WEBVTT

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This is a very good platform for the young buddies or young

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physicians to learn about a few medical problems that

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you face to face on the routine practice. So one of those

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kind of routine syndrome or syndrome you can say

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that is acute respiratory distress syndrome. So to begin with I would

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like to outline our next one hour. So we'll be introducing

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with the definition, then the clinical history of the patients, pathophysiology behind

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ARDS, how to diagnose and how to manage. So to begin with,

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let's discuss a case. So let's say if you are working in

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your ICU or ER and you have this male patient

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who is 35 years old and he had met with an accident

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and was admitted with tachypnea, dyspnea within 24 hours of

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admission. So once you examine, then you have pulse of 110,

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BP higher on a higher lower side that is 80/50. Patient is

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pallor, cyanotic, but there is no JVP. Heart sounds are normal,

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chest on auscultation suggests bilateral rails in mid

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and lower areas. Abdomen is soft and there is no bowel sound

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or any heart sound. ABC we did because of tachypnea, dyspnea and

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hypertension and on 50% of FiO2. PaO2 was 40%,

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PaCO2 45% and pH was 7.3. So

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more or less it's a kind of dyspnea or breathlessness. We did

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X-ray and X-ray suggestive of this. So you can make out what

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X-ray has to say and after that we

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treated the patient. So on X-ray and on clinical examination

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we can find out the patient might be in ARDS, right? So

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now what is ARDS? That is acute respiratory distress syndrome. So it's

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a syndrome, it's a clinical syndrome. Uh it's not a particular disease,

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but uh it's one of the step behind after a few diseases.

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So it's a clinical syndrome of dyspnea of rapid onset, hypoxemia

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and diffuse pulmonary infiltrates leading to respiratory failure. So

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in this what happens actually that we'll discuss about pathophysiology, but in

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a nutshell you can say that inflammatory cells and the proteinaceous fluid

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accumulate in the alveolar spaces and it leads to the decreased

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diffusion capacity and because of that patient is having hypoxemia. So

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what is the difference between ALI that is acute lung injury and

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ARDS? So ALI term is used when your PaO2 FiO2

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ratio is less than 300. So that is called as significant hypoxia.

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So both whatsoever may be the condition if PaO2

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and FiO2 ratio that is PF ratio if it is less than

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300, then you can say that patient is having acute lung injury.

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It can be anything. So ARDS is a subset of ALI because

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in ARDS PF ratio is less than 200. So there are a

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few more conditions as well in which PF ratio is between 200

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to 300. Now that is not ARDS, but that is ALI. So

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ALI is a broad term and ARDS is one part of ALI

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and both can be differentiated by PF ratio. So any PF ratio

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between 200 to 300 is not ARDS, but definitely it is ALI.

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So this is the difference you can say that between ALI and

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ARDS. So both are acute as the A

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stands the first and foremost letters. So both are acute. Uh as

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I told you the PA difference of PF ratio, so if it

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is less than 300, then it is a broad ALI. If it

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is 200, then it is specific ARDS. Both are having bilateral interstitial

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or alveolar infiltrates and in both PCWP that is pulmonary capillary wedge

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pressure is less than 18. Now if both are same and if

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in both PCWP is less than 18, then what would be the

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condition in which PCW could be more than 18? So you think

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over it and during this session we'll discuss if PCWP is

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more than 18 and if PCW is less than 18, then what

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could be our management plan? So how to diagnose ARDS?

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So it should be acute. There has to be a predisposing condition.

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It cannot occur by itself. It it is because of some diseases

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and which presents as respiratory distress. So that's what is we called

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as it's a clinical syndrome. In uh you have to have bilateral

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infiltrates. If infiltrates would be only one side, then maybe it is

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not ARDS. PF ratio must be less than 200. If it is

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less more than 200, then it is not ARDS, it could be

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ALI. And PCWP that is pulmonary capillary wedge pressure should be less

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than 18. If it is more than 18, then we'll consider it

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as a different pathophysiology. So make sure that if you have this

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findings available, all of these findings available, then you can stamp it

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as ARDS. Otherwise we have to think something else. So it has

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to be acute. You have to have a predisposing condition. Patient on

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X-ray or CT scan must have bilateral infiltrates. PF ratio should

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be less than 200 and pulmonary capillary wedge pressure should be less

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than 18. So this is must for ARDS. Now

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causes it could be direct lung injury, it could be indirect lung

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injury. So indirect lung injury, pneumonia first and foremost that we think

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of pulmonary contusion because of trauma, in patients with near drowning,

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inhalational injury in commercial places and aspiration of gastric

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contents can lead to ARDS. What

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are the indirect lung injuries? So sepsis, sepsis because of anything, severe

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trauma versus with shock of hyperperfusion, acute pancreatitis

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and transfusion of multiple blood products. So ultimately

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if I have to remember three or four most common causes of

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ARDS, then first would be sepsis, second trauma, third acute pancreatitis

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and fourth one is lung direct lung injury because

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of any of these. So pancreatitis, trauma, sepsis can

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lead to ARDS and once you are you are treating such

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patient, then you have to forecast that this patient can go into

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ARDS and steps must be taken to avoid ARDS. Once

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it is developed, then your treatment strategy would be different. So

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in my opinion, if we are having such patients, then ARDS is

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not the presenting complaint within 24 hours. It will develop gradually

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and once it is developed, then it is very difficult to treat.

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So make sure that your patients don't go into ARDS situation.

