We take care of sick patients. In doing so, we have various tools in our disposal including the physical exam, history, and hemodynamic parameters. We check the blood pressure on our patients and depending on that number, we do things for them (hopefully not to them).
We place the blood pressure cuff on their extremity, hopefully the right size, and cycle it. We have learned about the limitations of the oscillometric devices as I have covered that extensively and we have learned to trust the mean arterial pressure (MAP).
We all learned that the equation for MAP is:
MAP= [(2 x diastolic)+systolic]/3
We also learned that we should target a MAP of 65 based on the surviving sepsis guidelines and I generally agree with this. Sometimes I target a higher MAP, sometimes a lower MAP. Every patient is needs personalized care in my book.
Here's the other equation that we should know but don't.
MAP= (CO x SVR) + CVP
- CO= cardiac output, also HR x SV (and don't forget that the stroke volume is affected by preload, contractility, and afterload)
- SVR= systemic vascular resistance
- CVP= central venous pressure (tends to be zero in a spontaneously breathing patient). This value tends to be ignored for the sake of simplicity.
We all give IV fluids to increase the MAP, because that is what we see on the monitor, but that's the missing the point.
Fluid responsiveness is defined as an increase in stroke volume or cardiac output/cardiac index after being provided with a bolus.
Studies have shown us that only 50% of patients who are septic actually respond to fluid resuscitation. The other 50% who we blast with fluids, well, they just get overloaded and have complications secondary to that.
The point of this post is for us to think a bit more outside the box when we have a patient who is hypotensive. We can't just look at the blood pressure after being given a liter of fluid and call the patient fluid responsive.
The FENICE study looked at 2213 patients and 42.7% of the time, the clinicians gave IVF without looking at any hemodynamic parameters. Even when the patient had a "negative response" to the fluid bolus, 49.4% of the time, the clinician gave an additional bolus after that! I think you can call that insanity per the Einstein definition of it.
The clinicians were looking at primarily an increase of BP followed by urine output, decrease in HR, decrease in lactate rather than changes in CO or SV. Let's just say that we have all been guilty of this in the past but need to get better on the matter.
Here are some examples on where that thinking can lead us astray:
If the MAP is low but their CO or SV is looking great but their SVR is on the floor, they may need earlier vasopressors and nuanced fluid challenges. In the case of cardiogenic shock, you may find that the CO is on the floor and their SVR is in the clouds, those patients may benefit from some careful peripheral vasodilators with some inotropes. That undefined patient who is hypotensive and we give a liter of fluids to indiscriminately is quite dangerous at the end of the day. People come to the hospital to be helped, in those cases, we may actually be causing harm.
If we are going to call ourselves the best, we need to practice that way. Understanding hemodynamics are crucially important to saving lives.
-EJ
Cecconi M, Hofer C, Teboul JL, et al. Fluid challenges in intensive care: the FENICE study: A global inception cohort study [published correction appears in Intensive Care Med. 2015 Sep;41(9):1737-8. multiple investigator names added]. Intensive Care Med. 2015;41(9):1529‐1537. doi:10.1007/s00134-015-3850-x
