hey y'all this is the presentation on shock so we think about when we think about shock um it's kind of similar to respiratory failure in that shock is not a problem by itself shock happens because something else happened but it is so we consider it a syndrome and the issue with shock is decreased perfusion and cellular metabolism is impaired as well it's not just decreased tissue perfusion it's decreased tissue perfusion to the point that metabolism is impaired we also can think of this as microcirculatory collapse because that's where the perfusion happens that's where metabolism happens and that's where the problem in shock happens so what we have is an imbalance between supply and demand for both oxygen and nutrients so we classify shock in four different ways we talk about cardiogenic hypovolemic distributive and obstructive within hypovolemic shock we talk about absolute and relative hypovolemia so absolute lack of fluid and a relative hypovolemia is like there's fluid there but it's not where it's supposed to be within distributive shock we have three subtypes neurogenic shock which we talked about when we did neuro back in care too anaphylactic shock which we talked about in care too and septic shock which we're going to talk about in this quarter and then obstructive shock is not a form of distributive shock all right so we're looking at cardiogenic shock that happens because there is some sort of dysfunction in the heart and we have a low cardiac output because there is either usually left ventricle failure cardiogenic shock has a very high mortality rate up to 60 percent and there are a lot of different things get that can cause this drop in cardiac output so acute mi is one of those things you get that stunned myocardium that doesn't work an advanced cardiomyopathy those muscles have remodeled and stretched out and they're not doing anything a blunt cardiac injury so a cardiac contusion will injure cardiac myocardium to the point that it can't bump um severe hypertension will actually strain the heart enough that we get low blood flow cardiac tamponade you know about and then some metabolic issues can cause cardiac depression so there is your flow chart of cardiogenic shock and what i want you to see is that there are several different places where it starts but there's down at the bottom it's cellular oxygen supply decreased perfusion and with that combination impaired metabolism you're going to find that in most of these flow charts right so early in cardiogenic shock and the body is trying to compensate for this low cardiac output state we're going to see tachycardia because that's what the body does when there's low cardiac output you try to speed up heart rate hypotension we see that fairly early and its cardiac output is now down somewhere around 4 liters a minute or less and so you can see that's fairly low it looks a lot like acute decompensated heart failure it really does because what you have is low flow you've got myocardial inability to pump with both of those problems with it too you have increased myocardial demand oxygen demand because you've got this hype it's uh tachycardia that's going to cause increased work for the heart right on physical assessments you're going to see that tachycardia tachypnea you're going to have some pulmonary congestion so you're going to start hearing the crackles in the bases cool flammy skin that's related to the decreasing blood pressure with that with those low blood flow states you have decreased calf refill time because your cardiac output is low stuff's not getting to the end as quickly with these changes in cardiac output we see anxiety confusion and agitation because it's not just cap refill places they're getting shortchanged by cardiac output cerebral perfusion also drops if we have a pulmonary artery catheter in we could we would be able to see that we have increased pulmonary artery wedge pressure pulmonary capillary wedge pressure we would be able to see that as part of part of the system part of preload being elevated and then decreased perfusion for end organ a lot of times we're going to be looking at that urinary output because those kidneys are very sensitive to low blood flow all right with hypovolemic shock this is about not enough in the tank okay so absolute hypovolemia this is actually losing fluid volume so we could have hemorrhage that's usually a great place to lose intravascular volume and then if you look at these other things these are extreme diuresis or fluids being expelled from the body in one form or another so extreme vomiting and diarrhea fistula drainage so our patients with ileostomies and colostomys if they have issues with increasing drainage diabetes insipidus you guys should remember from care1 go back and retrieve all that stuff hyperglycemia that's going to pull extra fluid when it spills over in the kidneys and then diuresis from could be from any sort of diuresis so what that's doing is either blood is leaving the body or fluid is leaving the body and blood is becoming more concentrated but either way the number uh the amount of volume in the blood in the blood vessels is down okay so with relative hypovolemia what we've got is the total body water is not low but what happens is the fluid volume moves from the vascular space into a cavity or extreme anasaka so lots and lots and lots of edema think back to that patient that we looked at with the when we did burns in care 2 with all of that massive edema we call this third spacing it's moving from the vascular space into a potential space so we see ascites we see plural effusions we see this enormous fluid volume lost so what happens is the fluid goes there and the amount of fluid in the vascular space drops off so you can see from this patho map that whether it's relative or absolute you've got this continued