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!

Collar-Only Spine Immobilization?

It's been a while since the last post; if you've been ardently checking the site every day hoping for a new post (yeah, right!), I'm sorry!  The start of the semester and all the work that goes along with that, working the truck, a new four-legged fur baby (his name is Able, and he's a sweetie) all have conspired against me.  That, and I was wondering if there was anything new to say in the world of spine immobilization practices...by now, more and more people seem to be getting hip to the idea that strapping everyone to a long spine board and strangling them with a cervical collar may not be good medicine.  The National Association of EMS Physicians joined the American College of Surgeons' Committee on Trauma to publish a position paper on spine immobilization:

http://www.naemsp.org/Documents/Position%20Papers/POSITION%20EMS%20Spinal%20Precautions%20and%20the%20Use%20of%20the%20Long%20Backboard.pdf

I think this is a great step forward, but I have two main issues with it:

1)  There are no citations or evidence to support their recommendations.  I'm sure they did some research to form their conclusions, but I always like to see the strengths and weaknesses of the evidence behind them.

(Source:  one of my friend's Facebook page and www.roguemedic.com)

Around the same time period, the Wilderness Medical Society published their practice guidelines for spine immobilization in austere environments.  Even if you don't work in wilderness-y type places, it's a great review of the available literature (much of it from non-wilderness types of places) and recommendations that include levels of evidence.  If you're looking for recommendations with supporting evidence, it's a great reference:

http://wildernessmedicinemagazine.com/1041/articles/1041/Spine.pdf

2)  The NAEMSP/ACS-COT paper recommends that spine immobilization can be achieved with a rigid cervical collar and securing tightly to the EMS stretcher.

That statement worries me; I worry that, in our haste to abandon routine use of a backboard, our profession will jump in bed with a similarly unproven, possibly harmful piece of equipment!

Let's compare.....backboards;

• have not been shown to improve patient outcomes
• can impede respiratory effort
• can compromise the airway (lying supine + vomit = badness)
• can cause pressure ulcers

(All this has been discussed in many, many articles and online postings with references attached, so I won't bore you by repeating them here.  The evidence is there, and pretty easy to find with a good PubMed or Google search, depending on your preference.)

Cervical collars;

• have not been shown to improve patient outcomes
• may not actually restrict range of motion adequately (http://www.jem-journal.com/article/S0736-4679(11)00171-5/abstract)
• can compromise the airway by limiting mouth opening

(There is also a lot of literature about pressure ulcers developing from cervical collar use, but they seem to occur with prolonged application, i.e. days in an ICU, rather than the short frontcountry EMS transport times)

The literature I found demonstrated that spine immobilization as a whole impedes respiratory effort, but the studies didn't study cervical collars alone vs. collars with other devices (although they did test long boards vs. KEDs and found similar results).  So it's difficult to say whether or not a collar affects respiratory function like an LSB/KED does.

And of course, many are probably familiar with the small study published in Journal of Trauma back in 2010 that indicated that a cervical collar separates the cervical vertebrae, potentially making injuries worse.  In case you're not, however...http://www.ncbi.nlm.nih.gov/pubmed/20093981

What to make of all this?

Well, on the face of it, it seems that cervical collars, like long spine boards, have unproven benefit and pretty substantial risks.  We already have validated criteria for determining who might benefit (MIGHT being the operative word) from spine immobilization; why complicate the issue further?  Years of routine spine immobilization have ingrained half-hearted attempts (be honest....as important as padding the void spaces is, how often do you really do it?).  Now we're supposed to make choices between one unproven device and another?

Enough.

Spine immobilization, when it's indicated, should not be a half-assed procedure.  You either do it right (with a vacuum mattress, collar optional and probably not needed), or you don't.  The criteria to help you decide whether or not to perform it are valid.  Aside from a short-term way to save precious hands from manually holding the spine during something like rapid extrication, I don't think cervical collars have any place in EMS.  Unless, of course, you're a provider who likes to say "I want to play a game":

 

(Source:  images3.wikia.nocookie.net)

Stroke of Frustration, Part 2

In Part 1 of this post, I looked at the research surrounding the Cincinnati Prehospital Stroke Scale (CPSS), and found that 1) I wasn't particularly thrilled with the design of the tool 2) ditto the methodology of the derivation and validation studies, and 3) further studies demonstrated a wide range of sensitivity and specificity.  Specificity is the big property for what I need; at the service I work for, we routinely fly stroke patients to our local stroke center.  So I set out to find other stroke screening tools that have been published to see if there was something better.  Here's what I found;

1)  The Los Angeles Prehospital Stroke Screen (LAPSS).  In 2000, the developers of the LAPSS published a study in Stroke validating their screening tool.  Compared with the CPSS, the LAPSS includes history findings such as age, history of seizures/epilepsy, symptom duration, and ambulatory status.  It excludes speech testing from the physical exam.  Their study analyzed 206 patients who had an LAPSS form completed; 36 had a "target stroke".  They found a sensitivity 91%, specificity 97%, PPV 86% and NPV 98%.  Great numbers...but the original studies for the CPSS had similar numbers.  I wanted some additional reporting.

