19 ABSITE 2024 Critical Care_edited

All right. Welcome back to behind the knife. So we're discussing critical care. I'm here with Patrick. So one thing with critical care that I know it's a little deep dive here, but the things you want to know about formulas. So we're going to talk about certain specific formulas, what their components are and why they're important.

So Patrick, what's the formula for oxygen delivery? Sure. This is cardiac output times the total amount of oxygen. in the blood. And that is a detailed formula. We're gonna go through it right now and then talk about it a little bit. So that's hemoglobin times the oxygen saturation times 1. 34 plus PaO2 times 0.

003. So what's really important to take away from that is if you want to increase the total oxygen, you should really focus on increasing hemoglobin and or oxygen saturation. Whereas dissolved oxygen, the PaO2 has very little effect on this. Right. And this is used a lot in the critical care and specifically within the ICU to explain a lot of processes within the body, which we're not going to

go into specifically for the app site.

But you should be aware, like Patrick mentioned, if you want to improve your oxygen delivery, the easiest way to do that is to change your cardiac output, change your hemoglobin, or change your oxygen saturation. Alright, Patrick, what's the formula for oxygen consumption? Right, so this is cardiac output times the arterial oxygen minus venous oxygen.

Right. How about extraction ratio of oxygen? Yeah, so this is oxygen consumed divided by oxygen delivered. Right. Alright, let's go into some important values that we see in the ICU and prior rounds every day. So central venous pressure. Yeah, this is a surrogate for the end diastolic right ventricular volume.

Okay, pulmonary wedge pressure also surrogate. And this is for the end diastolic left ventricular volume. Okay, we talked about cardiac output. Well, what is it again? Stroke volume times heart rate. All right. And cardiac index. Yeah. So this is cardiac output divided by the body surface area. Okay, so let's move into some of the basis of most of critical care is a different

types of shock.

Okay. So we're going to, I'm going to give you a type of shock and we're going to see how that would affect your systemic vascular resistance your filling pressures and your cardiac output. So for hemorrhagic and hypo or hypovolemic shock, right? Yeah. So in this case, the systemic vascular resistance is up, right?

Your extremities are being squeezed to deliver oxygen to the important organs like your brain and your heart. The filling pressure or the CVP is going to be down. That's due to that low volume and cardiac output will be down as well. Again, heart cardiac output is heart rate time, stroke volume.

Stroke volumes going down with due to that blood loss. Right. And how about in cardiogenic shock? Okay. Again, systemic vascular resistance is up. You're filling pressures or CVP or pulmonary capillary wedge pressure also up, right? The pump is busted here and things are backing up in the system.

And by definition, your cardiac output is going to be low. Okay. septic shock. Yeah. Or distributive shock. Yeah. And in this case, you know, we mentioned for hypovolemic slash hemorrhagic and

cardiogenic, your SVR systemic vascular resistance is up. You're trying to move that blood to the central organs. In septic shock, your SVR is down.

And that's to all due to all the bad humors from an infection causing those vasodilation. And in this case, your filling pressures can be normal, can be low, and your cardiac output usually starts off high and in later stages of septic shock, it's going to fall off when it can no longer your heart can no longer compensate.

Right. And then finally, neurogenic shock. Yeah, neurogenic shock is easy. Systemic vascular resistance, filling pressures, the CVP, pulmonary capillary wedge pressure, and cardiac output are all going to be down. Okay. So there's a great chart in our in the Obsolete Companion. regarding vasoactive drugs.

We're going to talk about these drugs throughout the critical care portion here, but we're not going to go through each of them and the receptors, their actions and all those other things. So, we'll talk about them some more though. Yeah. And similarly, there's a great chart for hemorrhagic shock as well.

And we discussed this in detail in the trauma episodes. So let's go into each type of shock. And these are very

high yield. There's obviously a lot more in critical care that we could talk about for each one of these, but these are the questions that will come up on the app site. So for neurogenic shock.

What vasopressors are typically used with a neurogenic shock and why? Right, and so, in neurogenic shock, you have an injury to the spinal cord, and you lose vascular tone beneath that level of injury, and if your injury is high enough, specifically T1 through T4 sympathetic fibers with input to the heart, you can also have that paradoxical drop in heart rate.

