This is Sarah with RegisteredNurseRN.com and in this video we're going to continue our series on shock by talking about septic shock. And as always, after you watch this YouTube video, you can access the free quiz that will test you on this condition. So let's get started.
Septic shock occurs due to sepsis and this leads to a major decrease in tissue perfusion. So what happens is that the cells that make up our tissues and organs, for some reason, do not receive enough oxygen hence blood flow so they will start to experience what's called hypoxic injury and if this continues the cells will actually die and when cells die they take organs with them because organs are made up of cells so whenever we've talked about all these types of shock we have learned that depending on the type of shock will depend on why we are actually having this altered tissue perfusion. And for instance, with cardiogenic shock, why were these cells being deprived of blood flow of oxygen? Because with that type of shock, there was an issue with this heart. Most commonly, a myocardial infarction has damaged that heart and it can no longer maintain cardiac output.
So the blood flow going to those cells is altered. Now with septic shock, it's a little bit different of why we had an issue. with blood not flowing to those cells tissues. And the reason is because we have issues with how these small vessels are able to distribute blood flow. And it's going to come from some type of invasion from a microorganism, which is where the word septic comes from.
So at the beginning of the lecture, septic shock occurs due to sepsis. Well, what is sepsis? Well, sepsis is where you've had that invasion of that microorganism in the body.
And the microorganism can vary. It can be bacteria, which is the main cause of sepsis. It can be gram-positive or gram-negative. You can have a fungus, a virus, or a parasite. But regardless, whatever it is, the immune system is going to respond.
But in sepsis, that response is amplified system-wide. It sets off this inflammatory response system that's going to majorly damage these small vessels that actually deliver blood flow, hence oxygen, to these cells that make up our tissues and organs. So think of sepsis.
As sepsis progresses, it leads to septic shock. So septic shock is really the end result of sepsis. So we've really got to monitor our patient for this. And listen to this statistic by CDC.gov. One in three who die in a hospital have sepsis.
So as a nurse, we need to be able to recognize the early signs and symptoms of sepsis so they don't actually get to this point. And be aware of which patients that we have that are actually at risk for developing sepsis. Now what are the characteristics of septic shock?
How do we know if we have this patient in sepsis that they're actually entering into shock? territory. Well, we want to look for things that indicate that we have this decrease in tissue perfusion that's going to cause cell problems where they're not going to receive enough oxygen. One thing we can see, of course, you're going to see hypotension with sepsis, but this hypotension is going to be different when we start entering into shock territory. It will be persistent hypotension where that systolic is less than 90. will not go up even when they've had large amounts of fluid replacement.
In addition, in order to keep their mean arterial pressure, their MAP, greater than 65, they need vasopressors to achieve that, like Norad. epinephrine. And our map, what it does is it tells us how well those vital organs are being perfused. If it's less than 65, that pressure going to those organs really isn't maintaining them. Plus, they will have a serum lactate, if that is measured, greater than 2 millimoles per liter.
And think back to our stages of shock video. Why do we care about that serum lactate level? Well, remember, when cells are struggling, when they're not... receiving enough oxygen, they will switch from aerobic metabolism to anaerobic metabolism because they don't have any oxygen.
So they're going to metabolize without it. And because of that, that is going to produce lactic acid. And as it accumulates in the blood, your serum lactate will accumulate.
And that tells us we have altered tissue perfusion. Now let's talk about the pathophysiology of septic shock. And while we're having persistent hypotension and what is leading these small vessels...
to not be able to actually deliver. liver that oxygen to those cells. Well, septic shock is, like I said earlier, a distributive form of shock.
The other types of shock that are distributive are neurogenic and anaphylactic which we'll also be talking about in this series. So what What that means, again, is that there is issues with these small vessels being able to distribute blood flow to those cells so they can't get oxygen. Now, that is occurring not due to a cardiac outpouring. issue.
It's not because our cardiac output is so low it can't perfuse to those small vessels because in the early stages of septic shock you actually have a high or a normal cardiac output. It's fine but it's coming from a decrease in systemic vascular resistance which is due to this major vasodilation that is occurring throughout the body in these vessels. So these vessels have and whenever Whenever it widens, it decreases systemic vascular resistance.
So why in the world is that occurring? Okay, well, let's talk about what's going on. We have this microorganism that has invaded our body. The immune system in sepsis has responded in this like exaggerated way. So it thinks it's going to take care of it, but it's actually going to make things worse for a patient and progress them to septic shock if we can't take care of it.
