Categorical data were analyzed using the Fisher exact test. Continuous data systolic and diastolic blood pressure, heart rate, and hemoglobin values were analyzed with the Friedman analysis of variance. Volume kinetic parameter estimates are given as medians and 25th—75th percentiles.
These parameters are the results from nonlinear regression analyses and contain SEs. We considered an increase in plasma volume of ml after epidural anesthesia to be clinically relevant initial plasma volume assumed to be 3, ml, estimated SD of difference To account for variable subject responses, we included 12 subjects in the study. All subjects completed the study and followed the study protocol.
Two subjects received supplemental bupivacaine 25 mg because of insufficient sensory blockade. Median values are shown. Plasma volume did not change 90 min after epidural anesthesia compared with baseline all subjects or when subdivided into normotensive or hypotensive subjects table 1 and fig. Forty minutes after administration of HES, plasma volume was significantly increased by a median of ml, whereas no significant changes in plasma volume were observed after ephedrine administration table 1.
Erythrocyte volume did not change significantly during the study table 1 and fig. Peripheral hematocrit decreased significantly from 0. Body hematocrit did not change during the study table 1.
Mean corpuscular volume data were only available from six subjects and did not change during the study table 1. Final fit, one-volume model. The epidural is placed at 0 min, and infusion is started at 90 min. The experiment ends at min. This study was mainly undertaken to investigate the changes in blood volume after epidural anesthesia per se and to capture the behavior of fluid given intravenously during epidural anesthesia in a situation in which volume loading is controversial.
We found that plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume was increased with fluid administration but was unchanged with vasopressors, whereas both treatments had similar hemodynamic effects.
Hemoglobin concentrations were not significantly altered by either epidural blockade or ephedrine administration but were significantly decreased after HES administration. The observed decrease in systolic and diastolic blood pressure and heart rate after epidural anesthesia corresponds with previous observations in healthy volunteers, 7 and the time frame of these circulatory effects are also well known.
Previous studies during experimental hypovolemia have found a capillary refill to occur within 5 min, 2,8 and short-term studies 20—30 min with and without concomitant fluid administration after lumbar epidural anesthesia with hypotension have also suggested a capillary refill to occur based on hemoglobin measurements.
In several series of patients undergoing lumbar epidural anesthesia, a larger percentage of an infused amount of fluid was retained intravascularly in hypotensive compared with normotensive patients only indirectly measured by decrease in hemoglobin concentration, however. Initially, when a fluid load is given, most of the infused fluid shifts from the circulation to the interstitial compartment, thereby increasing its hydrostatic pressure.
When the arterial pressure decreases after 15—20 min, there is a fluid flux causing intravascular hemodilution. However, significant hemodilution 20 min after the onset of lumbar epidural anesthesia has only been observed when epidural anesthesia was accompanied by fluid administration.
However, when fluid was administered, there was a profound dilution and increased blood volume table 1 , which shows that epidural anesthesia per se had no effect on blood volume. Erythrocyte volume did not change significantly during the study but tended to increase with fluid administration table 1. The reasons for this are unclear because no changes in individual erythrocyte cell volumes occurred measured by MCVs.
However, to be accurate, the indicator dilution techniques required uniform distribution of the tracer. Previous findings have suggested that this is in fact not true during epidural anesthesia because 99 Tc-labeled erythrocytes sequester within the denervated area after epidural anesthesia assessed by gamma camera scan and plethysmography. Blood and plasma volumes are traditionally estimated by indicator dilution and mass balance techniques, 12,13 and in recent years, they have been supplemented by volume kinetic analyses, 14,15 a pharmacokinetic tool used to study more closely the time course of fluid shifts in various settings.
To look more closely at the fluid behavior during infusion, indicator dilution techniques in this study were supplemented by volume kinetic calculations. Hemoglobin analysis showed that when epidural anesthesia was applied, there was a very small dilution fig. When HES was administered, volume kinetic analysis showed a dilution of the plasma volume fig. The volume kinetic data delineate the time course of HES distribution, which cannot be assessed by tracer dilution technique.
