foreign what's up Ninja nerds in this video today we're going to be talking about shock this is a part of our clinical medicine section if you guys like this video it's you know it helps you it makes sense please support us you guys can do that by hitting that like button comment down the comment section please subscribe also it really goes a long way also highly suggest go down the description box below go to our website as I said before we have a lot of great things there notes illustrations we're developing exam prep programs for those of you taking your step one step two your pants Etc check those out and check out the merchandise that we got there all right without further Ado let's talk about shock there is a couple types of shock that we got to go into a little bit of depth on and that is hypovolemic obstructive distributive and cardiogenic shock out of all of these one of them has like some subtypes that will kind of like dive into a little bit we'll actually have separate lectures on all of those into more detail so first one is hypovolemic shock hypovolemic shock is super simple the volume within your vascular system is significantly reduced now when a patient lose volume you can lose volume in two ways one is you're losing volume from sources such as the git what will be a way that we could lose some fluid from your Git it doesn't take a genius to recognize if it's coming up from the top tube vomiting if it's coming from the bottom tube diarrhea another thing could also be like excessive NG tube suctioning as well or very very poor po intake from a decent amount of time this can cause hypovolemia the reason why is is if it's not getting absorbed across the GI tube you're not absorbing the volume so this is one particular reason why you drop your blood volume second one is excessive skin losses that would also lead to it and renal losses and again for skin losses it's again straightforward this would be a patient who has um usually excessive diaphoresis in other words they are sweating up a storm or and this could be from fevers so usually that'd be a big thing to think about so diaphoresis from fevers or burns like third degree burns that could be another big one and then Rhema losses is usually from things such as like diuretic abuse these scenarios will cause the patient not to be able to maintain a good blood volume right now if in these particular scenarios you reduce the blood volume that way that's going to lead to a problem you know generally the systemic circulation right you have the venous part and the arterial part the venous part is supposed to receive this volume if you will and take it where into the heart and allow for good venous return to allow for a good preload a good stroke volume cardiac output Etc if you have this problem where you're losing fluid this will lead to what a decrease in this particular scenario here a decrease in the venous return and if you decrease venous return you will drop your stroke volume and you will drop your cardiac output right so these are the underlying effects here because if you don't fill the heart you don't have enough volume of blood to pump out of the heart and one beat and then in one minute and that's the problem with this disease is you're losing fluid this way another way which is also catastrophic is it could be from blood loss if a patient has massive blood loss what would be some particular scenarios in this well we kind of talked about a little bit a triple A rupture would be pretty catastrophic I would say another one would be a GI bleed these are very very common or like a uterine bleed and you also can't go wrong with thinking about any type of trauma in that particular situation where it's like an external exanguination effect right so blood loss would be in this particular scenario and it's the same exact concept my friends where you're losing blood you're having a reduction in venous return in other words this process where blood is supposed to be going into the ventricles from the Atria is being reduced if you're reducing this process you're not having enough filling your edv is going down your stroke volume goes down cardiac output goes down now if we follow that process the amount of blood that's coming out of the heart is reduced and in that particular scenario that then drops as we said here your cardiac output and then if you drop your cardiac output what do you do to your your blood pressure you're dropping your blood pressure and so this will lead to a drop in What's called the mean arterial pressure which is the perfusion pressure if that drops you can't give oxygen to the tissues and this leads to something called organ malperfusion when you have organ malperfusion then this starts leading to organ dysfunction if not reversed in other words multiple organ systems can start to actually fail that is the concept of shock is where in this particular scenario the volume loss or blood loss is leading to reduction in venous return stroke volume cardiac output map and not perfusing the particular tissue and the organs such as liver kidney heart brain start to fail that's the concept there all right next one is obstructive shock in obstructive shock it's two particular etiologies here one is you are massively massively massively reducing the preload on the heart or you are massively increasing the afterload on the heart so it's one of the two there is a massive drop in the preload or there is a massive increase in the afterload so it's kind of like similar because if you think about a preload kind of goes with venous return right if you have a reduction of venous Trend you have a reduction in preload so just like you can see that in hypovolemia you may see that here but it has nothing to do with volume loss there's something obstructing the heart from filling because in this particular scenario as you couldn't fill same thing exists here where I can't get blood into the heart that same concept exists so there is a reduction in preload venous return then because of that if you drop your preload you drop your stroke volume and if I drop my stroke