Temporarily Out of Stock Online Please check back later for updated availability. Overview Publisher's Note: Products purchased from Third Party sellers are not guaranteed by the publisher for quality, authenticity, or access to any online entitlements included with the product. Your solution to mastering I. Therapy Demystified is your shortcut to mastering this essential nursing topic. This fast and easy guide offers: Learning objectives at the beginning of each chapter An NCLEX-style quiz at the end of each chapter to reinforce learning and pinpoint weaknesses Measurements labeled in SI units Indications for I.
Show More. Table of Contents I. Therapy Demystified 1. Basic Principles of IV Therapy 2. Fluids and Electolytes 3. IV Delivery Systems 4. Peripheral IV Therapy 5. Central IV Therapy 6. IV Therapy and the Nursing Process 7. Crystalloid Solutions 8. Colloid Solutions 9. Blood Component Therapy Therapy Demystified is your shortcut to mastering this essential nursing topic.
This fast and easy guide offers: Learning objectives at the beginning of each chapter An NCLEX-style quiz at the end of each chapter to reinforce learning and pinpoint weaknesses Measurements labeled in SI units Indications for I. Additional Product Features Dewey Edition. Therapy Demystified 1. Basic Principles of IV Therapy 2. Fluids and Electolytes 3. IV Delivery Systems 4. Peripheral IV Therapy 5.
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Central IV Therapy 6. IV Therapy and the Nursing Process 7.
Crystalloid Solutions 8. Colloid Solutions 9. Blood Component Therapy Parenteral Therapy Iv Pharmacological Therapy IV Therapy and Infants and Children IV Therapy and the Elderly Show More Show Less. There are a number of isoforms of the GABA A receptor, which determine its agonist affinity, probability of ion-channel opening, and conductance and also location and expression on the post-synaptic membrane. These pentameric GABA A complexes form chloride anion channels and are molecular targets for benzodiazepines, barbiturates, i.
Activation of the GABA A receptor leads to post-synaptic hyperpolarization of the cell membrane, inhibitory post-synaptic currents, and ultimately inhibition of neuronal activity. They are widely distributed within the central nervous system and are modulated by most inhaled general anaesthetics. Integrated neuronal network models of anaesthetic effect: Linking the effect of an anaesthetic at particular ion channel sites to its actual behavioural effects is fraught with difficulty.
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Much attention has focused on neural networks involved in sleep and arousal, including the ventrolateral preoptic area of the hypothalamus, the tuberomamilliary nucleus, and the ascending reticular activating system. Through its actions on GABA A receptors in the hippocampus and prefrontal cortex, propofol inhibits acetylcholine release. This action appears to be important for the sedative effects of propofol. Propofol also induces inhibition of NMDA receptors that may contribute to its central effects.
Etomidate was the first i.
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Ketamine inhibits the excitatory neurotransmitter glutamate at NMDA receptors. It functions at the thalamus which relays sensory impulses from reticular activating system to the cerebral cortex and the limbic cortex which is involved with the awareness of sensation. This can be conducive to bacterial growth, but addition of the chelating agent disodium edetate has reduced this.
Propofol can cause pain during injection which may be attenuated by co-administration of lidocaine or by formulation in medium chain, rather than long-chain triglycerides. It has a short initial distribution half-life 2—8 min. Propofol is rapidly metabolized in the liver by conjugation to glucuronide and sulphate, producing water-soluble compounds which are excreted mainly by the kidneys.
Clearance of propofol is extremely high greater than hepatic blood flow , suggesting additional extrahepatic, metabolism. After single-bolus injection, blood propofol levels decrease rapidly as a result of redistribution and elimination. The initial distribution half-life is 2—8 min and elimination half-life is 4—7 h. The longer elimination half-life is indicative of distribution to fatty tissues with low perfusion, which results in a slow return of propofol to the central compartment.
Because of this slow rate of return to the plasma compartment, propofol concentrations in the blood do not increase dramatically.
Therefore, emergence from propofol anaesthesia or sedation remains relatively rapid even after prolonged infusion. The pharmacodynamic effects of a number of i.
Systemic effects of i. Propofol reduces systemic vascular resistance, cardiac contractility, and preload. Patients with impaired ventricular function poorly tolerate significant reductions in cardiac output as a result of decreases in ventricular filling pressures and contractility.
Heart rate increases secondary to activation of baroreceptor-mediated compensatory mechanisms in response to the reduction in cardiac output and systemic vascular resistance. Like thiopental, propofol causes profound respiratory depression. A reduction in upper airway reflexes is helpful during intubation or laryngeal mask placements in the absence of paralysis induced by neuromuscular blocking agents. Propofol decreases cerebral oxygen requirements, cerebral blood flow, and intracranial pressure. It also has useful antiemetic effects. Although during induction, it may cause spontaneous movements, muscle twitching, or hiccups, it has predominantly anticonvulsant properties at high infusion doses and causes burst suppression on EEG.
It has been used successfully to terminate status epilepticus. There are now guidelines recommending maximum propofol infusion rates of 4. Thiopental is the most commonly used barbiturate and is derived from barbituric acid, a condensation product of urea and malonic acid.
It is insoluble in water and is prepared in a carbonate salt to maintain an alkaline pH. In patients with intravascular volume depletion, low serum albumin, or if the non-ionized fraction is increased e. After a single bolus, thiopental is rapidly distributed to highly perfused, low volume tissue e.
The uptake of thiopental by adipose tissue is a minor contributor to termination of the effects of an induction dose, because of minimal perfusion to fatty tissue and thiopental's slow removal from it. However, after a continuous infusion, termination of thiopental's effects becomes increasingly dependent on these slower processes of uptake into adipose tissue and elimination by hepatic metabolism. Thiopental causes direct myocardial depression, with decreased mean arterial pressure MAP due to inhibition of medullary vasomotor centre and reduced sympathetic outflow, resulting in dilatation of capacitance vessels.
It results in an elevation in heart rate due to baroreceptor-mediated sympathetic reflex stimulation of the heart in response to decrease in cardiac output and arterial pressure. Thiopental causes depression of the medullary ventilatory centre and decreases the response to hypercapnoea and hypoxia. It does not completely depress noxious airway reflexes and may predispose to laryngospasm and bronchospasm. It also has antanalgesic effects.
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Thiopental decreases cerebral metabolic oxygen consumption rate CMRO 2 , the cerebral blood flow, and intracranial pressure. Large doses cause electrical silence burst suppression on EEG, which may protect the brain from episodes of focal ischaemia. Owing to slow metabolism and prolonged elimination kinetics, thiopental is rarely used as a continuous infusion. No specific toxicity has been associated with it, other than extension of its known side-effects.