Types of Shock | Septic, Anaphylactic, & Neurogenic Shock

iron engineer so we're going to continue on talking about shock but we're going to focus right now about distributive shock so if you remember we talked over there about how certain situations like hypovolemic shock and cardiogenic shock and even obstructive shock we're causing this decrease in blood pressure and it was really due to a decrease in cardiac output they weren't able to get enough blood flow out into the actual circulation so the volume that was being distributed in the circulation was actually low and distributive shock is not really due to that type of issue it's actually due to a decreased tissue perfusion due to a decrease Systema class to the resistance so you guys remember we wrote over there that we've said that this low BP could be due to two different types of things right one is it could be due to a decrease in our cardiac output or a decrease in the systemic vascular resistance most of the shocks that we talked about over there were due to this situation a decrease in the cardiac output they want to be able to get enough blood flow to the peripheral circulation now for distributive shock the blood vessels are so expanded and dilated that now the systemic vascular resistance is actually going to decrease so the problem with these vessels is that the vessels are extremely dilated they're expanded and because they're so dilated it's going to decrease the tissue perfusion and if you decrease the tissue perfusion you decrease the oxygen delivery that hypoxia progresses to ischemia ischemia progresses to necrosis of the tissue and as the tissue starts dying the organ starts failing if not treated so let's go ahead and see now how septic shock it displays that type of activity all right so first thing you can see my little goldfish like looking microbes in there right cute little guys but dangerous let's just pretend that this microorganism here is some type of dangerous gram-negative bacteria I guess I'll just pretend it's some type of a dangerous gram-negative bacteria you know gram-negative bacteria what's so dangerous about gram-negative bacteria they have these things called endo toxins which are like those lipopolysaccharides and what happens is these guys can release those endotoxins and these endotoxins can cause so many different types of problems okay gram positive bacteria just understand that they can release chemicals that are similar to endotoxins okay but they're not endotoxins and released even something certain fungi even certain fungi can actually release certain types of chemical modulators that act like endotoxins but they are not endotoxins just so we're clear so gram positive and fungi can cause the same type of septic shock as gram negative it's just a little more common with the gram negative all right so what do these endo toxins do why are the culprits of all of these problems well let's go ahead and see so when and we're going to move to this brief is you guys have watched our video on the inflammation the inflammation part 1 part 2 part 3 part 4 that will really help you out because we are basically going to have a little quick recap of that super quick so what are these endotoxin is doing if you remember they were damaging the tissues and as they start damaging the tissues our tissues were starting to really certain chemical mediators remember the certain chemical mediators they're releasing like prostaglandins they're releasing chemicals like prostaglandins and leukotrienes leukotriene other some of those actual lipid mediator like messenger molecules that were broken down from arachidonic acid these guys here are coming over here in stimulating certain cells in this vicinity what are these certain cells some of these cells here are called mast cells and when these mast cells are stimulated by these chemicals they start releasing out a lot of different types of chemical mediators space they can start releasing like histamines they can also release leukotriene they can also release prostaglandins they can even release other different types of chemicals like protease ha's and they can even release certain types of chemo tactic agents why is all of this bad sounds like there's just a lot of inflammation well guess what let's see here whenever you're releasing a lot of histamines a lot of leukotriene a lot of prostaglandins these start coming over to the blood vessels and dilating the blood vessels so they dilate the blood vessels and they make the blood vessels really really leaky what is that call whenever you make the vessels really really leaky you're increasing the vascular permeability okay so as a result of this what are we going to do to the blood vessel we're dilating the blood vessel so it's going to get bigger so the vascular resistance is going to decrease so as a result here we're going to do two things we're going to vasodilate the blood vessel and we're going to increase the permeability of the amount of leakiness if this happens due to the fluid leaking out of this area into the actual interstitial spaces and stuff like that why is that so dangerous because that fluid can start accumulating a lot into these tissue spaces as the fluid starts accumulating a lot into the tissue spaces what starts happening to the blood volume the blood volume starts decreasing as blood volume starts decreasing this leads to a proportional decrease in the blood pressure that's why this is dangerous okay what else can happen here these chemotactic agents are going