to normoxic perfusate (no ethanol infusion) controls (n = 6). Perfusate alcohol levels progressively increased in experimental groups. Perfusate gas and pH values were normal and not altered by ethanol. PAP increased by the end of ethanol infusion from 9.7 +/- 2 to 26 +/- 13 mm Hg in the normoxic group and from 10.6 to 22 +/- 9 mm Hg in the hyperoxic lungs (p less than .02); no change occurred in control lungs. Severe pulmonary edema occurred in 83% of the ethanol exposed lungs (vs. 0% of perfusate controls). Postethanol wet/dry weight ratios were twice normal (p less than .02). Pulmonary arterial pressure rose in two stages. First there was a 25-100% increase before airway pressure increased, representing pulmonary vasoconstriction. This was followed by a precipitous 100-500% transmitted pressure rise as severe pulmonary edema developed. Thus, we conclude that the vasoconstrictor effect of ethanol on the pulmonary circulation occurs in rats as well as in lambs, dogs, and humans. In isolated perfused rat lungs, the response is locally mediated.
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PMID:Ethanol induces acute pulmonary vasoconstriction in salt-perfused rat lungs. 274 52

While in animal experiments neurogenically initiated pulmonary edema is a well known event and is supposed to be due to centrally initiated hemodynamic disturbances ("neurohemodynamics") in patients with severe cerebral lesions fulminant alveolar edema is reported to occur very rarely. The questions addressed by this study are: 1. whether and to what extent changes in extravascular lung water (EVTVL) can be demonstrated in patients with a severe isolated cerebral lesion; 2. whether a relationship between the severity of the cerebral lesion and accompanying EVTVL changes can be proven; and 3. whether or not EVTVL changes are associated with corresponding changes in intravascular hydrostatic and oncotic Starling parameters; i.e. cardiogenic or noncardiogenic pulmonary edema accompanying the cerebral lesion. This study included 44 patients presenting with a severe isolated cerebral lesion and decerebrate posturing on admission. EVTVL (by thermo-dye double-indicator technique), pulmonary gas exchange (AaDO2/pAO2), colloid oncotic pressure (COP) and mean systemic arterial (SAP), mean pulmonary arterial (PAP), and pulmonary capillary wedge pressures (PCWP) were measured from the day of admission to the 6th day after the acute cerebral lesion maximally; in addition the microvascular pressure in the pulmonary bed and intravascular filtration pressure were calculated from the above mentioned parameters. The neurological status on admission and throughout the observation period was scored using the Innsbruck Coma Scale (ICS) and the neurological outcome by the Glasgow Outcome Scale (GOS). Statistical analysis was performed using the distribution independent Kruskal Wallis test, the correlation coefficient r (Pearsan and Bravais), and the Spearman rank correlation (RSp); values are given as means +/- SEM; the significance has been set at P less than 0.05. Our results reveal an overall increase in EVTVL from 8.8 +/- 0.8 ml/kg on the day of admission up to 11.3 +/- 1.6 ml/kg on the 4th day. While survivors (n = 13) remained within the normal range of EVTVL (less than 9 ml/kg), non-survivors (n = 31) started at an already elevated level (10.05 +/- 1.04 ml/kg) and reached their maximum values (15.4 +/- 2.3 ml/kg) on day 3 to 4. In 3 non-survivors these increased initial EVTVL values were accompanied by pathologically increased intravascular pressures, indicating that hydrostatic mechanisms were involved in the EVTVL rises. While the hydrostatic pressures normalized spontaneously, EVTVL values stayed within the pathological range throughout the remaining observation period.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cardiovascular and pulmonary changes in patients with an isolated cerebral lesion. II. Extravascular lung water and pulmonary gas exchange ("neurogenic lung edema")]. 277 40

The effects of the serotonin receptor blocker, ketanserin, were studied in a porcine Pseudomonas adult respiratory distress syndrome model. Swine, weighing 14-30 kg, were anesthetized and ventilated with 0.5 FiO2 and 5 cm H2O positive end expiratory pressure. Three groups were studied: saline control (C, n = 9), continuous intravenous Pseudomonas aeruginosa, 5.0 X 10(8)CFU/kg/min (Ps, n = 8), and Pseudomonas and intravenous ketanserin, 0.2 mg/kg, given at 20 and 120 min after the onset of the Pseudomonas infusion (KET, n = 5). Pulmonary arterial (PAP) and systemic arterial (SAP) pressures, cardiac index (CI), thermal Cardio-Green extravascular lung water (EVLW), pulmonary albumin flux (slope index, SI), arterial blood gases, and whole blood serotonin levels were measured and pulmonary shunt and pulmonary (PVRI) and systemic (SVRI) vascular resistance indices were calculated. At 3 hr the Ps group demonstrated significant (P less than 0.05) increases in PAP (34 +/- 1 vs C 13 +/- 2 mm Hg), EVLW (14.4 +/- 2.2 vs C 4.3 +/- 1.2 ml/kg), SI (2.05 +/- 0.23 X 10(-3) vs C 0.38 +/- 0.09 X 10(-3) U/min), pulmonary shunt (67 +/- 15% vs C 9 +/- 3%), PVRI (1599 +/- 89 vs C 184 +/- 14 dyn X sec X cm-5/m2), and SVRI (4542 +/- 774 vs C 2087 +/- 129 dyn X sec X cm-5/m2) and decreases in CI (0.9 +/- 0.1 L/min/m2 vs C 2.8 +/- 0.2 L/min/m2), PaO2 (93 +/- 17 Torr vs C 203 +/- 15 Torr) and arterial blood serotonin concentration (23.5 +/- 13% decrease from basal). Treatment with ketanserin was associated with maintenance of PaO2 (KET 207 +/- 5 mm Hg vs C 203 +/- 15 mm Hg), pulmonary shunt (KET 8 +/- 3% vs C 9 +/- 3%), and CI (KET 2.3 +/- 0.1 L/min/m2 vs C 2.8 +/- 0.2 L/min/m2) at control levels and attenuated the Pseudomonas-induced increase in PVRI (873 +/- 37 vs Ps 1599 +/- 89 dyn X sec X cm-5/m2) and SVRI (2089 +/- 287 vs Ps 4542 +/- 774 dyn X sec X cm-5/m2), but did not alter the development of pulmonary edema. These data indicate that serotonin plays a role in the development of the V/Q mismatch and arterial hypoxemia observed in this model by a mechanism independent of changes in microvascular injury and permeability and was probably a result of reduced peripheral bronchiolar constriction.
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PMID:Serotonin receptor blockade improves cardiac output and hypoxia in porcine ARDS. 362 34

