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Medico Macha
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00:00:00So we'll talk about a very important topic now that is shock and every year in the entrance exam
00:00:14you have at least two questions from this topic. Also in your college exam this is usually a long
00:00:22question or a short note which you get. So I really want you to understand the concept behind
00:00:28shock and the newer modalities and the new developments in this field because that is a
00:00:33constant question in the entrance exam. Now the first thing which I want you to know is what is
00:00:39the definition of shock. Now this you must have covered in physiology as well and a very simple
00:00:45definition of shock is that it is hypoxia at the cellular level. It is hypoxia at the cellular
00:00:52level and there can be various causes of shock. The first one which we're going to talk about
00:00:58is the most common that is hypovolemic shock. So hypovolemic or hemorrhagic shock is the most
00:01:09common type of shock. In fact Bailey says that if a patient if a patient presents with shock
00:01:17shock and you are unsure about the etiology, you are unsure about etiology, it is safe to treat
00:01:34it as it is safe to assume that it is hypovolemic shock. So initially you can assume that the patient
00:01:50has hypovolemic shock and start treating the patient and then you can work up the etiology if you are
00:01:56unsure what exactly is the patient suffering from. Now hypovolemic or hemorrhagic shock, if you talk about
00:02:03hemorrhagic shock, it can be of two types. You can either have concealed bleeding, you can either have
00:02:16concealed bleeding which we cannot see or there can be revealed bleeding which exactly we can measure the
00:02:25blood loss and we can see the blood loss happening. Okay, now I'll just show you an image to depict the
00:02:32two. This is an image similar to a case which I saw when I was a first-year postgraduate. So there
00:02:40was a chef who was working and by some mistake we don't know exactly what happened but the chef's knife
00:02:46just went through his thigh and when he came to the hospital he had this huge gash on the thigh which
00:02:53was bleeding and he was actively oozing out blood from there and there were many spurters there. Okay,
00:02:59so you could actually see blood loss happening and that is revealed blood. You know that blood loss is
00:03:05happening and the patient is in shock. Okay, the other one is concealed hemorrhage. Concealed hemorrhage
00:03:12is when you can't see that blood loss is happening but it is accumulating somewhere. So what are the sites
00:03:19where blood can accumulate without us coming to know about it or actually seeing the blood loss? So you can
00:03:28have blood accumulation in the neck, in the thorax as you can see in this image, in the abdomen
00:03:35and in the pelvis and long bones like femur. So these are the concealed areas where blood loss can happen
00:03:49and the patient can go in shock without actually a single drop of blood being seen outside. Okay,
00:03:55one thing which I want you to remember here, this is very important for the exam.
00:04:00Isolated head injury and isolated head bleed can never give rise to,
00:04:10can never give rise to hypovolemic shock. This is a very important statement which I want you to remember.
00:04:20There is not enough space in the cranial cavity. Even if there is blood loss, the patient will not develop
00:04:29hypovolemic shock, right? So isolated head injury and isolated head bleed will never give rise to
00:04:36hypovolemic shock. If there is a patient, if patient has head injury and
00:04:45hypovolemic shock, then search for other sites of bleeding. Then we need to search for other sites
00:05:01of bleeding, right? And I've told you other sites are going to be, you can either look at the floor if
00:05:11there's blood loss or those concealed areas which I've just told you, right? So this is the first
00:05:17thing which I want you to remember. So another thing which I want you to remember that bleeding can
00:05:22either happen, it can either be an arterial source of bleeding or it can be a venous source of bleeding.
00:05:29Now arterial, you can have two types of injuries. Either there can be a transaction of the artery or there can just be a
00:05:41laceration of the artery. Now a question which is asked in the exam, transaction versus laceration, which one is going to bleed more?
00:05:52Transacted means it is completely cut into two pieces. Transacted. Lacerated means there's just a
00:05:57cut over the artery. Now lacerations of the artery bleed more. They bleed more as
00:06:07compared to transaction. Why? Because when it is transacted, you must have studied in
00:06:13pathology that whenever there is a vessel injury, the first response is vasospasm.
00:06:18There is spasm of the artery, right? So in transaction, the vasospasm will reduce the
00:06:24bleeding. Whereas when there is a laceration, because of the spasm, because of spasm, the opening
00:06:35increases, the opening increases and there is more bleeding. So this is point number one which I want
00:06:42you to remember that a lacerated artery bleeds more than a transacted artery. Now second venous
00:06:48blood, it is a gradual ooze. It is a gradual ooze. So because it is gradual ooze, more time for
00:06:58body to compensate. We will talk about the compensation when I discuss the parameters
00:07:04of hypovolemic shock but more time for body to compensate. And because the body can
00:07:10compensate more, these patients with venous bleeding will present late. I hope you understand this
00:07:23point because there is a gradual ooze, the body's mechanisms, the physiology can recalibrate and can
00:07:30adjust to that blood loss. So patients with the venous ooze will present very late when the BP suddenly drops.
00:07:37Okay, so this is another point which I want you to remember. Now when we talk about hemorrhage,
00:07:43supposing I am doing surgery and during surgery there can be hemorrhage or even after surgery
00:07:49there can be hemorrhage. So what are the various types of hemorrhages which you should know about?
00:07:55This is again a frequent MCQ asked in the exam. So you can have primary hemorrhage. Primary hemorrhage
00:08:01is the hemorrhage is the hemorrhage during surgery. When during surgery you have a bleed that is primary
00:08:07hemorrhage. The second one is the reactionary hemorrhage. This is the one which has been asked
00:08:12most commonly reactionary hemorrhage. Reactionary hemorrhage can occur 4 to 24 hours after surgery.
00:08:21Can occur 4 to 24 hours after surgery. Okay, so what are the causes of reactionary hemorrhage?
00:08:29The causes of reactionary hemorrhage would be increase in blood pressure or slippage of the
00:08:35knot. Slippage of knot. In previous modules we have spoken about surgical knots. Which knot would
00:08:43the surgeon have used which can slip easily? Yes, if you use a granny's knot then it can slip and it
00:08:50can give rise to a reactionary hemorrhage later on. Also what happens is that supposing when I am doing
00:08:57a surgery the anesthetist maintains the BP at a lower range than normal so that I have a bloodless
00:09:04field when I am doing surgery. Okay, but if I close at the same low BP and then the BP rises in the
00:09:13post-operative period then small oozes and vessels can start bleeding later on and I won't come to know
00:09:19about it until and unless it manifests in the drain. Okay, which is why as a surgeon before I start
00:09:28closing any wound, I ask the anesthetist is the blood pressure close to the baseline blood pressure.
00:09:35So, I will only start closing when the blood pressure is close to the baseline blood pressure
00:09:40so that I don't miss out on this reactionary hemorrhage later on. Okay.
00:09:46The final type of hemorrhage is secondary hemorrhage. Now, secondary hemorrhage will occur
00:09:55after a few days. After a few days and this usually occurs because of sloughing of the artery.
00:10:04Sloughing of the artery or the vessel and this can be secondary to infection. It is usually secondary
00:10:14to infection. So, these are the three types of hemorrhages which you should know about. Okay.
00:10:21So, what we have discussed till now, we have discussed that hypovolemic shock is the most
00:10:26common type of shock and we have discussed what are the various causes which can give rise to it.