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So pathophysiology there will be a diffuse alveolar damage. After

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that, lung capillaries would also be damaged. Inflammatory cells would be gathered

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into alveolar alveolar space and creates alveolar edema

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that gives rise to severe hypoxemia, decreased lung compliance and lastly pulmonary

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hypertension. Let's discuss one by one. So this is a normal alveoli

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on the left side. So in which you have type one cells,

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type two cells and surfactant layer and there are a few macrophages

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in the alveolar space. Outside alveoli you have interstitium and then blood

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vessels. In blood vessels also you have epithelial cell, endothelial cells

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and between these endothelial cells and epithelial cells of the alveoli there

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is a blood or gas exchange and there are very few microblasts

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or fibroblasts within the interstitial space. So interstitial space is very

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much looking transparent and easy gas exchange between normal alveolar space

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and the blood vessels. Now what happens if

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alveolus is injured during acute phase, then inflammatory reaction

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would come into place and because of that inflammatory reactions cytokine

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release IL-1, 2, 1, 6, 8, 10, TNF alpha,

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MIF would come into place and they don't activate the macrophages. Now

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this activated macrophages what they will do it will secrete leukotrienes, oxidants,

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PAF and proteases. Now these proteases would damage and apoptize

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or the type one and type two cells. And because of that

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there is a membrane disruption and because of that disruption there is

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an alveolar edema. The proteinaceous fluid will come into the alveoli. In

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interstitium there would be an edema. So widened edematous interstitium would be

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there. Neutrophils would be migrated from inside to outside and from another

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place to that place that secretes proteases and this proteases would further

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damage the alveolar cells as well as the endothelial cells. And

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now these endothelial cells again would decrease the transfusion of

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gases. So and there would be much of the fibroblast and procollagen

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within the interstitial space and that would create an inelastic

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or impermeable interstitial membrane. And because of this the

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transfusion of gases O2 and CO2 between alveoli to the blood vessels

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would be hampered and alveoli would be filled with

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proteinaceous fluid. There will be lack of surfactant layer and because

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of lack of surfactant layer and on fluids accumulation in the alveoli

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there would be collapse of alveoli. And because of that there would

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be increased dead space. So oxygenation would be decreased and because of

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lack of oxygenation patient would feel hypoxia. And whatever amount of FiO2

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you increase PaO2 will not be increased. And if PaO2 is not

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increasing in spite of FiO2, your PF ratio would go less than

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200. And if it is less than 200, then it fits into

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the definition of ARDS. So ARDS is nothing but the alveolar

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damage and because of the damage the whole cascade of inflammatory

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reaction come into place and because of that there will be collapse

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of alveoli. Proteinaceous fluid would be accumulated in the alveoli and

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decreased gas exchange between alveoli and blood vessels. And that

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would create this kind of picture in which fibronectin, myofibroblast,

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collagen cells and this the whole cascade would damage ultimately

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the alveoli and gas exchange. So this is the pathophysiology behind the

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ARDS. So if you see in the histopathology, then if a normal

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lung you can see in the lower picture. So the large alveolar

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volumes, septal spaces very thin, septa are very thin and

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no cellular congestion. And in comparison to the upper picture, there is

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a hyaline protein air in the spaces, cellular congestion, thickened interstitial

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walls. So this is typical uh histological findings in ARDS. So

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there would be alveolar inflammation, thickened septal from protein leak

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so that is the pink color and congestion and decreased alveolar volume.

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And because of this decreased volume decreased exchange and patient would be

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into hypoxia. So as we discussed, if you come into

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the clinical history part, then it's an acute condition. Okay, there is

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no chronicity. It's an acute condition. Patient would be critically ill because

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patient is into hypoxia. And because of this inflammation patient may be

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into the sepsis, septic shock. So multiple infusions, multiple transfusions, patient

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would be in the on the mechanical ventilation. So patient is ultimately

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falling into critically ill situation. Rapid breathing,

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rapid pulse and hypoxia. So that is trademark. So patient would have

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tachypnea, tachycardia, dyspnea, hypertension, maybe hypoxia

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as well. And it occurs basically within 12 to 24

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to 8 hours of precipitating events. After trauma within two days you

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can expect that patient may go into ARDS. So you have to

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be very careful while treating the patients with pancreatitis and trauma. Initially

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respiratory alkalosis would be there because uh you know there is increased

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work of breathing. So CO2 wash out will be there and because

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of that patient would be into respiratory alkalosis because of tachypnea. But

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later on, later on patient would go into respiratory

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failure. So there would be hypoxia. So type one respiratory failure you

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will come across after due course of time. So to

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know whether patient is going into hypoxia or not or hypercapnia or

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not ultimately ABG is the investigation of choice for us. So to

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begin with ABG because uh patient would be admitted because of trauma

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or pancreatitis or sepsis, septic shock or any of the lung pathology

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patient would be indoors. So you will be having a routine blood

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counts or RFT, CT if required, BNP, 2D cobalt,

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PCWP. So ultimately one of the most important investigation that I would

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like to send in this patient is ABG because I want to

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know what is the PO2 level, PCO2 level and pH level. If

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patient is not having any of the chest pathology, then now this

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is the time to get chest X-ray done. If it is chest

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X-ray is not good, then ultimately CTS or CT chest is required

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diagnose what actually it is going on inside. BNP is

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required to rule out heart failure. Now it's a time to discuss

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about uh cardiogenic and non-cardiogenic shock. So

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chest X-ray is required because in chest X-ray why we have the

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uh criteria to diagnose the infiltrates. So infiltrates would be on the