you know decreased stroke volume decreased cardiac output decreased perfusion ending with impaired cellular metabolism so what we're going to do about hypovolemic shock is going to depend on the reason that it happens so if it's a relative hypovolemia we're going to work on moving fluid back from wherever it's gone if it's an absolute hypovolemia we're going to need to either replace blood or fluid most people can accommodate about 750 mls of blood loss or fluid volume being down 750 mils after that we start having start seeing some symptoms it is going to be affected by it by injury if it's a result of hemorrhage from an injury age um the more co-morbidity someone has the less well they're going to do and if you look at these you're going to see a lot of similarities between hypovolemic shock and cardiogenic shock you're going to see the tachypnea tachycardia we're going to have lower stroke volume because there's there's just literally not that much to pump we're going to have urinary output dropping off because there's not as much to pump and usually if the blood loss is greater than 30 percent that's kind of the point where we start getting really serious about replacing blood all right neurogenic shock is kind of the odd um odd man out here so with distributive shock the problem is the fact that the tank got bigger okay it's not that the heart's not pumping and it's not that the the blood supply is low the problem is vasodilation so now there is a lot more space for the blood to go so it's not going to get back and be pumped back out this usually is going to happen neurogenic shock happens with c with t5 and above spinal cord injuries and it can last a really long time this is a long process to fix neurogenic shock so we can also see a temporary neurogenic shock when we're using spinal anesthesia because everything below the level of the um where the where we've done the procedure everything below it vasodilates so we have some hypoperfusion some vaso some um venostasis and sometimes we have to give them a little bit of a presser vasopressor to bring blood pressure back up um you guys that are in ob this quarter um you've probably seen a little bit of this when you go to do the c-sections where you go to watch the c-sections because basically that drop in blood pressure it's a form of neurogenic shock it's just very very short term now think about that for over a course of six weeks that's more like what we see in true neurogenic shock with our spinal patients all right so if you look at the the path for neurogenic shock what's here at the top is different so we've got loss of sympathetic tone but you start get down to about this point with the blood pressure and it starts to look like all the others it's decreased venous return decreased stroke volume decreased cardiac output decreased oxygen supply perfusion and ending with a metabolic state that the patient cannot survive with so from what we what you know about neurogenic shock we lose sympathetic nervous system stimulation so this is the only form of shock where what we have is bradycardia and the rest of them we're going to see tachycardia but the sympathetic nervous system in these patients is not going to kick heart rate up so we get hypotension and bradycardia with neurogenic shock they lose temperature control because everything is vasodilated so the skin is going to be warm instead of cool and glammy they're going to be warm particularly below the level of injury all right with anaphylactic reactions this is your allergic response with these um mediators so you get exposed to an allergen your body reacts to it those cytokines bradykinins and histamines bring that vasodilation not only that but they also make those capillaries leaky which is where all the edema comes from so you get all these vasoactive vasodilators released and then it becomes distributed it's not about how much blood there is it's about where it is distributed in the body that's distributive shock has to do with distribution of the blood supply so with anaphylaxis you you guys we've talked about anaphylaxis back in care 2 when we did allergies or sorry care 1 when we did allergic response so a lot of times what you're seeing is anxiety confusion these people have a sense that i'm going to die it's an impending doom sometimes they may have chest pain a lot of times we're having some sort of edema and some sort of respiratory distress and then along with that comes the circulatory failure from distributive shock may have a high risk of losing an airway from laryngeal edema may lose an airway from lips and tongue being swollen from angioedema and then the sec the last kind of distributive shock is septic shock so this is we think about sepsis as being an infection but it's really this whole inflammatory response that is has come as a result of infection it's not the infection itself it's this whole inflammatory inflammatory response if it's severe sepsis it's severe enough then we start having organ dysfunction so we have organs that start shutting down has mortality severe sepsis has mortality rates up to 50 percent so with sep septic shock we have a documented or suspected infection and we've got hypotension that is resistant to fluid resuscitation so if we have a hypovolemic shock related to an infection we can make that better with fluids you got less fluid you put fluid in you fix the problem with septic shock it's once again it's not about the amount of fluid that's in there it's about where it's gone so what we've got is inadequate perfusion related to this decreased cardiac output because of inflammatory mediators that have caused vasodilation so this um flow chart is a little bit more uh complex but you can see all this mess up here at the top this is all inflammatory system um interleukin cytokines um all this stuff up here