2)  The Miami Emergency Neurological Deficit (MEND) exam.  This exam was developed as part of the Advanced Stroke Life Support course; I've not taken the course, so I'm unfamiliar with the methodology and application of this exam.  It looks like it adds components of the NIHSS to the CPSS to expand the exam and provide some common ground with hospital-based clinicians.  I did find a poster presentation of a study that looked at 51 airlifted patients who had a MEND exam performed in the field; they found that the MEND exam correlated with the NIHSS scale performed at the hospital 90.2% of the time.  The participants of the study used the MEND exam, coupled with online medical consultation with a neurologist, to determine air transport.  Of the 51 airlifted patients, 78.4% were diagnosed with CVA.  The poster concluded that "The MEND exam is a valuable tool when assessing stroke patients in the field and determining the need for air transport".  Again, I've not been trained on the MEND exam (although now I'm looking for a nearby ASLS course!), but I'm not sure I agree; in the study, online consultation with a neurologist seemed to be the mechanism for "pulling the trigger" on air transport.  The MEND seems to be a great way to provide important information to hospital clinicians, but I can't find any research that spells out WHEN to call for air transport.
3)  The Melbourne Ambulance Stroke Screen (MASS).  Meanwhile, across the pond....some enterprising Aussie clinicians decided to combine the components of the CPSS and LAPSS and see if that improved diagnostic properties.  They studied 100 patients who had a MASS completed, and compared the MASS to the CPSS and LAPSS.  They found sensitivities of 90% vs. 95% vs. 78%, specificities of 74% vs. 56% vs. 85%, PPV of 90% vs. 85% vs. 93%, and NPV of 74% vs. 79% vs. 59%, all respectively.  (Note that in this study, the LAPSS didn't work as well as the original validation study, but still pretty respectable).

In the end...I decided that the MASS was probably the best screening tool for my use.  My next choice would be the LAPSS.  But, I think it's important to remember the classic saying "When you've seen 1 EMS system.....you've seen 1 EMS system".  We all have different needs for screening tools, diagnostics, and therapies.  Rather than blindly accept what you were taught, look around for the best tools to stock your toolbox.

A Stroke of Frustration (Part One)

Working on the ambulance a couple of days ago, I had my first scene flight in quite a while.  A 27 year old male reported classic stroke-like signs and symptoms (slurred speech, facial droop, unilateral weakness).  It was a bit of a confusing case because the patient was so young (but had several CVA risk factors) and not hypertensive.  However, my partner and I were able to rule out all those common CVA mimics like hypoglycemia, Todd's paralysis, drug intoxication, etc.  So we flew him (less than an hour from symptom onset, great times!).

And the patient was discharged from the ED later that day.

It was an uncommon enough case that I presented it to the paramedic class, and we all got into a great discussion about their experiences with CVA mimics, the Cincinnati Prehospital Stroke Scale, and so forth.  As a spinoff of that, I started digging into the research surrounding prehospital stroke scales and screens.  This post, I'll examine the research behind the most-commonly used scale (I think), the Cincinnati Prehospital Stroke Scale (CPSS).

Origin of the CPSS

The CPSS was first published in 1997, in Academic Emergency Medicine.  Here's a link to the free full-text PDF:

http://onlinelibrary.wiley.com/doi/10.1111/j.1553-2712.1997.tb03665.x/pdf

There are some issues I have with the methodology of the study, and the patient population.  The abstract says a "prospective, observational, cohort study" was performed.  When you read the methods section, however, both the "stroke" and "non-stroke" groups were pulled from a previously published study done on thrombolytic therapy.  What criteria did the authors use to include patients in the thrombolytic study?  Did that somehow bias the patient selection for this study?  I don't know.

Looking at the demographics of the two groups, there are a couple of anomalies.  The "non-stroke" group is almost exactly 3 times the "stroke" group.  Curiously, the "non-stroke" group was almost twice as old as well (the authors didn't report a range or standard deviation, so I'm not sure how wide the ages of the two groups were).  That's opposite of what I would expect, considering the epidemiology and risk factors for CVA.

Nonetheless, the authors pushed ahead and found, through statistical analysis, that presence of facial palsy, difference in arm strength, and dysarthria when assessed together in this small group of stroke patients, was 100% sensitive and 92% specific for predicting the presence of stroke.  They decided that dysarthria was going to be difficult to distinguish from aphasia, so they changed their model to "abnormal speech", reran the numbers, and decided that the modified test had 100% sensitivity and 88% specificity.

