All right. So, I'm going to cover your distributive shock. Uh, so sepsis, anaphilaxis, and that'll be it for this one. I'll do neurogenic on its own. All right. So, for your distributive shock, you can see your um pathophys here, precipitating event. This is going to depend on whether or not we're talking about sepsis or anaphilaxis all leading to vasoddilation. So your distributive is also your vasoddilatory. You'll see your activation of your inflammatory response. Mal distribution of intravascular volume leading to all the way down card decreased cardiac output and decreased tissue profusion. Your main issues here. Your clinical manifestations are going to be different for each of these. So we'll cover them separately. Right. So here you see um the SERS pathway. SERS is the systemic inflammatory response system which will or can I suppose progress into mods your multiorgan dysfunction syndrome which is that dysfunction in two or more organs. If we don't treat this aggressively your patient will go into system failure and death. So for CERS um what we're seeing here is your main causitive agent. This is your precipitating event um that get through the portals of entry skin respatory GI or GU tract. You'll have local inflammation. So redness, swelling, warmth and pain before we get to CERS, which is your activation of your inflammatory response where your patient becomes hypotensive, tachicardic, typnic, and they have a fever because it is an infection. This is your recognition of sepsis using sir's criteria. So your temperature is going to be um very low less than 36° C or very high greater than 38° C. Elevated heart rate your patient will be to kipnic you'll see breaths um per minute greater than 20 or your pCCO2 is going to be less than 32. And your white blood cell count either less than 4,000 or greater than 12,000. And if you're looking at the bands, you'll see le uh greater than 10% of immature band formation. So for SERS response, you'll have two or more of these criteria that you see on the left. When we talk about sepsis and your code sepsis or sepsis alert, whatever it is that you hear overhead at your hospital, two or more of these are present plus a confirmed or possible infection. So once we know that, then we can move towards that sepsis alert. For severe sepsis, this is where you're seeing sepsis and organ dysfunction. This could be mods if we progress that far. So septic shock, severe sepsis, but now you're having refractory hypotension and then we get more organs involved and they start to fail. That is when we see mods. So treating and managing sepsis. Um the most important thing with sepsis is prevention. So making sure that we're scrubbing all of the lines with alcohol um before we're using them. We use sterile dressing changes on all of our central lines. Good fully catheter care, removing any lines as soon as possible, recognizing your early signs and symptoms, and initiating measures to reverse any um complications. Start with two large bore IVs, again, an IO if you have to. We're going to get blood cultures for um two sets taken from different sites 15 minutes apart. And we need to get these cultures, urine cultures, wound cultures, whatever types of cultures before we administer any antibiotics. Lactic acid is going to be elevated. Um greater than two is considered elevated. Greater than four is considered a poor prognosis. Uh typically the goal here is to get all of these initial assessments done um within 3 hours of the sepsis diagnosis. Um but I have faith in you and we can get all of these accomplished very quickly, less than an hour. Uh if a patient has any indwelling catheters or lines that were present before the symptoms started, um the provider is probably going to ask you to remove those. uh before um we insert anything new. Uh and we also want to culture some of these. Um so if they have a central line and we're removing that, we just cut off the tip of that central line. Um the actual catheter inside the patient, not the things on the outside. Can't think of the word right now. Um, so make sure that you put that in a specimen container and send it down to lab. Usually just cut off the tip. Um, other interventions. So like I said, prevention is your main thing here. Providing oxygen, fluid resuscitation with 30 mls per kilogram bolus. Uh, if they are not responding to your fluid resuscitation, then we start vasopressors. You can also do a fluid challenge to see how your patient is going to respond to the fluids. This is simple. All we do is raise their feet while they're laying flat. If their blood pressure increases, we know it's a fluid issue. If it does not increase, we know we're going to need a little bit more heavyduty uh guns on this one. So adding your basil pressors, we're going to repeat our lactic acid after we give our fluid bololis and then any supportive therapy. That's pretty much it for sepsis. Um but I am going to skip through to anaphilaxis. I'll cover neurogenic shock in another video. Um so for your anaphilaxis uh your main concerns here are finding the causes um because this is how we can reverse this and distinguish anaphilaxis from other types of shock. So think um food medications, insect bites, stings, latex, environmental uh triggers, and then those oneoff patients who are seemingly not allergic to anything and have random anaphylactic episodes. There's a bunch of different kinds of antibodies or imunoglobulins in the body like IGG, IGA, IGM, IG D, and IG. And each antibbody is going to be designed to target a specific antigen or allergen. When the body encounters um that antigen, the antibbody, it is going to trigger the immune response in the body against that allergen or antigen. So this is how anaphilaxis occurs. What I'm going to