different types of shock

[CrystalBlackford]

I'm learning about different types of shock, and I need help understanding something. In hypovolemic shock, BP is decreased and the sympathetic nervous system is activated leading to vasoconstriction in an effort to raise BP. This causes systemic vascular resistance (SVR) to increase as a compensatory mechanism, correct? Does the same mechanism work in cardiogenic shock?

Basically, my question is... why is BP decreased/SVC increased in cardiogenic shock and hypovolemic shock, but BP is decreased/SVC decreased in septic and obstructive shock? Is the sympathetic nervous system not activated simply due to a decrease in BP? I was thinking that SVC should be increased in septic and obstructive as well, but my med-surg book says its decreased. Any help you can give me would be greatly appreciated!

[akulahawkRN, ADN, RN, EMT-P]

In a way, it is. However, this also (hopefully) gives you a better understanding of the concepts behind the shock states and why they present the way that they do. You'll delve deeper into those concepts later, but you'll have a much better foundation for when you visit the subject. When you review the book for this stuff, think about what's happening with the CV system and why it might be reacting in that particular way. Just keep the explanations simple. You'll thank yourself for that step later... why? You'll have to teach people (most of whom have no idea about this stuff) about various problems.

[CrystalBlackford]

Thank you for all of your help, akulahawk! I appreciate your tips and guidance. Sometimes, I just need someone to write out my thoughts to so I can sort things out. And you're right, sometimes I over-think things in an attempt to understand it, but my patient's will need simple explanations. I find this stuff so fascinating, though, and I love learning the details! If anyone else reading this has ideas on the subject, or would like to correct any of my own thoughts I discussed earlier, please feel free to do so!

[Esme12, ASN, BSN, RN]

I wanted to give you my thoughts on the PAWP and see if you can point me in the right direction.

I know I mentioned this earlier, but I wanted to put my thoughts down before I forget. So, PAWP is supposed to give you information about pressure in the left atrium. A catheter is put through the right side of the heart, through the right atrium and right ventricle into the pulmonary artery and then through another branch of the pulmonary artery. The balloon on the catheter is inflated and measures the pressure in the vessel. From my understanding, the pressure in the pulmonary artery represents the pressure in the left atrium because the same blood will make its way through the lungs, into the pulmonary veins, and into the left atrium and the pressure should remain the same. That makes sense to me.

But what about when you have a PE? Lets say a thromboembolism travels up through the vena cava, into the right atrium, through the right ventricle, through the pulmonary artery, and then gets lodged in a vessel in the lungs. Wouldn't blood eventually back up into the pulmonary arteries and the right side of the heart, thus causing pressure in the pulmonary arteries to increase (and cause an increased PAWP?) From what I researched, if there is less blood being sent to the left side of the heart, then the PAWP would be decreased, but how can that be if the arteries are occluded and pressure is increased? Am I not thinking about this right?

The is a good reference for the Swan Ganz/PA line...icufaqa.org

Actually the PCWP is a reflection of the LA pressure NOT the PA pressure.

PCWP is a reflection of fluid status and in the normal heart the CVP, RA, LA, PCWP and the LVEDP (left ventricular end diastolic pressure) will all be essentially equal....again in the normal undiseased heart.

Central venous pressure

Indirectly measures right ventricular end diastolic pressure. A measure of volume.

Systemic vascular resistance

Measures resistance to left ventricular ejection. Reflective of vasoconstriction or viscosity

Pulmonary vascular resistance

Measures resistance to entry of blood into the heart. Reflective of volume.

Pulmonary artery wedge pressure (also PCWP)

Reflects left ventricular end diastolic pressure.

Mostly because the PCWP reflects the pressures in the LEFT side of the heart..and emboli affect the right side of the heart...the PCWP will USUALLY stay unaffected by the Pulmonary emboli unless severe or a massive blockage of the PA.....this may also help.......http://www.in-isrc.org/docs/081013.HEMODYNAMICS.pdf

[CrystalBlackford]

Thank you, Emse12! That is very helpful!

[Esme12, ASN, BSN, RN]

I LOVE cardiac....

[nurseprnRN, BSN, RN]

I wanted to give you my thoughts on the PAWP and see if you can point me in the right direction.

I know I mentioned this earlier, but I wanted to put my thoughts down before I forget. So, PAWP is supposed to give you information about pressure in the left atrium. A catheter is put through the right side of the heart, through the right atrium and right ventricle into the pulmonary artery and then through another branch of the pulmonary artery. The balloon on the catheter is inflated and measures the pressure in the vessel. From my understanding, the pressure in the pulmonary artery represents the pressure in the left atrium because the same blood will make its way through the lungs, into the pulmonary veins, and into the left atrium and the pressure should remain the same. That makes sense to me. But what about when you have a PE? Lets say a thromboembolism travels up through the vena cava, into the right atrium, through the right ventricle, through the pulmonary artery, and then gets lodged in a vessel in the lungs. Wouldn't blood eventually back up into the pulmonary arteries and the right side of the heart, thus causing pressure in the pulmonary arteries to increase (and cause an increased PAWP?) From what I researched, if there is less blood being sent to the left side of the heart, then the PAWP would be decreased, but how can that be if the arteries are occluded and pressure is increased? Am I not thinking about this right?