Variations in oncotic pressure-pulmonary artery diastolic pressure gradient and in intrapulmonary shunt were studied in two groups of patients undergoing surgery with extracorporeal circulation for aortocoronary bypass of excision of an aneurysm. The two groups, differed only in terms of the E.C.C. bath (Group A: Ringer Lactate; Group B: DDextran 60,000). The effects of E.C.C. on these parameters were as follows: - decrease in both groups in the gradient (OP-PAP) (respectively P < 0.001 and P < 0.01) but with a more marked decrease in group A than in group B (P < 0.05) with non-negativisation of the gradient in that group; - non-significant variations in Qs/Qt in both groups without any correlation with gradient (OP-PAP). The onset of pulmonary oedema associated with a decrease in gradient (OP-PAP) leads to the suggestion of the use of Dextrans in pathological situations where OP is low or PAP high and all the more so when both of these factors are present.
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PMID:[Comparison of two E.E.C. baths by study of the oncotic pressure-pulmonary artery pressure gradient]. 610 3

The inhalation of toxic gases or vapours is capable of resulting in pulmonary oedema (P.O.), the mechanism of which corresponds, on the basis of a number of hemodynamic studies carried out, to that which characterises the so-called "lesional" pulmonary oedema, which is different from so-called "hemodynamic" oedema. Classically PAP, PCP and P wedge pressure have virtually normal values (normalisation of pulmonary arterial hypertension by correction of hypoxemia). CI and SWILV are normal or increased and pulmonary resistances are virtually normal. The origin of the oedema is thus related to an increase in alveolo-capillary permeability. The inhalation of toxic gases or vapours with a caustic or irritant action, or containing particles, however, usually adds on an obstructive syndrome, similar to a severe asthmatic attack. Under such conditions, the marked reduction in intrathoracic pressure during inspiration definitely favours pulmonary oedema by decreasing intra-alveolar pressure and by the accumulation of blood in the pulmonary circulation, and is capable of masking pulmonary arterial hypertension. Raised pressure, related to expiratory effort, on the contrary, decreases venous return and may result in collapse of the capillaries. Whilst the principal mechanism of PO by the inhalation of toxic gases or vapours is related to an increase in alveolo-capillary permeability, it is nevertheless important not to under-estimate the role of variations in intra-thoracic pressures which may constitute a provoking or at least aggravating element.
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PMID:[Pulmonary edema of toxic origin. Hemodynamic data]. 611 Dec 79

Pulmonary artery pressure (PAP systolic and diastolic) and heart rate (HR) have been recorded in conscious or anesthetized cats. Experiments have been carried out before and after bilateral vagotomy or section of vagal afferents at the level of the nodose ganglion. Animals were exposed to different levels of oxygenation using FIO2 from 0.11 to 1.00. The results show that: 1 Anesthesia with sodium pentobarbital did not affect PAP for a given level of FIO2 : changes in PAP caused by modifications of FIO2 were not affected by anesthesia. Heart rate was independent of FIO2, but remained always higher in the anesthetized animals (Fig. 4). 2 In anesthetized animals, pulmonary de-afferentation or vagotomy affected neither PAP, nor its variations with FIO2 nor HR (Fig. 5). 3 In conscious animals, PAP and its variations with FIO2 were not affected by vagotomy (Fig. 6 and 7) or pulmonary de-afferentation (Fig. 8). On the other hand, heart rate was always decreased after either vagotomy or pulmonary deafferentation. It is concluded that (1) PAP and its control by FIO2 are independent of the vagal innervation; (2) the pulmonary edema observed after vagotomy cannot be caused by an increase in lung vascular pressure; (3) anesthesia, on the one hand, and pulmonary afferents, on the other hand, can play a role in the control of the cardiovascular activity.
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PMID:[Vagus nerves and pulmonary artery pressure in the conscious and anesthetized cats using different levels of oxygenation (author's transl)]. 724 93

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


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