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

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.
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PMID:Cardiac-pulmonary edema and low pulmonary capillary wedge pressure. 50 73

After a subconjunctival injection of phenylephrine, cocaine and atropine, a patient's blood pressure rose to 220/180 mmHg. This rise was followed by hypotension, pulmonary edema, and subendocardial ischemia, all of which resolved spontaneously within 12 hours. This report reemphasizes the hazardous effects on blood pressure of phenylephrine applied to the eye.
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PMID:Systemic reaction to subconjunctival phenylephrine. 74 13

A standardized model of acceleration concussion in the rat was used for the study of cerebral energy metabolism during the acute concussive reaction. Impact velocities of 7 and 9 m/sec were used, and the cerebral metabolic state was determined 1, 4, and 15 minutes after the impact. A concussive response could be sustained with a normal energy state in the tissue, but with the more intense reaction to a 9 m/sec impact, energy depletion usually occurred. At 1 minute these changes were most pronounced in the brain-stem regions. At 4 minutes the reactions were more varied but a progression usually occurred during this time, while at 15 minutes restitution was indicated. Hypoxia due to neurogenic pulmonary edema aggravated the state. The findings are compatible with a high metabolic rate during concussion, but progressive changes indicate the rapid appearance of complicating factors, including hypoxemia and probably also ischemia.
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PMID:Exerimental head injury in the rat. Part 2: Regional brain energy metabolism in concussive trauma. 87 48

Fifteen postoperative surgical patients, in whom noncardiac pulmonary edema developed were studied. A presumptive diagnosis of left ventricle failure would have been based on historical evidence of heart disease (80%), electrocardiographic changes of ischemia or arrythmia (87%), or cardiogenic shock (20%). (see article) Fig. 6. PAEDP-PCW gradient. Note that arterial oxygen tension had an inverse relationship to this pressure differential. Roentgenographic findings included pulmonary edema (73%), pulmonary vascular congestion (60%), cardiomegaly or congestive heart failure (40%). Mean increase in A-aDO2 was 290 torr. Further cardiovascular investigation seemed to exclude left ventricular failure. Mean cardiac index was 4.1 plus or minus 1.3 L/min/m2; pulmonary capillary wedge pressure 4 plus or minus 2.7 torr, and stroke work was 87 plus or minus 8.7 gm-meters. Possible etiologic agents included elevated pulmonary artery pressure (67%), allergic reactions (27%), peritonitis or multiple system trauma (54%), or multiple transfusions (33%). Forty-seven per cent of the entire group survived. Therapy was directed toward the underlying noncardiogenic suspected etiology. Direct cardiovascular measurements were necessary to correct the erroneous though seemingly well founded suspected diagnosis of left ventricular failure in these patients.
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PMID:"Pseudocardiogenic" pulmonary edema. 111 52

Twenty-four dogs underwent in vivo left pulmonary hilar occlusion with the lung continuously expanded at 10 centimeters or 25 centimeters of water pressure to determine the period of pulmonary ischemia that may be tolerated before consistent pulmonary edema and congestion develop after lung revascularization. Consistent and prolonged pulmonary edema and congestion that caused death of the dog occurred in at least one-half of the dogs when the period of hilar occlusion was extended beyond six hours. Elevation of the left pulmonary artery pressure was only a rough measurement of the severity of the anoxic pulmonary injury. Expansion of the lung at 10 centimeters of water continuous pressure was more beneficial than was expansion at 25 centimeters of pressure. Cyclic ventilation with slight negative-expiratory pressure provided less support to the lung than did continuous expansion at either pressure tested. Intial decreases in both ventilation and perfusion isotope uptake and the percentage of the total volume of oxygen uptake per minute by the ischemic lung returned to near normal levels in three weeks in dogs that survived. Lung expansion during periods of ischemia appears to prevent alveolar collapse and to facilitate oxygenation.
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PMID:Evaluation of pulmonary function in the ischemic expanded canine lung. 125 71

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36

A traumatic transection of the upper descending thoracic aorta, undiagnosed, was complicated on the tenth day by an acute obstruction of the descending thoracic aorta. The upper body hypertension resulted in generalised convulsions and cardiac failure with pulmonary oedema. The lower body ischemia resulted in paraplegia, acute ischemia of the lower limbs, liver failure and anuria. An emergency revascularisation of the lower body was achieved by axillary-bifemoral bypass. The improvement of the clinical status allowed complete repair of the aortic transection two days after the extra-anatomic revascularisation. This case emphasizes the severity of the cases with impaired blood flow to the lower body and the benefit of the extra-anatomic bypass in pathology of the upper descending thoracic aorta when complete repair of the aortic transection is associated with an extremely high risk.
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PMID:[Traumatic rupture of the aortic isthmus revealed by acute obstruction of the descending thoracic aorta]. 128 8

