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So the initial insult in distributive shocks is either an immune response or an autonomic response, depending on the situation. Anaphylactic shock is an immune response because of an allergic reaction, and Septic shock is an immune response because of an infection. These immune responses cause inflammation which releases chemicals called Cytokines. Now, Neurogenic shock is caused by an autonomic response after a spinal cord injury. This causes decreased sympathetic nervous system activity. Both of these things, the cytokines and a loss of SNS activity, will interfere with vascular tone - or the ability of the vessels to contract - that causes massive peripheral vasodilation. For this lesson we’re going to focus on septic shock because it’s the most important and the one you’ll see most often.
So let’s see what happens in the body. You get this infection, it starts the immune inflammatory response, releases cytokines, and causes massive peripheral vasodilation. If all the blood vessels out in the periphery are dilated, all the blood is going to pool out there and can’t be “distributed” to the vital organs. That’s why it’s called distributive shock. So hemodynamically, we’ll see our SVR or our afterload decrease because of all the vasodilation - there’s practically no pressure there at all. We’ll also preload decrease because the blood can’t make its way back to the heart. This means our Cardiac Output and blood pressure will decrease, too - and remember our heart rate will increase to try to compensate. Now here’s where we see a big difference from the other two shocks. Because all the blood is pooling in the periphery and the non-vital organs like the skin - we’ll actually see the temperature go up. We might see warm, flushed skin, and maybe even bounding pulses in early stages. Don’t be fooled by this, they are still in trouble.
So what will we actually see? Well first, we’ll have some sort of suspicion of infection - maybe a UTI or a pneumonia? So you’ll see signs of that infection in addition to the signs of shock. The biggest thing, like I said, that differentiates septic shock from something like cardiogenic or hypovolemic shock is they’ll have a high temperature. Now by itself a fever doesn’t mean septic shock - we’ll also see evidence of perfusion problems. Remember, all the blood is pooling out here in the periphery and not getting to vital organs. It’s like taking a 5-lane highway down to one lane, the cars aren’t going to move. So think, if this person isn’t perfusing their vital organs - what other problems might they have? Brain - decreased LOC. Lungs - decreased SpO2, Kidneys - decreased urine output. Make sense? So blood pooling out here means high temp, warm flushed skin - blood not getting here means low blood pressure, high heart rate to compensate, and a decreased LOC, SpO2, and urine output. Make sense?
So therapeutic management of Septic Shock is guided by the Surviving Sepsis Campaign Guidelines. We’ve put a link to the most recent guidelines in the outline for you so you can see the details if you want, but we’re going to highlight the most important points for you to know. As always we need to treat the cause. The goal is to begin administration of broad spectrum antibiotics within 1 hour of recognition of sepsis - remember we have to draw blood cultures FIRST! With septic shock, we’ve found that they also benefit from aggressive fluid resuscitation, this helps to increase their preload and therefore their cardiac output - we’ll give about 30mL per kg body weight - so a 100kg man would get about 3 L of fluid. To maintain their blood pressure, we give vasopressors - first being norepinephrine, that’s the #1 choice. If needed we’ll add something like vasopressin or epinephrine. The goal is to keep their MAP above 65 mmHg - so they may need an arterial line so we can continuously monitor their blood pressure. Finally we are going to watch lactate levels. Lactate is released from the tissues when they aren’t getting enough oxygen. As we work to improve cardiac output in a septic shock patient, well want to see those lactate levels returning to normal. Check out the labs course to learn more about lactate.
So, there are a lot of nursing priorities for this patient - one of which being that they need to be in an ICU. But we’re gonna focus on the top 3 concepts here. Check out the outline, care plan, and case study attached to this lesson, you’ll see a ton of details about specific nursing interventions, and really get a good picture of what this looks like. As with the other shocks, the first concept is perfusion, we have got to monitor their hemodynamics and maintain a good cardiac output - again we give pressors to keep their MAP > 65. Then infection control, obviously septic shock is caused by an infection so we’ve gotta get that under control. Then oxygenation - not only are they going to have decreased oxygenation, but they may end up struggling to protect their airway because they’re exhausted and maybe have a decreased LOC - so always monitor their oxygenation status and intervene as needed.
So let’s review. Distributive shocks like septic shock are caused by some sort of immune or autonomic response that interferes with vascular tone and causes massive peripheral vasodilation. That blood pools in the non-vital organs like the skin and can’t get to the vital organs. We use the surviving sepsis campaign guidelines which promote early antibiotics and fluid resuscitation, the use of vasopressors, and monitoring lactate. As a nurse, we need to focus on perfusion, infection control, and oxygenation, and remember that this is an emergency, these patients need to be in an ICU and may even need to be on life support. So don’t be afraid to ask for help if you need it!
Make sure you check out the care plan, case study, and outline in this lesson to see more details about nursing care and interventions. We love you guys! Go out and be your best selves today! And, as always, happy nursing!
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