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

The ability of the portable roentgenography of the chest to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in 37 observations of 11 patients. Ten of the 11 patients had acute respiratory failure. The roentgenologic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer measured lung water and the pulmonary arterial wedge pressure. The roentgenologic scores for edema did not predict the shunt fraction or tracer measured lung water. The roentgenologic score for congestive heart failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the roentgenograms were false-positive and 11 per cent were false-negative. Roentgenologic findings lagged behind physiologic derangements. Thus, the roentgenogram could predict the shunt value of the preceding day. Results indicate that it is hazardous to accept a portable roentgenographic diagnosis of congestive heart failure as a cause of pulmonary edema.
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PMID:Limitations of portable roentgenography of the chest in patients with acute respiratory failure. 64 29

We have studied the effect of the ventrical height of the pulmonary wedge catheter in the lung on the pulmonary wedge pressure-left atrial relationship during positive end-expiratory pressure ventilation in oleic acid-induced pulmonary edema. Pulmonary wedge catheters were placed above and below the left atrium in normal dogs and in dogs with oleic acid-induced edema. Wedge pressure and left atrial pressure were measured simultaneously during positive end-expiratory pressure ventilation (range, 0 to 30 cm H2O positive end-expiratory pressure). Pulmonary wedge catheters below the left atrium correctly recorded left atrial pressure and change in left atrial pressure at all positive end-expiratory pressures studied. Pulmonary wedge catheters above the atrium consistently recorded pressures higher than the normal left atrial pressure. They did not correctly respond to increases in left atrial pressure until it was increased to a value higher than the initial upper pulmonary wedge pressure. Pulmonary arterial catheters, when properly placed, should be reliable indicators of left atrial pressure during positive-pressure ventilation in normal and edematous lungs.
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PMID:The effect of Swan-Ganz catheter height on the wedge pressure-left atrial pressure relationships in edema during positive-pressure ventilation. 64 23

Systemic venous hypertension (SVH) is a frequent finding in pulmonary edema. To study the possible contributory or even causal role of SVH in pulmonary edema, a dog model was developed in which balloon catheters were placed in the left and right atria. Inflation of the left atrial balloon produced a tendency to pulmonary edema by causing pulmonary venous hypertension (PVH) (pulmonary artery wedge pressure of 20 mmHg). Inflation of the right atrial balloon produced SVH (central venous pressure of 15 mm Hg). After 2 hours, dogs with SVH with or without PVH demonstrated a greater amount of lung fluid accumulation (P less than 0.01) compared to controls or PVH alone. There was no significant difference in lung water in SVH dogs with or without PVH. Pulmonary blood flow was not significantly different between the experimental groups, each of which was less than control. Impairment of pulmonary lymphatic flow is one possible mechanism producing the worsening edema; however, bronchial venous hypertension or neurogenic reflexes cannot be excluded. We conclude that the contribution of systemic venous hypertension to the development of pulmonary edema may have therapeutic implications.
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PMID:Contribution of systemic venous hypertension to the development of pulmonary edema in dogs. 68 59

This is a prospective study on 24 patients with chronic renal failure. Thirteen of them had evidence of acute uraemic encephalopathy. Of those 9 patients were found to have dilutional hyponatraemia, two patients severe salt and water depletion and one patient septicaemia. Hyponatraemia was associated with pulmonary oedema in 3 patients. Correction of salt and water disturbances and treatment of heart failure improved cerebral functions in 10 (77%) patients. It is therefore concluded that dilutional hyponatraemia probably leading to cerebral oedema is a reversibe major factor in the development of acute uraemic encephalopathy. This, if left uncorrected, may prove fatal especially in tropical countries.
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PMID:Acute uraemic encephalopathy in tropical countries. 70 18

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.
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PMID:Effect of pulmonary microembolism on arteriovenous shunt flow. 70 53

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.
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PMID:Effect of afterload reduction on plasma volume during acute heart failure. 70 95

Monocrotaline, a plant alkaloid shown histologically to produce pulmonary endothelial damage and edema, was used in dogs to produce an acute model of noncardiogenic pulmonary edema. Following intravenous injection there was no change in pulmonary vascular pressures or heart rate; cardiac output fell and pulmonary vascular resistance increased. After 2 h measurement of lung water demonstrated modest pulmonary edema in all animals. The degree of edema produced was more consistent and reproducible than that following alloxan or alpha-naphthylthiourea.
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PMID:Monocrotaline model of noncardiogenic pulmonary edema in dogs. 73 Jun 1

Pulmonary oedema has been reported in severe cases of acetyl salicylic acid (ASA) poisoning. Liberal use of intravenous fluids, to establish a forced diuresis, is usually thought to be the precipitating cause. A case of severe ASA poisoning and respiratory failure was found to have increased pulmonary vascular resistance and signs of intravascular hypercoagulability. The patient recovered rapidly on mechanical ventilation with a positive endexpiratory pressure of 18 cm H2O and systemic steroids.
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PMID:Adult respiratory distress syndrome precipitated by massive salicylate poisoning. 73 81

Seven cases of submersion in the Dead Sea are described. The clinical picture varied in severity and consisted of signs of pulmonary edema, chemical bronchitis, hypermagnesemia and hemoconcentration. Two of the patients died of hypotension and cardiac arrhythmia. The clinical findings were similar to those found in cases of drowning in seawather, but the presence of hypermangesemia is unique to this entity. The amount of aspirated water causing severe clinical signs seemed to be much smaller than is seen with ordinary seawater. Therapeutic guidelines, including assisted respiration, infusion of hypotonic solutions and corticosteroid therapy, are suggested.
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PMID:Near drowning in the Dead Sea. 85 66

After successful rescue from drowning there may develop a situation which is called secondary drowning, resulting in acute respiratory distress characterized by interstitial pulmonary oedema, hypoxaemia, hypercapnia and acidosis during drowning, direct alteration of the alveolar membrane by aspirated water and particulate matters and a volume overloading by adsorption and--not seldom--inept therapy. This situation requires mechanical ventilation and forced diuresis, combined with high doses of steroids, antibiotics and digitalis. We present the case of an eleven year old patient whose clinical course demonstrate the necessity of exact clinical observation after rescue from drowning. After development of acute respiratory distress only the immediate utilization of the therapeutic modalities of an intensive care may result in a satisfactory outcome. Four months later our patient had normal pulmonary function except for a moderate reduction of compliance.
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PMID:[Acute respiratory distress syndrome after near-drowning (author's transl)]. 90 76


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