00:10:30So, this is a very important table which we are going to discuss about hypovolemic shock and every
00:10:36year this is asked in the exam. So, what we are going to discuss here, there are four classes of
00:10:42hypovolemic shock. So, you have class 1, class 2, class 3 and class 4 and the various parameters which
00:10:52we need to discuss in hypovolemic shock are percentage of blood volume lost. This is the most important
00:11:02parameter percentage of blood volume loss, asked a lot of time. Amount of blood loss. Amount of blood loss.
00:11:12The other parameters which we need to discuss are pulse rate, systolic blood pressure,
00:11:18diastolic blood pressure, pulse pressure. Pulse pressure you know is systolic blood pressure minus
00:11:25diastolic blood pressure. You have a respiratory rate, urine output, mental status.
00:11:32You have base deficit. Base deficit, I will tell you what exactly is base deficit and you have management.
00:11:45So, these are the various parameters which we need to discuss in all four classes of hypovolemic shock.
00:11:52Now, I know it looks like a lot of parameters but I am really going to simplify this table for you.
00:11:58Right? And it will be very easy for you to understand it. So, the first thing which we need to discuss is
00:12:04what is the percentage of blood volume loss in each class of hypovolemic shock. And before I tell you
00:12:11this, I want to show you a video which will clarify a lot of things for you.
00:12:15Okay? This is a video which I always show in my class and this is a video of two great
00:12:22tennis players Federer and Djokovic. This is the US Open finals. Right? Federer is the one in red and
00:12:29Djokovic is the one in yellow. And you can see Djokovic has served and I just want you to see what
00:12:37Federer does in this point. So, it looks here as if he's going to lose the point but he just pulls out
00:12:43an amazing shot and I want you to watch the slow motion to really understand what
00:12:48exactly did Federer do. And this gave him match point and he ultimately won the
00:12:57championship. So, you can see here that it looks as if he is losing the point. He just
00:13:01casually runs back and hits the ball between his legs for a winner. Right? So, between his legs for a
00:13:08winner. Right? So, there are a couple of things which I want you to learn from this video. So,
00:13:15in the post-match interview, Federer was asked that was it a fluke shot or did you practice this shot
00:13:23quite a lot of times? So, Federer said in the post-match interview that it wasn't a fluke.
00:13:28I've practiced this shot more than thousand times. Right? And he said that the first 200-300 times I
00:13:36used to get it wrong. But after that, the frequency at which I was getting it right
00:13:41increased tremendously. Okay? So, one thing which I want all of you to remember is that practice is
00:13:48what is going to make you perfect. If you don't solve MCQs, if you don't practice your MCQs,
00:13:54it'll be difficult for you to crack your entrance exams. So, keep on practicing MCQs. Yes, initially,
00:14:00you will make mistakes. But as you practice them more, you'll get better at them. Okay? Now,
00:14:06the second thing which I want to tell you is that the scoring of a tennis game, most of you must be
00:14:13knowing is 00, that is love all. And then you have 15, 30, 40 and game over. And that is what I want you
00:14:23to remember to memorize the classes of hypervolemic shock. So, the classes of
00:14:29hypervolemic shock, very easy to remember. Just remember the scoring of a tennis game. Right? So,
00:14:35you have 0 to 15 percent, that is class 1. 15 to 30 percent is class 2. 30 to 40 percent is class 3. And
00:14:45game over for the patient, that is more than 40 percent is class 4. So, very easy to remember. Now,
00:14:53again, the amount of blood loss, this is approximately 400 to 500 cc. And you just keep on adding 500, 500 to
00:15:02each class. So, this is going to be 1 liter. This is going to be close to 1.5 liters. And this is more
00:15:09than 2 liters. Right? So, just keep on adding 500, 500 in each class. Now, let's talk about class 1
00:15:18hypovolemic shock or class 1 hypovolemia. Okay? Now, you have a patient who's lost around 400 to 500 cc of
00:15:26blood. I'm sure a lot of you watching this video must have donated blood as well. And if you donate
00:15:34blood, like I donate blood every 2 to 3 months, my hemoglobin is on the higher side. I have a
00:15:40hemoglobin of close to 17. So, the doctors have told me every 3 months I have to donate blood. Okay?
00:15:46So, if you donate blood, they take approximately 450 to 500 cc of your blood. Right? Now, if you've
00:15:56given that much blood, you've experienced class 1 hypovolemia. Now, tell me, all of you, those who've
00:16:02donated blood, what happens to your parameters once you've donated blood? Well, I don't know about you,
00:16:09but for me, nothing changes. Everything remains normal. Right? Nothing changes. Even my mental
00:16:17status remains normal. The base deficit. Base deficit, you need to understand. Base deficit,
00:16:26that means a deficit in base means an excess in acid. Right? And when there is shock, there is bound
00:16:32to be acidosis. Okay? But class 1, nothing is changing. So, base deficit is also normal. It is 0 to
00:16:41minus 2. It is 0 to minus 2 milliequivalents per litre. Okay? And once you've donated blood,
00:16:52what do they give you after blood donation? Well, I fondly remember that you get a fruity and a packet
00:16:58of biscuits. Right? So, that's what you get after blood donation. So, the management of class 1
00:17:03hypovolemia is oral liquids. That's all you require. Okay? Let's talk about class 2 shock now. Now,
00:17:13class 2 shock is known as the compensated phase of hypovolemic shock. This is very important.
00:17:20This is the compensated phase of hypovolemic shock. Why are we saying it's the compensated phase?
00:17:26Let's look at the physiology of class 2 shock. So, if you look at the physiology of class 2 shock,
00:17:32when there is blood loss, you know that the sympathetic system is stimulated. Right? You
00:17:40must have read this in physiology that the sympathetic system is stimulated. And when the sympathetic
00:17:48system is stimulated, adrenaline and norad are released. And adrenaline and noradrenaline are
00:17:56released from the system. Now, what is the first change which adrenaline and noradrenaline will bring
00:18:02about? You've read this in pharmacology that the first change which adrenaline and noradrenaline
00:18:09will bring about is tachycardia or increase in pulse rate. And this is the earliest indicator
00:18:18of hypovolemia. This question has also been asked many times. This is the earliest indicator
00:18:23of hypovolemia tachycardia. Okay. What else is ADR and norad going to do? ADR and norad are also
00:18:34going to cause peripheral vasoconstriction. They will cause peripheral vasoconstriction.
00:18:40Now, when the peripheral vasoconstriction happens, blood is not going to flow to the peripheries
00:18:49and the peripheries are going to become cold. So, you'll have cold peripheries. The hands and legs
00:18:55are going to become cold. Okay. Now, you know that when these arterioles vasoconstrict, what is going
00:19:03to happen to the peripheral vascular resistance? Common sense that if you have a constricted vessel,
00:19:10there is more resistance to the flow of blood to the peripheries, right? Which is why blood is not
00:19:16going into the peripheries, right? So, peripheral vasoconstriction will give rise to increased
00:19:22peripheral vascular resistance. PVR is peripheral vascular resistance. So, a simple rule of thumb which
00:19:32I want you to remember for all shocks which we discuss later on as well. Any shock with cold
00:19:38extremities, the peripheral vascular resistance increases and any shock with warm extremities,
00:19:47the peripheral vascular resistance is going to decrease. So, just remember the simple rule of thumb.
00:19:54Okay. Now, why is the body causing peripheral vasoconstriction? Another common sense question.