volume I'll also drop my cardiac output and that'll drop my mean arterial pressure and then the same concept here exists the difference in this scenario though is that there's something else reducing the filling one is you have the pericardium pushing on the heart and it's not allowing good filling of the heart or you have a lot of the lung pressing on the heart because the pressure inside of the pleural cavity is crazy high so it's either pericardial pressures are high or plural pressures are high what are the two diseases this is actually pretty straightforward one here would be a tension pneumothorax that will cause the plural pressures to go high and compress the heart and prevent it from Philly the second one would be tamponade and that would be the pericardial pressures are high compressing the heart preventing it from filling and these two scenarios these will massively drop your preload drop your perfusion to the tissue and so subsequently the patient develops organ malperfusion and again we'll talk about all the organs that can be malperfused and what that looks like a little bit later but that's the concept of shock now other things actually do happen here that not only does the heart actually get compressed but it also does like really quickly here cause something called septal shift so you shift the actual septum into the left ventricle which impairs its fillingness process as well but either way you're not filling right here's one with increased afterload if you increase your afterload what do you do to your stroke volume in your cardiac output you reduce it right so the reason why is afterload is the amount of pressure that you have to exert to push Blood Out Of The ventricle whether it's right or left into the aorta or into the pulmonary artery if it's too high can you get a lot of blood out no so your stroke volume and subsequently your cardiac output will drop and so will your map so in this particular scenario it's the exact same it's just a different mechanism but the question is coming what is causing this massive afterload increase look at that big chunky clot in the right right in the pulmonary artery what is that called pulmonary embolism now I can't get blood out of the heart why because the afterload's high because something's blocking that flow and then because of that if I can't fill the pulmonary arteries I won't be able to fill the left atrium and fill the left ventricle and if I can't fill the left ventricle I can't get a good stroke volume cardiac output map drops I don't perfuse tissues what in the heck did I just say it can cause this a pulmonary embolism so a p e is one of the potential etiologies that can really stimulate this okay so we have these etiologies here and these etiologies here that's obstructive shock for distributive shock it's a little bit different this one's interesting so the whole primary pathophysiology here for all of these is the vessels are vasodilated so let's actually put that right here you see how these vessels look at this one compared to this one compared to this prior one these suckers are huge right so these patients have massive vasodilation all right when you have massive vasodilation of your vessels now blood can easily flow through here without very little with very little resistance what happens to the svr I just told you and I told you the svr is going to drop right so vasodilation occurs intensely this drops your systemic vascular resistance when you drop your systemic vascular resistance what does that do to your blood pressure we already know cardiac output is equal to heart rate times stroke volume and blood pressure is equal to cardiac output times svr so if svr goes down blood pressure goes down so then what happens the map drops you don't perfuse your tissues and more organ malperfusion begins to ensue and that is the problem here but the question then arises here that we have to try to figure out is what in the stink is causing vasodilation massive vasodilation one other thing here's a big thing that's really really important we'll talk a little bit more get into the complications but whenever your svr if you'll notice something and this shock here this is the only one out of all the shocks where the svr is really low and all of these other shocks the svr is usually High the reason why is cardiac output is low cardiac output is low and in this one cardiogenic shock cardiac output is low remember the formula we said blood pressure is equal to cardiac output times svr if cardiac output goes down what has to happen to the svr it has to go up and if svr goes down what has to happen to the cardiac output it has to go up so sometimes these patients will exhibit what's called a reflexive increase in cardiac output in other words their hearts banging away it's important remember we'll talk about a little bit later but let's come to the question what in the heck is causing this vasodilation one is you're losing your sympathetic tone the norepinephrine and epinephrine that are supposed to naturally bind here to your alpha-1 receptors and you've got Alpha One receptors here it's just not happening for some reason there's some type of Disconnect there is just this disconnect where they aren't being released so there's like these lower levels of norepinephrine epinephrine they're not hitting the alpha-1 receptor so this is inhibited Alpha One respect receptors are supposed to cause vasoconstriction if you don't have them they'll produce vasodilation what is the reason why I'm having this disconnect usually the reason is some type of spinal cord injury it's usually a spinal cord injury sometimes a spinal anesthetic and this is called neurogenic shock neuro genic shock and we usually see these and I'm going to abbreviate this in spinal cord injuries all right there's a lot of different reasons why these can happen besides spinal cord injuries but this is the big one the other thing that's important to remember just to add in here is that these epinephrine epinephrine also hit the just as a little quick note a little side note it also has beta receptors on the heart beta 1 receptors so this may be the only type of shock besides maybe cardiogenic shocks that can also if there's less norepinephrine epinephrine hitting these receptors the heart rate will be a little bit lower so remember neurogenic shock is a weird one where they can have hypotension and bradycardia but look for some type of neurological catastrophe all right let's come back here neurogenic shock is one probably one of the least common this is going to be by far the most common type of distributive shock and this is called septic shock and this is usually due to a nasty type of infection so usually you have some type of bacteria that has reached its way into the bloodstream when it gets into the bloodstream it's called bacteremia but when the bacteremia starts leading to effects like hypotension fevers infectious types of properties now we're talking about septic shock so what happens is the bacteria we're not going to go through the entire mechanism here we'll do this in the pathology lectures but these bacteria activate our immune system cells and these bad boys release Bunches of cytokines and these cytokines some of the interleukins and tumor necrotic factors Etc what they do is they have the capability of precipitating oh wow vasodilation and that's going to cause this whole downward Cascade another thing is that they also do cause the vessels to become super leaky so fluid also leak is leaks out as well so they get a little bit of volume hypovolemic too the last one here is usually anaphylaxis okay with anaphylaxis this is usually an allergic reaction of some sort by a bee ate something that they're super super allergic to have a contrast allergy they got contrast what happens is that allergic reaction causes them to activate the immune system massive cytokines be released causing vasodilatory shock how do you differentiate these it's usually in the context of some type of spinal cord injury an obvious infection leukocytosis fevers whereas they have some type of angioedema upper Airway obstruction hives a recent exposure but that's some of the big ways of differentiating these from one another as a Distributive shocky theology all right we come down to the last one this is preferably one of my favorite ones in comparison to septic shock Cartesian shock is really really interesting in the sense that it can happen in two different ways one is it can be mechanical or it can be arithmogenic so let me explain here let's say here we have a patient who has cardiogenic shock they have some type of problem with their myocardium in other words they have a poor contractility that is their disease process let's say they have a reduction in the contractility and what's reasons why you can have a reduction in contractility one is you have an MI the second one is you could have heart failure usually with a reduced EF so an MI is one heart failure with a reduced ejection fraction will be another example right so this area is damaged and you're losing the ability to get blood out if contractility drops I am going to now have a problem getting blood out of the heart so what is that called stroke volume right in in one kind of beat and then if that's the case I may also over a process of a minute drop my cardiac output and so this is something that you could potentially see is a drop in stroke volume and a drop in cardiac output due to a drop-in contractility another thing to think about is is there a valvular damage oftentimes when valves are super super damaged and the one that I really would want to point out here is if there is damage to the aortic valve sometimes the mitral valve as well in acute let's say acute aortic regurgitation or mitral regurgitation and these scenarios what happens is is you have a constant backflow of blood right so you push blood out but the blood comes right back in and that can cause patients to go into an acute heart failure so it's the same kind of concept it kind of volume overloads them in the heart but you can't get blood out same concept so think about a catastrophic mitral or aortic regurgitation or recent Mi or do they have acute heart failure so usually this is heart failure where they reduce ejection fraction but it's usually acute not chronic in other words they decompensated if they have chronic or they developed acute heart failure or something to that effect in this particular scenario if you have a reduction in cardiac output what do you do to your map you drop your map you don't perfuse the tissues and what ensues my friends organ malperfusion so we're getting the concept here that some problem is there is a reduction of perfusion to the tissue and the tissues start becoming dysfunctional and all of these reasons just occur based upon the different pathophysiological process all right that's one way cardiogenic shock can ensue acute valvular regurgitation or reduction in contractility and just remember acute aortic regurgitation of mitral regurgitation can be a factor that can cause heart failure an acute heart failure okay next one here the other scenario that maybe causes us to get less blood out of the heart so less stroke volume and as a response less cardiac output and then if there's less cardiac output there has a lower map this concept here would be its arithmogenic so I have an arrhythmia that is preventing me from getting blood out of the heart there's two types of arrhythmias it's not too hard right one is the heart rate is going way too dang fast or it's going way too dang slow and this would be if you have a tachy arrhythmia this has to be really fast though guys I'm talking like a patient who is going like 150 or greater ventricular rate so we see this particularly in vtac maybe v-fib or atrial fibrillation sometimes SVT all right that it can potentially do this but I'd say it's more these top three the concept behind this super high heart rate is that what you do is you impair filling so what it's supposed to do is this is you're supposed to have blood coming into the heart this will be inhibited in the situations of tachycardia so this massive tachycardia will actually do