Thirdly, a marked bradycardia with a reduction in cardiac output and severe hypotension can occur suddenly in a few subjects at some time after the mother moves to the supine position. This reflex effect is the relatively uncommon supine hypotensive syndrome of pregnancy SHSP. Holmes 8 proposed that compression of the inferior vena cava by the gravid uterus caused hypotension after spinal anaesthesia because venous return was reduced and thus cardiac output decreased.
The theory of caval compression and supine hypotension was based largely on studies by Scott and colleagues, 11 who measured cardiac output by dye dilution in eight patients. Clearly, this study reported a heterogeneous group of patients, and the patients with bradycardia developed the supine hypotensive syndrome, which is a different phenomenon from the hypotension seen in the other patients in that study.
An extensive review of SHSP found a wide range of case selection, clinical features, definitions, and degrees of hypotension. In some patients, hypotension only occurred after 20 min in the supine position. The possible reasons given for hypotension in these patients were either vena caval obstruction or a vagal reflex bradycardia, which is a well-known phenomenon associated with poorly filled heart.
Undoubtedly, the vena cava is affected by the gravid uterus. Femoral venous and distal inferior caval pressures were greater in the supine position. In the lateral position, venous pressure was less, but still not as low as non-pregnant levels. The abdominal vena cava remained partly occluded in the lateral position.
No early studies involved spinal anaesthesia because general anaesthesia and increasingly epidural anaesthesia had, by that time, largely replaced spinals for Caesarean section in the UK. The proponents of the caval compression theory suggested three ways to prevent hypotension after spinal block, but none has withstood careful examination. First, infusion of crystalloid or colloid was proposed to compensate for the venous blood said to be trapped in the legs, but initial reports of success in preventing hypotension 17 were not replicated in subsequent studies.
Secondly, leg compression was attempted but was relatively ineffective, despite the success of the anti-G suit in preventing lower limb pooling and hypotension in aerospace medicine. Although widely used, this procedure is variably applied, 19 and does not prevent hypotension after spinal anaesthesia. Despite this, current books suggest routine use of strategies based on these putative explanations, 4 and current teaching uses these concepts.
The original hypothesis underlying the mechanism of hypotension was that a reduction in central venous pressure would reduce cardiac output, and thus reduce arterial pressure. This concept should be reconsidered. The hypothesis was based on the view that central venous pressure controls cardiac output, as suggested by the experimental studies of Paterson and Starling 20 and Guyton. They were of an isolated heart, supplied with blood from a venous chamber which could be raised or lowered to adjust the atrial pressure.
The supply to the venous reservoir was externally adjusted by the investigator to keep the atrial pressure constant. By raising the reservoir to increase inflow pressure, the stretch of the ventricular muscle was increased, and thus ejection volume increased.
To maintain the atrial pressure, the atrial reservoir had to be replenished more rapidly. In these circumstances, atrial pressure regulated cardiac output. This did not mean that the increased flow from the venous reservoir had increased the cardiac output, only that the flow had to be increased to sustain the reservoir pressure. The entirely separate studies of Guyton in which he related atrial pressure and venous return were equally artificial.
Venous return was controlled using an adjustable pump. The inextricable link between venous return and cardiac output, and the unrealistic question concerning which is the cause and which is the effect, was recognized by Guyton, despite his considering venous pressure to be an independent variable.
Even at the time, this highly artificial experiment was recognized as unlikely to be applicable to the intact animal. The important feature of the venous system is its compliance, not its resistance, and we can relate the central venous pressure to the volume held in the veins. For example, the splanchnic component of this capacitance drains directly into the vena cava via the hepatic vein which is not directly compressed by the uterus.
However, we lack basic information on these aspects of venous dynamics. Comparison of cardiac function and venous return curves. Download the PDF to view the article, as well as its associated figures and tables.
A fall of blood pressure accompanies each spinal anesthesia. It is the one possible danger associated with this form of anesthesia and may cause death. Its low point is usually ten minutes after the injection, and most fatalities have occurred at that time.
After fifteen minutes, one is working away from the danger point, not toward it as in other general anesthetics. Given a reliable method of holding up blood pressure for the first fifteen minutes, and modern spinal anesthesia in trained hands is free of danger. Epinephrin given intravenously is the only reliable drug in desperate cases of blood pressure collapse. Acta Anaesth Scand Acta Anaesth Scand [Suppl] Abstr. Reg Anesth Reiz There are no affiliations available. Personalised recommendations.
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