00:20:01The body is causing peripheral vasoconstriction because it wants that the blood should go to the
00:20:06vital organs. The heart, the brain and the vital organs, right? So, it wants to shunt blood from the
00:20:12peripheries to the vital organs and that is why this vasoconstriction is happening. This is going to
00:20:18shunt blood to vital organs.
00:20:22And because this shunts more blood to vital organs, the cardiac output and the systolic blood pressure
00:20:33are going to remain normal. Because more blood is returning to the heart, the cardiac output and
00:20:38the systolic blood pressure remain normal which is why we are saying this is the compensated phase
00:20:44that despite blood loss, the body has adjusted and there's been no loss in systolic blood pressure.
00:20:51Okay. So, let's fill out the table now.
00:20:56We know that pulse rate is increasing. This is the earliest indicator of hypovolemia.
00:21:02Systolic blood pressure is normal. What happens to the diastolic blood pressure?
00:21:06You've read in physiology that if the peripheral vascular resistance increases then the diastolic
00:21:15blood pressure will also increase, right? So, diastolic blood pressure increases.
00:21:22Now, understand one thing. This is our systolic blood pressure. It is remaining normal.
00:21:28This is my diastolic blood pressure. Systolic blood pressure minus diastolic blood pressure
00:21:32is pulse pressure. Systolic is here, diastolic is here. Systolic is not moving but diastolic
00:21:39is increasing. So, if diastolic increases, the difference between the two reduces. So, the
00:21:47pulse pressure is going to become narrow. The pulse pressure becomes narrow. Okay.
00:21:56Respiratory rate is going to remain the same. Urine output is normal or slightly reduced.
00:22:04The mental status. Patient is going to be thirsty and anxious.
00:22:10Patient is going to be thirsty and anxious. And the base deficit is going to be minus 2 to minus 6
00:22:19milliequivalents per liter. So, some amount of acidosis has started happening now, right? So,
00:22:27minus 2 to minus 6 milliequivalents per liter is the base deficit. And these patients are going to
00:22:34require IV crystalloids. You know crystalloids. I've discussed in the chapter in nutrition and fluid
00:22:43about crystalloids and we can use normal saline or ringer lactate here in form of crystalloids to manage
00:22:51these patients. Now, class 3 shock is the decompensated phase of hypovolemic shock. This is the
00:23:00decompensated phase of hypovolemic shock. What do we mean by the decompensated phase? That now the body
00:23:08has lost so much of blood that now the systolic blood pressure cannot be maintained. So, now systolic BP
00:23:15will start to fall, okay? Because body has lost so much of blood. So, what is going to happen here
00:23:21that there is going to be further tachycardia. Tachycardia increases, right? You have a rapid
00:23:29thready pulse. Systolic blood pressures now starts to fall. This is again a very very important MCQ.
00:23:37In which class of hypovolemic shock does systolic blood pressure fall for the first time? Class 3
00:23:47shock, okay? So, systolic BP falls for the first time in class 3 shock. Remember that, please.
00:23:54The diastolic blood pressure also falls. Why? Because there is loss of circulatory volume.
00:24:03So, although there is vasoconstriction, so the peripheral vascular resistance is increasing but
00:24:12now because blood is being lost, so much of blood is lost that now diastolic blood pressure will also
00:24:17fall. So, the pulse pressure becomes even narrower because now both are falling. So, the pulse pressure
00:24:26becomes even more narrow. Respiratory rate is going to increase. Patient will have tachypnea.
00:24:33Urine output now starts to fall dramatically, okay? And this patient is now confused.
00:24:41Patient is now confused.
00:24:44And the base deficit is minus 6 to minus 10 milliequivalents per liter.
00:24:51Minus 6 to minus 10 milliequivalents per liter. Now, these patients cannot be managed alone with
00:24:58crystalloids. So, they have to be given IV crystalloids
00:25:02plus colloids.
00:25:07And colloids, I showed you in that
00:25:10table in the chapter on fluids. You can give
00:25:14albumin, Hestarch, there can be
00:25:17dextran, various types of
00:25:19colloids can be there. But even
00:25:21blood products are colloids.
00:25:23So, class 3 shock patient,
00:25:25you can give blood products as
00:25:27well, right? So, we'll
00:25:29give crystalloids and colloids.
00:25:30And crystalloids to colloids are given
00:25:32in a 3s to 1 ratio.
00:25:353 parts of crystalloids
00:25:36to 1 part of colloid.
00:25:40Okay?
00:25:40So, class 4 shock is also very
00:25:42easy to remember. The patient has lost
00:25:44so much of blood that everything
00:25:46is non-recordable, right?
00:25:48So, you will have pulse rate is
00:25:50non-recordable, right?
00:25:52You'll have pulse rate non-recordable.
00:25:55You will have BP non-recordable.
00:25:58You can't record the pulse pressure.
00:26:01The respiratory rate
00:26:03increases even more.
00:26:05The patient has anuria.
00:26:07No urine production is there.
00:26:09This patient will be in a state of
00:26:11coma. And
00:26:13it will be more than minus
00:26:1610 milliequivalents per liter.
00:26:19The base deficit is more than
00:26:20minus 10 milliequivalents per
00:26:22liter, right?
00:26:24So, these are the 4 classes of
00:26:26hypovolemic shock.
00:26:28And in this patient with class 4
00:26:30hypovolemic shock, what do we do?
00:26:32We have to give these patients
00:26:33massive blood transfusion.
00:26:35We have to give these patients a
00:26:42massive blood transfusion.
00:26:44And I'm going to talk about massive
00:26:46blood transfusion in a few minutes
00:26:48time. Very important topic.
00:26:50A pet favorite for the AIMS and the
00:26:52Central Institute exams.
00:26:54But class 4 shock patients require
00:26:56massive blood transfusion, okay?
00:26:58So, this table is very important for
00:27:01you to understand.
00:27:02I've tried to simplify it as much as
00:27:05I could for you.
00:27:06Let's solve one question here so that
00:27:08you understand what kind of practical
00:27:10questions are asked from this table.
00:27:12So, let's look at this question now.
00:27:14You have a 70 kg man who's come to the
00:27:17emergency following a stab injury to
00:27:20the abdomen, right?
00:27:22His pulse rate is 110.
00:27:24So, there is tachycardia and BP is 90 by
00:27:2860 means systolic is also falling and
00:27:31diastolic is also falling and he
00:27:34appears confused.
00:27:36What percentage of blood volume has he
00:27:39lost?
00:27:40So, very simple.
00:27:41How do we approach these questions?
00:27:44There is tachycardia here, right?
00:27:49So, it cannot be class 1 shock.
00:27:51Has to be either class 2, class 3 or
00:27:53class 4, right?
00:27:54First thing.
00:27:56Second thing, systolic BP has started
00:27:59falling.
00:28:00It is 90 systolic.
00:28:01So, systolic BP has started falling.
00:28:04So, when does systolic BP fall for the
00:28:06first time?
00:28:07In class 3 shock.
00:28:10Why isn't this class 4 shock?
00:28:12Because you can still feel the pulse,
00:28:14you can still record the BP.
00:28:15It is not non-recordable, right?
00:28:18So, this would be class 3 shock and
00:28:23class 3 shock.
00:28:24Again, remember the scoring of a
00:28:26tennis game?
00:28:27Class 1 was 0 to 15, class 2 was 15 to
00:28:3030, class 3 was 30 to 40 percent.
00:28:33So, 30 to 40 percent blood loss has been
00:28:37there in this person and the patient is
00:28:41suffering from class 3 hypovolemic shock.
