Intern Content: Approach to Shock – OnlineMedEd



you shock is a very difficult concept we're going to talk about it over the next three lectures finishing with a particular type of shock septic shock in this first lecture what I want to do is give you a method for approaching hypotension in general and see how it correlates to shock I will warn you because I have come up with these concepts and these words and these nomenclatures myself and I use them a little different and they are in the literature so if you go read about shock you're going to hear the same words but in those papers they're regarding something a little different so as you begin this I want you to just explore a method for approaching hypotension and then a framework for what the body looks like in reference to different types of shock this is going to set you up for the approach to shock before we move into how to pick a base oppressor and then finally septic shock let's start off with the first method for building a differential and it's a good equation it is the mean arterial pressure is equal to the cardiac output times systemic vascular resistance cardiac output is made up of heart rate and stroke volume stroke volume is preload times contractility the first thing to recognize is that the body wants to maintain a mean arterial pressure such that if the cardiac output Falls it will compensate by increasing systemic vascular resistance if any one of these three components of cardiac output fail the body will attempt to adjust by increasing them all and systemic vascular resistance if systemic vascular resistance Falls the body will compensate by increasing cardiac output by increasing any of the three elements of cardiac output that it can adjust the classic way of looking at shock doesn't help you choose what to do next which is why I don't use it but let's discuss briefly I'm going to put it down here in really small print so that you know to mostly ignore it the classic models of shock include distributive shock cardiogenic hypovolemic and obstructive and you'll see the dashed line down here this dash line correlates to the dashed line that's up in our equation the idea is that distributive shock and systemic vascular resistance are the same thing whereas these are components of cardiac output but as you'll see we will use this nomenclature in the equation but what you will learn from my method is what's the next step this formulation does not do that so as you read literature about shock these are the words you'll see but as you learn to deal with patients who are in shock you will learn that these don't help let's go back up to the equation and see how this correlates in mean arterial pressure equals the cardiac output time systemic vascular resistance and there's a dashed line through the X Y because all causes of shock on this side I'll have to do this system agnostic Euler resistance and all shock on this side have to deal with cardiac output and that's the first element to the approach to shock what I want you to see is that systemic vascular resistance is tone it is how constricted the blood vessels are cardiac output is how much womp is on top of that tone see this as diastole and this is systole let's play with us a little bit the quintessential blood pressure is 120 over 80 if someone has increased systemic vascular resistance but no change in the cardiac output so if someone not in shock I want you to see diastole as tone if they increase systemic vascular resistance the diastolic tone goes up the diastolic pressure goes up let's say it goes up by 20 points the systolic WAMP is 40 we've increased since Nemec vascular resistance by 20 the womp hasn't changed 140 over 100 so you see that the diastolic component has gone up as this person begins to go into cardiogenic shock that is they lose the womp the womp begins to disappear and all of a sudden the pulse pressure is narrow as they begin to go into shock itself they lose the blood pressure they still have a narrow pulse pressure but now their blood pressure is lower so I want you to see that a narrow pulse pressure equals shock from cardiac output no systolic womp this is the diastolic tone represents an increase in systemic vascular resistance that's the womp disappears the blood pressure slowly trickles down the body tries to maintain as much tone as it can but as the patient goes deeper and deeper into shock the blood pressure continues to fall the systolic whomp still is nothing and the blood pressures begins to fall until they die but also notice that an increased systemic vascular resistance means something to peripheral circulation and consider what happens to you when you get cold sitting in a lecture hall your fingers get cold that's from vasoconstriction your fingers and your toes Auto regulate so when it's cold it shunts blood back to the core but your shins and your ankles will not have been cold because they still get full perfusion when a person goes into shock and they have a narrow pulse pressure the diastolic tone is trying to sustain the blood pressure so there's so much vasoconstriction that no blood flow gets to the extremities thus if someone is in a cardiac output shock and the systemic vascular resistance is attempting to accommodate the low blood pressure from a low cardiac output what you'll get is a narrow pulse pressure and a cutting off of the blood vessels so you'll also have a cold extremity so when you walk into the ER and you see a patient you've been console tada you might need to go to the unit you see that blood pressure is 70 over 60 and you touch their extremity and it's cold that's probably cardiac output in nature being compensated by systemic vascular resistance let's go the other way let's say the person is going into shock from a decreased systemic vascular resistance initially the cardiac output is going to maintain itself but what you're going to see is a drop in the diastolic tone the pulse pressure begins to widen and as the person gets deeper into shock the cardiac output can't keep up and the blood pressure begins to fall so what you'll see in shock from a loss of systemic vascular resistance is going to be a wide pulse pressure and because there is a loss of systemic vascular resistance you're going to get peripheral vasodilator that means blood flow is going to go to the extremities when it shouldn't be it should be being shunted back to the core to maintain the diastolic perfusion of the coronary vessels insists all a profusion of the brain but it's not because the systemic vascular resistance is broken so if you touch their extremity it's going to be warm and this is important it's not their hands and their feet because those Auto regulate differently it is their shins and their forearms if they're warm and there's a wide pulse pressure it's a problem systemic vascular resistance if there's a narrow pulse pressure and they're cold it is a problem with cardiac output in systemic vascular resistance is attempting to compensate so those are two physical diagnosis clues you can use to determination of shock let's go over an actual differential based on this equation first let's do systemic vascular resistance these are going to be the things that cause the diastolic tone to be lost that is the loss of sympathetic tone that causes vasoconstriction and whether that's going to be inflammatory mediators that overwhelm the vase of constructive response or loss of sympathetics it doesn't matter if you don't have any one component you've debeso dilate inappropriately the big one is going to be sepsis there is similar to sepsis you know this is inflammatory mediated by interleukin 1 it's anaphylaxis and aful axis is histamine related but both of these cause halation spinal trauma can do it by transecting the sympathetics as can anesthesia particularly the epidural that became intradural and Addison's disease it's strange and bizarre but pheochromocytoma a kind of a letdown of the Pheo flare can cause and reduce systemic vascular resistance but I'm not putting it up there sepsis NFL active spinal trauma anesthesia and Addison's are what you should think of for problems of systemic vascular resistance we move over to cardiac output we make our loop around the different elements of cardiac output for heart rate it's either too fast or too slow period it doesn't matter what the rhythm is if they're in shock you're going to fix it and if you remember from the ACLs in a nutshell they're too fast and in shock you shock them they're too slow and in shock you