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Medico Macha
  • 7/8/2025
Transcript
00:00let's make a table regarding the other types of shocks now so we've already
00:12discussed hypovolemic shock hypovolemic we've already discussed the other type
00:20of shocks can be cardiogenic shock so this is related to cardiac causes then
00:28another very important one is neurogenic shock this is also been asked in the
00:34exam quite frequently you have anaphylactic shock anaphylactic shock
00:43and you have septic shock septic shock you know is divided into a warm septic
00:51shock and a cold septic shock two more terms which you need to know you can
00:59have obstructive shock this I'll cover in some time you can have distributive shock
01:07after making this table I will cover these two terms and the third one is
01:13endocrine shock right so these are three more types of shocks I'll tell you about
01:20them once I've made this table regarding these five types and the various
01:25parameters which we need to consider in this table are pulse rate cardiac output
01:35systolic blood pressure JVP JVP is jugular venous pressure and peripheral vascular
01:44resistance so first let's write peripheral vascular resistance and JVP PVR is
01:50peripheral vascular resistance JVP is jugular venous pressure or the CVP central
01:56venous pressure now hypovolemic shock we've already covered and we are assuming
02:02that we have a patient in class 3 hypovolemic shock we are assuming a patient
02:07in class 3 hypovolemic shock let's fill in the blanks we know that there is going to
02:11be tachycardia and class 3 hypovolemic shock the cardiac output is going to
02:16fall cardiac output falls and we know that systolic blood pressure also falls
02:22for the first time in class 3 shock peripheral vascular resistance now we've
02:29discussed that the extremities are going to be cold right and whenever we have
02:34cold extremities why do we have cold extremities because there's peripheral
02:39vasoconstriction and when there is peripheral vasoconstriction what will
02:44happen to the resistance it is going to go up so the peripheral vascular
02:49resistance is going to be raised please don't get confused yes initially
02:55peripheral vascular resistance rise is going to give rise to increase in
03:00diastolic blood pressure but as the blood volume loses from the body as the blood
03:06volume is lost from the body then the diastolic blood pressure is also going to
03:11fall okay jvp also falls because there's loss of circulating blood volume so these
03:20are the parameters for hypovolemic shock cardiogenic shock there can be multiple
03:25causes of cardiogenic shock you can have myocardial infarction you can have
03:30arrhythmia you can have tamponade there can be various causes of cardiogenic shock we
03:40can consider anyone let's consider a patient who's had a myocardial infarction
03:45so when there is a myocardial infarction the cardiac output is reduced the heart is
03:51not working properly because the cardiac output is reduced the systolic blood
03:55pressure is reduced and because the cardiac output is reduced blood is not flowing to
04:03the extremities properly so the extremities are extremities are cold extremities are cold
04:13there is vasoconstriction in the extremities so because there's vasoconstriction there is
04:21increase in peripheral vascular resistance which is there and also you need to remember that because
04:29the heart is not working the cardiac output is low the preload preload is the blood which is there
04:36which the hardest to pump out right so the preload is accumulating and this leads to increase in jvp and
04:46you have engorged and dilated neck veins okay so this is regarding cardiogenic shock if you have to fill
04:54in the table now pulse rate can either be increased or decreased why because in arrhythmias you might have
05:03a high heart rate whereas if there is a patient who has a heart block which can also give rise to
05:09cardiogenic shock there will be bradycardia so you can either have increase or decrease in pulse rate
05:14cardiac output is going to reduce systolic bp is going to reduce extremities are again cold so
05:21peripheral vascular resistance increases and because the heart is not pumping out blood there is raised jvp
05:29engorged neck veins moving on to very important neurogenic shock neurogenic shock has been asked almost
05:37the same number of times as hypovolemic shock now neurogenic shock we are going to consider the example
05:44of we are going to consider the example of a transacted spinal cord a transacted spinal cord after a road
06:01traffic accident in the trauma module I've told you that cervical spine is very important for us if there