And, in this case, we want to get that squeeze back. Okay, and we start with by getting fluid resuscitating. But also we need pressors typically, and most commonly that's phenylephrine or norepinephrine. Yeah, and then if you have a very high spinal lesion or injury and you lose that inotropic effect, that you would get a neurogenic shock, what other things could you add in?

Yeah, that's where dopamine could be considered. Yeah. Okay, going forward with sepsis and septic shock. So what scoring system do we use to

identify patients with a suspected infection? This is specifically outside the ICU and then also those patients that have the greatest risk for poor outcome. Yeah, and in septic shock, I think it's worth for the ab site and in life in general is to check out the most recent updates from the surviving sepsis guidelines.

They're now a couple of years old at the time of this recording. But things kind of have changed and the scoring systems have changed. So the new scoring system you really have to be aware of is QSOFA or the quick sequential organ failure assessment. And this includes There's three components. First is altered mental status.

So GCS is less than 15. The second is high respiratory rate, which is greater than 22 times per minute. And the third is low systolic blood pressure defined as less than 100 millimeters of mercury. Now, as you mentioned, this is a screening tool used to identify sick patients in the hospital. And that is certainly can pick up patients who have septic shock, but it's not necessarily just a patient's septic shock.

Right, exactly.

Yeah, so the QSOFA score is based off the sequential organ failure assessment or the SOFA score. This is another scoring system that will use the assessed performance of several organs within the body. The higher the score, the higher the likely mortality. It is best to use the SOFA score when comparing patients on how to best allocate resources.

which became a thing during COVID, right? It allows for objective quick triage. It's not really typically used as a screening tool, and it should not be used as so. Right, and you're not going to need to know the components of the SOFA score for the test because there's tons of them. I mean, it's a big score, and it requires a lot of data.

And so, again, you want to know the QSOFA, altered mental status, high respiratory rate, low systolic blood pressure. All right. What is this definition of sepsis and septic shock? Sure. So the definition of sepsis is a life threatening organ dysfunction due to dysregulated response to infection. Mortality rate for all comers is around 10 percent now that's a pretty broad definition.

Sepsis

shock. The definition for that's a little more clinically useful. The definition here is vasopressor requirement.

And for this subset of patients, mortality is much higher, which is around 40%. Yeah. And the things you want to look at in your questions for the app site is the early symptoms concerning for septic shock and those that can be listed out. So we have unexplained hypotension. temperature dysregulation, fever and or hypothermia, sun and explained dyspnea, confusion, decreased urine output, excessive bleeding, metabolic acidosis, or jaundice.

That's basically everything you can go wrong with your body. But those are the things that you can look out for septic shock. All right, so we in critical care and for the app site, they do sometimes ask about diagnostic adjuncts. So Patrick, what is procalcitonin and how do we use it? Sure. There's a whole bunch to unpack here that we're not going to get into, but procalcitonin for the purpose of the ab site is best used as a guide for when to stop antibiotics.

So when that procalcitonin level comes down and becomes more normal

that can be a time in which you stop antibiotics. It's best studied in folks with pneumonia. Okay. What can we use specifically for fungal infections? Sure. This is the one at three beta D glucan or BDG assay. Okay. All right. So moving into sepsis management.

Now there's, you know, multiple textbooks and papers written about how we should manage sepsis, but we dialed this down for the abseil. So Patrick, walk me through the key points of managing a patient that walks into a sepsis. Right. And so the big three things you want to think of initially are getting that patient antibiotics as soon as possible.

Within one hour, you're gonna start broad spectrum antibiotics. You want to get some culture sent off ideally before antibiotics are started, but you don't want to delay those antibiotics if that's the case. And you're going to fluid resuscitate and you're going to specifically bolus with 30 cc's per kilogram of crystalloid.

If that lactate is above four. This is highly controversial, but again, that 30 CC per kilogram bullets is what you're going to know for the test. And we also want to consider,

especially if these folks are, or patients are not responsive to fluid or suscitation starting pressers and in the latest SCCM guidelines, considering starting pressers early.

Our number one presser of choice is norepinephrine. Yeah. And you might see that come up on the app site now especially with that change from. you know, late presser initiation and the intent to reduce that fluid therapy in the beginning. So you want to start pressers earlier now. So there are some adjunct therapies.