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both sides. And both sides infiltrates can be seen in cardiogenic as

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well as non-cardiogenic pulmonary edema. Now ARDS is non-cardiogenic pulmonary

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edema. So we need to rule out the cardiogenic pulmonary edema. Now

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how to rule out? First thing is BNP. If BNP is normal,

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then you can say this is not patient is in not into

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cardiogenic pulmonary edema and 2D echo to see what is the ejection

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fraction. Ejection fraction is normal if there is no uh IVC

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dilatation and if there is no any signs of left ventricular dysfunction,

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then you can say this is not a cardiogenic pulmonary edema. It

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must be because of non-cardiogenic pulmonary edema because you may see have

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patient with HFrEF or HFpEF. So what is HFpEF? That is a

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heart failure with preserved ejection fraction. And now this preserved ejection fraction

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with heart failure can be seen in non-cardiac pathologies like CKD,

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like MR, like uh hyperproteinemia. So there are

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different different pathologies in which you have HFpEF. So we need to

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rule out whether patient is having HFpEF or ARDS. So cardiogenic pulmonary

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edema is in the bilateral side. Even non-cardiogenic it is also bilateral,

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but in cardiogenic you have tendency of infiltrates on

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the lower side. But in non-cardiogenic you have diffuse. Uh in

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cardiogenic you have curly B lines and cardiomegaly whereas in non-cardiogenic

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you have homogeneously distributed throughout the lung and there is no curly

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B lines. So this is a very important point to rule

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out in chest X-ray whether patient is having cardiogenic pulmonary edema or

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non-cardiogenic pulmonary edema. So patch infiltrates in bases

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that is as seen in cardiogenic pulmonary edema and homogeneous fluffy opacities

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in non-cardiogenic pulmonary edema. In cardiogenic you have pleural effusion. In cardiogenic

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non-cardiogenic pleural effusion is generally not there. In cardiogenic you have curly

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B lines, whereas in ARDS there is no curly B lines. In

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cardiogenic you have cardiomegaly. In non-cardiogenic you don't have any kind of

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cardiomegaly. In cardiogenic you have pulmonary vascular redistribution that is bat wing

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appearance, but here it there is no pulmonary vascular redistribution. So in

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cardiogenic you have excess fluid in the alveoli, clear fluid. Whereas in

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non-cardiogenic you have proteinaceous inflammatory cells and fluid in

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the alveoli. So that is more dangerous than cardiogenic pulmonary edema. So

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early signs you can see these are maybe the lower side, but

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in late signs you have almost diffuse cardiogenic pulmonary edema

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so uh in ARDS. So these are the very clear-cut signs on

228
00:18:31.500 --> 00:18:36.000
chest CT scan. So there is a septal thickening and more severing

229
00:18:36.000 --> 00:18:40.400
lung bases, whereas here there is no patchy septal uh thickening. There

230
00:18:40.400 --> 00:18:45.900
is a diffuse alveolar infiltrates, atelectasis of the dependent lobes usually

231
00:18:45.900 --> 00:18:51.400
seen in ARDS. So very typical, very clear-cut

232
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differentiation between cardiogenic pulmonary edema and non-cardiogenic pulmonary edema. So

233
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you should know when you treat your patient with hypoxia and you

234
00:19:00.500 --> 00:19:05.200
have chest X-ray with bilateral infiltrates, then as the primary consultant you

235
00:19:05.200 --> 00:19:10.200
should be able to differentiate between cardiogenic and non-cardiogenic. And lastly, once

236
00:19:10.200 --> 00:19:15.700
you have a confirmed diagnosis of ARDS, then there are therapies

237
00:19:16.000 --> 00:19:21.100
that should be implemented. So first and foremost treatment

238
00:19:21.100 --> 00:19:25.000
of underlying cause. So we have direct lung injury as well as

239
00:19:25.000 --> 00:19:30.000
the causes which cause or the diseases which cause indirect lung

240
00:19:30.000 --> 00:19:35.200
injury like trauma, sepsis, pancreatitis or multiple blood transfusions.

241
00:19:35.600 --> 00:19:40.900
And in direct lung injury like pneumonia or what

242
00:19:41.000 --> 00:19:45.900
you can say the contusions. So these will give rise to the

243
00:19:46.400 --> 00:19:49.800
direct lung injury in ARDS. So treat the underlying cause as soon

244
00:19:49.800 --> 00:19:54.800
as possible to reduce the chances of ARDS. Then second comes the

245
00:19:54.800 --> 00:20:00.400
cardiogenic support if patient is having hypoxia or hypertension or tachycardia,

246
00:20:00.400 --> 00:20:05.900
then it is required to support the cardiac and pulmonary status.

247
00:20:06.700 --> 00:20:10.700
There are few specific therapies that can be targeted to the lung

248
00:20:10.800 --> 00:20:15.200
injury in ARDS. And then the rest of the supportive therapy that

249
00:20:15.200 --> 00:20:19.800
you generally give in ICU setting. So underlying cause we'll not discuss

250
00:20:19.800 --> 00:20:23.700
much because we know that you know how to treat pancreatitis or

251
00:20:23.700 --> 00:20:27.000
how to treat trauma or how to treat multiple lung multiple blood

252
00:20:27.000 --> 00:20:32.900
transfusions. Just we'll focus mainly on cardiogenic support and ARDS.

