Ignite Creation Date:
2025-12-24 @ 6:58 PM
Ignite Modification Date:
2025-12-31 @ 7:11 AM
Study NCT ID:
NCT06573957
Status:
COMPLETED
Last Update Posted:
2024-08-27
First Post:
2024-08-24
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Comparison of the Effects of Dexmedetomidine and Lidocaine on Blood Pressure and Heart Rate Response
Sponsor:
Universitas Padjadjaran
Organization:
Study Overview
Official Title:
Comparison of the Effects of Intravenous Administration of Dexmedetomidine 0.5 μg/kg Body Weight With Intravenous Lidocaine 1.5 mg/kg Body Weight on Blood Pressure and Heart Rate Response During Laryngoscopy and Endotracheal Intubation
Status:
COMPLETED
Status Verified Date:
2024-08
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Endotracheal intubation is considered a definitive therapy and the gold standard for airway management. However, this procedure carries several risks, including sudden increases in blood pressure and heart rate. These spikes in blood pressure and heart rate can be tolerated by healthy individuals, but for patients with cerebrovascular and cardiovascular risk factors, they can be extremely dangerous and even life-threatening. Various techniques and drug choices can be employed to prevent the hemodynamic surges associated with endotracheal intubation, including the use of anesthetic drugs from the α2-adrenergic agonist and amide classes. One of the α2-adrenergic agonists commonly used to prevent hemodynamic surges during endotracheal intubation is dexmedetomidine, while one of the amide drugs frequently used for this purpose is lidocaine.
Detailed Description:
Dexmedetomidine works very selectively on noradrenergic receptors distributed both within and outside the central nervous system, particularly in the pons and medulla. Presynaptic stimulation of α2 receptors can reduce the release of norepinephrine and the activation of postsynaptic α2 receptors. Lidocaine works by inhibiting sodium channels within cells, preventing the occurrence of action potentials and the transmission of impulses along nerves. Lidocaine also acts by blocking calcium and potassium channels as well as N-methyl-D-aspartate (NMDA) receptors.
Study Oversight
Has Oversight DMC:
True
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
False
Is an FDA AA801 Violation?: