Full transcript
0:00Let's say a general hospital in a local
0:02area here in Mexico . Mortality can
0:04skyrocket to 80 % . It's very high . I
0:07stand next to the patient , I examine
0:08them , I look at capillary refill time ,
0:10I look at lauresis , I look at altered
0:12mental status . Clinically , that patient
0:14already meets my definition of shock .
0:17We could estimate that 70 to 80 % of
0:19cogenic shocks are due to an acute
0:21myocardial infarction , always
0:23accompanied by the most objective
0:25measurement possible in order to have a
0:27guided intervention . Okay ? No , no , not
0:31so much doing it empirically by just
0:33giving them NORED or BUT or giving them
0:35a fluid load . There comes a point where
0:38the drugs have a limit
0:40and the NORED is already stratospheric
0:42doses and you say , " No more , I have to
0:44move on to a device now . " And for that
0:48we look for a care strategy , we do the
0:50work of the heart . So , it is the
0:53interventions that generate changes in
0:56the patient's prognosis . Even the
0:58security guard needs to know that this
1:01is a disease which is dependent on time
1:04. There will never , ever be any other
1:07hemodynamic monitoring that can replace
1:11the doctor's commitment to the
1:13patient's bedside . Welcome to another
1:21episode of Interconsulta , the medical
1:23podcast . I'm Ider Samarrón , an
1:25emergency intensive care specialist ,
1:26and welcome here to this YouTube
1:28channel , Training in Critical Care
1:29Areas . If you're watching on Spotify or
1:31listening to it , remember to follow us
1:34on Training in Critical Care Areas on
1:36YouTube and vice versa . Today we're
1:39going to address one of the most
1:41complex emergencies with the highest
1:43mortality rate in critical care
1:45medicine : cardiogenic shock .
1:47Recognizing it early , identifying its
1:50cause , and starting appropriate
1:51treatment can make the difference
1:53between life and death . And to discuss
1:57this topic , we're joined by a
1:59specialist in cardiovascular intensive
2:01care , my friend Dr. Luis Morgado Villa .
2:05Sir , we're going to ask him from start
2:08to finish , how is this condition
2:10currently treated ? Welcome , Luis . How
2:13are you ?
2:13Thank you very much , Eder . Very well ,
2:14it's a pleasure to be here with you .
2:16Thank you very much for the invitation .
2:17Well , let's get started . That's right .
2:19Look , not normally , I'll introduce you
2:22to the guest . He's a friend of mine for
2:25many years . I met him when I was an
2:28intensive care resident , and now he has
2:31very focused and advanced training in
2:35cardiology , cardiovascular emergencies ,
2:38and critical cardiology . And it's a
2:42pleasure for me that he's talking about
2:44this topic because he truly has all the
2:46credentials to do so , since he does it
2:47both in theory and in practice . Could
2:50you briefly tell us about your training
2:51?
2:52Yes , of course . I had the opportunity
2:54to specialize in medical-surgical
2:56emergencies at the Autonomous
2:58University of Tamaulipas in Reyosa ,
3:00Tamaulipas . Afterward , I completed a
3:04subspecialty in intensive care in
3:06Torreón , Coahuila , at the UMAE71
3:09hospital , and later I became passionate
3:11about the field of cardiology , which I
3:14truly love , but specifically from the
3:16perspective of critical care medicine ,
3:19alright ? The cardiologist , well , the
3:22consultation , treating patients with
3:24chronic heart failure ; but I was more
3:26interested in starting to evaluate
3:28these patients in the acute
3:30cardiovascular area , and I had the
3:32opportunity to do highly specialized
3:34training at the Ignacio Chávez
3:36National Institute of Cardiology
3:38Hospital , where I developed the skill
3:41of critical care echocardiography .
3:43Later , I also did cardiovascular
3:45emergencies there at the National
3:48Institute of Cardiology and later
3:50applied to do highly specialized
3:52training in cardiovascular intensive
3:55care and later ECMO and specialist ,
3:57which is all the circulatory ,
3:59respiratory and extracorporeal
4:01ventricular support for cardiovascular
4:04patients . So , passionate about that ,
4:05right ? Right ? And the truth is that I
4:08am passionate about doing it with
4:10patients to be able to help them and
4:12also to spread these topics that are
4:14truly needed . Here we are going to be
4:17and I hope , well , I promise to try to
4:19bring up not only this topic , but some
4:21others to come . Sure , sure .
4:23And to begin , what interests us is what
4:26you trained in , but what you know , so
4:28that we can all learn from you . And
4:32what exactly is cardiogenic shock and
4:35why does it continue to be one of the
4:37pathologies with the highest mortality
4:39in intensive care ?
4:41Cardiogenic shock , uh , incredible . It
4:45is a very fascinating subject and is
4:48characterized by a state of generalized
4:51tissue hypoperfusion , which can be
4:54represented clinically , biochemically ,
4:57secondary to the heart's inability to
5:00meet the metabolic demands of the
5:03tissues . This develops a low cardiac
5:07index , the inability to generate
5:10cardiac output and develops interesting
5:14behavior . Although we have already
5:17considered hypodynamic shock states ,
5:19the main characteristic of cardiogenic
5:22shock is that they will have increased
5:25filling pressures . If we are talking
5:29about right ventricular dysfunction , we
5:31are talking about increased central
5:32venous pressures . If we are talking
5:35about left ventricular cardiac
5:37dysfunction , we are talking about
5:39increased pulmonary capillary pressure
5:42or wedge pressure . So , it is a state of
5:45biochemical and clinical tissue
5:47hypoperfusion characterized by the
5:50pump's inability to maintain cardiac
5:53output , an economy in the entire
5:55cardiovascular system . Now it is
5:58time-dependent , it is a completely
6:01time-dependent emergency . Early
6:05recognition of a patient in cardiogenic
6:07shock is what could be shown to reduce
6:10mortality and increase the probability
6:12that the patient will survive . So ,
6:17mortality is expressed at approximately
6:2130 to 50 % in centers well-trained and
6:25specialized in treating cardiogenic
6:28shock . In a hospital that is not a
6:32priority center for evaluating
6:34cardiogenic shock , let's say a general
6:36hospital in a zone here in Mexico ,
6:38mortality can skyrocket to 80 % . It is
6:42very high . So , early recognition and
6:45having the therapy that will reverse
6:48the cause of the state of shock , which
6:50we now know that cardiogenic shock is
6:53multifactorial . We mainly have ischemic
6:56heart disease , acute myocardial
6:58infarction that causes cardiogenic
7:00shock , and early reperfusion in a
7:01percutaneous coronary intervention room
7:03. Access to this has been shown to
7:06reduce mortality . So , the fact that we
7:09do not have a therapy available to
7:11reperfuse a patient in need , that also
7:13significantly increases mortality . I
7:16would prefer recognition , I would
7:18prefer deficiency in treating the cause
7:20.
7:23Pharmacological treatment , which we
7:25will discuss later , and ventricular
7:27circulatory support , still lacks
7:29significant evidence in many studies ,
7:32because at the end of the day , they are
7:34support therapies , support to gain time
7:37while the patient arrives to treat the
7:39cause . I would prefer early recognition
7:44, I would prefer basic therapy for the
7:47cause that led to the shock and I would
7:50prefer the implementation of , uh , Heams
7:52; yes , the possibility of expanding
7:55knowledge not only to cardiovascular
7:57intensive care , but also to the
7:59cardiologist , also to the
8:01anesthesiologist , also to
8:03cardiovascular nursing , so that we all
8:06have the same language to implement
8:09better results with patients . Well ,
8:12well , the other therapies are bridging
8:15therapies , support therapies , therapies
8:18to gain time . We're going to go into
8:21much more detail now , but it's great
8:23that you mentioned it , that mortality
8:25rate is so high , up to 80 % in places
8:27where we are not specialized , including
8:29polyvalent therapies , obviously . And as
8:32you rightly say , even more so if the
8:34etiology that has led to the pump
8:35contractile failure is not resolved , or
8:37contractile failure , whether systolic
8:39or diastolic , left , right or global ,
8:40which we will go into more detail about
8:42now ; but without a doubt that is
8:43something that we must take into
8:45account , because then we become
8:46overconfident , Luis . And I have even
8:49heard comments , or I think many people
8:51have heard it , saying : " Now the
8:53mortality rate from cardiogenic shock
8:55has decreased significantly . " In other
8:58words , it may now be 50 % or less . Yes ,
9:02but as you rightly say , if it is
9:04managed in a specialized way in terms
9:06of support and etiology so that the
9:08patient does not become overconfident ,
9:10mortality will not decrease
9:12just by supporting it , but by managing
9:14the etiology . Exactly . Yes . Something
9:18important that has happened in the
9:20latest updates on the management of
9:22cardiogenic shock is the implementation
9:24of the Sky classification . Yes ,
9:26the Sky classification was a watershed
9:29because now we speak the same language
9:31regarding the severity , prognosis , and
9:34mortality of the patient . Previously ,
9:37we had several studies that even spoke
9:40of several definitions , and this made
9:42cardiogenic shock very heterogeneous .
