This is Sarah with RegisteredNurseAriene.com and in this video we're going to be going over the stages of shock and this video is part of an NCLEX review series over shock and as always after you watch this YouTube video you can access the free quiz that will test you on these stages. So let's get started. First let's start out talking about what is shock. Well shock results from a cause of some type and there's various forms of shock but regardless of whatever form of shock we're talking about, that type of shock is going to lead to decreased tissue perfusion.
So in this video what we're going to do is we're going to lay the foundation for shock by talking about the stages that these patients will go through. Then in the next videos within this series we're going to talk about these individual types of shock and talk about their nursing interventions. So what are the various types of shock? Well we have septic shock and this is where a patient has a severe infection. Another type is hypovolemic shock.
This is where the patient has lost a massive amount of fluid. There's also cardiogenic and this is where the heart is just really weak. It can't pump. If the heart can't pump correctly, it can't put out blood.
So the cardiac output decreases, hence tissue perfusion decreases. And a big cause of cardiogenic shock is like an acute myocardial infarction. There's also anaphylactic and this is due to some type of allergic reaction. You can have neurogenic where the neuro system has become damaged like a severe spinal injury or we can also have obstructive shock and this is where there is an impediment of blood flow and Something that can cause this is like cardiac tamponade now You may also see distributive and what distributive is is it's taken Septic anaphylactic and neurogenic and put it under there under distributive So if you see that that's what that means, but regardless of this type of shock Whatever shock it is, it leads to decreased tissue perfusion. Now, if we have decreased tissue perfusion, we can't perfuse our organs in our body, hence the cells that make up those organs that allow it to work because they're not getting enough oxygen from this heart that would receive oxygen from the lungs and pump it throughout the body.
So the cells start to suffer and experience hypoxia. Now, as I go through these stages... you're going to see how these cells start responding to this decreased tissue perfusion. You're going to see that they're trying to really save themselves by switching to different types of metabolism. The body also tries to compensate by stimulating the sympathetic nervous system, by causing the kidneys to activate the renin-angiotensin system, all trying to save these cells from dying.
Because if we can't correct the shock that is going on, what will happen is is that we will experience multiple organ dysfunction syndrome, M.O.D.S., where those organs are going to completely shut down and eventually lead to death. So whenever a patient is in shock, they need very aggressive treatment to save their life. So what are the stages of shock?
Well here they are in order. We have the initial stage, and then after that the patient will enter into the compensatory stage. The compensatory stage is reversible. if we can correct whatever's going on with this whatever form of shock, the patient can make a full recovery.
But if not, they will progress to the progressive stage. And then the last stage, which we don't want the patient to get there, is the refractory stage. And this is where it's irreversible.
It's not manageable anymore. And this leads to mods and then eventually death. Now let's talk about the individual stages of shock.
Okay, that first stage of shock is the initial stage. Now the big thing I want you to take away from this stage is how that cell starts to behave due to hypoxia. It's not receiving a lot of perfusion, so it's not receiving a lot of oxygen.
And to help it survive, it switches the way it metabolizes. So the cell is going to switch from anaerobic metabolism, which is metabolism with oxygen, it can't do this because it's not receiving a lot of oxygen, to anaerobic metabolism without oxygen. And whenever it does this, type of metabolism, it produces a waste product called lactic acid.
And as we go through the stages, you're going to see how lactic acid is going to be a big problem for our patient who is in shock. So let's say we have a patient who is in hypovolemic shock. They've had a massive amount of fluid loss. Now, let's talk about this for a moment.
Okay, if we don't have a lot of fluid in our body, our heart doesn't have... A lot of fluid aka blood to pump throughout our body and your heart is that central station for tissue perfusion because your heart specifically the left side receives oxygenated blood from the lungs then it shoots it up the aorta, which the aorta is a pretty amazing structure because it goes and branches off in a network of arteries and feeds your brain, your liver, your kidneys, your gut, everything. And those cells take all that nice oxygen oxygenated blood, take that specifically that oxygen from that blood and they work and they do their job.