vasocon vasodilation permeability all of this mess up here is inflammatory response but what we get out of this inflammatory response we get endocardial or myocardial depression but you look down here at the bottom we've got decreased oxygen supply we have decreased tissue perfusion and impaired cellular metabolism it this the end state is decreased perfusion decreased metabolism all right so when we're looking at septic shock there are a few things that are a little bit different with septic shock we get microthrombi and occlusion of some microvasculature we also get increased coagulation so blood is clotting and it's not being broken down and this is a result of some of those inflammatory response changes initially we get increased cardiac output and decreased vascular resistance because we've initially got this tachycardia and vasodilation together but the distribution that's why we call it distributive shock has to do where the blood flow is going is a problem we also get a decreased ejection fraction and you get a little bit of dilation of the ventricles they start stretching out to increase stroke volume so that cardiac output stays up what we're going to see with these patients we see tachypnea and hyperventilation remember hyperventilation is going to blow off more carbon dioxide so they're going to have a respiratory alkalosis as they move towards respiratory failure then we may start seeing an acidosis but with that hyperventilation and tachypnea that's going to push them towards a respiratory alkalosis we're also going to see decreased urine output altered neurostatus so some of these other signs of decreased tissue perfusion and end organ perfusion sometimes we also see gi issues because part of the fight-or-flight system is to turn off the gut so that's your your body de-prioritizes the gi system to shunt blood elsewhere all right so obstructive shock this happens when deep when cardiac output drops off because there is something anatomic something blocking um blood flow so maybe from compression like we would see in cardiac tamponade or tension pneumothorax we may have it see it from compartment syndrome so patients with a lot of fluid shifting into you know as a psyche so fluid shifts into the belly swelling of bowel where that abdominal compartment gets tighter that can actually decrease blood flow it can compress decrease blood flow coming in sometimes you get aortic pressure that's going to decrease blood flow on the way out so there is your flow chart and if you look down here at the bottom once again oxygen supply tissue perfusion cellular metabolism that is the common common pathway between all of these types of shock so with obstructive shock we're going to have decreased cardiac output the afterload is going to be increased because there's a blockage that's keeping blood flow from flowing out so we're going to have a higher pressure in the afterload system and those filling pressures are going to be all over the place we have to figure out very quickly what's going on and immediately treat so if you think back to what we know about tension pneumothorax and cardiac tamponade those things have to be dealt with very quickly so when we look regardless of the category of shock we talk about four different stages and they're not quite as discreet as we would like to say there are four stages and people are either in one or the other it's more like a continuum so with the initial stage we're not really seeing a whole lot of clinical manifestations at this point at this point the metabolism has changed at the cellular level and it's now on anaerobic metabolism because it's not getting the o2 it means and so we end up with this lactic acidosis the liver's got to filter all the lactic acid it can't do that because it can't get oxygen either with the compensatory stage the body is trying to shift things around and adapt to this anaerobic metabolism and keep everything stable there are some neural hormonal and biochemical compensatory mechanisms this is the compensatory stage of shock if you wish to stop the video at this point and take a look at that that would be fine but you look down here at the end result and it is still you know this is how we fix it down here all right in the compensatory stage this is where those baroreceptors are sensing that the blood pressure is dropping that the cardiac output is dropping and it's going to kick that sympathetic nervous system this is where it engages so that it's going to try to shunt blood to the heart and brain particularly it's going to de-prioritize some organ systems and try to protect heart and brains can protect vital functions all right so this sympathetic stimulation anytime you have sympathetic stimulation you're increasing myocardial contractility increasing myocardial oxygen demand and that is going to you know temporarily increase blood blood flow but it's you've got a low flow state so it will only keep it up for so long it only compensates so much um some of this is involves a vq mismatch that gets done it starts bypassing part of the lungs you get some vasoconstriction in areas of lungs so that blood gets back to the heart faster unfortunately that means that arterial oxygen levels are going to go down in order to compensate for that the body kicks up respiratory respiratory rate to try to pump oxygen in and out and make the best of the situation with gi motility that's going to slow down and there's really a big risk for paralytic ilias with these patients they usually look cool and pale um accepted patients may be mormon flushed and early neurogenic shock is warm and flushed so this decreased yet decreased endorphin perfusion to the kidneys and at that point the kidneys start screaming for things kid the angiotensin renin system gets kicked in you get more venous return and you get