06:08is a cervical spine injury that can give rise to spinal shock there can be transaction of the spinal cord
06:14cord and it can give rise to neurogenic shock in patients okay so here I just want you to remember
06:23one thing if you just remember this one term the entire physiology would become very easy for you to
06:29understand and that one term is that when the spinal cord is transacted there is loss of sympathetic tone
06:38there is loss of sympathetic tone just this one term is enough to understand the physiology when there is
06:49loss of the sympathetic system or loss of sympathetic tone you know what is going to happen there is going
06:56to be vasodilation is going to be there right we are going to have vasodilation and these patients are
07:08also going to have bradycardia because there is loss of sympathetic tone so there is going to be
07:14bradycardia that means the heart rate is low and there is vasodilation in the periphery because the
07:22sympathetic tone has gone now when there is peripheral vasodilation extremities are going to be warm because
07:32there is more blood accumulating there so you have vasodilation warm extremities and this is going to
07:40give rise to pooling of blood why is there pooling of blood because our poor patient is lying on the ground
07:47after the accident his spinal cord is transacted cannot move and all the blood is there in the peripheries but
07:55the blood is not returning back right blood is not returning back so there is pooling of blood
08:03there is decreased venous return now if there is decreased venous return common sense question
08:10what is going to happen to the preload the preload is going to reduce so decrease jvp because less blood
08:18is returning decreased preload means decreased cardiac output which means decreased systolic blood pressure
08:28so this is the physiology behind neurogenic shock right let's fill in the blanks now in the table
08:37so neurogenic shock you can see there is bradycardia occurring cardiac output is also reducing systolic bp is
08:46also reducing peripheral vascular resistance is reducing why because the extremities are warm
08:53and jvp is also falling because the return is less so all the parameters have reduced and the question
09:03which has been asked umpteen number of times is bradycardia
09:09and hypotension are seen in which shock it they are seen in neurogenic shock
09:19they are seen in neurogenic shock please don't confuse this with bradycardia and hypertension
09:27which is seen in head injury bradycardia hypertension and head injury is cushing reflex i've covered that in
09:35the head injury module right don't confuse that with neurogenic shock neurogenic shock is brady and hypotension okay
09:46let's talk about anaphylactic shock now anaphylactic shock we are going to consider the example of a mismatched
09:53blood transfusion right so anaphylaxis you can have mismatched blood transfusion
10:00now when there is a mismatched blood transfusion
10:07histamine is released and histamine is the driver for this anaphylaxis and anaphylactic shock
10:14you know large quantities of histamine are released now i want you to very carefully observe what is
10:20happening in this shock okay and this is the correlation which i want you to understand
10:25so when histamine is released you know histamine is a potent vasodilator
10:32right potent vasodilator so look carefully
10:37vasodilation
10:39this is going to give rise to warm extremities
10:42this will again give rise to pooling of blood
10:44again give rise to decrease venous return
10:48again give rise to decreased
10:50jvp again decrease cardiac output decrease systolic blood pressure
10:55so the story is exactly the same as
10:59neurogenic shock but what is the difference here
11:05but sympathetic system is normal
11:10sympathetic system is normal
11:13therefore pulse rate is going to increase
11:19so everything is the same as neurogenic the only difference is that there is going to be
11:24tachycardia in anaphylactic shock rest is the same as
11:30neurogenic so easy to remember
11:32anaphylactic shock
11:33tachycardia rest everything reduces as neurogenic shock okay
11:44moving on to septic shock septic shock
11:47you have two phases of septic shock so in the warm phase of septic shock
11:51i just want you to remember one term
11:54the term which i want you to remember in warm septic shock is hyper dynamic
12:01circulation
12:05is hyper dynamic circulation that is the only term which i want you to remember
12:09in warm septic shock so what is happening the heart is working
12:14quickly when you have fever there is tachycardia heart is working quickly
12:18blood is quickly going through the body and coming back
