hey everyone welcome to the module 6 exam review video my name is Justin and I am the EMT instructor at Baton Rouge this video is part one of three and will primarily cover the highlights of chapter 15 shock and resuscitation I want to preface that this week's module is very large containing a lot of information across six chapters we often call this set of chapters medical emergencies one and the exam will introduce even more scenario based questions than you have seen in the previous exams since we have lot to cover let's go ahead and get started and remember that you can pause or rewind the video at any time so we first need to start by defining what is shock and to do that we need to recall the term perfusion which is the adequate delivery of oxygen and nutrients to the cells as well as the removal of waste and shock is simply known as hypoperfusion or inadequate tissue perfusion whenever we have a disruption for the components necessary for adequate perfusion your patient is now at risk of going into a State of Shock and these issues are usually caused due to inadequate volume inadequate pump function and inadequate vessel tone inadequate volume is probably the most common ideology of shock and this is when you have a decrease in blood volume so just imagine your patients that are severely dehydrated or they've suffered some trauma and they're bleeding out everywhere um if you don't have enough blood to deliver your nutrients and oxygen then that is going to lead to hypo profusion probably come up with more obvious examples of loss of volume but just remember to do a patient assessment and make sure you take a thorough history to rule out any other causes for loss of volume such as frequent urination or even excessive diarrhea for the past few days next theology we'll cover is in adequate pump function and this one is as straightforward as it can be right if your pump is not working then you are not delivering nutrients you're not delivering blood and you're definitely not removing any waste from the body most common examples of inadequate pump function is a heart attack otherwise known as myocardial infar you all should be able to break up that term myocardial infar as death of heart muscle and plainly put if the heart muscle is dying or is not working then that will lead to the pump failing a couple other examples we'll highlight here is the pericardial tanod and the tension numo thorax uh we'll probably talk more on these later in the cardiac and respiratory chapters but for now these are just a couple extra examples and so the last ideology of shock will'll cover is inadequate vessel tone and this relates more so to the vessel size due to massive vasil dilation what you have to understand is as the blood vessel vasod dilates to the point where the systemic vascular resistance decreases too much you're now going to have a drop in blood pressure um try to recall from module 2 in your amp chapters where we discussed that an increase in blood pressure generally means that you have improved or better perfusion whereas a drop in blood pressure means inadequate perfusion or inadequate uh blood pressure and so that's why we always Mark that 90 systolic as our cut off for what is considered you know too low this slide is just to kind of give you guys a visual representation of how Vaso dilation or massive Vaso dilation will lead to a decrease in blood pressure right so a normalized blood vessel is full of blood you have enough systemic vascular resistance to generate an adequate blood pressure and when that that vessel gets way too large you just don't have enough volume to fill all that space and that's going to decrease the resistance therefore leading to hypop perfusion or shock so next we're going to cover the four major categories of shock and that's going to include hypovolemic distributive cardiogenic and obstructive some techs like to list a fifth category when the metabolic and respiratory shock uh for the purpose of this exam and what we usually talk about in class we tend to leave out that fifth category but if you want to review it later for your final exam or for the nrmt exam um I'm going to talk about it a little bit too as we progress through the slides for the purpose of this exam you do need to be very familiar with the four categories of shock and we should be able to provide examples for each so hypovolemic shock is probably the most common type of shock out there um and it is also most commonly caused by hemorrhagic shock or the loss of blood um we have a few other examples like Burns and dehydration that can cause low blood volume but just remember that hypovolemic you're thinking about a loss of volume I want to stress that it is due to a loss of volume because I think some students get trapped into thinking that it's only blood loss but hemorrhagic shock is just you know one specific type of hypovolemic shock um we have to consider other examples where a patient is either not getting enough fluid intake or they're losing fluids by other means and so that will fall into the category of nonhemorrhagic shock or uh non-hemorrhagic hypop fmia getting a little redundant here but this is hemorragic hypmic shock and again this is due to a loss of whole blood um as a result you're going to have decreased profusion