EPA Playbook: Perioperative Care of Critically Ill Patient

Welcome back to the EPA Playbook, a series of episodes where we dig into the key and trustful professional activities through case scenarios. I'm Dr. Kniery and with me today are two of my behind the knife surgical education fellows, Agnes Prim Kumar from Creighton, and Emma Burke from Baylor. Today's episode is focused all about critical care Agnes: and to recap EPAs matter because they translate the abstract language of competencies into the real work that you do every day. As a surgical resident, each EPA such as managing a critically ill patient defines a professional activity that you must eventually be trusted to perform independently. EPAs can also make feedback more meaningful by increasing the objectivity and by providing more data points across time, specialty case type, and case complexity. When you demonstrate consistent entrustment on these EPAs, it can accelerate your progression towards independent operating and decision making, and that's why we've created this series. It's a perfect way for junior residents to dominate EPAs. Kevin: Okay, so today we'll be diving into all things shock related.

So before we go any further, Emma, can you tell us a little bit about each type of shock? Emma: Absolutely. There's four main types of shock, each with their own unique presentation. These are high yield for the Abset exams, and truly understanding these will help you manage a critically ill patient. The first type of shock is hypovolemic shock, which is usually due to hemorrhage, dehydration, burns, et cetera. This is typically our patient that doesn't have enough blood returning to their heart, and they're tachycardic, hypotensive, and they have cool pale skin and flat neck veins. The main management is closely monitoring and managing their resuscitation, whether it's crystally for your non hemorrhagic cases or with blood products for hemorrhagic shock. Next up, we have distributive shock. Think of your severely septic or anaphylactic patient. This category also includes the patients who are in adrenal crises. The key pathophysiology is vasodilation and capillary leaking, leading to third spacing. Here. These patients are warm with flush

skin, but they're still hypotensive. They do have a widen pulse pressure here. Once again, we wanna pay close attention to resuscitation antibiotics for those septic patients, and source control epinephrine if it's due to anaphylaxis or steroids and adrenal crisis. And then we can add on our vasopressors as needed. Neurogenic shock is often grouped with distributive shock. This is where we have spinal cord injury leading to loss of sympathetic tone. Patients are hypotensive, but importantly, they're Brady cardiac and they still have that warm flush skin. The important aspect here is management to ensure that the mean arterial pressure goals are met for adequate spinal perfusion. Kevin: Okay. Uh, did you talk about spinal shock? What is spinal shock, and is that the same thing as a neurogenic shock? Agnes: Great question. I always get these two things mixed up, but spinal shock is not actually a hemodynamic shock. It's a temporary loss of all neurologic activity below a certain level of injury. So you'll have a

reflexive depression phenomenon where the reflex pathways are stunned and there's a depression in the spinal cord function. Their vital signs are normal. Their skin is not usually flushed or warm like neurogenic shock is. But you do see that areflexia loss of sensation and the loss of bowel or bladder function. So spinal shock, as we said, is temporary. So once it's resolved, you see those reflexes coming back, such as the bobo cavernous reflux, and that management is usually centered around supportive treatment just to get until they resolve it on their own. Kevin: Okay, so make sure you know this important distinction. Alright, Emma, finish us off of the last two types of shock. Emma: Yeah, so the next group up is cardiogenic shock, where the heart is not pumping effectively. Most commonly, this occurs after a myocardial infarction or after arrhythmias, or even with severe CH. These patients will have cool clammy skin with an elevated JVD and pulmonary edema. Here, the treatment revolves around treating the underlying

cause, such as a PCI for an mi. It's also important to support these patients with inotropes, such as epinephrine and dobutamine and vasopressors as needed, and diuresis as well for any volume overload. And then lastly, we have obstructive shock, which is due to things like a massive pe, attention pneumothorax, cardiac tamponade, et cetera. This presentation might vary slightly depending on the underlying cause, but they often have dyspnea, hypotension, and JVD. If there's a massive pe. On the other hand, for attention, pneumothorax will have hypotension with absent breath sounds. And then in co cardiac tamponade, we have to think about that. Beck triad hypotension with JVD and muffled heart sounds. Here you wanna treat the cause appropriately. So for a PE that's gonna be thrombolytics or thrombectomy decompression with a chest tube for a pneumothorax and a pericardiocentesis, or a surgical window for cardiac tamponade. Kevin: Okay. That was a great overview. Uh, let's walk