Heady claims.

My take on the article:  This was a small group of patients (299 total, only 74 of which were diagnosed with stroke).  The inclusion criteria may have been biased by grabbing patient data from a thrombolytic therapy trial (which presumably had some pretty tight inclusion criteria because of the inherent risks of tPA and the like).  Overall, I'm not really comfortable with how the CPSS was created.

Validation Studies

Of course, like any good clinical prediction rule, after being created, the CPSS needed to be validated.  So three of the original authors grabbed two other MDs and published a study entitled "Cincinnati Prehospital Stroke Scale:  Reproducibility and Validity".  Here's a link to the PubMed citation; unfortunately, the article isn't available free full-text:

http://www.ncbi.nlm.nih.gov/pubmed/10092713

Since the article isn't available full-text, let me summarize.  The authors took a total of 2 MDs and 24 EMTs and paramedics, and had them score patients identified as "stroke" or "non-stroke".  The patients were drawn as a convenience sample from the ED, and from patients on the neurology ward (with CVA, TIA, and several other neuro conditions).  The convenience sample in the ED?  The authors wrote "An attempt was made to identify patients with chief complaints that were suggestive of stroke or of other diseases that could be mistaken for stroke".  The numbers, again, were a little disproportionate; 49 in the "stroke" group and 122 in the "non-stroke" group.  Interestingly, the mean age between the two groups was flip-flopped from the original study; 55.8 in the non-stroke group and 62.5 in the stroke group.  (That sounds a little more like what I'd expect).  For the analysis of sensitivity and specificity, the authors eliminated 11 patients with a diagnosis of TIA, further lowering the "stroke" group to 38 (vs. 122 non-stroke patients).  For results, the authors stated that a single abnormality on the CPSS had a sensitivity and specificity of 66% and 87% for physicians and 59% and 89% for prehospital providers, respectively.  3 abnormalities has values of 11% and 99% for docs and 13% and 98% for medics (also respectively).  Their conclusion from the abstract: "The CPSS has excellent reproducibility among prehospital personnel and physicians.  It has good validity in identifying patients with stroke who are candidates for thrombolytic therapy, especially those with anterior circulation stroke."

My take on the article:  Reproducibility, sure.  Validation I'm not so sure of.  The patient group sizes were pretty similarly unequal.  The study doesn't identify any specific inclusion criteria for the ED patients; whoever the doc thought the test might work on in the ED at that particular time made the cut.  I think that the age differences between the patient groups were a little more realistic.  However, the study was conducted in the hospital, not in the environment that EMTs and paramedics would be using the CPSS.  And the sensitivity values for this study were far different from the original published sensitivity from the chi-square calculator; 66% and 59% instead of 100%.  (Additionally, the range in sensitivity for the MD group for 1CPSS abnormal finding was 49-80% to reach a 95% confidence interval.  That seems like a pretty broad range!)

And thus, the CPSS became "validated" and approved for prime-time use.  There were a few other studies I found in my PubMed/CINAHL search that gave me some data on the CPSS; these were studies published to test a different stroke screening device.  I'll point out the other tests in the "Part 2" of this topic, but here's a quick table summarizing the predictive values of the CPSS in those studies:

 

Study	# Patients	CPSS Sensitivity	CPSS Specificity
Kothari R, et al (1997) (original study)	299	100%	88%
Kothari R, et al (1999) (validation study mentioned above)	160 (those that made the analysis)	66% (best of two groups)	89% (best of two groups)
Bray J, et al (2005)	100	95%	56%
Mingfeng H, et al (2012)	540	88.77%	68.79%
Studnek JR, et al (2013)	416	79%	23.9%
Frendl, et al (2009)	154	74%	41%

One caveat; some studies reported sensitivity and specificity values for 1, 2, or 3 items on the CPSS being abnormal.  On the chart above, I listed the values for 1 criteria abnormality.  Actually, let's look at the two studies that did examine multiple-variation sensitivities and specificities:

Study	CPSS-1 Sensitivity	CPSS-1 Specificity	CPSS-2 Sensitivity	CPSS-2 Specificity	CPSS-3 Sensitivity	CPSS-3 Specificity
Kothari, et al (1999)	59%	88%	27%	96%	13%	98%
Frendl, et al (2009)	74%	41%	37%	64%	21%	73%

As you can see, the specificities from a study performed in the field (Frendl) don't even come close to those reported in the ED-based study (Kothari).  I think that's important because we're using these scales/screens to identify patients who might benefit from thrombolytic therapy and get them preferentially to a hospital capable of doing that.  That's a common goal; however, depending on the service you work for, it takes different logistical forms.  At the EMS job I used to have, this entailed driving the patient about 15 minutes further.  At the EMS job I currently have, it entails bringing in a helicopter.  The greater the risk to the patient, the more sure I want to be that the juice is worth the squeeze; for my old job, high sensitivity and lots of false positives are acceptable in the face of the risk.  At my current one, false positives are risky for everyone; I want something with great specificity.