Reperfusion of ischemic hindlimbs leads to leukotriene B4 (LTB4) and polymorphonuclear neutrophil (PMN)-dependent lung injury. Pulmonary mast cells are capable of synthesizing LTB4 and are potential mediators of this inflammatory response. This study tests their role in PMN sequestration and pulmonary edema after hindlimb ischemia. Anesthetized, mast cell-sufficient mice (n = 8) or their congeneic mast cell-deficient strain (n = 8) were subjected to 3 hours of hindlimb ischemia. After another 3 hours of reperfusion, plasma LTB4 levels rose to 651 pg/ml, higher than sham ischemic control (n = 8) values of 202 pg/ml (p less than 0.05). At this time there was sequestration of neutrophils in the pulmonary microcirculation (54 PMN/10 high-power fields [HPF]) and an increase in lung wet/dry weight ratio (W/D) of 4.4. Both these values were higher (p less than 0.05) than those in sham ischemic animals that showed sequestration of 18 PMN/10 HPF and a lung W/D of 3.1. In contrast, mast cell-deficient mice showed an attenuation of ischemia- and reperfusion-induced rise in plasma LTB4 (507 pg/ml), fewer sequestered neutrophils (34 PMNs/10 HPF), and a reduction in lung W/D to 3.9 (all p less than 0.05). To test the role of lung LTB4 in determining PMN sequestration, rats (n = 78) were subjected to 3 hours of hindlimb ischemia. After 3 hours of reperfusion, plasma and bronchoalveolar lavage (BAL) LTB4 concentrations rose to 956 and 211 pg/ml, respectively--higher than sham values of 460 and 121 pg/ml (both p less than 0.05). After 4 hours, plasma LTB4 levels had returned to baseline, whereas BAL LTB4 had increased further to 658 pg/ml, indicating lung origin. Treatment of other rats by localized lung lavage of the lipoxygenase inhibitor diethylcarbamazine (80 mg/kg in 0.1 ml twice) prevented the ischemia- and reperfusion-induced rise in BAL LTB4 (267 pg/ml) and limited local neutrophil sequestration (from 51 PMN/10 HPF after saline aspiration to 36 PMN/10 HPF) and lung W/D (from 4.5 to 4.1) (all p less than 0.05). The data indicate that after hindlimb ischemia pulmonary mast cells and localized LTB4 synthesis mediate, in part, the lung inflammatory response.
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PMID:Mast cells and leukotrienes mediate neutrophil sequestration and lung edema after remote ischemia in rodents. 132 74

Ischemia and reperfusion of the lower torso lead to leukotriene- and neutrophil (PMN)-dependent lung injury characterized by lung PMN sequestration, increased permeability, and noncardiogenic edema. It is thought that PMNs require adhesion to endothelium to alter barrier function. This study tests the role of CD 18, the PMN adherence receptor, in mediating lung permeability after lower torso ischemia and reperfusion. Anesthetized rabbits (n = 9) underwent 3 hours of bilateral hind limb ischemia. Ten minutes after the release of the tourniquets, plasma leukotriene B4 levels increased to 395 +/- 85 pg/ml, higher than 129 +/- 35 pg/ml in controls (n = 9, p less than 0.01). At this time there was a reduction in circulating white blood cells (x 10(3)), 3.56 +/- 0.49/mm3 relative to 6.07 +/- 0.61/mm3 in controls (p less than 0.01). PMNs were sequestered in the hind limbs, indicated by increased myeloperoxidase activity of 1.06 +/- 0.19 units/g compared with 0.56 +/- 0.09 units/g in controls (p less than 0.05). Four hours after tourniquet release, PMNs were sequestered in the lungs, 52 +/- 4 PMNs per 10 high-power fields, a value higher than 31.5 +/- 3 PMNs per 10 high-power fields in controls; bronchoalveolar lavage fluid protein content increased to 554 +/- 90 micrograms/ml relative to 277 +/- 46 micrograms/ml in controls; and there was lung edema, measured by increased wet weight-to-dry weight ratios of 5.19 +/- 0.10, higher than 4.29 +/- 0.21 in controls (all p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of neutrophil adherence receptors (CD 18) in lung permeability following lower torso ischemia. 135 25

The ischemic extremities treatment in a precarious phase has been standardized in the two last decades with a significance extremities savement. But the ischemia of the interdigital vessels and at the microcirculation is still a defiance. We expose the hiperemiant surgery past. We describe the experience of four years in Centre Hospitalari-Unitat Coronaria, Manresa, with 21 lumbar sympathetic ablation in patients without distal pulse, ankle/arm index by Doppler effect between 0 and 0.6 and angiographies without distal bed images, with 13 successes, 2 exitus by M.A.I., 3 amputations and a lung edema. We finish with a futuristic vision that suggest alternatives for the usage of the lumbar sympathectomy according to the medical advances in the coming time for available the ischemic extremities.
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PMID:[The past, present and future of lumbar sympathectomy]. 141 31


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