cardiophysio question

[daisygirl]

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First aid states that afterload = diastolic arterial pressure. Lilly's cardio states that afterload may be approximated by using systolic ventricular pressure OR systolic arterial pressure. 😕

First aid states that contractility increases with a decrease in extracellular sodium levels 😕 . I have no idea why and I haven't been able to reason with this 😕

Thanks 😀

 

[omarsaleh66]

First aid states that afterload = diastolic arterial pressure. Lilly's cardio states that afterload may be approximated by using systolic ventricular pressure OR systolic arterial pressure. 😕

First aid states that contractility increases with a decrease in extracellular sodium levels 😕 . I have no idea why and I haven't been able to reason with this 😕

Thanks 😀

First Aid says afterlaod = diastolic arterial pressure? maybe that means that after systole (left ventricle pumps out the blood), it goes directly to diastole and hence, the diastole arterial pressure is the pressure of the blood that the left ventricle pumped out (systole) but it reaches the arteries in diastole so hence, afterload = diastolic art. pressure?

this is a big guess ya'll.

and if extracellular NA+ decreases, isnt it going into the cells, so that means action potential, larger amt. of Na+ coming in (remember the big spike that comes in the ventricular cells) hence, stronger contraction.

someone please check my answers

peace

 

[daisygirl]

First Aid says afterlaod = diastolic arterial pressure? maybe that means that after systole (left ventricle pumps out the blood), it goes directly to diastole and hence, the diastole arterial pressure is the pressure of the blood that the left ventricle pumped out (systole) but it reaches the arteries in diastole so hence, afterload = diastolic art. pressure?

this is a big guess ya'll.

This doesn't make sense to me since my understanding of afterload is that it is the resistance to which the left ventricle needs to 'pump' against in order to eject its fraction of blood. Maybe I'm not making a connection here since cardio has not been my best subject 😳

and if extracellular NA+ decreases, isnt it going into the cells, so that means action potential, larger amt. of Na+ coming in (remember the big spike that comes in the ventricular cells) hence, stronger contraction.

For some reason, I've got a sneaking suspicion that something else is going on. However, I'm really fuzzy on this stuff- I remember learning how extracellular ion gradients screw around with the heart, but I don't exactly remember how (i.e. K levels changing from normal can lead to arrythmias- I think this has to do with the pacemaker stuff and the 'funny current' activating earlier due to repolarization). I'm just having a tough time figuring out how a decrease in extracellular sodium is leading to increased contractility especially since the myocytes ability to contract is dependent on intracellular calcium level.

Thanks for your help 🙂

 

[omarsaleh66]

man i am curious to how this stuff works too...; My USMLE is coming up next June

holler

 

[Idiopathic]

This doesn't make sense to me since my understanding of afterload is that it is the resistance to which the left ventricle needs to 'pump' against in order to eject its fraction of blood.

Yes, this is why systolic BP has to be greater than diastolic BP. It is the 'weight' of the blood in the circulation and the TPR of the vessels.

 

[Idiopathic]

First aid states that contractility increases with a decrease in extracellular sodium levels 😕 . I have no idea why and I haven't been able to reason with this 😕

This is essentially the digitalis principle. There is a Na+/Ca++ exchanger that is indirectly blocked by digitalis, keeping Ca++ in the myocyte. A similar situation exists when extracellular Na+ is diminished, as intracellular Ca++ cannot be exchanged for Na+. Contractility is increased because there is a greater concentration of intracellular Ca++.

 

[daisygirl]

This is essentially the digitalis principle. There is a Na+/Ca++ exchanger that is indirectly blocked by digitalis, keeping Ca++ in the myocyte. A similar situation exists when extracellular Na+ is diminished, as intracellular Ca++ cannot be exchanged for Na+. Contractility is increased because there is a greater concentration of intracellular Ca++.

I'm still confused though. That na/ca exchanger depends on the na/k atpase pump. From what I understand of digitalis- it binds to the k channel which then inhibits na/k atpase from 'working', and this leads to an accumulation of na inside the cell hence the na/ca exchanger (which works on gradients) does not work very well since there is too much intracellular na (so the intracellular calcium increases).

So is first aid saying that the extracellular sodium is low due to it being in the cell? If so, then I get it now.

Thanks, and sorry for having to expose everyone to the disorganized nature of my thinking 😳

 

[Idiopathic]

No, but the concentration gradient is relative. Low extracellular Na+ is analagous to high intracellular sodium with a non-working Na+/Ca++ exchanger, right? If it aint there (low extracellular) then it cant be taken in to spit out the calcium.

 

[daisygirl]

No, but the concentration gradient is relative. Low extracellular Na+ is analagous to high intracellular sodium with a non-working Na+/Ca++ exchanger, right? If it aint there (low extracellular) then it cant be taken in to spit out the calcium.

