Cardiac output

[chiddler]

Why does contraction of smooth muscle in the walls of large veins cause more cardiac output?

And regarding oncotic pressure: it's a form of osmotic pressure by blood proteins causing fluid influx into blood vessels. If blood proteins are absent, then blood will be too dilute causing fluid loss and edema. Yes?

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[MT Headed]

And regarding oncotic pressure: it's a form of osmotic pressure by blood proteins causing fluid influx into blood vessels. If blood proteins are absent, then blood will be too dilute causing fluid loss and edema. Yes?

I can vouch for this

Not sure about the first question.

 

[MedPR]

Why does contraction of smooth muscle in the walls of large veins cause more cardiac output?

And regarding oncotic pressure: it's a form of osmotic pressure by blood proteins causing fluid influx into blood vessels. If blood proteins are absent, then blood will be too dilute causing fluid loss and edema. Yes?

Are you sure this is right? You would think decreased venous return would decrease cardiac output... right?

I can vouch for this

Not sure about the first question.

MT doesn't know the answer? First time ever! Not trying to be a jerk, it's actually a compliment.

 

[chiddler]

i should of written this in original post. sorry :<

"...This would increase the filling pressure (the pressure gradient) driving blood into the right atrium thus increasing venous return, stroke volume, and cardiac output."

but i don't understand how simply increasing the pressure would cause more stroke volume because if less diameter of vessels, then less flow, right?

 

[davcro]

I thought cardiac output was supposed to be constant. Otherwise blood would get backed up (what's the proper term for this?).

Assuming constant output, than by poisilles eqn, a decrease in radius would be compensated with an increase in pressure

 

[chiddler]

I thought cardiac output was supposed to be constant. Otherwise blood would get backed up (what's the proper term for this?).

Assuming constant output, than by poisilles eqn, a decrease in radius would be compensated with an increase in pressure

Is it? I'd think not because we're given formula:

Output (L/min) = stroke volume (L/beat) * heart rate (beat/min)

with this formula, why would our heart rate increase when we exercise if cardiac output is the same. in that case it would remain constant.

 

[Misfit138]

It's because of the Frank-Starling mechanism. I don't know all the minute details, but basically, the force of the heart's contractions varies depending on how filled the ventricles are. Increased venous return leads to increased filling pressure, which causes greater myocyte stretching. This stretching leads to a more forceful contraction (something to do with sarcomere length). More forceful contraction = increased stroke volume = increased cardiac output.

 

[davcro]

Okay, I'm definitely wrong. CO does change. I see that your question comes from the Princeton review bio (p 290). I don't understand their reasoning either. I thought constriction would increase resistance.

Here's a possible explanation. Veins have valves. When they constrict they behave like a pump and push blood into the right atrium. This would temporarily increase CO. At least until the next heart beat.

 

[MedPR]

i should of written this in original post. sorry :<

"...This would increase the filling pressure (the pressure gradient) driving blood into the right atrium thus increasing venous return, stroke volume, and cardiac output."

but i don't understand how simply increasing the pressure would cause more stroke volume because if less diameter of vessels, then less flow, right?

Contraction in veins will move blood along more quickly (very technical terms here), thus increasing venous return. Increased venous return leads to increased EDV, leading to increased SV, leading to increased CO.

Also, if we think about Bernoulli's and the continuity equation, doesn't a constricted vessel have increased flow velocity compared to a dilated vessel? v1A1=v2A2?

 

[Charles_Carmichael]

CO output isn't always constant. Think about when you're exercising. Your cardiac output increases tremendously to support the increased metabolic demand of your muscles.

Veins normally have a large storage capacity for blood. When you have venoconstriction, you're returning more blood to the heart (ie. increased venous return). You're essentially decreasing the venous system's storage capacity and shifting blood to the arterial side.

Like someone mentioned, there's a very important relationship, known as the Frank-Starling relationship, which basically states that the volume of blood pumped out of the ventricle depends on the volume of blood present in the ventricle at the end of diastole (which, in turn, depends on how much blood is returned to the heart). This way, the heart couples venous return with cardiac output.

Hope this helps.

 

[SLC]

Why does contraction of smooth muscle in the walls of large veins cause more cardiac output?

And regarding oncotic pressure: it's a form of osmotic pressure by blood proteins causing fluid influx into blood vessels. If blood proteins are absent, then blood will be too dilute causing fluid loss and edema. Yes?

Kaushik above me explained the venoconstriction concept well. You either "store" blood through venodilation, or increase venous return to the heart through venoconstriction. Issues with this concept will become the basis of approaching CHF, Blood Pressure treatment, and a whole host of other cardiology treatments.

As far as oncotic pressure, yes you're right. I like to think of it as a "goldilocks" situation with the plasma proteins. Too little and you're going to get edema as the fluid leaks from capillaries in an attempt to restore plasma protein concentration to "just the right" level. Conversely, if the plasma proteins are too concentrated, then oncotic pressure will be very low and fluid will tend to leak into the capillaries from the interstitial space until "just the right" level of concentration is achieved.

There are two main mechanisms to Edema and interstitial fluid loss, Oncotic pressure and Hydrostatic pressure. Hydrostatic pressure has more to do with volume and actual fluid pressure in the traditional sense than Oncotic pressure. I.e. if there is too high a volume of blood in the capillaries, then hydrostatic pressure drives fluid into the interstitial space creating edema etc.

To take it one step further, the Oncotic pressure's contribution to edema becomes an integral concept when dealing with renal failure and/or liver failure as the plasma proteins could either be lost to the urine through a damaged kidney, or not produced in sufficient quantity by a damaged Liver, or even a combo of the two.

 

[chiddler]

thank you very much for the thorough response