Kabimidine Special Precautions

Continuous electrocardiogram (ECG), blood pressure and oxygen saturation monitoring are recommended during infusion of Dexmedetomidine. Caution should be exercised in patients with preexisting severe bradycardia disorders (i.e. Advanced heart block), or patients with preexisting severe ventricular dysfunction (e.g. ejection fraction <30%) including congestive heart failure and cardiac failure in whom sympathetic tone is critical for maintaining hemodynamic balance. Dexmedetomidine decreases sympathetic nervous activity and therefore, these effects may be expected to be most pronounced in patients with desensitized autonomic nervous system control. Prevention of hypotension and bradycardia should take into consideration the hemodynamic stability of the patient and normovolemia prior to administration of Dexmedetomidine. Patients who are hypovolemic may become hypotensive under Dexmedetomidine therapy. Therefore, fluid supplementation should be administered prior to and during the administration of Dexmedetomidine. Based on clinical experience with Dexmedetomidine, if medical intervention is required, treatment may include decreasing or stopping the infusion of Dexmedetomidine, increasing the rate of IV fluid administration, elevation of the lower extremities, and use of pressor agents. Elderly patients over 65 years of age or diabetic patients are more prone to hypotension with the administration of Dexmedetomidine. Transient hypertension has been observed primarily during the loading dose infusion associated with initial peripheral vasoconstrictive effects of Dexmedetomidine and relatively higher plasma concentrations achieved during the loading infusion.
In such causes reduction of the infusion rate may be considered. Following the loading dose infusion, the central effects of Dexmedetomidine dominate and the blood pressure usually decreases. Clinical events of bradycardia and sinus arrest have been associated with Dexmedetomidine administration in young, healthy volunteers with high vagal tone or with different routes of administration including rapid intravenous or bolus administration of Dexmedetomidine. In clinical trials, glycopyrrolate or atropine was effective in the treatment of most episodes of Dexmedetomidine induced bradycardia. However, in some patients with significant cardiovascular dysfunction, more advanced resuscitative measures were required. Dexmedetomidine may cause reduced lacrimation. Lubrication of the patient's eyes should be considered when administering Dexmedetomidine to avoid corneal dryness. Parental drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
Withdrawal: Although not specifically studied, if Dexmedetomidine is administered chronically (for >24 hours) and stopped abruptly, withdrawal symptoms similar to those reported for another α2-adrenergic agent, clonidine, may result. These symptoms include nervousness, agitation and headache, accompanied or followed by a rapid rise in blood pressure and elevated catecholamine concentrations in the plasma. Dexmedetomidine should not be administered for greater than 24 hours.