and decreased oxygen carrying capacity so you know best way to manage this is for one stop the bleed remember that we re we treat those uh those bright red spurting bleeds you know with direct pressure and if it doesn't work we slept on a tourniquet um outside your scope but maybe in the hospital they could replace blood or start uh replacing blood components and all that is to hopefully uh bring back some function of what was lost so another example of hypmic shock is burn shock and I think a lot of students don't take enough perspective into how much Burns affect uh your fluid retention we have to remember that your skin plays a major role in regulating fluid retention in the body and so if if you have enough Burns across a wide enough body surface area um your patient is now at risk of losing fluids um beyond that your capillaries when they become damaged from the Burns will become more permeable and what that means is that you're going to start leaking these uh plasma proteins or your plasma into the interstitial spaces and that's going to lead to edema or swelling in the area uh now we're moving on to the next major category of shock which is distributive shock I feel like students tend to have a harder time understanding the concept of distributive shock or come up with examples but this is the one that is caused by Massive Vasa dilation so recall that we talked a few slides ago that this when the blood vessel gets a lot bigger your systemic vascular resistance goes down and therefore your blood pressure goes down and again without enough blood pressure you're going to lack profusion so a very common example of distributive shock is anaphylaxis or anaphylactic shock we're going to talk more about anaphylaxis in module 7 but this is a severe allergic reaction where your body releases a lot of chemicals to combat the allergen and this is causing massive systemic Vasa dilation and increased capillary permeability so we highlight that epinephrine is the medication of choice for anaphylaxis and just recall that epinephrine contains you know those Alpha and beta properties to you know to give Vaso constriction or increase your heart rate and so it's going to directly counteract the effects of the allergen sepsis or septic shock is another type of distributive shock and this is very similar to anaphylaxis except instead of reacting to an allergen it is reacting to a bacterium or virus or even a fungal infection so again this is going to lead to Vasa dilation and increased capillary permeability and as an EMT you're going to focus more on managing their Airway their ventilation and oxygenation but this patient would benefit from IV fluids or medications to constrict the vessels as well as antibiotics so you know we just highlight here that you could consider contacting ALS or you know just make sure your patient makes it to the hospital promptly so this slide is just a table highlighting the screening tools used to identify sepsis these have like different criterias or scales that uh various systems might use to label a patient as in sepsis or not not it is not relevant to this exam but I leave it here in case you want to review it for the nrmt exam or if you're just curious about it and you want to take this knowledge with you out into the field example of distributive shock is neurogenic shock and this is caused by any spinal cord injury where our nerves are no longer communicating to your blood vessels to vasoconstrict so we call this the loss of sympathetic nerve fer functions and that's also going to lead to the loss of blood vessel tone um so with that loss of systemic vascular resistance again we're keeping into that theme of the blood vessel is vasod dilating or nothing is helping it vasoconstrict and now you are losing systemic vascular resistance and therefore a drop in blood pressure the next major category of shock is cardiogenic shock and this is caused by the inability of the heart to contract a effectively so this kind of goes back to our example of inadequate pump function where you have a heart attack or you have uh heart failure where the ventricles have failed to pump effectively um and so your stroke volume your cardiac output is going to go down and again if your pump is not moving blood well then you're going to have hypo profusion on this slide I'm just highlighting how a heart attack is a c CA of cardiogenic shock remember that if you have damaged heart muscles um it's going to reduce your force of contraction and therefore you're not going to have as much stroke volume and if your cardiac output goes down too much then your blood pressure will also drop and again loss of blood pressure loss of perfusion next major category of shock is obstructive shock and as the slide States it results from a condition that obstructs forward blood flow so we have to consider that the volume is adequate the heart isn't damaged and the vessels are all of normal size with adequate resistance um just something is preventing the blood from moving forward uh typically the causes include a pulmonary embolism where you have a clot in the within the pulmonary arteries uh other great examples are like the tension numo thorax or paracardial tanod where we have a pressure either in the in the plural space or within the pericardial