aldosterone release which stimulates adh so you start trying to retain fluid bulk up the blood supply so some body is able to change compensate for some okay at this point we can if we if we can fix it we can the patient's gonna emerge relatively unscathed if not if we can't fix it at this point then the patient is going to move on to a more progressive and worse off state so at this point those mechanisms that sympathetic nervous system the aurin angiotensin system they all begin to fail and these patients are going to the unit period all right there is the progressive stage of shock this is kind of where we go from we flip from that um anaerobe this um respiratory alkalosis to a metabolic acidosis because we get more of that anaerobic metabolism more of that lactic acidosis and the body can no longer compensate with the respiratory system can't make up for that right so with the progressive stage we're getting more and more decrease in perfusion to the cell at the cellular level and as a result all those cytokines and that whole inflammatory process that gets released when anaerobic metabolism happens causes more and more edema interstitial edema and as proteins leak into that space it's going to pull more fluid more water into that space as well what we see in progressive stage we get because of that those proteins leaking through water following the proteins we get absolutely it's called anasaka and profound edema doesn't even begin to describe what's going on everything gets leaky and swollen so this is one of those places where we can add obstructive shock from fluid leaking into solid organs and other tissues it still cranks down blood flow from pulmonary cavalry so we're going to get even less oxygen moved across and a lot of hypoperfusion so getting really weak or absent peripheral pulses and we can also have vasoconstriction to the point where we lose circulation to the periphery so hands feet may actually become ischemic with the metabolic and oxygen distribution changes that we see in progressive stage of shock this is where we start seeing myocardium suffer from the oxygen deprivation so we get those dysrhythmias ischemia possible mi and eventually cardiovascular collapse we also see fluid going into the interstitial pulmonary space so it's moving out of not just the periphery but also moving out in the lungs as well so we'll see that pulmonary edema bronchoconstriction all of those kind of full irritated airways and the patient won't be able to maintain respiratory capacity so with those respiratory changes it's just like any any other disorder with lots of fluids so edema you get decreased surfactants so you get more atelectasis actually get crackles work of breathing goes up you get gi ischemia because we've remembered the body has deprioritized gi circulation in order in a last-ditch effort to save heart and brain so that mucosal barrier is pretty fragile and requires has a fairly high blood supply requirement so at this point we're having ischemic bowel and which you know ulcerates has gi bleeding and anytime you have ischemic vowel bacteria is going to move out of the gi space either into circulation or into the peritoneal space and so you've got a risk of bacteremia or peritonitis or both okay with that hyper hypoperfusion you also get decreased circulation to kidneys which isn't just about um urine output it's not just about filtering things but you actually get kidney ischemia at this point tubular ischemia those nephrons start to die off and sometimes we're using nephrotoxic drugs that are going to make this worse we will see decreased urine output both from perfusion and from loss of renal function and you'll see those the bu and creatinine go up and part of what you're going to see from this renal failure is a metabolic acidosis that's part of it's from the renal failure and from the lactic acidosis all right with the liver failure as the liver loses oxygen supply you get loss of immune function you get coagulation difficulties may have dic with a lot of bleeding you may have drugs that build up because they can't be metabolized now in refractory stage you just kind of take all of this dreadful stuff we've already talked about and turn it up okay so there is much great increase in anaerobic metabolism because you not only have this hypoperfusion but now you have all this extra fluid within the interstitial spaces that is also delaying oxygenation oxygen diffusion and carbon dioxide diffusion and lactic acid movement out of the tissues and into the bloodstream and as that happens those tissues become more fragile they become those capillaries get even more permeable and so it's just really an ugly cycle and with the refractory stage of shot this is where it's really difficult to do anything about this at this point that's why we call it refractoring so you have worsened tachycardia you've got multi-system organ failure and a patient in refractory shock it's very unlikely that they will survive right so diagnostic studies like i said shock is a syndrome that's related to something else it's not a disorder of itself it doesn't happen without something else attached to it so there's not really any single study diagnostic test imaging that's going to say yes this patient has distributive shock or yes this patient has hypovolemic chalk so we're putting this together from hemodynamic monitoring we can look at lactic acid levels that tells us about anaerobic versus aerobic metabolism they're going to need continuous ecg monitoring we may get a chest x-ray looking for sepsis we're looking for heart failure and then the hemodynamic monitoring is going to help us as well if we can prevent shock that's always a better option than treating shock so we need to be able to look at our patients and know what their risk is what is their risk for sepsis what is