12:22right so blood goes quickly comes back quickly
12:25there is a hyper dynamic circulation which is there
12:29so there's going to be tachycardia
12:34there's going to be tachycardia because the heart is working over time
12:39there is cardiac output is going to be increased
12:43so when the cardiac output is increased
12:45systolic blood pressure will also be increased or normal
12:50right extremities are warm it's there in the shock itself warm extremities
12:56so warm extremities means peripheral vascular resistance is low
13:01extremities are warm and what is happening to the jvp so understand this
13:06this is very important whatever the heart is pumping out
13:10it is coming back and again the heart is pumping that out
13:14right so pump comes back pumps comes back it pumps again there is no
13:20backlog which is occurring here right no backlog of preload
13:25so jvp is normal jvp is normal in these patients okay
13:32this is warm septic shock cold septic shock i want you to remember
13:38that in late phases of sepsis in late phases of sepsis
13:47what happens bacterial toxins
13:52bacterial toxins inhibit the myocardium
13:57the bacterial toxins inhibit the myocardium therefore late septic shock
14:02late septic shock or cold septic shock is equal to cardiogenic shock
14:12is equal to cardiogenic shock so the parameters of cold septic shock
14:18are exactly the same as cardiogenic shock so this is another easy correlation
14:24for you so that you can remember this for the exam
14:29now these three terms which i mentioned obstructive distributive and endocrine shock
14:35what exactly do these mean first let's talk about obstructive shock
14:39so obstructive shock by definition is a shock in which a shock in which
14:53the preload
14:57so obstructive shock by definition is a shock in which the preload is reduced
15:03due to mechanical impairment in cardiac filling due to mechanical impairment
15:18in cardiac filling
15:24right so what exactly does this term mean let's consider the examples of obstructive shock you can
15:31have cardiac tamponade cardiac tamponade i've covered in the thoracic trauma module
15:37cardiac tamponade you know that there is rapid accumulation of blood around the heart
15:43rapid accumulation of blood around the heart and because of this the heart cannot relax
15:48if the heart cannot dilate or relax filling will not happen right and if filling does not happen
15:55cardiac output will not get generated okay so this is one example cardiac tamponade
16:01another one is another one is a massive pulmonary embolism
16:10a massive pulmonary embolism is also going to hamper cardiac filling and when cardiac filling gets
16:17hampered the cardiac output and the systolic blood pressure reduce so this is obstructive shock
16:23distributive shock
16:29so distributive shock is
16:33when the blood redistributes to the peripheries
16:39when the blood redistributes to peripheries
16:43the peripheries thereby thereby reducing
16:54cardiac output
16:57right so when there is more blood which accumulates in the peripheries less blood is coming back to the heart
17:04and that is going to give rise to shock so what are the examples of distributive shock
17:11they are going to be neurogenic
17:15you will have anaphylactic
17:16and you will have warm septic shock so all the three shocks in which the extremities are warm
17:29they classify as distributive shock so easy way to remember
17:33any shock with warm extremities is an example of distributive shock
17:38and endocrine shock
17:48endocrine shock can be a combination of
17:53endocrine shock can be a combination of distributive
17:59and hypovolemic
18:08and cardiogenic shock
18:11right it can be a combination of these shocks
18:14and endocrine shock you can get in
18:18hypo hyperthyroidism
18:20and adrenal problems
18:31and in patients with adrenal problems okay so these are three more definitions which you should know
18:38and this covers the various types of shocks which you need to know for the exam now we are going to
18:45talk about septic shock in detail because that is a very important topic for the exam so we will talk about sepsis
18:55so there are certain definitions in sepsis and septic shock which are asked frequently in the exam
19:01the first one which you need to know is SIRS
19:06SIRS stands for systemic inflammatory response syndrome
19:10in simple terms what is this in simple terms this is the body's response
19:27this is the body's response to inflammation
19:32it is the body's response to inflammation
19:34now this inflammation this inflammation can either be infective
19:43or non-infective
19:46so it can be secondary to
