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1. |
Pathophysiology and care of respiratory failure |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 170-170
WILLIAM SHOEMAKER,
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ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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2. |
Pulmonary gas exchange in the critically ill patient |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 171-180
JOHN WEST,
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摘要:
A new method for determining the distribution of ventilation-perfusion ratios in critically ill patients in the intensive care setting is described. The method is based on the infusion of a mixture of inert gases into the venous circulation with a subsequent measurement of the gas concentrations in arterial blood and mixed expired gas by gas chromatography. Young normal subjects show very narrow distributions of ventilation and blood flow with respect to ventilationperfusion ratio. These distributions broaden with increasing age. Oxygen breathing causes the development of shunts in both normal and abnormal lungs, particularly in patients with lung disease. The mechanism of this is discussed. Measurements of shunt after 100% oxygen generally result in overestimates. In some abnormal lungs, positive end-expiratory pressure decreases the amount of shunt and also results in increased amounts of ventilation going to units with very high ventilation-perfusion ratios. Preliminary results suggest that the new test may be of diagnostic value in some settings; eg, detecting pulmonary embolism in critically ill patients.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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3. |
The role of the central nervous system in shockThe centroneurogenic etiology of the respiratory distress syndrome |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 181-185
GERALD MOSS,
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摘要:
The central nervous system seems to play a major role in triggering lung damage.A complete anatomical and physiological picture of the respiratory distress syndrome can be produced by perfusing the brain of experimental animals with blood low in oxygen, ie, simulating the stagnant hypoxia of shock at the brain level.In other experiments relative to oxygen toxicity, there is evidence that a site remote from the lung where high oxygen tensions trigger lung damage. Here again, a centroneurogenic factor seems to be implicated.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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4. |
Pulmonary microcirculationCellular pathophysiology in acute respiratory failure |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 186-199
JAMES WILSON,
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摘要:
Pulmonary failure associated with shock from myocardial infarction, sepsis, trauma, and numerous other situations can be related to a cellular metabolic problem. Perhaps the most important emerging concept in cellular physiology and microcirculatory research today is that the lung exhibits a uniform response to injury, whether mediated via the vasculature or the airways. The serious and often fatal nature of syndromes and diseases affecting the lung requires that every physician treating patients familiarize himself with the cellular morphologic and physiologic data presently available. An awareness of the hazards of oxygen, a knowledge of sophisticated pharmacologic therapy, a high index of suspicion for developing acute respiratory failure, and good clinical judgment tempered by experience may allow the salvage of a higher percentage of patients with pulmonary failure.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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5. |
Pattern of pulmonary hemodynamic and functional changes in shock |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 200-210
WILLIAM SHOEMAKER,
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摘要:
Death from pulmonary failure in clinical shock is largely due to alterations in pulmonary venous admixture with ventilation-perfusion (V/Q) abnormalities which are related to very early increases in pulmonary vascular resistance; the latter is an important early predictor of survival.Sequential hemodynamic, oxygen transport and pulmonary venous admixture measurements were performed in experimental animals as well as in shock patients remote from therapy. In surviving patients, the early physiologic response consisted of hypotension, increased PVR, normal arterial pH, and normal central blood volume. There was an increased cardiac output with normovolemia and usually decreased cardiac output in the presence of hypovolemia. During the early period of shock, the nonsurvivors had lower cardiac output, higher central blood volume, higher PVR, greater acidosis, and lower oxygen consumption.Increased PVR occurred early, often before development of maximal hypotension and low cardiac output in both clinical and experimental conditions. The magnitude of the PVR increase was roughly related to the extent of the trauma and hemorrhage; the increase was significantly greater in nonsurvivors. The increased PVR was associated with acidosis during hypovolemia, increased central blood volume after volume deficits were restored, and with the subsequent appearance of pulmonary shunting.These data indicate that trauma, hemorrhage and other forms of stress produce pulmonary vasoconstriction from neural influences; initially at least, this is a compensatory mechanism which tends to redistribute blood flow upward. However, the increased PVR may be exaggerated by metabolic, hormonal, and rheologic factors. The persistence of a high PVR leads to the backup of blood behind the lesser circulation and uneven blood flow in the microcirculation. Thus, ventilation-perfusion abnormalities are produced by maldistributions of regional or zonal pulmonary blood flow as well as maldistributions of flow at the microcirculatory level. Therapy is directed toward the reduction of PVR by correction of acidosis, the use of plasma expanders and steroids, and the avoidance of vasopressors and saline.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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6. |
Infection control in critical care units |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 211-216
JAY SANFORD,
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摘要:
Inhalation therapy equipment is a potential vector of gram-negative bacilli. Small-volume Venturi nebulizers have a potential but are infrequently implicated in the dissemination of bacteria. Large volume nebulizers of all designs are the major source for aerosolized bacteria. Ventilators and humidifiers have minimal potential.Any system of decontamination requires the meticulous application of a procedure at least once every 24 hours. The degree of contamination should not exceed that of hospital air.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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7. |
Monitoring respiratory function |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 217-220
JOHN OSBORN,
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摘要:
The status of patients on respirators can change very suddenly; therefore, continuous airway monitoring which can provide data on the immediate status of respiratory function can be life-saving as well as contribute to the making of sound clinical decisions.A system for continuous monitoring and analysis of respiratory gas, pressure, and flow is presented.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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8. |
New light on pediatric respiratory problems |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 221-224
A. BROENNLE,
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摘要:
The prevention, and treatment of respiratory distress syndrome continues to evolve and improve with the predictive use of the lecithin-syringomyelin ratios in determining optimal delivery time for some infants and in the application of continuous positive airway pressure and other techniques of providing positive transpulmonary pressure. CPAP may be effectively applied with nasal prongs and reduce the need for endotracheal intubation. Current criteria for instituting the various levels of respiratory support are outlined. Intermittent mandatory ventilation is briefly described.
ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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9. |
Rational ventilator modes for respiratory failure |
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Critical Care Medicine,
Volume 2,
Issue 4,
1974,
Page 225-225
HENRIK BENDIXEN,
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ISSN:0090-3493
出版商:OVID
年代:1974
数据来源: OVID
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