their risk how much blood did they lose are they at risk for hypovolemic shock what does that myocardium look like what is how big was that am i are they at risk for cardiogenic shock how high is that spinal cord spinal injury are they at risk for neurogenic shock so it's really important that we look at our patients with an eye as to rescue i would rather prevent than have to rescue so we need to put together the patient's history our clinical findings so we're going to be putting together a lot of pieces to decide to decide who's going to be at risk and who's in early shock so a lot of our interventions are going to be targeted at fixing the problem eliminating the cause so if the cause is hypovolemia then we need to put more volume in the tank if the problem is cardiogenic shock we need to fix the pump if it's neurogenic shock we need to make the tank smaller if it's obstructive shock we need to fix whatever the obstruction is it's all about eliminating the cause of the shock state while we're doing that we're going to be doing supportive care we can't just support we got to fix the problem too so for some of our problems we're going to be rehydrating we may be giving medications that improve myocardial contractility we may be supporting renal function supporting liver function generally we want a patient who's responsive we want a patient with an airway and we want to make the most of the oxygen delivery system so increasing supply we need to we may need to do fluid replacement we may need to transfuse especially if they've had blood loss we need not just gas in the tank but we need trucks to carry oxygen so we need more hemoglobin what we get that is transfusion we may need to supplement oxygen or if they are on their way to respiratory failure mechanically ventilate these patients but we have to stop the hypoxic state all right for septic hypovolemic and anaphylactic so your low blood pressure flow states the first thing that we got to do is fill the tank so large for iv is preferably two may use an intraosseous device or a central line and they're going to get both crystalloids and colloids so we usually think three liters of crystalloid to a unit of colloids that's sort of the rule of thumb we're going to want to use isotonic crystalloid so saline or lactated ringers remember if they're going to need if you're plant looking at planning to give blood you're going to want saline over lactated ringers if they're going to the or anesthesia likes lactating ringers colloids would include albumin the head of starches plasma blood anything that's not a crystalloid all right with that volume expansion we really decide how do we know it worked well vital signs stabilize the heart rate comes down blood pressure goes up um we have good urine output we have good cap refill so those are our signs that we have filled the tank and that really is truly how we do that with large volumes of with large amounts of fluid resuscitation um there is always a risk if you dump three liters of crystalloids room temperature crystalloids in somebody you are going to induce hypothermia so we prefer to use warmed fluids sometimes units have warming fluid warming systems sometimes we're using fluid out of a fluid warmer it looks kind of like a big freezer but it warms like a blanket warmer but the top has a different temperature and it's appropriate for fluids sometimes with the large volume expansion those coagulation factors get diluted and so we may have coagulopathies we can address that with plasma administration because fresh frozen plasma has coagulation factors in it if we have filled the tank and filled the tank and they're still hypotensive that's really when we look at adding a vasopressor because we don't just want to keep filling the tank with crystalloids especially we may need to add a vasopressor until we can finish solving the problem that started this in the first place all right that's all just talked about those things colloids crystalloids colloids and colliding factors and warm it up if you can all right so when we're looking at drugs what we're trying to do is correct a perfusion problem so not necessarily a volume problem we're looking at perfusion we want if we have to we're concentrating on end organ perfusion we want a map somewhere between 60 and 65 and like i said we're gonna we're gonna try fluid resuscitation first and if that doesn't work to get us that map then we may move to pressers sometimes with the pressers we can actually impede end organ perfusion depending on how much we have to run to keep that map up so we we do try to very we're very cautious about making sure that we're monitoring urine output because that's kind of our our that's the canary in the coal mine about perfusion and looking also at cerebral blood supply so looking at those level of consciousness changes sometimes we have to have vasodilator therapy and we're still looking at that map between 65 so we may need to decrease afterlife especially with our obstructive shocks i have had patients that i had vasodilators and vasoconstrictors running at the same time so that we could get that map right in that sweet spot of 60 to 65. all right so we also we want oxygen to the end organs but we also have to provide building blocks for healing and other forms of other fuel for metabolism so we need to if possible feed them early if they have bowel sounds we need to get it started as quickly as possible um if we can't do internal feeding so if they've got a paralytic ileus if there's no bowel function then we're going to have to move very quickly to parenteral nutrition so move into tpn we know that this is going to decrease morbidity and that's really what we want to do we want to decrease morbidity and mortality so we want to start very slow if we're doing enteral feeding we want to start