A study in Intensive Care Med reminds me of how arterial blood pressure is a crappy substitute for proper invasive monitoring or echo when treating hypovolemic sepsis patients.
One of our most common interventions when treating sepsis patients is giving fluid challenges. We give 250-500 ml fluid and see if it increases cardiac output. If cardiac output increases by 10-15% we say the patient was hypovolemic, is a fluid responder and assume the improved cardiac output is a result of our bolus pushing the patient´s heart to a better place on the Frank-Starling curve.
Without invasive monitoring or echo we are often tempted to make that call based on changes in the patient´s blood pressure. After all flow is a function of pressure differences and resistance. To what extent does increased arterial blood pressure after a fluid bolus really reflect improved cardiac output? If a patients MAP increases after a fluid bolus, what is the likelihood of that really reflecting an improved cardiac output?
Observational study that included sepsis patients who had received a fluid challenge during their ICU stay. Hemodynamic variables like arterial pressure, heart rate, cardiac index, CVP was recorded at baseline and at the end of the fluid challenge.
51 patients were included.
The important stuff is in the graph where changes in MAP is plotted against change in cardiac output. (CI, cardiac index)
A responder is defined as a patient whose CI increased by more than 10% after a fluid challenge was given. Non-responders had no significant increase in cardiac index.
When giving fluid boluses, increases in blood pressure does not reliably track increases in cardiac output in sepsis patients.
Study lives here:
Can changes in arterial pressure be used to detect changes in cardiac index during fluid challenge in patients with septic shock?
Pierrakoa C, Velissaris D, Scolletta S, Heenen S, De Backer D, Vincent JL.
Intensive Care Med. 2012 Mar;38(3):422-8. doi: 10.1007/s00134-011-2457-0. Epub 2012 Jan 26.