Predicting Hypotension Related to Spinal Anesthesia

Overview

This study aims to identify women at risk of low blood pressure (hypotension) after the usual cesarean anesthetic - a spinal anesthetic. Hypotension may be caused by dehydration. We believe we can predict who will get hypotension by using two anesthesia monitors together with a passive leg raise (PLR) (legs elevated after a period spent reclining). The PLR will cause a shift of blood from the legs to the heart, and the monitors will detect the heart's response to tell if a subject is dehydrated. We want to see if these dehydration tests can also predict hypotension after a spinal anesthetic.

We aim to predict the development of spinal anesthesia related hypotension in subjects already receiving a prophylactic infusion of phenylephrine (PE) who are having a cesarean delivery (CD). Hypotension arising in this fashion may signify that a subject is actually relatively fluid-deplete, and might benefit from intravenous (IV) fluid replacement. We will observe the association between hypotension and results of pre-anesthesia tests with two non-invasive monitors used in conjunction with a dynamic cardiovascular fluid challenge (by using a passive leg raise (PLR) maneuver). The use of any therapeutic intervention such as a fluid infusion would be the object of a subsequent study. We propose that a minority of parturients present for elective CD being relatively fluid deplete. It is our hypothesis that the characteristics of passive leg raise (PLR) induced changes in the plethysmography variability index (PVI generated by the Masimo Radical 7™) and cardiac output (CO as derived from the Non Invasive Cardiac Output Monitor (NICOM) produced by Cheetah Medical™) will identify these subjects and that without large volume fluid administration they are likely to develop hypotension despite the use of a prophylactic PE infusion Justification: Hypotension is the most common cause of spinal anesthesia related morbidity in cesarean delivery. Hypotension is very common and without treatment can affect over 80% of women. The mechanism is usually twofold: Firstly preload to the right ventricle (RV) is reduced as a result of venodilation from spinal sympathetic blockade. Unfortunately attempting to improve preload by infusion of IV fluid alone doesn't make much difference to the rates of hypotension (only 16% reduction in one large study). The second mechanism results from afterload reduction through arterial vasodilation which directly causes a reduction in blood pressure (BP). The treatment for this is most commonly a PE infusion, and when used this makes a significant difference reducing rates by over 50%. Unfortunately again there are a few who don't seem to respond (the residual of hypotension remains about 30%). Increasing the doses of PE only increases the rate of side effects, without affecting hypotension rates. However, giving both fluid and a PE infusion does seem to prevent hypotension in almost all subjects, suggesting that those who were resistant to PE alone actually did need some fluid. These subjects however are the exception not the rule, and giving fluid to these relatively "fluid deplete" as well as the rest may result in an increase in fluid related side effects. We believe that fluid therapy could be tailored better if we could identify which subjects are actually fluid deplete in the first instance. Testing to predict fluid responsiveness has been studied in the intensive care unit (ICU) but not in obstetric subjects. Using a PLR increases the return of blood to the right ventricle (RV). In a fluid deplete individual this significantly improves venous return such that CO changes dramatically. In a well hydrated individual venous return is already adequate so the change in CO is less. The NICOM will directly detect the CO change induced by a PLR. The Masimo detects variations in the pulse oximetry plethysmograph trace that result from subtle variations in the cardiac output caused by changes in the intrathoracic pressure from breathing. Intrathoracic pressure increases during expiration in a spontaneously breathing subject and causes a reduction in venous return to the RV which causes a subsequent fall in CO. The variation in the plethysmography signal with respiration is displayed as a percentage index of the baseline signal strength which correlates with how much venous return to the RV is affected by respiration. If a subject's preload is low the plethysmography variability index (PVI) will be high from the dramatic fluctuation in CO with changes in intrathoracic pressure. Unfortunately with spontaneously breathing subjects this value is not consistent enough between individuals for PVI itself to give an accurate indication of fluid volume state. However changes induced in the PVI within an individual subject from a challenge such as fluid infusion or a PLR appear to be better at indicating fluid responsiveness. We plan to use both the NICOM and the Masimo in conjunction with a PLR to assess fluid state (deplete or otherwise) preoperatively. We will then observe whether or not the pre-anesthesia testing correlates with development of PE infusion resistant hypotension during the routine spinal anesthetic. The primary objective of this study is to correlate the results of pre-anesthesia testing with actual development of PE infusion resistant hypotension. Secondary outcomes are discussed in statistical analysis below.

Conditions

Eligibility

Locations (1)

Outcomes