They do this by decreasing the permeability of the nerve cell membrane to sodium ions which decreases the rate of depolarization of the nerve membrane, which increases the threshold for electrical excitability, and prevents action potential. It is believed that this done by competing with calcium for membrane binding sites which control membrane permeability to sodium. Catecholamine stores are not released due to the sympathetic blockade resulting from this effect on excitable membranes, which affects the nervous system and therefore the heart rate and blood pressure levels (Medscape, 2001; Nagelhout & Zaglaniczny, 2001; Stoelting, 1978; Takki, Tammisto, Nikki, & Jaattela, 1972).
An endotracheal tube is inserted through the larynx into the trachea (Morgan & Mikhail, 1996).
Aqueous lidocaine hydrochloride, 5 ml in a 2% mixture, administered IV, 4 minutes before endotracheal intubation (Morgan & Mikhail, 1996).
Aqueous lidocaine hydrochloride, 5 ml in a 4% mixture, sprayed topically to the upper airway and vocal cords 4 minutes prior to endotracheal intubation (Morgan & Mikhail, 1996).
For this study the blood pressure change will include an increase in systolic blood pressure of 10 mmHg or more at five, ten, and fifteen minute intervals, compared to pre-induction blood pressure.
For this study the heart rate change will include an increase in heart rate of 10 beats per minute at five, ten, and fifteen minute intervals, compared to pre-induction heart rate.
What is the difference in the effectiveness of topical and intravenous application of lidocaine for the blunting of increased heart rate and blood pressure in patients undergoing laryngoscopy and intubation.
Study delimitations include the timing of lidocaine administration, the amount of drug given, and the length of laryngoscopy. Study limitations include the use of retrospective chart review which may not reveal exact measurements of these variables.
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