253
00:20:34.200 --> 00:20:38.700
So if patient is spontaneously breathing, so in early stages ARDS the

254
00:20:38.700 --> 00:20:44.200
hypoxia may be corrected by 40 to 60% of inspired oxygen. So

255
00:20:44.200 --> 00:20:48.500
if you feel that patient is having hypoxia and hypoxia and tachypnea,

256
00:20:48.500 --> 00:20:53.700
then you can start the full 100% FiO2 oxygen through NRBM. And

257
00:20:53.700 --> 00:20:58.800
then see how it goes and how patient improves. So the first

258
00:20:58.800 --> 00:21:03.400
and foremost thing is to give oxygen through mask that is NRBM

259
00:21:03.600 --> 00:21:07.600
and check what the SpO2 level, what is the level of tachypnea.

260
00:21:07.800 --> 00:21:11.400
If patient is improving, then continue with that. But if patient is

261
00:21:11.400 --> 00:21:15.400
deteriorating, then you need to go one step higher. So if the

262
00:21:15.400 --> 00:21:20.400
patient is well oxygenated on less than 60% of expired oxygen

263
00:21:20.400 --> 00:21:25.400
and apparently stable without CO2 retention, so we need we do ABG

264
00:21:25.600 --> 00:21:30.500
and see what is the PaO2 and PaCO2 level. Then monitoring would

265
00:21:30.500 --> 00:21:35.800
be feasible and continuous oximetry and regular blood gases

266
00:21:35.800 --> 00:21:40.800
are required to check whether this therapy is

267
00:21:40.800 --> 00:21:46.000
effective or not. Now what are the indication for mechanical

268
00:21:46.000 --> 00:21:51.300
ventilation? So inadequate oxygenation with P so that is PaO2

269
00:21:51.300 --> 00:21:56.700
less than 60 with FiO2 more than 60% rising or elevated PaCO2

270
00:21:56.700 --> 00:22:01.300
level that is more than 50 mmHg and if you feel that

271
00:22:01.700 --> 00:22:06.900
patient is going into respiratory failure, patient is going into fatigue and

272
00:22:06.900 --> 00:22:12.000
other signs of mechanical ventilation like GCS is worsening, like

273
00:22:12.000 --> 00:22:17.100
hypotension is there and patient needs to be ventilated, then yes mechanical

274
00:22:17.100 --> 00:22:20.700
ventilation is a good choice to implement. So you have to be

275
00:22:20.700 --> 00:22:24.600
very careful while treating the patient on NRBM because at any moment

276
00:22:24.600 --> 00:22:29.900
patient may require mechanical ventilation. So it is very very

277
00:22:29.900 --> 00:22:34.200
important to understand the severity of the patient on NRBM than the

278
00:22:34.200 --> 00:22:38.600
mechanical ventilation because on mechanical ventilation you are safe because airway is

279
00:22:38.600 --> 00:22:43.900
protected and machine is delivering whatever we want. But in NRBM

280
00:22:44.300 --> 00:22:49.400
patient's airway is not protected and patient is breathing on his own.

281
00:22:49.500 --> 00:22:54.900
So you have to be very watchful on patients with NRBM. Don't

282
00:22:54.900 --> 00:22:57.600
take it lightly as patient is only on NRBM, that's okay. Patient

283
00:22:57.600 --> 00:23:02.700
is not critical. Even on NRBM we have to think that patient

284
00:23:02.700 --> 00:23:07.700
is critical and we have to give utmost care to

285
00:23:07.700 --> 00:23:13.000
the patient on NRBM. So in mechanical ventilation

286
00:23:13.000 --> 00:23:18.000
the aim is to increase PO2 while minimizing the risk of

287
00:23:18.100 --> 00:23:24.000
further lung injury. So this ventilator induced lung injury. So

288
00:23:24.000 --> 00:23:29.200
mechanical ventilation doesn't only come with benefits, it has disadvantages, it has

289
00:23:29.200 --> 00:23:34.200
complications and it is causing lung injury. So

290
00:23:34.200 --> 00:23:39.600
you have to be very watchful while doing mechanical ventilation. So ideal

291
00:23:39.800 --> 00:23:44.800
ARDS net protocol. So patient should be on ventilator uh volume

292
00:23:44.800 --> 00:23:49.800
assisted control mode, back mode, tidal volume of around 6 ml

293
00:23:49.800 --> 00:23:54.600
per kg. So if patient is uh 60 kg, then you can

294
00:23:54.600 --> 00:23:59.000
put it as a 350 to 400 ml. Plateau pressure of it

295
00:23:59.000 --> 00:24:03.700
should be less than 30 cm of water. Rates 6 to 35

296
00:24:03.700 --> 00:24:07.800
whatever you are feeling convenient. IE ratio should be 1 is to

297
00:24:07.800 --> 00:24:12.000
1 to 1 is to 3. So expiratory is more than inspiratory.

