Records and their imaginaries: imagining the impossible, making possible the imagined

© 2015 Springer Science+Business Media Dordrecht This paper argues that the roles of individual and collective imaginings about the absent or unattainable archive and its contents should be explicitly acknowledged in both archival theory and practice. We propose two new terms: impossible archival imaginaries and imagined records. These concepts offer important affective counterbalances and sometimes resistance to dominant legal, bureaucratic, historical and forensic notions of evidence that so often fall short in explaining the capacity of records and archives to motivate, inspire, anger and traumatize. The paper begins with a reflection on how imagined records have surfaced in our own work related to human rights. It then reviews some of the ways in which the concept of the imaginary has been understood by scholarship in other fields. It considers how such interpretations might contribute epistemologically to the phenomenon of impossible archival imaginaries; and it provides examples of what we argue are impossible archival imaginaries at work. The paper moves on to examine specific cases and “archival stories” involving imagined records and contemplate how they can function societally in ways similar to actual records because of the weight of their absence or because of their aspirational nature. Drawing upon threads that run through these cases, we propose definitions of both phenomena that not only augment the current descriptive, analytical and explicatory armaments of archival theory and practice but also open up the possibility of “returning” them (Ketelaar in Research in the archival multiverse. Monash University Press, Melbourne 2015a) as theoretical contributions to the fields from which the cases were drawn

The influence of positive-pressure ventilation on cardiovascular function in the critically ill

The overall effect of artificial ventilation on cardiovascular performance has not been completely defined, primarily because of the difficulties inherent in assessing the phasic and steady-state characteristics that determine cardiac performance. However, on the basis of the studies reviewed here, certain generalizations can be made regarding the hemodynamic effects of artificial ventilation. If ventilatory maneuvers are divided into those generating negative swings in ITP (for example, spontaneous respiration with or without CPAP and spontaneous breaths during IMV) and positive swings in ITP (for example, positive-pressure ventilation, CPAP and PEEP), the effects of these maneuvers can be separated into factors that alter venous return to the RV, ventricular interdependence, and LV afterload. Venous return is the primary limiting factor determining cardiac output when cardiac function is normal. Increases in Pra induced by positive-pressure ventilation will decrease cardiac output by increasing the back pressure to venous blood flow. This decrease in venous return will be especially pronounced in hypovolemic states (hemorrhage, dehydration) and in patients in whom vasomotor tone is decreased (sepsis, spinal shock, autonomic blockage). In these clinical settings, increases in ITP induced by any means, whether by positive breathing, CPAP, or hyperinflation in patients with airflow obstruction, will be associated with a decrease in cardiac output. Decreasing venous return induced by positive-pressure breathing may be responsible for the often observed cardiovascular collapse seen in some patients immediately following endotracheal intubation and 'bagging' for acute respiratory failure. Since the falls in blood pressure and cardiac output are due to decreases in venous blood flow, appropriate treatment would be to restore the normal pressure gradient for venous return. This can be accomplished by fluid resuscitation, elevation of the legs, a pressure suit (military antishock trousers: MAST), and measures designed to minimize the increase in ITP, such as decreased inspiratory time, decreased tidal volume, and the minimal amount of PEEP necessary to maintain lung inflation. IMV, by interspersing spontaneous breaths with mechanically derived ones, is also useful in minimizing the increase in ITP. However, it may confound the management of hemodynamic instability, especially in patients in ventilatory failure. If fluid resuscitation and ventilator manipulation fail to improve cardiovascular performance, vasopressors may be indicated. However, additional fluid resuscitation often is needed. If patients requiring fluid resuscitation are at significant risk of developing pulmonary edema, LV filling pressures and cardiac output should be measured by pulmonary arterial catheterization as a guide to fluid and vasopressor management. In the hemodynamic evaluation of such patients, it is important to remember that pulmonary artery occlusion pressure may not accurately reflect LV filling when hyperinflation or high levels of PEEP (more than 12 cm H2O) are present. In such settings, other indicators of blood flow, such as mixed venous oxygen saturation, arteriovenous oxygen differences, and urine output can be monitored. When pulmonary artery pressure rises acutely, RV systolic performance can be compromised. Hyperinflation, excessive use of PEEP, pulmonary thromboembolism, and hypoxic pulmonary vasoconstriction can, in the appropriate setting, induce acute cor pulmonale. As Pra increases, venous blood flow decreases. The dilated RV impinges on the LV, decreasing LV diastolic compliance, which further decreases cardiac output. Minimizing hyperinflation by bronchodilator therapy, an adequate ratio of expiratory to inspiratory time, minimal necessary levels of PEEP, and supplemental oxygen will decrease PVR. However, increasing RV filling pressure by volume infusion will result in improved cardiac output in all but the most advanced forms of cor pulmonale and may allow time for other selective forms of therapy to become effective. In LV failure states, intrathoracic blood volume increases, and spontaneous inspiration only increases it further. If pulmonary venous pressure is elevated by either volume overload or severe LV failure, pulmonary edema may develop, decreasing pulmonary compliance and alveolar gas exchange and increasing the work cost of breathing. If methods directed at reversing these processes, such as peripheral vasodilators, inotropic agents, and diuretics, are not successful, or when severe hypoxemia associated with pulmonary edema necessitates endotracheal intubation, positive-pressure breathing (including CPAP) may improve cardiac performance by increasing ITP and will decrease intrathoracic blood volume by decreasing venous return. This should manifest itself as either an improvement or no change in cardiac output associated with a decreasing LV filling pressure