00:28:43So, these are the kind of practical
00:28:45questions which can be asked from the
00:28:46table which we've just discussed.
00:28:48So, we've discussed the classes of
00:28:50hypovolemic shock and I've broadly
00:28:51outlined the treatment for you.
00:28:54Now, it is also very important that such
00:28:56patient should be monitored at a regular
00:28:58basis.
00:28:59So, how do we monitor a patient with
00:29:02hypovolemic shock?
00:29:04That's a very important concept for you
00:29:06to understand.
00:29:07Now, there are two common questions and
00:29:09these two questions have been asked at
00:29:11least 20 times in your exam.
00:29:13The first question is, which is the best
00:29:16indicator to determine amount of fluid
00:29:23required, best indicator to determine
00:29:27amount of fluid required in shock, right?
00:29:36And the second question is, which is the
00:29:38best clinical indicator, which is the best
00:29:42clinical indicator of fluid resuscitation,
00:29:47of fluid resuscitation in shock, okay?
00:29:55Now, what is the literal meaning of these
00:29:58two definitions?
00:29:58The first question is asking that when a
00:30:01patient comes to me in the emergency,
00:30:03how do I determine how much fluid to give
00:30:07to that patient, right, of shock?
00:30:10How much fluid is to be given?
00:30:12Which is that indicator?
00:30:14And the second question is, that once I have
00:30:17given fluid to this patient, how do I know
00:30:21whether that was adequate fluid or
00:30:23inadequate fluid?
00:30:25So, I hope you've understood the two
00:30:27questions.
00:30:27Now, the first question is, how to
00:30:29initially determine how much fluid to give?
00:30:33There, the answer is pulmonary capillary
00:30:36wedge pressure is a better answer than
00:30:39CVP.
00:30:41This is pulmonary capillary wedge pressure
00:30:44and CVP, all of you know, is central
00:30:51venous pressure.
00:30:52So, for all practical purposes, it is the
00:30:56central venous pressure which is what we
00:31:01use to determine how much fluid to give.
00:31:05But theoretically speaking, pulmonary
00:31:08capillary wedge pressure is a better
00:31:10answer than CVP because it gives you an
00:31:13accurate indicator of the left-sided heart
00:31:16pressures.
00:31:17Whereas, CVP is giving you an indicator of
00:31:20the right-sided heart pressures, okay.
00:31:23So, theoretically, pulmonary capillary
00:31:25wedge pressure is a better answer.
00:31:28Otherwise, for practical purposes, it is
00:31:30CVP.
00:31:31And pulmonary capillary wedge pressure, you
00:31:34know that we use a Swann-Gans catheter
00:31:38and then we measure the pulmonary capillary
00:31:45wedge pressure, okay.
00:31:47So, this question has been asked many times.
00:31:49You should remember this.
00:31:51Now, once you have given fluid, how do we
00:31:53know whether that fluid has been adequate
00:31:55or inadequate?
00:31:57So, that is determined by the urine output.
00:32:03That is determined by the urine output.
00:32:05Very, very important question.
00:32:07These two questions have been asked at
00:32:09least 20 times in the exam.
00:32:11So, you should read the question carefully
00:32:12and then answer after assessing what is
00:32:16the examiner trying to ask you, okay.
00:32:18Now, the urine output for adults in a
00:32:22patient with shock, the urine output for
00:32:24adults should be maintained more than
00:32:270.5 ml per kg per hour.
00:32:30Whereas, for children, our aim should be
00:32:33that it should be more than 1 ml per kg
00:32:35per hour.
00:32:37Now, in addition to this, there are certain
00:32:39new endpoints of fluid resuscitation as
00:32:42well.
00:32:43These have been listed in Bailey and
00:32:45they are very important for the exam
00:32:47asked a lot of times in the last couple
00:32:49of years.
00:32:50So, what are the new endpoints of
00:32:52resuscitation?
00:32:54The new endpoints of resuscitation for
00:32:56systemic perfusion.
00:32:57So, for systemic perfusion, the new
00:33:04endpoints of resuscitation which you need
00:33:06to remember for your exam is MVOS.
00:33:11This is mixed venous oxygen saturation.
00:33:16I will talk about this in detail in two
00:33:18minutes.
00:33:19Mixed venous oxygen saturation.
00:33:22The second one is base deficit which I have
00:33:25already told you is because there is
00:33:28acidosis and the third one is serum
00:33:31lactate.
00:33:33So, these are the three for systemic
00:33:35perfusion.
00:33:37These are the new endpoints and if you
00:33:39have to choose the single best endpoint
00:33:41of resuscitation, it is MVOS.
00:33:47Right?
00:33:48So, for any future exam, if they ask you
00:33:52which is the best endpoint of fluid
00:33:54resuscitation and you have urine output
00:33:58also mentioned there, you have MVOS also
00:34:00mentioned there, you will mark MVOS.
00:34:04Right?
00:34:04That is the single best endpoint of
00:34:06resuscitation.
00:34:07If they ask clinical endpoint, you will
00:34:10mark urine output.
00:34:12Okay?
00:34:12So, please no confusion there.
00:34:13For muscle perfusion, for muscle
00:34:20perfusion and for brain perfusion, it is
00:34:23the same.
00:34:24For muscle perfusion and brain perfusion,
00:34:27the endpoints of resuscitation are NIRS
00:34:30that is the near infrared spectroscopy.
00:34:34NIRS is near infrared spectroscopy and
00:34:38tissue oxygen electrode.
00:34:41Tissue oxygen electrode.
00:34:43So, these are the two endpoints of
00:34:45resuscitation for muscle and brain
00:34:47perfusion.
00:34:48For gut perfusion, there are three of
00:34:55them, sublingual capnometry, gut
00:34:59mucosal pH and laser Doppler
00:35:02flowmetry.
00:35:04Okay?
00:35:04So, you have sublingual capnometry, gut
00:35:07mucosal pH and laser Doppler flowmetry.
00:35:11You have to remember these endpoints.
00:35:15This is a table directly from Bailey.
00:35:17But, please remember that MVOS is the
00:35:19single best endpoint of resuscitation.
00:35:22One more thing which I want to tell you
00:35:24here and I've covered this in the
00:35:27stomach module as well.
00:35:28that the gastric mucosa, that the gastric mucosa
00:35:35is the most sensitive mucosa, it is the
00:35:41most sensitive mucosa in GIT to
00:35:48hypovolemic insult.
00:35:49So, whenever there is a hypovolemic insult
00:35:55in the body, it is the gastric mucosa
00:35:58which is the most sensitive, right?
00:36:00What is the practical importance of this?
00:36:04Because the gastric mucosa is most
00:36:06sensitive, that is why you can get stress
00:36:09ulcers.
00:36:10Whenever there is hypovolemic shock,
00:36:14patient can develop stress ulcers and
00:36:18that can lead to bleeding.
00:36:20So, these two types of stress ulcers which
00:36:22I've discussed in both upper GI hemorrhage
00:36:25and the burns module are Cushing and
00:36:28curling ulcers which develop in a
00:36:30stressful condition.
00:36:31So, this is how we monitor a patient with
00:36:36hypovolemic shock.
00:36:39Before I move further and tell you more
00:36:41indices, let me tell you about MVOS.
00:36:44What exactly is MVOS?
00:36:47So, this stands for mixed venous oxygen
00:36:52saturation.
00:36:57Right?