But if they can't receive that, we have issues. So if a patient has lost a lot of fluid, what's that heart pumping? It's not really pumping anything. So cardiac output has become low.
And again, cardiac output is just the amount of blood the heart pumps per minute. So when our cardiac output drops, it can't support tissue perfusion. and the oxygen demands of the tissue's organs slash cells. And whenever this happens in this first initial stage, the signs and symptoms in your shock patient are very subtle.
They're not going to be outright obvious compared to those other stages, like the compensatory, especially progressive, and then the last stage, the refractory. So subtle signs and symptoms. Now, because we have low cardiac output, can't meet the needs of our cells. Our cells are like, hey, we're going to switch the way we metabolize.
metabolize. So that big takeaway, they're going to switch their metabolism to anaerobic metabolism without oxygen, but that's going to create lactic acid. Now, normally our body can deal with lactic acid because we produce this sometimes.
And what structure deals with lactic acid? Our liver. Our liver will normally take this lactic acid and we'll convert it into pyruvic acid, which will then go into glucose.
through gluconeogenesis but our liver is suffering as well because cardiac output is not very well it's it's low so if cardiac output is low all the arteries that feed our liver that come through that heart the liver is not receiving as much oxygen as it should so it can't really deal with the lactic acid because those cells that deal with the lactic acid are suffering so lactic acid starts to build up in our blood and that is not good. Whenever we've talked about our acid-base imbalance videos, whenever we throw a patient in an acid-base problem, we have issues. So we get an imbalance, this acid-base imbalance will damage our cells even more.
The patient can go into lactic acidosis and you can measure a lactic acid level. A normal serum lactate is less than 1 millimoles per liter and a patient who is in lactic acidosis where that lactate level is less than 1 millimoles per liter, acid levels really high it would be greater than 4 millimoles per liter now let's talk about the compensatory stage okay in a nutshell what's going on during this stage is that the body is using its systems to rescue itself so just like the name says the body's trying to compensate because in the first stage what's going on our cells are experiencing hypoxia they're releasing lactic acid and our body knows if this continues that cells are going to die that make up our organs and our body is going to die so what it wants to do is it wants to increase tissue perfusion so these cells don't die and we have these natural structures in our body that can help do that so the big takeaway I want you to get from this stage is that our body is going to use a biochemical neural and hormonal team to fight the effects of that anaerobic metabolism and it's going to help increase our blood pressure increase our cardiac output which in the long run is is going to increase our tissue perfusion, give those cells the oxygen it needs so they can continue working and we don't have the death of these organs. Now if a patient enters this stage, it is reversible.
So it's very important that we recognize the signs and symptoms of this stage and get the patient the appropriate treatment. Because if it's not corrected, they will go to the next stage, which is the progressive stage and pretty much what that stage is, is the failure of the body. to compensate and we see the effects of that. So at first during this compensatory stage the body's going to succeed at increasing the blood pressure, increasing the cardiac output, but it can only do it for so long. That's why we have to correct the cause of shock and give them the appropriate treatment.
But how does it compensate? Now this is where we really want to hone in on what's going on. So what happens is that the body senses that they are There is a drop in blood.
pressure and cardiac output. Because of that, it knows that there's going to be a decrease in tissue perfusion. Our cells need that oxygen to survive. And if they don't get the oxygen to survive, bad things start happening.
So as I said, we have these natural structures in our body that are going to kick into gear and save the person's life so one of these neat little structures are called baroreceptors and they are the found in the carotid sinus and the aortic arch whenever they sense that we're having drop in blood pressure drop in cardiac output arterial pressure all that what it does is it stimulates the sympathetic nervous system fight-or-flight response now whenever that gets stimulated what's going to be released or catecholamines so we're gonna have the release of epinephrine and norepinephrine now these awesome substances they cause vasoconstriction which is sort of what we need right now and what that's going to do is that's going to increase blood pressure pressure, increase the heart rate, increase the contractility of the heart, and help with our tissue perfusion, make ourselves happy. Now with this increased perfusion, the body knows that first we need to take care of our vital organs, which is our heart and our brain. Because if we don't have a brain that works and we don't have the heart that works, what's the point?
