Hypovolemic Shock: Stages and Assessment (Nursing)

00:01 Let's take a look at the different stages and the assessment findings in those stages.

00:06 Now, when you're preparing for practice, and for the NCLEX, you're gonna want to keep in mind Clinical Nursing judgment.

00:13 How do you do that? When you look at the measurement model, that's the one that the NCLEX is based off of.

00:18 It's just a way of demonstrating how you should think like a nurse.

00:23 Layer Zero thinks about the client needs and client decisions.

00:26 Layer One is clinical judgment.

00:29 And that's where you're gonna really start to use your critical thinking.

00:32 Now on the second layer, you form your hypothesis, you refine it, you evaluate it, but here's where I want you to zero in.

00:39 That third layer, where you're recognizing queues, analyzing queues, prioritizing your hypothesis, generating solutions, taking actions and evaluating them.

00:49 This is where the the majority of the exam questions are going to come from.

00:54 Now that fourth and final layer to environmental and other examples.

00:57 Just hang on to that because we're going to focus in on Layer Three.

01:02 Now let's take a look at recognizing queues and analyzing queues.

01:07 Now you see we've got on your screen, four stages their: Initial, compensatory, progressive, and refractory.

01:15 Now the cues in shock are gonna vary depending on the stage of shock that the client is in.

01:20 Okay? So from the top, things are okay.

01:23 All the way down to the bottom things are so not okay.

01:27 So let's start with the initial stage.

01:29 And remember, we're talking about hypovolemic shock.

01:33 And these cues vary, it's along this continuum.

01:36 So it depends on where you are.

01:38 Now, think about this, in this very first stage.

01:40 Your cells are saying, "We need oxygen." Because during a hypovolemic shock, they lose compensatory mechanisms are not enough.

01:49 That's why we're in shock.

01:51 So even though when there's less volume, the body's compensatory mechanisms kick in, right? The heartbeats faster, moves things around more quickly, the heart's beating stronger trying to make up for the lack of oxygen being delivered to the cells.

02:05 But you reach a point where it just can't keep up anymore.

02:09 That's when you have hypoxemia.

02:11 Not enough oxygen in the cells.

02:13 We've got those little guys there to remind you, they don't like that when they don't have enough oxygen to carry around to the body. And then the cells can't function.

02:23 So as the hypoxemia worsens, and causes impaired cellular metabolism.

02:28 Yeah, that's a serious as it sounds.

02:30 Cells need oxygen for normal metabolic needs.

02:34 If these cells can get their oxygen delivered to them, they can't function normally.

02:40 So they have some big changes.

02:43 Cellular metabolism switches from aerobic oxygen to anaerobic.

02:48 Here's the problem.

02:49 When you switch from aerobic to anaerobic, you end up with a lactic acid build up.

02:54 Yeah, that's the problem.

02:56 So low volume can't get enough oxygen to the tissues to the cells.

03:01 So they have to switch from aerobic to anaerobic metabolism, that causes a huge lactic acid buildup.

03:08 Now, lactic acid is just this waste product is removed by the liver, normally.

03:14 Oxygen, this is what's needed for the liver to get rid of the lactic acid.

03:18 Now, it's not available because we don't have enough well perfused tissues.

03:23 So what's the problem? Lactic acid is going to build up in the body and that is no good.

03:29 Because the body is overwhelmed, the liver can't get rid of it like it normally would, it doesn't have enough oxygen.

03:34 That's why we end up with lactic acid buildup.

03:37 Now, I'm going to talk about some signs that you can't necessarily see.

03:41 This is in the compensatory stage.

03:43 So we're hit the initial stage. We're starting to see problems.

03:47 Now we're going to move into the compensatory stage.

03:50 Now we already know that the cellular metabolism is switched from aerobic to anaerobic.

03:55 We've got a bunch of lactic acid building up.

03:57 We told that's not really great, right? Stroke volume, with the hardest putting out is decreased.

04:05 Now hopefully that's making sense to you.

04:07 With less volume in the intravascular space, the stroke volume is going to be lower, as will the cardiac output.

04:15 Because it doesn't matter how fast the heart is pumping, if the volume isn't there to pump, both of these are going to be down or less.

04:23 Now the hypoxemia will just continue to worsen, and it's going to cause even more impaired cellular metabolism.

04:30 Now you're going to have something called tachynea.

04:32 Remember, this is what you will notice in this face, Tachy means fast. And we're dealing with breath.

04:38 Tachypnea. So they're going to be starting to breathe faster than normal.

04:43 Why would they do this? Well, it's trying to compensate for the metabolic acidosis that this patient is heading into.