00:36:57So, this is the amount of oxygen which is
00:37:01returning back to the heart after being
00:37:05utilized in the body, that is MVOS.
00:37:08So, let me simplify this for you further.
00:37:11So, supposing 100 molecules of oxygen
00:37:13are pushed from the heart into the body.
00:37:16Right?
00:37:17Now, the body is going to utilize this
00:37:19oxygen.
00:37:20So, supposing the body utilizes 50
00:37:24molecules of oxygen and 50 molecules are
00:37:28returning back to the heart.
00:37:29So, that is the MVOS.
00:37:33The percentage of oxygen which is returning
00:37:36back to the heart is mixed venous oxygen
00:37:39saturation.
00:37:41Right?
00:37:42So, accurate measure of MVOS
00:37:45can be done by drawing blood
00:37:56by drawing blood from a catheter
00:38:00from a catheter in the right atrium.
00:38:08That is going to give you the accurate measurement.
00:38:11Why not the SVC?
00:38:14If blood is drawn from the SVC,
00:38:18if blood is drawn from the superior vena cava,
00:38:24then you can get an inaccurate measurement.
00:38:26You can get an inaccurate measurement.
00:38:32Why?
00:38:34Because there is more oxygen extraction
00:38:38because more oxygen extraction occurs in the lower limbs.
00:38:44So, you will get a false value here, falsely high value
00:38:52because more extraction is happening from the lower part of the body
00:38:56or the lower limbs.
00:38:57So, for accurate measurement, it should be from the right atrium.
00:39:00Now, the normal value of MVOS is between 50 to 70%.
00:39:07That is the normal value of MVOS.
00:39:11Less than 50% MVOS.
00:39:16Less than 50% MVOS.
00:39:18Where are we going to get less than 50% MVOS?
00:39:21So, it's a common sense question.
00:39:22One is if the heart is pushing less oxygen, right?
00:39:28Or the second is if the body is utilizing more oxygen.
00:39:33Those are the two situations when you are going to have a low MVOS, right?
00:39:39So, low MVOS will be seen in patients with cardiogenic shock
00:39:43because the heart is unable to pump out oxygen
00:39:47and you will have it in hypovolemic shock.
00:39:54Why in hypovolemic shock?
00:39:56Because I told you there is peripheral vasoconstriction, right?
00:40:02And there is stasis of blood which is happening
00:40:04and because the circulating blood is less,
00:40:08there is less oxygen which is being sent.
00:40:10So, because less oxygen and stasis is there,
00:40:16the body extracts more oxygen.
00:40:18The tissue is going to extract more oxygen
00:40:20and less oxygen is going to return.
00:40:24So, that also leads to a low MVOS.
00:40:28So, these are the two types of shocks
00:40:30where you can get low MVOS.
00:40:34Now, where can we get high MVOS?
00:40:37will be seen in patients with septic shock.
00:40:44Why septic shock?
00:40:47Septic shock, we are going to discuss later.
00:40:50The warm phase of septic shock is a hyperdynamic phase, right?
00:40:55The warm phase is a hyperdynamic phase.
00:40:59So, because there is a hyperdynamic phase,
00:41:02there is quick circulation.
00:41:05Quick circulation is there
00:41:06and this leads to less extraction of oxygen.
00:41:15Also, there is impaired tissue oxygen extraction in septic shock.
00:41:23Impaired tissue oxygen extraction.
00:41:25So, these two reasons lead to a high MVOS
00:41:31in patients with septic shock.
00:41:34So, I have told you what is MVOS?
00:41:37I have told you the causes of low and high MVOS.
00:41:40This you should remember for the exam.
00:41:42So, even in distributive shock, right?
00:41:45Distributive shock like anaphylactic shock
00:41:48and neurogenic shock also you can get a high MVOS
00:41:52because there also the same thing is happening
00:41:56that you have stasis of blood.
00:41:59So, more oxygen is being extracted in these patients, okay?
00:42:04So, this was regarding MVOS.
00:42:08Now, there are certain indices which I want you to remember.
00:42:12They have been asked in the AIMS exam.
00:42:13These are also used to monitor shock.
00:42:17One is shock index.
00:42:21So, the first index which I want you to know is the shock index.
00:42:27Shock index is heart rate by systolic blood pressure, okay?
00:42:33The other one is modified shock index.
00:42:36The other one is modified shock index.
00:42:39Modified shock index is heart rate divided by mean arterial pressure.
00:42:44MAP is mean arterial pressure.
00:42:47And the third one is rope.
00:42:51Rope stands for rate over pressure difference.
00:42:56Stands for rate over pressure difference.
00:43:02That is rope.
00:43:04So, rate means heart rate and pressure difference.
00:43:08What is pressure difference?
00:43:09Systolic minus diastolic is pulse pressure.
00:43:12So, heart rate by pulse pressure is rope.
00:43:18Now, out of these three,
00:43:20modified shock index is the most sensitive indicator.
00:43:26Modified shock index is the most sensitive indicator.
00:43:29This point has also been asked in the exam.
00:43:31Another thing which I want you to remember is that a shock index.
00:43:42If you have a shock index ratio of more than 0.9,
00:43:47then there is higher mortality.
00:43:49This is very important.
00:43:50This is from a large scale study which was done.
00:43:55And this found out that if shock index is more than 0.9, higher mortality.
00:44:00And if the rope value is less than 3, patient remains stable.
00:44:06But if rope, that is rate over pressure difference, is more than 3,
00:44:11then it is indicative that the patient might develop decompensated hemorrhagic shock.
00:44:17So, if you can for the central institute exams,
00:44:21please remember these two values.
00:44:22Shock index of more than 0.9 and rope of more than 0.3.
00:44:27Again, higher mortality, poor outcome.
00:44:31So, I have told you various things how to monitor hypovolemic shock.
00:44:35Now, I have to discuss a very important point that is massive blood transfusion.
00:44:47Massive blood transfusion, you need to remember for the exam
00:44:51because almost each year there is a question which is being asked from this topic.
00:44:56First, what is the definition of massive blood transfusion?
00:44:59The definition of massive blood transfusion is when we replace the entire circulating volume
00:45:10in 24 hours.
00:45:16That is number 1.
00:45:18Or, if more than 10 units of blood
00:45:21are given in 24 hours.
00:45:27That is number 2.
00:45:28And number 3 is if more than 4 units of
00:45:33PRBC or blood products
00:45:35are given in 1 hour.
00:45:39So, these are 3 definitions which you need to remember
00:45:42for massive blood transfusions.
00:45:44The definition itself has been asked
00:45:46many times in the exam.
00:45:49Now, you know when such large quantities of blood
00:45:52is required, there has to be a protocol.
00:45:55So, there is a massive blood transfusion protocol which is initiated
00:46:00whenever we anticipate that a patient would require such large quantities.
00:46:06Okay.
00:46:07Before I joined my post-graduation,
00:46:09I had done an externship at Cornell and Harvard.
00:46:13And at Cornell, I was at a level 1 trauma center in Bronx.
00:46:17Now, Bronx is one of the areas in New York
00:46:20but it is notorious for crime, right?
00:46:24And that level 1 trauma center was in the middle of that high violence zone.
00:46:30And every night I was on call, you could hear at least 3 or 4 gunshots happening outside.
00:46:35So, one such patient landed up to the ER with 4 gunshot wounds to the abdomen, right?
00:46:43And the patient had non-recordable vital signs when the patient came in.
00:46:49Patient was resuscitated and we activated the massive blood transfusion protocol.