to try to signal our immune system they're going to let go immune system come out here so they're going to kind of try to call out the monocytes you know you have monocytes in here we even have some neutrophils these guys are going to try to fight off this bacteria and it's due to these chemotactic agents these chemotactic agents going to pull them out what else gets pulled out to this area complement proteins is remembered the complement proteins like c3 and c5 they were those little guys that actually had to get activated by these proteases so when c3 and c5 come over here these protease is released by the mast cells activates the c3 a and c5 a and these guys help to be able to do a couple things they actually stimulate the endothelial cells to become very very permeable and they'll cost some other things to be released as well so they're going to increase the permeability and they're actually going to enhance the inflammatory response they're also going to play a role in chemotaxis so so far what do we know the endotoxins are damaging the tissue causing chemical mediators to be released stimulating the mast cells to release a ton of different chemicals like histamine zuv leukotriene the prostaglandins dilating the blood vessel increasing the actual permeability causing more things to leak out it's also releasing chemotactic agents that draw light a lot of white blood cells to the area and it's going to cause the complement proteins like c3 and c5 to get activated which can activate the endothelial cells dilating and also increasing the immune response and it's going to cause more white blood cells to come to the area now when these white blood cells come over and start trying to fight off this endotoxin look what happens here these actual white blood cells will come over here let's say that we have a lot of site here and it's got this gram-negative bacteria over that it's trying to fight off here so there's that like little bacteria where there was a little let's actually draw it like this here's our little bacteria right here and it's trying to fight off this bacteria whenever it comes into this area and starts trying to fight off the bacteria it starts releasing a bunch of chemicals some of the chemicals are going to be like interleukin 1 - man aquatic factor alpha your even have a lot of other chemicals released like interleukin 6 interleukin 8 a lot of different stop substances what's the whole situation with this and you're looking 1 & 2 min aquatic factor alpha if released in significantly high amounts they're going to go to your hypothalamus so these are going to go to the actual hypothalamus in a specific area in the hypothalamus where the actual temperature regulation is occurring and when they go to the hypothalamus they're going to reset the actual hypothalamic temperature system and this is going to lead to the release of process of pge2 which is a prostaglandin and this prostaglandin is going to change our thermometer our body's thermometer readings and it's going to cause us to develop an increase body temperature very high body temp but we don't call it this we say it gets so high that we actually develop a fever okay we start developing a fever so that's one of the things that you're going to miss about septic shock they're going to develop a fever they're gonna have really dilated blood vessels a lot of permeability a lot of inflammatory cytokines release you know what else happens it's interleukin 6 it also goes to your bone marrow in your arm I'm sorry that's your bone marrow goes to your liver your liver is responsible for producing a lot of different types of proteins one of the really important things about the liver and the liver is actually going to respond to this interleukin 6 and it's going to produce a lot of these things called acute phase reactive proteins so acute phase reactants and these proteins are going to be like C peptide and half the globin and surreal plasma a whole bunch of different proteins that basically are an indicator that there's a lot of inflammation going on okay a lot of inflammation that's really bad what else interleukin 8 can actually go and signal other white blood cells to increase their actual phagocytic activity so that we can come out and start eating out more bacteria so this is going to cause the actual white blood cells to increase their phagocytosis processes okay that's going to increase cameo to chemotaxis too so now what's going to get into toxins neither they're really mean I really mean suckers sometimes they can actually come up to our endothelial cells and they're two things one is they're going to tell the endothelial cells to increase the expression of what's called a platelet I'm sorry plasminogen activator inhibitor type one why is this bad because the others die enzyme you know that there's a process here called plasminogen and plasminogen gets converted into what's called plasma and plasma likes to break up the clots it tries to cause fibrinolysis well this is carried out by TPA tissue plasminogen activator if you increase the expression of plasminogen activator inhibitor what do you think you're going to do you're going to inhibit this guy right here the tissue plasminogen activator he can't activate plasma as plasma levels start decreasing you aren't able to be able to break up the clots so what does that mean I'm going to develop actually some clots so I'm going to develop some micro vascular occlusions this is bad if I start developing like like right here a micro vascular occlusion