Now I get it. Thanks so much. For some reason I just couldn't make this connection. Medical school makes me feel so stupid at times 😳

 

[azzarah]

I still don't get the afterload explanation....

As I understand it, end-diastolic pressure is preload--load encountered by the ventricle just before it begins to contract.

Afterload is the pressure the ventricle encounters as it actually ejects--the aortic pressure.

So wouldn't afterload be equal to systolic arterial pressure? which is proportional to peripheral resistance? 😕


The Ca2+/Na+ explanation makes perfect sense. Thanks Idiopathic.

Someone please correct me if I'm wrong...and do it quick! Daisygirl is taking her exam soon!

 

[daisygirl]

I still don't get the afterload explanation....

As I understand it, end-diastolic pressure is preload--load encountered by the ventricle just before it begins to contract.

Preload is the volume of blood returned back to the left heart (via venous return). The end diastolic pressure is the pressure that the heart must eject its contents against (arteries and arterioles, etc..). The end-diastolic pressure can be found using the pressure-volume curves- it is the point at which the left aortic valve opens. So, end-diastolic pressure is achieved at the end of isovolumetric contraction by the left ventricle.

Afterload is the pressure the ventricle encounters as it actually ejects--the aortic pressure.

Afterload is the end-diastolic pressure. The pressure that the left ventricle must overcome in order to get its ejection fraction out.

So wouldn't afterload be equal to systolic arterial pressure? which is proportional to peripheral resistance? 😕

Systolic arterial pressure arises due to the left ventricle forcefully ejecting its contents into the aorta. The forceful contraction of this blood leads to the 'new' pressure which is the systolic arterial pressure. The systolic arterial pressure can be determined by using the pressure-volume loop- it is the maximum point, and this point is found between where the aortic valve opens and the aortic valve closes (just to be completely anal- the systolic pressure achieved by the ventricle is read off of this point; the actual systolic arterial pressure is 2-3 mmHg less than the systolic arterial pressure read off of the curve 🙂 ).

I hope that I've finally gotten this concept 😳 . I didn't 'get' the pressure stuff until I did a qbank question on it last night. Q-bank explained the question using the pressure-volume curve. After doing that question- this happened to me

 

[Idiopathic]

So wouldn't afterload be equal to systolic arterial pressure? which is proportional to peripheral resistance? 😕

No, because if it were, then no blood would move. Afterload takes two things into account: the volume of blood in the circulation (and its viscosity), and the 'stiffness' of the vessels. Systolic pressure most overcome this to force blood through.

This also helps explain why, in anemia and endotoxic shock, there is a widened pulse pressure, due to either decreased viscosity (anemia) or decreased resistance (shock), both of which lower the diastolic pressure.

Im sure everyone knew this.

 

[azzarah]

Alright...I am pretty confused. I will check this out in the library and see if that helps! Thnaks guys! 😀

 

[azzarah]

"For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled. The afterload of the ventricle is the pressure in the artery leading from the ventricle. In figure 9-7, this corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. (Sometimes the afterload is loosely considered to be the resistance in the ciruculation rather than the pressure.)"

Page 103, 10th Edition of Guyton and Hall Textbook of Medical Physiology.


So today I was at the library and looked this up in Guyton....It seems that afterload=systolic P.
I hope this helps....

 

[Idiopathic]

"For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled. The afterload of the ventricle is the pressure in the artery leading from the ventricle. In figure 9-7, this corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. (Sometimes the afterload is loosely considered to be the resistance in the ciruculation rather than the pressure.)"

Page 103, 10th Edition of Guyton and Hall Textbook of Medical Physiology.


So today I was at the library and looked this up in Guyton....It seems that afterload=systolic P.
I hope this helps....

Sorry...I think you are reading this wrong. 'afterload is considered to be resistance in the ciculation/pressure in the exiting aorta'

This is the definition of afterload/diastolic pressure, since it is the pressure that the heart must generate to move blood at all. Its the force that is already there (from the viscosity of blood and the diameter of the vessels). The systolic pressure is what the heart actually generates, which accounts for why blood moves.

 

[azzarah]

Wouldn't you expect the systolic pressure to be > than or = to the arterial diastolic pressure in order for the blood to move?...that's what makes me think that afterload should equal to systolic pressure and not just the arterial diastolic pressure....

I guess this is really easy for other people to understand...sorry I am just having a hard time grasping this afterload/preload thing.

Maybe when we do path next year this will all become crystal clear. Darn, I did so well on my cardio phys exam too! 😱

 

[Idiopathic]

afterload is diastolic pressure, because it must be overcome for blood to move. It is overcome by systolic pressure.

 

[azzarah]

Thanks idiopathic...I will never ever forget this! 🙂 😳