You're doing a good job figuring this out. :flwrhrts:

It's helpful if someone can step back first and think of what the anatomy of the circulatory system is supposed to accomplish. It's supposed to move a fluid around in a bunch of blood vessels, pumped out at high pressure from the left side of the heart, returned to the heart by passive squeezing in the veins and kept from sloshing backwards by valves in the vessels. Then the right side of the heart is supposed to push it through the lungs (at a lower pressure, because it only has to perfuse the lungs right next door, not all the way down to the toes like the arterial system) to do the gas-exchange thing. Then the fluid goes back to the left side of the heart and out to the body again.

Ventricular filling pressure is just the pressure that is in the ventricles at the end of diastole (LVEDP, left ventricular end-diastolic presssure). For a given volume delivered to a ventricle, pressure can be lower if the ventricle is nice and soft and flexible and empty, ready to accept a new load, than if it's hard and scarred up or has leftover blood in it from the last systole because the AV is hard to open OR because its contractility was so lousy that it didn't empty well. Another term that is used could be "preload," pre- meaning "before systole," and load, well, being the load of blood delivered to the ventricle that it is gonna have to move out in systole. You can measure load as weight or volume, but the way we look at it is by measuring the pressure that occurs there. Pressure changes tell us what's going on in there. Think about a soft balloon (low pressure) and a hard one (high pressure). Which has more air in it?

Let's look at the blood flow in a linear fashion. I regret that I cannot give these in color so you can see the blue of venous, the red of arterial. But hey. Draw them on a piece of paper in color. The lungs are pink :)

Body > Veins > Vena Cava > Right Atrium > tricuspid valve > Right Ventricle > pulmonic valve > Pulmonary Artery > LUNGS >Pulmonary Vein > Left Atrium > mitral valve > Left ventricle > aortic valve > Aorta/arteries > Body

Think about when the valves between two chambers are OPEN. By definition, each chamber must be at the same pressure, right? So, at the end of diastole, just before systole, the pressure in the LV is the same as LA pressure is the same as the pressure in the pulmonary vein (no valve in the way there) and in the pulmonary capillary bed. And since there are no valves in the pulmonary capillary bed, tracking backwards, you can see that LV end diastolic pressure equals end-diastolic PULMONARY ARTERY PRESSURE, which is, conveniently, what we look at when we are wondering what's going on in the left heart. You can even follow it back all the way to the right atrium, and the vena cava-- central venous pressure! Wow!

OK. Now, why do we care about LV end-diastolic (filling) pressure? It's because that's where the work of supplying the whole body goes. For that, I wish I could draw you a nice little curve here. I can't, so I will describe it and YOU will draw it on a piece of paper to look at while we chat.

Horizontal axis: label this "preload" or any other term you like. Filling pressure, PA diastolic pressure is the same thing (see above) and you can even extrapolate all the way back to central venous pressure, for a rough trend-setting bit of data.

The vertical axis you will call "cardiac output," or "blood pressure," because the line we are going to draw is going to explain something really cool.

Start lowish on the left, near the vertical axis-- low filling pressure means low BP. Think: hemorrhage, hypovolemia, makes your BP low, right?

Slant the line upwards to the right, showing that blood pressure (cardiac output) increases the more blood you put into the heart. (Tank up that hypovolemic guy, and BP improves.) But at some point, that upward-going curve peaks, flattens out...and then it DROPS as the preload keeps increasing. This is because cardiac muscle is like a rubber band-- the more you stretch it, the harder it contracts...to a point, at which point it gets too stretched out and actually contracts less well. Draw a little asterisk at the top of that curve, where it starts to fall, then let it fall a little bit. That asterisk marks the best cardiac output you can get-- preload and output are optimal for that heart. Beyond that point, where the line slopes downwards, lies congestive heart failure- the heart is too full, has more than it can handle, and it fails. (This is, BTW, called the Frank-Starling Law of the heart, and you just drew the Frank-Starling curve) Pressure backs up into the pulmonary capillary bed making the lungs get wet and heavy. This is when people get diuretics (to decrease that excessive preload) AND drugs to improve their contractility.

Of course, if contractility is lousy because of coronary artery disease, previous MI, or whatever, this whole curvy line thing will kinda slide over to the left-- the myocardium will fail with lower pressures than it would if it had better contractility. Better contractility (a right shift) means it will handle more preload (higher filling pressures) and make better BP out of it. Draw a second curve to the right of the first one, parallel to it, to see that. With me so far?

I think you can see how CAD/CHF will give you higher filling pressures-- when the heart is failing a bit, it goes past the top of its curve more easily because its contractility is diminished.

Mitral STENOSIS will, in fact, decrease your LV preload, but it will increase pressures back into the lungs and, eventually, the right heart, because of the resistance to flow from the right side to the LV. Mitral REGURGITATION, on the other hand, will result in higher filling pressures because when the ventricle contracts in systole, some of the blood goes backwards, leaving excess sloshing around between the atrium and ventricle; the ventricle will have to accept a higher reload at diastole, and it doesn't like it. Over the top of the curve again.

Pulmonary embolus in the artery where the end of your particular Swan-Ganz sits will not give you useful pressures for the reason you intuit-- there isn't free blood flow through it. But the chances of the PA catheter being in that one little artery -- remember, there are a lot of them of the size of the balloon at the end of th catheter-- are small.

Well, I hope this hasn't confused you. I used to tell my students they had to know this because we saw lots of people with all sorts of deficits, but if they didn't have hearts and lungs, they were dead and we didn't have to take care of them anymore. Works in every possible area you could work, except pathology. Please ask me if I've confused you anywhere.