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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five healthy rhesus monkeys were ventilated with intermittent mandatory ventilation and 20 torr positive end-expiratory pressure (PEEP) for 8 hours. PEEP was increased to 25 torr and the monkeys were ventilated for 4 more hours. Lactated Ringer's solution and human salt-poor albumin were used to expand plasma and extracellular fluid volume throughout the entire period of study. Homologous blood was administered to maintain hematocrit at control levels and maintenance fluids were infused to maintain transmural pulmonary capillary wedge pressure at 5 to 15 torr. Although cardiac output, mean aortic blood pressure, oxygen consumption, venous admixture, transmural pulmonary capillary wedge pressure, HCO3- and in-vivo base excess were not changed when intermittent mandatory ventilation was employed, cardiac output and blood pressure were significantly depressed by brief periods of controlled mechanical ventilation when alternated with intermittent mandatory ventilation. Sporadic increases in arterial-venous oxygen content difference occurred. Arterial carbon dioxide tension was elevated moderately, with a concomitant depression of arterial pH. No pneumothorax occurred. High PEEP was well tolerated with intermittent manditory ventilation, intravascular volume expansion, and careful cardiovascular monitoring.
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PMID:Cardiorespiratory effects of high positive end-expiratory pressure. 81 Nov 32

Clinical and roentgenographic findings were compared in patients 40 years of age and over and in those under 40 who were treated for acute unilateral pneumothorax. Dyspnea and anxiety were pominent in the older individuals, although pneumothoraces were usually small. Because physical findings were often unreliable, roentgenograms were required. In the presence of pulmonary emphysema, loss of retractility prevented total collapse of the underlying lung. Increased intrapleural pressure caused over-expansion of the chest wall and the depression of the diaphragm without much mediastinal shifting. Partial collapse of emphysematous lobes demonstrated bullae that were not previously obvious. Respiratory failure developed in five patients over 40 years of age, but four of them recovered after relief of the pneumothorax. Mortality for the group was low and related to associated pulmonary diseases.
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PMID:Pneumothorax complicating pulmonary emphysema. 117 69

The diagnosis of myocardial contusion is often difficult, as traditional methods such as serial electrocardiograms, cardiac enzyme (creatine kinase [CK-MB]) analysis, and echocardiography lack sensitivity and specificity. Recent reports have shown that 111In labelled antimyosin scanning has high sensitivity for detecting cardiac injury. However, no prior studies have been reported for antimyosin imaging with patients suspected of sustaining a cardiac contusion. Accordingly, 17 patients with severe multisystem trauma (intrathoracic vascular injury in eight patients, pneumothorax and pulmonary contusion in 13) underwent antimyosin scintigraphy, echocardiography, 12-lead electrocardiograms, and CK-MB determinations. Arrhythmias were noted in seven patients, four of whom died. All patients has elevated CK levels but CK-MB isoenzyme was greater than 4% in only three. Abnormal ST segments were noted in nine subjects, only one of whom had CK-MB elevation. Echocardiography revealed pericardial effusions in four patients but was technically suboptimal in 53% of the studies. Blinded interpretation of the antimyosin scans revealed only one with focal myocardial uptake; this same patient had the only discrete wall motion abnormality on the echocardiogram and also had ST depression with ectopy but normal CK-MB. Thus in patients with suspected myocardial contusion, echocardiography is frequently limited technically and the electrocardiogram and CK analysis appear to lack diagnostic accuracy. In contrast, monoclonal antimyosin imaging may be performed in patients with trauma without limitation and yields results that are concordant with echocardiograms. In patients with suspected myocardial contusion, focal antimyosin uptake is uncommon despite severe thoracic injury, which suggests that extensive myocardial necrosis is not the primary method of injury.
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PMID:Focal myocardial injury following blunt chest trauma: a comparison of indium-111 antimyosin scintigraphy with other noninvasive methods. 157 35

