Recent years have seen a move away from large-volume intravenous hydration as prophylaxis against post–spinal hypotension. 1,2Although controversy still exists, there is accumulating evidence that crystalloid solutions are particularly ineffective in preventing hypotension after extensive sympathetic blockade associated with spinal anesthesia. One reason crystalloid solutions may not be effective is their short intravascular half-life. In this issue of ANESTHESIOLOGY, Ueyama et al. 3provide data to support the limited and transient effect of 1,500 ml (more than 20 ml/kg) crystalloid on blood volume and cardiac output compared with hydroxyethyl starch 6%(HES). They suggest that to effectively prevent hypotension associated with obstetric spinal anesthesia by intravenous volume administration, augmentation of blood volume must be large enough to result in a significant increase in cardiac output.
The widespread prophylactic use of crystalloid solutions followed work in gravid ewes that showed the value of rapid intravenous fluid administration in partly restoring uterine blood flow after spinal hypotension. 4Blood pressure usually is maintained in the face of vasodilation (other than that caused by central nerve blockade) by a reflexive increase in cardiac output. However, in the presence of spinal induced venodilation, venous return is reduced to an extent that cardiac output cannot increase and is often reduced. 5The result is severe hypotension with reduced uteroplacental perfusion. Therefore, efforts were made to increase cardiac preload before instituting spinal blockade in the hope of preventing subsequent hypotension; the concept of intravenous “preload” was born.
Initial clinical studies of crystalloid prehydration in obstetric spinal anesthesia appeared to be promising, 6,7but the results were clouded by issues such as the presence of labor (which decreases the incidence of hypotension), aortocaval compression, and study design. Although intravenous fluid preload became an established part of anesthetic practice, it soon became apparent that it was not completely effective in preventing hypotension. 8However, it was assumed that, because the theory was sound, more preload was required in some patients. Hence, large volumes (up to 30 ml/kg) were increasingly used or studied. 9,10Nevertheless, the problem remained.
A number of studies have shown either no 1or a clinically insignificant 11reduction in the incidence of spinal hypotension after crystalloid preload, leading some to abandon it altogether and others to remove it from routine mandatory practice. The use of colloid solutions for spinal preloading met with mixed results. Gelatin solutions may be ineffective and have not achieved the degree of success seen with modified starch solutions. 12,13This may be a result of the difference in intravascular half-life between the two, supporting the argument used to explain crystalloid failure. However, does this necessarily relate to the concept of preload?
The indocyanine green dilution method used by Ueyama et al. 3to estimate blood volume and cardiac output does not permit a simultaneous assessment of cardiac preload. Nevertheless, similar modest increases in blood volume produced by 1,500 ml lactated Ringer's and 500 ml HES (8 and 10% respectively) were associated with modest increases in cardiac output (11 and 14%), without a significant reduction in the incidence of subsequent hypotension. Doubling the increase in blood volume (to 19%) by use of 1 l HES more than tripled the associated increase in cardiac output (to 43%). Because heart rate did not change substantially, the change must have been a result of an increase in stroke volume. Because there was no change in arterial pressure associated with volume administration, this implies a decrease in vascular resistance. Increases in cardiac output occur with normovolemic hemodilution. An increase in cardiac output of 29% may be seen after isovolumic reduction of hematocrit to 33%. 14It is likely that hypervolemic hemodilution would produce an even greater increase in cardiac output via a number of possible mechanisms, including increased cardiac preload, decreased blood viscosity, and peripheral vasodilation caused by reduced arterial blood oxygen content. Increased cardiac filling alone might reduce afterload via atrial stretch receptors and atrial natriuretic peptide. Which of these factors is responsible for the reduced incidence of hypotension? Parturients with an increased baseline systemic vascular resistance index or systolic blood pressure have been shown to be at increased risk of subsequent hypotension after regional anesthesia. 15Is it possible that the key to prevention of post–spinal hypotension is a sustained increase in cardiac output and reduction in afterload before central sympathetic blockade, rather than a transient increase in cardiac preload?
Despite its short intravascular half-life, intravenous crystalloid has been shown to significantly increase cardiac filling pressures before spinal anesthesia. 16,17However, this increase is rapidly reversed after the onset of sympathetic blockade. In the absence of data showing a sustained increase in atrial pressure or left ventricular end-diastolic volume during spinal anesthesia without hypotension, the whole concept of fluid preload might be called into question. Rapid administration of crystalloid solutions can cause hemodilution and increase cardiac output, 18but the volumes required to produce the same degree of change seen with 1 l HES would not be practicable, and even then would be relatively transient. The increase, albeit transient, of cardiac preload seen with crystalloid suggests the possible role of other mechanisms in the prevention of hypotension by colloids.
Whatever the mechanisms of hypotension and its prevention, there are some practical issues regarding the use of large volumes of intravenous colloids before spinal anesthesia for cesarean section. Even with the use of 1 l HES, the incidence of hypotension was 17%(upper 95%, confidence limit 48%). Would it be possible to reduce this even further by use of larger volumes, and, if so, by how much more? After delivery of a neonate, there is an autotransfusion of blood from the contracted uterus. Would this constitute a risk of pulmonary edema in the presence of an already expanded blood volume? There is a small risk of allergy to colloidal solutions, and they are expensive. Before the prophylactic use of colloids becomes part of routine practice, the potential problems and cost need to be balanced against the value of improved outcome and the cost and value of other methods of prevention, such as prophylactic administration of vasopressors. It is likely that the use of colloid alone will not eradicate post–spinal hypotension. Even if it could, is this sufficient reason to use it?
Is “prevention better than cure” applicable to spinal hypotension? Although hypotension can be catastrophic and pose a threat to both mother and infant, it is not always severe, is readily treated, and, if short-lived, does not significantly affect neonatal outcome. Studies showing significant differences in the incidence of hypotension may fail to show a significant difference in umbilical blood gas and acid–base status at delivery between infants born of hypotensive and nonhypotensive mothers. 10Even studies that show significant biochemical differences may not show any clinical differences in Apgar or neurobehavioral scores. 19
In summary, the study by Ueyama et al. , 3although confirming the ineffectiveness of crystalloid, does not persuade us to immediately change to prophylactic colloid administration to prevent spinal hypotension associated with cesarean section. However, it does lead us to question the concept of preloading in this situation. As there is no method that is guaranteed to prevent spinal hypotension and improve neonatal outcome, we continue to advocate vigilant monitoring of maternal blood pressure at least every minute after spinal injection, with immediate treatment of hypotension by bolus intravenous ephedrine.