okay so a thrombus basically and it's not getting broken down I'm going to start affecting the blood flow beyond that area to the tissue what's that problem with that that can lead to a scheme you so this can add to the ischemic problem so we already have a problem getting oxygen to tissues because of the vessels are so Veysel dilated now we just add it to the problem by actually causing this a thrombus to actually develop and this micro vascular thrombus is actually decreasing the blood flow to the tissues causing ischemia another thing that can happen is the endotoxins can actually increase the rushon of another type of protein these little suckers are a little little mean guys they increase the expression of these proteins here on the membrane and these proteins here are called tissue factor in case you factor is really important because it helps to generate the actual collaboration cascade so if you increase the actual expression of this tissue factor then what's going to happen then if you have a lot of this tissue factor you're going to increase this whole process of where you're going to have a lot of these clots developing here so increase the expression of this tissue factor is going to add to the problem in causing a lot more blood clots to be affected because you're increasing increase in the coagulation activity this also leads to another problem like because of an increase in the Pai Pai the plasminogen activator inhibitor that's inhibiting this causing micro vascular collusions tissue factor is also causing this micro vascular occlusion by increasing the coagulation activity you if this happens in various parts of the body intact which can happen in septicemia with a septic shock right is that it can lead to what's called disseminated intravascular coagulation what's called di C and D IC is terrible it's where you actually bleed because you're consuming so much of your clotting proteins you have so many different widespread blood clots throughout the body that you've consumed almost all your clotting proteins and when you need to clot you can't clot and these people start bleeding from like different orifice like from their eyes or from their mouth or from their their ears it's terrible so that's also another problem that can happen here another thing that can happen here is not only have we develops where we develop here so far we've developed a fever of these people they've increased their production of the acute phase reactants we've actually caused a lot of vasodilation a lot of permeability which is leading to what that's leading to a decrease in the blood pressure because we're losing a lot of volume here and this is the big problem because we're not getting enough oxygen to the tissues and they're becoming ischemic and then pay possibly necrotic we're causing a lot of micro vascular occlusions by increasing the PAI production and by increasing tissue factor guess what there's even other things in our white blood cells that are called the neutrophils whenever they're trying to fight off these bacteria sometimes what they'll do is they'll release certain chemicals to try to fight at all one is the release was called reactive oxygen species unfortunately though they released so much during this time period that it actually starts damaging the actual endothelial cells as you starts damaging the endothelial cells guess what happens according to virtuous triad he says that one of the things that can increase hemostasis or blood clots is whenever there's endothelial cell dysfunction guess what can start happening you can start developing increase incidences of thrombi so that's another problem here okay so a lot of things are going to happen here within this individual and you want to make sure that you understand how this whole process is working okay so in other situations there's going to be the production of Ross the reactive oxygen species and even other things which are called extracellular traps which is like basically histone proteins a little bit of DNA that are released onto the actual circulation to bind onto bacteria and try to tag them but this is kind of a big big thing one other thing that I want to mention the last one here is interleukin 1 a two-minute rhotic factor often some of these other interleukins they can have another devastating thing that they can do they can actually cause the depression of the heart function they can actually depress myocardial contraction this is bad and how one of the things that happens is because you're not getting enough oxygen delivery to the tissues you start developing a lot of lactic acid and a lot of lactic acid can actually cause a lot of problems here so not only is the lactic acids one of the problems of decreasing myocardial contractility but also the interleukins like interleukin 1 and 2 min aquatic factor alpha they also have a depressive activity on the myocardium of the heart so that's also going to add to the problem so but here's what's really weird here's what's really weird getting to the bottom of this when these individuals who have septic shock because of all these different problems their blood pressure starts dropping right their blood pressure starts decreasing when their blood pressure starts decreasing their BP is decreasing it's really due to what these blood vessels really really dilating and increasing their permeability that's another thing that this interleukin 1 and 2 minute chronic factor alpha also can do they can also come over here and also contribute a little