Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the effect of acute upper airway obstruction upon pulmonary edema (PE) formation, we studied seven dogs that were subjected to inspiratory obstruction for three hours. Hypoxia was avoided by the administration of supplemental oxygen during the study period. Six dogs developed pulmonary vascular congestion, and four developed histologic findings of PE. Inspiratory intrapleural pressure decreased to -28 +/- 4 mmHg in dogs that developed PE and to -23 +/- 2 mmHg in dogs that did not. Transmural pulmonary artery pressure and pulmonary artery wedge pressure did not increase significantly. Central venous pressure during inspiration (CVPi) increased in all dogs, and CVP at end expiration (CVPe) was significantly higher in dogs with PE. Dogs that developed PE experienced a decrease in cardiac output and an increase in systemic vascular resistance. Furthermore, alveolar ventilation declined in dogs with PE, ultimately resulting in ventilatory failure. Pulmonary edema formation was not preceded by an increase in pulmonary vascular pressures but was associated with higher CVP, pulmonary vascular congestion, and hypercarbia.
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PMID:Pulmonary edema associated with upper airway obstruction in dogs. 830 97

1. The possible contribution of endogenous endothelin (ET) to the pathogenesis of seizure-associated pulmonary oedema was examined in mechanically ventilated rats after intravenous bolus injection of the gamma-aminobutyric acid (GABA) antagonist, bicuculline (1.2 mg kg-1). 2. Recurrent seizure activity elicited by bicuculline injection led to rapidly developing pulmonary oedema. Within 4 min after bicuculline application (1.2 mg kg-1), arterial O2 partial pressure (PaO2) significantly dropped from 17.49 +/- 1.20 kPa to 7.51 +/- 2.21 kPa (P < 0.01) and arterial CO2 partial pressure (PaCO2) significantly increased from 4.64 +/- 0.56 kPa to 8.15 +/- 0.99 kPa (P < 0.01). Gradually a progressive acidosis developed. Moreover, mean arterial blood pressure (MABP) and end-inspiratory airway pressure (Paw) rapidly increased. 3. Concomitantly there was a time-dependent increase of big ET-1 and ET-1 levels in bronchoalveolar lavage (BAL) as determined by combined reverse phase high performance liquid chromatography (h.p.l.c.) and radioimmunoassay. BAL levels of both peptides increased up to 8 min after bicuculline injection and slowly decreased subsequently. In contrast, BAL from animals injected with vehicle did not contain detectable amounts of ET. 4. Pretreatment with the endothelin-converting enzyme inhibitor, phosphoramidon (5.4 mg kg-1, i.v.) for 5 min significantly (P < 0.001) reduced peak ET-1 levels in BAL fluid by 65.4 +/- 9.9% at 8 min after bicuculline injection. Simultaneously it afforded protection from hypoxia. PaCO2 did not increase and PaO2 decreased only slightly from 14.63 +/- 1.00 kPa to 12.97 +/- 0.61 kPa (P > 0.05) after phosphoramidon pretreatment. In contrast, vehicle-treated animals that received bicuculline showed both significant hypercapnia as well as profound hypoxia. Phosphoramidon significantly diminished the maximum increase in Paw by 76.7 +/- 12.4% (P <0.005), but only slightly affected the MABP. Phosphoramidon pretreatment had no effect on the acidosis.5. Pretreatment with the ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.), for 5 min did not affect the levels of ET-1 in the BAL fluid at 8 min after bicuculline injection but did ameliorate the development of hypoxia. No hypercapnia developed and Pa02 decreased only moderately from 16.65 +/-0.25 kPa to 14.19 +/-2.15 kPa (P>0.05) in BQ-123-treated animals. In contrast, vehicle-treated animals that received bicuculline exhibited significant hypercapnia as well as profound hypoxia. BQ-123 significantly reduced the increase in Paw by 51.3 +/- 12.8% (P < 0.01). It affected MABP only slightly and had no effect on the acidosis.6. These results suggest that ET peptides play a significant role in this model of neurogenic pulmonary oedema and may act as mediators of respiratory distress. The deleterious effects of endogenous ET in this model are primarily mediated via the ETA receptor, for they were inhibited by the ETA receptor antagonist, BQ-123. ETA receptor antagonists may therefore be of potential therapeutic value in respiratory distress.
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PMID:A role for endothelin in bicuculline-induced neurogenic pulmonary oedema in rats. 854 73