All these other structures, they can't survive without those. So we need to preserve function to them first. So they get more...
perfusion and it's shunted away from those non vital organs like the GI system, the skin, the lungs, and the kidneys, especially the kidneys, which is here in a moment when we talk about the kidneys, you can see whenever the kidneys receive decreased blood flow, they actually activate their own system, which will help actually play a role in this compensatory stage. Now, in addition, because we have the drop in the blood pressure and the cardiac output, we're going to have decreased arterial pressure. of course so that means whenever we have a decrease in arterial pressure we have a decrease in capillary hydrostatic pressure now what is this fancy word this is just the amount of pressure that the blood exerts on that capillary wall so if we have a drop in blood pressure we have a drop in pressure that that blood is exerting on that capillary wall right so whenever that happens the body sees that it says hey we need to get more fluid into that intravascular system because we have a drop in like the blood pressure in there.
So what it does is it causes fluid to move from the interstitial compartment to the intravascular compartment. So you have more fluid move in there and that's going to increase the venous blood return to the heart. So you have more fluid coming back to this heart structure and what's that going to do? That's going to increase cardiac output, increase the blood pressure, and increase tissue perfusion. So it's a neat little help.
to help us increase the fluid going back to the heart. So think of it like this whenever we give a patient an IV fluid bolus in their vein we're giving them some extra fluid so it can go to the heart and it can increase cardiac output and blood pressure. Now let's talk about how the kidneys play a role in this compensation.
Okay whenever they receive decreased perfusion they're like oh no we've got to do something to stop this and what they're gonna do is they're gonna activate the renin angiotensin system and what this neat little system is going to do is it's going to cause some vasoconstriction and it's going to help increase blood volume so what it does is renin is released and whenever renin is released it stimulates angiotensinogen and this creates angiotensin 1 which turns into angiotensin 2 and I want you to remember angiotensin 2 because this is a huge player with the kidneys okay angiotensin 2 is going to do two big things. First thing it's going to do is it's going to cause major vasoconstriction. And I'm talking about vasoconstriction to the arterial and venous system, which is really going to help us out because causing vasoconstriction to the arterial system is going to increase pressure, which we need. Causing vasoconstriction to the venous system is going to equal more blood return to the heart.
So those two things together is going to increase cardiac output, increase our perfusion to our cells. make ourselves happy and not be as hypoxic. In addition, what angiotensin 2 does is whenever the adrenal cortex senses that this substance is present, it knows that there is a problem.
So it releases aldosterone and aldosterone is a great substance whenever you need some blood volume because it helps the kidneys keep sodium and water which in turn is going to increase our blood volume. Now because the kidney are keeping that sodium it's going to cause the urine to have a higher sodium content which will lead the urine to have a high osmolality. Now because it has a high osmolality this is going to signal to the posterior pituitary gland that the body is trying to increase blood volume because there is an issue in the body hence shock where it needs some more blood volume to maintain its hemodynamic status. So it's going to release ADH, which is an antidiuretic hormone and ADH, what does it do?
It prevents your body from excreting water. So in turn, that increases blood volume even more. And all that together is going to help increase blood volume, increase cardiac output, and increase perfusion.
Now, our gut, our skin, and our lungs are also going to be affected by this decreased perfusion. So let's look at what's going to be going on with that. Okay, our GI system.
If you have decreased blood flow going to this stomach and to the gut, what's going to happen? Well, it's going to signal to the gut, hey we probably need to stop working and so it's not going to work as well as it should because those cells aren't getting the oxygen and the nutrients it needs. So it's going to work slower, you're going to have decreased peristalsis and during this time the patient is at risk for a paralytic ileus where literally the bowel is just like frozen and it's not working. So listening to those bowel sounds.
