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

The role of CO2 in hyperbaric oxygen toxicity was investigated by administering acetazolamide (Diamox), Tris buffer [tris(hydroxymethyl)aminomethane], and sodium bicarbonate by i.p. injection, and by exposure of other groups of animals to an atmosphere of 5% CO2 and 95% O2. All animals were placed in a pressure chamber and maintained at 50 psig in 100% O2 until death. The Tris buffer and the sodium bicarbonate buffer significantly extended time to onset of convulsions and to time of death. Acetazolamide and also 5% CO2 shortened time to onset of convulsions and significantly shortened survival time. These results suggest that increased tissue levels of CO2 play an important role in hyperbaric oxygen toxicity. The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension.
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PMID:Acetazolamide and CO2 in hyperbaric oxygen toxicity. 680 59

High-frequency jet ventilation (HFJV) was compared with conventional ventilation ventilation during oleic acid-induced pulmonary edema in dogs. HFJV, when combined with positive end-expiratory pressure (PEEP), returned arterial PO2 (PAO2) and venous admixture to preoleic acid levels, even with tidal volumes as low as 4.8 ml/kg and rates of 300 min-1. When HFJV was compared with conventional (low-frequency, high tidal volume) ventilation at the same Flo2 and level of PEEP, Pao2 was lower and venous admixture higher with HFJV. However, venous admixture was lower with HFJV when comparisons were made at the same peak airway pressure, because of a higher level of PEEP compared with conventional ventilation. At each level of PEEP, cardiac and stroke indices were not different between the two methods of ventilation. The ability to eliminate CO2 with lower peak airway pressures or to increase PEEP without further increases in peak airway pressure are the primary advantages of HFJV during severe lung injury. Oxygenation is as efficient during HFJV as during conventional ventilation in this model of pulmonary edema when comparisons are made at the same peak airway pressure, but less efficient at the same PEEP.
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PMID:Comparison of venous admixture during high-frequency ventilation and conventional ventilation in oleic acid-induced pulmonary edema in dogs. 704 7

The course of the illness of a 56 year old female patient is reported, who is still surviving one and a half years after developing advanced, presumably progressive, so called "shock-lung syndrome". Following two episodes of hemorrhagic shock due to intestinal hemorrhage and post-operative secondary hemorrhage, interstitial lung edema developed, which was resistant to therapy. During the following weeks this was followed by bronchopneumonia with symptoms of sepsis persisting over several weeks. Between the third and seventh week of artificial ventilation X-ray of the lungs showed significant progressive changes of the interstitial tissues. This correlated with a progressive deterioration in gas exchange for O2 and CO2, which reached its peak in the seventh week with a paO2 of 71 mm Hg at a FIO2 = 1 and a paCO2 of 68 mm Hg at a minute volume of 15,51. The compliance of lung and thorax was severely reduced at 19 m1/cm H2O. At this apparently unfavourable time the patient was weaned off the respirator, and subsequently, over a period of three weeks, from oxygen insufflation. After eleven weeks of therapy, transfer to the medical ward was possible, with discharge from the hospital following three weeks later. The lung function tests at the time of discharge revealed a high grade reduction of all lung volumes and capacities without a significant obstructive component. The findings have shown a definite improvement during the following one and a half years. In retrospect the polypragmatic intensive therapy measures do not allow valid generalised therapeutic guidelines to be derived. We conclude, however, from this single observation, that therapeutic nihilism is not justified even in a progressive shock-lung syndrome which appears clinically and radiologically to be at an "irreversible" end stage.
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PMID:[Pulmonary fibrosis following ARDS. Case report of successful intensive therapy (author's transl)]. 711 41

In an effort to duplicate a previous model of neurogenic pulmonary edema (NPE), we maintained intracranial pressure (PIC) at 20 Torr below mean arterial pressure in six closed-chested dogs anesthetized with alpha-chloralose and urethan. This was accomplished by infusing 1) isotonic saline (NS), 2) a gas mixture of 80% helium and 20% oxygen (HeO2), or 3) 100% carbon dioxide (CO2) through a trephined hole into the subdural space. Three more animals were studied with the same protocol after thoracotomy to permit Doppler examination for bubbles in the left pulmonary artery. Significant increases in pulmonary artery pressure, pulmonary vascular resistance, physiological shunt, dead space fraction, and hypoxemia were recorded when Pic was elevated by HeO2 infusion but not during infusion of NS or CO2. Pulmonary gas-bubble embolism was suggested by an increase in the fraction of helium in expired gas during HeO2 infusion and confirmed by Doppler recordings. We conclude that increasing Pic with air produces the physiological changes of air embolism; this is not a satisfactory model for investigating NPE.
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PMID:Increasing intracranial pressure with air causes air embolism, not neurogenic pulmonary edema. 722 70

Only 53%-58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. PATHOPHYSIOLOGY. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6-12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. CALCIUM ANTAGONISTS. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. HYPERVOLAEMIC HAEMODILUTION. Volume expansion and haemodilution to a hematocrit of 30%-33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10-12 mm Hg and 15-18 mm Hg, respectively. But there is no evidence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. INDUCED ARTERIAL HYPERTENSION. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. CONCLUSION. Treatment of cerebral vasospasm following a SAB aims to avoid any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
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PMID:[Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Therapeutic value of treatment with calcium antagonists, hypervolemic hemodilution and induced arterial hypertension]. 778 50