00:46:55Okay.
00:46:55In 24 hours, this patient was given 14 vats of blood products.
00:47:03Okay.
00:47:03So, classified as massive blood transfusion.
00:47:06Now, when you are giving such large quantities of massive blood products or blood products,
00:47:12there are bound to be certain complications as well.
00:47:15So, what are the complications of massive blood transfusion?
00:47:21The complications of massive blood transfusion, you know that blood when we get from the blood bank,
00:47:27it is cold, right?
00:47:30And normally, if I have to transfuse just one unit of blood,
00:47:34we will take our own sweet time for the blood to come to room temperature
00:47:39and then we start transfusing.
00:47:40I am sure as interns, all of you must have done that.
00:47:43But in patients where we are in a hurry, we have to transfuse 10 units in 24 hours or 4 units in 1 hour,
00:47:51then we don't get enough time to warm up this blood, right?
00:47:55So, in these patients, when we are giving blood so rapidly, these patients can become hypothermic.
00:48:03There can be hypothermia.
00:48:06Okay.
00:48:07Now, you also know that when we are giving blood,
00:48:12blood, when you are storing blood, it has an anticoagulant with it.
00:48:17And these days, the anticoagulant used is citrate.
00:48:22So, citrate is the anticoagulant which we are using these days.
00:48:26And because citrate is going to chelate calcium and magnesium,
00:48:38these patients can develop hypocalcemia and hypomagnesemia.
00:48:45Now, normally, there is 80 ml of citrate which is there.
00:48:59Okay.
00:49:00This 80 ml of citrate is normally metabolized by a normal person like us can metabolize it in 10 minutes.
00:49:07But patients who are in shock cannot metabolize the citrate effectively.
00:49:13So, massive blood transfusion can also give rise to citrate toxicity later on.
00:49:21This can give rise to citrate toxicity later on and it can worsen the metabolic profile of the patient.
00:49:28So, potassium, you can either have hyperkalemia or there can be hypokalemia.
00:49:43Why?
00:49:45Hyperkalemia because you know that stored RBCs can lice.
00:49:49Stored RBCs can lice and when stored RBCs lice, potassium is released.
00:50:00Also, later on when there is acidosis, that can also increase the potassium.
00:50:09Hypokalemia, why?
00:50:10Because RBCs after transfusion can actively take in potassium and that can give rise to hypokalemia as well.
00:50:35There can also be metabolic alkalosis initially.
00:50:41Why will there be metabolic alkalosis?
00:50:44This is due to citrate toxicity.
00:50:47Citrate metabolism is going to give rise to metabolic alkalosis.
00:50:51But later on this is then replaced by metabolic acidosis.
00:50:57So, both alkalosis and acidosis later on there is acidosis.
00:51:02Of course, you can have the blood transfusion reactions which are there.
00:51:07Because we are giving so much of blood, the blood transfusion reactions which are the febrile reactions.
00:51:14You can have febrile reactions which are the most common.
00:51:20And rarely you can also have an anaphylactic reaction if there is a mismatched blood transfusion.
00:51:26Other problems which can happen in these patients.
00:51:33There are two terms which I want you to know.
00:51:35These two terms have also been asked in the exam in the last two years.
00:51:40Taco and trolley.
00:51:42What is taco?
00:51:43Taco is transfusion associated.
00:51:47Taco is transfusion associated.
00:51:50Cardiac overload.
00:51:55Transfusion associated.
00:51:56Cardiac overload is taco.
00:52:00And trolley is transfusion related.
00:52:02Acute lung injury.
00:52:07Transfusion related.
00:52:08Acute lung injury is trolley.
00:52:11Now, as interns, I am sure you people must have transfused blood to patients.
00:52:18And sometimes you must have transfused two or three units as well.
00:52:22Sometimes what happens when you transfuse blood, there can be volume overload.
00:52:28And how will that volume overload manifest in the patient?
00:52:31That volume overload will manifest as puffiness, puffiness of the face and edema.
00:52:39And these can be signs of cardiac overload.
00:52:42And this will develop as you are transfusing blood.
00:52:46Within some time of that only, you will notice these changes.
00:52:49And I am sure all of you must have seen that when you notice these changes,
00:52:54your senior comes and your senior says,
00:52:56well, this is due to fluid overload.
00:52:58What do we need to do here?
00:52:59We need to give this patient lasics, right?
00:53:03We need to give this patient diuretics or lasics.
00:53:07And that is going to take care of this problem.
00:53:12So, diuretics are to be given if you have taco.
00:53:16Trolley, on the other hand, is transfusion related acute lung injury.
00:53:21Now, trolley usually develops within six hours of transfusion.
00:53:29Within six hours of transfusion, you are going to have trolley.
00:53:34And it is hypothesized that this is due to anti-HLA antibodies.
00:53:41And this is going to give rise to a picture of ARDS, acute respiratory distress syndrome, right?
00:53:50You've write acute respiratory distress syndrome in medicine in great detail.
00:53:54So, you'll have bilateral chest infiltrates.
00:53:57There will be tachypnea.
00:53:59Saturation would be low.
00:54:00But the good thing is that if trolley is detected early and treated adequately,
00:54:06then it has a good recovery rate as well.
00:54:08So, these two terms you need to remember, taco and trolley.
00:54:13One final point regarding massive blood transfusion.
00:54:16The most common cause of death,
00:54:19the most common cause of death in massive blood transfusion,
00:54:24this question has been asked multiple, multiple times,
00:54:29is coagulopathy.
00:54:30It is not trolley, it is coagulopathy.
00:54:38So, why is coagulopathy occurring in these patients?
00:54:42Coagulopathy is occurring because of hypothermia.
00:54:51Because of hypothermia.
00:54:53You remember the chapter of trauma where I have spoken about abdominal trauma.
00:54:59I had spoken about damage control surgery.
00:55:03There I told you the terrible triad of trauma.
00:55:07The terrible triad of trauma is hypothermia, acidosis,
00:55:14hypothermia, acidosis and coagulopathy.
00:55:18So, all three are related.
00:55:25Right?
00:55:25The other cause is,
00:55:29as I mentioned, there can be acidosis
00:55:31and the most important thing is
00:55:34dilutional coagulopathy is there.
00:55:38There is dilutional coagulopathy.
00:55:41What do we mean by this?
00:55:42We know that
00:55:43the blood which we are transfusing
00:55:46is stored blood is poor in,
00:55:49stored blood is
00:55:52not rich in platelets,
00:55:56not rich in platelets
00:56:00and it has decreased clotting factors.
00:56:07It has decreased clotting factors.
00:56:10So, there can be dilutional coagulopathy here.
00:56:14Now, how to deal with this problem of
00:56:18coagulopathy in massive blood transfusion?
00:56:21So, to deal with this problem,
00:56:24the massive blood transfusion protocol
00:56:26and this has also been asked two or three times
00:56:29is that
00:56:29The ratio of PRBC
00:56:33to FFP
00:56:35to platelets
00:56:38in massive blood transfusion
00:56:41should be
00:56:421 is to 1 is to 1.
00:56:45So, PRBC is
00:56:46packed RBCs.
00:56:50FFP is
00:56:51fresh frozen plasma.
00:56:54FFP is
00:56:56fresh frozen plasma
00:56:57and you have platelets.
00:57:01So, the ratio should be
00:57:031 is to 1 is to 1
00:57:05when we are
00:57:07doing massive blood transfusion
00:57:09in order to avoid
00:57:11coagulopathy.