298
00:24:13.200 --> 00:24:19.200
Our target of PaO2 is 7.3 to 10.7 kPa and SpO2

299
00:24:19.200 --> 00:24:24.200
of around 90 to 95. So peep and FiO2 set

300
00:24:24.200 --> 00:24:28.400
according to the predetermined combination that is peep should be between 5

301
00:24:28.400 --> 00:24:32.400
to 24. Peep should not be less than five. So it should

302
00:24:32.400 --> 00:24:40.000
be low volume or low tidal volume ventilation to avoid any further

303
00:24:40.000 --> 00:24:45.000
lung injury. So how to wean? Once patient

304
00:24:45.000 --> 00:24:48.800
is put on ventilator, so patient is improved, then we have to

305
00:24:48.800 --> 00:24:54.500
wean. Now before weaning we have to follow these protocols like

306
00:24:54.600 --> 00:24:57.900
spontaneous breathing trial should be given on daily basis. And you are

307
00:24:57.900 --> 00:25:02.400
satisfied with the spontaneous breathing, then you can think of weaning. Systolic

308
00:25:02.400 --> 00:25:06.000
blood pressure should be more than 90 mmHg without any kind of

309
00:25:06.000 --> 00:25:10.700
vasopressors. There should not be any neuromuscular blockade. So patient should be

310
00:25:10.700 --> 00:25:15.300
fully conscious and oriented. Two hour trial with TPs and one to

311
00:25:15.400 --> 00:25:20.200
with 1 to 5 cm water of CPAP should be given. Continuous

312
00:25:20.200 --> 00:25:25.500
ABG respiratory with monitoring is required. And if patient is tolerating

313
00:25:25.500 --> 00:25:30.800
for 30 minutes, then you can consider for extubation.

314
00:25:31.300 --> 00:25:36.500
So extubation is very tricky. And after extubation

315
00:25:36.500 --> 00:25:39.400
if you have to reintubate the patient, then it is very traumatic

316
00:25:40.000 --> 00:25:45.300
for you, for patient and for relatives. So you

317
00:25:45.300 --> 00:25:48.700
cannot just go ahead and extubate the patient. You have to follow

318
00:25:48.700 --> 00:25:54.200
certain criteria to wean and then consider extubation.

319
00:25:56.000 --> 00:26:00.500
So there are a few recommendations. Uh evidence-based recommendation for ARDS therapy.

320
00:26:00.500 --> 00:26:04.400
So low tidal volume is the level A recommendation. So you have

321
00:26:04.400 --> 00:26:09.500
to follow uh low tidal volume principle in treating the patient with

322
00:26:09.500 --> 00:26:14.500
ARDS. High PEEP and minimize LFP. Okay, B

323
00:26:14.500 --> 00:26:19.500
recommendation. High PEEP C, type C recommendation. Prone position. Yes, it is

324
00:26:19.500 --> 00:26:25.000
type C recommendation. Recruitment maneuvers. Again time C. High frequency

325
00:26:25.000 --> 00:26:29.200
ventilation. Type D. So not of much value along with corticosteroids, surfactant

326
00:26:29.200 --> 00:26:34.000
replacement and inhaled NO or others. These are of type D recommendation.

327
00:26:34.000 --> 00:26:37.000
So we'll not go into detail of this much, but low tidal

328
00:26:37.000 --> 00:26:43.900
volume is that you should think of with minimizing LFP. So

329
00:26:43.900 --> 00:26:48.400
in this one thing uh we have to discuss is uh I

330
00:26:48.400 --> 00:26:53.500
forgot to discuss about PCWP that is pulmonary capillary wedge

331
00:26:53.600 --> 00:26:58.800
pressure. Now this pulmonary capillary wedge pressure in cardiogenic and non-cardiogenic pulmonary

332
00:26:58.800 --> 00:27:04.100
edema it should it is normal in non-cardiogenic pulmonary edema

333
00:27:04.100 --> 00:27:08.800
as while it would be increased in cardiogenic pulmonary edema. So nowadays

334
00:27:08.800 --> 00:27:13.200
we don't generally measure PCWP, but theoretically you should remember that if

335
00:27:13.200 --> 00:27:17.700
PCWP is increased, then it is cardiogenic pulmonary edema. If PCWP is

336
00:27:17.700 --> 00:27:22.800
normal, then it is non-cardiogenic pulmonary edema. So

337
00:27:22.800 --> 00:27:28.000
these are few differentiating point between cardiogenic pulmonary edema and non-cardiogenic

338
00:27:28.000 --> 00:27:33.400
pulmonary edema. So now you should be able to differentiate between

339
00:27:33.400 --> 00:27:38.300
cardiogenic pulmonary edema and non-cardiogenic on clinical examination, on investigations and on

340
00:27:38.400 --> 00:27:42.700
X-ray. And depending upon that you can go ahead and treat the

341
00:27:42.900 --> 00:27:48.200
patient. So low tidal volume ventilation that is very very important

342
00:27:48.200 --> 00:27:53.400
in reducing alveolar associated lung injury. So in ARDS

343
00:27:54.100 --> 00:27:58.900
there is a large amount of poorly compliant or non-ventilating lung and

344
00:27:58.900 --> 00:28:02.600
a small amount of healthy and compliant lung tissue as most of

345
00:28:02.600 --> 00:28:07.700
the lungs are collapsed. Now if you give large

346
00:28:07.700 --> 00:28:12.800
volume, then it can lead to overinflation of healthy lungs and resulting

347
00:28:12.800 --> 00:28:18.100
in ventilator-induced lung injury of that healthy tissue. So we are ventilating

348
00:28:18.100 --> 00:28:23.100
only few percentage of lungs, not the whole lung.

