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Epidural anesthesia modifies cardiovascular responses to severe hypoxia in dogs
Author(s) -
Shibata K.,
Taki Y.,
Futagami A.,
Yamamoto K.,
Kobayashi T.
Publication year - 1995
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1995.tb04164.x
Subject(s) - medicine , anesthesia , hypoxia (environmental) , catecholamine , epinephrine , anesthetic , hemodynamics , heart rate , blood pressure , chemistry , organic chemistry , oxygen
Hypoxia is a critical and sometimes fatal complication of anesthesia. Since there is little information on the cardiovascular response to hypoxia during epidural anesthesia, we assessed the effects of epidural anesthesia on the cardiovascular response to hypoxia and on survival in dogs. We randomly assigned 36 mongrel dogs to one of three groups according to the anesthede technique used: the thoracic group (n=12) received thoracic epidural anesthesia plus general anesthesia, the thoracolumbar group (n=12) received thoracolumbar epidural anesthesia plus general anesthesia, and the control group (n=12) received general anesthesia alone. We monitored hemodynamics and plasma catecholamine concentrations and assessed survival in these groups during normocapnic hypoxia (FiO 2 , 0.09 for 120 min). During hypoxic challenge, PaCO 2 and PaO 2 values were similar in all groups. In both groups that received epidural anesthesia, heart rate, systolic and diastolic arterial pressures, and plasma epinephrine and norepine‐phrine concentrations were lower and arterial pH was greater than in the control group. There was no significant difference in survival among groups. Epidural anesthesia modified both the physiologic cardiovascular and catecholamine responses to hypoxia. Epidural anesthesia of the thoracic region did not appear to accelerate cardiac arrest, but it attenuated the development of metabolic acidosis during hypoxia.