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• W4253320199 abstract "Dexmedetomidine is an α2-adrenoreceptor agonist recently approved for short-term sedation in the intensive care unit (ICU). Many beneficial effects of α2-adrenoreceptor agonists have been reported, such as a decrease in sympathetic tone with attenuation of hemodynamic and neuroendocrine responses to stress (1), reduced anesthetic and opioid requirements (2), and an analgesic effect. Side effects are mild to moderate cardiovascular depression, with a slight decrease in blood pressure (BP), heart rate (HR), and cardiac output (3). We report a case of tachycardia unresponsive to β-adrenergic blocker therapy that resolved with the initiation of a dexmedetomidine infusion. Case Report A 73-yr-old man with an anterior myocardial infarction 2 days before admission was scheduled for off-pump coronary revascularization (OPCAB). The patient had no history of diabetes, hypertension, hyperlipidemia, or obesity and was only taking 325 mg of aspirin a day. After placement of a radial artery catheter and a pulmonary artery catheter, anesthesia was induced with thiopental (250 mg), fentanyl (500 μg), and vecuronium (10 mg). Preinduction hemodynamic variables were all within normal range: BP was 140/72 mm Hg, HR was 63 bpm (sinus rhythm), central venous pressure was 10 mm Hg, and pulmonary artery pressure was 22/10 mm Hg. The preinduction arterial blood gas analysis showed pH 7.46, Po2 76 mm Hg, Pco2 34 mm Hg, base excess 0 mmol/L, hematocrit 38%, Na 136 mmol/L, K 3.8 mmol/L, and glucose 131 mg/dL. Isoflurane was administered with end-tidal concentrations of 0.8%–1.5%. An additional dose of 500 μg of fentanyl was given before starting the infusion at 2.1 μg · kg−1 · h−1. The bispectral index (BIS) value was 53 after tracheal intubation. During the minutes after the induction and intubation, the BP increased to 150/80 mm Hg; all other variables remained unchanged. A nitroglycerin infusion was started (2 mg/h); BP decreased to 120/60 mm Hg within 10 min and HR increased slightly to 75 bpm, with all other variables remaining constant. Throughout the hour after incision, while the surgeon was dissecting the internal mammary artery and starting the graft anastomoses, the HR increased in a constant manner to a persistent sinus tachycardia of 115 bpm. BP increased simultaneously to 140/65 mm Hg (Fig. 1). Central venous pressure, pulmonary artery pressure, and BIS values remained unchanged. No additional drugs had been administered. The arterial blood gas analysis showed pH 7.39, Po2 301 mm Hg, Pco2 36 mm Hg, base excess −3 mmol/L, and glucose 157 mg/dL. Furthermore, throughout the entire operation the pulse oximeter read saturations of 100%, the end-tidal CO2 concentrations ranged from 28 to 32 mm Hg, and the patient was not febrile. Incremental bolus doses of esmolol were administered over a 5-min period to a total of 200 mg and had minimal effects on HR and BP. In the rapidly changing setting of OPCAB surgery, we did not want to use a longer-acting β-adrenergic blocking drug and therefore started dexmedetomidine, which is usually administered for ICU transfer and ventilator weaning. The initial loading dose, which is usually started after chest closure, was initiated just after protamine administration in this case. A loading dose of dexmedetomidine 1 μg/kg was given over 10 min, and an infusion was started at a rate of 0.3 μg · kg−1 · h−1. Within 15 min, the HR decreased to 80 bpm and remained at that value throughout the remainder of the surgical procedure. BP decreased within 30 min to 105/55 mm Hg and remained in that range until the patient was transferred to the ICU. The BIS values were unchanged, at 52–57, throughout the operation. The dexmedetomidine infusion was continued in the ICU for almost 4 h until extubation, and the HR remained at 80–90 bpm over 24 h.Figure 1: (⇓) The important decrease in blood pressure before the start of the dexmedetomidine loading dose was due to manipulation (lifting) of the heart for better surgical exposure and was therefore not taken into account. Syst = systolic; diast = diastolic; BP = blood pressure; PAP = pulmonary artery pressure; CVP = central venous pressure; BIS = bispectral index; BE = base excess.Discussion We used dexmedetomidine in this case as a novel approach, taking advantage of its sympatholytic side effects, to treat persistent sinus tachycardia during OPCAB surgery. Although additional β-adrenergic blockade with longer-acting drugs may have been effective, we wanted to avoid their long duration of action in the rapidly changing environment of OPCAB surgery. Tachycardia increases myocardial oxygen demand and can lead to ischemic episodes and increased mortality in a patient with coronary artery disease (4). Although our patient did not show signs of ischemia, we considered it necessary to reduce the HR from 115 bpm. We initially chose β-adrenergic blockade, feeling confident that the depth of anesthesia was sufficient (fentanyl total loading dose of 12.5 μg/kg followed by a continuous fentanyl infusion of 2.1 μg · kg−1 · h−1; the isoflurane end-tidal concentration was 1.5% during tachycardia, and BIS values were unchanged at 52–57). To our surprise, the administration of esmolol (200 mg over five minutes) had minimal effect in our patient, with insignificant changes in BP (±10 mm Hg) and HR (±5 bpm). Dexmedetomidine is an α2-adrenoreceptor agonist that binds to receptors located throughout the body, including the peripheral and central nervous system, vascular smooth muscle, and platelets, as well as tissues supplied by the sympathetic nervous system, such as liver, pancreas, kidney, and eye. At least three different α2 isoreceptors have been defined (5), but generally the differentiation is made according to their pre- or postsynaptic location. Presynaptic activation of α2-adrenoreceptors inhibits the release of norepinephrine, terminating the propagation of pain signals, whereas postsynaptic activation of α2 receptors in the central nervous system inhibits sympathetic activity and produces a decrease in HR and BP (3). This last mode of activation, specifically in the locus caeruleus, is also responsible for the sedative and anxiolytic effect of α2 agonists (3). Dexmedetomidine also leads to increased intraoperative hemodynamic stability because of the attenuation of the stress-induced sympathoadrenal responses with significantly lower plasma norepinephrine levels (6). We therefore started a standard dexmedetomidine loading dose, followed by an infusion of 0.3 μg · kg−1 · h−1. The HR decreased from 115 to 80 bpm within 15 minutes and remained around that value until extubation in the ICU. It was notable that the BIS value did not decrease, with nearly constant values from 52 to 57, even after the α2 agonist administration and with an unchanged concentration of inhaled anesthetic. This is important because α2 agonists have been shown to reduce anesthetic and opioid requirements because of a synergistic effect with all intraoperative anesthetics, regardless of their method of administration (IV versus inhaled) (1,2). It suggests that the tachycardia was not due to insufficient anesthesia. Furthermore, the nitroglycerin infusion started after the induction was administered at a constant rate and did not induce any changes in filling pressures, so a discrete vasodilating effect did not seem to be linked to the patient’s tachycardia. In summary, we report a case of persistent tachycardia during OPCAB surgery that failed to respond to esmolol but that responded to dexmedetomidine. Although β-adrenergic blockade is often a useful therapeutic approach, it may not always be practical in the setting of preexisting bronchospasm or reactive airway disease. Because of the potential adverse effects of tachycardia on myocardial ischemia, especially during beating-heart surgery, we believe that dexmedetomidine represents a potentially useful therapeutic approach when treating such patients." @default.
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• W4253320199 title "Treatment of Persistent Tachycardia with Dexmedetomidine During Off-Pump Cardiac Surgery" @default.
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