Are they absent or severely hypoactive that can represent a paralytic ileus? Now your skin, decreased perfusion to the skin, how's that going to present? Well the skin should be cold, moist, it should be pale except in early stages of septic shock.
In this stage when you have a patient with septic shock, their skin is going to be hot and flush because with septic shock you have massive vasodilation. the type of state that they're in is actually going to make their skin feel warm in this stage. The lungs, if you have decreased perfusion going to the lungs, well certain areas of this lung tissue isn't going to be perfused and our lungs are very vascular because they help play a role with gas exchange. Well if we're not perfusing certain areas of the lungs, whenever the person goes in to breathe to take that oxygen to transfer across that capillary membrane, brain, well that's not there to happen.
You're not going to have that gas exchange occurring because it's not being perfused. So you get decreased oxygen level in the body, you're going to get a ventilation perfusion mismatch which is a VQ mismatch and what the body's going to try to do is going to try to increase the respiratory rate, have hyperventilation, trying to increase the oxygen level. Now let's talk about the progressive stage of shock. Okay in a nutshell what's going on in this stage is that the body systems are failing. In the previous stage, they were rescuing, but now they are failing.
And what's happened is that the body can no longer compensate. So the body's really progressing now to multiple organ dysfunction syndrome. All these organs right here, their cells are being deprived of oxygen and every system is starting to shut down, which will progress to death. And that will be in our very last stage.
So the big takeaway I want you to get from this stage is that we have no more compensation going on, which is leading to a complete drop in cardiac output. This heart is not putting out a lot of blood per minute. This is going to cause a drop in our perfusion because if we have such a significant drop in our cardiac output, we can't get blood to these organs.
Can't get blood to the organs that are not being perfused. What happens to the cells that make up those organs? They start...
die and the cells will be so deprived of oxygen at this point that they're going to start experiencing hypoxic injury you're going to get a change to their ion pump where the cell is just going to swell in addition you're going to have increased capillary permeability this one caused a lot of problems and what happens is that literally the floodgates are just open from the intravascular system that we just built up with our compensatory stage remember all the those little hormones that are playing a role in helping us build up our blood volume back to the heart well this just undone it and it's going to take that fluid from the intravascular system to the interstitial space and that's going to pull fluids and proteins we pull proteins proteins regulate oncotic pressure so it's going to take even more fluid with it and this is going to cause the loss of blood volume you lose blood volume You drop cardiac output, drop tissue perfusion, and massive edema throughout the body. So whenever we're looking at the signs and the symptoms, how this patient is presenting, all we have to do is look at each body system that's made up of cells and ask ourselves, well, when this cell starts to die, what's going to start presenting? So let's start with our brain, neuro.
Well, decreased cardiac output, major drop in blood pressure, so our mean arterial pressure. This is where you calculate it with your diastolic blood pressure. You can multiply that by two, add that to systolic blood pressure, divide that by three.
You get your mean arterial pressure, and that's telling us how well perfusion is happening. And whenever it gets less than 60 millimeters of mercury, things aren't great. So that's where we're getting at in this point. And the brain is not being perfused. And your mean arterial pressure, your mat, plays a role in calculating your CPP.
you take your intracranial pressure with your map and you get your CPP. So our cerebral perfusion pressure is dropping and whenever that CPP is dropping that's telling us in a nutshell that our brain tissue is not being fed. So when the cells that make up the brain are not being fed what are you really going to see? This is where you're going to start to see major mental status changes with your patient. So they're going to have slow speech, they're going to be confused, agitated, restless, not responding to stimulation like pain like they should.
Next are lungs. What's going to happen with our lungs? Well remember we have increased capillary permeability, they're receiving decreased perfusion.
We already knew that in the previous stage that some spaces in the lungs are not being perfused like they should so we're having a drop in oxygen. Now we're throwing in increased capillary permeability. Well this is going to lead to ARDS, which is acute respiratory distress syndrome.
