In the classic movie "Apocalypse Now" Willard (Martin Sheen) is staring at a number of decapitated heads on sticks on land under the control of the now psychotic Colonel Kurtz (Marlon Brando). An American photo journalist played by Dennis Hopper tries to explain away the murdering by saying "The heads. You're looking at the heads. Sometimes he goes too far. He's the first one to admit it." This is undoubtedly what has happened in Critical Care with fluid resuscitation in septic shock. We were all swept away by the Early Goal Directed Therapy data with early aggressive resuscitation being associated with improved outcomes. Hell, long before the Rivers EGDT trial my mentor, Charles J. Fisher, Jr. M.D. , emphasized the importance of providing adequate resuscitation to improve organ function and decrease vasopressor needs when he said "You can't drive a car on empty tank". We had seen countless patients transferred to the MICU at Cleveland Clinic on 3 vasopressors, ischemic limbs and a CVP of 3. As residents we would stay up all night giving fluid bolus after fluid bolus in hopes that we would have our patients off pressors and making urine by morning rounds. We would pass off the "Michelin Man" appearance of our patients as a matter of cosmesis that would resolve in time.
We were, of course, proven to be dead wrong in our assumptions about the harmless nature of edema and anasarca. We now have a number of studies showing that positive fluid balance during an ICU stay is associated with greater need for renal replacement therapy, a longer duration on mechanical ventilation and a worse outcome. The question has become how do we give enough fluid but not too much. To give you Physiology course flashback nightmares it comes down to how do we get to the sweet spot on the Frank-Starling curve where the stroke volume is maximized with the preload. We want to know if fluid will improve stroke volume and the patient is "fluid responsive".
Studies have now demonstrated that so called "static" variables such as heart rate, systolic blood pressure and CVP are not helpful in determining fluid responsiveness. The use of "dynamic variables" such as stroke volume in response a fluid challenge however has been found to useful. The fluid challenge can be exogenous i.e. 500ml IV crystalloid or endogenous in the form on passive leg raising (PLR) from a semi-recumbent position. PLR is equivalent to a 500-700ml fluid challenge.
In the June 28, 2017 issue of the Journal of Critical Care ( J Crit Care 2017;42:42-46), Steven Simpson and his colleagues at University of Kansas presented data on the value of using stroke volume to guide fluid resuscitation. The method for measuring stroke volume was the non-invasive bioreactance method NICOM (Cheetah Medical). In their paper, the authors compared outcomes in patients who had stroke-volume guided fluid resuscitation compared with usual standard of care in a retrospective cohort study. In the stroke volume group patients were given fluid boluses only when the response to a bolus led to an increase of at least 10% in the stroke volume index (SVI). In the stroke volume group only 50% of patients demonstrated an increase in the SVI by 10%. The use of stroke volume was associated with a smaller positive fluid balance (1.77 vs 5.36L), shorter length of ICU stay (2.89 days) ,shorter duration of time on vasopressors (32.8 hours) and lower requirements for mechanical ventilation and hemodialysis (6.25% vs 19.5%).
To sum up, we can no longer flood the patient with septic shock and expect everything to be fine once the waters recede. Stroke volume guided resuscitation appears to be a valuable approach.
Please note I receive no compensation and have no equity interest in Cheetah Medical (the maker of the NICOM device).
We were, of course, proven to be dead wrong in our assumptions about the harmless nature of edema and anasarca. We now have a number of studies showing that positive fluid balance during an ICU stay is associated with greater need for renal replacement therapy, a longer duration on mechanical ventilation and a worse outcome. The question has become how do we give enough fluid but not too much. To give you Physiology course flashback nightmares it comes down to how do we get to the sweet spot on the Frank-Starling curve where the stroke volume is maximized with the preload. We want to know if fluid will improve stroke volume and the patient is "fluid responsive".
Studies have now demonstrated that so called "static" variables such as heart rate, systolic blood pressure and CVP are not helpful in determining fluid responsiveness. The use of "dynamic variables" such as stroke volume in response a fluid challenge however has been found to useful. The fluid challenge can be exogenous i.e. 500ml IV crystalloid or endogenous in the form on passive leg raising (PLR) from a semi-recumbent position. PLR is equivalent to a 500-700ml fluid challenge.
In the June 28, 2017 issue of the Journal of Critical Care ( J Crit Care 2017;42:42-46), Steven Simpson and his colleagues at University of Kansas presented data on the value of using stroke volume to guide fluid resuscitation. The method for measuring stroke volume was the non-invasive bioreactance method NICOM (Cheetah Medical). In their paper, the authors compared outcomes in patients who had stroke-volume guided fluid resuscitation compared with usual standard of care in a retrospective cohort study. In the stroke volume group patients were given fluid boluses only when the response to a bolus led to an increase of at least 10% in the stroke volume index (SVI). In the stroke volume group only 50% of patients demonstrated an increase in the SVI by 10%. The use of stroke volume was associated with a smaller positive fluid balance (1.77 vs 5.36L), shorter length of ICU stay (2.89 days) ,shorter duration of time on vasopressors (32.8 hours) and lower requirements for mechanical ventilation and hemodialysis (6.25% vs 19.5%).
To sum up, we can no longer flood the patient with septic shock and expect everything to be fine once the waters recede. Stroke volume guided resuscitation appears to be a valuable approach.
Please note I receive no compensation and have no equity interest in Cheetah Medical (the maker of the NICOM device).
Comments
Post a Comment