bit to some vasodilation activities and so can't interleukin 6 & 8 there's a lot of different things here but the whole idea here is that vasodilation is actually going to be causing the blood vessel to get a lot bigger as that happens that decreases the systemic vascular resistance right so this is a decrease in systemic vascular resistance due to the vasodilation causes that decrease in blood pressure and that's what's really really dangerous what's weird is is that these individuals would have septic shock in the early stages they actually have a high cardiac output okay and that's one of the weird things that can happen in these people and it's because even though it's actually affecting some of the volume in the return and the depressing the myocardial contraction the ventricular walls are actually getting thinner so it's kind of compensating for that and because that it's helping to maintain a decent cardiac output so in these individuals that are in septic shock just watch out because they have an increase in cardiac output a decrease in stem systemic vascular resistance they also have a decreased blood pressure hypotension and obviously they can have a fever they can have acute phase reactive proteins being produced they can have increased incidences of micro vascular occlusions which can lead to di C can we do a lot of different problems they also can lead to ischemia too so very dangerous situation here now the thing is how would you treat this person okay you treat this person right away by putting them on antibiotics you definitely want to do an IV antibiotics that's that's obviously the most important thing that you're going to want to do with this situation is you're going to want to put them on IV antibiotics okay now the question is is okay well Zack what if I don't know what type of bacteria they're on that's when you have to send out a culture so you obviously have you have to do a culture but even if then you can put them on broad-spectrum antibiotics like you can use what's called your news is called ceftriaxone okay so you can use ceftriaxone and you can combine them with what's called zosyn which is basically what's called pip Tazo it's Pipper saline and T's will back them and you can use these as a combination for the broad-spectrum and then once you figure out all if they actually have an intra-abdominal infection okay we'll put on metronidazole and maybe some type of clindamycin oh well they have they don't have a spleen okay we'll put them on ceftriaxone to prevent them from being infected by Nasseri meningitis or streptococcus pneumoniae Haemophilus influenzae so obviously again the whole point is do a culture but the first thing you want to do is put them on broad-spectrum antibiotics and not just antibiotics what else what you want to put them on they're losing some of the fluid into the tissue spaces give them fluids so another thing that you want to give these people as you're also going to want to give them fluids so try to give them some actual fluids to put them on crystalloids right so give them certain types of like a ringers lactate so give them like a normal saline or ringers lactate also if they're not responding to the fluids you might have to put them on basal pressors so if you give them fluids and they're not properly responding to the actual fluids correctly within over a certain amount of time you can give them vasopressors to help to be able to constrict the blood vessels and get some of that actual volume circulating again a big thing is treat the underlying issue which is going to be giving the antibiotics and then again if it's certain types of bacteria obviously treat for that so for example if it's like MRSA give them vancomycin if it's some type of situation like a Pseudomonas give them gentamicin obviously make sure that you find out the type of bacteria before that put them on broad-spectrum antibiotics give them fluids and try to be able to restore their blood pressure that's how septic shock is going to work okay let's go on to the next one anaphylactic shock anaphylactic shock is just basically an allergic reaction it's a severe systemic allergic reaction so really important for this one it's basically an allergic reaction and this one usually it's due to a first exposure so let's say say that on you here most people if they take penicillin like you know they have a penicillin allergy or some other type of drug like maybe morphine accoding they break out they can go to anaphylactic shock there could be a lot of different causes a lot of it could be even bee stings like certain insect bites like bee stings or even like certain like bugs that actually certain insects that I can actually bite you know that devii the venom within them could even be like food allergies some people may be severely allergic to certain foods so food allergies drug allergies no one else is another one you know one that sometimes they have to put contrast into the individual to look at the certain situations they do it IV certain types of IV contrast people can actually have a severe allergic reaction too so the whole point here is it's a severe allergic reaction it could have many different types of but what's the whole idea here let's say that I'm exposed to this allergen at first is usually don't go into anaphylactic shock off your first exposure to it but let's say that here's the allergen here's the allergen and I'm exposed to this allergen the first time usually what happens is is this allergen is going to get processed by