04:51 When they increase your respiratory rate, you blow off CO2, CO2 is acidic. So if you can blow off some of that we're gonna try to reestablish homeostasis, and not be as acidotic, but move back towards a more normal pH.

05:05 This isn't going to last long if the hypovolemia isn't corrected.

05:11 So, what I mean is, tachypnea can try to help us but it's not going to help us it's not a long term solution.

05:17 First of all, it's going to exhaust the patient and it's not going to be able to keep up with a huge change in pH.

05:25 Breathing gets faster, so does your heart rate.

05:28 Now you're getting heart rate that is fast tachycardia because you're trying to compensate for that low cardiac output.

05:35 The heart realizes, "Wow." "This is a lot less volume than I'm used to doing." So, it thinks, "I don't have very much but what I do have, I'm gonna move around a lot faster." That's why you see a heart rate that's high.

05:47 Classic sign of hypovolemia is a heart rate that's elevated and a blood pressure that's decreased.

05:57 Now let's think about what happens when somebody's cardiac output drops or their blood pressure drops, those baroreceptors activate the sympathetic nervous system.

06:04 Well, what happens then? We have this vasoconstriction, and it tries to redistribute blood flow to the non vital organs.

06:13 Well, listen. If I'm kidneys, I'm thinking I'm real vital, right? But the brain and the heart are super greedy.

06:20 Everything is going to be shunted to them.

06:23 So the periphery is going to be cut off.

06:25 Some of the other organs are gonna get significantly under perfused, in order to maintain blood and oxygen supply to the brain and to the heart.

06:35 Less volume means a lower blood pressure.

06:38 I bet you've already put that together, because we've talked about it, if you did just celebrate.

06:43 Everyone needs a victory in nursing school.

06:46 Less blood volume in the intravascular space equals less or lower blood pressure.

06:52 Now there is a side note.

06:54 there can be individuals who have such high chronically high blood pressure, hypertension.

06:58 It might seem unusually high to you.

07:01 If normal is 120/80, that's NCLEX world, this patient may not meet what we typically expect to see if someone has hypovolemia. It might be a little elevated.

07:11 That's why it is so important to know your patient's baseline.

07:15 What are their normal vital signs? So, in hypotension and hypovolemia, we normally would expect the blood pressure systolicly to be less than 90.

07:26 Also got a mean arterial pressure of less than 65.

07:29 Same concept, less blood in the intravascular space should lead to a lower than normal blood pressure.

07:37 I can tell you on the NCLEX, 120/80 is assumed to be normal for everyone.

07:44 So because everything is kind of shifting toward my brain and my heart, what happens to my extremities on the periphery? Well, they're pale, because they're not as well perfused.

07:55 What other signs can I see? Well, once you get to 15 to 30% of a loss of volume, your central nervous system really kicks in that sympathetic nervous system response, right? That's the mediated response. So what happens when the sympathetic nervous system is stimulated? That brain has said, "Whoa, let's go at it." Well, typically, everything gets faster.

08:19 It's trying to tell you, I sense my brain that I need more oxygen delivered to my cells.

08:26 So how do I do that? Well, heart rate, it's going to go faster and harder.

08:29 Respiratory rate is going to go faster.

08:32 Remember, we've talked about that tachypnea and tachycardia.

08:35 And in general, sympathetic nervous system speeds everything's up, because almost like you're getting ready to run really fast, and you need more oxygen.

08:44 In this case, the patient may just be lying there.

08:47 But because there is less volume in their intravascular space, delivering oxygen to the cells and tissues, it feels like they're really running a hard race.

08:58 Now, oxygen is normally, right? All the way throughout the tissues.

09:02 But here's what kind of happens, your gas exchange is impacted.

09:07 Remember, at that stage where blood is being shunted to the heart into the brain.

09:12 So the blood flow has been redistributed.

09:15 Now, when you have decreased blood flow to the lungs, it increases the patient's physiological dead space.

09:21 Now what happens in deadspace? Not CO2 enough to exchange.

09:26 So, some of the areas of the lungs that are being ventilated will not be perfused, because of the decreased blood flow to the lungs.

09:32 Remember, where's it going? Heart and brain. Good.

09:36 The arterial O2 levels will decrease and the patient will have this compensatory increase in the rate and depth of their respirations.

09:44 We've called that tachypnea.

09:45 So now we're explaining even more why the patient will have tachypnea.

09:50 Then there is the RAAS. Now you're familiar with this.

09:54 We talked about it in pharmacology, we talked about it a multiple series because it's all over reactions in your body.

10:01 So when there's decreased renal perfusion, right, the kidneys pick up, "Hey, I am not getting what I normally get." It kicks out Renin. You end up with this whole process, and at the end, you end up with Aldosterone and Angiotensin II.

