different types of shockRegister Today!
- by CrystalBlackford Apr 28I'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!
- While I'm not going to give the answer, remember that the circuit through system is composed primarily of three basic parts: the pump, the container (blood vessels), and fluid. With each type of shock, think about what parts of that system is being affected, and why! Septic shock is a distributive shock, why? What is it that's causing it to be this kind of shock? Ask yourself the same questions about the other types of shock and then look a little more deeply into how those kinds of shock occur.
Like hypovolemic shock is a loss of fluid, so the body compensates by making the pump run faster and the container smaller...
I'm glad you're curious... keep looking and keep that going because you'll need that to understand the problems behind what you're seeing.
Just don't expect to get a direct answer... we might point you toward the answer, but if you do the work, you'll remember the answer much more concretely!
So, for this one, tell us the answer you think it might be and why. Don't be afraid to be wrong, but you'll get to the answer and know it well when you're done!Last edit by akulahawk on Apr 28
- Thank you for your response! I do like figuring things out on my own, I just sometimes need some guidance, so I appreciate your comments. I will continue to think about this and hopefully come up with some answers soon!
- Apr 28 by emtb2rnAkula gave you a huge hint. Follow through on that thought process.
- Apr 28 by Esme12I think this will help.......Cardiovascular Critical Care Tutorials
Why is BP decreased/SVC increased in cardiogenic shock and hypovolemic shock, but BP is decreased/SVC decreased in septic and obstructive shock?
OK.....The B/P is decreased in cardiogenic shock because the heart is weakened and not perfusing the vital organs sufficiently enough so the bodies "fight flight" takes over and vaso constricts the vessels to try to channel the blood to the vital organs further decreasing the B/P because it is to weak to pump against resistance. I have always considered obstructive shock (pulmonary artery obstruction with massive emboli and cardiac tamponade) with cardiogenic shock....so it would be low B/P high SVR. So you either understood it wrong or the book is wrong...in my opinion.
Septic shock has both low B/P and low SVR because of the histamine release and vasodilation that occurs.
- Esme provided an excellent reference for you. Read through that and come back to us and tell us what you think! Don't be afraid to be wrong. Better to be wrong here and learn than it is to be wrong, not know it, and have it affect a patient.
- That website gave me one of the answers I was looking for about septic shock and the sympathetic nervous system so thank you!
Ok... so here are my thoughts. We are just covering Cardiogenic, hypovolemic, septic, and obstructive shock right now, so I will give you my thoughts on these and please let me know if I'm on the right track or not. This may be kinda long, so please stay with me :-)
In Cardiogenic Shock, the heart is not pumping effectively. This will result in decreased Cardiac Output (CO) and decreased BP. In response, the HR increases and the sympathetic nervous system (SNS) is activated, causing vasoconstriction in an effort to maintain perfusion. Blood is shunted away from kidneys, GI tract, skin, and lungs, and sent to the heart and brain. This vasoconstriction leads to increased Systemic Vascular Resistance (SVR) and increased Pumonary Vascular Resistance (PVR).
The left ventricle (LV)will not be pumping out enough blood, so it will back up into the pulmonary veins. This will cause an increase in Pulmonary Artery Wedge Pressure (PAWP). If it's backing up in the pulmonary arteries, it will back up into the pulmonary vasculature and then the pulmonary arteries. This is similar to heart failure - left sided heart failure can lead to right sided heart failure. Then, increased pressure on the right side of the heart will lead to increased pressure in the vena cava (increased Central Venous Pressure [CVP]), which will lead to hepatomegaly and splenomegaly.
There is decreased blood volume, either from things like hemorrhage or GI losses (absolute hypovolemia) or from third spacing as seen in burns (relative hypovolemia). The decreased blood volume will lead to decreased BP, increased HR, and increased SVR due to SNS activation in attempt to maintain perfusion to tissues. Pulmonary vasculature is also constricted in order to shunt blood to brain and heart, causing an increase in PVR.
There will be a decrease in venous return, so CVP is decreased and thus PAWP is decreased. (Does the PAWP always follow the CVP? I'm having a hard time wrapping my mind around how putting a catheter into the pulmonary arteries on the right side of the heart gives you info about the Left atrium... Is PWAP affected by CVP, SVR, or both? How can PVR be increased, but PAWP be decreased?) Do you know of a good resource I could look at to understand this better?) B/c there is less blood returning to the heart, less blood is being pumped out the left side of the heart so CO is decreased.
Microorganisms release toxins which cause damage to cells. The inflammatory response is activated, which leads to vasodilation, increased capillary permeability, and activation of the clotting cascade. Nitric oxide concentrations also rise in septic shock (thank you again for the awesome website reference! This is the info I was looking for!) and it plays a role in organ resistance to catecholamines, such as epinephrine and NE. There is also a deficiency of vasopressin. Therefore, the body will not respond to the SNS and hypotension results from the massive vasodilation that occurs.
Vasodilation leads to decreased BP and decreased SVP. HR increases to try to circulate more blood to the tissues.
Fluid leaks out of the vasculature into interstitial spaces. Because the body is not responding to the SNS, the pulmonary vessels are not affected (???) and thus the PVR remains unchanged.
Because fluid is leaking out, there is decreased blood volume, decreased venous return, and decreased CVP. Less blood is being pumped through the heart so PWAP decreases and CO decreases. (SVR is decreased and PVR remains unchanged, so there is less pressure in the pulmonary arteries.)
Last one! Obstructive shock:
something is blocking blood flow, which causes decreased CO and decreased BP. In response HR increases. My book is saying that SVR would be decreased, but I thought it would be increased in response to the SNS. Am I missing something here? I'm also thinking PVR would be increased due to action of the SNS.
Like if you have a pulmonary embolism, blood flow is blocked in the pulmonary circulation so less blood reaches the left side of the heart. (What happens with the PAWP? - I'm thinking because PVR is increased, PAWP should be increased also)
The PE reduces blood flow to the left side of the heart. Blood backs up into the pulmonary arteries, then the R ventricle and atrium, and eventually the vena cava, causing increased CVP.
If something happens to prevent the right side of the heart from filling, as in abdominal compartment syndrome, venous return will be decreased. There will be decreased CO, decreased BP, increased HR, and increased SVR (in response to the SNS). I'm thinking CVP would be decreased, PAWP would be decreased, and PVR would be increased (as result of SNS).
Phew...I'm tired of typing! Your opinion on my thought process would be greatly appreciated!
- Sounds like you're on the right path to understanding the topic! Good work. The more you delve into this, the better you'll understand it and (hopefully) be more able to apply what you've learned to caring for the patient that's presenting in some kind of shock state.
- 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?