00:57:12Okay.
00:57:13Now, these blood products,
00:57:15their storage,
00:57:17how do we transfuse them
00:57:19has been covered in great detail
00:57:21in pathology by Dr. Rilla
00:57:23in the blood banking module.
00:57:25Right.
00:57:25I want you to listen to that module
00:57:27along with this shock module
00:57:30because those values
00:57:32are asked in the exam.
00:57:34The reason why
00:57:35I don't want to tell you
00:57:36the values here
00:57:37because we compared
00:57:38and the values in Bailey
00:57:40and the values in Robbins
00:57:41are different
00:57:42and blood banking,
00:57:44there is a standard book
00:57:45for blood banking.
00:57:46So, Dr. Rilla
00:57:47has covered values
00:57:48from that standard book.
00:57:50So, I want you to
00:57:51remember those values
00:57:52rather than the ones
00:57:53which are mentioned in Bailey.
00:57:56So, this is how we prevent
00:57:57coagulopathy.
00:57:58Now, another thing
00:57:59which I want you to know here,
00:58:01there are two scores
00:58:02which are
00:58:03for massive blood transfusion.
00:58:06These are
00:58:06scores which help
00:58:09in taking decisions
00:58:10regarding massive blood transfusion
00:58:11especially in trauma patients.
00:58:13You have the ABC score.
00:58:15It has three parameters
00:58:17penetrating trauma mechanism,
00:58:20systolic BP less than 90,
00:58:22heart rate more than 120
00:58:23and positive fast.
00:58:26And you have the TASH score.
00:58:28You need to remember
00:58:29the full form of TASH score.
00:58:31It is trauma associated
00:58:33severe hemorrhage score
00:58:35and it has seven parameters in it.
00:58:38These two scores
00:58:39have not been asked
00:58:40in the exam as of now
00:58:41but I just want you
00:58:42to remember the names
00:58:43and the full form of TASH.
00:58:47You also need to remember
00:58:48about blood substitutes, right?
00:58:50Sometimes,
00:58:51we don't get blood.
00:58:53Supposing,
00:58:54you know that
00:58:54we are in a very tricky situation
00:58:56with China right now
00:58:58and it is in a place
00:59:01like Ladakh
00:59:01and you have,
00:59:03if there is going to be a fight,
00:59:05it's going to be
00:59:05on high altitudes
00:59:07where you don't have a blood bank,
00:59:08you don't have stored blood
00:59:10there as well.
00:59:11So, in places like those,
00:59:13you need to have
00:59:14blood substitutes also
00:59:15to maintain the patient's life
00:59:18till you can shift the patient
00:59:19to the hospital, okay?
00:59:21So, these blood substitutes,
00:59:23you have first generation
00:59:25substitutes like
00:59:26perfluorocarbons,
00:59:27second generation
00:59:29astroma-free hemoglobin
00:59:30and the latest generation,
00:59:32the next generation
00:59:33which is being evaluated
00:59:34these days
00:59:35is polyethylene glycol hemoglobin,
00:59:38hemospan,
00:59:40hemospan,
00:59:41a lot of trials
00:59:41have been done
00:59:42in hemospan,
00:59:43this is
00:59:44PEG conjugated
00:59:45human hemoglobin
00:59:46and you have
00:59:47pyrotoxylated hemoglobin,
00:59:50polyoxyethylene conjugate,
00:59:52PHP,
00:59:53this has also been evaluated.
00:59:55So, I just want you
00:59:55to remember the names,
00:59:57again,
00:59:57this has not been asked
00:59:58in the exam
00:59:59till now.
01:00:00I have also told you
01:00:03about this
01:00:04anti-shock garment
01:00:06when I was talking
01:00:08about pneumatic
01:00:09anti-DVT stockings,
01:00:11I told you about
01:00:12this anti-shock garment
01:00:13as well.
01:00:15This anti-shock garment,
01:00:17you have numbering
01:00:18from 1 to 6
01:00:19and this is used
01:00:21in patients
01:00:21with hypovolemic shock.
01:00:26So, where do we use it?
01:00:28Supposing you have a lady
01:00:29who has delivered
01:00:31in a primary health center
01:00:32and she starts having
01:00:34postpartum hemorrhage.
01:00:36Now, the primary health center
01:00:38is not well equipped
01:00:39to manage this
01:00:40postpartum hemorrhage
01:00:41and you need to
01:00:42shift the patient
01:00:43to the hospital
01:00:43but the hospital
01:00:45is 1 hour away.
01:00:46So, of course,
01:00:47you are going to give
01:00:48fluids to the patient
01:00:49but you will also
01:00:50tie this garment
01:00:51and this garment,
01:00:53there is sequential
01:00:54compression,
01:00:56maximum compression
01:00:57here
01:00:57and least compression
01:01:01here
01:01:01as we go up.
01:01:03So, what this does
01:01:04is that this
01:01:05squeezes out blood
01:01:07from the limbs
01:01:07and sends it
01:01:09to the heart
01:01:09so that the blood pressure
01:01:11can be maintained
01:01:12for some time
01:01:13till the patient
01:01:14is shifted
01:01:14to the hospital.
01:01:16Okay?
01:01:17So, this was regarding
01:01:18massive blood transfusion.
01:01:21Another thing
01:01:21which I want you to know,
01:01:22there are some
01:01:23key definitions
01:01:24which I want you
01:01:24to remember
01:01:25in hypovolemic shock.
01:01:29One is
01:01:30occult hypoperfusion.
01:01:31This is the new term
01:01:32which is there
01:01:33in Bailey
01:01:34and you need
01:01:34to remember this.
01:01:36So, occult hypoperfusion
01:01:38means
01:01:38that the patient
01:01:40is going to have
01:01:41normal
01:01:41cardiovascular
01:01:43parameters.
01:01:46The patient
01:01:46is going to have
01:01:47normal cardiovascular
01:01:48parameters
01:01:49that means
01:01:49pulse rate BP.
01:01:51Patient is going
01:01:52to have
01:01:52normal urine output.
01:01:55Normal urine output
01:01:56but
01:01:57there is going
01:02:00to be
01:02:00low
01:02:01MVOS
01:02:02and
01:02:04acidosis.
01:02:07Right?
01:02:08So, this is
01:02:09the preclinical
01:02:11state
01:02:11of
01:02:12hypotension.
01:02:13This is
01:02:13occult hypotension
01:02:15where the parameters
01:02:16are normal.
01:02:17Your cardiovascular
01:02:18and urine output
01:02:19but there is
01:02:20low MVOS
01:02:21and there is
01:02:22acidosis
01:02:23in this patient.
01:02:24Now, what is
01:02:25the importance
01:02:25of occult hypoperfusion?
01:02:27That if
01:02:28occult hypoperfusion
01:02:30if it lasts
01:02:32for more
01:02:33than 12 hours
01:02:34then there
01:02:37is a poor
01:02:37outcome.
01:02:38So, we need
01:02:39to identify
01:02:40occult hypoperfusion
01:02:42early
01:02:42and we need
01:02:44to manage
01:02:44it on time.
01:02:45What is
01:02:48dynamic fluid
01:02:49response
01:02:49in shock?
