Cardiac output

[Brandon O]

We're always taught that the body compensates for shock by -- among other things -- increasing the heart rate. That's why we look for it as a sign.

Some time ago, though, I was pointed towards this site -- http://cardiovascular.cx/video.htm -- which is all about cardiac output and its determinants. The narrator there (Dr. Robert M. Anderson) pretty convincingly argues a number of cardiological points, and one of the big ones is that, as a passively-filling pump, cardiac output is NOT determined by heart rate. Well, to a minimal extent it is; obviously if your HR is 0 then your output is also 0. But past a certain minimum, beating faster is not moving any more blood, because the pump is simply filling less each time; it doesn't "suck" and can only pump out whatever flows into it between contractions, so pumping faster is just trading volume for rate with the same overall result.

On some level this makes a great deal of sense, and we do hear a lot about venous return being determined more by vessel compliance and other factors than by how fast the little sucker beats. On the other hand, it seems impossible not to think of the cardiovascular system as an essentially closed system, in which case you have to ask -- doesn't each "output" into the circulation (from the heart) have a corresponding "input", i.e. filling for the next beat? Sure, it's a compliant system, so there will be some fudge and some lag, but it's still a basically closed loop, so if I push blood faster I'd expect to get it back faster as well. If not, where's it going?

In short, this is all a little hard to understand. The description from Anderson is very convincing, but it seems to directly contradict much of what we're taught in our EMS training, which emphasizes the role of the heart in directly influencing the flow of blood. So what should I make of this? If I listen to him, I feel like I have to basically ignore the basis of a lot of seemingly-obvious signs, like an accelerated pulse during compensated shock or even after a hard run.

Anyone have some better understanding for a poor EMT? Everyone I've spoken to about this seems to, upon careful examination, basically have no idea what they're talking about and is unable to resolve the conflict.

 

[Lifeguards For Life]

What exactly did you learn that Dr. Anderson is directly contradicting? If your inquiring as to learn by all means ask away, but if you are waiting to test or are still in basic class, and this is confusing you don't fret over it. Basic is a class that teaches you how, if you want to learn more Paramedic is the class that teaches you why.
I'd be interested if you could elaborate a little bit more on what exactly you are confused about?

 

[Brandon O]

I have my cert. This is not for a test.

The question is basically: above some minimum, and other things being equal, does an increase in heart rate yield an increase in cardiac output? Our basic training seems to say yes; Anderson's information seems to say no.

 

[WuLabsWuTecH]

Cardiac Output (in units of Volume per time) = Stroke Volume x Heart Rate

There is a point of diminishing returns. If the heart rate is pumping so fast that volume is not close to the normal capacity, then yes. But until you get to that point, an increase in hear rate ==> increase in cardiac output.

You can almost think of it as a 3D graph with a theortical maximal plane.

 

[Lifeguards For Life]

Well, to a minimal extent it is; obviously if your HR is 0 then your output is also 0. But past a certain minimum, beating faster is not moving any more blood, because the pump is simply filling less each time; it doesn't "suck" and can only pump out whatever flows into it between contractions,.[/QUOTE

Cardiac output is the total volume of blood pumped through the ventricle per minute. You can calculate cardiac output as simply the total product of the heartrate times the stroke volume. Stroke Volume is about 70ml. So it looks like you were right in your above quote. An increased heartrate leads to an inceased cardiac output

 

[Lifeguards For Life]

oh well woolabs? beat me to it

 

[usafmedic45]

The question is basically: above some minimum, and other things being equal, does an increase in heart rate yield an increase in cardiac output?

Yes and no, because once it gets to a certain rate- which will depend on the patient's age, cardiac health and the status of their intravascular fluid volume- one no longer sees a increase in cardiac output and if you exceed that rate you will actually see a drop in cardiac output as the heart begins to not have enough time to fill between beats. I think you might be referring to this well documented fact (this is one reason why really fast organized rhythms can cause hypotension with the other being poor electromechanical coordination) and simply misinterpreting what was said.

Just keep in mind that it's not a linear relationship (1 change in X causes 1 change in Y) sort of issue since there are several factors at play here (more than one gets from the standard HR x SV = CO equation most new EMS providers are taught), especially when you get towards the higher rates where things start to get more complicated.