Sac that's compressing on the heart or you know the veins leading to the heart and that's going to cause um obstruction of blood flow and here we have some examples to help illustrate causes of obstructive shock where you have a pulmonary embolism there it's blocking the arteries preventing blood flow and with the tension in with orx you have a buildup of air in that plural space surrounding the lungs and as that pressure increases it'll also compress on the heart to prevent cardiac output with the pericardial tanod you'll see this Blood build up around the pericardial Sac that is also going to put pressure on the heart and prevents cardiac output so you know for your exam you really need to know the examples of obstructive shock will highlight you know the tension numor thorax and the pericardial tanod for the purpose of the exam yall don't really need to know too much about the metabolic or respiratory shock um some sources list this as a fifth category I think in our class we tend to just identify those like issues as what they are so for example if it's carbon monoxide poisoning that interferes with the ability of hemoglobin to carry oxygen we just call it carbon monoxide poisoning um if you want to review or just kind of keep in mind a fifth category in case the nrt asks about it uh here's the slide otherwise we can just move on next we're going to review the body's response to shock so if you call from module two we talked a little bit about the sympathetic nervous system and uh the release of epinephrine and norepinephrine as two major compensatory mechanisms first we're going to talk about direct nerve stimulation and so this is referring to the sympathetic nervous system which is pretty immediate in its effect and we're going to see an increase in heart rate an increase in the force of contraction uh your blood vessels will constrict and it's going to stimulate the release of epinephrine and norepinephrine I know I moved on from the last slide but I kind of want to touch base on neurogenic shock and just kind of help youall keep in mind that if you have a spinal injury where your nerves are no longer connected to the body and it's not communicating to your blood vessels or your heart Etc then you're not going to have those typical symptoms that you see with sympathetic response with the increased heart rate or the vessel constriction and that's kind of the whole point to neurogenic shock is that as you separate that that communication your vessels are going to end up dilating and your heart rate is not going to react to compensate with it um here in this slide we're talking about the body's response to shock in reference to hormones so we said that the sympathetic nervous system will stimulate the release of epinephrine and norepinephrine and these hormones are going to have effects on the adrenal receptors if you remember the alpha 1 beta 1 and beta 2 if you forgot about the effects of alpha 1 beta 1 beta 2 this slide is here for you to kind of just help summarize what they all do um that way you don't have to go back to module two to reread this but I would be very comfortable with the effects of each moving on you definitely need to know how to identify the differences between compensatory shock versus decompensatory shock and compensatory shock is essentially what it means your body is compensating for whatever is causing the body to lack profusion how to tell if your patient is compensating or not and it's a pretty easy your patient might have that pale cool clammy skin appearance and that's due to the blood being shunted away from nonvital areas such as the surface of your skin uh but what you really should Define as compensatory is whether the body is able to maintain the normal blood pressure and therefore perfusion of your vital organs so it's two main criteria we look at the blood pressure being above 90 systolic or if your patient is becoming Al altered or having you know they're losing Consciousness then we're going to say they are not compensating anymore if they're no longer compensating then they are decompensating and so this means that whatever your compensatory mechanisms are doing whether it's through an increased heart rate increased force of contraction or vessel constriction none of that is working anymore and now your blood pressure is starting to drop so where we said that compensatory shock is when your blood pressure is above 90 systolic and you have a normal mental status decompensatory shock is when your blood pressure Falls below that threshold of 90 and you start to see signs and symptoms of confusion or In and Out Of Consciousness or they're losing responsiveness so the biggest takeaway from this slide is you should not rely on any one finding sign or symptom so if a patient just has pale cool clamy skin you can't just say that your patient is in shock or if they have a high heart rate you can't just automatically assume they're in shock you have to have the whole picture so you need to have a good history you need to do a good physical assessment you got to have you know a little bit of common sense to what happened before you were called and then how your patient is currently presenting and if you can recognize signs of shock then you know that's the key to the whole thing cuz