19:48infection or it can even be secondary to trauma so it's not necessarily that it's all because of infection or sepsis only
19:56this is the body
19:59this is mediated by IL-1, IL-6 and TNF-alpha
20:06mediated by IL-1, IL-6 and TNF-alpha these
20:10interleukins have been asked in the exam which
20:15control the SIRS response of the body
20:18what are the parameters the parameters are
20:21temperature less than 36 degree centigrade or more than 38 degree centigrade
20:31WBC count less than 4000 or more than 12,000
20:40or more than 10 percent band forms in peripheral smear
20:47this last one is something which students forget so please make sure you don't forget this this has been asked in the UPSC exam many times
20:57third parameter is respiratory rate more than 20 per minute
21:03or pCO2 less than 32 millimeters of mercury
21:10right and the final parameter is pulse rate
21:14more than 90 per minute so these are the four parameters which you need to remember regarding
21:22SIRS
21:23so these are the four parameters which you need to remember regarding SIRS and if any two parameters are met
21:31if any two parameters are met
21:39then we say that the patient is having SIRS systemic inflammatory response syndrome
21:45what are the other definitions the other definitions are sepsis
21:49so sepsis is SIRS plus a known site or known foci of infection
22:01means supposing if somebody has a boil and that boil is giving rise to SIRS
22:07then we will say that the patient has sepsis because the patient has parameters of SIRS
22:13but the cause is that boil so we are going to say that the patient is in sepsis
22:21septic shock
22:25septic shock
22:26is sepsis plus hypotension
22:32sepsis plus hypotension which fails to respond to fluids
22:39which fails to respond to fluids
22:43septic shock
22:45that is septic shock
22:49M O D S multiple organ dysfunction syndrome
22:57multiple organ dysfunction syndrome
23:02so M O D S is
23:04when there is failure of two or more
23:11two or more organ systems
23:17that is when we say the patient has M O D S
23:21this has a high mortality rate
23:23now one thing which I want you to understand is
23:26that kidneys will be one organ system
23:28it's not as a one or both kidneys have failed
23:31so you won't count it as two organs
23:33so kidneys would be one organ system
23:36respiratory system would be another organ system
23:38cardiac would be another organ system
23:41CNS would be another organ system
23:43right so if there is failure of two or more organ systems
23:47we label it as
23:49M O D S
23:53so these are certain definitions which you need to remember
23:56now there has been certain new updates regarding sepsis
24:00and those updates I want you to know
24:02the first update is
24:05this SOFA score
24:07this is the sepsis related organ failure assessment score
24:13this is the SOFA score
24:15and if you have a SOFA score of two or more than two
24:22plus known foci
24:23plus known foci
24:28then we call it sepsis
24:32right
24:32a SOFA score of two or more than two plus a known foci of infection would classify as sepsis
24:39but what you need to understand here is that this SOFA score is such an elaborate score
24:44that it becomes difficult for us to measure each and every parameter
24:48so to circumvent that problem of having so many parameters
24:53they've also come out with a Q SOFA score
24:56what is Q SOFA
24:58this is quick sequential
25:02this is quick sequential organ failure
25:08assessment score
25:09Q SOFA score is Q SOFA and what are the parameters which are included in Q SOFA
25:20you have systolic BP less than 100
25:24altered mental status
25:26and tachypnea more than 22
25:29please please don't get confused
25:32here tachypnea is more than 22
25:35but in SIRS tachypnea guideline was more than 20
25:40so they're different don't get confused between the two
25:44now if you have a score of two or more than two
25:48it indicates a poor outcome
25:51so you need to remember Q SOFA you need to remember the parameters
25:55in the last four years there have been six questions and various exams regarding Q SOFA
26:01this is very very important for your exam
26:04so sepsis 3.0 these are the latest guidelines
26:08what are the updates which we need to remember
26:11the definition of sepsis now has changed
26:14one definition I've told you is SOFA score of two or more than two plus known foci of infection
26:21another one is life-threatening organ dysfunction
26:25caused by a dysregulated host response to infection
26:29right so that is another definition of sepsis
26:33septic shock the definition has changed very important
26:36it is the need for vasopressors
26:40and a serum lactate more than two millimoles per liter