slow slow continuous feeding we need daily weights we need protein albumin pre-albumin levels we need because that's going to give us some some important information bun for renal function glucose because tpn always interferes with glucose and then electrolytes because these patients are going to have issues with electrolyte shifts all right cardiogenic shock is kind of one of the odd man out because what we have to do is restore blood flow to the myocardium so we've got to do something the whole end organ perfusion issue is coming from a pump failure so we have to fix that problem so they may need angioplasty to treat um ischemic infarcted myocardium we may need an emergency bypass we might need an emergency valve replacement these patients are going to need hemodynamic monitoring we have to know what all those pressures are in there they may be on nitro to deal with to open up coronary arteries may have diuretics and some of this may actually seem kind of counterintuitive i mean their blood pressure is low so we're going to give them nitrates and diuretics and vasodilators what we're trying to do is decrease afterload so that that heart can pump more efficiently this is where we may use the aortic balloon pumps and dry aortic balloon pumps to assist pumping function right there that's what i just said we also may end up having needing heart transplant sometimes these patients are in extensive cardiogenic shock and may need these assist devices until transplant all right with hypovolemic shock we're looking at first we have to put stuff in the tank the fluid resuscitation but we're also we have to stop whatever is wherever the leak is wherever the loss is whether it's bleeding or vomiting whatever the source of the hypovolemia is we got to stop it otherwise we're just going to end up pouring more fluid in so like i said fluid resuscitation is three ml per one mil so every one mil of blood loss we're putting three in and then these patients with septic shock they're also going to get fluid resuscitation we're going to be titrating it a little bit differently because we're going to have hemodynamic monitors so we're going to be looking at afterload and preload and trying to hit that sweet spot a lot of times they will need vasopressors and then sometimes we need vasopressin usually with the vasopressors we're using norepinephrine dopamine is kind of old school but sometimes we end up using vasopressin with septic shock sometimes we need corticosteroids because remember this is about a systemic inflammatory response so sometimes we need corticosteroids to tamp down that inflammatory response with sepsis we're going to culture and antibiotics within an hour this is a priority um we're going to give broad spectrum antibiotics and then narrow it down when cultures start coming back right with septic shock we don't really want to keep glucose quite so tight we're not looking at 180 80 to 110 we just want it to be less than 180. we know that the tighter we keep it you know these patients have an incredible metabolic demand and so if we can keep those glucose levels a little bit higher they're going to have more fuel more fuel to fight we do want stress ulcer prophylaxis with these patients so they're going to get ppi's they're going to have vte prophylaxis so get your heparin or your anoxiparon ready with our neurogenic shock with our spinal cord patients we need to stabilize that spine um we're going to treat the hypotension and bradycardia because remember neurogenic is hypotension bradycardia we're going to treat the bradycardia here with atropine we're going to treat it with atropine because it's bradycardia with hypotension plain bradycardia we're not going to treat if they're if they're 50 beats a minute is keeping a normal blood pressure we're not going to worry about it if they're hypotensive and bradycardic that's when we treat hypoten treat the bradycardia the hypotension we're going to treat with vasopressors we usually don't bolus these patients with fluid because it's not a fluid problem it's not a pump problem it's where is the fluid where is it gone problem and these patients are at risk for hypothermia all right so with anaphylactic shock we've talked about how we deal with anaphylaxis so that's going to be just like any other severe allergic reaction we're going to fix the problem which is epinephrine antihistamines ranitidine so epi epi benadryl and renitidine um we have a priority on airway because of the risk of airway loss due to the edema with the bronchospasm we need bronchodilators so this is you know treating anaphylactic shock kind of focuses initially on stopping the anaphylaxis we may need to intubate or strike these patients or do a cricothyroidotomy to save an airway and with shock with these patients we are going to be very aggressive with crystalloids um corticosteroids says corticosteroids if significant um they're going to get cardio steroids much earlier than a shock situation as soon as they have some systemic allergic response they're going to get corticosteroids with obstructive shock we need to make sure that we are recognizing this early so those mechanical decompressions so with tension pneumothorax making sure that we recognize that with cardiac tamponade that we're recognizing that if they have a large pulmonary embolus that is an obstruction making sure that we get those thrombolytics done getting them to the cath lab so that they can retrieve a clot with a mass that may be obstructing emergency removal of that mass or debulking of that mass and if they have swelling in the gut that is causing it we may need to open their belly um and decompress then their belly may stay open until that swelling goes down and then we'll go back and close all right anytime we see patients in shock it goes back to the abcs airway breathing