like certain cells like maybe my macrophages and whenever this macrophage in there is actually encountered by this allergen it's going to express that allergen on its membrane with an MHC 2 complex right so to express it on its membrane with an image d2 complex and then what it will do is it will take it to a t-cell so it'll take this to a T helper cell this T helper cell will then have specific proteins on its membrane like a target cell receptor and we'll have another different type of protein expressed on its membrane too so it has a lot of different proteins on its membrane so this is actually going to be like a macrophage so this could be like a macrophage and what happens is this macrophage is bringing the MHC 2 complex as well as bringing here this antigen when he comes he'll bring it to this T helper cell and the T helper cell will have a TCR and alas not another protein are called a cd4 molecule when these guys interact the T helper cell responds to this and starts producing certain types of chemical mediators these chemical mediators that is going to start releasing could be various different types of interleukins okay it could be like interleukin 2 interleukin 4 interleukin 5 the whole purpose is it starts releasing tons of cytokines these cytokines come over here and stimulate another cell this cell is called a D cell and what it'll eventually do is will convert the B cell so let's say here's our B cell it'll convert into what's called a plasma cell this plasma cell is really important because what it will start doing is of a start secreting antibodies but the thing is due to this interleukin 5 interleukin 5 tells the B cell to make a special type of antibody and this antibody is called an I GE antibody why is this such a problem they are now going to be firmly implanted onto a special host cell let's draw this bad boy right up here let's say here is this this is this is the problematic cell this is the guy that's causing a lot of the problems here this cell is called a mast cell and mast cells can be basically found anywhere around your circulation system so they can actually be found around it like peri vascular it can be find a lot of like our areolar connective tissue on the mast cell it has a special type of protein I guess everything's like predestined right now because some people are genetically predisposed to this but what happens is this IgE antibodies plugs right in to this actual receptor here what is this receptor called it's called an FC epsilon R one receptor that's not a heck of cord there right so this FC epsilon or one receptor binds with this IgE antibody now this mast cell is ready anytime that person is exposed to that allergen in this case we could be it could be anything this allergen but one of these usually anytime they're exposed to it again they might have an over a hyperactive immune response to that so some people they might just produce a little bit of histamines if they're exposed to it again but some people might be very very sensitive hypersensitive to it that's why this is the type of hypersensitivity if they're exposed to the allergen they'll produce tons more than normal amounts of inflammatory mediators so let's say that they get they for some reason they're like I don't I didn't know if they took penicillin and then they take it again without knowing that they're severely allergic to it that penicillin binds onto the mast cell and that mast cell goes ham and what does that mast cell going to start doing let's say that we have the mast cell right here the mast cell is going to start D granulating and it's kind of start producing tons and tons of the chemical mediators here so here's my IgE antibody and truly it takes a couple allergens really to to activate this IgE antibody usually has to be dimerized anyway when you activate the mast cell the mast cell starts producing all these chemical mediators the main one the main one that's going to be causing a lot of these problems here we'll mention two of them one is going to be leukotriene this is one really bad one the other one is going to be histamines and this is the culprit this one is really really bad because they produce a lot of histamines why is this bad histamines have two big functions one is they can go to blood vessel so let's pretend here I have like a small blood vessel here so there's two things let's say here's the smooth muscle because it can act on smooth muscle and it can act on blood vessels and it can act on other different things too so let's save it here I have a smooth muscle here and let's say here I have a blood vessel one thing you can do it's actually most affected in the heart of the actual Airways within our respiratory system our skin those are the main areas that can cause this severe anaphylactic shock what happens is these histamines come over here to these blood vessels and they bind on to receptors on the blood vessels and what they do is is they'll stimulate the blood vessels to become dilated and when these vessels dilate and become very permeable a lot of fluid leaks out why is that a bad thing let's say it's within this respiratory airway I took a cross-section of like a bronchial let's say that a lot of fluid starts building up out here a lot of fluid starts building up in this area what's it going to start doing it's going to start squeezing and actually become very very Adam a sh Asst we're strict in the airway but guess what histamines are like hey let me actually come over here bind onto the smooth muscle within the