A packet-based dual-rate PID control strategy for a slow-rate sensing Networked Control System.

This paper introduces a packet-based dual-rate control strategy to face time-varying network-induced delays, packet dropouts and packet disorder in a Networked Control System. Slow-rate sensing enables to achieve energy saving and to avoid packet disorder. Fast-rate actuation makes reaching the desired control performance possible. The dual-rate PID controller is split into two parts: a slow-rate PI controller located at the remote side (with no permanent communication to the plant) and a fast-rate PD controller located at the local side. The remote side also includes a prediction stage in order to generate the packet of future, estimated slow-rate control actions. These actions are sent to the local side and converted to fast-rate ones to be used when a packet does not arrive at this side due to the network-induced delay or due to occurring dropouts. The proposed control solution is able to approximately reach the nominal (no-delay, no-dropout) performance despite the existence of time-varying delays and packet dropouts. Control system stability is ensured in terms of probabilistic Linear Matrix Inequalities (LMIs). Via real-time control for a Cartesian robot, results clearly reveal the superiority of the control solution compared to a previous proposal by authors.

[Hemodynamic changes in hypoglycemic shock]. / Alteraciones hemodinámicas en el choque hipoglucémico.

Severe hypoglycemia may be present in seriously ill patients; if it is not corrected opportunely a series of neuroendocrinal mechanisms take place aimed at correcting metabolic alterations. These mechanisms can produce hemodynamic alterations as well. Nine mongrel dogs were studied with continuous registration of: blood pressure, central venous pressure, cardiac frequency, respiratory frequency, electrocardiogram and first derivative (Dp/Dt). Six dogs received crystalline (fast acting) insuline intravenously (group 1). After hemodynamic changes were registered hypoglycemia was corrected with 50 per cent glucose solution. Complementary insuline doses were administered to three dogs (group 2); in this group hypoglycemia was not corrected. In group 1 during hypoglycemia there was an increase in blood pressure, central venous pressure, cardiac frequency, respiratory frequency and Dp/Dt, and changes in QT and T wave on the EKG; these changes were partially reversible after hypoglycemia was corrected. The above mentioned alterations persisted in group 2, breathing became irregular irregular and respiratory arrest supervened. It can be inferred that the hemodynamic response to hypoglycemia is predominantly adrenergic. The role of catecolamines, glucocorticoides, glucagon, insuline, cyclic AMP in metabolic and hemodynamic alterations consecutive to hypoglycemia are discussed.