pace them it's not about rhythm interpretation if you see someone is in hypotension as a result of an onset of arrhythmia fix it you should always start here because you can fix it in seconds and reverse the shock and then work your way around the equation for preload it can be one of two things you can simply be preload down that is volume down which is remember by the mnemonic the four DS diarrhea dehydration diuresis and hemorrhage which captures anemia and blood loss but there could also be other things that compromise preload conditions that don't allow enough volume to get back into the ventricle the two things that impair venous return to the right side are a tension pneumo or a pericardial tamponade tension pneumo and pericardial tamponade impair filling to the right side there's enough volume but something is preventing from getting in things that prevent filling of the left ventricle are going to be pulmonary hypertension and a pulmonary embolism these four by the way are obstructive shock the Green is hypovolemic the heart rate in red was cardiogenic and we finish with other causes of cryogenic shock under contractility which are going to be essentially CHF MI and myocardial contusion you as a medicine doctor will not see myocardial contusion that's in severe trauma so I want you to just recognize why I do this the way I do it I'm going to ask you if someone has a tension pneumothorax and they are suffering from shock what do you think the initial step is going to be if they are preload down the answer should be obvious you give them volume now you know to do a needle decompression but who has a knee already if they're sitting in front of you give them some volume try to expand the venous return to the RV if their volume down what are you going to do it's a preload issue you give them some preload give them volume if they have a pulmonary embolism and they're in shock what's your first step their preload down give them more volume yes you're going to use TPA to break up the PE but the idea is as you go around and think about what is deficient that it what type of shock it is is less important than which of the equation is broken because if there's an issue with contractility you're going to support the contractility if there's an issue with preload you're going to give them preload it was a problem with heart rate you fix the heart rate and there's a problem with systemic vascular resistance you fix this is the make vascular resistance and this classic model of shock that you're not going to see again in this video doesn't account for that so as long as you know that these four are obstructive and the volume down is hypovolemic you can then correlate this method into the classic method so so far we have just a list of differentials so when you see someone who is hypotensive when you see someone who has orthostatics when you see someone who's in Frank shock this is what you should do now it's based on the equation and yes you have to memorize what your needs which is in each one but I will tell you that in clinical practice when I approach a rapid response or approach a patient in the ER who is in shock I actually go around this loop asking questions and obtaining laboratories which will help me evaluate for each one this is a method for remembering what diseases are involved in shock let's talk about how you identify shock in the first place that is to say there is obvious overt shock and this is a person who has a systolic blood pressure less than 90 as you enter the intensive care unit what matters more your Maps or someone who has a map less than 65 but there's two other types of shock that people miss one is a cult shock and the other is a shock index that is people who are not in Frank obvious shock but who you should at least be considering taking to the unit even though the numbers don't say so some of the shock index has a heart rate that is greater than the systolic blood pressure this can happen in younger healthier people that 23 year old sickle-cell who has a UTI her heart rate might be 170 but her blood pressure 101 over 50 she's walking around asking to go to the bathroom she is still in shock as she has a shock index but she can compensate her cardiac output is good enough to sustain a heart rate of 170 because she's so young she may not need to go to the unit well you could justify her admission by the positive shock index but if you've got an 80 year old whose heart rate is 110 their blood pressure is a hundred Golic you should start thinking something's wrong because chances are that person does not have a low blood pressure at baseline and that shock index is indicative of them going the wrong way likewise you in a cult shock what you'll see this is difficult to do because you need to have a system with lots of continuity you see them someone in clinic and they constantly come in uncontrolled their blood pressure and all of a sudden sitting in the emergency department they look great and you might bypass this 120 over 70 if you didn't have these values from Clinic and say well the blood pressure is fine actually low look and fantastic but really they're supposed to be on five different antihypertensives and even off those antihypertensives their blood pressure is normal that's actually a cult shot because their blood pressure is lower than in-seat than they're used to and this person her blood vessels have already adapted to this and her she needs this hypertension in order to sustain perfusion through those diseased vessels this doesn't cut it she may actually be in shock this is how to identify someone who might be in shock the equation is used for the differential let's talk about one more way of thinking about the body before we move into talking about which type of vasopressors you use and in septic shock I want you to think of the body as a tank the brain is suspended the top there's a motor that pushes the fluid towards the brain against gravity and the goal is to get the water level over the brain this is an adequate perfusion a tank and normal-size with love water and a motor to get it there there's three ways that this system can break that will present with the brain being poorly profused and after all that's the purpose of our body is to perfuse our brain and make us us the first is that the tank could be too big the motor still works but there's just not enough volume to get to the brain systemic vascular resistance has increased the tank is too big and now there's not enough fluid to fill the tank this is an issue with the tank and reflects systemic vascular resistance you might lose the pump tank is normal-sized but now without the pump there's enough fluid to get to the brain but not enough force to get it there this is a broken pump and is the center of potentially contractility one way the pump can break is with the heart rate that's too slow or too fast and finally if you're following along you could just have a hole in the tank brain doesn't get perfused the pump is trying to push fluid up to the brain but all that happens is that it leaks out this is the fluid and is issues with volume or preload and this is where you have to be careful this is the terminology I use it makes sense to me it probably makes sense to you but you'll see tank and pump and fluid in terms like it in the literature in some ways of thinking about it which are a little different which I know is frustrating but this is the way it works for me it's worked for students under me I suggest you thinking about it like this because we're going to use these concepts as we talk about vasopressor activity and in septic shock so to review the biggest thing you should take away from this lecture is this equation the mean arterial pressure is cry up attempt this times the colic vascular resistance cardiac output it's heart rate times stroke volume stroke volume is preload times contractility and anytime you encounter a patient who has hypotension write this out then you should begin committing to memory the different potential diagnoses and recognize that systemic vascular resistance represents the diastolic tone when cardiac output represents the systolic WAMP so you can use the blood pressure and your physical exam to start you down the major pathway so you know what to do next we're going to talk more about that in the coming lectures that is shock one introduction to shock we make these videos for free and we need your help please donate because without your donations we can't make any more videos please donate