this now bradycardia is really cool because when the heart rate is super super low such as in an AV block right this is interesting because it directly drags down the cardiac output if you increase the heart rate you'd be like oh well cardiac output is equal to heart rate time stroke volume so if I increase the heart rate I would increase my cardiac output sex that doesn't make sense it's if your cardiac output is so high it reduces diastolic filling then it can drop your cardiac output but in the other scenario cardiac output is equal to heart rate times stroke volume a heart rate drops so does cardiac output that is direct correlation relationship so these are two particular scenarios here where you can see heart rate driving a reduction of stroke volume cardiac output map and organ malperfusion so with all of that being said we've covered the different types of shock now what I need is to really kind of understand here is how do we really look at the complications and some other differentiating factors for patients with shock I'm reference so now we're going to talk about shock particularly the complications that can arise from shock and that is usually multi-system organ failure as the result of organ malperfusion regardless of any etiology of shock this is the problem so to quickly recap again and those patients who have cardiogenic shock obstructive shock or hypovolemic shock all of their problems is a result of their cardiac output being reduced so the problem is in these particular patients is their cardiac output is reduced again which types of shocks would do this my friend this would again be just as an aside here this would be cardiogenic 100 would be cardiogenic the second one would be obstructive and the last one would be hypovolemic all of these via different mechanisms reduce the cardiac output right so that's what we know about these particular shocks here is that these very specifically reduce the cardiac output now if we reduce the cardiac output what that tells me is that I am not getting enough blood out of the heart right so this process here is significantly reduced right so I'm getting a reduction in cardiac output which reduces my mean arterial pressure leading to organ malperfusion right and that's the concept here and we'll talk about those organs that get malperfused one thing that I want to also mention here is when a patient has a low cardiac output some things happen you guys remember this formula here that BP is equal to cardiac output time systemic vascular resistance the cardiac output in this disease is doing what it's dropping which will drop your blood pressure all right so the cardiac output is dropping this will drop your blood pressure what does your body have to do to compensate here increase the systemic vascular resistance let's do this in a different colors do the pink so this will have to increase now what that will look like is super super interesting when you increase your systemic vascular resistance you clamp down on those vessels like you squeeze the living heck out of them so you have intense Vaso constriction what that will do is is that will reduce the blood flow through the arteries in your extremities and when you go and look at these patients on exam what you will know is is they will have cold extremities pale extremities and they will have modeling of the extremities so this is what you will notice cold extremities pale extremities and modeling of their extremities all because their vessels are super super constricted that's super common cold pale modeled extremities very common in cardiogenic obstructive and hypovolemic shocks because of this mechanism here right so this is one thing I want you to understand the other thing is that whenever your cardiac output drops there's another formula that you want to remember and this is cardiac output is equal to heart rate times the stroke volume well in all of these types of shocks with the exception of cardiogenic shock which is the bradycardia related if your cardiac output is dropping what should be the reflexive reaction to your heart rate it should go up and so oftentimes these patients will develop what's called a reflex tachycardia so we call this a reflex tachycardia and this is common in all of these shocks there is an exception AV blocks would be one particular exception uh and and anything that a bradycardia so AV blocks or like a beta blocker overdose and this would all be related to Beta like a braided cardio all right so these are the concepts that I want you guys to understand here and low cardiac output related shocks your body increases resistance and increases your heart rate super important the other scenario here is we have the vessels that are jacked up so the systemic vascular resistance is the problem and the other types of shocks so whenever we have the systemic vascular resistance is really low what does that do to your mean arterial pressure that also will lower your mean arterial pressure and what are the shocks that lower your systemic vascular resistance my friends you should already know this once so again it's going to be which type of shock here oh son of a gun this will be distributive shocks distributive and so when a patient has distributive shock their systemic vascular resistance is massively going to be reduced this would be septic shock this would be neurogenic shock and this would be anaphylactic shock now what happens here is when a systemic vascular resistance is low think about the equation so BP is equal to cardiac output times systemic vascular resistance if we think about this formula when the systemic vascular resistance is going to be low then we know that the blood pressure will be low and so your body will have to increase its cardiac output so it'll beat harder and beat faster but here's the other concept what's the svr it's low so if you have a low svr your vessels are what we call dilated so that's why we call this a vasodilatory shock or a Distributive shock are they going to have good blood flow through them yeah because they're going to be pump and plump and leaky so they