that's when you're going to decide how immediate this transport is uh What treatments you can even consider useful and where this patient needs to go a key takeaway from this slide is that if you do a thorough history you might figure out from your sample that your patient takes certain medications we're going to highlight here that beta blockers and calcium channel blockers can alter the patient's response to shock so these drugs typically act on the heart where they may lower the heart rate in order to lower and manage the patient's blood pressure and if the patient has any of these medications in their system then their body might not be able to compensate as well so like you might not see typical signs of uh increased heart rate if they're taking a beta blocker for example here we are talking about the physical exam and the vital role that plays so again if they are compensating their vital signs might look normal you're going to have an maybe a slightly elevated heart rate you might have a normal blood pressure and your spo2 will appear fine but if you're a patient I don't know flew out of the windshield and now they're laying in the street and you know they're walking around with pale cool clammy skin they got a giant bruise across their abdomen um that's a pretty good sign that your patient is in shock and just simply compensating right now also want to have some age considerations so elderly people they tend not to compensate well at all they uh deter detate very quickly whereas children or young you know young adults they tend to compensate very well but then when they do crash they crash very quickly and so just you know keep these ages in mind and how they influence the development or management of shock um you know it's a it's a crapshoot either way so as we wrap up shock um I just kind of want to highlight that shock means you know in an Essence that your patient is is dying so the whole point of recognizing shock and learning the management of shock is to extend the time of how much your patients have before they eventually meet their demise and so hopefully you've made it to a hospital in time hopefully they've made it to the appropriate centers for surgery or whatever treatment they need to reverse the symptoms of shock or reverse whatever place them into a State of Shock And if you don't make it or if uh you know despite all our best efforts efforts sometimes your patients will expire and now we go into our talk about resuscitation and cardiac arrest um we're going to Define cardiac arrests is when the ventricles of the heart are not Contracting or maybe they are Contracting but the output is not enough like it's in effective to where you can't feel a pulse therefore nothing is being profused anymore so here in this slide we highlight that your brain cells will begin to die within 4 to 6es minutes uh following a cardiac arrest and you know this definition of cardiac arrest where patients are described as having suffered sudden death within 1 hour of the onset of the signs and symptoms we often say that the patient goes through three phases of cardiac arrest before they lead to biological death and it's highlighted here as the electrical phase the circulatory phase and the metabolic phase I want to talk more about the electrical phase because this is considered you know the first minutes of cardiac arrest where the heart still has supply of oxygen and glucose and you still have uh favorable conditions and therefore you know defibrillation is very important here so if you witness a cardiac arrest and the patient is in vtac or V FIB something that is a shockable rhythm then our aeds can quickly be attached and we want to defibrillate as soon as possible and this is going to give us the best chance of resuscitation once we go beyond the electrical phase things get a little bit harder so now your oxygen stores are depleted your heart cells are switching to the anerobic metabolism and so they're producing all this lactic acid and you know you're having the destruction of cells and cell function so this is where good compressions high quality CPR comes into effect and you're going to restore your supply of oxygen and glucose as best you can um and hopefully your patient will still be responsive to defibrillation if they have a shockable rhythm and again not as good as the electrical phase but we're still kind of holding on to Hope here that we can resuscitate the patient successfully when we get to the metabolic phase which is the last phase of cardiac arrest this is when things start to look uh very Grim um these take a while you know 10 minutes after cardiac arrest according to the slide but essentially your heart muscle is so acidic so es schic that they're dying and they're at the point of no return and so you know once your cell dies there's no bringing those cells back to life because of the extensive damage that was done due to the buildup of metabolic waste and here you have your chances of resusitation are very unfavorable and not very likely your patient probably isn't in a shockable rhythm anymore at this point they're more likely presenting an asy or even paa on this slide we're talking about withholding resuscitation so we're kind of recalling those DNR orders those do not resuscitate orders uh just keep