9:45We currently know that a Sky A is a
9:47patient who already has a
9:48cardiovascular situation that puts them
9:50at risk . A patient with an acute
9:53myocardial infarction may progress to
9:55cardiogenic shock . A patient who has
9:57valvulopathy , who already has heart
9:59failure with low fever , may develop
10:01cardiogenic shock . A post-cardiotomy
10:03patient , who has undergone cardiac
10:05surgery , may also develop cardiogenic
10:06shock . So , these are patients who
10:09already have a stage A ,
10:11yes , high risk . B is when clinical
10:13manifestations begin , tachycardia
10:16begins , and there is hypotension . That
10:19patient who already has cardiovascular
10:22disease and there is clinical progress
10:24begins , it is already the beginning of
10:27a stage B. C is when norepinephrine and
10:29dobutamine are required to maintain
10:32perfusion pressure and cardiac output ;
10:34and if the patient continues to
10:36deteriorate , I have a class D and then
10:39I have an extreme class E. So , this
10:43implementation of Sky has allowed us to
10:46speak the same language in
10:47cardiovascular intensive care to know
10:50when it is time to activate an ECMO
10:52code , for example , which we are going
10:55to mention now , or when , well , we are
10:57going to give reperfusion , strategy ,
10:59support , etc. Okay .
11:02I like , I really like your concepts and
11:04you just mentioned something that needs
11:06to be highlighted . In other words , the
11:08diagnosis is made clinically or
11:10biochemically . Well , let's continue
11:13with the question that is from the
11:15initial assessment so that it is useful
11:17to all of us from the moment we have
11:19contact for the first time . What are
11:22the clinical data that should suspect
11:24cardiogenic shock ? And something very
11:27important , if you can link it , how can
11:29we differentiate it from other types of
11:31shock ?
11:31Perfect . Yes . Excellent . The diagnosis
11:34of cardiogenic shock is still clinical .
11:37We also rely on other diagnostic tools
11:39such as echocardiography , that is
11:40certainly the case . Or invasive methods
11:42, of course . But early recognition of a
11:46patient who already has a
11:47cardiovascular history , who has already
11:50had a cardiovascular event ; but the
11:52patient is no longer urinating , has
11:55oliguria , has cold extremities , has a
11:57capillary refill time which is vital ,
12:00is prolonged more than two , more than
12:02three seconds , has an altered
12:04neurological status , which are the
12:06clinical windows of shock . Add to this
12:10a state of sustained arterial
12:12hypotension with a systolic blood
12:14pressure less than 90 mm of mercury ,
12:16which the guidelines currently say , "
12:18Don't focus so much on pressure , the
12:20patient may already be in shock , but
12:22still have increased or normal blood
12:25pressure levels . " So , clinically , I
12:28stand next to the patient , I examine
12:30them , I look at the capillary refill
12:32time , I look at the lauresis , I see the
12:34altered mental status , that patient
12:36clinically already meets my definition
12:38of shock , regardless of blood pressure .
12:41Now I have the opportunity to do some
12:44secondary biochemical analysis and look
12:47for evidence of tissue hypoperfusion
12:49with biochemistry . Lactate has also
12:51been mentioned above two , above three .
12:56There are some other markers , central
12:58venous saturation , perhaps a CO2 delta ,
13:00and other markers that we could include
13:02. Yes , we can also rely mainly on
13:06lactate . Well , we are going to do the
13:09differential , because a patient with
13:11septic shock can also give me capillary
13:14refill time , clinical and biochemical
13:16windows of shock ; but the main
13:18characteristic of this type of shock is
13:20the inability of the heart to maintain
13:23a cardiac index and the cut-off point
13:25is still 2.2 with increased filling
13:30pressures . So , it is very important
13:33that now with echocardiography we can
13:36estimate , surrogate , not measure , but
13:38have the idea that the heart is not
13:41moving and that it has increased
13:43filling pressures . You look at the
13:46lungs and you see pulmonary B lines ,
13:49that patient has increased left
13:50pressures . Now , I see data of
13:53congestion , congestive vena cava more
13:56than 21 mm . That is indicating to me
13:59that the patient has increased filling
14:01pressures on the right side . So , I have
14:04to look at the heart and I have to take
14:06the heart as the cause of the shock
14:08state . A heart can be the protagonist
14:10or it can be the spectator in the state
14:13of shock and in this case it is the
14:15protagonist . I really liked that . Yes ,
14:18of course , of course , of course . Okay .
14:19I mean , later we are going to do some
14:21episodes of shock in general , of
14:23dynamic monitoring , but right now I
14:25wanted to get the most out of you in
14:26cardiogenic shock . Hey , and within the
14:29definitions that there are multiple ,
14:32well , if you want to mention them now ,
14:34the multiple ones that exist to
14:37diagnose cardiogenic shock more
14:39specifically , which one do you like the
14:41most ? And which one is perhaps the one
14:45that is most used in the large centers
14:46where you have been training ?
14:50Yes , in hemodynamics , they talk about a
14:52cardiac index . We are talking about a
14:55cardiac index below 2.2 . Cardiac index ,
14:58cardiac output divided by met² body
15:00surface area to index it to the patient
15:02, less than 2.2 . And a pulmonary
15:06capillary pressure , previously it was
15:08said above 18 , the cut-off point now is
15:1015. We are at 15. Above 15 would
15:12already be evidence of an increase in
15:15the telediastolic filling pressures of
15:17the left ventricle . Now , it is
15:21important that there is a clinical
15:23shadow between hiding this retor and
15:26seeing the presence of pulmonary B
15:28lines . What is that line ? that
15:31approximately 25 mm of mercury of
15:34pulmonary capillary pressure is what is
15:36approximately required to be able to
15:39auscultate rales .
15:41So , between 15 and 25 we have that line
15:44and that is where the ultrasound comes
15:46in to show that the patient has
15:48increased filling pressures between 15
15:51and 25 , that is , above 15. Now we can
15:53estimate them through transmitral flow ,
15:59uh , uh , the E wave on the raw tissue E
16:02waves to look for pulmonary capillary
16:04pressure by Naget . Yes , what interests
16:08me ? That it is above 15. That patient
16:10already has increased pressures and the
16:12cause is cardiac , yes or yes .
16:14Or the ultrasound is cool . I mean ,
16:16before hearing the pulmonary edema , you
16:20can see it . You
16:22can see it . Indeed ,
16:23right ? Yes , of course . And that , like
16:25all the context , already helps you . And
16:26of course , I also always tell them , the
16:28clinical picture is very important . In
16:29fact , sometimes I arrive , I do
16:31hepatojugular reflux and I see that it
16:33is present , this , I try to examine it ,
16:36but as you rightly say , the ultrasound
16:38sees beyond the obvious , like the sword
16:40of omen . So , if you are seeing an
16:43ultrasound of Benacaba or jugular ,
16:45where there is very little variability ,
16:47something is already preventing blood
16:49from passing , I would say , from right
16:51to left , that is , the heart is not
16:53emptying properly .
16:55And there is pulmonary congestion ,
16:58venous congestion and obviously , in
17:01this case , an increase in cardiac
17:03pressures , right ?
17:05How interesting . How interesting .
17:06Anything else you want ? This is very
17:08exciting .
17:09Yes . What happens is that we have to
17:11understand that the relationship
17:13between the right ventricle and the
17:15veins is to unload them , to keep the
17:17pressures low . So , if there is a pump
17:20failure , these pressures will appear
17:23high with signs of congestion . If we
17:25are talking about the right ventricle ,
17:27then these are all the pressures that
17:29all the veins should discharge onto the
17:31right ventricle , including the portal
17:32vein . For us , the portal vein in
17:35ultrasound evaluation is very important
17:37to see venous congestion , let's leave
17:38it like that . And of the left ventricle
17:42, lungs , pulmonary capillaries . That is
17:46what we focus on to evaluate , estimate
17:48filling pressures , which we can
17:50estimate a little more advanced with
17:52formulas and estimates of transmitral
17:54flow velocities . Yes , yes , we also do
17:57it to estimate that the pressures are
17:59increased . That is the characteristic
18:02of cardiogenic shock ,
18:03the behavior .
18:05Interesting , interesting the pump
18:07failure as it brings all those
18:08repercussions . Well , right now I have
18:11many questions , but let's go in order .
18:13Let's go step by step , as Jack the
18:15Stripper would say . Now ,
18:17right now you have already introduced a
18:20concept that has come , I think , to
18:23facilitate and speed up the
18:25identification and management of the
18:27patient , which is
18:30critical ultrasound in general . Okay ,
18:33the echocardiography that you mentioned
18:35, but then what I understand is also
18:37critical ultrasound in general , because
18:39it also includes venous insonation ,
18:41pulmonary insonation , for the diagnosis
18:43of cardiogenic shock and , well , spoiler
18:45of all types of shock . So , what current
18:48role does critical ultrasound have in
18:52the diagnosis and decision-making of a
18:55patient with cardiogenic shock ?
18:58Pillar , fundamental . The evaluation of
19:03a patient in cardiovascular intensive
19:05care , in a cardiovascular emergency ,
19:07must be done with an ultrasound at the
19:10bedside , okay ? Why do we have to
19:13evaluate ? We can evaluate etiology , we
19:16can evaluate valve disease , we can
19:18evaluate right ventricular function , we
19:21can evaluate left ventricular function ,
19:23both in its systolic function and in
19:26its diastolic function . We can evaluate
19:30pericardium , cardiac tamponade , we can
19:33extend to having a cause that I can
19:36resolve , identify quickly to offer
19:38timely treatment to the patient . I can
19:43see segmental contractility disorders ,
19:45a wall that is completely non-moving ,
19:48which is appropriate , and I begin to
19:50integrate a complete diagnosis . I have
19:53an electrocardiogram that may have two
19:55out of three ABF with positive ST
19:57segment elevation and the patient has
20:00signs of tissue hypoperfusion , I do an
20:02echo and I see that the inferior wall
20:04is not moving . So I say , " You know what
20:06? Quick , we have to think about
20:09reperfusion , fibrinolysis , PCI , etc. It
20:11depends on which center I am in , but
20:14echocardiography is essential to
20:16evaluate the patient every day . We see
20:19it every day and when the patient
20:21arrives we evaluate them immediately
20:23with ultrasound . Okay , fine . Regarding
20:28etiologies ,
20:30well , you have been in highly complex
20:33centers , in medical centers
20:35specializing in cardiology , how do they
20:38behave in terms of etiologies ? In other
20:42words , which are the most frequent ones
20:43that are described or that they manage ?
20:46In Mexico , and I believe in Latin
20:48America and the United States , ischemic
20:50heart disease and acute myocardial
20:52infarction continue to be the leading
20:54cause of cardiogenic shock . We could
20:57estimate that 70 to 80 % of cardiogenic
20:59shocks are due to acute myocardial
21:01infarction . It will then depend on the
21:03center where we are . For example , the
21:06National Institute of Cardiology . Well ,
21:08see patients who have undergone
21:10post-operative cardiac surgery and
21:11there we are faced with a scenario of
21:13cardiogenic shock , post-cardiotomy .
21:15Okay . Okay . Uh , patients who could even
21:19fail after a heart transplant or think
21:22that we have to endure this patient to
21:24take him to a heart transplant and that
21:27he is in cardiogenic shock . This is
21:30also another scenario that we could
21:31find ourselves facing . We would say
21:34that we have ischemic heart disease , we
21:37have cardiogenic shock post-cardiotomy ,
21:40we have valvulopathies of cardiogenic
21:42shock and we also have heart failure .
21:46Heart failure that begins with
21:48diastolic dysfunction and later causes
21:51systolic dysfunction and leads to
21:53advanced heart failure . Within the
21:57progression , the evolution of heart
21:59failure , in the end , this patient ends
22:01up presenting cardiogenic shock , very
22:04reduced febrile cardiac output , uh 5-7 %
22:06we have faced and that there is no
22:11other way to help them survive . That
22:14patient then evolves into cardiogenic
22:16shock .
22:16Sure . And as some say , he can be lame
22:19and lethargic . at the same time . In
22:21other words , those who have heart
22:23failure , perhaps due to chronic
22:25hypertensive uncontrol , which first
22:27causes concentric hypertrophy , then
22:29eccentric hypertrophy , and then
22:31practically causes left ventricular
22:33failure with low FBP , but then it is
22:35also associated with some anginal chest
22:38discomfort ,
22:40which , well , could be that one thing
22:42also compensates for the other because
22:44I told you that I had it the other time
22:45, well , let's see if I can do an
22:47ultrasound . I sent this ultrasound to
22:50Dr. Morgado , a patient already had
22:52chronic heart failure , but lately his
22:55functional class had begun to
22:56deteriorate more , that is , now it was
22:58dyspnea on minor exertion and angina .
23:02So they did some tests there and he
23:04showed signs of cardiac ischemia , they
23:06put him in for catheterization and
23:08after the catheterization , they did
23:09work on the right coronary artery and I
23:11think an anterior descending artery ,
23:13they put in a stent and when he came to
23:15us , I think only the first pressure was
23:17normal . After that , he began to have
23:21hypotension , he began to have
23:23respiratory difficulty , he began to
23:25being tachycardic and , as Dr. Morgado
23:27mentioned , that is , delayed capillary
23:29filling , I did cardiac insonation and
23:32he was all hypochondrial , a little bit
23:34of pericardial effusion . But yes , that
23:38patient , well , we started to give him
23:41hemodynamic support , in that case ,
23:42vasopressor , norinephine , which is a
23:45vasopressor and also has a neotropic
23:47effect . I mean , and with that you give
23:49him the dose and that's not enough , you
23:51give him a pure nonotropic , but the
23:52patient never improved . I mean , that
23:55patient is more complex with mechanical
23:57ventricular support , blah blah , right ?
24:01I don't know , and then a bridge to a
24:03heart transplant , but a patient in
24:05their 80s is already difficult .
24:07Yes , yes , it's difficult . There are
24:09also stent thrombosis ,
24:11right ? Probably or it has to be
24:14investigated , that patient is tolerated
24:16and returns to coronary intervention to
24:19evaluate how the coronary anatomy is .
24:21Yeah . It could be another situation .
24:25In this case , the patient , I think , I
24:27told you in about an hour , 2 hours , he
24:29stopped and obviously the
24:31mortality rate is very high ,
24:32very high , very , very high , very high .
24:34Yes . Wow , what questions . Now , let's
24:38get into
24:39this more . Much more into the subject ,
24:42because this is getting quite
24:43interesting . Remember to give it a
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24:59enemies who are health professionals . I
25:03tell you
25:04so that they can have fun . Perfect . Now
25:06, let us create a scenario , Master
25:08Homgado , so that this can become a
25:10little bit easier for us to understand .
25:13A patient with unstable angina or with
25:16a myocardial infarction , let's go
25:18directly to the anterior face , this
25:21patient is elevated there in B1 to B4 ,
25:23chest pain , about 2 hours of evolution ,
25:26the patient has data of tissue
25:28hypoperfusion and with this situation ,
25:31that is , we already have the diagnosis
25:34of cardiogenic shock . Initial
25:37management . What would your initial
25:40management be ? Fluids , vasopressors ,
25:42inotropes , what do I do for the
25:44respiratory system ? Yes , it is
25:48complex , complex , complex . Yes ,
25:50normally I will have a patient with
25:52arterial hypotension , with a state of
25:53tissue hypoperfusion , elevated lactate .
25:55I will have , uh , oligoguanuria ; I will
25:58have , this , that the patient has
26:00delayed neocapillary time and yes , of
26:02course , they may be hypoxemic . We must
26:04remember that the patient may have
26:06signs of congestion and that could lead
26:08to hypoxemia . What is recommended ?
26:10Focus on hemodynamics . Yes , it does not
26:13mean that we are not going to
26:14understand the respiratory system , but
26:16we are going to prioritize hemodynamics
26:18. What is the goal of fluids ? Regarding
26:21fluids , it does not mean that we do not
26:23use them . In fact , there are
26:26post-cardiac surgery patients who
26:28require volume to achieve a adequate
26:30ventricular filling , but we have to be
26:33very judicious when using fluids and
26:35try to assess the patient's volume
26:37responsiveness at that time . Now ,
26:41ideally I achieve a perfusion pressure ,
26:44a perfusion pressure MAP and then I
26:46look through insonation , through some
26:49tool , to see how the contractility is .