I have a whole video on that if you're studying that. If you want to go over it, I talk about all the stages of it and go in depth with it. But what's happening is that those alveoli sacs are being affected.
You have increased permeability. You have fluid collected in those sacs, causes the sacs to collapse. And as the progress, the lungs lose compliance. They become stiff.
Hence, it starts causing respiratory failure. They need to be intubated, mechanical ventilation. You have increased respiratory rate, decreased oxygen.
So that starts to happen. Heart will be affected as well. What happens when the cells that make up our heart start to die?
Well, a couple things. First of all, remember we have an electrical system in our heart. We have the SA node, the bundle of Hiss, just to name a few little structures.
And they're made up of cells that... create an electrical activity in our heart and we want our heart to be a normal sinus rhythm because that allows it to pump the most efficiently. But when these cells start to die in here that control our electrical activity, we start having dysrhythmias, lethal rhythms that like VTAC, VFib that can kill the patient. In addition, we have cells that make up our heart that allow our heart to pump.
So if our coronary arteries that sit on top of our heart aren't able to deliver blood to that tissue, the heart isn't going to pump and sometimes what can happen is it can lead to a myocardial infarction where these ventricles die those muscle cells that make up that ventricle actually die and the heart will just not pump anymore also affected will be our kidneys so whenever the kidneys are not being perfused we're here at this state where these cells compensation cannot help them anymore What happens is that the functional unit of our neph, which is our nephron, starts to really quit working in the kidney. And we're really talking about those tubules. So they start to experience acute tubular necrosis, which eventually will lead to renal failure. So that nephron within the kidneys just is not working, doing what it's supposed to. So what will happen is that your patient's urinary output is going to go dramatically down.
They're not going to be put be putting out a lot of urine because the kidneys aren't working to do that. In addition, their BUN is going to go up, their creatinine is going to go up. All that represents how well those kidneys are performing.
When that's elevated, kidneys are not performing very well. In addition, you're going to see an increased amount of waste in the blood because the kidneys aren't clearing it. So we're talking about acids. which is going to lead to metabolic acidosis because your kidneys, which help play a role normally in balancing that out with bicarb, isn't able to keep bicarb.
So you're going to see that. Another system affected is our gut. So whenever the gut loses blood flow to itself, we talked a little bit about this in the compensatory, but this is going to be so severe where the cells that make up that lining that help protect our gut, from the natural acid that's in there will lose its protective mechanism like the bicarb. So ulcers will start to develop and this can lead to GI bleeding, massive GI bleeding, which ties to our liver because our liver helps create those clotting factors.
So if we're having issues with that, we get a bleeding ulcer in our gut, we can have some major problems. So our liver can be affected. You have decreased blood flow to the cells in the liver. The liver is really cool organ because it plays a role in filtering waste, drugs, filtering out viruses, bacteria, and it plays a role with those clotting factors.
So if it's not working like it should, we're going to have an increase of waste in our body like ammonia, bilirubin, things we don't need there. In addition, we're at risk for a germ invasion so they can get bacteria in their blood and clotting so they can... have bleeding problems which leads us to another complication that can develop with shock is DIC and this is where little micro clots will form within the vessels throughout the body this is going to deplete the platelets and clotting factors in the body and what's going to happen they have massive clotting and then all of a sudden they're going to have massive bleeding that is that you can't control out of every orifice on the body so always watch at those IV sites anywhere something's been punctured for a little bit of oozing of blood because that could represent that. So whenever a patient is in this progressive stage, it's a very dangerous stage, they need very fast dynamic treatment to prevent from the patient actually going into mods.
And this leads us to our last stage which is the refractory stage and the word refractory means unmanageable and whenever a patient hits this stage it cannot be managed and it cannot be reversed. The end result is death. And this is where all the organs are going to shut down. So everything that was happening in that progressive stage is getting worse.
It gets so worse where you already seen how the function was already deteriorating. It's just going to keep going and going until it completely stops and everything shuts down. Okay, so that wraps up this review over the stages of shock.
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