01:02:52So, any
01:02:52patient with
01:02:53shock
01:02:54we have
01:02:54discussed
01:02:54that we
01:02:55have to
01:02:55give fluids
01:02:55to these
01:02:56patients
01:02:56and
01:02:57whenever we
01:02:59get a
01:02:59patient with
01:02:59shock
01:03:00we give
01:03:00a bolus
01:03:01of fluid
01:03:02which is
01:03:07250 to
01:03:08500 cc
01:03:09bolus
01:03:10we give
01:03:10as soon
01:03:11as we
01:03:12get this
01:03:12patient
01:03:12and a
01:03:13normal
01:03:14response
01:03:14after giving
01:03:15this is
01:03:15that the
01:03:16CVP
01:03:17increases
01:03:18by 2 to
01:03:195 centimeters
01:03:20of water
01:03:21CVP
01:03:23rises by
01:03:232 to
01:03:245 centimeters
01:03:25of water
01:03:26and it
01:03:29gradually
01:03:30normalizes
01:03:31it
01:03:33gradually
01:03:33normalizes
01:03:34in
01:03:3820 minutes
01:03:39or so
01:03:40so this
01:03:42is normal
01:03:43response
01:03:43now there
01:03:44can be
01:03:44three types
01:03:45of
01:03:45responses
01:03:47in a
01:03:48patient
01:03:49with
01:03:49shock
01:03:50you can
01:03:51have
01:03:51responders
01:03:52once you
01:03:54give this
01:03:55fluid
01:03:56you can
01:03:56have
01:03:56responders
01:03:57I have
01:03:59just told
01:04:00you that
01:04:00they will
01:04:01be a
01:04:03CVP
01:04:03rise
01:04:04and it
01:04:05will then
01:04:06normalize
01:04:07like I have
01:04:07just told
01:04:08you
01:04:08then you
01:04:09can have
01:04:09non-responders
01:04:11non-responders
01:04:14when there
01:04:15is no
01:04:17change
01:04:17and you
01:04:20can have
01:04:21transient
01:04:21responders
01:04:22and you
01:04:25can have
01:04:26transient
01:04:26responders
01:04:27transient
01:04:31responders
01:04:31will show
01:04:34a rise
01:04:35in
01:04:35CVP
01:04:36will show
01:04:37rise in
01:04:38CVP
01:04:39but
01:04:41CVP
01:04:44again
01:04:44returns
01:04:46to
01:04:47pre-treatment
01:04:50value
01:04:50that
01:04:53means
01:04:54again
01:04:54low
01:04:54CVP
01:04:55in
01:04:5810 to
01:04:5915
01:04:59minutes
01:05:00so
01:05:01initially
01:05:01they show
01:05:02a spike
01:05:03they show
01:05:03increase
01:05:04but then
01:05:05it returns
01:05:05to the
01:05:06pre-treatment
01:05:06value
01:05:07in 10 to
01:05:0815
01:05:08minutes
01:05:08so
01:05:09these are
01:05:09the three
01:05:09kind of
01:05:10responses
01:05:11which we
01:05:11can get
01:05:11when we
01:05:12give fluids
01:05:12to a
01:05:13patient
01:05:13of
01:05:13shock
01:05:14how does
01:05:15this
01:05:16help me
01:05:16as a
01:05:17clinician
01:05:17non-responder
01:05:19means that
01:05:20the patient
01:05:20is losing
01:05:21so much
01:05:21of blood
01:05:22that the
01:05:23rate at
01:05:24which I am
01:05:24giving is
01:05:25not able to
01:05:26match with
01:05:26the rate
01:05:27of loss
01:05:28so we
01:05:29need to
01:05:29evaluate
01:05:30what is
01:05:30the cause
01:05:31of loss
01:05:31and we
01:05:32need to
01:05:32treat that
01:05:33transient
01:05:35responder
01:05:36means that
01:05:36there is
01:05:37ongoing
01:05:38losses
01:05:38happening
01:05:39so again
01:05:40these patients
01:05:41we need to
01:05:42monitor
01:05:42carefully
01:05:43and we
01:05:44need to
01:05:45identify
01:05:46the cause
01:05:46and treat
01:05:47that as
01:05:47well
01:05:47okay
01:05:48so these
01:05:49are the
01:05:50three types
01:05:51of responses
01:05:51which we
01:05:52can get
01:05:52in a
01:05:53patient
01:05:53with
01:05:53shock
01:05:54another
01:05:55important
01:05:56update
01:05:57in the
01:05:5727th
01:05:58edition
01:05:58of
01:05:58Bailey
01:05:58is that
01:05:59the
01:05:59perioperative
01:06:00blood
01:06:01transfusion
01:06:01guidelines
01:06:02have been
01:06:03changed
01:06:03perioperative
01:06:04transfusion
01:06:06means after
01:06:07surgery
01:06:07if a
01:06:08patient
01:06:08is to
01:06:09be given
01:06:09blood
01:06:09or not
01:06:10given
01:06:10blood
01:06:10those are
01:06:11now determined
01:06:12by these
01:06:13guidelines
01:06:13and you
01:06:14need to
01:06:14remember
01:06:14this
01:06:15this is
01:06:15very
01:06:15important
01:06:16that if
01:06:18the hemoglobin
01:06:19is less
01:06:19than 6
01:06:20if the
01:06:20hemoglobin
01:06:21is less
01:06:22than 6
01:06:22then there
01:06:24is going
01:06:24to be
01:06:25benefit
01:06:25from
01:06:27transfusion
01:06:28if the
01:06:29hemoglobin
01:06:29is 6
01:06:30to 8
01:06:31only give
01:06:32blood
01:06:33we only
01:06:35give blood
01:06:35if
01:06:37ongoing
01:06:37losses
01:06:38are there
01:06:39if
01:06:40ongoing
01:06:41losses
01:06:41are present
01:06:42then only
01:06:43we give
01:06:43blood
01:06:44and
01:06:44more
01:06:45than
01:06:458
01:06:45there
01:06:46is
01:06:46no
01:06:46indication
01:06:47of
01:06:48giving
01:06:48blood
01:06:50transfusion
01:06:50if the
01:06:51hemoglobin
01:06:51is more
01:06:52than 8
01:06:52so please
01:06:53remember
01:06:53these
01:06:54parameters
01:06:55one final
01:06:56thing
01:06:56which I want
01:06:57you to
01:06:57know
01:06:58this was
01:06:58asked in
01:06:58the
01:06:58AIMS
01:06:59exam
01:06:59a couple
01:06:59of
01:06:59years
01:07:00back
01:07:00when we
01:07:01are giving
01:07:01blood
01:07:01there is
01:07:02a special
01:07:02filter
01:07:03which we
01:07:03can use
01:07:04here
01:07:04this is
01:07:05known as
01:07:05a
01:07:05leukoreduction
01:07:06filter
01:07:07this is
01:07:10a
01:07:10leukoreduction
01:07:11filter
01:07:11again the
01:07:12details have
01:07:13been covered
01:07:14in the
01:07:14blood banking
01:07:15module by
01:07:16Dr.
01:07:16Rilla
01:07:16so
01:07:17leukoreduction
01:07:18filter
01:07:18it reduces
01:07:20the incidence
01:07:21of
01:07:24febrile
01:07:25reactions
01:07:25it reduces
01:07:28the incidence
01:07:29of
01:07:29febrile
01:07:30reactions
01:07:31so this
01:07:32takes care
01:07:32of
01:07:33hypovolemic
01:07:33shock
01:07:34it is
01:07:34a
01:07:34very
01:07:34very
01:07:35important
01:07:35topic