in mind that you have to work your patients unless you know proof of this DNR order exists and it has to be signed by the physician and the patient has to be you know within the proper date and again the original copy should be presented on scene for you to withhold resuscitation otherwise you're going to work the patient otherwise uh if you have injuries incompatible with life so if the person is stiff and they have been dead for several hours then we don't necessarily have to work them another obvious sign of death is you know decapitation and I always joke with my class if I ever catch any of you guys doing CPR in the body and ventilating the head that's like several feet away you know I'm just going to pretend I don't even know you that being said uh going back to the beginning we want to defibrillate our patients early um assuming that they are a workable patient and the most frequent initial rhythm in sudden Cardiac Arrest is called ventricular fibrillation and so that is when your ventricles they're not necessarily cont racting all at once they're fibrillating and when we say fibrillating it's described as like a quiver and so the most effective treatment for V FIB is to defibrillate it and when you defibrillate you're sending like a large amount of energy through the heart to basically you know hit it as hard as we can in hopes that we can stop all that nonsense and by stopping that nonsense we're hoping we can restart uh a normal functioning Rhythm however for the fation to be successful we also need very effective CPR so we want to stop the viib as soon as possible but we also need to perform high quality CPR getting good chest compressions and ventilations in so that we can supply that heart muscle with more oxygen and glucose and all the good stuff that it needs as well as removal of waste um this way the heart is primed and ready so that when you do defibrillate it it is going to go back to a working rhythm you know hopefully this should all just be kind of reviewing your BLS CPR but remember to push hard and fast your compression should be at a rate of at least 100 a minute and your compression and ventilation ratio will be 30 to two you should try to minimize interruptions or not be off the chest longer than 10 seconds and uh avoid excessive ventilation so we can't talk about defibrillation without talking about a ads aads are in the ENT scope of practice and they are very useful and that they are safer usually you can stay hands off with the ad as in after you apply the pads and it's time to defibrillate the patient no one has to touch anything except for the shock button um some argue that it is more efficient monitoring because the manual ads require interpretation from a person or paramedic and so the AED is not as likely to mess up um I don't know I always argue that the paramedic is still faster but you know they do have a chance of getting things wrong so the drawback to the a is it cannot determine if your patient has a pulse or not so once you slap it on it's going to analyze the Rhythm and it's just going to determine whether it needs to deliver a shock or not but you as The Rescuer provider needs to determine if the patient has a pulse or not and whether CPR should be started and whether you even need an AED to begin with when the AED is on and it's analyzing the patient it's looking for V FIB or vtac as its shockable rhythms and The nonshockable rhythms are asy and pulseless electrical activity otherwise known as pea while it is analyzing the patient no one should be touching the patient at all uh during the analysis stage and obviously you shouldn't be touching the patient during the shock delivery as well um any movement will interfere with the Rhythm analysis and then you're going to kind of trick it into thinking its Rhythm that it's not uh the safety risk here is that energy can be transmitted to anyone touching the patient so we always want to make sure we clear the patient before we analyze and before we shock the patient um I will kind of add on here that once your AED is applied to a patient even though you get a pulse back or if you've delivered a shock you never turn the AED off right so we're always going to leave the pads attached and keep the AED on uh for the remainder of that call until you get to the hospital as a note we always say that manual defibrillation is preferred for patients that are younger than a year old um we can kind of control the amount of energy being delivered because we can calculate the patient's weight and size uh but here on the slide I just kind of wanted to show the placement of the pads it's going to be the exact same as you would on an adult um if you're if you're only stuck with adult pads instead of the Pediatric pads shown they kind of still fit in the same vicinity on that TP top right and the bottom left but if it doesn't fit then you just put one on the front and then one on the back as we're talking about infants uh if they have a heart rate that is is should say less than 60 with inadequate ventilations then you need to start CPR and so if you have the BLS team performing CPR so if it's a single rescuer you have 30 to2 ventilations but as soon as you have two Rescuers or a team is present then you're going to modify it to 15 to two so that's 15 