Reduced tolerance to high altitude may be associated with a low ventilatory and an increased pulmonary vascular response to hypoxia. We therefore, examined whether individuals susceptible to acute mountain sickness (AMS) or high altitude pulmonary oedema (HAPE) could be identified by noninvasive measurements of these parameters at low altitude. Ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) at rest and during exercise, as well as hypoxic pulmonary vascular response (HPVR) at rest, were examined in 30 mountaineers whose susceptibility was known from previous identical exposures to high altitude. Isocapnic HVR expressed as difference in minute ventilation related to difference in arterial oxygen saturation (delta V'E/ delta Sa,O2) (L.min-1/%) was significantly lower in subjects susceptible to HAPE (mean +/- SEM 0.8 +/- 0.1; n = 10) compared to nonsusceptible controls (1.5 +/- 0.2; n = 10), but was not significantly different from subjects susceptible to AMS (1.2 +/- 0.2; n = 10). Hypercapnic ventilatory response was not significantly different between the three groups. Discrimination between groups could not be improved by measurements of HVR during exercise (50% maximum oxygen consumption (V'O2,max)), or by assessing ventilation and oxygen saturation during a 15 min steady-state exercise (35% V'O2,max) at fractional inspiratory oxygen (FI,O2) of 0.14. Pulmonary artery pressure (Ppa) estimated by Doppler measurements of tricuspid valve pressure at an FI,O2 of 0.21 and 0.12 (10 min) did not lead to a further discrimination between subjects susceptible to HAPE and AMS with the exception of three subjects susceptible to HAPE who showed an exaggerated HPVR. It is concluded that a low ventilatory response to hypoxia is associated with an increased risk for high altitude pulmonary oedema, whilst susceptibility to acute mountain sickness may be associated with a high or low ventilatory response to hypoxia. A reliable discrimination between subjects susceptible to high altitude pulmonary oedema and acute mountain sickness with a low ventilatory response to hypoxia is not possible by Doppler echocardiographic estimations of hypoxic pulmonary vascular response.
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PMID:Ventilatory and pulmonary vascular response to hypoxia and susceptibility to high altitude pulmonary oedema. 862 Sep 46

Cystic fibrosis (CF) is a disease characterized mainly by altered exocrine gland function that eventually produces irreversible dysfunction of the pancreas and lungs. The respiratory insufficiency that develops in CF patients in the advanced stages of disease can only be corrected at this time by lung or heart-lung transplantation. We describe our experience with 6 terminal phase CF patients who underwent sequential double lung transplantation (SDLT). Anesthesia was intravenous, with exhaustive hemodynamic and respiratory monitoring. During surgery the most frequently encountered hemodynamic complications were low minute volume, arterial hypotension and irregular heart rate. The main respiratory complications were hypoxemia, hypercapnia and pulmonary edema of the implanted lung, which developed in all cases to varying degrees related to the organ's state of preservation and duration of ischemia. Other complications were the need for extracorporeal circulation in 1 case, oliguria and blood loss requiring multiple transfusions. The most critical moments were at the time of clamping the pulmonary artery, the period after revascularization of the donated lung, and at the start of patient ventilation through the first implanted lung so that the second could be implanted. Although our series is small, it is of interest given the limited Spanish experience with lung transplantation in CF patients, and the good early results obtained, which are similar to those reported for other diseases.
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PMID:[Anesthetic complications in sequential bipulmonary transplantation in patients with cystic fibrosis. Apropos of 6 cases]. 884 34

Laparoscopic surgery is very popular among physicians and patients because this technique is associated with safety, shorter hospital stay, early return to normal activity, and cosmetic acceptance of the operative scar. Although the procedure involves minimal invasion and tissue damage, it has potentially serious complications, including cardiopulmonary effects that result mainly from hypercarbia and raised intraabdominal pressure caused by pneumoperitoneum. Absorbed carbon dioxide from the peritoneal cavity tends to cause acidosis. Leakage of the gas into tissue spaces may induce subcutaneous emphysema, pneumothorax, pneumomediastinum and pneumopericardium. Cardiac effects include arrhythmias, hypotension, cardiac arrest, gas embolism, pulmonary edema, and myocardial ischemia or infarction. Some of these effects, though rare, are serious and potentially fatal. Physicians should anticipate these problems in their patients undergoing laparoscopic procedures. This review discusses the technique of and physiologic considerations in laparoscopic surgery as well as its potential complications.
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PMID:Laparoscopic surgery and its potential for medical complications. 901 21

Surgeons have often been reluctant to use cardiopulmonary bypass (CPB) during single (SLTx) and double lung (DLTx) transplantation surgery because of the potential adverse sequelae of CPB including haemorrhage and activation of complement leading to sequestration of neutrophils and platelets in the pulmonary capillary bed, endothelial damage, increased capillary permeability and pulmonary oedema. To clarify the effect of CPB on lung transplant recipients, we reviewed our last four years' experience in 74 patients of whom 30 required CPB support. Indications for CPB were mean pulmonary artery pressure of greater than 50 mmHg, haemodynamic instability, hypoxia or hypercarbia. Patients undergoing SLTx were placed on CPB via the femoral artery and vein, while those undergoing DLTx were cannulated in the standard fashion using the ascending aorta and right atrium. All patients were administered aprotinin prior to CPB. Intraoperatively and postoperatively, haemorrhage was not a major problem. The 30-day mortality in the CPB group and the non-CPB group were 20% and 4.6%, respectively which was not statistically significant (p = 0.06). We conclude that CPB during lung transplantation is a safe, effective method to support these severely ill patients and should not be avoided because of concerns over adverse sequelae of CPB on postoperative graft function.
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PMID:Cardiopulmonary bypass (CPB) for lung transplantation. 916 Mar 61