Let's say we're failing and we are kind of a concern about adrenal insufficiency septic shock. What things can we consider doing? Sure. This is steroids here, hydrocortisone, 200 milligrams per day. You can either give that out as a drip or 50 milligrams every six hours. We should also note that that's, Part of the indication is also once you add that second vasopressor on which in this case The second vasopressor you should add after norepinephrine is vasopressin if the patient's still not responsive.

You want to consider starting steroids, right? And if you're if they're absolutely bringing you a question on adrenal

insufficiency What would be the associated labs you want to look for in the question step? Yeah, this is a good one low sodium high potassium And hypoglycemia are the main three that you'll notice and should kind of, point you in that direction when it comes to adrenal insufficiency.

Okay. And in finishing out sepsis management, what about glucose control? Also highly controversial, but I think most institutions have the, they use this type of approach to this now. Yeah. Glucose of less than one 80. Oh yeah. So tight glucose control has been associated with worth worse outcomes in general.

Okay. Moving on to cardiogenic shock. What vasopressors are likely to be beneficial in cardiogenic shock. Yeah. Again, review that vasopressor and inotrope table for all the details, but we can use epinephrine, dobutamine, and or milrinone as these all have a direct effect on cardiac contractility.

Okay. Moving on to respiratory failure. John, what are type one and type two respiratory failure? Yeah, so type one is hypoxemic respiratory failure

where you have a PA two of less than 60. Yeah. And type two. Type two is hypercapnic plus or minus hypoxemia. So that's where you have a PACO2 of greater than 50.

Sure. So what are, well, I guess I should say there's a number of different potential causes for hypoxia in a hospitalized patient. Let's go through a few of these. So you often hear this term VQ mismatch. What are some of the clinical syndromes that lead to VQ mismatch? Yeah. If you see VQ mismatch pop up, they might give you a scenario with that.

You wouldn't be thinking pleural fusion, PE. Pneumonia or phrenic nerve paralysis. And the highest of that list is definitely PE for VQ mismatch. So how about alveolar capillary membrane abnormalities? Yeah, that's a mouthful, but you want to think of emphysema, interstitial lung disease, pulmonary contusion, pulmonary edema, or early ARDS.

Yeah. So alveolar capillary membrane abnormalities, the highest that are going to top that list are ARDS and or pulmonary edema. How about small airway obstruction?

Here you want to be thinking about pulmonary edema, asthma, and COPD. Yup, COPD and asthma at the top of that list, versus large airway obstruction.

That's where you have to worry about a mass, such as thyroid or thymus, tracheal malacia, hematoma, or angioedema. Right, so angioedema or something pushing on the airway. Patients who have altered compliance can also have hypoxia. What are some things that lead altered pulmonary compliance? Yeah, here you would have restrictive lung disease, rib fractures, pulmonary contusions, pneumothorax or morbid obesity.

Anything that doesn't allow your lungs to expand. That's right. And a few other testable topics include oxygen transport abnormalities. And or poisoning of the cellular oxidization enzyme. So what are the oxygen transport abnormalities, John? Yeah. So you have carboxyhemoglobinemia and methemoglobinemia.

Yeah. And then the oxidation enzymes getting all screwy. Yeah. Cyanide toxicity. Right. What do you think about? Sure. These are high yield topics. Let's start with carboxyhemoglobinemia. So this is exposure to carbon monoxide

from a fire with an enclosed space. Remember that carbon monoxide has 240 times the affinity for hemoglobin compared to oxygen.

So patients will present with headaches, they'll be nauseous, dizzy, and more extreme cases they could have seizures or present in a coma. And so you can diagnose this by looking at a blood gas and checking the carboxyhemoglobin levels. Normal is around 3%. Normal for smokers though is around 10%. And interestingly, pulse oximetry cannot differentiate between carbon monoxide and oxygen.

And so your SpO2 is actually going to be normal. And treatment in this case is oxygen and to slowly displace that carbon monoxide. Next is methemoglobinemia. This is when your iron atom goes from two plus to a three plus state or is oxidized. And this can either be congenital or acquired. And for an acquired methemoglobinemia, you'd have to be exposed to topical anesthetic agents, dapsone or nitric oxide.

