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!

The Truth About Blood Pressure, Part 2: (measuring) Resistance is Futile

In the last post, we saw how blood pressure is not a measure of perfusion, because perfusion is all about flow.  We also saw how resistance within a tissue bed or organ can significantly affect flow:

(image source: www.cvphysiology.com)

So, can we use blood pressure as a measure of vascular resistance to get a sense of the biggest factor that determines blood flow?  At one point, I believed that diastolic blood pressure was a good indicator of "afterload", which I interpreted as systemic vascular resistance.

Let's look at the factors that affect resistance; in a single blood vessel with non-turbulent flow we can use Poiseuille's equation:

(image source: my computer.  I can't remember which website I got this from)

There are three main things that effect resistance (R); length of the blood vessel (L), the viscosity of blood ("n" is the closest I can get to the symbol you see), and the diameter or radius of the vessel (r).  The viscosity of blood stays within such a small range except in extreme cases that it's typically considered to be a constant.  As you can see, vessel radius has a huge impact on resistance; small decreases in resistance can cause dramatic increases in resistance and decreases in flow.

We typically assume that all portions of the arterial vasculature have equal responsibilities of blood distribution and resistance, but that's not the case.  Large arteries play a much larger role in distribution than in resistance; the arterioles have the biggest impact on resistance because of their size (less than 200 micrometers).  Where do we typically measure blood pressure?  A large artery.

Blood pressure isn't a good measurement of vascular resistance.

Now, Poiseuille's equation might lead us to believe that since the radius of a blood vessel is so important at determining resistance, small changes to the size of a large artery (say, the brachial one) during hypotension can significantly decrease distal blood flow to the capillary beds and cause hypoperfusion.  However, there's another factor to consider; arterioles, capillaries and venules exist in parallel networks to bathe the individual cells with opportunities for microcirculation.

(image source: http://yr8science2011.wikispaces.com/Siobhan)

Even this image can't accurately describe the sheer number of tiny blood vessels in the tissue bed of an organ; there are thousands, probably tens of thousands of them.  This is hugely important, because parallel vessels decrease the overall vascular resistance of the tissue bed or organ.  We also have to consider that the total resistance in this vascular bed is the sum of the individual vessel resistances;

Total resistance (Rt)=RA + Ra + Rc + Rv + RV 

(A=artery, a=arteriole, c=capillary, v=venule, V=vein)

The take-home point to this is that decreasing the diameter of a large or small artery will have very minor effects on the total vascular resistance of the tissues in question because it's such a small percentage of blood vessels involved in perfusing that area.  As a matter of fact, a large or small artery has to have it's diameter increased by more than 60-70% before it starts to have a significant effect on tissue perfusion!

The reason our tissues can get away with this goes back to the relationship between resistance and flow; even at low perfusion pressures you can increase flow to the tissues by decreasing resistance in the arterioles (known as "autoregulation").  And it just happens that I have some research to support this :)

http://www.jccjournal.org/article/S0883-9441(12)00060-3/abstract

In this study, researchers measured mean arterial pressure and microcirculatory flow in hemodynamically unstable patients; they found that microcirculatory flow changed significantly despite a relatively unchanged MAP.

Hypotension does not always mean hypoperfusion.

So, at this point we've determined that:

1) Blood pressure doesn't measure perfusion, or even perfusion pressure.

2) Blood pressure doesn't measure vascular resistance.

3) Because of the concepts of total vascular resistance, hypotension in an artery doesn't always equate to hypoperfusion in the tissue bed.

In the next post, we'll wrap it all up by looking at traditional blood pressure measurement versus mean arterial pressure, and figure out how to use blood pressure measurement in the clinical environment.  Stay tuned!

The Truth About Plood Pressure, Part 1: Don't Keep Up the Pressure, Just Go With the Flow!

Happy belated New Year everyone!

My New Year's resolution was to be more consistent about blogging on here; major changes to my classes' curricula last semester kept me chained to the lesson plans and LMS (on the plus side, the semester ended on a good note).  So for my first post of 2014, I wanted to make up for the lack of posts by talking about one of the most misunderstood, poorly-taught concepts in EMS education.

Blood pressure.


Many of us were taught that blood pressure is a marker of perfusion, and in our clinical practice, we use blood pressure measurements to make decisions on whether or not the patient is suffering from hypoperfusion.  That's not necessarily a bad thing, but without a good understanding of how the cardiovascular system works, and the physical laws of bloodflow, we're in danger of misinterpreting blood pressure measurements.  Think of your favorite definition of perfusion; it's probably something similar to "Blood flow through an organ or tissue".  Sounds good, but we're making a crucial error when we equate a measurement of vessel pressure with bloodflow through that vessel.

Pressure does not equal flow.

If we're seeking information about perfusion, we should be looking at blood flow, not blood pressure.  Ohm's law applied to hemodynamics as much as electrical flow:

(image source: www.cvphysiology.com)

(sorry about the background of the picture...I can't seem to get it to show up with a white background)

Don't get me wrong; you need pressure in order to have flow (F).  However, you need a change in pressure from one point to another ("triangle"P).  In the setting of tissue perfusion, that change becomes the pressures of the arterioles (Pa) and venules (Pv) of the vascular bed in question.  If we wanted to measure blood flow quantitatively, we'd need a way to measure arterial pressure, venous pressure, and resistance within the vessel or system of vessels.  Blood pressure only provides us with one-third of that!

You can see that resistance (R) plays a big role in determining flow.  In fact, resistance and flow have an inverse relationship; you can dramatically reduce flow by increasing resistance, and vice versa:

(image source: www.cvphysiology.com)

In the next post, we'll talk more about the role resistance plays in tissue perfusion, and how blood pressure doesn't tell us diddly about that either.  Until next time!