Despite more than 25 years of extensive research, the mortality of ARDS patients remains high. The inflammatory process within the lung and the associated gas exchange disturbances require an aggressive ventilatory regimen, which itself may harm the lung. Therapeutic measures which are used to reduce iatrogenic damage to the lung are pressure controlled mechanical ventilation in combination with PEEP and permissive hypercapnia, dehydration and extracorporeal gas exchange. At present, new strategies such as intratracheal instillation of surfactant, partial liquid ventilation and inhalation of nitric oxide (NO) are being evaluated. Surfactant reduces the surface tension, forming a monomolecular layer at the air/tissue interface. It thereby decreases the forces necessary to expand the alveoli and prevents alveoli with small diameter from collapsing. In ARDS, a disturbance of surfactant synthesis, function and re-uptake is the rationale for treatment with exogenous surfactant. Initial clinical results suggest a limited positive effect independently of the surfactant preparation used, the dose and the application mode. Experience with partial liquid ventilation with perfluorocarbons in ARDS has also been reported. Perfluorocarbons are liquids with a high binding capacity for oxygen and carbon dioxide. During normal mechanical ventilation with gas, repetitive doses of perfluorocarbons are instilled into the lungs up to a volume equal to the functional residual capacity. The liquid is pushed into collapsed alveoli and keeps them open by reducing the surface tension. First clinical studies have demonstrated the possible improvement in pulmonary gas exchange. In ARDS, inhalation of NO may cause a predominantly selective vasodilation in blood vessels of ventilated lung regions, resulting in an increase in PaO2 and a decrease in pulmonary artery pressure. The effect of NO on the pulmonary vasculature also induces a reduction in right ventricular afterload and also in pulmonary capillary pressure, which may lead to a faster resolution of pulmonary edema. However, in spite of the promising results of these new strategies, further studies are needed to evaluate their influence on morbidity and mortality.
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PMID:[Perspectives in mechanical ventilation in ARDS]. 928 30

Although the physiological effects of positive pressure ventilation are numerous, sometimes undesirable and have varying degrees of significance, positive pressure ventilation still plays a major role in the resuscitation and treatment of critically ill patients. Advances in the various methods of delivering positive pressure, especially when incorporating spontaneous breathing, have reduced the severity of complications. Despite serious complications, mechanical ventilation has advantages. When it is instituted for ventilatory and hypoxaemic respiratory failure, the benefits can be viewed in the context of the work of breathing. Spontaneous breathing normally requires 5% of total oxygen delivery to meet its demands. In lung disease, the ratio of oxygen consumption by the respiratory muscles to whole body oxygen consumption can increase to 25-30% (Henning 1986, Pinksy 1990). Mechanical ventilation reduces the energy demand of respiratory muscles and increases the oxygen delivery to other vital organs. When mechanical ventilation improves hypoxaemia and/or hypercarbia, or significantly decreases the work of breathing, it may also normalize associated changes in heart rate (Perel & Pizov 1991 p53). When cardiac output is increased in response to the increased work of breathing and associated stress, the institution of mechanical ventilation may beneficially lower the cardiac output simply due to the decrease in oxygen demand; thus the physiological reduction in cardiac output may not necessarily be regarded as a complication. The effects of raised intrathoracic pressure during mechanical ventilation may be beneficial when used to prevent or reduce pulmonary oedema, though problematic in some other situations. Mechanical ventilation is a life-saving treatment which has many associated complications; nurses have to accept the unavoidable hazards and adapt their nursing care to minimize their effects.
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PMID:Physiological changes occurring with positive pressure ventilation: Part Two. 956 54

Non-invasive continuous positive airway pressure (CPAP) seems to decrease the need for intubation in patients with severe cardiogenic pulmonary oedema (CPO) in the intensive care unit. The goals of our study were to delineate indications for CPAP in the emergency department, and to confirm its usefulness in such a setting. We retrospectively assess the evolution of all patients ventilated under CPAP for an acute hypoxaemic respiratory failure over a 1-year period (n = 64 patients). Hypercarbia and respiratory acidosis were present in most patients with CPO (PaCO2 = 54.4+/-22.3 mmHg; pH = 7.27+/-0.13), according to respiratory exhaustion, although initial PaCO2 was low in the pneumonia group. There was a significant improvement of arterial blood gases after 1 hour of ventilation in the CPO group (PaO2 = 254.1+/-121.0 mmHg; PaCO2 = 44.0+/-12.6 mmHg; pH = 7.34+/-0.08; p < 0.0001 for both parameters). In the pneumonia group, oxygenation was also improved but with the persistence of a significant shunt (PaO2 = 157.6+/-84.4 mmHg). Fifty-four patients (84%) were considered as successfully ventilated under CPAP, with no need for intubation and a favourable evolution, mainly in the CPO group. No side effects were reported. In conclusion, CPAP is a useful and easy-to-use ventilatory device in the emergency department. It is now one of our first line treatments during prehospital and emergency care of patients with CPO.
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PMID:Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department. 982 33

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70


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