preload

[mjl1717]

What definitions do you guys hear for preload? Can someone explain it "cold" in terms of mathematically, in medical terms, and in laymans terms?

I hear things like venous return which I think is too simple Kaplan says load on the ventricles at end of diastole. Pleasse what increases it and what decreases it? This "preload haunts you in the basic sciences and the clinicals.

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[Vox Animo]

What definitions do you guys hear for preload? Can someone explain it "cold" in terms of mathematically, in medical terms, and in laymans terms?

I hear things like venous return which I think is too simple Kaplan says load on the ventricles at end of diastole. Pleasse what increases it and what decreases it? This "preload haunts you in the basic sciences and the clinicals.

never heard the term before in my life.

 

[Taus]

the lay terms are all you really need to know......pre-load=amount of blood returning to the heart....more blood in ventricle=ventricle must stretch more and subsequently contracts more forcefully (frank/starling law stuff).....any condition causing more blood to return to the heart causes an increase in preload...common example = inspiration (raise negative intrathoracic pressure sort of "sucks" blood back up to the heart)

 

[Ezekiel20]

What definitions do you guys hear for preload? Can someone explain it "cold" in terms of mathematically, in medical terms, and in laymans terms?

I hear things like venous return which I think is too simple Kaplan says load on the ventricles at end of diastole. Pleasse what increases it and what decreases it? This "preload haunts you in the basic sciences and the clinicals.

Pre-load is synonymous with 'end diastolic volume'. Thus if a person has aortic regurgitation, pre-load will be increased.

This increase in pre-load can be compensated (Starling's law of the heart), as increased stretch leads to increased contractility. But above the threshold of compensation, it can damaged the heart muscle.

I'd recommend reading Robbins pathology for a more detailed description.

 

[mjl1717]

anyone else want to chime in , please!! Previous responders thank you!!
What increases preload and what decreases it?? Anyone else want to chime in, please!!!!

 

[Shodddy18]

anyone else want to chime in , please!! Previous responders thank you!!
What increases preload and what decreases it?? Anyone else want to chime in, please!!!!

increased intravascular volume... like in chf, laying down... this is why chf'ers have orthopnea (shorness of breath when laying down... why they sleep w/ 3-4 pillows and almost sitting up). Breathing... hence the splitting of s2 on inspiration. Pulmonic and Aortic Regurge. Dilated cardiomyopathy.

 

[surgical06]

pre-load. think of it in relation to the amount of water that is in a balloon (heart) while you fill it for a water fight. remember in the old days you attach the balloon to the sink and let it fill. well the sink in medical terms would be your superior and inferior vena cava. as long as you hold the balloon to the sink spout, the preload increases. as the preload increases the balloon (heart) stretches and this makes your end diastolic volume. the heart can only stretch so far, remember your actin and myosin cross links.

when does pre load decrease. it decreases when you have severe bleeding, drug that dilates veins such as nitroprusside,. both of which can decrease volume thus limiting central venous return (the amount of water running from the sink to your balloon

pre load increases. generally in a volume overload state. in severe cases, thats when you will see a JVD. or if you give a drug that increases CVP. most drugs do this by vasoconstricting peripherally therefore increasing the amount of blood circulating centrally.

 

[surgical06]

i forgot to add,
preload increases when there is a demand for increased cardiac output.

central venous return is very important. in patients with heart failure, the Central venous pressure (SVC/IVC volume of blood) will be high because the heart is failing and the preload this patient has is huge however, the heart is no longer operation under starling principles and is supplying an inadequate cardiac output.

if your CVP is low, this can be due to cardiac arrest , but is generally a sign of hypovolumia or severe shock. remember the CVP is the amount of blood in the SVC/IVC returning to the right atrium is low. thus the preload the heart gets from the two veins is low.


you have to know these dynamics cold, many patients you see, especially criticall will have volume issues.

surgical06 MSIV

pre-load. think of it in relation to the amount of water that is in a balloon (heart) while you fill it for a water fight. remember in the old days you attach the balloon to the sink and let it fill. well the sink in medical terms would be your superior and inferior vena cava. as long as you hold the balloon to the sink spout, the preload increases. as the preload increases the balloon (heart) stretches and this makes your end diastolic volume. the heart can only stretch so far, remember your actin and myosin cross links.

when does pre load decrease. it decreases when you have severe bleeding, drug that dilates veins such as nitroprusside,. both of which can decrease volume thus limiting central venous return (the amount of water running from the sink to your balloon

pre load increases. generally in a volume overload state. in severe cases, thats when you will see a JVD. or if you give a drug that increases CVP. most drugs do this by vasoconstricting peripherally therefore increasing the amount of blood circulating centrally.

 

[PoorMD]

preload is the volume of blood in the heart the instant before contraction (systole) begins. Hence others have used the term end-diastolic volume

 

[8744]

Preload: The majority of a pornographic movie.

 

[Shodddy18]

Preload: The majority of a pornographic movie.

 

[RaaMD]

end diastolic volume

 

[Blade28]

So I take it there isn't much afterload in these films then.

Wow that's a long time to prepare that comeback line! 🙂

 

[kouhiiko]

Our Card. block lect. (and Costanzo's Physiology) summed it up like this:

Preload is the stretch on the muscle just prior to contraction.
It is measured in terms of end-diastolic volume of the ventricles or end diastolic pressure.

The reason stretch matters is because it increases the overlap of actin and mysosin filaments in the muscle (increasing the number of possible sites for cross bridge formation). It increases the peak tension generated during systole. Increasing preload increases the performance of the heart.