through a scenario now. So we have a 60-year-old male who underwent a sigmoid colectomy five days ago for diverticulitis. He was doing well until this morning when his vital signs suddenly deteriorated. He's now hypotensive with a map of 55. He's febrile to 102.5. He's tachycardic to one 20 and requiring increased oxygen supplementation. His abdomen is mildly descended and his initial lactate is five. Agnes, what do you think this is? Agnes: So this presentation with that recent surgery five days ago, it sounds like an anastomotic leak to me. It seems like the leak is pretty bad that it's leading to an intraabdominal sepsis picture and septic shock. So I wanna start by managing him like a septic patient. According to the surviving sepsis guidelines, we wanna measure the lactic acid, which we've done. We know it's five. We wanna start off by drawing some blood cultures and then initiating antibiotics. These antibiotics should be broad spectrum. And then lastly, you wanna initiate fluid resuscitation at 30 ccs per kg of Crystal Lloyd fluid immediately within that first

hour. All these things together should help him with his hypotension and his lactic acidosis. Kevin: That aggressive initial fluid recitation is key to addressing the hypovolemia inherent in this type of shock. Emma if he remains hypotensive despite this initial fluid challenge, what is the next step in hemodynamic management? Emma: So for septic shock, which again is a type of distributive shock due to loss of vasomotor tone and decreased systemic vascular resistance. If the hypotension is persisting after those fluids, we should start vasopressor support with a goal of maintaining a map of over 65. The main vasopressor that we use in septic shock is norepinephrine because it has a mix of both alpha and beta functions. After we start norepinephrine, we need to monitor our endpoints of resuscitation, such as mental status, urine output, and lactic acid clearance to make sure that our patient's responding appropriately. Agnes: And when that norepinephrine gets to higher than 10, that's usually a sign that the patient is vasoplegic and is not responding the best as they can to your

pressors. So you can add vasopressin in this case. The thought process is that vasopressin can cause arterial smooth muscle contraction through a non catecholamine receptor pathway. So since the catecholamines are not working as well, this is a useful adjunct. But usually Levo is that first line pressor and vasopressin is added when Levo reaches high doses. If that patient is vasoplegic and not responding to vasopressors, you can also supplement with steroids during that acute shock management phase. And while all this resuscitation is ongoing, you need to shift your focus is surgery. We think that that suspected source is an intraabdominal sepsis picture, so we need to get source control and we need to decide when is the best time that we can take him to surgery. Kevin: Yeah, exactly. That timing is critical. Can we stabilize him enough for transfer while recognizing that delaying source control allows the multi-system organ failure to progress. Alright. We also see that he's becoming more abumed. What are you worried about, Emma, and what would you do? Emma:

Yeah, so that altered mental status is super important to pick up on a patient who's obtunded and cannot protect their airway should be intubated. And there's a couple different mnemonics to think about for the different needs for intubation. And one example that I like is the SOAP mnemonic. S stands for secretions that are excessive and cannot be cleared OS for inadequate oxygenation. A is for airway compromise or obstruction. These patients will sometimes have ominous, high pitched upper airway sounds or strider, and then that P is for pulmonary function, not meeting ventilatory needs. Since our patient is obtunded and in shock, he's at very high risk for aspiration and we'll need to intubate him immediately. Kevin: Good call. Remember to always approach each patient systematically and treat the life-threatening issues first. What drugs are you going to use for rapid sequence intubation? Agnes: Yeah, so usually intubating in the ICU means that the patient is unstable, so we wanna tailor our medications to the hemodynamics and the mental status of our patient. So usually we wanna give

an induction agent, then followed by a paralytic. Your choices for induction agents are ate, ketamine, propofol, or midazolam. ATE is hemodynamically stable. It's fast onset, but it usually comes with the cons of possible adrenal suppression. Ketamine, on the other hand also is hemodynamically stable and it maintains that blood pressure and it can bronchodilate your airways, so it's good for patients who have asthma or COPD exacerbations, and it can also provide analgesia as well. The cons for ketamine are that it's. Potential for hypertension and tachycardia. And some patients describe an emergence phenomenon. You have your classic propofol, which is fast, but it usually causes hypotension. So usually in your unstable patient, that's not a good first choice. And then our lastly, we have midazolam, which is slow, and it has a high risk of prolonged sedation, so it's usually a second line medication. Then if we shift gears to think about our paralytics. The big camp is either Syl choline, which is depolarizing

neuromuscular agent, and it's usually used because it's fast and short acting, and it's ideal for a rapid sequence intubation. But remember, this is one of those questions that we get all the time. Succinylcholine should be avoided in hyperkalemia burns, and if the patient has neuromuscular. You also have rocuronium or vecuronium, which are non depolarizing neuromuscular agents. They're safe and hyperkalemia, burns neuromuscular disease, but they're longer in action so they can lead to a prolonged paralysis. Kevin: Great. Yeah. Always remember induction before paralytic. You do not want to be awake and paralyzed. Okay. Let's talk tubes because picking the wrong size can make bronching suctioning or ventilating way harder than it needs to be. Emma: Yeah, so that perfect tube size depends on if your patient is male or female, and then their overall size. Typically, in adult women, we aim for a 7.0 or a 7.5, whereas in adult men it's typically gonna be a 7.5 to an 8.0. If there's a lot of secretions and