So these chemicals are being released. by the microorganism toxins. It's damaging the surrounding tissues with its toxins and the immune system sees this and it's like okay we've got to respond but it responds in an amplified way and it releases cytokines and pro-inflammatory mediators. That's what's going to make our vessels and what's happening in septic shock a lot worse. So these chemicals right here are going to lead to the following.
You're going to get vasodilators. dilation. So these vessels system-wide are going to open up and whenever that happens, blood as it really flows, it's not really going to flow, it's going to pool.
So you're going to limit the amount of blood flow that's going to those cells and that's leading to our decreased systemic vascular resistance. In addition, these chemicals are going to change the permeability of these vessels. It's going to make them leak. So the fluid that that's in our circulatory system is going to start leaving it.
It's going to leave the intervascular system and that fluid is going to move out into the interstitial tissue. What's this going to do? This is going to lead to hypovolemia, specifically relative hypovolemia, and that's going to limit even more blood flow, hence oxygen being able to travel to those cells because they are depending on that blood flow to come to them. But if we have vasodilation and we're losing our fluid due to leaky vas... vessels, that's not happening very well.
In addition, to make things worse, what's also going to be released is called platelet activating factor. And what this does, the substance, is it causes platelet aggregation. Because in these vessels, we're having inflammation, we're having damage. So all these small little clots are going to start forming in these vessels. And we're talking system wide.
Now, if we're forming clots system wide, what's that going to do to our clotting factors? It's going to use them up. So the patient is at risk for DIC where they can bleed out of every orifice of their body.
So watch for oozing of blood. And these clots are going to create an even more of an obstacle for blood flow. If we have all these clots in our microcirculation, how's blood going to flow to those cells?
It's not. It's going to decrease the ability of that to occur. So if you have vasodilation, increased permeability, clot formation in vessels system-wide, you can see how those cells...
are being deprived of oxygen and we're having decreased tissue perfusion. So when we talk about treatment here in a moment, nursing interventions, you're going to see why treatment is going to try to undo this vasodilation and undo the clots and all this system-wide inflammation that is going on in the body. And then later on, what's also going to occur because of this process taking place, you have those cytokines that are present. Well, if you have abundance of these cytokines present throughout the body, it can affect the myocardial function, your heart's function. And specifically we're talking about tumor necrosis factor and interleukin-1.
And what this can do, it can decrease ejection fraction which is the percentage of blood ejected by your heart with each contraction. Now let's talk about the risk factors for septic shock because the chances are if you're taking an exam over this topic there may be a question that says which of the following patients is at risk for developing We know that the patient develops sepsis they are definitely at risk for entering into septic shock. So remember these risk factors and to help us remember that we're going to remember the mnemonic sepsis. Okay our first S is suppressed immune system. So any patients who have HIV, AIDS, or they're on immunosuppressive therapy, they're taking steroids, chemo, they're pregnant, have malnutrition issues, they're all at risk for an altered immune system.
For extreme age, this can be really young patients like infants and elderly at risk for developing sepsis. For people who have received an organ transplant or at risk. For surgical procedures, anything invasive, anything that's going to go in there and possibly introduce a microorganism into the body that normally shouldn't be there. For indwelling devices, anything that's going to be there.
that's inside your patient puts them at risk for a microorganism. So if the option says that a patient has something inside of them, like a Foley, a central line trach, think at risk. They have that risk factor for introducing a microorganism.
And then our last S is sickness. And these are chronic conditions. And it can be anything from diabetes, mellitus, to hepatitis, alcoholism, renal insufficiency, etc. That can alter a patient's patient's ability to fight infection. And another thing to consider would be the most common sites of sepsis.
So be thinking about the GI system, specifically the abdomen or the respiratory system, the lungs, or the urinary tract. All these are common sites where sepsis develops. Now let's talk about the signs and symptoms of septic shock.
And to do that, we're going to look at the early signs and symptoms versus the late signs and symptoms. Because as a patient is in shock, signs and symptoms... symptoms are going to vary depending on what stage they're in, especially septic shock, because it's a little bit different than those other types of shock we've talked about in their stages, because we have this massive vasodilation.
So early on, we're going to have some signs and symptoms that are a little bit different than what may, let's say, occur in cardiogenic shock. So let's look at the early signs and symptoms first. Okay, this is sometimes referred to as the warm stage of septic shock. It's where we have...
sensation going on and the patient's in this hyperdynamic state because of this phasodilation. And what you're going to see is warm slash flush skin. When you feel that skin, it's going to be warm and it can be flush.
Now later on, once we're in the late stages, it's going to be cold and clammy. So remember that difference. In addition, their blood pressure is going to be low, their heart rate is going to be up, and their respirations are going to be up. In addition, they're going to have a fever. So if you're looking at this patient, they have a fever, their blood pressure is low, their heart rate is up, they're breathing fast, and they have warm flushed skin.