The aim of this study was to assess the value of peridural thoracic analgesia (ATP) to prevent pain observed during pleural symphysis with tetracycline (STP) for pneumothorax (PNO). 12 patients (age 27 +/- 6 years) having a spontaneous PNO benefited from 13 SPT (1 gm, tetracycline diluted in 60 cc of normal saline) under cover of an APT (at the D5-D6 level) with Fentanyl (0.1 mg) and Bupivacaine 0.5% adrenalin (1 mg/kg). The protocol was used on three successive days. Repeated determinations of blood bupivacaine levels were performed in 9 patients on the first day. No patient had an intolerable pain which required injection of parenteral morphine and/or an interruption of the protocol. For two patients (one of them having a right symphysis and then a left symphysis one month later) the treatment sessions to achieve a symphysis were totally painless. 10 patients experienced moderate pain, mainly on the first day, which was relieved by reinjection of peridural bupivacaine (25 mg) (n = 9) or by the parenteral injection of non morphine analgesia (n = 1). No patient had a respiratory depression, collapse or bradycardia. The blood bupivacaine levels were always significantly less than the toxic levels (1.6 mg). The results observed suggest that APT, (Fentanyl and Bupivacaine) is an effective method, non toxic and well tolerated for the prevention of intolerable pain which is seen in SPT for PNO.
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PMID:[Pleural symphysis with tetracyclines for pneumothorax. The value of thoracic peridural analgesia]. 203 49

The subclavian artery is the most important landmark of the supraclavicular brachial block. However, it is difficult to locate the artery by palpation in the patients with poor landmark. The present study was aimed to compare two localizing methods of the subclavian artery by a pulse oximeter or by palpation. One hundred patients were divided into three groups. Group A (Slim Group): 6 patients, Group B (Normal Weight Group): 75 and Group C (Obese Group): 19. All patients received both methods to locate the subclavian artery. The first method was by palpating the pulsation of the subclavian artery. The second was by observing the wave depression of the pulse oximeter while pressing supraclavicular area. It was found that the detection rate of the first method was 83.3% in Group A, 52.0% in Group B, 26.3% in Group C and 49.0% in overall patients. However, the detection rate of the second method was 100% in each group. It shows a significant difference between the two methods in Group B, Group C and all patients (P less than 0.001), but no difference in Group A (P = 0.68). There were 13 patients among the 100 patients undergoing surgery of the upper extremity. Seven of them whose pulsation was not clearly palpated but could be located exactly by pulse oximeter. Supraclavicular brachial block was still completed successfully in these 13 patients. No pneumothorax was found. Utilizing pulse oximeter in supraclavicular block provides a high detection rate of the pulsation of the subclavian artery and improves the reliability of the block, especially in the patients with poor landmark.
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PMID:The application of pulse oximeter for supraclavicular brachial block. 235 63

A 27-year old man was admitted with a right-sided pneumothorax of 2-3 weeks duration. A chest tube was inserted and connected to an underwater seal drainage system without the application of external suction. Three hours later, the patient developed unilateral re-expansion pulmonary oedema and severe hypotension. Active management consisted of ventilating the patient with the addition of PEEP, and the administration of liberal amounts of fluids, including plasma and gelatin solution. The mechanism of re-expansion pulmonary oedema is different from that of cardiogenic pulmonary oedema, and the treatment consequently different. The cause of the hypotension may be due to hypovolaemia, from rapid pooling of fluid within the thorax, pre-existing volume depletion and myocardial depression. One must specially be aware of this possible complication when the pneumothorax is large and of more than 3 days, and it is to be stressed that suction should never initially be used in the treatment of a pneumothorax.
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PMID:Life threatening re-expansion hypotension and pulmonary oedema following treatment of a pneumothorax. 261 7