26:54If I'm talking about cardiomyopathy or
26:55an acute myocardial infarction , then
26:57I'm going to have contractility
26:59disorders . So , first I put a
27:02vasopressor before the fluids , I put
27:04norepinephrine , I adjust the dose to
27:07reach 65 on average and then I look at
27:10the contractility and perhaps I have to
27:13use dobutamine to improve contractility
27:16at that time in that patient . Now we
27:20have to investigate , it could be
27:22another cause , it could be heart
27:24failure ; and there , if I give volume to
27:26a patient who already has data of
27:29global congestion , is enargued , has
27:31increased filling pressures , perhaps
27:33giving volume is not the best idea ,
27:35perhaps that patient benefits from
27:38diuretic and start evacuating this
27:40patient . This patient now shows signs
27:43of hypoperfusion , so I administer
27:45norepinephrine , assess contractility ,
27:47always accompanied by the most
27:49objective measurement possible in order
27:52to have a guided intervention , okay ?
27:56Not so much doing it empirically by
27:58just administering norepinephrine or
28:00buta or giving them a fluid load , but
28:02rather doing an ultrasound scan and
28:03through the ultrasound scan assessing
28:05the hemodynamic pattern , the behavior
28:07of my patient and working on that .
28:11Regarding breathing , ventilation ,
28:13ideally you should try to delay
28:15intubation as much as possible . Why ?
28:20Because sometimes we have to use those
28:23patients who have a low cardiac output
28:25behavior that compensates with systemic
28:28vascular resistance to maintain blood
28:30pressure . If I administer propofol as
28:34an inducer to a patient who is already
28:36hemodynamically unstable , I will
28:38basodilate them and then that patient
28:40will become hypotensive and the
28:42hemodynamic evolution of my patient
28:44will be worse . So , I have to make that
28:46judgment . Preferably not to intubate ,
28:49offer something noninvasive , perhaps
28:52tips , a mask , even something
28:54noninvasive . In case you have to
28:58intubate , perhaps some etomidate ,
29:00ketamine or fentanyl to be able to
29:03achieve hemodynamic stability and then
29:06offer some invasive mechanical
29:09ventilation . But ideally , it is trying
29:12to be a little conservative with these
29:14patients and prioritize hemodynamics .
29:17That's it . Exactly . Very good . I think
29:20that's the concept and general rule .
29:23Always prioritize hemodynamics over
29:26respiratory . And here it's exactly the
29:29same . This , in your case I like it
29:33because in your case , since you're an
29:35intensivist , now they call us general
29:37intensivists , what's up ? You're a
29:41general intensivist , but also a
29:43cardiovascular intensivist , so you have
29:45both tools : both as an expert in
29:47mechanical ventilation , both
29:48noninvasive , as you say , invasive with
29:51high flow , a CPAP support or a bipup
29:53that can also be used . They can use
29:56invasive ventilation if required ; that
29:59is interesting , and also your
30:01specialized training in hemodynamic
30:04support , which is something interesting
30:07that you must have . Now , if you support
30:11, you achieve goals , for example , of
30:13tissue perfusion , you achieve
30:15oxygenation goals , what else ?
30:18And seek to resolve the cause ,
30:20mainly seek to resolve the cause . If it
30:23is a valvulopathy , then you would have
30:25to see what type of , uh , what structure
30:27of valvulopathy it has , if it has
30:28stenosis , has insufficiency and seek to
30:30optimize hemodynamics as much as you
30:32can . Maybe that patient requires
30:34surgical treatment ,
30:36then you support them , you
30:39seek the form of surgical treatment and
30:42then you take them to surgery if it is
30:44a valvulopathy .
30:46Of course . We
30:48always place the highest priority on
30:51hemodynamics and seek to optimize the
30:53patient's condition . Sometimes a single
30:57norepinephrine or a single dobutamine
31:00is not enough . Of course ,
31:03sometimes you need to use
31:04norepinephrine , vasopressin and not
31:07just dobutamine . Perhaps we should also
31:11evaluate right ventricular function and
31:13see how that resistance and right
31:15contractility are , because perhaps the
31:17neurotropic drug of choice might be
31:19milrinone . So , that is another behavior
31:23. Right ventricular failure , very
31:25sensitive to changes in volume , very
31:27sensitive to changes in pressure . We
31:29should evaluate how right ventricular
31:31behavior is in that patient , because
31:33perhaps the neurotropic drug should be
31:35changed to milrinone . Other patients
31:39have used dobutamine , even levosimendan
31:41at the same time to improve
31:42contractility through another mechanism
31:45of action . If I have a patient who
31:47previously had heart failure , we know
31:50that they are going to be on sacubitril
31:52, balsartan , this spironolactone , they
31:54are going to be on dapagliflozin and a
31:57beta-blocker . If I give them dobutamine
31:59, then the beta receptors will already
32:01be blocked . So I have to use another
32:03inotrope or inodilator that helps
32:05contractility through another mechanism
32:07of action , such as a sensitizer to
32:09calcium channels .
32:10Levocosimitendal .
32:11Levocosimitendal . In this scenario , the
32:14behavior and phenotype of shock that is
32:17occurring will depend on whether there
32:19is an increase in filling pressures ,
32:21perhaps benefiting from a diuretic ,
32:23contractility , what type of failure
32:25does he have on the right or left , and
32:28being able to assist .
32:30Regarding the phenotypes , which ones
32:33would you identify or describe for
32:35management ?
32:37Pure right ventricular failure , pure
32:39left ventricular failure , biventricular
32:42failure . Those would be the most
32:45representative phenotypes of
32:46cardiogenic shock .
32:48Some literature indicates that
32:52cardiogenic shock is characteristically
32:55hypodynamic or low output or they call
32:58it cold ,
33:00that is , initially , but they also later
33:02describe some hemodynamic behavior ,
33:05such as warm or dilated vessels . That
33:10is , it may be that or it may reach a
33:12final phase or what could you explain ,
33:14right ? And for example , for example ,
33:17septic shock has the characteristic of
33:19being so heterogeneous that it can
33:21begin as a vasodilated distributive
33:24shock and ultimately cause septic
33:26cardiomyopathy and the patient ends up
33:28with biventricular failure or left
33:30ventricular failure or a tacotsubo that
33:33we would have to endure . Obviously , a
33:37state of shock can be heterogeneous and
33:39cardiogenic shock at the beginning , the
33:42patient will even have a systolic of
33:44100 or 110 but that begins with signs
33:46of hypoperfusion . So that patient will
33:50develop cardiogenic shock , but at the
33:53moment , at this moment , he is behaving ,
33:56well , perhaps , as a state that is not
33:58so hypodynamic and has not yet lost
34:00those vascular resistance compensation
34:03systems , which in the end will end in
34:06that , but , uh , probably , it is the
34:08evolution of cardiogenic shock over
34:10time , how it behaves . Yes , as you
34:14rightly mentioned , I mean , imagine
34:16cardiac output and vascular resistance .
34:19I always put them like little hands .
34:21Cardiac output is determined by the
34:22heart rate and the stroke volume .
34:24Stroke volume by preload , afterload ,
34:26contactivity , and ventricular
34:27extensibility . I mean , I'm talking to a
34:30cardiointensivist , I have to bring up
34:33this one too , which many of us skip ,
34:35but obviously ventricular extensibility
34:37is also important . Here it is . With
34:40these functions , you get a good stroke
34:42volume and multiply it by the heart
34:44rate to get cardiac output . When your
34:46cardiac output drops , the compensation
34:49mechanism is resistance . But if it goes
34:52a long time without management , without
34:54support , blah blah blah , or an
34:56infectious process is added , then you
34:59also lose resistance and then there's
35:01no , as they say , God the Father . Well ,
35:04yes , I mean , I don't want to get
35:05involved , but even miraculous things
35:07like that won't be able to save you ,
35:08because if you have no output and no
35:10resistance , there's
35:11no perfusion .
35:12Exactly . And another concept , as you
35:15said , cardiac output is equal to heart
35:17rate times stroke volume , but we also
35:19have another concept of heart rate . A
35:23patient can end up presenting low
35:25cardiac output at the expense of both
35:27from an increase in sympathetic
35:28activity as well as an increase in
35:30parasympathetic activity , that is , an
35:32atrial block or fibrillation with
35:33accelerated ventricular response , for
35:35example . Then you have the concept of a
35:39state of hypoperfusion , but secondary ,
35:41not due to loss of stroke volume , but
35:43to a disorder of heart rate . And that
35:46is still being treated as a diagnosis
35:48of , well , strictly speaking it will be
35:50cardiogenic shock , but let's say due to
35:52arrhythmias such as ACLS , that is , an
35:54unstable bradyarrhythm or an unstable
35:56tachyarrhythma .
