Dexmedetomidine is a highly selective agonist at α 2 -adrenoceptor with a wide range of pharmacological properties. It has a strong sympatholytic effect by reducing the release of norepinephrine from sympathetic nerve endings. Sedation reduced due excitation coeruleus noradrenergic basic nucleus which is located in the brainstem. Acting on this portion has dexmedetomidine sedation (similar to natural sleep without rapid eye movement), while simultaneously allowing the patient to be in the active state and awakened. Dexmedetomidine has anesthetic and a moderate analgesic effect; analgesic effect has been demonstrated in patients with chronic pain in the lower back. Effect on cardiovascular system depends on the dose; at lower infusion rates dominates central action, which leads to a decrease in heart rate and blood pressure. At higher doses predominate peripheral vasoconstrictor effects, which leads to an increase in systemic vascular resistance and blood pressure, while bradycardia becomes more pronounced. Dexmedetomidine has almost no inhibitory effect on the respiratory system.
Orion Corporation, Finland
1 ml – 118 micrograms of dexmedetomidine hydrochloride that corresponds to the content 100 micrograms of dexmedetomidine
Excipients: sodium chloride – 8.83 mg water d / and – up to 1 ml
Sedation mild to moderate in ICUs during or after intubation.
Hypersensitivity to dexmedetomidine or any of the excipients of the drug.
On the part of metabolism and nutrition. Often: hyperglycemia, hypoglycemia; rare: metabolic acidosis, hypoalbuminemia.
Mental disorders. Common: agitation; rare: hallucinations.
Cardio-vascular system. Very common: bradycardia, hypotension; often: ischemia or myocardial infarction, tachycardia; rare: AV-blockade of I degree, decrease cardiac output.
The respiratory system. Uncommon: dyspnea.
From the digestive system. Common: nausea, vomiting, dry mouth; Uncommon: abdominal distension.
General disorders and reactions at the injection site. Often: withdrawal syndrome, pyrexia; rare: ineffectiveness of drug craving.
How to accept, acceptance rate and dosage
Only for hospital applications.
The dose for adult patients.
Patients who already intubation performed and which are in a state of sedation can be translated into an initial rate Deksdor / v infusion of 0.7 ug / kg / h, which can be gradually corrected within – 0.2-1.4 ug / kg / hr to achieve the desired level of sedation. For weakened patients should consider the usefulness of the lowest initial rate of infusion. It should be noted that dexmedetomidine is a potent drug, therefore, the infusion rate indicated by one hour.
Typically the shock loading dose is not required. Patients who need a more rapid onset of sedation can be administered first load infusion 0.5-1.0 ug / kg body weight over 20 minutes, i.e. an initial infusion of 1.5-3 mg / kg / h for 20 min.
The rate of infusion after initial loading infusion of 0.4 ug / kg / h, which can be further corrected.
Patients in this age group dosage adjustment is not usually required.
Impaired renal function.
Patients with impaired renal function Dosage adjustment is not usually required.
Abnormal liver function.
Deksdor metabolized in the liver, so it should be used with caution in patients with impaired hepatic function. Consideration should use low maintenance dose.
The duration of the course depends on the patient’s need to stay in a state of sedation. No experience with Deksdora more than 14 days.
Deksdor introduced only health professional who has experience in the treatment of patients requiring intensive care. The drug is used only as diluted in / infusion using an infusion device with regulation of the rate of administration. Ampoules and vials are intended only for personal use in one patient.
Preparation of p-ra
Before applying Deksdor may be diluted in 5% dextrose in D-p, p-D Ringers, mannitol or 0.9% solution of sodium chloride in D to achieve the desired concentration of 4 mcg / ml. The table below shows the volumes needed to prepare the infusion.
Displacement Deksdora concentrate for preparing p-ra infusion ml
Displacement solvent, ml
The total volume of infusion ml
After cooking gently shake to mix well rr.
Before applying cooked rr should be visually inspected for foreign particles and discoloration.
Deksdor suitable for fluids and medications: lactate rr Ringers, 5% solution of dextrose, 0.9% solution of sodium chloride, 20% mannitol, sodium thiopental, etomidate, vecuronium bromide, pancuronium bromide, succinylcholine, atracurium besylate, mivakuriya chloride, rocuronium, glycopyrolate bromide, phenylephrine hydrochloride, atropine sulfate, dopamine, norepinephrine, dobutamine, midazolam, morphine sulfate, fentanyl citrate and plasma expanders.
At temperatures above 25 ° C. After reconstitution store at 2 to 8 ° C for 24 hours.
Simultaneous application Deksdora with anesthetics, sedatives, hypnotics and opioid drugs may result in potentiation of their effects. Specific studies have confirmed the potentiation of effects while the use of sevoflurane, isoflurane, propofol, alfentanil and midazolam.