should have warm and they should have it should not be pale and it should not be modeled and in fact we should actually use this term there should be warm and pink slash red so warm and well perfused which means that they're pink and red so it should be warm pink and red and not modeled this is going to be your distributive shocks okay the last thing here is whenever your systemic vascular resistance drops your map drops your cardiac output has to increase the only other thing to remember here is is that whenever the svr reduces and as happens it also will try to create a reflex tachycardia the only exception to this process here is going to be neuro genic shock all right that is the only type of exception so all of these you should have a reflexive tachycardia a reflex increase in cardiac output that is the big Concepts that I need you guys to understand so neurogenic shock will have bradycardia and AV blocks or beta blocker overdose we'll have bradycardia all right now that we have a good understanding of that when your map's low you stop perfusing organs so I lead to a lot of problems here I don't perfuse generalized tissues when tissues don't get perfused they produce something called lactic acid and lactic acid what it will do is is it will actually drop your pH and when it drops your pH that is going to create a metabolic acidosis that then does something really interesting it triggers your lungs to have to breathe faster and so one of the ways that you can see disease in these patients is their respiratory rate is increased look for that in shock another one is they don't perfuse the brain and they can it can actually start to experience things like encephalopathy they also don't perfuse their coronaries and if you can't perfuse your coronaries enough guess what this heart starts to become a little bit sad and becomes a little bit ischemic and this is called an N stami this is super common the other one and you know what's interesting encephalopathy obviously they're present with confusion lactic acidosis they can present with a low PH if you check a gas but they'll also have tachypnea for in stemi they may present with chest pain but sometimes the way that this is found is some numbskull checks a troponin and these troponins will be elevated and the other thing is they may have an EKG that gets worked up for because they're in shock and they can have St depressions or T wave inversions they may not present with chest pain just remember that the other thing here is that they don't perfuse the kidneys and when you don't profuse the kidneys these poor kidneys they can develop what's called an acute kidney injury and acute kidney injury is usually the way that you'll see this is the urine output will drop off and their creatinine will rise and that is the big things to look for with an acute kidney injury the next thing is if you I mean it is multi-system right my friends is you don't perfuse the git and if you don't perfuse the git this can lead to what's called acute mesenteric ischemia and this will precipitate terrible abdominal pain usually out of proportion to what your exam is so watch out for this potential finding and lastly you may not perfuse the liver and these patients can develop what's called ischemic hepatitis and and these particular scenarios when I've seen them these patients usually have lfts that are through the roof like into the thousands and so this is another way that you'll be able to see this is because you just don't profuse the liver as well in these scenarios we see how if a patient develops any shock cardiogenic obstructive hypovolemic shock distributive shock they don't perfuse these tissues these are the complications that ensue we also understand that in patients with distributive shock they're vasodilated they're warm pink red not modeled and those with cardiogenic obstructive hypovolemic they're vasoconstricted they're cold they're pale they're modeled both can have reflex tachycardia with the exception and these AV blocks beta blocker overdose and here neurogenic shock let's now go into the Diagnostics of shock how do we diagnostically approach shock well first thing is calculate the shock index and the way that you can do that is by taking the heart rate and dividing them by the systolic blood pressure in all shocks with the exception of a bradycardic shock or neurogenic shock the heart rate should be high and the systolic blood pressure should decrease so if you think about that if that shock index is greater than one that supports shock what else supports shock lactate if lactate is super elevated that means that you're not perfusing organs potentially and that could also support shock and then ask yourself okay are there any features of decreased organ perfusion in other words do they have any encephalopathy is there any evidence of acute kind of changes in their EKG or troponins is their abdominal pain is there any features of acute kidney injury like an increase in creatinine and decrease in their urine output is there any bump in their lfts if that is the case that supports shock as well now the question is how do we determine which shock it is we do not do this in every patient but on your boards you will have to determine this based upon a swan guns catheter or a right heart calf you place this catheter into the jugular vein run it down into the right atrium right ventricle pulmonary artery into the pulmonary capillary area and inflate the balloon and it'll give you some pressures what it'll do is it'll give you these different numbers that'll help you to differentiate the type of shock so the first one is hypovolemic I want you to remember that this was a cardiac output low so the way that we look at cardiac output is cardiac index and svo2 these should both be low the next thing is svr in any shock except for distributive should always be high what's the only things that aren't kind of like we didn't talk about CVP and Pulmonary capillary wedge pressure this means that the actual heart is usually in some way shape or form having a hard time getting blood out of it and so in this