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Does plasma expansion and adrenaline administration improve haemodynamic alterations secondary to lumbar epidural analgesia in splenectomized, open-chest sheep?
Does plasma expansion and adrenaline administration improve haemodynamic alterations secondary to lumbar epidural analgesia in splenectomized, open-chest sheep?
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In an experimental sheep model, the combination of plasma expansion and adrenaline effectively counteracts systemic arterial hypotension induced by lumbar epidural analgesia.
Haemodynamic alterations secondary to the induction of lumbar epidural analgesia (LEA) were investigated in splcnectomized, open‐chest sheep. A considerable reduction in systemic arterial blood pressure (P Aa ) and total peripheral resistance (TPR) occurred. Cardiac output (Q pa ) was reduced non‐significantly as a fall in heart rate (HK) was counteracted by an increase in stroke volume (SV). Myocardial blood flow (MBF) was reduced in parallel with myocardial oxygen consumption (MV O2 ), so that myocardial oxygen extraction (O 2 uc myocardium) remained unchanged. No convincing signs of compensatory vasoconstric‐tion were noticed in the non‐blocked area, and the proportion of Q PA diverted to the blocked area (Q ap/ca ) was increased only non‐significantly. Administration of dextran 70 was followed by an increase in Q PA , mainly due to an increase in SV. P Aa increased only slightly as TPR was further reduced. MUF rose only non‐significantly, but O 2 uc myocardium increased somewhat. A reduction of vascular resistance in the blocked area was recorded, and in comparison with the control value Q ap/ca was markedly increased in most animals. The effect of adrenaline in three different dosages (0.362, 1.91 and 3.62 μg/min) was studied on the circulatory changes induced by the combination of LEA and dextran administration. The smallest dose resulted in a still further reduction of TPR, but in an increase in Q pa , so that P Aa remained unchanged. The two largest dosages resulted in increases in P A2 as Q pa increased with unchanged TPR. It is postulated that the rise of Qpa was a result of improved niyocardial contractility and increased venous return to the heart. MV O2 as well as MBF increased, but O 2 uc myocardium was unchanged. Plasma expansion alone is considered insufficient to counteract the systemic arterial hypotension caused by LEA, but the additional administration of adrenaline in dosages of around 0.1 μg/kg/min restores systolic arterial blood pressure without any untoward effects upon regional perfusion.
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Ottesen et al. (1978) studied this question.
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