You can almost think of it as a 3D graph with a theortical maximal plane.

What he said. :lol: You can tell I'm not an engineering student. :lol:

Our basic training seems to say yes; Anderson's information seems to say no.

Actually it sounds like a problem combining what was taught with additional information. From what you said, it doesn't sound like he's saying anything contradictory.

NOTE: I have not checked out the link that you provided. My comments are just an educated guess as quite a few students I've taught over the years tend to have a problem grasping the idea that stroke volume can drop if the rate gets fast enough because of impaired passive filling which will cause the cardiac output (and often, in turn, the blood pressure) to drop despite an elevated heart rate. This is the Cliff Notes version of it, but I don't know how much you really understand about hemodynamics so I don't want to start by talking over your head. If you want more detail, just ask.

 

[Shishkabob]

Easiest way to picture it: V-tach with a pulse.

The heart is beating so fast that the ventricles simply are not able to fill with fluid before their next contraction.

 

[Brandon O]

Yes and no, because once it gets to a certain rate- which will depend on the patient's age, cardiac health and the status of their intravascular fluid volume- one no longer sees a increase in cardiac output and if you exceed that rate you will actually see a drop in cardiac output as the heart begins to not have enough time to fill between beats.

Okay, then it sounds like the point of contention may be just where this "point of diminishing returns" lies. You seem to be indicating -- and this is more in line with what I was taught with regards to tachycardia etc. -- that you have to reach some very high HR (maybe ~200 BPM) before further increases will yield no greater output. Anderson seems to be indicating that this rate is much lower, something closer to 70 BPM or so.

Granting that all of these numbers vary according to system pressure and so forth, this is still a very big difference -- not just numerically, but qualitatively, because if the latter is true, then "most" of the HR variances we see in non-bradycardic patients would seem to have no actual effect on circulation.

I do recommend that you guys check out that video (there's textual material on that site as well but that's more or less just the same thing in greater detail and rigour) as that would add much clarity to this discussion. Plus it's good stuff anyway.

 

[ResTech]

One thing that I would add is a increase in heart rate up to a certain point will increase cardiac output. Just the same as increasing your respiratory rate will improve oxygenation up to a point. The faster you breathe, the more oxygen is being taken in up until the point where your resp rate is so fast that it decreases tidal volume. Same kinda applies with the heart.

The faster the rate, the more blood (output) being delivered until the rate becomes so fast that it limits the filling time of the ventricle and preload is reduced.

However, say for example in hypovolemic shock, not only does the heart rate increase, but peripheral vascular resistance increases as well from catacholamine release which causes a higher pressure and increased preload (ie more blood volume returned for pumping and fills the ventricles with higher blood volume before each contraction). So the body actually ejects more blood not only because of the increased rate, but also because of the increased preload from increased vascular resistance and also from the increased force of contraction... all from the epinephrine and norepinephrine release in addition to the Angiotensin II depending on how long the Shock state persist.

Heart rate, preload, and increased force of contraction all play a part in cardiac output.

An exception would be spinal cord injury that produces neurogenic shock.... basicly the brain loses its communication pathway and the compensatory mechanisms aren't able to be turned on and actually relaxed.. normal or bradycardia would be seen.

Its generally said that hemodynamic compromise begins to occur at rates around 150 in an adult... give or take.

 

[Brandon O]

However, say for example in hypovolemic shock, not only does the heart rate increase, but peripheral vascular resistance increases as well from catacholamine release which causes a higher pressure and increased preload (ie more blood volume returned for pumping and fills the ventricles with higher blood volume before each contraction). So the body actually ejects more blood not only because of the increased rate, but also because of the increased preload from increased vascular resistance and also from the increased force of contraction... all from the epinephrine and norepinephrine release in addition to the Angiotensin II depending on how long the Shock state persist.

Yes, everyone seems to agree on the important role of the peripheral compliance/resistance as far as filling goes.

 

[ResTech]

Just wanted to make mention of that because I didnt see in any of the post where that was mentioned.

 

[usafmedic45]

Easiest way to picture it: V-tach with a pulse.

