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I. Thoracic Epidural Analgesia An Experimental Study in Sheep of the Effects on Central Circulation, Regional Perfusion and Myocardial Performance during Normoxia, Hypoxia and Isoproterenol Administration
Author(s) -
Ottesen S.,
Renck H.,
Jynge P.
Publication year - 1978
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.1399-6576.1978.tb01411.x
Subject(s) - medicine , vascular resistance , cardiac output , hypoxia (environmental) , heart rate , anesthesia , hypoxic pulmonary vasoconstriction , stroke volume , blood pressure , perfusion , circulatory system , cardiology , contractility , blood flow , blood volume , vasoconstriction , oxygen , chemistry , organic chemistry
Some circulatory effects of thoracic epidural analgesia (TEA) were investigated in splenectomized, open‐chest sheep during normoxia, hypoxia and isoproterenol administration. During normoxia, TEA caused comparatively marked reductions in systemic arterial blood pressure, total peripheral resistance and cardiac output. A fall in heart rate was not compensated for by any rise in stroke volume. Myocardial contractility (LV dp/dt/IP) was not affected by TEA. The proportion of cardiac output diverted to the blocked area was markedly increased. Compensatory vasoconstriction was not observed within the unblocked area in six out of nine animals. Myocardial blood flow showed a pronounced reduction in accordance with the calculated changes of heart work, so that myocardial oxygen extraction remained unchanged. Studies under hypoxia revealed that cardiac responses to hypoxia in the sheep are mediated chiefly by neurogenic factors. TEA abolished the hypoxia‐induced rise in heart rate but did not affect the increase in pulmonary vascular resistance caused by hypoxia. The administration of isoproterenol during TEA increased systemic arterial blood pressure, but due to further fall in total peripheral resistance it was not fully normalized. Cardiac output and heart rate increaied markedly. Myocardial oxygen consumption and blood flow increased but did not reach control levels.