So if you have a question

stem. where a patient presents with cyanosis or hypoxia, the most common agent they will have been exposed to are topical anesthetic agents. And you can diagnose methemoglobinemia on a blood gas. The patient's PAO2 is actually going to be normal. And the other thing that's going to give it away in your question stem is that for methemoglobinemia, your pulse oximeter is going to read 85%.

regardless of the patient's oxygen saturation and treatment. Here's methylene blue and last is cyanide. And so cyanide secondary to fires or exposure to fires, especially industrial type situations. And so the question stem would likely be an industrial fire. And this cyanide interrupts oxidative phosphorylation and this results in anaerobic metabolism and a rise in lactic acid levels.

And so that high lactic acid is key to the diagnosis. Patients will present with headaches. dizziness. They have arrhythmias. They can also have liver and renal failure. And interestingly, this, this almond odor to them. So that's another key. Something may be

presenting the question stem. And for diagnosis, you want to see that lactic acid level up and you can check a cyanide level.

This is time dependent, depending on when the patient was exposed. And so we're going to treat based on clinical suspicion. So right up front and we're going to give the patient either a cyano kit or other forms of hydroxy cobalamin. All right, let's move on to ventilator settings and management. We should say that this is a very low level review.

That's absolutely appropriate. And so, John, how does the ventilator cause lung injury? Yeah. So ventilator induced lung injury is caused by increased volumes increased pressure leading to barotrauma. and eventually oxygen toxicity. Yeah, so volutrauma, barotrauma, oxygen toxicities. Alright, let's talk oxygenation and ventilation.

So, what are some of the things we can do to affect oxygenation? Yeah, so things on the ventilator we can change. You can change your FIO2, your PEEP and your mean airway pressure. Okay, how about ventilation? The two

you're looking for here are respiratory rate and tidal volume. Right, and if you multiply respiratory rate by tidal volume, that is your minute ventilation.

So we have a bunch of different pressures, right, that we follow on the ventilator. Let's go through a few of those, John. What's peak pressure? So that reflects the pressure in the large airways. Okay. Compare that to plateau pressure. Plateau pressure reflects the alveolar pressure. And the only way to get a plateau pressure is to do an inspiratory pause to allow the pressures to equivalate.

Right. And so what if there's a big difference between the peak? Let's say our peak is really high and our plateau is pretty decent. Yeah, so then we have to be thinking of a large airway obstruction or a bronchospasm. Right, so something in the actual airway that could even be a clog or gunk right? What if the peak pressure and the plateau pressure are both high?

Here we'd be thinking of alveolar lung disease, which you'll see most commonly with ARDS. Okay, John, if plateau pressure is measured with an inspiratory pause, then what is measured with an expiratory pause? Yeah, that would give you your total peak.

All right. So moving on. So ventilation modes can vary by institution and different types of ventilator.

All right, John. So this is a real challenge to break down and to talk about on a podcast. We're going to keep it very, very simple. We're going to focus on three different modes. The first would be volume control. Second is pressure control. And third are spontaneous pressure supported breaths. So let's start with volume control.

For volume control setting, you are determining the tidal volumes, that's really important, the respiratory rate, the PEEP, and the oxygen level. Now the dynamic variable, or how the lungs respond, are going to be the peak airway pressure and the plateau airway pressure, so pressures. So the risk with the volume control is that you set the tidal volume too high, and you lead to trauma to the lungs because the pressure is too high.

Let's compare that to pressure controlled settings. In this circumstance, you are setting the inspiratory pressure level, the PEEP, the respiratory rate, and the

FiO2. Now in this case, the dynamic variable is tidal volume. So the risk here is that you are giving too little pressure and that your minute ventilation and tidal volumes are too low.

Now let's move on to pressure support ventilation. Here you're going to set the inspiratory pressure. The end expiratory pressure, or PEEP, and the FIO2. And just like we had our pressure control setting, tidal volumes are going to be variable. And it's important to note that for pressure support settings, all breaths are spontaneous, meaning they're initiated by the patient.