Five patients on maintenance haemodialysis were exposed to varying degrees of hypernatric dialysate, leading to acute hypernatraemia (plasma sodium concentrations 158 mmol/l to 179 mmol/l). With the exception of one patient, who developed pulmonary oedema, symptoms were minimal and in each case hypernatraemia was corrected without residual complications. The hypernatric dialysate resulted from a granular and less soluble batch of sodium bicarbonate powder. The extra effort required to dissolve the powder caused CO2 to be shaken out of solution, producing sodium carbonate and raising the pH. Mixing calcium from the 'acid' concentrate with excess carbonate in the 'bicarbonate' concentrate led to rapid precipitation of calcium carbonate on the conductivity monitoring cells. Dialysate conductivity was incorrectly sensed as low by the coated conductivity cells, so that an increasing amount of 'acid' concentrate, with its accompanying electrolytes, was delivered to the patient. When the granular powder was ground to a fine powder, passed through a 125 microns sieve and gently dissolved, the machine operated normally. We recommend that sodium bicarbonate powder is supplied with a sieve size no greater than 125 microns, kept dry to prevent the formation of large crystals, and dissolved gently.
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PMID:Acute hypernatraemia during bicarbonate-buffered haemodialysis. 780 Feb 20

The aim of this prospective study was to analyse the contribution of the measurement of alveolar arterial gradients of CO2 during forced expiration in the diagnosis of pulmonary emboli occurring in chronic airflow obstruction (COPD) as a result of smoking. The study was carried out on 178 patients: Group 1: 54 subjects without emboli (14 controls, 33 COPD and 7 patients with chest pain); Group 2: 72 patients with proved emboli (49 non COPD, 23 COPD); Group 3: 52 patients COPD presenting with varied non-embolic broncho-pulmonary pathology (pneumonia, bronchospasm, pulmonary oedema, bronchial neoplasm). The diagnosis of pulmonary emboli was confirmed by scintigraphy in patients with non COPD or angiography (in patients with COPD). The maximal fraction of CO2 was measured using a capnologue during a forced expiration which was long and prolonged until residual volume was achieved. The PaCO2 was measured simultaneously by an analysis of arterial blood gases. The D index was calculated according to the formula [(PaCO2-PEM CO2)/PaCO2] x 100. The D index was significantly lower in Group 1 (3.42 +/- 3.8% p < 0.0001) than in Group 2 (20.8 +/- 10%) and Group 3 (17.6 +/- 11.7%) (not significant between Groups 2 and 3). In patients with COPD the specificity and sensitivity and the predicted positive and negative value were 100% for a D limit of 7%. In COPD patients these values were respectively 82, 95, 75 and 96% for a D limit of 7%; on the other hand for a D below 5% the values were 60, 100, 64 and 100% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The significance of maximal expiratory concentrations of CO2 (MEC CO2) in the negative diagnosis of acute pulmonary embolism in chronic obstructive bronchopneumopathies]. 789 65

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

The purpose of this study was to determine the effect of inverse ratio ventilation (IRV) on gas exchanges and circulatory systems in 56 mongrel dogs with oleic acid induced pulmonary edema. The dogs were divided into 9 groups and were ventilated with 9 kinds of ventilatory modes such as I:E ratio of 1:2 (control), 2:1 (2:1 IRV), 3:1 (3:1 IRV), 1:2 with 5 cmH2O PEEP (1:2 PEEP 5), 2:1 with 5 cmH2O PEEP (2:1 PEEP 5), 3:1 with 5 cmH2O PEEP (3:1 PEEP 5), 1:2 with 10 cmH2O PEEP (1:2 PEEP 10), 2:1 with 10 cmH2O PEEP (2:1 PEEP 10) and 3:1 with 10 cmH2O PEEP (3:1 PEEP 10), using a Servo ventilator 900C. IRV could not improve arterial oxygenation in dogs with oleic acid induced pulmonary edema, but PEEP could significantly improve arterial oxygenation depending on PEEP level. Although in the control group, PaCO2 increased gradually, PaCO2 was kept constant for 8 hours in the 3:1 IRV groups. In the 2:1 group, PaCO2 did not change significantly until 6 hours, but in IRV with 10 cmH2O PEEP groups, PaCO2 showed the highest increase. There was no significant alteration in hemodynamics after ventilatory modes were changed to IRV. Although oxygen delivery was the best in the 3:1 IRV group, there was no statistical significance between the 3:1 IRV group and others. It was concluded that IRV did not improve arterial oxygenation but showed a favorable effect for CO2 elimination, in dogs with oleic acid induced pulmonary edema.
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PMID:[Effects of inverse ratio ventilation and positive end-expiratory pressure on gas exchanges in dogs with oleic acid induced pulmonary edema]. 818 79

A case of successfully treated multiple venous air embolism occurred in a man aged 41 operated on for cerebellar tumour. Postoperatively exceptionally serious complication developed in the form of neurogenic pulmonary oedema. Attention is called to a number of aetiological factors in this case. The anaesthesiological management in such cases should include careful monitoring of end-tidal CO2 concentration and insertion of catheter into right atrium.
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PMID:[Multiple venous air embolism during cerebellar tumor surgery. Case report]. 823 43


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