They're probably septic, sepsis, septic shock. We have that going on. In addition, they can have the high cardiac output.
So either that can be normal or high. Later on, it will be low because that's where we have the failure. of our heart and our organs.
Mental status wise, they'll be restless, anxiety. Now as the septic shock progresses, we're going to go out of compensation. We're going to go where we're uncompensated.
So this is like the late stage. We consider this the cold stage of septic shock. They're hypodynamic and what's going on is all the systems are really failing.
So you're going to see signs and symptoms that are going on with that. We really don't want to get our patient here. So scan instead of being warm and flushed.
It's going to be cold and clammy. We have vasoconstriction going on. Things are just not being perfused because our heart is failing now at this point. So our cardiac output is decreased.
They will have severe hypotension. Heart rate can be high. Respirations high. Respiratory failure.
Everything going on. Urinary output, augleric. That is one thing that's so simple to look at to tell us if we're getting enough blood flow to those kidneys. If it's not at least 30. mls per hour or more our kidneys are not being perfused very well and they're starting to shut down so we're going to get renal failure another easy thing to look at is mental status are they in a coma not responding at all that's telling us that our brain is not being perfused and they can have hypothermia and again they just can't regulate their body temperature because every system of the body is failing now let's wrap up this lecture and let's talk about nursing interventions and treatments and to help us understand why we're doing these certain nursing interventions and implementing these certain...
treatments, we have to understand our goals for these patients. And those goals are really going to be around what is going on in these small vessels that are disrupting blood flow to those cells. We want to reverse that so we can increase perfusion. So some goals would be, of course, to increase tissue perfusion. This can be done several ways by giving them large amounts of fluid replacements if that doesn't work, vasopressors like norepinephrine.
epinephrine to help constrict the vessels instead of having major vasodilation cause vasoconstriction that can increase our pressures. Then we want to make sure they are oxygenated. If that patient is being perfused but there's not enough oxygen in that blood, we're not really doing a great job. So we want to make sure that we're keeping the oxygen saturation greater than 95%. The problem with patients in septic shock is that they are at risk for developing respiratory failure due to acute respiratory distress syndrome.
And remember with that disease, we talked about this in depth. What's going on is that whenever you have increased capillary permeability going on in the body, like how we do with septic shock, that's going to affect the vessels in the lungs, especially around those alveoli sacs. So fluid is going to leak into those sacs and cause them to collapse. And the patient's going to be in respiratory failure.
So a lot of times these patients have to be intubated and have mechanical ventilation to breathe. So we'll be looking at that. In addition, we want to fight that microorganism. So we want to obtain cultures as soon as we can to see what we are fighting against so they can receive the appropriate treatment. Start antibiotic therapy if this is a bacteria so we can get rid of that microorganism.
In addition, decreasing that system-wide inflammation that's going on. Sometimes that has to be done to help increase perfusion. So they may be started on like low dose corticosteroids. corticosteroids, or on activated protein C to help that, which has anti-inflammatory and anti-thrombotic effects. Because remember, we have claw issues as well.
And we'll talk about that here more in a second. And nutrition, we want to make sure that they get early nutrition because when we have decreased tissue perfusion, especially going to our gut, that can alter gut integrity. So we can start nutrition early through those feedings.
We can ink. increased gut integrity, help prevent those stress ulcers that can happen and improve our patient's outcomes. In addition, we want to control blood glucose.
This is really a big thing today because hyperglycemia alters the way that the immune system can work. So we want to make sure that we're keeping their blood glucose controlled. They may need to be on an insulin drip to help achieve that. Now let's take all that information and let's put it into an easy to remember new model.
on, septic shock. So whenever you're trying to pull for your exams what you're going to do for this patient, think of this word. So S, first S is start antibiotics.
This will be administered within the first hour of septic shock. This helps improve the patient's outcomes and typically a broad spectrum antibiotic is used until that microorganism is identified and you will want to collect cultures before actually starting the am. antibiotic. However, don't delay antibiotic therapy. Next is E, enteral nutrition.
This will need to be started early. By starting it early, it helps preserve GI integrity because there can be a risk of altered tissue perfusion to that gut. And plus, nutrition is going to help play a role with immune health, helping it to work as optimally as possible, helps with healing, and with the prevention of stress ulcers. Now, to help prevent stress ulcers, ulcers, the patient may be ordered some GI drugs like famotidine to help with ulcer prevention. And that is the brand name Pepsin.