As mentioned here, I didn't say anything about setting the respiratory rate. All right, moving on. What are our extubation criteria? What are we thinking about when we're talking about extubation every day? Yeah. So we want to get that tube out as quickly as possible. There's a lot of problems that come along with folks being ventilated or on the ventilator, and that includes ventilator associated pneumonia.

Oftentimes, sedation is required because it's super uncomfortable to have a breathing tube

across your vocal cords. So we want to get that tube out as soon as possible. So the patient's overall condition should have improved, whether that's a primary pulmonary condition. or maybe neurologic or maybe abdominal sepsis.

These conditions should be improving before we think about extubating the patient. And every day in the ICU, we want to perform a spontaneous awakening trial where sedation is held and a spontaneous breathing trial where we kind of test the patient out and see if they're ready to get that breathing tube out.

In general, when we put the patient on a spontaneous breathing trial, this is a spontaneous or pressure support mode of ventilation. The peak is less than eight. The FIO2 is less than 50 percent and we're going to watch and see what the patient does and how they respond. Typically, a spontaneous reading trial lasts for about 30 minutes to 2 hours.

And again, we're watching and looking for failure. So failure would be tachypnea, oftentimes defined as a respiratory rate greater than 35, hypoxia or

SpO2 less than 90%, and respiratory acidosis or pH is less than 73. We're also going to eyeball the patient. If they have an increased heart rate, increased work of breathing, if they're diaphoretic, if their tidal volumes are falling, these are all signs of failure.

There's also quantitative indices that we can use to assess patients and their readiness for extubation. The most testable one is the Rapid Shallow Breathing Index, or RSBI. This is the respiratory rate divided by the tidal volume in liters. Okay. Respiratory rate divided by the tidal volume in liters, and it should be less than 105.

We also, if the patient is able to, want to test negative inspiratory force or NIF. We like to see this at least negative 30 centimeters of water or more. You can also ask the patient to take a big old breath and say, hey, you know, breathe in deeply, and you can check and see what their force vital capacity is.

We want to see those breaths ideally at least five or 600 cc's or more. And you want

to assess the patient for a cuff leak. You should either be able to hear audible air leak or calculate it on the ventilator. All right, with that, let's move on to our next highly testable topic. Acute respiratory distress syndrome or ARDS.

This is defined by the Berlin criteria. John, what is that? All right. The Berlin criteria are defined by the four following criteria. So respiratory symptoms that developed within one week of insult. You have characteristic bilateral capacities on imaging. You have symptoms and radiology findings that cannot be explained by other pathologies such as cardiac failure and you have a PDF ratio less than 300.

The PDF ratio can be divided by severity. So mild is a PDF ratio, which is your PaO2 divided by your FiO2 between 2 and 300. Moderate is a PDF ratio between 1 and 200. And severe is a PDF ratio less than 100. All right, Patrick, let's talk about management of ARDS. So what are some of the ventilator strategies we can do to deal with ICU?

Yeah, this is a really important and again, highly

testable because there's only one thing you can do on the ventilator to improve mortality in patients who have ARDS. And that is use lung protective settings. And so these are relatively low tidal volumes of six cc's per kilogram of ideal body weight.

So again, that's the ARDS net criteria, super high yield, super testable. What other things must we think about in management of ARDS? Sure. So there's actually good data to support proning. And with everything that happened in COVID, that was sussed out even farther. So proning can definitely help folks who are failing our standard strategies.

Neuromuscular blockade is used very frequently. It may or may not be helpful. And in folks who are quite ill and hypoxic, you can consider pulmonary vasodilators, like inhaled nitric oxide or prostaglandins or prostacyclins. And this will increase the oxygen level, but it's not been shown to improve mortality.

All right, John, let's talk pulmonary embolism. So what's the most common vital signs change when a patient has a PE?

So tachycardia or tachypnea and dyspnea are the most common. You also may see respiratory alkalosis due to that tachypnea. Sure. And you can also see hypoxia as well, right? So hypoxic patient with respiratory alkalosis, think PE.

Okay, John, what is the most common EKG finding with PE? So the most common EKG finding is sinus tachycardia. It's not the classic S1Q3T3 which is relatively uncommon. Sure. And how do you diagnose PE? So the gold standard is CT pulmonary arteriogram. Sure. So what's the role of D dimer when it comes to diagnosing PE?