22 thoughts on “Intern Content: Approach to Shock – OnlineMedEd

  1. Just thought of a mnemonic for remembering the causes of Hypovolemia:
    But warning itโ€™s very dirty!!

    Diarrhea
    Dehydration
    Diuresis
    Vomiting
    Bleeding
    So DDDVB
    Just remember if there are Three Dicks and one Vagina, there is going to be Blood.
    Ur welcome.

  2. Great teaching skills, understandable & memorable. But, his brain drawing looks more like a butt crack ๐Ÿ˜‚

  3. i still did not get it !why when we have narrow pulse pressure it's problem of cardiac output?an when we have wide PP ,the problem is with SVR????!!can someone explain it for me please

  4. Thanks very much. An excellent, clear and very informative lecture. Thanks for your effort. |Great man.

  5. When you say, Tank size increases, it means SVR has decreased, right. That would be why we give them pressors.??

  6. and if TPR or diastolic increase by 20 points,,then will the systolic or CO should nt decrease?? as u mention tht if TPR increase ,,CO will decrease and if CO decrease,,TPR will increase?//??

  7. sir u say bp is 120/80,,the diastolic pressure goes up by 20 points then you say systolic womp is 40 how this 40 comes from??

  8. one question though –
    wasnt there a mix up in what causes RV / LV filling problems?
    in the video:
    RV – PTX and temponade
    LV- PE, Pulmonary HTN

    im not so sure,
    isnt PE causing RV damage?
    pretty sure that pulm hypertension causes problems to the right heart also….

  9. Hi There !
    I'm not a native english speaker and i'm really not making sense out of one word.
    Could someone please give me a hint ?

    "consider SVR as tone, and CO as … ??? "

    … Wamp ? womp ? Can't figure it out ..

    Love your videos ๐Ÿ™‚

Leave a Reply

Your email address will not be published. Required fields are marked *