Abstract

BackgroundSpinal anesthesia induced hypotension and bradycardia are common and hazardous in elderly patients. Many techniques are being tried to prevent and treat these problems even if there is a controversy. The effects of prophylactic atropine on prevention of spinal anesthesia induced hypotension and bradycardia in geriatrics for urologic surgeries are not well-established. ObjectiveTo assess the effects of prophylactic atropine in prevention of spinal anesthesia induced hypotension and bradycardia in geriatrics undergoing urological surgeries at a resource limited setting in Central Ethiopia from December 1, 2017 to February 28, 2018 G C. MethodsThis is a prospective cohort study that recruits 76 patients who underwent elective urological surgeries. Independent t-test and Manny Whitney tests were used for numeric data while Chi-Square or Fisher exact test was used for categorical variables. P-values < 0.05 were considered as statistically significant. ResultsThere was no significant difference in baseline heart rate, mean arterial pressure, type & duration of surgery and total fluid administrations. There was a statistically significant difference in mean heart rate and mean arterial pressure at different times of measurement between the exposed and un-exposed groups. Total 1 h vasopressor consumption was minimal in the exposed group (P = 0.038). ConclusionProphylactic atropine with in 1 min of induction of spinal anesthesia in elderly patients undergoing urological surgery might reduce the incidence of hypotension and bradycardia.

Highlights

  • Spinal anesthesia induced hypotension and bradycardia are common and hazardous in elderly patients

  • Total one hour vasopressor consumption was minimal in the exposed group (P = 0.038)

  • Prophylactic atropine with in one minute of induction of spinal anesthesia in elderly patients undergoing urological surgery might reduce the incidence of hypotension and bradycardia

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Summary

Introduction

Spinal anesthesia induced hypotension and bradycardia are common and hazardous in elderly patients. The first and widely accepted mechanism is systemic vasodilation induced by sympathetic blockade, resulting in venous pooling of blood and reduction in systemic vascular resistance [4] This could be treated by administering peripheral vasoconstrictors thereby increasing the systemic vascular resistance and facilitating the venous return [5]. The second cause is believed to be the blunted reflex tachycardia This may result from the blockade of cardioaccelerator sympathetic fibers at T1 to T4, and due to the “reverse” of the Bainbridge reflex. To prevent this mechanism, prophylactic use of intravenous (IV) atropine might have importance [6]

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