I'm expecting to have to bronch the patient pretty frequently, I might upsize them closer to an 8.0. If there's a ton of airway edema or you think it's gonna be a difficult airway, set yourself up for success and air on the side of a smaller tube. Kevin: Yeah, there's a lot of details associated with who will be an easier versus harder airway. You can check their thyroid mental distance, a mal and potty score, neck circumference and neck mobility. But often in the ICU with a crashing patient, you don't have the luxury to check all these things before intubating. Have your fallbacks ready. Have a video, laryngoscope a bougie, and if all us fails, a cricothyroid autotomy kit. Alright, moving on. We can talk for hours on ventilator management alone, but can you give us a quick overview? Emma: Yeah, absolutely. Ventilatory modes are split into volume controlled and pressure control strategies in volume control or VC modes. Think of the machine giving the same amount of tidal volume with each breath. On the other hand, pressure control or PC is where you set a target

inspiratory pressure, and then that can lead to different volumes delivered by the machine, depending on how compliant the lungs are and if the patient is having any effort to breathe. There are some more nuanced modes such as pressure support ventilation, where the patients are placed on a spontaneous mode that helps with breaths initiated by patients, an A PRV or airway pressure release ventilation that maintains high airway pressures for oxygenation. You wanna aim for a tidal volume that's typically six to eight mils per kg of ideal body weight. An ideal body weight corresponds to the height of the patient, and most of the ventilators, at least in our hospital, have a nice handy calculator where you put in the patient's height and it'll spit out their ideal body weight. In some scenarios such as a RDS, you might wanna use four to six mils per kg to protect the lung. And then on the other hand, an obstructive lung disease you might wanna use closer to the end of six to eight mils per kg. Kevin: Good. Like we mentioned earlier, there are a lot more details and nuances to deciding the best ventilation strategy, but these are

a few of the basics. Agnes, your patient is stabilized on the ventilator compressors. You're able to take him to the or. His prior anastomosis was leaking fent material into the belly, so you overs sowed the distal in and brought up a colostomy. Now he's back in the ICU. What are you thinking of and what management priorities take over at this point? Agnes: So now our focus shifts into managing the multiple organs that were affected during that initial insult. So I wanna start him off on broad spectrum antibiotics or continue them, I should say, and leave him intubated and allow his mentation to clear before extubating. Based on what you said, it sounds like it was a dirty case. So I wanna keep a close eye on his incisions and make sure that they're healing properly within the next few days. And make sure that I keep an eye out for any skin breakdown or abscesses that might form. Emma: I also like to always get a fresh set of labs. When a patient comes back from the OR to check for a few common things, we wanna see if he has an a KI. That's a really common complication with shock, and usually the treatment's supportive by watching urine output and providing fluids as

needed. However, if the patient develops severe volume overload, hyperkalemia. Or metabolic acidosis. Renal replacement therapy might be indicated, and we delve into the nuances of RRT in another episode, so be sure to check that out. I'd also wanna take a look at his glucose level. Hyperglycemia is common and is an independent risk factor for adverse outcomes. Our goal here is to maintain a glucose of less than 180, which can sometimes mean starting an insulin drip during the acute phase. Agnes: And lastly, always be thinking about nutrition for that patient. Patients who are critically ill are in a catabolic state, so daily during rounds. Ask yourself that patient can get any internal nutrition yet, 'cause that is the best way to maintain that gut integrity and decrease infection rates. But if your patient can't get any internal feeds, they should at least get started on PPN or TPN. Kevin: Great. Yeah. This is my favorite question to ask. The ICO attendings, can we extubate my patient? How do we decide, when

can we extubate the patient? Emma: Yeah, one of my attendings says The job of the intensivist is to get the patient to look good for the surgeon. The patient's ready for extubation when they have appropriate mental status. They're on minimal sedation. They have intact airway reflexes, a good cough, and the ability to breathe well without excessive support. I also always like to look at their chest x-ray and their P two F ratio on their gas to just see how their lungs are doing. We should be doing daily SVTs or spontaneous breathing trials in our patients in the ICU to work them out. This is where the patient breathes on minimal support with the ventilator, such as pressure support or CPAP for about 30 minutes. You track if the patient's able to do this and then take note if they're unable to, you're gonna watch for their vitals. Work of breathing and overall oxygenation status. If you feel that a patient's doing well on their SBT, you can get some objective measures to help guide your decision. First is gonna be the rapid shallow breathing index or Riss B, which is calculated as respiratory rate divided by