Pharmacokinetic interaction between Deksdorom and isoflurane, propofol, alfentanil and midazolam have been identified. However, due to possible pharmacodynamic interactions with the application of such agents in combination with Deksdorom may be necessary to decrease the dose of concomitant Deksdora or anesthetic, a sedative, hypnotic or opioid drug.
Should consider the possibility of strengthening the hypotensive and bradycardic effects in patients receiving other drugs that cause such effects, although additional effects in an interaction study with esmolol were modest.
Deksdor is intended only for use in intensive care units. During the infusion Deksdora all patients should be continuously monitored cardiac function. Patients who have not carried out intubation, should monitor respiratory function.
As is the case with all sedative drugs, caution should be exercised when combining Deksdora with other drugs that have a sedative effect and affect the cardiovascular system because of the possibility of additive effects.
By virtue of the pharmacodynamic effects of Deksdora Caution should be exercised when using the drug in patients with severe bradycardia, advanced heart block (AV-block II-III degree, except when using a pacemaker), hypotension, or in patients with severe dysfunction of the heart ventricles. Deksdor reduces the activity of the sympathetic nervous system, and in patients with hypovolemia, chronic hypertension and in the elderly can expect more severe hypotension / bradycardia. Patients with good physical preparation and low resting heart rate may be particularly sensitive to bradycardic effects agonists α 2 -adrenoceptor; There are reports of temporary stop of sinus node activity. Hypotension and bradycardia generally do not require treatment, but if necessary, hypotension should be treated with a vasoconstrictor agent and / or the fluid, and bradycardia – anticholinergics.
Caution should be exercised to avoid substantial arterial hypo- or hypertension in patients with ischemic heart disease, which are used Deksdor because there is a theoretical possibility to reduce coronary blood flow due to α 2 -mediated peripheral vasoconstriction. Consideration should be given a dose reduction or discontinuation of therapy in patients which confirms ECG signs of myocardial ischemia.
Patients with impaired activity of the autonomic nervous system (e.g. due to spinal cord injury) may draw more pronounced hemodynamic changes after initiation of Deksdora because care should be taken to use this drug in these patients.
Temporary AG detected mainly during loading dose that was associated with a peripheral vasoconstrictor effect Deksdora. Hypertension treatment is usually not required, but recommended to decrease loading dose or infusion rate.
Compared with propofol and midazolam, patients receiving sedation Deksdorom usually easier to wake up, better communicate with your doctor and are able to better communication, while remaining generally in a state of rest and relaxation. However, the clinical profile indicates that Deksdor as an independent agent may not be the drug of choice when it comes to the need for deep sedation or full obezdvizhimosti patient. If necessary muscle relaxation (including during endotracheal intubation) patients should receive additional alternative sedative at therapeutic doses, so they do not come to mind during the procedure.
Introduction bolus doses Deksdora to dramatically increase the level of sedation was not evaluated, it is not recommended for use. In case of insufficient sedation, especially during the first hours after the transition to Deksdor can be applied bolus doses alternative sedative.
Deksdor probably does not inhibit seizure activity, and therefore can not be used as a single agent for treatment of status epilepticus. Experience of using Deksdora with severe neurological disorders such as head trauma, is limited, so in such cases it should be used with caution, especially if deep sedation is required. Like other sedatives, Deksdor may reduce cerebral blood flow.
Agonists of α 2 -adrenoceptor rarely associated with reactions canceling the sudden cessation of long-term application. This possibility should be considered if the patient develops agitation and hypertension shortly after discontinuation of Deksdora.
It is unknown whether the use of safe Deksdora in individuals susceptible to malignant hyperthermia, so its use in these patients is not recommended. In the case of prolonged unexplained fever drug treatment should be discontinued.
No experience with Deksdora more than 14 days.
Ability to influence the reaction rate when driving and operating other machines.
The drug is indicated for use in a hospital environment.
In clinical studies and post-marketing reports of several cases of dexmedetomidine overdose.
Maximum dexmedetomidine infusion rate, which was reported in these cases reached 60 ug / kg / h for 36 minutes, and 30 ug / kg / h – for 15 min in 20-month old child and adult respectively. The most frequent adverse reactions that have been reported in connection with overdose in these cases included bradycardia, hypotension, excessive sedation, somnolence and cardiac arrest.
In cases of overdose with clinical symptoms of infusion rate Deksdora should be reduced or discontinued. Advantageously expected cardiovascular effects, treatment was performed for clinical reasons. At high drug concentrations hypertension may be more pronounced than hypotension. In clinical studies cases stop sinus node activity were spontaneously or respond to treatment with atropine or glycopyrolate. In some cases of severe overdose, which led to cardiac arrest, require resuscitation. None of the overdoses did not lead to death.