it's usually kind of scenarios of obstructive shock or cardiogenic shock so we would expect these numbers to be low and patients with hypovolemic shock so again low cardiac output based upon these two numbers High svr present in all of these other types of shocks generally okay the only difference is CVP and Pulmonary capillary wet pressure should be low obstructive shock CVP should be high because you're not going to have good filling into the right heart and the reason why you're not going to have good filling into the right heart is because you have something pushing on it like attention or a tamponade or you have no blood leaving the right heart because they have a pulmonary embolism so in those scenarios the CVP should be high but again if it's an obstructive hypovolemic or cardiogenic cardiac output should be low so that's based upon these two numbers here their svr should be high as the compensation and their CVP will be high the only thing that is different here is their pulmonary capillary wedge pressure should be low there's only one exception in obstructive shock where the pulmonary capillary wedge pressure is high and that is tamponade otherwise that is the big defining difference here between obstructive and hypovolemic is this CVP is high low here these should be the same The Only Exception is cardiac tamponade cardiogenic shock the problem is getting blood out of the heart okay you can't get blood out of the heart so the CVP and it's actually hard again and these patients they have problems with being able to get blood out of the heart and they can't actually get blood out of the heart and so they kind of call them become overfilled and congested so CVP should generally be high in cardiogenic shock pulmonary capillary wedge pressure is a measure of left atrial pressures left atrial pressures are usually always high in patients with cardiogenic shock so you see how that's the big defining feature here between these is pulmonary capillary wedge pressure is high that's super suggestive of cardiogenic shock and again these shocks all have a low cardiac output so cardiac index should drop and svo2 should drop svr should always be high in all three of these shocks but the only defining features between these is cvp's low CVP is high pulmonary capillary wedge pressure is low pulmonary capillary wedge pressure is high The Only Exception here is cardiac tamponade last one is distributive so in this one we already know that their svr should be super low that's the defining feature of this shock and then what's the compensatory response an increase in cardiac output so these should be high and then pulmonary capillary wedge pressure and CVP are low because you're having an easy time filling the heart it's not a problem of filling the heart okay so you should be low and that's the ways that I want you guys to differentiate the types of shock based upon the swan guns catheter okay now we move into the next step which is how do we treat Chaka depends upon the type of shock the type of bulimic you have to ask is it fluid loss give them fluid is it blood loss give them blood how do I do that give them IV fluids if they're losing fluids give them blood if they're losing blood simple as that obstructive treat the cause it was tamponade stick a needle in pull that fluid off pericardiocentesis is it attention pneumothorax chest tube relieve the air there is it a PE TPA or embulectomy if they're hemodynamically unstable cardiogenic you have to treat the cause it is a reduction in contractility due to myocardial infarction they have to go to the cath lab is it an aortic valve that's acutely blown or a mitral that's acutely blown then you've got to give them a valve replacement is it bradycardia that second degree mode is two or third degree okay then we need to do a pacemaker is it a need potentially because of beta blockers and calcium channel blockers that have caused this patient to go into a bradycardic rhythm okay then we need to reverse that beta blockers with glucagon calcium channel blockers with calcium and then is it because they're going way too fast then we need to give them a cardioversion if they're an afib or if they're in vtac next concept here is if a patient's in cardiogenic shock and we've tried to treat the underlying cause but their perfusion is still being reduced and the examples of that is usually myocardial infarction and sometimes you may need to initiate inotropes things like dobutamine or mil Renown and if that doesn't work sometimes mechanical circulatory support so things like an aorta interrated balloon pump or VA ECMO we talked about that again in CHF and we talked about that a little bit in mi distributive shock is another one so this one is again the different types so anaphylactic shock is the systemic allergic reaction usually the best treatment for these patients is epinephrine give it to them as soon as you possibly can then after that you can do things like antihistamines and steroids for septic shock it's all about antibiotics you've got to get them on antibiotics you can give them a 30cc per kg slug of fluid initially but it's antibiotics and Source control of the infection that's going to prevent them from continuing to be in shock one thing that's important to remember is and patients with distributive shock you want to really support their blood pressure any type of shock you want to support the blood pressure but distributed most commonly they need a lot of vasoconstriction and so when you vasoconstrict the blood vessels you increase their svr which increases their blood pressure and increases their perfusion so you want to give drugs that squeeze the heck out of the blood vessels things like phenylephrine things like norepinephrine things like epinephrine or things like vasopressin so this will help to keep their blood pressure up long enough for the primary cause to be treated which is treating the anaphylaxis treating the sepsis okay all right my friends in this lecture we talk about shock I hope it made sense I hope that you guys enjoyed it and as always until next time [Music] [Music]