PROPOFOL Propofol (2,6-diisopropylphenol) is a lipid-soluble anesthetic agent that is supplied in an emulsion of soybean oil and purified egg phosphatide, which most egg-allergic patients should tolerate, since it contains no protein. The emulsion is responsible for frequent burning on injection and contains no preservatives, resulting in the risk of bacterial growth in improperly handled solutions. When given by infusion, the onset of sedation is rapid (5 to 10 min), and it resolves rapidly (5 to 10 min) upon discontinuation of the infusion.19 Amnesia, however, is not reliably produced in doses used for sedation. The drug possesses antiemetic properties. Propofol produces significant cardiovascular depression, with dose-related declines in systolic blood pressure of up to 25 to 40 percent when given in induction doses. This effect is more pronounced in those with hemodynamic compromise and in the elderly.
The use of propofol for ED CS is controversial, and its use outside the operating room by nonanesthesia personnel may be restricted by hospital policy. However, Swanson and colleagues employed a regimen of 2 pg/kg fentanyl and a propofol infusion at a loading rate of 0.21 (mg/kg)/min, followed by a maintenance rate of 3 to 6 (mg/kg)/h in 20 ED patients who required CS. This provided rapid onset of sedation (mean, 6.6 min) and rapid recovery (mean, 6.1 min), with high patient and physician satisfaction scores. Three patients had pain on injection, one had pain and brief hypotension, and two had brief episodes of apnea; 75 percent had amnesia for the procedure at 24 h.19
Propofol is a promising agent for CS in the ED because it rapidly produces sedation that quickly abates when the infusion is discontinued. In doses usually used for CS, however, both analgesic and amnestic agents may be required, which may result in hypoventilation and potentiate the already significant hemodynamic effects of propofol. Further study is required before the routine use of propofol in the ED can be recommended.
KETAMINE Ketamine is a phencyclidine derivative that has analgesic and anesthetic properties. Ketamine anesthesia is often called "dissociative," reflecting electroencephalographically demonstrable discontinuity of the corticothalamic and limbic systems. The patient's eyes often remain open, with spontaneous horizontal and vertical nystagmus. Muscle tone may be increased, and corneal reflexes and spontaneous swallowing are preserved; occasional purposeful movements unrelated to the environment occur. Emergence reactions, characterized by disturbing dreams and vivid, sometimes frightening hallucinations, occur in 5 to 30 percent of patients. Patients at greatest risk for emergence reactions are over 16, female, normally dream, have personality disorders, or receive droperidol or atropine. These phenomena may be attenuated with benzodiazepines given before or at the completion of the procedure.
Ketamine is highly lipid soluble and has a pKa of 7.5, accounting for the rapid (within 1 min) onset of hypnosis following IV injection. Peak brain and plasma concentrations develop within 1 min; rapid redistribution to peripheral tissues results in a mean hypnosis time of 6 min (1.0 mg/kg) to 10 min (2.0 mg/kg). Ketamine is metabolized by the hepatic P-450 system to several active metabolites, the chief among which is norketamine. Norketamine appears within 2 min of a bolus injection and is one-tenth to one-third less potent than the parent drug, but does not appear to penetrate the CNS in quantities sufficient to produce hypnosis. Subsequent metabolites are conjugated and renally excreted, but, because they are much less active, the dose appears not to require adjustment in patients with renal insufficiency. Drugs which induce the P-450 system increase the metabolism of ketamine, whereas inhibitors prolong the duration of effect.
The hemodynamic response to ketamine is complex. It is a direct myocardial depressant and vasodilator, but these effects are typically overshadowed by stimulation of significant CNS sympathetic outflow, resulting in tachycardia and vasoconstriction. (The author's experience is that fentanyl, 1 to 2 Mg/kg given 3 to 5 min prior to the procedure, attenuates this effect but increases the frequency of hypoxemia, especially when ketamine is given rapidly.) However, profoundly hypovolemic patients or those with little sympathetic reserve (e.g., cocaine users) may develop hypotension, particularly at rapid rates of injection.
The pulmonary effects of ketamine make it an appealing agent. Although it produces bronchodilation and bronchorrhea, it rarely causes significant respiratory depression unless given by rapid injection (over less than 60 s) or coadministered with other agents. Patients usually retain protective airway reflexes, but this is not a certainty, and careful monitoring is necessary when ketamine is used.
Before giving ketamine, it is important to consider the drug's likely nontherapeutic effects. If a hyperdynamic state or bronchorrhea may not be well tolerated, then appropriate premedication (opioids or glycopyrrolate) should be given or another agent chosen. A specific discussion of the emergence phenomenon with the patient, family, and friends will reduce the impact of this occasionally dramatic event.
The dose of ketamine commonly used for analgesia is 0.5 to 1.0 mg/kg over 60 s. Anesthesia is produced by doses of 1 to 2 mg/kg. When anesthetic doses are administered, midazolam should be given during the emergence phase to attenuate emergence phenomena.
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This guide Don't Panic has tips and additional information on what you should do when you are experiencing an anxiety or panic attack. With so much going on in the world today with taking care of your family, working full time, dealing with office politics and other things, you could experience a serious meltdown. All of these things could at one point cause you to stress out and snap.