The Truth About Blood Pressure: Conclusion (for now)....

Since my new semester of classes is due to start in less than 24 hours, I wanted to put up a tentative ending point on this discussion of blood pressure.  With all the talk about Ohm's law, the major role of arterioles in autoregulation, and major changes to flow based on vessel resistance, I feel a little like Thomas Dolby:

(Image source: www.uproxx.com)

To use blood pressure measurements appropriately, we need to both appreciate what it's actually measuring (which we've done) and consider what we use the monitoring tool for.  I would suggest that we use blood pressure monitoring for two main purposes;
1) Detect hypoperfusion
2) Initiate and guide therapies like intravenous fluid and inotropes/vasopressors to correct hypoperfusion

Let's look at how we can use blood pressure appropriately for both these goals.

Detecting Hypoperfusion

Until new technologies like microcirculatory flow monitoring becomes available in the field (are you listening, Zoll and Physio???), we can't actually quantitatively measure perfusion where it matters, the capillary beds.  Making guesses about perfusion based partially on blood pressure is the best we can do.  However, using the traditional measurement of systolic/diastolic blood pressure is a poor way to go about it.  Remember, systolic and diastolic pressures are measured at the extremes of the cardiac cycle; height of contraction and depth of relaxation, respectively.  A more true measure of arterial blood pressure is calculating the mean arterial pressure; most monitors will do this automatically for you at this point, and if not there are simple calculators available online and in app stores for this.  A caveat; the calculation is based on relatively normal heart rates; as heart rate increases the duration of diastole decreases.  I've not yet found a formula or calculator that adjusts for heart rate.

However, keep in mind the major limitation; whether it's systolic/diastolic or MAP, it's still a pressure reading above the site of the action!  Autoregulation via the arterioles can go a long way to maintaining flow, so it's not just about the numbers.  Look for additional signs of hypoperfusion instead of an arbitrary threshold number.

Initiating/Guiding Therapies

Once you've decided made an educated guess that the patient is suffering from hypoperfusion, often times you need to do something about it.  Depending on the clinical situation, we often turn to either fluid therapy or medications such as inotropes or vasopressors.  There's obviously a cutoff point where additional fluids are bad; when I was in paramedic school it was drilled into me to listen to lung sounds before starting a fluid bolus, and periodically to make sure that the patient wasn't fluid-overloaded.  Waiting until you've put your patient into pulmonary edema to switch to something different is ridiculous...we need to be looking for something better.

Unfortunately, looking for changes to systolic blood pressure or MAP isn't particularly sensitive.  Measuring the diameter of the inferior vena cava with portable ultrasonography makes great theoretical sense and is currently being used in some hospitals, but exactly how accurately it predicts the need to switch to vasopressors is still being debated and studied.

One potential way is to measure the pulse pressure over time; remember, pulse pressure is calculated by subtracting the diastolic blood pressure from the systolic blood pressure.  Doing so theoretically represents the amount of blood ejected by the left ventricle, or stroke volume.  Theoretically, then, pulse pressure could be multiplied by the heart rate (and probably some sort of coefficient) to determine cardiac output.  There's an abstract I found that studies just that, and it looks promising.  Think about it...a non-invasive way to quantitatively measure cardiac output!

However, there's more....following that same train of thought, changes in pulse pressure measured over time (pulse pressure variation) can help us determine if the patient will respond to additional IV fluids.  This is a topic for a whole other blogpost, which I intend to do, but the short version is that measuring the pulse pressure can help us figure out where the patient is on the Frank-Starling curve:

(Image source: http://ccforum.com/content/11/3/131)

Some research has been published demonstrating that pulse pressure variation might determine "fluid responders" in various types of critical illness or injury; that is to say, pulse pressure variation might help you decide when the patient's had enough fluid and it's time to try something different.  I've not had a chance to really read anything but the abstracts yet, so I don't think this is ready for use in clinical practice yet, but it's certainly interesting enough that I want to know more about it!

The Bottom Line

Now that we've reached a temporary stopping point about blood pressure, let's recap what I think is appropriate use of blood pressure measurements:

1. Throw away the notion that blood pressure or mean arterial pressure alone identifies hypoperfusion.  Most of my protocols define hypoperfusion as "systolic blood pressure >90mmHg".  It's not about the numbers, it's about the numbers AND the patient.
2. Mean arterial pressure is more representative of arterial pressure than systolic/diastolic measurements of blood pressure.  I'm going to continue to focus on the MAP rather than systolic blood pressure measurements alongside other clinical indicators to detect hypoperfusion.
3. We can potentially use both measurements of blood pressure (MAP and systolic/diastolic) to measure  hemodynamic parameters previously unavailable in our patients; pulse pressure variation may turn out to be a very useful clinical tool in measuring cardiac output, as well as guiding management of hypoperfusion

As always, let me know what you think...do you agree, disagree?  Also as always, don't blindly believe what I say; hit the search engines, read the studies, and come to your own conclusions!

Until next time!