Preoperative treatment with clonidine (4 microgram/kilogram) prevents the deterioration of renal function after cardiac surgery. This effect might be due to clonidine-induced reduction in the sympathetic nervous system response to coronary artery bypass graft surgery.
Intrathecal morphine in a dose of 0.1 and 0.2 mg provides effective analgesia for up to 48 h without any need for systemic opioids at all in many patients.
This study was designed to evaluate the dose-response effects of different doses of clonidine on the stress response to laryngoscopy and endotracheal intubation. In a randomized, double-blind study, 48 coronary artery bypass grafting (CABG) patients received 0, 2, 4, or 6 micrograms/kg clonidine as an intravenous (IV) infusion during a 15-min period 30 min prior to induction of anesthesia with etomidate (0.3 mg/kg), fentanyl (5-7 micrograms/kg), and pancuronium (0.1 mg/kg). Sedation was assessed prior to induction of anesthesia. Cardiovascular variables and catecholamine plasma levels were measured at predefined intervals. Additional bolus doses of etomidate and fentanyl for suppression of stress-induced reactions were administered if predefined limits of heart rate and blood pressure were exceeded. Clonidine 4 and 6 micrograms/kg significantly attenuated hemodynamic and adrenergic reactions to stress, reduced pharmacologic interventions, and increased sedation. However, clonidine 6 micrograms/kg was not more effective than 4 micrograms/kg, and clonidine 2 micrograms/kg was equally effective as placebo. We conclude that clonidine 4 micrograms/kg IV is the appropriate dose to attenuate the stress response to laryngoscopy in CABG patients. Side effects limiting the use of IV clonidine were not observed.
Intensive care patients often require inotropic support to stabilise circulation and to optimise oxygen supply. In this context, the catecholamines norepinephrine (noradrenaline), epinephrine (adrenaline), dopamine and dobutamine are still the mainstay of therapy. They provide, to different extents, a variety of adrenoceptor-mediated actions comprising vasoconstriction (via alpha-receptors) as well as vasodilatation (via beta 1-receptors), and an increase in cardiac output by enhancing inotropy and heart rate (again via beta 1-receptors). Because of their favourable pharmacokinetic profile (plasma half-lives of about 2 minutes) their actions can easily be controlled. Combinations of different catecholamines with each other or with other drugs such as phosphodiesterase inhibitors or nitrates lead to a broad spectrum of possible haemodynamic actions. However, the use of catecholamines is limited by side effects like tachycardia, hypertension and disturbances of organ perfusion caused by vasoconstriction. Furthermore, as a result of receptor downregulation during long term therapy, the efficacy of catecholamine treatment decreases. These shortfalls stimulated the search for alternatives to catecholamine treatment. Among these, phosphodiesterase inhibitors (e.g. enoximone and amrinone) appear to be the most promising drugs which have been introduced into acute clinical practice up to now. They act via inhibition of the phosphodiesterase isoenzyme III, leading to higher intracellular calcium levels by increasing cyclic adenosine monophosphate (cAMP) levels. These agents improve cardiac performance by enhancing contractility, reducing left ventricular afterload and improve diastolic relaxation. In cases of failing catecholamine therapy due to receptor downregulation, treatment with phosphodiesterase inhibitors may still be effective since their action is not receptor-mediated. Inhibition of the phosphodiesterase enzyme in vascular smooth muscle leads to vasodilatation. Therefore, in low cardiac output states combined with increased total peripheral or pulmonary vascular resistance, phosphodiesterase inhibitor therapy is particularly effective. Depending on the dosage and the speed of intravenous administration, the use of phosphodiesterase inhibitors sometimes results in pronounced decrease of blood pressure which may require vasopressor therapy. Other drugs including histamine H2-agonists are currently under investigation. Their value in the treatment of intensive care patients has still to be evaluated.
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