26:47and a serum lactate of two millimoles per more than two millimoles per liter
26:52the term severe sepsis has been removed
26:56and SIRS is out and Q SOFA and SOFA are used
27:01one more thing this is not there in Bailey but it's there in Subistan
27:05the surviving sepsis guidelines and you had a question in the NEAT exam
27:10last to last year from the surviving sepsis guidelines
27:14now these guidelines say that within the first six hours of resuscitation
27:19of a septic patient
27:23we need to achieve all these goals what are the goals which we need to achieve in a
27:28patient with sepsis who's undergoing resuscitation
27:31we need to get a CVP of 8 to 12 millimeters of mercury
27:37MAP mean arterial pressure of more than equal to 65 millimeters of mercury
27:44urine output of more than equal to 0.5 ml per kg per hour
27:48and MVOS mixed venous oxygen saturation of 65 or more
28:00I told you some time back that MVOS and sepsis is increased
28:06and we have to maintain it that way so that adequate oxygen reaches the tissues
28:12so the MVOS in sepsis should be kept between 65 to 70
28:18okay also we need to normalize lactate in these patients
28:25now if you have a patient with septic shock
28:30if you have a patient with septic shock septic shock first give fluids
28:38we have to first give fluids and
28:41if they are not sufficient if they are not sufficient
28:51then we can start the patient on inotropes
28:57and vasopressors
29:00then we can start the patient on inotropes and vasopressors
29:04like you can start the patient on dopamine, dobutamine, noradrenaline
29:12but all of these are started only once the patient has failed on fluid resuscitation
29:19okay so this is the management of septic shock
29:22I have told you the definitions which are important for the exam
29:26and this brings us to the end of this module
29:28I have told you time and again that this module is very very very important
29:33from the point of view of all exams
29:36before we end let's just solve few MCQs
29:41so which one of the following is seen in
29:45massive blood transfusion
29:48now I have told you that both metabolic alkalosis and acidosis can be seen
29:55but what is more important and more common is metabolic acidosis
30:00so if you are given a question like this you will choose metabolic acidosis
30:06the capillary refill time is prolonged in all types of shock except
30:12right so capillary refill time prolonged when will capillary refill time be prolonged
30:20when there is vasoconstriction and less blood is flowing or when there is vasodilation and more blood is flowing
30:28of course when less blood is flowing that is when capillary refill is going to be delayed
30:34so or prolonged so that is going to happen in hypovolemic shock
30:39it is going to happen in cardiogenic shock obstructive shock you know as a type of cardiogenic shock only
30:45so here you will have cold extremities cold extremities cold extremities
30:52so the capillary refill time will be prolonged septic shock you know you have warm extremities
31:00so here the capillary refill time will not be prolonged okay this is another practical application of that table
31:08which we have discussed
31:12you have a 26 year old man with road traffic accident he had a pelvic fracture and was transfused blood
31:20within a few hours the patient develops fever oliguria and hypotension cvp is normal but there is bleeding
31:28from the site of the iv line through the riles tube what is the most common diagnosis
31:35this was asked in the aims exam fat embolism you know can occur after a long bone fracture but it
31:43occurs after around 24 to 48 hours so this is out adrenal insufficiency there is no indication that this
31:53patient might have adrenal insufficiency hemorrhagic shock if there was hemorrhagic shock
31:59cvp how will cvp be normal for cvp to be normal cannot be hemorrhagic shock in hemorrhagic shock cvp or jvp will
32:09be reduced we've discussed this so this is also out so even by elimination we can reach to blood transfusion
32:18reaction but the classic keyword here which is a throwaway that it is a blood transfusion reaction
32:26is that there is bleeding which is happening from the iv lines from the riles tube so there is coagulopathy
32:33which has started happening and you can see this is a direct picture from bailey where
32:41if antibodies are present in incompatible transfusion this is going to result in acute hemolytic reaction
32:49so hemolysis is what is happening there and that is what is giving rise to the transfusion reaction in
32:56this patient which is not a complication of massive blood transfusion so we know hyperkalemia can occur we
33:05know hypocalcemia can occur we know hypokalemia can occur so hypercalcemia will not occur okay this was