Things that affect preload are blood volume (more blood/greater venous return stretches the heart muscle more, which increases preload) venous pressure, venous tone, and ventricular compliance.

Hope this helps.

 

[osli]

I'll have to throw in my 2c here...

Technically: preload is the stretch or tension on muscle fibers just before contraction is initiated.

That's it. That is all you really need to know for the "technical" definition, and as far as I'm concerned this suits just fine for the "layman's" definition as well.

Now, you'll most often hear preload spoken of in terms of end diastolic volume. But you need to realize that preload is the stretch of the muscle, not necessarily the size of the chamber. Why is that difference important? What about a dilated ventricle? It might have a significantly increased end diastolic volume vs. the norm, without having any appreciable increase in muscle fiber tension.

You'll often also hear it spoken of in terms of end diastolic pressure. This might be a closer approximation in most cases, but again you need to remember that the exact definition of preload relates to muscle fiber tension, not ventricular pressure. Why is this difference important? What about a hypertrophied ventricle? It might harbor a significantly increased pressure inside, but that pressure is contained by a thicker cross section of muscle tissue, and thus may also have no appreciable increase in preload tension.

But in practical terms, if you think of an individual's heart and compare its "norm" to an "increased preload" state, then both end diastolic pressure and volume are increased relative to its "norm." This is for a hypertrophied or dilated (or both) heart... while its preload "baseline" might be different than another heart, anything that increases end diastolic volume/pressure will increase preload relative to its own baseline.

Thus, clinically, f you think of an acute situation in an individual, anything that increases venous return will also increase end diastolic pressure and volume, and thus will increase preload. But an increased end diastolic measure in one individual vs. another (or a "norm" value) at any one point in time is not sufficient to conclude that the preload on the former's heart is greater than the latter's.

 

[45408]

preload is the volume of blood in the heart the instant before contraction (systole) begins. Hence others have used the term end-diastolic volume

exactly

 

[mjl1717]

You guys were great.. Any brave doc wanna comment on some of the ORDERS you would write -if you admitted an 85 y o man with unstable angina/MI who has had numerous previous episodes of angina, EKG show possible LBBB and an occasional PVC and he ran out of angina medication.. whose B.P. is 100/60, pulse is 60, respiration 16, temp. 98 degrees.. he is stable and talking to you.. [Anything you can add] Ill start: Chest Xray, Normal Saline 100 ml/hr..

 

[Blade28]

You guys were great.. Any brave doc wanna comment on some of the ORDERS you would write -if you admitted an 85 y o man with unstable angina/MI who has had numerous previous episodes of angina, EKG show possible LBBB and an occasional PVC and he ran out of angina medication.. whose B.P. is 100/60, pulse is 60, respiration 16, temp. 98 degrees.. he is stable and talking to you.. [Anything you can add] Ill start: Chest Xray, Normal Saline 100 ml/hr..

Why are you asking this? Is this a case question? Real-life example?

Kaplan can't be covering this in their course...

 

[mjl1717]

Why are you asking this? Is this a case question? Real-life example?

Kaplan can't be covering this in their course...

Its a case I saw with my attending... And I was just reflecting and anticipating on some of the orders that could be written..
[Im also trying to be Osler like in my institution, without getting too many grey hairs or losing my hair..]

 

[osli]

So let's say (in theory, not like I was asked this on a test or anything 😉) that a professor asked you straight out on an exam which of the following is the best approximation of preload and had both EDV and EDP as options. Which do you choose?

Wow, well that would be a ****ty question but I could see it showing up on someone's exam. You could choose EDV because that is what you see most often in texts... and because people usually speak of increased venous return volume and not pressure. But I might reason that you should choose the one corresponding to the smaller incidence... dilated ventricles or hypertrophied ventricles. Whichever is smaller will mean that your "approximation" holds true more often in practice. If dilated is less common, then go with EDV. If hypertrophy is less common, go with EDP.

And then I'd bitch at the professor. 🙂

But in reality, both choices are equally valid because they are essentially synonymous. If you are talking about an individual's heart, then EDV and EDP are proportional to one another, and to preload. This is because as EDV increases the tension (preload) in the muscle increases, raising EDP. So while the three are not technically measuring the same thing, they all rise and fall together within an individual.

 

[osli]

Our school seems to be mostly fair about reevaluating exam questions. Often before our grades are even posted and we have a chance to review the exam there are a couple of questions that have either been thrown out or multiple "correct" answers allowed.

There is a stastical report given to several faculty members to review which they use to identify suspect bad questions. e.g., the class only performed slightly better than random guessing on a question and the top quartile didn't do appreciably better than the bottom quartile. Or there is a strong bimodal distribution where half the class chooses "A" and the other half chooses "C" with few if any going for other options. So they review those questions to see if a mistake was inadvertently made in either the stem or the answer choices... bad wording, two correct or no correct answer choices given, etc.

When we review our exams we have a chance to ask for "clarification" of questions we think are poorly written or contradictory to notes or whatever. Requests for clarification are forwarded to the question writer and a couple of faculty who review them as well. If it is obviously a bad question, the faculty review group can strike the question from the exam, accept a different answer choice, etc. If it is just a question of "that isn't what you taught/said/insinuated/etc. in class or in your notes" then the question writer has final say I believe.

But to be honest, I think I'd rather have a "no challenge" rule. I think it is more frustrating to know a question is bogus and the "powers that be" refusing to strike it for whatever reason, than knowing it is bogus but there is nothing you can do about it. 🙂