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Nonbarbiturate Anesthetics
Case Synopsis
A 53-year-old, 75-kg man with a past medical history significant for poorly controlled hypertension and non–insulin-dependent diabetes is scheduled for an external fixation of a femur fracture sustained after a fall off a ladder 2 days ago. The patient has been NPO since the accident and on maintenance fluids of lactated Ringer’s solution at 75 mL/h. He has no known drug allergies and takes hydrochlorothiazide, lisinopril, and metformin at home. On arrival to the operating room, his heart rate is 96 beats per minute, his blood pressure is 105/50 mm Hg, and he is saturating 98% on 2 L nasal cannula. During induction, he receives 150 μg of fentanyl, 80 mg of lidocaine, 150 mg of propofol, and 8 mg of vecuronium. After easy mask ventilation, the airway is secured with an endotracheal tube. Postinduction blood pressure is 65/43 mm Hg with a heart rate of 108 beats per minute. Minimal response is noted to initial boluses of 100 μg of phenylephrine and 10 mg of ephedrine. Ultimately, the patient’s hemodynamics stabilized after a bolus of 1 L of crystalloid solution.
Problem Analysis
Definition
In addition to ketamine (see Chapter 89 ), nonbarbiturate anesthetics include midazolam, dexmedetomidine, etomidate, and propofol. Midazolam and dexmedetomidine are more commonly used as sedative-anxiolytic agents and often as adjuncts to other induction agents. Both etomidate and propofol are used as intravenous (IV) induction agents; the former is often preferred for patients with or at risk for hemodynamic instability.
Recognition
Mechanism of Action
Benzodiazepines, propofol, and etomidate all exert their effect via interaction with γ-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the central nervous system. Midazolam is a benzodiazepine that increases the frequency of chloride channel opening by facilitating GABA-receptor binding, causing cell membrane hyperpolarization and thus producing an inhibitory effect on neural function.
Dexmedetomidine is an α 2 -agonist that causes activation in the locus coeruleus and spinal cord that results in a decrease in sympathetic nervous system outflow (norepinephrine and epinephrine) and cellular hyperpolarization through the reduction of cyclic adenosine monophosphate.
Etomidate is an imidazole derivative. It also causes hyperpolarization of the neuronal cell membrane, thereby inactivating the reticular activating system. Etomidate may also increase GABA-receptor availability.
Propofol is an alkylphenol. It is presumed to act on GABA receptors in the central nervous system to increase the frequency of chloride channel opening. Thus propofol too has a neuroinhibitory action.
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