35:57Yes . That is what we treat .
35:59Sure , sure . Yes . It is not because you
36:01say cardiogenic shock that you are
36:03going to give inotropic vasopressor . It
36:05says cardiogenic shock of
36:06rate . Exactly . So , early recognition
36:11and knowing which hemodynamic factor is
36:13altered is what we are going to try to
36:15correct , optimize and then take it to
36:17definitive treatment .
36:19Sure . That , that , exactly . Now , gosh ,
36:22many of those who are watching us
36:24probably remember that . of that patient
36:27who was already given what Dr. Morgado
36:29said . It is an acute coronary syndrome ,
36:32maybe he has already been admitted to
36:34the hemodynamics room , they were even
36:36able to catheterize him well and
36:38perform percutaneous coronary
36:40intervention . They inflated the balloon
36:43, left good ST flows , but he is still
36:45in shock and they are not even
36:47achieving perfusion goals and he is
36:49already given a vasopressor , he is
36:50already given another vasopressor , he
36:52is already given a non-sinotropic agent
36:54and the patient is still hypoperfused .
36:57Now , what about ? I mean , here I am
37:01thinking a lot , well , this is the end ,
37:03right ? Here there is another concept
37:06which is circulatory support and
37:08mechanical ventricular support .
37:11Exactly .
37:12Well , now he tells us if they are the
37:14same or two different concepts . At what
37:16point should we consider circulatory
37:18support or mechanical support ?
37:20Excellent , excellent question ,
37:22excellent question because we have to
37:24go back to the Skype classification .
37:27Sure .
37:27Yes . In the past we would say , " I have
37:30given the patient two vasopressors , two
37:33inotropes ; it's not working . " " You
37:35know what ? Well , now talk to the ECMO
37:38people or talk to the people and we'll
37:40start activating the circulatory
37:43support protocols late , late . We've
37:47currently dropped to Sky C
37:49classification . From Sky C , when the
37:53patient starts , give them nore , give
37:55them dobuta , that's when I start
37:57supporting the patient with drugs . I
38:01start to think about the possibility
38:03that my patient is going to require
38:05some type of assistance , okay ? The
38:08assistance that we use the most to
38:11support is circulatory support . Okay .
38:15Circulatory support is eMO ,
38:18venoarterial eMO . And that's an
38:21important concept because sometimes we
38:23think that ECMO is going to help the
38:26left ventricle and that it's a
38:27ventricular assist device , but it's not
38:30quite the opposite . In fact , if we
38:34connect it to the patient in a
38:36peripheral configuration where I
38:38extract venous blood from an efemoral
38:40vein , pass it through a turbine and
38:43push it against a membrane where the
38:45exchange takes place and returns it
38:48arterially in the direction of the
38:50artery . retrograde femoral , it will
38:53increase the afterload of the left
38:55ventricle . That means that it will
38:59complicate the left ventricle more . But
39:02what do I gain with ECMO ? Organic
39:05perfusion . And it is very interesting
39:08that we connect to ECMO and in less
39:11than 4 hours , 6 hours , I begin to
39:13reduce the vasopressors and sinotropics
39:16immediately . Why ? Because I am already
39:19perfusing the patient . So , the
39:21oxygenated blood to the brain arrives
39:23through ECMO and not from the native
39:25heart , because the native heart is
39:27receiving blood but in reverse . Well ,
39:30there are complications of this .
39:32Complications can occur . If I have a
39:34heart that has a Febi of 5 % -7 % and I
39:37also increase the afterload to the left
39:40ventricle , I can end up overdistending
39:42it . That is called left ventricular
39:44extension syndrome . And then I have to
39:47think of a strategy to unload that left
39:50ventricle . Okay ? We are talking about
39:53circulatory assistance devices , which
39:55is ECMO , but I have ventricular assist
39:58devices . where Now I'm going to try to
40:01reduce the blood that's inside the
40:04ventricle , suction the blood inside the
40:07ventricle through a mechanical device
40:10and that's a device , for example , the
40:13Impela .
40:15The Impela is a device that enters
40:17percutaneously through the femoral
40:19artery , it goes up or through the
40:21axillary , if it's a 5.5 , for example ,
40:23or a CP , it can enter in this way , uh ,
40:25uh , below through the femoral artery .
40:29It reaches the horta , it positions
40:31itself and then it's a turbine that
40:33begins to extract blood from the left
40:35ventricle and it's a ventricular assist
40:38device where now what I'm doing is
40:40reducing the afterload of the left
40:42ventricle . I'm reducing the afterload
40:45and I'm suctioning to improve , uh , uh ,
40:47the left ventricle . In
40:49other words , the left ventricle has now
40:51helped with that turbine to extract
40:52blood to the horta
40:54and then to the entire systemic
40:55circulation . That cardiogenic shock
40:58secondary to acute myocardial
41:00infarction in the Danger Shock study
41:02published last year in New England
41:04decreased mortality when They take
41:06patients to Impela . Okay . Another
41:10ventricular assist device could be the
41:12intraventricular balloon pump ,
41:15which we also use in conjunction with
41:17ECMO . What for ? To be able to discharge
41:21the balloon pump , which has the benefit
41:23of improving coronary perfusion by
41:25increasing diastolic pressure and
41:27lowering the left ventricular
41:28end-diastolic pressure , and that
41:30increases cardiac output . So it
41:33provides ventricular assistance ,
41:35which is assistance as a bridge to
41:37recovery . Of course ,
41:39because they say that this does not
41:41reduce mortality . But for example , if
41:44you do not have an Impela , then they
41:46could use or in large centers they
41:48still use balloon pump .
41:50Yes , yes , yes , yes , yes . It is still
41:52used and what we are looking for is ,
41:54for example , the ECMO configuration has
41:56four possible destinations . I take the
42:00patient to a bridge to recovery , for
42:03example , a patient who has peripartum
42:06cardiomyopathy , okay ? Circulatory cyst
42:10in 5 or 7 days , myocarditis in 5 or 7
42:12days , I know that she will recover when
42:14reduce the inflammation of the
42:16myocardium and then I cannulate it from
42:18ECMO and that ventricular function
42:19improves . Post-operative cardiac
42:22surgery patients who are on heart-lung
42:24bypass pumps . The heart is stunned , I
42:27assist it for 5 to 7 days , I'm talking
42:29about an average . 5 to 7 days recovers
42:32ventricular function , I remove it . They
42:35are bridge to recovery , bridge to
42:37transplant . We have had patients with
42:47Chagas , you take them to a bridge to
42:49transplant , you cannulate them on ECMO ,
42:52you hold them while we have a possible
42:54transplant , you transplant them and
42:56then you try to decannulate the patient
42:58from ECMO . Another would be bridge to
43:02decision . Bridge to decision , for
43:06example , very frequent in , uh , we call
43:08it ECPR , which is ECMO in cardiac
43:10arrest ,
43:11right ?
43:12Uh , you cancel the patient until you
43:14have to take them out of cardiac arrest
43:15, you have to put them in care . From
43:18there , we see other countries assist in
43:21organ procurement .
43:23Yes . Okay . And the other would be
43:27bridge to the extended assist device ,
43:30such as a Herzmate 3 , which is a device
43:34that connects to the ax of the left
43:37ventricle , sucks the blood and sends it
43:41outside the heart to the aorta . So , we
43:45are bypassing the left ventricle and we
43:47are bypassing the aortic valve . It is a
43:49device that comes out , okay ? It is a
43:52Herzmate 3 , it is implanted . or a
43:54Centrimac . A Centrimac is also a
43:58circulatory device , yes , ventricular
44:00assist , but without oxygenation . The
44:04native lungs are functioning without
44:06any problem , Canada . The patient can be
44:10talking , can be rehabilitating , can be
44:12exercising and is on those devices
44:14while we can take them to a transplant
44:16or something else , but those devices
44:18last longer , it is not like the ECMO
44:20that you can take for a longer time in
44:22those patients .
44:25How interesting . How interesting . Any
44:27case that you remember that has been
44:30bypass A and that has served all the
44:32circulatory and mechanical ventricular
44:34support ? Yes , many .
44:36Anything left for us ?