circulation those always come first then we're going to look at those tissue perfusion so skin color level of consciousness cap refill what are their pulses like what's that blood pressure are they making any urine and then we need a brief history what happened before they got here um how long has this been going on um for for example our ketoacidosis patients diabetic ketoacidosis how long have they been vomiting how long has their sugar been up when was the last time they took their insulin what was last week well okay we know what we're dealing with um looking at the health histories have they had vaccinations have they been out of the country recently um the this is a list of possible ineffective tissue perfusion possibilities so we have ineffective tissue perfusion is your pro your actual one i would not connect all of these together i would not say risk for all of this mess i would just say ineffective tissue perfusion related to and then whatever the related t was and then of course anxiety this is kind of a terrifying thing um is your patient's really really sick and everybody around them is moving very quickly and shouting at each other trying to get things done so it's really terrifying for the patients goals are we think about the goal as being get that blood pressure up but that's really not it the goal is to improve tissue perfusion because we can't stop that metabolic failure until we have tissue perfusion so it's not just about blood pressure that's part of one of the signs that we're making progress we want organ function to be stable we want to avoid those that acute kidney injury and that those ischemic ischemic bowel and all that other stuff that happens with hypoperfusion so looking at patients who are at risk our older patients are at risk for everything a lot of times they have cardiac morbid comorbidities and so that's going to put them at risk for cardiogenic shock patients who are immunocompromised or have chronic illness have an increased risk of sepsis and our surgery trauma patients they're at risk for hypovolemia right so looking to prevent shock we need to monitor their fluid balance um make sure that we are doing scrupulous hand washing to prevent nosocomial infections or to prevent spread of infection acutely it's going to require a lot of attention to detail um their emotional status their physical status looking at those small changes like you're an output level of consciousness that may clue you in that something bad is about to happen something is going on and then making sure that we're looking at interventions we're going to have to evaluate we're going to have these outcomes that we're going to be titrating all these medications doing all these therapies and we have to make sure that we're not just checking boxes and doing orders but that we are truly assessing how these interventions are working the patients and their families are going to need a lot of emotional support this isn't an event that they plan for this is something that sneaks up and happens suddenly so they are going to need a lot of support and then a lot of coordination with respiratory and lab and pharmacy and chaplaincy service and physicians and everybody is going to have to be on board with the same plan of care neurologically we want to do a lot of things that are going to try to decrease icu delirium so making sure that we're orienting looking at those times and things keeping the light levels down keeping the the noise down so that we're decreasing their stimulation and keeping them on a day-night cycle that seems reasonable from a cardiovascular standpoint we need to make sure we're going to be monitoring a whole bunch of sounds we're going to be listening for s3s s4s because remember one is hypertension one is heart failure um we don't want to treat hypotension with head down positioning we used to do that but we don't really want to we know that's not really good for the patient respiratory status a lot of these patients particularly in late compensatory and progressive shock they're going to be on the ventilator we're going to be intubating on the ventilator trying to regulate some of these metabolic derangements we need to make sure that we're doing continuous pulse ox keep in mind though that for a patient with a hemorrhage or hypovolemia they may have a reasonable pulse ox but because of low levels of hemoglobin they still may be at risk for hypoxia renal status that's going to be urine output and bun creatinine need to make sure that we are looking at those temperature changes with the rapid fluid resuscitation they're at risk for um hypovolem hypothermia our patients with neurogenic shock are on their way to becoming one with the room temperature our patients with sepsis may be febrile or they may beginning to slip into a hypothermic situation standpoint we're going to need to listen to bowels make sure that we're not feeding someone with no bowel sounds that we select the appropriate kind of nutrition for them need to make sure that we are looking for occult blood because if we have ischemic bowel we may have be finding occult blood we need to turn regardless we need to make sure that we're watching those sets when we're doing our nursing activities because even a bath increases oxygen demand emotional support we need to you guys know how to do this drugs only if we need them but making sure that we're talking that we're involving their caregivers that we're giving them privacy and then making sure that we're getting these patients rehabilitated we've we have to correct the cause um we have to prevent complications and then we're also going to be looking at okay what sequelae do they have from from their episode of shock evaluation we're going to want adequate tissue perfusion normal function without complications and we want them to be comforted