A Comparative Study Between Intranasal and Intravenous Dexmedetomidine and Hemodynamic Responses During Endotracheal Intubation
Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy. This randomized comparati...
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Published in | Curēus (Palo Alto, CA) Vol. 15; no. 2; p. e35196 |
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Main Authors | , |
Format | Journal Article |
Language | English |
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United States
Springer Nature B.V
19.02.2023
Cureus |
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Online Access | Get full text |
ISSN | 2168-8184 2168-8184 |
DOI | 10.7759/cureus.35196 |
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Abstract | Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy.
This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline.
In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses.
Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising. |
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AbstractList | Introduction: Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy.Materials and methods: This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline.Results: In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses.Conclusion: Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising. Introduction: Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy. Materials and methods: This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline. Results: In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses. Conclusion: Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising. Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy. This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline. In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses. Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising. Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy.INTRODUCTION Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to laryngoscopy and endotracheal intubation, many medication combinations have been tried with varying degrees of efficacy.This randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline.MATERIALS AND METHODSThis randomized comparative study was double-blinded and included 106 subjects. Patients including those aged 18-60 belong to the American Society of Anesthesiologists (ASA) 1 and 2. These subjects were divided into two study groups. Group A received dexmedetomidine 0.5mcg/kg (200mcg diluted in 50ml syringe with normal saline (NS) up to 50cc 4mcg/ml) through an infusion pump over 40min before induction. Group B received dexmedetomidine intranasally (1mcg/kg) in undiluted which is prepared from parental preparation (100mcg/ml) and an equivalent dose of NS to the other group. The intranasal drug was dripped into both nostrils in equal volume using a 1ml syringe in a supine head-down position about 40min before induction. Both groups received an intravenous placebo and an intranasal placebo with normal saline.In our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses.RESULTSIn our study, intranasal and intravenous groups were compared. There was no statistically significant difference in hemodynamic variables like heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) between the two groups (majority p value >0.05). Hence both routes can be preferred for attenuation of pressor responses. Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising.CONCLUSION Study findings demonstrate dexmedetomidine can be utilized as a premedication to lessen hemodynamic surges during endotracheal intubation with more or less the same efficacy via intranasal and intravenous routes. This result could be attributable to the fact that both intravenous and intranasal dexmedetomidine stop central catecholamine levels from rising. |
Author | Nelamangala, Kiran M.K, Padmasree |
AuthorAffiliation | 1 Anaesthesiology, Sri Devaraj Urs Medical College, Kolar, IND |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36968881$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1034/j.1399-6576.2001.450815 10.1016/j.aat.2011.11.010 10.1002/14651858.CD004087 10.1111/j.1460-9592.2009.03207.x 10.1111/j.1399-6576.2006.01174.x 10.4103/0019-5049.198404 10.4103/ija.IJA_320_19 10.1111/j.1365-2125.1991.tb05505.x 10.1213/01.ane.0000269488.06546.7c 10.1016/B978-1-4377-2764-7.00007-5 10.4103/ija.IJA_61_17 10.1007/s40265-015-0419-5 10.4103/ija.IJA_1_18 10.1097/BCR.0b013e3181abff90 |
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Snippet | Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to... Introduction: Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor... Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the pressor response to... Introduction: Tracheal intubation and laryngoscopy may cause sympathetic stimulation, which can cause tachycardia and hypertension. To abolish the... |
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SubjectTerms | Age differences Analgesics Anesthesia Anesthesiology Blood pressure Emergency Medicine Heart rate Hemodynamics Intubation Laryngoscopy Pain Management Patients Standard deviation Variance analysis |
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Title | A Comparative Study Between Intranasal and Intravenous Dexmedetomidine and Hemodynamic Responses During Endotracheal Intubation |
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