focus on though is Ig because this is the one that's responsible for anaphilaxis. When Ig encounters that allergen, it triggers the mast cells. And the mast cells are going to release chemical mediators, your histamines, eosinaphils, prostaglandins. Histamine is your first chemical mediator in your immune and inflammatory responses. It can reach its peak effect in 5 to 10 minutes. uh you'll see athemma, localized edema in the form of wheels, pruritis, bronchial smooth muscle contraction. So this is where you get your bronco spasms and wheezing. Histamine is released in the form of histamine 1 and histamine 2. Your histamine 1 receptors are located in that bronchial smooth muscle and vascular smooth muscle. Histamine 2 are in your gastric parietal cells. So that's why for allergic reactions, we're going to commonly administer two different types of medications. We're going to give dyenhydramine for your histamine one and your pepsid or your fmotedine for your histamine 2. Both of these block both one or one and two respectively for your diaphragm and your pepsid. Einophils also play a role in um fighting an infection in the body. uh when there's an antigen in um in the body that's causing that allergic reaction. So they release substances that are going to fight off and destroy foreign organisms and create inflammation and heat. So could be localized or systemic depending on the situation. But one of those um substances are cytoines which cause inflammation and cause heat systemic fever or localized heat as well as lucatrines. Your prostaglandins cause inflammation. Basod dilation, capillary permeability, increased pain associated with inflammation. So we're going to give incaids for this. They can also cause edema, athemma, and heat. So there is your systemic inflammatory response system as well. All of these work together to cause allergic reactions. And it could be mild, severe, depending on how the body reacts. Usually a person is just going to have an initial exposure to the antigen and then build up antibodies for it. So a person may have no reaction, mild reaction to a substance the very first time that they're introduced to it and then they'll end up having a more severe reaction to the second exposure. Some people always just have a mild reaction with each exposure and some people always have a severe. This is why anaphilaxis is so dangerous because somebody may be allergic to something severely whereas another person is going to have variable reactions. Allergies can be hereditary. So if somebody in a patient's immediate family has allergies to something, there's a high probability that their children will also be allergic. So patients should be taught to avoid allergens as much as possible. Read the food labels, avoid areas highly populated by insects that they're allergic to, wear insect repellent and protective clothing, carry the EpiPen. We need to be able to teach patients with hands-on demonstration and practice how to use this so that it is actually effective and they are not hurting themselves. This is another reason why it's so important for us to assess for allergies before we give any medications. If a patient is getting a scan done, we need to make sure that we assess allergies, especially to dye, shellfish, iodine. Think back to when we insert fully catheters. Assessing for latex and iodine or shellfish shellfish allergies, excuse me, is so important before we start the procedure. Other things that are very common like a pure wick, things that are made out of latex, always assess for that. Your treatment for anaphilaxis is going to depend on how severe it is. So it can be mild or very severe, very life um threatening. The time of onset is correlated with how severe the reaction is going to be. And it also depends on how much antigen the person is exposed to and for how long. If it's mild, the onset is usually within 2 hours of exposure. They're going to have nasal congestion, fullness in the mouth and throat, sneezing, hives, tingling sensations, and warmth. Uh if it's moderate, this is going to be within two hours of the exposure. All signs and symptoms from your mild exposure plus flushing, anxiety, coughing, airway edema, and you'll hear wheezing. For our severe anaphilaxis, this occurs within minutes of exposure. All of the same signs and symptoms from mild to moderate plus bronco spasms possibly angioadeema and airway closure cyanosis strider hypotension diarrhea vomiting and possibly cardio um cardiac arrest. If a patient is getting epi we need to monitor them because it's going to increase their heart rate. we need to put them on the cardiac monitor and then sometimes the antigen in the body will remain longer than the medications. So there can be a reoccurrence of the anaphilaxis usually within 48 hours after exposure and the initial reaction. So, if the antigen was ingested or the patient had a severe reaction, they may need to be longer um monitored longer like a 24-hour obs unit for our medications. We'll keep it here. For our medications, epi.3 mg I am for adults in the 1 to 1,000 concentration. For our kiddos, we use 0.01 mg per kilogram for peds. Still I am we're only going to do IV epi if a patient's coding and then you give the 1 milligram but we give the 1 to 10,000 ratio. 1 to 10,000 concentration means that there's 1 gram of epi in 10,000 milliliters versus the 1 to 1,000 concentration is 1 g of epi in 1,000 milliliters. So you can see how the IM version is way more concentrated than the IV version. We're never going to give the 1 to 1,000 version IV. We can also give some lodtosteroids like solumedrol as well as our dipidhydramine and pepsid. That's going to be it for your obstructive shocks. I'll do neuro um distributive shocks. I'll do neuro on a different one.