44:37Yes , a patient , we had a patient , this
44:39one was actually a patient that was
44:41sent to us from the United States , the
44:44first 5.5 Impela in Mexico .
44:46Could you explain what the 5.5 Impela
44:48consists of ? Because many , I mean , I
44:50have more or less the orientation that
44:53it is the liter capacity that is going
44:55to improve , but so that people are also
44:57probably very expert . As I have read it
44:59. Wow .
44:59Sure . Yeah . And in Mexico , it is more
45:03common to find a CP . A CP can generate
45:082.5 or 3 L depending on the patient's
45:11blood pressure . Sonia .
45:13Yes . of cardiac output , of 2 cardiac
45:15output . So , it will depend on the needs
45:18of this patient at that time so that
45:20the device can satisfy the metabolic
45:23needs and that the patient still has a
45:25supply three , four , five times more
45:30than the oxygen consumption . Okay . But
45:33a 5.5 or 5 is a device that rotates
45:36very quickly , it does not generate as
45:38much hemolysis and it is a device that
45:41can be in place for a long time and is
45:43generating up to a cardiac output of 5
45:46L.
45:47Phew ! So it is a device that has a
45:49greater capacity to meet the metabolic
45:52demands of a patient who is in
45:54ventricular dysfunction . Because at the
45:56end of the day , we return to the
45:58definition of cardiogenic shock , it is
46:00a state of hypoperfusion with pump
46:01incapacity . So I replace it with a pump
46:05device .
46:06Yes . No longer mechanical , I mean no
46:08longer pharmacological as we discussed
46:10at the beginning , but circulatory .
46:12There
46:12comes a point where the drugs have a
46:15limit
46:16and the redox
46:18is already stratospheric doses and you
46:20say I no longer have to advance to a
46:23circulatory or ventricular assist
46:25device .
46:26And that patient was brought from the
46:27United States .
46:28From the United States . Yes . Mexican .
46:30They brought him from the United States
46:31. He arrived with the device , he had an
46:34underlying neoplastic disease and had
46:36chemotherapy treatment and that caused
46:38him cardiotoxicity , a young patient . So
46:41, he was entered into the protocol , the
46:43oncologists and hematologists saw him
46:45and they ruled out that , well , they
46:47assumed that he had already
46:50resolved the of the underlying disease
46:51and then he was a candidate for
46:53transplant . So we had him supporting
46:55himself in Impela . It was approximately
46:58120 days in Impela and then he was
47:00transferred to transplant . The patient
47:03then develops dysfunction due to
47:05transplant and is transferred to ECMO .
47:08Wow .
47:08Mm . And he was also on ECMO , he came
47:11off ECMO and the patient had good
47:13results . The patient did well , let's
47:15say , that post-transplant dysfunction
47:18was self-limited .
47:19Yes . Yes . At the end of the day , it is
47:21a structurally healthy heart . Yes . But
47:24as you stop it , cool it , and perform
47:26the cardioplegia , the heart is left in
47:30a stunned state .
47:32So , while the transplant is being
47:36placed , so to speak , you assist it , the
47:38ventricular function begins to improve
47:41and and you take him off ECMO . Now ,
47:43how common is that ? I mean , because ,
47:45well , one would think that not , I mean ,
47:47you transplant him and that's it ,
47:48right ? Yes , it is common . Yes , it is
47:50common . And a heart transplant must
47:53involve a heart recipient , it must
47:55follow a study protocol that must be
47:57done through direct measurements of
47:59pulmonary artery pressures , which is
48:01where swangan ganans comes into play .
48:04Yes , yes . I'll tell you something . I
48:07mean , my friend Pablo Martínez Rubio ,
48:10who is a cardiothoracic surgeon , he is
48:12a transplant specialist , he both
48:14transplants hearts and he is going to
48:17bring hearts . So he says that he has to
48:22do an echocardiogram , swang gas , a
48:24complete evaluation , that the function
48:27of that brain-dead patient is adequate ,
48:29he removes the heart and brings it ;
48:31that is , in the cold chain and all that
48:34, I mean , it is not so , uh , I mean ,
48:36they have to make sure that the heart
48:38is fine , in good condition . If they see
48:42a heart that is not suitable because it
48:44has dysfunction , already has heart
48:46failure , already has pulmonary
48:48hypertension , I mean , he says , " Well ,
48:50it is not going to be appropriate to
48:52put this patient in someone who has an
48:55adequate pulmonary circulation system ,
48:57in this case . "
48:58Exactly .
48:59Yes , he explained all that to us .
49:00If you take a heart and put one in it ,
49:03at the end of the day , these are
49:05anastomoses that are going to be done
49:08in a heart transplant . If you take a
49:11heart , and speaking mainly of the right
49:13side , it has pulmonary hypertension ,
49:15and if you put it on the right side , it
49:16will dilate and cause right ventricular
49:18dysfunction , and those are the worst
49:20prognosis for transplants . So , yes , you
49:24have to categorize and specify very ,
49:26very , very well which patient is a
49:28candidate for a transplant . Of course .
49:31Gosh , he told me some cases that are ,
49:33I'll tell you
49:34later if I tell you about them or not .
49:38But well , well , well , well , well , we're
49:40going to land quickly , says Professor
49:43Jorge Olivares . This whole thing about
49:47cardiogenic shock has been a world and
49:49well , they won't let us , we're falling
49:51short because this is a world , this is
49:53just a little mess of this podcast
49:55episode , but I know it will sow doubt
49:56in you so that you Let's delve deeper
49:58into all this . Now , what are the most
50:02frequent complications during the
50:03evolution of these patients with
50:05cardiogenic shock ? And well , it may
50:07already be inferred , but what
50:09strategies do you use to prevent these
50:10complications from progressing ?
50:12The main complication is multiple organ
50:14failure . Why ? Because the tissues are
50:17left without oxygen supply , the supply
50:19drops , the patient is in shock and
50:20there is an imbalance between supply
50:22and demand . That leads to lactate
50:24production and the patient has multiple
50:26organ failure . It starts with kidney
50:28failure , liver failure , coagulation
50:30failure . Uh , patients also have
50:33cerebral hypoperfusion . So , the main
50:36complication of cardiogenic shock is
50:38the secondary one , the inability of the
50:40heart to meet metabolic demands . And
50:43for that we look for a support strategy
50:46, we do the heart's job . With what ?
50:48With devices , for example , ECMO , which
50:51prevents multiple organ failure by
50:53perfusing , and it's great because the
50:55patient can be in cardiogenic shock for
50:586 hours and not urinate at all ; When
51:00you have nore , vaso , dobuta , eh levo
51:03and it doesn't work , you connect it to
51:05ECMO and , as the flow enters
51:07retrogradely , the kidneys begin to
51:09perfuse and they urinate and urinate
51:11and urinate and urinate . So the lactate
51:14is cleared very quickly . In 6 hours ,
51:17from 17 lactate , 15 lactate that you
51:19had , you take it to five , four lactate ,
51:21seven lactate , you have already lowered
51:23it . Which of course , is a way of
51:26evaluating perfusion , but we are also
51:29evaluating lauresis , capillary water
51:31time , etc. ,
51:32right ? And in ECMO it is a different
51:34monitoring .
51:34It is a different monitoring , indeed .
51:37And , uh , what we seek is that , to avoid
51:39multiple organ failure . So , we assist
51:42the patient , either pharmacologically
51:44with devices .
51:45Yes . And note that there is something
51:47called noxischemic encephalopathy ,
51:49which many of us believe is only for
51:51the patient who had a cardiac arrest .
51:54prolonged cardiac arrest or who was not
51:56adequately resuscitated and that is why
51:58the patient will remain , well , for a
52:00time with absence of cerebral
52:01circulation , cerebral oxygenation and
52:03with cognitive motor or cognitive motor
52:05damage , and that is just the patients ;
52:08but patients with prolonged shock ...
52:09they
52:11can also present it and sometimes we do
52:13not consider it and say , " Hey , why did
52:14he end up with sequelae ? " Oh , who knows
52:17why . Well , because he was in shock for
52:19a long time and was not given adequate
52:21support .
52:21Sure , sure , of course . Have
52:23you ever encountered a patient who
52:25has these issues ? Even when a patient
52:28undergoes cardiac surgery and the pump
52:30times are very long , there is also
52:32evidence of cerebral hypoperfusion and
52:34then you wake the patient up , you
52:36emerge , you extubate them and the
52:38patient has delirium , has noxoischemic
52:40encephalopathy or has seizures . We have
52:44to protocolize it : to do a tomography ,
52:46an MRI ... maybe there's bleeding , maybe
52:48we use anticoagulation during where ,
52:51during extracorporeal circulation , we
52:53use this , they are left in cardioplegia
52:55, or patients who are , well , operated
52:57on , on the carotid arteries that have
53:00to be entered , or on the aortic arch
53:02that also has to be entered there to
53:04find a way to perfuse the brain . We
53:08also face those challenges . Perfect .
