hi my name is rich Savelle I am the director of the surgical intensive care unit here at Maimonides Medical Center and this is the introductory educational video for house officers rotating here in the surgical ICU in this video we're going to help you understand the basics of the different categories of shock States I'm going to talk about the differential diagnosis of when a patient is having cardiopulmonary arrest I'm going to spend a few minutes talking about the three hour and six hour bundles for patients with severe sepsis syndrome importantly I want to take some time and try to help you understand how an intensivist thinks about acid-base disorders and how we take a structured approach to patients with this problem finally over here I'm going to take a few minutes and speak to you about how we define a RDS and how we use the ARDS net protocol as a standardized approach to managing patients who have the acute respiratory distress syndrome we will take a few minutes and talk about the abdominal compartment syndrome and then at the very end we will talk about the ventilator bundle and the catheter-related bloodstream infection bundle in terms of differential diagnosis of shock there are some important categories that you need to keep in mind when you're caring for the critically ill patient as you can see here hypovolemic distributive cardiogenic and non cardiogenic obstructive primarily you will be caring for patients who have septic shock while you're here in the surgical intensive care unit Surgical septic shock septic shock is a subcategory of distributive shock other examples of distributive shock include spinal shock and Donna Falak DIC shock hypovolemic shock is commonly seen in patients who are bleeding hemorrhagic shock but also in patients who have diabetic ketoacidosis cardiogenic shock is important but not primarily something you'll see while you're here in the surgical intensive care unit where the primary problem is pump dysfunction this is a very important category because it can be known or used to be known as cryptogenic shock non cardiogenic obstructive it's as though there is pump failure but fundamentally the heart is working fine examples include pericardial tamponade pulmonary embolism tension pneumothorax and importantly especially in this intensive care unit the abdominal compartment syndrome it's very important that you keep these in mind when you're caring for a patient who's meeting criteria for shock here is an important differential diagnosis that's important when you're caring for a patient who requires CPR why am i coding it's important that the person who's running the code explicitly go over these items during the code does the patient have hypovolemia hypoxia hypothermia hypo or hyper Kaylee Mia massive mi pericardial tamponade pulmonary embolism tension pneumothorax overdose or acidosis these are important especially when you're actively running a code to think about these things that might be treatable hiding lis here is a description of the three hour and six hour bundles for the surviving sepsis campaign guidelines or as you can see here surviving sepsis for reasons I still don't understand at three hours it you are expected for a patient who meets criteria for severe sepsis syndrome and we've talked a lot about this infection and tour more code two or more service criteria as sepsis sepsis or the cute sepsis induced organ dysfunction is severe sepsis syndrome and if the patient remains volume remains vasopressor dependent after appropriate volume resuscitation the patient meets criteria for septic shock what you're supposed to do in that setting and we have a sepsis order set and we will be discussing that but type in sepsis into Sunrise clinical manager and it will pop up you check a lactate by three hours check a lactate level get cultures prior to antibiotics start broad-spectrum antibiotics and there are antibiotics that are pre done for you in the order set that are appropriate and give at least a 30 ml per kilo crystalloid bolus initially at six hours you should have the patient on vasopressors if they remain persistently hypotensive with a mean arterial pressure target of greater than 65 millimeters of mercury you should be considering if a central line hasn't already been placed place one and if you have placed one check a central venous pressure the targets of those are going to be between 8 & 10 or 8 to 12 and re measure lactate if your initial serum lactate is elevated now on acid-base status in the intensive care unit it's very important to have a fundamental understanding of this so that you can deal with it this is not something that I'm doing for academic purposes it's really important we use this to make real-life decisions in the intensive care unit as intensivists we break things down into metabolic acidosis and metabolic alkalosis first we'll start with metabolic acidosis you have to calculate the anion gap and if the anion gap is elevated the differential diagnosis as you can see here is mud piles and we'll go over that methanol uremia diabetic ketoacidosis paraldehyde iron or inh lactate ethylene glycol and if you want to get fancy salicylate toxicity with a metabolic acidosis and a respiratory alkalosis the most important here is obviously in this unit on this rotation is an elevated serum lactate from patients who have some form of shock most of the