10:18 So this is a patient that doesn't have much volume.

10:21 One way that might be able to treat as a whole make those vessels smaller, right? That might help raise our blood pressure, And then tell your body to absorb reabsorb sodium and water and increase the volume.

10:33 Under normal circumstances, this might be enough.

10:36 But if someone is in hypovolemic shock, this is not enough to fix the problem.

10:42 Now we're moving into the progressive stage.

10:45 This patient starts to start to be anxious and confused.

10:48 They're really not perfusing their brains well.

10:50 They have hypoperfusion in their central nervous system.

10:53 And that's what makes them very anxious and very confused.

10:55 It's kind of their body's way of telling them, "We're going to die if we don't do something drastic to fix this." Now their hands before were kind of pale.

11:05 Now they're cold and clammy.

11:08 There is no circulation getting to those hands.

11:11 Start to have some weird dysrhythmias.

11:13 This patient is in extreme danger.

11:16 They could have a myocardial ischemia, they might have a myocardial infarction, they're gonna see some weird rhythms. This is huge.

11:23 Now, if you did a Swan-ganz catheter, if you inserted it, or if you have maybe another way to measure these pressures, you'll see in our picture. There's a heart.

11:33 And you've got the Swan-ganz catheter into the right atrium, right ventricle, and right up heading into the lungs, right? That's where capillary wedge pressure is measured.

11:42 Now normal wedge pressure would be 4 to 12.

11:45 But we're thinking of something being in hypovolemic shock, it's going to be on the lower end.

11:51 So the most important thing is to remember, wedge pressure will be lower.

11:56 Definitely probably less than 8.

11:58 And I do recognize that it's normal 4 to 12.

12:01 Now CVP, this one gets a little more controversial.

12:04 Remember, Swan-ganz as kind of a big deal.

12:07 That's really invasive.

12:08 You may not have those numbers to deal with, but you know what the impact will be on the wedge pressure, or the PCWP pressure. It'll be on the lower end.

12:17 Central venous pressure monitoring is in the right atrium.

12:21 Now, doing this in the critically ill is an established practice. A lot of places do it.

12:26 But there's kind of a lot of, let's say, argument about it.

12:30 And people are challenging that.

12:32 There's a large body of evidence pulling toward that.

12:35 So, I'm just going to tell you that for a CVP, you would expect it to be reduced, alright? Normal is 2 to 6. I would expect it to be less than 2.

12:44 So if you have that information, and an exam question, you'll know how to answer it.

12:49 In real practice, know that this practice is changing all the time on what types of measurements are appropriate in treating shock.

12:57 So, if you have these toys at your disposal, those would be the readings that you would expect to find at this point in hypovolemic shock.

13:06 Now, let's take a look at acute respiratory distress syndrome.

13:10 This is when the patient has both tachypnea and crackles.

13:15 Fluid is backing up into the lungs. This is extremely problematic.

13:19 So when we're talking about things that have happened, right, they're going to be anxious and afraid because their brain has been hyperperfused.

13:25 Even when it has been greedy and tried to shunt as much blood to the heart into the brain.

13:31 The lungs could progress into acute respiratory distress syndrome.

13:35 Breathing rapidly, you hear crackles in the lungs.

13:38 The gut is also going to struggle.

13:40 It's not going to be able to absorb nutrients that the body needs.

13:43 Puts the patient at risk for ulcers and GI bleeding.

13:46 You can end up with renal tubular ischemia.

13:49 Okay, this is all kinds of problems.

13:52 It's leading cause is that poor perfusion, because see if tissue over a long period of time has decreased perfusion, now we're going to have this mucosal barrier that's usually really protective and good, starts to become ischemic, and that is beyond problematic.

14:10 So, this ischemia predisposes the patient to be at risk for things like ulcers and GI bleeding.

14:16 And that's why we have some of the GI problems that come with that.

14:19 It also increases the risk for the bedbugs to migrate from the GI tract to the blood into the lungs, which could lead to something like sepsis.

14:28 So, not good. Any of the tissues that don't get perfused, these are just some of the things that you can see happen in shock.

14:37 Now we're at the refractory stage. Now, this is the saddest one of all.

14:42 This is when you look at the CNS system, the pupils are nonreactive, the patient is unresponsive.

14:48 The hypotension is not just low, but it's profound, and we're not able to raise it. They're in respiratory failure.

14:55 One by one, all the organs are responding to the lack of oxygen being delivered to them.

15:02 The gut is even involved in it's an ischemic gut.

15:05 They cannot control their body temperature and they have severe hypothermia.

15:10 Those hands it used to be kind of pale, then they got clammy, now they are cyanotic.

15:16 The kidneys aren't putting out any urine.

15:20 They're anuria.