53:12Now , I'm still going to give you two
53:14final questions , but before that , a
53:16brief parenthesis . We haven't talked
53:20much about it , we only touched on it or
53:22you touched on it briefly and
53:24indirectly due to some issues when you
53:26mentioned cardiac index or when you
53:29mentioned pulmonary artery occlusion
53:31pressure or wedge pressure . But what
53:34role does Swan Gans play in cardiogenic
53:37shock ?
53:38Vital . This question is going to step
53:41on toes . What are the current
53:43indications for administering
53:45cardiogenic shock ?
53:47Pulmonary hypertension is another . For
53:49diagnosis , classification ,
53:50vasoreactivity testing is another .
53:53Heart transplantation is another . This
53:57is direct pressure monitoring . Remember
54:01that echocardiography is very useful ,
54:04vital , and important , but ultimately it
54:06does not measure pressures , it
54:08estimates them based on flow velocities
54:10, but these flow velocities can be
54:12underestimated or overestimated due to
54:15the patient's blood volume . So , these
54:18are markers that are multi-variable and
54:21will be modified . So , the only way to
54:25have an accurate measurement of
54:27pulmonary artery pressure is through
54:30right heart catheterization , how is the
54:32ventricular pressure and not only that :
54:35we can make gradient measurements , but
54:37not dependent on flow , transpulmonary
54:39gradient , pulmonary diastolic gradients
54:42, etc. , and with that we can realize if
54:44the patient has increased pulmonary
54:47vascular resistance , secondary to heart
54:49failure that would be postcapillary , or
54:53precapillary , which would be
54:55post-pulmonary disease . So , with that ,
54:58we can classify ourselves in pulmonary
55:00hypertension . But also in the
55:02resuscitation of patients with
55:04cardiogenic shock , we can metrically
55:06evaluate how the pulmonary artery
55:09occlusion pressure is going . So , we do
55:12cardiac output , optimize cardiac output
55:15, cardiac index , and try to reduce
55:17pulmonary capillary pressure through
55:19inodilators , diuretics , and when the
55:21pulmonary capillary pressure drops ,
55:24then we try to exit the pulmonary
55:26capillary pressure with some device ,
55:28dobutamine , or some other assistance .
55:31Okay . Okay .
55:32Yes . I also tell you something , I say ,
55:35I know that the ideal thing is to put a
55:36swang gans in and have it done by
55:38someone who knows how to do it , by
55:39someone who knows how to interpret it ,
55:41by a center that specializes in that .
55:43That's also why some studies do suggest
55:46a benefit of this intervention , but
55:49also if you don't have it , don't be so
55:52sad , it's like saying , I mean , ah , I'm
55:55going to make a diagnosis of acute
55:57appendicitis . The ideal thing is a
55:59tomography , for example , but I don't
56:01have it . With what I have , they have to
56:03do the best they can . Here , I think
56:06it's something similar , but as
56:08academics , one of the usual indications
56:11is the Sangan catheter . Now , could you
56:15briefly or conceptually explain what
56:17the Sangan catheter consists of ? In
56:20other words , how is it that through
56:22pulmonary artery occlusion we can then
56:24know if we are in the right ? How are we
56:27going to evaluate left-sided function ?
56:28In other words , what many people
56:30sometimes can't do ,
56:31what we really measure is the right
56:33cardiac output .
56:34Yes ,
56:35yes , because I have an injection in the
56:38right atrium through the PVC that
56:41enters and exits at the end through the
56:43thermistor . So , what I'm really
56:46measuring is the right cardiac output
56:48and I assume that the right cardiac
56:50output is the same as the left cardiac
56:51output , but in reality what I'm
56:53measuring is the right cardiac output .
56:55Now , the Suang Gans catheter is a
56:58catheter that measures 110 cm . It
57:01enters through the right atrium with
57:02the balloon inflated , passes the
57:04tricuspid of the right ventricle ,
57:05passes the pulmonary artery , and goes
57:07to one of the branches . It is very
57:09important that it is in the third zone
57:10of West , which is where there is
57:12greater pulmonary capillary perfusion .
57:14And there , with the balloon inflated , I
57:16stop . It is the same as an inspiratory
57:19pause in the ventilator . I stop the
57:21flow , there is no flow , zero flow , and
57:23then I can measure the pressure . What
57:26pressure ? The pressure of the left
57:28atrium , which in the absence of mitral
57:31pathology will give me the
57:32telediastolic pressure of the left
57:34ventricle ,
57:35okay ? Which would be the D2 of the LV .
57:39But , well , it has its biases and its
57:41things and its indications . I would
57:45stick with the importance of the swang
57:47guns . Yes , of course , but more than the
57:50importance of the swang guns is knowing
57:52how to interpret it and make decisions .
57:54It's like ultrasound . What's the point
57:57of
57:57me grabbing the ultrasound machine ,
57:59putting it on the patient , and seeing ,
58:00" Oh , he doesn't move ? " Oh , well , but I
58:01don't do anything , I don't give him
58:02Dobuta . So , it's the interventions that
58:06generate changes in the patient's
58:08prognosis . If I just stick with
58:11measurements and don't take action ,
58:13then there's no point in taking those
58:14measurements or piercing the heart with
58:16a swang gans . So , let's
58:19not expect the swang gans to reduce
58:22mortality by itself , but rather the
58:24actions that accompany the prognosis .
58:27That's what's going to give me the
58:28prognosis . Now , the interpretation of
58:30that information has to be vital to
58:32also avoid therapeutic biases or going
58:35around doing things that aren't right ,
58:37right ?
58:37Yes . Note that I sometimes have a
58:41phrase regarding critical ultrasound
58:43where I say that a good doctor will do
58:46an excellent job . In other words , a
58:50good doctor who is excellent will
58:52become even more excellent , but a bad
58:55doctor can become dangerous . It's
58:58something similar here ; I mean , if you
59:00lack the capacity and the training
59:02required to place and interpret it ,
59:04then regardless of how sophisticated
59:06the assessment may be and even if it is
59:08backed by evidence to diagnose ,
59:10hemodynamically locate , and monitor the
59:12patient , obviously , the simple act of
59:14placing it will inevitably lead to
59:16causing complications for the
59:18individual involved in the process .
59:20And in the post-surgical period of
59:21complex cardiac surgery , heart
59:23transplants , it is definitely managed
59:25with SUAS . Of course , that's something
59:27I'd be interested in in another episode
59:29. I mean , those who are already part of
59:31the critical areas training membership
59:33on YouTube ,
59:34we have a class on post-surgical
59:36management in cardio-surgical units ,
59:39but an episode on that would be good
59:41later because it's a world that very
59:43few of us know about , even those of us
59:46who work in intensive care , because
59:48we're in the multipurpose unit , not
59:52in a cardiovascular unit . I mean , in my
59:55case , I manage post-operative
59:57hemodynamics , but not post-surgery
1:00:00because it's a different world . But hey
1:00:04, even arrhythmias are managed
1:00:05differently , bradycardias don't respond
1:00:07to tropine , that's crazy , so this is
1:00:09very interesting . Well , there it is .
1:00:13That's going to be the part that I
1:00:14think is most controversial , but I do
1:00:16say it's not controversial because
1:00:17those who really manage cardiogenic
1:00:19shock and their specialized units do
1:00:20what you're describing .
1:00:22Of course .