Chest wall protrusion and depression deformities, also known as funnel chest and pigeon chest, are nosologically a uniform entity. Our own histopathological studies revealed secondary changes, found likewise in arthroses, scolioses, aseptic osteonecroses and inflammatory processes, as well as changes found in so-called primary collagenous diseases of unknown aetiology. Investigation of the collagen metabolism did not disclose differences from the normal II-type collagen either qualitatively or quantitatively. The aetiology of funnel chest and pigeon chest can be defined as follows: A hereditary disturbance of metabolism results in weakening of the wall of the parasternal cartilage, effecting a deformation secondary to mechanical strain by respiration and growth. Psychocosmetic reasons are recognised as indication for operation. In our opinion, the optimal age for operation is the second to the sixth year of life. During 20 years, 765 patients were operated on at our hospital without lethality. Postoperative complications were pneumothorax (4%), pneumonia (2%), after bleeding (2%) and disturbed wound healing (7%). Late results 5 years following surgery were excellent in 57%, good in 27%, satisfactory in 10% and unsatisfactory in 6% of the cases, thus adding up to 84% good results.
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PMID:[Clinical aspects and problems of pigeon breast and funnel chest]. 328 94

Patients with severe air-flow obstruction receiving mechanical ventilation are at risk of inadvertent pulmonary hyperinflation with morbidity and mortality caused by pneumothorax and circulatory depression. Nine patients with severe air-flow obstruction (5 asthma, 4 chronic air-flow obstruction) requiring mechanical ventilation were studied while sedated and therapeutically paralyzed. Pulmonary hyperinflation during steady-state ventilation was quantified by measuring total exhaled volume during 20- to 40-s apnea (end-inspiratory lung volume, VEI). Patients were studied at 3 levels of minute ventilation (VE) (10, 16, and 26 L/min) and at each VE, 3 levels of tidal volume (VT) (0.6, 1.0, and 1.6 L) and 3 levels of inspiratory flow (VI) (40, 70, and 100 L/min for VT = 1.0 L). There were progressive increases in VEI when VT was increased or when expiratory time (TE) was decreased either by an increase in rate (and hence VE) or by a decrease in VI (at a constant VE) reaching lung volumes as high as 3.6 +/- 0.4 L above FRC. Alveolar, central venous, and esophageal pressure rose in parallel with lung volumes, and hypotension was seen in most patients at highest lung volumes. Peak airway pressure (Ppk) was predominantly related to inspiratory flow and did not reflect changes in lung volume. Levels of ventilation required for normocapnia prior to paralysis (15.7 +/- 2.3 L/min) were associated with hypotension in 7 patients and probable hyperinflation in excess of 1.96 +/- 0.17 L above FRC. VEI is a simple, reproducible measurement of pulmonary hyperinflation and may be more important than Ppk in the causation of barotrauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe air-flow obstruction. 366 41

Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and anuria after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure, disseminated intravascular coagulation, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.
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PMID:Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax. 394 Jul 93

The chest radiographs of 86 patients with suspected aortic rupture from blunt chest trauma were reviewed. Seventy-three patients had no evidence of aortic rupture on aortography or surgical exploration, and 13 patients had surgically confirmed rupture. Sixteen radiographic findings were analyzed for sensitivity and specificity in detecting aortic rupture. The following findings were not statistically significant: hemothorax on either side; rib fractures on either side; pneumothorax on either side; lung contusion; widened left paravertebral stripe; and widening of the mediastinum, along with an increased ratio of mediastinal width to chest width. The most helpful findings leading to suspicion of aortic rupture included nasogastric tube or tracheal deviation to the right at the T4 level; depression of the left mainstem bronchus; and loss of the aortic contour or knob and left apical cap. False positives and false negatives occurred with each radiographic sign, indicating that there is no single finding that is absolutely reliable in predicting or excluding significant injury in every patient with suspected aortic rupture. Analysis of combinations of findings found that when the aortic contour and knob are normal and the nasogastric tube and trachea are not deviated, there was no case of aortic rupture in four consecutive years of experience. These four signs can be used to exclude aortic rupture.
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PMID:Blunt chest trauma and suspected aortic rupture: reliability of chest radiograph findings. 401 12


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