So D dimer is very sensitive. It's good for ruling out PE. But it has a very high false positive rate, right? And especially in the surgical patient population, whether you've just done surgery or they had a traumatic injury or their septic, that D dimer is likely to be high in most of our patients. All right, John, you've diagnosed PE.

How are we going to treat it? So typically in a hospital we do a heparin bolus followed by a drip, or you can also use

Lovenox. The goal PTT for a heparin drip is between 60 and 90. We also use factor 10A. levels as well when we're when we're dosing Levinox, right? So a hospital specific for that, but you're, you're on the higher end of the spectrum compared to treating acute coronary syndrome.

When you're thinking about anti coagulating what, what are the indications for systemic thrombolytics? Cause that's another treatment. Yeah. So hemodynamic instability is obviously the number one. And then right heart strain found on echocardiogram, right? And if needed to some institutions are performing embolectomy, you know, direct embolectomy and suction thrombectomy.

If this PE is severe enough. Yeah. In addition, catheter directed thrombolysis kind of falls in that same spectrum using IR, IR guidance. All right, let's move on to liver failure. John, what are the findings that are present in patients with acute liver failure? Yeah. So you need to have an INR greater than or equal to 1.

5. You know, evidence of acute liver injury through hyperbilirium anemia or transaminitis,

encephalopathy, the symptom onset must be less than 26 weeks from the diagnosis and no prior history of cirrhosis or other liver disease. Right. So in your stem, you're going to notice that less than 26 weeks of onset, so something relatively recent.

What are some of the potential causes for acute liver failure? Yeah, there's a lot of them. Most commonly, most common causes are acetaminophen or other drug induced liver injury, viral hepatitis. Wilson disease autoimmune hepatitis ischemia or help syndrome in pregnancy as well as toxins toxins like alcohol, right?

Yeah, and then I think the number one cause right is Tylenol induced. Mm hmm How about hepatovenal syndrome? This is something that's complicated. How can you how do you explain that? Yeah, it's very simplistic for the app site So you have portal hypertension? That leads to splenic vasodilation Decreased effective arterial blood volume and decreased renal perfusion activates the renin angiotensin system and sympathetic nervous system activation that decreases your

GFR.

All right, portal hypertension leading to splenctin vasodilation leading to a decreased effective arterial volume that activates the renin angiotensin system and then leads to decreased GFR. How do you diagnose it or can you? So it's a diagnosis of exclusion. The findings you'd see in hepatorenal syndrome are oliguria, increased serum creatinine.

You'd typically get urine labs. You'd have a urine sodium less than 10, urine RBCs less than 50, and urine protein less than 500 milligrams a day. And then another way of kind of testing it and looking for hepatorenal syndrome is doing, you'd have no improvement in kidney function. with the administration of crystal or colloid and while holding diuretics.

Okay, so a diagnosis of exclusion. So how are you going to manage it? The mainstay is octreotide that leads to splenctin vasoconstriction. Mitadrine, which leads to system vasoconstriction. It's an alpha adrenergic agonist. And then obviously a lot of these progress to dialysis. So greater than six weeks of dialysis should also trigger your liver

kidney transplant evaluation.

Okay. All right. Let's talk about endocrine dysfunction So how should steroids be managed periodically? So specifically let's say I have a patient who's been on less than three weeks of steroids and or less than five milligrams a day of prednisone. Yeah. So high yield stuff here. So no additional glutocorticoids perioperative are needed, right?

So then if we go long term steroids, so greater than three weeks or at higher doses, more than five milligrams per day of prednisone, those patients can be at risk for adrenal insufficiency. And so we think about stress dose steroids. John, what are stress dose steroids? How would you? Yeah, we, it changes based on the, if it's a major or minor procedure, right?

So for minor surgeries, IV hydrocortisone, 25 to 50 milligrams on a day of surgery. And then you, you just resume the normal dose afterwards for major surgeries you do IV hydrocortisone 50 to 75 milligrams Q eight for 24 to four, eight hours, and then you can resume the normal dose. Yeah, and a lot of times this ends up being more of a

gestalt thing.