1:00:23Now , if they're not in a cardiovascular
1:00:25unit and they have cardiogenic shock ,
1:00:27they should try to refer them to a
1:00:29specialized center as much as possible ,
1:00:31obviously with all the possible
1:00:33variations or limitations . It's like
1:00:36when we have a patient with a major
1:00:38burn , they're going to benefit more in
1:00:39a major burn unit . Okay , now to wrap
1:00:43things up , what are the most common
1:00:45mistakes you see in the management of
1:00:48cardiogenic shock and what
1:00:50recommendations could you make to avoid
1:00:53it ? The first mistake I would like to
1:00:56make is the lack of early recognition
1:00:58of patients in cardiogenic shock . I
1:01:01have a heart attack patient who has
1:01:02Levin's sign in the emergency room and
1:01:04who is sitting there and no one has
1:01:06paid attention to him . They already did
1:01:08an EKG , so he has a heart attack and is
1:01:10about to come , but it is without ST
1:01:11elevation . So , leave him there , give
1:01:14him aspirin , clopy
1:01:15or unstable angina . Unstable angina and
1:01:18those patients , watch out , I have to
1:01:20think , " Hey ,
1:01:22this patient is starting to have
1:01:24tachycardicity , today he is starting to
1:01:26have hypotension , watch out , this
1:01:28patient is already developing
1:01:30cardiogenic shock . " So early
1:01:32recognition is important in the
1:01:34prognosis of patients with cardiogenic
1:01:37shock . Two , the lack of implementation
1:01:41of an H team . Yes , it is essential that
1:01:45our hospitals and medical care centers
1:01:47have doctors and nurses who are
1:01:49properly trained . This is why
1:01:52institutional heart attack codes are so
1:01:55vital , as even the security guard must
1:01:57understand that this is a condition
1:02:00where every single second counts . The
1:02:03person who receives a patient with a
1:02:05heart attack must be aware and fully
1:02:07understand that this patient requires
1:02:09time-dependent care for their treatment
1:02:11. Your team , well , anesthesiology ,
1:02:15nutrition , psychology , intensive care ,
1:02:21cardiology , hemodynamics , everything
1:02:26related to your team , cardiovascular
1:02:28surgery , etc. , should be available in
1:02:30our centers . That would be ideal . Of
1:02:32course .
1:02:33Three , do not guide monitoring , do not
1:02:40guide therapy based on hemodynamic
1:02:43monitoring . And I am going to refer to
1:02:45the ultrasound . If we have an
1:02:47ultrasound at the bedside , I can guide
1:02:50a hemodynamic monitor in a patient with
1:02:52cardiogenic shock . Administering
1:02:55medications like dobutamine or
1:02:57levosimendan without an objective
1:02:59assessment makes it highly probable
1:03:01that we will commit errors when we take
1:03:04those clinical actions . Therefore ,
1:03:07training in ultrasound care would be a
1:03:10very important investment in the care
1:03:13of these patients . I would
1:03:17also like to point out the lack of work
1:03:20on the underlying etiological cause , if
1:03:22it is ischemic heart disease , taking
1:03:25them to percutaneous intervention ,
1:03:27reperfusing fibrinolysis . If it is a
1:03:31patient who has valvulopathy or if they
1:03:33have post-cardiotomy cardiogenic shock ,
1:03:35then we have to think about a way to
1:03:36care for this patient . I would focus on
1:03:40these four points , which would be the
1:03:43most frequent errors and which can be
1:03:45associated with higher mortality in our
1:03:48patients . Drugs , well , drugs have not
1:03:51yet demonstrated that if you administer
1:03:54a drug , it will improve the patient's
1:03:56prognosis . You can support it , that's
1:03:59what we intend , support it with
1:04:00medications , but work on the underlying
1:04:03cause
1:04:04in a hypothetical situation or make a
1:04:07decision for your life . If from now on ,
1:04:10they told you that only for management ,
1:04:12for monitoring cardiogenic shock ,
1:04:14you're going to have swansong or
1:04:15ultrasound . What do you say ? I'll stick
1:04:20with the ultrasound ,
1:04:22betraying your school .
1:04:23No , no , no , no , no , no . I'll stick with
1:04:26the ultrasound because it's what I have
1:04:28faster at the bedside , I grab it , I
1:04:29sound it , I see it and I make decisions
1:04:31. But now with more precise monitoring .
1:04:34Yes ,
1:04:34more precise . Yes , I'll go with the
1:04:36swangans . It
1:04:36should be both . So , it
1:04:38should be both . Exactly . I think that
1:04:41school of having them compete , which is
1:04:43better ? Ecco , Swan , no , we're talking
1:04:47about different scenarios , we're
1:04:49talking about different information ,
1:04:51we're talking about going back to the
1:04:54Swanang Guns , I think that in highly
1:04:56classified , selected patients , who
1:04:58require that information , it's vital ,
1:05:01it's important .
1:05:03Yes , of course . And it's not a matter
1:05:05of egos or debates between doctors , but
1:05:07rather which tool would be best for the
1:05:10patient . Yes , at the end of the day ,
1:05:13the answer to the question you asked me
1:05:14is , " I would stick with both , perhaps I
1:05:16would start with the echo and then I
1:05:17would try to put a swap . " It's already
1:05:21recorded . Okay , perfect . And final
1:05:25message or , uh , let's say , final advice
1:05:28that you want to send to all our
1:05:30followers , health professionals here on
1:05:32Interconsulta , the medical podcast ,
1:05:34where you can find it in training in
1:05:36critical areas on YouTube and also on
1:05:38Spotify . On Spotify we appear as
1:05:41Interconsulta , the medical podcast . The
1:05:44commercial . Yes .
1:05:45Well , the last message is , the
1:05:46cardiovascular patient is a patient who
1:05:48evolves very dynamically . Attachment ,
1:05:51I'll stick with this , the doctor's
1:05:53attachment to the patient's bedside .
1:05:57There will never , ever be any other
1:06:00hemodynamic monitoring that can replace
1:06:03the doctor's attachment to the
1:06:05patient's bedside . If we are glued to
1:06:09perfusion , we are detecting a patient
1:06:11who is becoming seriously ill and it is
1:06:13a patient that I have to take action on
1:06:15, measure , interpret , act and reassess .
1:06:17Our patient is always glued to the
1:06:18serious condition ,
1:06:19the famous pee .
1:06:20The famous pee .
1:06:21Measure , interpret , act and reassess .
1:06:25Exactly . Well , thank you very much , Dr.
1:06:28Morgado . We have learned a lot .
1:06:30Personally , I always learn from you . It
1:06:32is a way of saying things , or you have
1:06:37a way of saying things , that I think is
1:06:39very well understood , despite the fact
1:06:41that they are quite complex situations ,
1:06:43sometimes , you learn through reading or
1:06:45through the explanations of even people
1:06:47who , perhaps , have more years in this ;
1:06:50but I think it is very understandable .
1:06:53If you thought so , well , we can invite
1:06:55you to another episode . The truth is
1:06:57that I'm very interested in cardiac
1:07:00critical care but also post-surgical
1:07:02care . ECMO would also be very
1:07:05interesting , man . There are a lot of
1:07:07cardio issues that we can discuss with
1:07:09Dr. Morgado . This is about cardiac
1:07:11arrest , but in terms of post-surgical
1:07:13care because that's
1:07:14another issue .
1:07:16Yes , yes , yes . There are many names for
1:07:18it , right ? But cardiac arrest in
1:07:20patients who have undergone cardiac
1:07:22surgery is also another issue . But
1:07:24anyway , thank you very much again . Any
1:07:27plans or upcoming projects that you
1:07:29would like to discuss ?
1:07:32Well , we are going to publish the book
1:07:36on critical cardiology and ...
1:07:38Yes . Well , I could help you with
1:07:40something , obviously . Obviously , with
1:07:42your training . I remember when Morgado
1:07:44was going to tell you something like
1:07:45that . Like gossip . He sent me a message
1:07:49: " Doctor Zamarrón , this is Luis
1:07:51Morgado , sir , I am an intensive care
1:07:54resident , second year , or rather first
1:07:56year , first year ,
1:07:58first year . " Yes , you were just
1:07:59starting out in therapy . I want to take
1:08:01the mechanical ventilation course . I
1:08:02tell him , " Oh , where are you from ? " He
1:08:04already told me . I tell him , " Well , I
1:08:06don't think you're ready to take it .
1:08:09You're here to help us . What do you
1:08:11think ? " And no , of course you are . I
1:08:12know ventilation and you know good
1:08:14concepts , honestly . So we've already
1:08:16seen you and I tell Morgado , well ,
1:08:18ready , come on , give a workshop .
1:08:21Morgado , well , welcome . We're going to
1:08:24give him a programming workshop , get
1:08:26started , and here he is giving courses
1:08:28on mechanical ventilation and all
1:08:30critical care . And right now , he's an
1:08:33expert on critical cardiovascular
1:08:35issues and he's a great asset to our
1:08:37work group and to all of you who have
1:08:39seen him here on Interconsulta , the
1:08:41medical podcast . Thank you very much
1:08:43again
1:08:45and we hope he soon releases that book
1:08:47on cardiovascular emergencies and
1:08:49critical cardiology . That's
1:08:51right . That's right .
1:08:52See you next time . Give it a thumbs up ,
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1:09:00Ciao .