Disadvantages of sedating neurologic patient
These agents are used at induction of anaesthesia, to maintain sedation, to reduce elevated intracranial pressure, to terminate seizure activity and facilitate ventilation.The intent of their use is to prevent secondary brain injury by facilitating and optimising ventilation, reducing cerebral metabolic rate and reducing intracranial pressure.In the central nervous system (CNS), activation of α-2 receptors reduces norepinephrine release, reduced sympathetic activity and sedation.In the cortical blood vessels activation of presynaptic α-2-adrenoreceptors decrease norepinephrine release, whereas postsynaptic α-2-adrenoreceptors may directly increase vascular smooth muscle tone.Propofol, benzodiazepines, narcotics, barbiturates, etomidate, ketamine, and dexmedetomidine are reviewed and compared.
Pain is a common problem and may be worsened by invasive and unpleasant procedures. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Several different classes of sedative agents are used in the management of patients with traumatic brain injury (TBI).The replacement of an endotracheal tube by a tracheostomy reduces the discomfort associated with an artificial airway and may often remove the need for sedation entirely.Thus, modern day sedation involves more than tube tolerance and is now focused on the multifactorial individual needs of the patient.
Heavy sedation in critical care to facilitate endotracheal tube tolerance and ventilator synchronization, often with neuromuscular blocking agents, was routine until relatively recently.