So you have a patient in your ICU who's struggling. Who is not responding to things like vasopressors and they have a history of steroid use. You may empirically treat them with stress dose steroids and see if you get an improvement. Okay, to round off our endocrine section, a lot of folks are on SGLT2 inhibitors for either diabetes management or weight loss.

How should those be managed preoperatively? Yeah, so the SGLT2 inhibitors should be discontinued three to four days preoperatively. Other oral anti hypoglycemic medications should not be taken the morning of surgery. Right, but can be taken up to the the day before surgery. Right. Alright, let's move on to nutrition.

Let's talk metabolics. So what is the respiratory quotient? So the respiratory quotient is your CO2 production divided by your oxygen consumption. And so what is the respiratory quotient useful for? How do you use that result? Yeah, it's, it's useful to identify carbohydrate overfeeding in intubated patients.

which then results in a higher CO2

production and difficulty weaning from the ventriloquy. This is something you actually see clinically. Okay. Alright, we have to mention nitrogen balance, even though this is not something that either of us use in practice or have seen. It may be testable, so how do you measure nitrogen balance?

Yeah, this requires a 24 hour collection and measurement of urine nitrogen. Okay, so if a patient has a negative nitrogen balance, It's a catabolic state and a positive nitrate balance. That's an anabolic state. Great. Let's talk calories, John. So how many calories are in the carb? 4k cals a gram and lipids 9k cals a gram and protein is 4k cals a gram.

Great. So in general, about 75 percent of non protein calories should be carbs. The other 25 percent should be fat and the total protein per day. It should be one to two grams per kilogram per day. That's highly testable. So one to two grams per kilogram per day. Okay. And when feeding, we always want to use the gut first, if at all possible.

If we need to use TPN, that is obviously doable as well. Let's move on to

nutritional deficiencies. John how do I treat beriberi? So that's a thiamine deficiency, so we give thiamine. Okay. Macrocytic anemia. It's a folate deficiency. Ricketts. Vitamin D deficiency. Arr, scurvy. Vitamin C deficiency.

Coagulopathy. Vitamin K deficiency. Alright, I got a rash. I have alopecia and vision changes. What do I need? Zinc deficiency. Alright, and then a combination of microcytic anemia, pancytopenia, and osteopenia. Yep, that'd be copper. Some folks talk a lot about immunonutrition, things like omega 3 fatty acids, glutamine, arginine, etc.

What's the possible or purported benefit for these supplements? Yeah, you see these in the ICU, depends by institution. But they're associated with lower infectious complications, but they're still being studied. All right, let's talk about abdominal compartment syndrome. Patrick, what is intra abdominal hypertension?

Okay. Intra abdominal hypertension is an intra abdominal pressure that's greater than 12 millimeters of mercury. The normal intra abdominal pressure should be less than five.

Okay. How is this different than abdominal compartment syndrome? Sure. So abdominal compartment syndrome is 20. We measure this usually using a Foley catheter, but greater than 20.

Plus organ failure. Right. And so, we ought to consider this when the patient presents with a distended abdomen. If it's tense, if there's oliguria, if a systemic vascular resistance goes up, but really most importantly, if airway pressures goes up. So, you know, the right clinical context, a tense abdomen, urine output drops, peak pressures on the venter high.

Right. And this is not a patient is going to walk in with a street of double carcinogens. This is a typically patients in the ICU. who have undergone some other sort of injury or abdominal operation or sepsis from other news or other reason. Okay, let's move on to brain death. So Patrick, we have a patient who is in our irreversible coma with a known cause demonstrated on imaging.

What should be included in our clinical examination to determine brain death? Right. And so this is a clinical diagnosis. So the patients have to be normothermic. They have to have no

residual drug effects. So things like paralytics and phenobarbital, other things that can depress the nervous system have to be cleared.

They should have a relatively normal acid base electrolyte and endocrine balance. They should have no spontaneous respirations. And we're going to come back to this when we talk about the formal apnea study. And last, the patients have to have a systolic blood pressure greater than 100 or a MAP greater than 60.

And to reach this goal, vasopressors are allowed. So we, we talk about brainstem reflexes. Can you walk me through these? All right, here we go. This is going to be a bit of a mouthful, but the following reflexes have to be absent. So pupillary reflex, oculocephalic or doll's eyes reflex, the oculovestibular reflex, which is tested with cold calorics and that should result in nystagmus in a patient who has a brainstem function.

