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

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14

A 4 hr intravenous infusion of Escherichia coli endotoxin in a total dose of 100 mg/kg produced significant morphological and functional pulmonary alterations in pentobarbitone anesthetized rats. Lung vascular permeability index was increased from 2.11 +/- 0.34 in normal rats to 4.82 +/- 0.65 in untreated endotoxemic rats. Treatment of endotoxemic rats with recombinant human superoxide dismutase (r-HSOD) in doses of 0.1, 0.215, and 0.464 mg/kg.min i.v., infused concomitantly with endotoxin, dose-dependently reduced the permeability index to 3.28 +/- 0.96, 2.83 +/- 0.55 (P less than 0.05), and 2.16 +/- 0.65 (P less than 0.05). The wet lung weight was 523 +/- 15 and 664 +/- 46 mg/100 g bwt in normal and in untreated endotoxemic rats, respectively. r-HSOD dose-dependently inhibited the endotoxin-induced increase in wet lung weight to 617 +/- 40, 577 +/- 31, and 559 +/- 39 (P less than 0.05) mg/100 g bwt. r-HSOD (0.464 mg/kg.min) did not affect permeability index and wet lung weight in normal, nonintoxicated rats. Endotoxin infusion produced a significant increase in respiratory rate (max. +69%) and blood gas alterations, indicating a hyperventilatory hypocapnia in endotoxemic control rats. Infusion of r-HSOD (0.464 mg/kg.min) significantly inhibited the endotoxin-induced tachypnoe (max. +13%) and blunted the alterations in arterial hydrogen carbonate content and carbon dioxide tension. In conclusion, infusion of r-HSOD dose-dependently and significantly inhibited pulmonary edema formation and hyperventilatory dyspnoe in endotoxemic rats.
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PMID:Effects of recombinant human superoxide dismutase on increased lung vascular permeability and respiratory disorder in endotoxemic rats. 217 95

Cytotoxic agents may cause interstitial or eosinophilic pneumonitis, alveolar proteinosis, pulmonary venous occlusive disease, pulmonary fibrosis, pneumothorax, or pulmonary oedema. These agents may also potentiate lung injury caused by radiotherapy or high oxygen fractions in inspired air. Clinical and roentgenological features of lung damage induced by cytotoxic drugs are usually non-specific, and differential diagnoses include progression of the malignant disease and a plethora of opportunistic infections. Monitoring of blood gases and carbon monoxide transfer factor may facilitate early detection of drug induced lung injury. Fiberoptic bronchoscopy, bronchoalveolar lavage, transbronchial biopsy, or open lung biopsy may be necessary for reliable diagnosis. Early detection of lung damage and immediate withdrawal of the responsible agent(s) are essential. Steroids may be of therapeutic value in some patients.
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PMID:Pulmonary toxicity of cytotoxic and immunosuppressive agents. A review. 218 2

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87

A computer program, which calculates the required minute volume using fuzzy set rule incorporating the authors' clinical experiences, was developed to keep a stable PCO2 during anesthesia, and its clinical usefulness was examined on 30 consecutive patients. The program requires the value of end-tidal CO2 concentrations at present, and 5 minutes before, and arterial-end-tidal CO2 tension difference (aEDCO2), and generates the adjustable value of minute volume to maintain the constant PaCO2 (acceptable range; 37 to 33 mmHg). Twenty-three cases were successfully controlled after adopting the calculated minute volume, which closely coincided with our clinical experiences. Seven cases, on the other hand, did not show the anticipated PaCO2 change, because of incidental leakage of endotracheal cuff (2 cases), larger aEDCO2 than the expected value of 4 mmHg (4 cases), or mild pulmonary edema (1 case). It has become clear that in the steady anesthetized patients, the program based on the authors' clinical experiences, which was made possible with the concept of fuzzy set rule, can be used to control the PaCO2 within the strict range during variable anesthetic situations.
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PMID:[Application of fuzzy algorithms for ventilatory control during clinical anesthesia]. 225 49

A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.
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PMID:The pathophysiology of carbon monoxide poisoning and acute respiratory failure in a sheep model with smoke inhalation injury. 230 76

The effects of the mechanical factors involved in ventilation on pulmonary edema are only partially understood. To clarify the effect of ventilation on the adult respiratory distress syndrome (ARDS), we examined the effect of reducing rate and tidal volume on oleic acid-induced low-pressure pulmonary edema in dogs, hypothesizing that hypopnea would reduce lung edema. We placed the experimental animals on venous-venous extracorporeal membrane oxygenation (ECMO) for CO2 clearance and oxygenation 1 h after the injury. This allowed reduction of the ventilatory rate from 17.2 +/- 4.8 to 3.3 +/- 0.8 breaths/min and tidal volume from 20 to 16 ml/kg, effectively resting the injured lung. After 5 h of hypopnea there was no reduction in edema by gravimetric or extravascular thermal volume measurements. The ECMO-facilitated hypopnea reduced airway pressure and pulmonary artery pressure while improving arterial oxygen saturation but increased venous admixture. These results suggest that there may be a supportive role for ECMO-assisted hypopnea, but there was no direct beneficial effect of hypopnea on edema.
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PMID:The effect of hypopnea on low-pressure pulmonary edema. 238 95

Diabetes mellitus produces serious complications in several major organ systems. The pulmonary complications, although uncommon and not well recognized, may be life-threatening. We describe a 20-year-old patient with diabetic ketoacidosis in whom pulmonary zygomycosis developed. This condition was complicated by stenosis of the left upper lobe bronchus despite successful treatment of the zygomycosis. Bronchial obstruction has become a well-recognized complication of pulmonary zygomycosis. In addition to infections caused by Zygomycetes, mycobacteria, viruses, and bacteria, the pulmonary complications described in patients with diabetes include pulmonary edema, disordered breathing during sleep, and reductions in elastic recoil of the lungs, diffusing capacity of the lungs for carbon monoxide, and bronchomotor tone. Other reported complications are respiratory alkalosis, cardiorespiratory arrest, pneumothorax, pneumomediastinum, plugging of the airways with mucus, and aspiration pneumonia attributable to diabetic gastroparesis.
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PMID:Pulmonary complications in diabetes mellitus. 250 1

Inhalation injuries most often occur with cutaneous burns, and the likelihood of an inhalation injury increases incrementally with age of the patient and size of the burn. Damage to the pulmonary parenchymal tissue manifests as increased capillary permeability leading to excessive lung fluid formation and increasing hypoxia. An inhalation injury may be diagnosed using observation of indirect criteria in conjunction with fiberoptic bronchoscopy, xenon 133 radiospirometry, and/or measurement of extravascular lung water. Initially, carbon monoxide poisoning threatens the patient's oxygenation capacity. High-flow oxygen therapy reduces the half-life of carbon monoxide to an acceptable period. The patient proceeds through three stages: pulmonary insufficiency, pulmonary edema, and bronchopneumonia. Treatment is directed toward supporting oxygenation using endotracheal intubation with mechanical ventilation, humidification of inspired air, early mobilization, chest physiotherapy, antibiotics for documented infection, and adequate systemic hydration.
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PMID:Managing smoke inhalation injuries. 258 65

Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.
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PMID:Combination of constant-flow and continuous positive-pressure ventilation in canine pulmonary edema. 267 48


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