So what does all this data mean?  In my opinion (and this is just that, an opinion.  Read the articles yourself and draw your own conclusions.  And bear in mind I have very little formal training in statistics or research methodology; so if I'm drawing incorrect conclusions, let me know!)....

I think the original patient group that the CPSS was derived from is a little "hinky".  I don't think it was validated as conclusively as the original authors claimed.  Other studies with more subjects have shown a wide variety of specificity values from 23-68%.  I question whether or not the CPSS has actually been "validated" at all.  And I'm looking for an alternative that offers greater specificity, more consistently based on the risks to my patients.

In part 2, I'll post some info about alternative prehospital stroke scales/screens and discuss the strengths and weaknesses of those.

Father's Day and Vasopressors

First of all, Happy Father's Day to all the dads out there!  Especially to my father, who taught by example what it means to be a man, and who's been nothing but supportive about my career choices and directions.  But enough of that stuff....I'll be calling him this evening :)

In the last post I shared some interesting research I found about using inotropes and vasopressors to treat shock; from that study (incidentally probably some of the best in terms of methodology and sample size), it seems that norepinephrine (a vasopressor) works AT LEAST as well as dopamine (inotrope) in most kinds of shock, and shockingly (ooh, that was a bad pun!) works better in cardiogenic shock.

How can this be?

I found, while messing around online, a great video from the SMACC (Social Media and Critical Care) 2013 conference.  In it, John Myburgh takes a look at the published evidence surrounding various adrenergic agents.  He spent a good deal of time talking about the fact that epinephrine and norepinephrine (or adrenaline and noradrenaline) are molecules inherent to the body, as opposed to things like dobutamine and milrinone.  But I still couldn't wrap my head around why a drug like epi nor norepi, which increases vascular resistance, is less damaging to patients with cardiovascular problems.  And then the lightbulb went off.

(Incidentally, I posted a link to the SMACC video on the Socratic Medic Facebook page.  You have "Like"d it, right?????)

My feeling is that a lot of clinicians, like me, equate "vascular resistance" with arterial vasomotor tone.  That's where the impossibility seems to lie; the heart has to work against greater pressures, which can't be good for the sick heart!  However, "vascular resistance" means much more than arterial tone; it means venous tone as well.  And there lies the answer!

(unfortunately, I can't remember from which website I got this picture.  No copyright infringement is intended!)

There are a couple of things that need to be pointed out:
1)  Perfusion (pressurized flow) depends on two things; pressure and volume.  Different types of blood vessels optimize those two factors.  Arteries, due to their thick walls, have much more to do with pressure than do veins.  As the circled area shows, almost three-quarters of your blood volume is located in the veins at any one time!
2)  The thick walls of the arteries resist dilation much better than the veins do.  Veins have such a tendency to dilate at normal physiology, in fact, that the legs of the muscles act as a "venous pump" to help ensure return of blood to the heart.

All very interesting, but why does a vasopressor improve cardiac output when it really shouldn't, based on increased vascular resistance and an ineffective pump?

Keep in mind, veins get innervated by sympathetic nerves too.  Increasing sympathetic stimulation will cause the veins to constrict, in addition to the arteries.  So what happens when veins constrict?  Pressure increases; the vein walls are more resistant to dilation, and one-way valves in the veins keep blood from backflowing.  So the blood can't go backwards, can't go sideways; it must go forward.

And preload increases.  Since preload increases, stroke volume increases, and the Frank-Starling law behaves as it always does.

CO = SV x HR

What about dopamine?

Dopamine is an inotrope; it increases activity at beta-1 receptors in the heart.  The result is that heart rate and contractility both increase.  But where's the fluid for the heart to pump?  The heart is a positive pressure pump; it can't suck blood in to the ventricles.  Increasing the heart rate and pumping strength without increasing the delivery of blood to the heart (through the veins) isn't a good solution.  It makes sense, then, that adding dopamine (or other inotropes) to increase pumping ability without first assuring adequate preload (with fluid boluses and/or vasopressors) doesn't improve outcomes.  And it also might give insight into why dopamine has so many adverse events like arrhythmias; increase the myocardial oxygen demand without increasing the oxygen supply, and what do you get???

Vasopressors do not just affect the arteries; they affect the veins as well.  Inotropes affect the heart.  If you increase the heart's pumping effectiveness, you'd better also have given it more blood to pump; venous vasoconstriction offers that.  Misuse the drugs on your ambulance at your patient's peril.