Corneal reflexes will be gone. That's you simply touch the cornea and look for a blink. Absence of facial or extremity motor response to painful stimuli. And absent gag and

cough reflexes. So these patients are intubated and you can initiate the gag reflex by pulling on the endotracheal tube and the cough reflex by passing a suction catheter to the carina.

All right, Patrick, you completed the clinical brain death exam. What do you do next? Sure. So all patients need to have formal apnea testing. This is a core component of brain death testing because it assesses brainstem function. Now the goal of apnea testing is to trigger the respiratory centers in the medulla by allowing the serum carbon dioxide levels to rise sufficiently.

And the absence of respiratory effort with a pH of less than 7.3 and a PA CO two of greater than 60 millimeters of mercury is consistent with brain death. So again, if the patient doesn't breathe and you've reached a PA CO two of greater than 60, that is consistent with brain death. Okay. Alright, let's move on to our quick hits.

John, hypotension associated with bradycardia and warm extremities. Okay, so this is neurogenic shock, and you have loss

of supraspinal control of the sympathetic nervous system. Okay, for septic shock, what's the first line vasopressor, and the second line vasopressor? So norepinephrine, and then you want to use vasopressin.

Okay. What about a patient who has hemoptysis after they undergo Swann Gans balloon inflation? So this is the classic ruptured pulmonary artery. And how do you treat it? Now we treat it with angioembolization. Okay. A patient has a tachyarrhythmia, EKG shows torsades. How do you treat it? So IV mag. What are the indications for renal replacement therapy?

So this is inability to correct your AEIOU, so your acidosis, electrolyte abnormalities, the intoxicants, fluid overload, and uremia. Okay. When talking about RSI we may give a specific drug that can depress adrenal function. We actually like to use in the trauma setting because it does not cause a lot of hypotension.

What drug is that? So you want to avoid it. Tom and a inpatients who have a risk for

adrenal insufficiency because it inhibits steroid synthesis. Okay. And what patients should suck some coal and not be used in? Yeah. Have you heard this one pop up a few times before? Because it does show up on the outside.

So burn patients and patients with crush injuries, patients with hyperkalemia, those with significant spinal cord trauma. What is the definition when it comes to the PDF ratio of severe ARDS? So that's a PDF ratio less than 100. Moderate is PDF ratio of 1 to 200. And mild is anything between 2 and 300.

What is Virchow's triad? So that's venous stasis, hypercoagulable state, and endothelial injury. What's the most common post operative complication in patients who are over 65 years old? Now, if you ever worked in a hospital, this is delirium. Sure. Let's say you've given a patient frequent IV Haldol doses.

What do you need to keep an eye out for? So you have to worry about prolonged QT, and you can diagnose this with an EKG. Okay. I got a patient who has a

positive urinalysis, their MAP is 60, their lactate is 4. 5. They meet criteria for what? So this patient's in septic shock. I have a 5 year old patient who comes in after trauma and they become bradycardic during an attempted intubation.

How can I treat that in addition to ensuring they're well oxygenated? Yeah, so this is a high risk population for bradycardia. We would treat it with atropine. So a post op CABG patient has hypertension and their CVP is elevated and wedge pressure is 20. So we worry about cardiac tamponade. What are indications for thrombolysis in a patient with pulmonary embolism?

So you have an unstable patient with evidence of right heart strain. Patient undergoes large volume paracentesis for ascites. They are a cirrhotic patient by the way. And then they have oliguria and their creatinine rises. You check the urine sodium and it's low, it's less than 10. What's the diagnosis?

So I'd be concerned about hepatorenal syndrome. We treat this with albumin and vasopressin and we'd consider a transplant if dialysis extended greater than

six weeks. Okay, what are the electrolyte abnormalities found following, or in the setting of refeeding syndrome? So everything's decreased. So decreased potassium, decreased magnesium, and decreased phosphorus.

All right, what's the gold standard for diagnosing PE? CT angiogram, specifically a CT pulmonary angiogram. Okay, who should be discussing organ donation with a patient's family? So the organ donation representative, not the physician.