33:14another question asked in the exam right in hemorrhage larger arterioles vasoconstrict in response to the
33:25sympathetic nervous system yes that is why there are cold extremities when there is hemorrhage which
33:32categories are associated with vasodilation of large arterioles so don't get confused by such technical
33:42questions and technical terms try to simplify it for yourself okay the examiner is saying that in
33:49hemorrhage shock there is vasoconstriction so the extremities are cold now he is asking which are the
33:57shocks where there is vasodilation so if there will be vasodilation extremities are going to be what
34:04extremities are going to be warm so which are the shocks where extremities are warm you have septic
34:12shock neurogenic shock so the answer becomes a and c following a recent abdominal surgery the patient is in
34:22the icu with sepsis below what level of hemoglobin would a transfusion be indicated i've told you that
34:30transfusion now is indicated when it is six or close to six that's when you're going to do transfusion if
34:38it's six to eight then there has to be ongoing losses then only we transfuse okay so this is a very
34:47important question this is where you're given a clinical scenario and these are the options which
34:54you have to choose from whether the patient has sirs sepsis mods septic shock or severe sepsis so let's
35:03look at the statements and see what the patient has you have a 44 year old male he has an ileal perforation
35:12on the third post-operative day he has pain and an ultrasound reveals that there has been a leak
35:22so there is a leak after surgery there has been a leak his pulse rate is 100 per minute tachycardia
35:31bp is 100 by 80 wbc count is 15 000 respiratory rate is 20 per minute
35:39the urea is 70 creatinine is 1.5 he is conscious and oriented but complaining of pain so what does this
35:48patient have okay let's start step by step like i told you the definitions does this patient have sirs yes
35:58or no let's see his counts are raised and his respiratory rate is more than 20 so two parameters are met
36:08yes he has sirs now does he have does he have a foci of infection
36:20that is the next question i need to ask myself when i'm approaching such questions yes he does have
36:27a foci of infection there is an ileal perforation leak which has occurred after repair there has been
36:34a leak so i know that sirs plus foci is equal to sepsis so this much i know that this patient is
36:46having sepsis does he have mo ds
36:52does he have mo ds you know mo ds is failure of two or more organ systems
37:00so if you look here his kidneys urea is 70 kidney function is deranged kidneys are gone so one organ
37:08system is gone but he is conscious and oriented so cns is intact so only one organ system is affected
37:18here so does he have mo ds no he does not so what is the answer here the patient has sepsis
37:26i hope this is clear because you can expect many more questions like this in your next exam in your
37:36ini cet exam you will be shown clinical vignettes like this and you'll be asked questions and i've
37:43just told you the approach to such questions okay let's look at another patient will follow the same
37:49approach you have a 65 year old diabetic patient who's been brought with four years gangrene four
37:56years gangrene you know is necrotizing fasciitis of the perennial region the pulse rate is 110 so
38:03tachycardia BP is 90 systolic BP is also falling on giving fluids BP does not improve okay he started on
38:13dopamine in noradrenaline and debridement is planned his liver functions are marginally deranged but other
38:21blood parameters are normal so let's do the same analysis as we did here does this patient
38:30does this patient have sirs yes why because there's tachycardia and there is hypotension so two parameters
38:42are met yes he has sirs does he have a known foci of infection yes he has four years gangrene
38:50so he has sirs and he has four years so he has sepsis this much also we know
39:03is there septic shock
39:08is there septic shock well there is hypotension and it does not improve with fluids does not improve with
39:17fluids so yes there is septic shock in this patient is there mo ds no there is no mo ds because his only
39:27his liver functions are deranged rest of the parameters are normal so here the answer is going to be septic
39:35shock so you can see different clinical scenarios and how have we utilize the definitions which i told you
39:44to answer these clinical scenarios this is very important for your future exams this brings us to
39:51the end of this very important module on shock thank you