tidal volume in liters. Aris SBI should be less than 1 0 5 to indicate a good likelihood of the patient passing their extubation. Next up is the negative inspiratory force or nif, a measure of inspiratory muscle strength, and that's calculated when the patient's asked to take in a really deep breath that's measured by the ventilator. This should be more negative than negative 20 to negative 30 centimeters of water. And lastly, patients should be able to generate an adequate tidal volume, typically greater than four to six mils per kg of ideal body weight during spontaneous breathing. And the respiratory therapists are the best people to ask to show you how to do these things and how to interpret them. Agnes: And another component is a cuff leak. This is where the respiratory team deflates the cuff on that ET tube and sees if they can hear air leaking through a negative cuff leak can suggest that the trachea is really edematous, and that's gonna increase your likelihood of failing extubation. And if you're worried about tracheal edema, you can give dexamethasone to reduce that swelling and you can check the cuff

leak the next day. Kevin: Great. Remember, reintubation are common as well, so after excavating a patient, make sure you're monitoring their respiratory status. Let's pivot to a circulatory collapse with a different etiology. Our second patient is a 72-year-old male, three days post major abdominal surgery. He's known to have severe aortic stenosis. He is hypotensive with a map of six C, has low urine output and on exam exhibits, signs of jugular venous distension, and pulmonary congestion, signs of marked volume overload. Agnes, how does this hemodynamic picture differ from the septic shock we just discussed? Agnes: This sounds like cardiogenic shock, because the patient has significantly decreased cardiac output from a pump failure. Unlike that hypotensive septic patient we talked about, who usually has a low SVR, and seen a distributive shock. The cardiogenic patient compensates with increased sympathetic output leading to increased. Systemic vascular resistance and this high SVR combined with that

low cardiac output is a defining sign for pump failure. Kevin: Emma, how does that physiology impact fluid in pharmacologic management? Emma: Yeah, so unlike our septic shock patients where we need to give them a lot of fluids in these patients with cardiogenic shock, we wanna be extremely cautious with fluids. The positive response in cardiogenic shock if you give them a small bolus, is pretty quickly lost as the filling pressures rise even higher, and that causes the cardiac output to fall further down that Frank Starling curve. The key strategy here is to use both inotropic and chronotropic support. We would wanna use agents like dobutamine, which is a synthetic catecholamine, which can augment heart rate and contractility via its beta one actions. While its beta two. Vasodilatory effects can help decrease left ventricular preload. Agnes: There's two other vasopressors that are used in the ICU that we haven't really touched on thus far, and that's epinephrine and dopamine. So epinephrine is a very strong alpha one, beta one, and beta two agonist. That can lead to increased

ionotropic and chronotropic, and at high doses can lead to increased SVR. We can also use epinephrine and cardiogenic shock, especially if they have poor left ventricle output. But other scenarios that you might see epinephrine are anaphylactic shock and in post ROSC patient. The other vasopressor is dopamine, which is usually not first line, but it has distinct effects based on the dosage at low doses. It's been known to lead to renal vasodilation. It hasn't really been shown to be useful for any renal protection. Usually we use it at either the medium or high dose. Medium dose leads to beta one effect with increased heart rate and contractility. In high doses, you see predominantly an alpha one vasso construction, so you can get an increased SVR and blood pressure. Dopamine is a strong chrono tr, so you can use it for patients who are in shock and they're have symptomatic bradycardia, usually within the ICU. Norepinephrine or Levo is the king and used most often. But we wanted to briefly just discuss these as well. Emma:

And back to our patient. If he does not respond to the pharmacologic therapy, we might have to utilize advanced modalities such as an intraaortic balloon pump, or IABP or another ventricular assist device. These are all bridges to cardiac recovery, and you'll need to talk to your cardiology and cardiothoracic colleagues if you think your patient might benefit from. Kevin: Yeah. The takeaway here is that interpreting hemodynamic data is crucial. A low cardiac output and high SVR mean ionotropic support steering away from aggressive fluid loading, typical of distributive shock. We've covered managing urgent interabdominal septic shock, and stabilizing the postoperative cardiogenic shock. Any final thoughts? Emma: Yeah, I just wanna highlight that, and this is one of the reasons I love the ICU. It's all a team effort. Other disciplines are crucial in managing these patients. So be sure to engage your respiratory therapy and nursing colleagues and even medicine colleagues as well in managing each of these patients. Agnes: And goal-based discussions are also really crucial. It's important that we fulfill what the

patient would've wanted and what their wishes would be since they're not usually able to advocate for themselves. So you should take the time to talk with the patient's, families and the palliative care team early and making sure that the patient can be in the center of the care that we provide for them. Kevin: Awesome. Thank you guys for a great episode. Emma: Thanks to all of you guys for listening. This is one episode in a series entitled The EPA Playbook, where we delve into each of the EPAs outlined by the American Board of Surgery. You can find more information about EPAs at the a BS website. Thanks again for listening, and as always, dominate the day.