time it's severe sepsis syndrome and septic shock the idea here is the reason we check this is because we consider this to be a cosmetic metabolic acidosis and it isn't about treating the fundamental it isn't about treating the acidosis but figuring out why the patient is acidotic and treating part of metabolic acidosis is a non anion gap metabolic acidosis the way I would like you to think about that is to remember that the patient is either losing is either losing bicarb from their gut or their kidney or has been resuscitated with a bicarb poor substance like normal saline when I say they're losing bicarb from their gut usually that's in the form of diarrhea and when I say they're losing it from their kidney they're what I'm referring to here is a renal to Buhler acidosis now this can be intimidating don't let it intimidate you let it wash all over you this is important so there's type 1 2 & 4 1 is distal 2 is proximal where the body is not reabsorbing bicarb and then importantly and excitingly the type for RTA and it has taken me years to be able to get my mind around this enough to teach it to you so a type 4 RTA is a form of hypoalle dosterone ism it's an equal sign type for RTA is hypoalle dosterone ISM and so then the question is is it primary hyperaldosteronism does the patient have adrenal insufficiency from sepsis or does this patient have some form of drug-induced hypoalle dosterone ISM and this is actually really important because you that's right you when you're on call you will be called with a patient who has an elevated potassium and a normal creatinine and you should think that patient has a type 4 RTA due to a drug most likely and the common drugs as we've talked about a lot here on this rotation include ACE inhibitors NSAIDs and surprisingly and importantly heparin so heparin induced hypoalle dosterone ISM is an important cause of hyperkalemia that is otherwise of unclear etiology in the intensive care unit the next thing to talk about is the differential diagnosis of a metabolic alkalosis metabolic alkalosis is a little bit more confusing and it is clearly the unsung hero of acid-base disorders in the critically ill patient but it's important I'll give you an example a patient with COPD comes in with a CHF exacerbation already my minds worrying COPD a with a CHF exacerbation so a COPD or somebody with a chronic respiratory acidosis with metabolic compensation then they come in with a CHF exacerbation and they need to be dire east which makes their Singham bicarb go up even more and their response to that is to retain even more co2 so you can see that an understanding of acid-base disorders can be the difference between life and death for a patient with something as simple as COPD and CHF so let's take a look here at how you work up or think about somebody with metabolic alkalosis you're supposed to send off a spot urine chloride and look if it's less than 20 or less than 25 or greater than 40 this breaks these entities down into chloride responsive and non chloride responsive metabolic alkalosis one of the most important ones commonly is especially in a surgical intensive care unit is vomiting or NG tube suctioning this is very common it makes sense you're sucking out acid the patient develops and alkalosis one of the important points I want to remember is the relationship between hypokalemia and a metabolic alkalosis they feed off of each other and are tightly linked to each other and that you often can't get rid of your metabolic alkalosis until the patient's potassium and magnesium have been appropriately supplement the treatment for a chloride responsive metabolic alkalosis is to give saline okay that makes sense but here's where it gets complicated if your urine chloride is greater than 40 you have a constellation of diagnoses where I try to keep it all together by thinking of the fact that you have revved up the rena angiotensin aldosterone system so hyperaldosteronism pseudo hyperaldosteronism which is called Liddell's syndrome actively using a diuretic so again that can be seen and it makes sense why the urine chloride would be elevated in addition there are two entities barters and Gittleman syndrome which are these channel APPA thiis where the body is acting like it has its own diuresis and it's very much analogous to actively using diuretics licorice is important and interesting because it has to do with the mineralocorticoid receptor and the there's a molecule in licorice glycerine ik acid that inhibits eleven beta hydroxy steroid dehydrogenase and allows the mineralocorticoid receptor to be constitutively firing a again causing an elevated cortisol an elevated steroid State other examples include ask exogenous steroids and ectopic ACTH so again you break it down into chloride responsive and non chloride responsive metabolic alkalosis I think the important things to keep in mind big picture when you're thinking about acid-base is does this patient have an anion gap or non ion gap metabolic acidosis or both does this patient if they have a non anion gap do they meet criteria for a type 4 RTA in terms of hypoalle dosterone ism and I hope you've seen the nice yin and yang of hypoalle dosterone ISM and hyperkalemia and hyperaldosteronism and hypokalemia this is not something trivial it's very important so try to keep all this in mind when you're thinking about your critically ill patient