349
00:28:23.300 --> 00:28:27.500
And that's why uh the tidal volume from 10 ml per kg

350
00:28:27.500 --> 00:28:31.300
should be reduced to 6 ml per kg because we don't want

351
00:28:31.300 --> 00:28:36.300
the healthy tissue to get damaged. And peep would support us to

352
00:28:36.300 --> 00:28:41.200
prevent further lung injury due to shear forces by keeping airways patent

353
00:28:41.200 --> 00:28:46.500
and during expiration. So it peep will prevent the

354
00:28:46.500 --> 00:28:53.100
collapse of the lung and gradually it will increase the uh recruitment

355
00:28:53.500 --> 00:28:58.100
of lungs. And then you can increase the tidal volume. So the

356
00:28:58.100 --> 00:29:03.100
initial therapy should be with low tidal volume mechanical

357
00:29:03.300 --> 00:29:08.800
ventilation. So uh there were studies or trials

358
00:29:08.800 --> 00:29:12.300
done and you can see that high tidal volume versus low tidal

359
00:29:12.300 --> 00:29:17.400
volume uh the model rate was higher in tidal volume than low

360
00:29:17.400 --> 00:29:22.900
tidal volume. And in high peep versus low peep 13 versus 8

361
00:29:23.000 --> 00:29:27.000
there is no difference. So peep should be read uh I mean

362
00:29:27.000 --> 00:29:32.100
kept between 5 to 8 not more than that. And

363
00:29:33.800 --> 00:29:37.800
what one study suggested that optimal peep was 15 cm of water

364
00:29:37.900 --> 00:29:40.700
H2O, but in my opinion peep should be 5 to 8 not

365
00:29:40.700 --> 00:29:45.000
more than that with low tidal volume that would prevent further lung

366
00:29:45.000 --> 00:29:49.800
injuries and slowly and gradually as lungs would be drying up, there

367
00:29:49.800 --> 00:29:54.400
would be more and more accumulation or recruitment of alveoli into the

368
00:29:54.400 --> 00:30:00.000
ventilatory system. A study was done on inverse ratio relationship. So

369
00:30:00.000 --> 00:30:05.100
it reduced the peak airway pressure. So IE ratio if we keep

370
00:30:05.300 --> 00:30:10.800
4 is to 1, then it is required in severe hypoxic

371
00:30:10.800 --> 00:30:15.000
respiratory failure. So in which there should be the ratio of IE

372
00:30:15.000 --> 00:30:20.000
should be reversed to 4 is to 1. Hypercapnia

373
00:30:20.100 --> 00:30:25.100
we can keep up to 55. So pH up to 7.25

374
00:30:25.100 --> 00:30:30.300
is okay. pH should not go down. pH should be between 7.25

375
00:30:30.300 --> 00:30:35.600
nearly 7.25 and PCO2 nearly 55. And a controlled hypoventilation

376
00:30:35.600 --> 00:30:40.700
can be given a chance along with proning. So proning is required

377
00:30:40.700 --> 00:30:44.900
because in supine condition if we sleep, then our heart that is

378
00:30:44.900 --> 00:30:49.300
on the anterior side would compress the lungs from ventilation. So it

379
00:30:49.300 --> 00:30:51.900
will give its weight on the lungs. So lungs would have a

380
00:30:51.900 --> 00:30:57.100
difficulty in expansion. And secondly, if you lie down supine,

381
00:30:57.100 --> 00:31:02.100
then the abdominal content would gradually push the diaphragm

382
00:31:02.100 --> 00:31:06.800
up. And then again there are less space required for the lung

383
00:31:06.800 --> 00:31:13.400
to expand. So to cover up both the factors proning

384
00:31:13.400 --> 00:31:18.600
is recommended so that the ventilation is easier and

385
00:31:18.600 --> 00:31:22.900
without much troubles. So proning would help in this two situation, but

386
00:31:22.900 --> 00:31:26.300
again as we saw that it is level C or D recommendation.

387
00:31:26.900 --> 00:31:30.600
And you can try, you don't try, that's up to you if

388
00:31:30.600 --> 00:31:35.700
depending upon your comfort zone. So other methods, high flow

389
00:31:35.700 --> 00:31:41.000
ventilation, so nasal cannula, ECMO. ECMO is a

390
00:31:41.000 --> 00:31:44.700
recent and advanced therapy that is being given in the patients of

391
00:31:44.700 --> 00:31:49.800
ARDS. We have seen many ARDS patient during COVID. And we had

392
00:31:49.800 --> 00:31:53.100
put a lot of patients onto ECMO and it has given wonderful

393
00:31:53.100 --> 00:31:58.100
results. So ECMO is nothing but the artificial lung. So lungs would

394
00:31:58.100 --> 00:32:02.600
be at a rest and slowly they would improve, they would heal.

395
00:32:02.800 --> 00:32:06.100
And then once they are properly healed, then we remove the ECMO

396
00:32:06.100 --> 00:32:10.000
and put the patient in a normal ventilation. And there's last thing

397
00:32:10.000 --> 00:32:14.500
is partial fluid ventilation that even I don't think much of use.

398
00:32:15.000 --> 00:32:20.900
So ultimately ECMO is the last resort for us to prevent patients

399
00:32:20.900 --> 00:32:26.100
from dying and give time to for to learn to heal.