bronchi and I'm going to stimulate the smooth muscle within the bronchi to constrict so now the actual smooth muscle is going to constrict if it starts constricting it's going to reduce the amount of air coming in through the airway what is that going to do that's going to cost severe respiratory distress so it's going to cause severe respiratory distress this is why it's so dangerous because it can constrict the Airways and affect the amount of air that's coming into the individual's lungs another thing so it's actually causing increase in the actual itthat's basal dilating the blood vessels and why is that a problem because when you gaze or dilate the blood vessels what how does that affect it basal dilating the blood vessels decreases the amount of fluid that's remaining within the actual blood vessel so that decreased the blood volume which decreases the actual blood pressure also as all this fluid is leaking out into the peripheral areas not only will it cost the stimming hypotension but if you can't deliver enough oxygen to your tissues they're going to become a scheming because it become ischemic they become necrotic if they make up necrotic over a long period of time the organs can fail now another thing that can actually happen with this anaphylactic shock not only can it constrict the Airways but it can constrict another really really important one if this starts developing it becomes very dangerous so it's causing vasodilation which is basically causing a lot of edema one of the dangerous ones that can cause edema here in the larynx you have a lot of a demon and swelling starts developing around the larynx this is causing laryngeal edema this couldn't be more dangerous okay so laryngeal edema this is bad news bad news bears here because as the edema starts developing around the larynx and swelling up the larynx you can't get air in you're obstructing your respiratory passageways that is bad so that can cause severe problems and lead to death very quickly so what else could happen if they're having such respiratory distress right so they can have a lot of respiratory distress because of the constriction of the blonko of bronchioles the fluid accumulation in that area even around the larynx where it's going to happen you know angioedema can develop around the lips too it can also develop in other different areas like we said like the larynx and even the in eyes - you need a little bit angioedema which is swelling with an eyes another thing can happen is that these actual histamines and other different chemical mediators can come over to the skin and it can cause a lot of reactions within the skin that can lead to itching okay they can lead to itching of the skin and it could lead to rashes and hives of the skin so that's another thing that you might notice within a person going into anaphylactic shock so what would you like Santa flock of shocked you notice the person has a decreased blood volume like the actual amount of volume circulating within the blood the actual blood vessel so they're gonna have systemic hypotension okay bee why the reason they have systemic hypotension is because the blood vessels are dilating so the vasodilation is decreasing what vasodilation is leading to it decrease what so if we remember over here this is the main culprit vaso dilation is doing what it's decreased in the systemic vascular resistance which is decreasing the blood pressure as you decrease the blood pressure you decrease the oxygen delivery to the tissues which leaves dye poxy ischemia necrosis failure you get it now the question is how would you treat the patient how would you treat them you're going to want to be able to give them epinephrine why because epinephrine is going to come in there and constrict the blood vessels so if you give them epinephrine to constrict the blood vessels to help to be able to retain the blood pressure also what's the culprit histamines give them anti histamines give them benadryl give them Renata D which is basically going to block those histamine receptors where histamine is binding so that's another thing that you do another thing is you have to really be careful people go an advil acting shock you have to monitor them for a couple hours the reason why is there's a small percentage of the population like 20% that after they have their first initial attack about three or four hours later they can have another attack it's called a biphasic phenomenon so in certain situations you do want to monitor the patient but again treat them with giving them epinephrine you can first give them at the EpiPen like I am injections if that's not working you should get them to the hospital and try to be able to get the IV line setups to get them epinephrine and again put into the IV give them this antihistamines like benadryl or ranitidine which is basically blocking those histamine receptors preventing histamine from causing all this vasodilation itching redness laryngeal edema angioedema all these different types of problems that could kill the individual okay that covers anaphylactic shock now for the last one to finish it all off is neurogenic shock neurogenic shock is actually pretty much what it says in the name in this situation the nervous system is actually the problem so usually what happens is this is the most common cause of this is usually an acute spinal cord injury okay so some type of situation where you injured the spinal cord now acute spinal cord injury or maybe even another one is like if certain people when they going to go