Then P for protein activated C. And this is what I was talking about that has that anti-inflammatory and anti-thrombotic effects because we need that with what's going on. We have massive inflammation and we have these small little clots forming throughout our body.
And medication that does that is drotracogen alpha. And this is most effective if it started within 24 to 48 hours of septic shock. Now, because it has that anti-thrombotic effect, you'll want to monitor for bleeding. T for titrate vasopressors to keep that mean arterial pressure greater than 65 millimeters of mercury.
An example and first choice drug is norepinephrine. So what this will be used for is when fluid replacement is unsuccessful. So fluid replacement is... first. If we can't get that blood pressure pressure up, they're going to switch to vasopressors.
And what vasopressors are going to do is they are going to cause major vasoconstriction because we have vasodilation going on. And this is going to increase systemic vascular resistance, which we majorly need because we, in septic shock, we have decreased systemic vascular resistance. And by titrating this to keep our mean arterial pressure greater than 65, that's going to help perfuse our organs.
Again, that map is the amount of pressure in the arteries during one cardiac cycle. What it does is it shows us how well our vital organs are being perfused. Then I for inotropics, an example of a drug that can be used in septic shock that can provide this type of effect is called dobutamine.
This drug may be added if there's still low tissue perfusion going on. They can add this with the presser and it helps increase the strength of the heart. contractions.
C for crystalloids or colloid solutions. These are used with that first initial treatment to help get that blood pressure up but if it's not working then vasopressors are added to treatment. Now how can you evaluate if your IV solutions are being successful? Well you can look see is blood pressure going up? Is our systolic getting higher?
Well it's working and if the patient has hemodynamic monitoring because when these patients are in septic shock they're gonna be in the eye ICU and they're going to have these special devices that can monitor, for instance, the CVP, which is a central venous pressure. And we talked about this a lot in cardiogenic shock, but just to recap, central venous pressure is that filling pressure on the right side of the heart. So it's how much blood is really returning to that heart.
And in septic shock, we have hypovolemia, relative hypovolemia. So remember a lot of fluid left that vessel and went into the interstitial tissue so we depleted our circulatory system and if we're giving them fluids we should be replacing that fluid that has left that vessel and we're going to increase the venous return to the heart so as that blood is flowing into the right side our central venous pressure should be going within normal range and a normal cvp is 8 to 12 millimeters of mercury now if it was unsuccessful these fluids just really aren't doing the job you would be seeing persistent hypotension Hypotension, it's not really changing that blood pressure. They're hypotensive still and that CVP is Less than eight millimeters of mercury.
So there isn't a lot of feeling pressure Occurring in that right side of the heart because our circulatory system is depleted of fluid as for steroids What can be used is like low dose corticosteroids and this is used in some Patients to help decrease that amplified inflammation that's occurring due to that immune system Remember it's occurring system-wide and if that patient isn't really responding to those vasopressors, that vasopressor isn't really helping get that response that we need. So they may be started on this as well. H for hemodynamic monitoring. They're going to have that. Like I said, they're going to be treated in the ICU.
They will have a central venous slash arterial catheter to help assess tissue perfusion and those filling pressures in the heart because that tells us a lot of what's going on with our patient. Example, that CVP was that filling pressure in the right side. And then you you can look at what's called a pulmonary arterial wedge pressure and this is a filling pressure in that left side of the heart. O for oxygenate.
You want to keep the oxygen saturation greater than 95% because those tissues need oxygen. If we're making sure the blood's getting there, if we don't have oxygen in it, then it's not really doing great. So we want to make sure that they're having plenty of oxygen in their blood and again they're at risk for ARDS and they may need to be intubated with with mechanical ventilation to help assist them with breathing.
C for cultures. This will need to be collected before starting the antibiotics, but of course do not delay antibiotic therapy. And this will help identify the microorganism that's causing the infection so appropriate antibiotics can be ordered and target that microorganism. And then last, K.
Keep glucose less than 180. We want to prevent hyperglycemia because hyperglycemia... affects the immune system, and how it can heal. So a patient can be started on an insulin drip to control blood sugars. Other interventions that will be initiated, of course, is monitoring that serum lactate level.
Levels greater than two to four millimoles per liter are abnormal. And this again shows that cells are struggling for oxygen and have switched to anaerobic metabolism because they don't have any oxygen to metabolize. And of course, you want to monitor their urinary output, Foley insertion, they're going to have that.
And you want to make sure that the kidneys are putting out at least 30 mLs per hour of urine. And if it's low, that tells us that our kidneys are failing due to decreased tissue perfusion. Okay, so that wraps up this review over septic shock.
Thank you so much for watching. Don't forget to take the free quiz and to subscribe to our channel for more videos.