400
00:32:27.500 --> 00:32:33.400
So this is routine ECMO system that is bypassing lung and

401
00:32:34.400 --> 00:32:39.800
gives proper oxygenation patients. Uh few

402
00:32:39.900 --> 00:32:45.100
supportive therapies like fluids to be conservative. Uh you can

403
00:32:45.100 --> 00:32:49.600
choose a normal or low fluid therapy. And it will reduce the

404
00:32:49.600 --> 00:32:54.000
ICU stay and duration of ventilation, steroids in the initial days or

405
00:32:54.000 --> 00:32:59.000
initial time. Steroids may be useful before the proper

406
00:32:59.000 --> 00:33:04.000
inflammation is set in. After the proper inflammation is set in, then

407
00:33:04.000 --> 00:33:07.300
there is no much use of steroids. So what you can do

408
00:33:07.300 --> 00:33:10.800
is give his entire prednisolone 2 mg per kg and then taper

409
00:33:11.300 --> 00:33:14.400
1 mg per kg in one to two weeks. But it should

410
00:33:14.400 --> 00:33:19.400
be started in early stages of inflammation. And then

411
00:33:19.400 --> 00:33:21.400
sepsis, antibiotics. Yes, uh empirical antibiotics. And if you have culture, then

412
00:16:44.600 --> 00:16:44.600
culture oriented or targeted antibiotics you can give. Avoid nephrotoxic

413
00:16:49.600 --> 00:16:54.100
drugs

414
00:33:29.900 --> 00:33:35.500
because patient is going to stay long in your ICU. And

415
00:33:35.500 --> 00:33:39.700
a few more for the complications are expected like DVT and bed

416
00:33:39.700 --> 00:33:43.700
sore and web. So please make sure that you don't give any

417
00:33:43.700 --> 00:33:48.200
medicine that would further hamper kidney function and enteral feeding to support

418
00:33:48.200 --> 00:33:52.900
the nutrition. It is again very important. Other modality is that you

419
00:33:52.900 --> 00:33:59.000
can think of that is nitrous oxide, uh ketoconazole, pentacifyline,

420
00:33:59.000 --> 00:34:04.000
NSAIDs and acetylcysteine. These are all treatments that you can give, you

421
00:34:04.000 --> 00:34:08.800
don't give, but there are few very few studies that can give

422
00:34:08.900 --> 00:34:14.000
a concrete opinion on using this. So prognosis in such patients

423
00:34:14.600 --> 00:34:19.100
mortality ranges from 26 to 44%. So it is very high. So

424
00:34:19.100 --> 00:34:23.600
ARDS model prognosis is very high and uh what we feel as

425
00:34:23.600 --> 00:34:28.000
an uh doctor, as a doctor that we don't when we are

426
00:34:28.000 --> 00:34:31.900
very helpless when such situations set in. So we try as much

427
00:34:31.900 --> 00:34:35.900
as possible, but ultimately 44% that is one out of two patients

428
00:34:35.900 --> 00:34:39.500
is dying, then even we feel helpless at this end of the

429
00:34:39.500 --> 00:34:43.700
day that we could not do much. Even though we have given

430
00:34:43.700 --> 00:34:48.500
best of us. But that is very discouraging. So make sure that

431
00:34:48.700 --> 00:34:51.900
ARDS should be prevented and once it is set in, then from

432
00:34:51.900 --> 00:34:54.500
day one you have to be very very aggressive. You don't just

433
00:34:54.500 --> 00:34:58.200
wait to patient go into certain kind of other complications. So risk

434
00:34:58.200 --> 00:35:02.500
factors as I told you that chronic uh advanced age, chronic kidney

435
00:35:02.500 --> 00:35:06.900
disease, chronic liver disease, these are very prone to develop ARDS because

436
00:35:06.900 --> 00:35:12.300
of you know uh multi-organ dysfunction ultimately, chronic alcohol abuse

437
00:35:12.500 --> 00:35:16.700
and chronic immunosuppression. So that would also trigger sepsis, septic shock and

438
00:35:16.700 --> 00:35:21.800
ultimately ARDS. So uh and if ARDS is because of direct lung

439
00:35:21.800 --> 00:35:26.600
injury, then it is having a double mortality rate. So it is

440
00:35:26.600 --> 00:35:31.600
very very important. So ARDS is very common uh manageable,

441
00:35:31.800 --> 00:35:36.100
but again as I told you that it is disappointing. Once patient

442
00:35:36.100 --> 00:35:40.000
you dies in front of you after so many efforts you have

443
00:35:40.000 --> 00:35:43.400
put in. So these are my references that you can go ahead.

444
00:35:44.000 --> 00:35:48.000
So thank you very much for patient listening. Sir uh when should

445
00:35:48.000 --> 00:35:53.900
you consider advanced airway management in acute respiratory distress? So

446
00:35:54.700 --> 00:35:58.100
as I told you that acute respiratory distress you begin with uh

447
00:35:58.100 --> 00:36:02.000
NRBM. So once patient is fully conscious surrounded, but as you feel

448
00:36:02.000 --> 00:36:07.100
that patient is going into certain kind of poor GCS or worsening

449
00:36:07.100 --> 00:36:12.600
in altered sensorium and other parameters like blood pressure is falling, then

450
00:36:12.700 --> 00:36:17.900
uh early intubation would help uh because you know that would prevent

451
00:36:17.900 --> 00:36:21.200
the lungs to go into further damage because if patient is breathing

452
00:36:21.200 --> 00:36:23.700
at the rate of 25 40 and patient is breathing at the

453
00:36:23.700 --> 00:36:28.500
rate of 12 15, then definitely the chances of lung injury much

454
00:36:28.500 --> 00:36:31.400
higher if we are breathing is at 35 to 40 rates. So

455
00:36:31.400 --> 00:36:34.300
we don't want patients to go into further trouble and we need

456
00:36:34.300 --> 00:36:39.200
to give proper rest. So if you consider yourself you're in viral

457
00:36:39.200 --> 00:36:42.900
fever, so you cannot run marathon in viral fever. You need rest

458
00:36:43.200 --> 00:36:46.900
for proper healing. It is same kind of principles you can apply