The heart is beating so fast that the ventricles simply are not able to fill with fluid before their next contraction.

Yes and no....there is some limited evidence (mostly from electrophysiological and echocardiographic studies) that it is both the rate and a failure of the myocytes to respond to the eletrical stimulus at a "local" level that contributes to the hypotension that may be seen in pulsatile VT. Think of it as EMD/PEA on a regional rather than global (entire heart) scale.

that you have to reach some very high HR (maybe ~200 BPM)

Like ResTech said, the "normal" ("normal" meaning based on studies done mostly in young health males and backed up by stress echocardiographic studies) point where the maximal increase from heart rate are seen and anything beyond it causes a decrease in cardiac output is usually cited as somewhere between 150-180.

Anderson seems to be indicating that this rate is much lower, something closer to 70 BPM or so.

I've never seen any credible evidence to that fact, unless there is something else clouding the issue (vasodilation, decrease in cardiac contractile force (negative inotropic change to use the technical term, etc).

I do recommend that you guys check out that video (there's textual material .....plus it's good stuff anyway

I would not go so far as to say that it's "good stuff". There are far better resources on hemodynamics out there. The only thing this seems to be good for is as an example that just because someone has MD after their name does not mean they are not above making broad based statements without sufficient corroborating evidence to back it up.

A lot of what you seem to be seeing as a "positive" finding (meaning it supports this doc's ideas) is simply an illusory correlation. The fact that his contentions are based on his model which seems to contradict findings based upon human experiments would make his statements suspect in my book. Seeing as that video is nearly a decade old and nothing has really come of his stances, it would be another nail in the coffin that somehow this collection of a pump and some tubes has rewritten hemodynamics so far as I am concerned. As the saying goes, "In God we trust, all others bring evidence." His little model is not evidence or rather, is not sufficient evidence.

 

[Brandon O]

I suppose I just meant that it was an easily-comprehensible and well-illustrated presentation of the material. Figuring out what facts to walk away with is the whole point of this thread (and the topic of my uncertainty), after all.

 

[usafmedic45]

I suppose I just meant that it was an easily-comprehensible and well-illustrated presentation of the material. Figuring out what facts to walk away with is the whole point of this thread (and the topic of my uncertainty), after all.

As I said, there are better teaching opportunities out there that don't lead to misconceptions. Once you get a false idea implanted into someone's brain (especially if that person isn't the sharpest tool in the shed) it's really difficult in a lot of cases to correct their misconceptions.

 

[Brandon O]

Once you get a false idea implanted into someone's brain (especially if that person isn't the sharpest tool in the shed) it's really difficult in a lot of cases to correct their misconceptions.

Well, I was dropped on my head as a kid, so you nailed that one. Sometimes I'm not sure how I manage to put on my pants without causing an MCI.

 

[usafmedic45]

Well, I was dropped on my head as a kid, so you nailed that one. Sometimes I'm not sure how I manage to put on my pants without causing an MCI.

LOL, that wasn't directed at you. It was just a general statement from someone who spends a large percentage of his time clearing up misconceptions and disproving outright untruths both on here and otherwise.

 

[Brandon O]

I guess that's fair. The trouble with EMS -- at least at the BLS level -- is that half of our training might be unsubstantiated tradition and the other half is sound medicine but simplified into falsehood for those of us whose heads are filled with oatmeal, so trying to come up with really good info is generally like navigating a hall of mirrors and very frequently requires shooting above our level of training.

But I digress...

 

[Shishkabob]

No, the problem is training vs education.









(God I can't believe I just said that. What's happening to me?! I'm turning into medic417!)

 

[Lifeguards For Life]

I guess that's fair. The trouble with EMS -- at least at the BLS level -- is that half of our training might be unsubstantiated tradition and the other half is sound medicine but simplified into falsehood for those of us whose heads are filled with oatmeal, so trying to come up with really good info is generally like navigating a hall of mirrors and very frequently requires shooting above our level of training.

But I digress...

I agree. In my Basics class i feel we were taught a "cookbook recipe" approach to all scenarios. The anatomy, physiology, and anything that required the bare minimum of thinking was avoided. we were taught a 1-2 step if you do this everytime, you cant go wrong.