regional anesthesia they can also develop a neurogenic shock tube but again the most common type is a cause of this is acute spinal cord injury if you damage the spinal cord let's say that you damage the main air is here that is delivering these action potentials out to the heart so remember here we have the vasomotor center and I'm going to keep it the same color here for the cardiac accel Tory Center and it was coming down here and it was activating these neurons within the spinal cord right around t12 l2 right and what these guys were doing is they were taking information to the heart to the myocardium of the heart into the SA node an AV node and stuff like that they were also taking information to the blood vessels to do what one thing is it wanted to constrict the blood vessel so one thing is it wants to cause vasoconstriction that's a big one okay to constrict the blood vessels to squeeze them to aim to be able to increase the blood pressure when you need to the other thing is it goes to the heart and when it goes to the heart of tries to increase the heart rate it's positive coronal complication and is trying to increase the actual contractility which is acting as a positive inotropic agent but in some type of acute spinal cord injury guess what you've done guess what you done did you don't correct these things off they even an autonomic blockade so now you've you've affected them with an autonomic blockade because there's an autonomic blockade and you damage these actual fibers that are moving from the thoracic lumbar Regional spinal cord do you think that you're going to be able to increase the heart rate now anymore no so guess what remember the vagus nerve the vagus nerve was actually coming over here and was actually affecting the heart rate - guess what he's unopposed now so now you have unopposed wake up a venomous well opposed unopposed vagal tone why is that bad because this can lead to Braddock Ardea so in these patients you'll notice that they're going to have Braddock are do so that's one big thing another thing is they're not going to be able to cause vasoconstriction of the blood vessels if they can't raise them constrict the blood vessels what are you going to notice with these individuals so I'll have a decrease heart rate and they can't vasoconstrict so naturally their blood vessel is going to be vaso dilated what did I say was the problem with these individuals they have whenever the blood vessels are vasodilator this decreases the systemic vascular resistance as you decrease the systemic vascular resistance this decreases the blood pressure that was the problem with all of these because you decrease the blood pressure what happens you're not delivering enough oxygen to the tissues if you can't deliver enough oxygen to the tissues what's going to happen it's going to result hypoxia ischemia necrosis and then possibly organ failure if not reversed so these people are going to have a loss of vasomotor tone so they can have a very little blood pressure and that's why this can become very very dangerous now with that being said how would you treat the patient how would you treat them generally what you're going to want to do is you're probably going to want to put them on basal pressors that's probably the big one you're going to want to give them the basal pressors okay so vasopressors is going to be a significant one and again you can give them dobutamine you can give them so what could you give me to give them dobutamine you could give them isoprene alene you could give them epinephrine you could give them atropine there's a lot of different drugs that you could give to be able to treat this patient right another thing is you're going to put them on fluids so you're probably going to use some type of IV fluids okay to be able to stabilize the blood line bring it up a little bit sometimes in certain situations they even respond positively to corticosteroid therapy so sometimes they even do some sometimes you can use it sometimes you cannot you could use corticosteroids so why is that a problem then again if you aren't able to stimulate the heart to be able to increase the heart rate you're not going to be able to bring it down and it's going to be on the vagus nerve is unopposed so now it's going to significantly decrease the heart rate the contractility isn't going to be able to be increased beyond what it normally is anymore also you can't vasoconstrict the blood vessels so what starts happening to these bad boys these bad boys start four and dilating and as they start dilating it affects the actual tissue perfusion and as you affect the tissue perfusion you're not going to be able to get enough blood flow to this actual tissue area it's going to affect the oxygenation of the tissues lead to ischemia leads into kosis and then again the problem is that this can lead to organ failure all right engineers I can't say thank you enough guys if you guys stuck in throughout the whole video both series the part 1 part 2 I can't thank you enough I really appreciate it guys I really made sense I know this was a beast and it was a lot to go through and I hope it helped I really do it fit guys if you guys did like the video if it made sense please hit the like button comment on the comment section and please subscribe visionaires as always until next time

Channel: Ninja Nerd

Views: 476,558

Keywords: septic shock, anaphylactic shock, neurogenic shock, types of shock

Id: UbJRZTFLKdw

Length: 35min 41sec (2141 seconds)

Published: Fri Aug 04 2017