459
00:36:46.900 --> 00:36:50.400
that if lungs are at risk, lungs are damaged, then they need

460
00:36:50.400 --> 00:36:54.700
rest. And if patient is in altered sensorium, then you cannot put

461
00:36:54.700 --> 00:36:59.000
BiPAP, you cannot put NRBM. Ultimately it is the decision to intubate

462
00:36:59.000 --> 00:37:04.300
the patient put in on mechanical ventilation. All right, sir. Sir moving

463
00:37:04.300 --> 00:37:08.000
on to the next question that is and this is I think

464
00:37:08.000 --> 00:37:13.100
very important because I also hear it many times from different

465
00:37:14.000 --> 00:37:18.000
uh physicians. So how frequently should you reassess a patient with acute

466
00:37:18.000 --> 00:37:23.500
respiratory distress after initial stabilization? So after initial stabilization

467
00:37:23.500 --> 00:37:28.400
ABG uh see patient would be on monitor. So SpO2 pulse blood

468
00:37:28.400 --> 00:37:32.800
pressure should be almost measured every 5 10 minutes. And ABG you

469
00:37:32.800 --> 00:37:36.200
can consider checking every 6 hours so that you know can come

470
00:37:36.200 --> 00:37:39.900
to know what is the PO2 FiO2 ratio. So patient would be

471
00:37:40.000 --> 00:37:43.100
initially you know ALI so PaO2 PF ratio should be less than

472
00:37:43.100 --> 00:37:46.700
300, but at one moment you feel that PF ratio is less

473
00:37:46.700 --> 00:37:50.400
than 200. PF ratio is more less than 100. So if patient

474
00:37:50.400 --> 00:37:52.400
PF ratio is less than 100, then you can say it is

475
00:37:52.400 --> 00:37:56.300
severe respiratory distress syndrome. If PF pressure is between 100 to 200,

476
00:37:56.300 --> 00:37:58.800
then you can say it is moderate. And if it between 300

477
00:37:58.800 --> 00:38:02.400
to 200, then you can say it is mild. So depending upon

478
00:38:02.400 --> 00:38:06.800
the PF ratio you can differentiate between mild, moderate and severe. And

479
00:38:07.000 --> 00:38:09.800
mild, moderate and severe what you have to do is that it

480
00:38:09.900 --> 00:38:13.900
has to be predefined. So once you are studying and reading the

481
00:38:13.900 --> 00:38:17.300
textbook, then you should have your notes or you know uh in

482
00:38:17.300 --> 00:38:21.500
pharmacology we were studying P drugs. Yeah. So it is our personal

483
00:38:21.500 --> 00:38:25.300
drugs that we want to give to certain conditions. So in ARDS

484
00:38:25.300 --> 00:38:30.100
also you have to have your personal protocols for mild ARDS, moderate

485
00:38:30.100 --> 00:38:34.600
ARDS and severe ARDS. So whenever you come across any of the

486
00:38:34.600 --> 00:38:37.900
ARDS, it has to be on your tip of tongue what to

487
00:38:37.900 --> 00:38:42.400
do in this patients. All right, sir. Sir moving on to the

488
00:38:42.400 --> 00:38:46.400
last question for today's session that is sir what are the potential

489
00:38:46.400 --> 00:38:52.000
complications of endotracheal intubation in emergency department settings? So

490
00:38:52.000 --> 00:38:57.100
in emergency uh endotracheal intubation it's an invasive procedure. So an invasive

491
00:38:57.100 --> 00:39:01.700
procedure would have a few complications. So if we define complications then

492
00:39:02.200 --> 00:39:06.000
of the procedure, then you can have bleeding and damage to the

493
00:39:06.000 --> 00:39:10.500
oral cavity and trachea. While putting the endotracheal tube we have seen

494
00:39:10.500 --> 00:39:14.800
or the patients coming from outside the tracheal tear is there. Uh

495
00:39:16.000 --> 00:39:20.300
while intubation we give RSI drugs. So the drugs would have their

496
00:39:20.300 --> 00:39:25.300
own complications. Uh tube dislodgement while shifting the patient from one place

497
00:39:25.300 --> 00:39:30.400
to another. Tube blockage is another complication. During intubation tongue

498
00:39:30.700 --> 00:39:35.400
uh I mean tongue injury or tooth injury or pharyngeal injury that

499
00:39:35.600 --> 00:39:40.700
gives bleeding and ultimately if patient is on the antiplatelets and anticoagulants,

500
00:39:40.700 --> 00:39:44.300
then it will bleed a lot and it will cause another kind

501
00:39:44.300 --> 00:39:48.300
of you know pneumonitis. So these are the complications that you can

502
00:39:48.300 --> 00:39:52.800
uh think of while intubating the patient. So technique first and foremost

503
00:39:52.800 --> 00:39:56.900
is technique is very important. Visualization of trachea and larynx is very

504
00:39:56.900 --> 00:40:02.500
important. And avoid any uh procedure related

505
00:40:02.500 --> 00:40:07.100
injuries. All right, sir. Sir with this I would like to conclude

506
00:40:07.100 --> 00:40:09.800
today's session. Thank you so much for your time. And like I

507
00:40:09.800 --> 00:40:12.600
said the session was very very insightful. I'm sure our viewers will

508
00:40:12.600 --> 00:40:15.700
get to extract a lot of information from here. I'm really looking

509
00:40:15.700 --> 00:40:18.100
forward to hosting you again on our platform. Thank you so much.

510
00:40:18.100 --> 00:40:19.200
Thank you. Thank you.