compressions two ventilations if you have more than one rescuer on I don't want to rehash all the details of doing CPR on adults again but I do want to highlight this last bullet point here that if you are dealing with the pregnant patient then we have to displace that uterus laterally um so that means that you know we're going to just kind of push it over to the side while we do chest compressions and it's probably better to push it to the patient's left side because we want to get that weight off of the venne Cava that inferior vnea that's running along the right side of the body um again sorry if I'm speaking fast I'm just trying to wrap this up to stay close to 30 minutes I know I just went over this in the previous slide but here it is again um for you guys to read it and just kind of digest that information so when you encounter a patient in Cardiac Arrest we don't want to just load and go you typically want to lay the patient Supine and start compression start CP are if you have an AED attach that as soon as you can if not then you need to send someone to retrieve it um if ALS is not responding then you can transport but only if the patient regains a pulse or if your protocol indicates you know you guys have reached a certain point where it's time to load and go uh but for most agencies most protocols we want to stay on scene and work the patient at least a little bit whether it's delivery of at three shocks or work him for at Le at least 10 to 15 minutes before we even think about moving that patient so assuming you do get rasque or return a spontaneous circulation you know now you got to figure out well you know we got them back what do we do next so if we can feel a pulse after the ad indicates that no shock is advised then it means that you have return of spontaneous circulation if the patient starts breathing on their own I don't really like that one because sometimes your patient will have uh you know some kind of respiratory response even though that their heart isn't functioning um and if your patient begins to move again this has to be more so like your patient is moving you know I don't want to say consistently but more purposefully uh when you shock or defibrillate your patients they tend to do like a sudden jerk you know where where their hands might like kind of flop up so that's not the movement you're looking for you're looking for them to almost be like responsive to the pain um type of movement and here we're just going to go over some special considerations for the a remember that we want to make sure that everyone is clear and not touching the patient during the an analysis phase as well as during delivery of a shock uh we don't want to defibrillate a patient that is like covered in water or at least like sitting in a pool of water so we want to dry them off as best we can after removing them uh we don't want to well we got to be careful about Metal surfaces so just like we said it can jump from one person to another well we should kind of recognize that metal or metal surfaces are also High conductors of electricity so you know if we can help it maybe try to move them to a surface that doesn't conduct electricity well or put something underneath them um we want to remove any transdermal medication patches on the chest and so like if you have a you know a fentanyl patch or any other medication patch nicotine patch that's on the chest you want to get it out the way and of course if there's excessive chest here then we should shave it off so that we can get better placement with those pads and uh not burn the patient I will say a lot of emphasis is placed on the operations of the ad or even the you know the progression of CPR and progress It's it's one of those calls that gets really hectic in the first few minutes and it takes a lot of practice a lot of understanding of what your role is in the in the cardiac arrest between you and your partner and so you know we want to just kind of nudge you guys to refresh and maintain your skills you know talk to your qi see talk to your partner uh the AHA will update make updates every few years or so and you have to recertify every two years so this is always a helpful thing to just revisit and constantly stay in tune with so that you can always be a deliverer of great CPR the biggest thing I'm trying to highlight from this slide is the placement of cardiac pacemakers so like if there's a if there's a pacemaker implanted under the patient's skin you don't want to put the AED pads directly on top of it we kind of want to just move it off to the side um so we're relatively in the same area that we're supposed to be but just off to the side and not directly on top of the pacemaker for those of you that have never seen one it can kind of look like this and then planted pacemaker under the skin and this is just to highlight that besides pacemakers some patients also have implanted defibrillators which we'll work on its own again never put your ad pads directly on top of it if it's working on its own then try to let it complete its cycle before you attach your AED um on that note that's going to wrap up chapter 15 shock and resuscitation I hope that it'll help you for the exam and we have have two more videos to cover respiratory and cardiac emergencies and then the rest