Hemodynamic Changes in Shock (Nursing)

by Corey Hardin, BSN, RN, CCRN-CMC, CV-BC

My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides Hemodynamic Changes in Shock Nursing.pdf
    • PDF
      Download Lecture Overview
    Report mistake

    00:01 Now that we've covered the four parts of blood pressure, let's look at shock in relation to those four parts of blood pressure.

    00:08 What shock is that we do not have enough blood pressure or mean arterial pressure to perfuse the body, we're not getting enough oxygen somewhere.

    00:16 So when you're trying to identify the different classes of a shock, we need to look at what is affected in those four parts of blood pressure.

    00:26 So if it's cardiogenic shock, it's going to be your contractility or your heart rate that is affected.

    00:32 Hypovolemic is your preload, there's not enough fluid volume status.

    00:37 And if it's sepsis, it might be vasodilation.

    00:40 So let's look at these a little bit more in depth.

    00:42 When we're talking about cardiogenic shock, what is affected? Well, it's your left ventricle.

    00:49 So which part of the four parts of blood pressure is affected? Well, we definitely know if my left ventricle can't contract hard enough because it's damaged, then it's going to be our contractility, that part of the four parts are blood pressure.

    01:03 Our blood pressure is low because we don't have enough contractility.

    01:06 Your heart rate can also be affected depending on if the right side of the heart is affected as well.

    01:12 So you might have a low cardiac output because we don't have enough contractility and we may not have enough heart rate.

    01:18 So how does the body compensate for that? When the blood pressure gets low, the body will always try to compensate to increase it.

    01:26 Well, can the body compensate with increasing contractility? It can't in cardiogenic shock, because the LV is damaged.

    01:33 Can it increase heart rate? Possibly, but it may be that mechanism may be affected as well.

    01:39 Can it pool volume into the vascular space? Not quickly.

    01:45 So it's not going to it's not going to change by that.

    01:47 How will it compensate? It'll vasoconstrict.

    01:51 So you'll see your SVR being really hard, you're trying to maintain a map.

    01:57 In turn because the SVR is really high, you're going to see that your CVP and your PAD is going to be elevated as well.

    02:05 Now, with hypovolemic shock, what is our issue here? In hypovolemic, we don't have enough blood volume.

    02:12 And so without enough blood volume, our CVP and our PAD or wedge pressure is going to be too low.

    02:18 We don't have enough preload going into those ventricles to maintain a mean arterial pressure.

    02:24 How will our cardiac output be affected by that? Well, we learned a little bit earlier that if our CVP and our PAD are low, we're not going to have blood volume going into the ventricles.

    02:35 So we're not going to have enough blood volume going out of the ventricles.

    02:37 So our cardiac output and index will be low.

    02:41 Now, how does the body try to compensate in relation to the four parts of blood pressure? Well, can it increase heart rate? Yes, it can increase heart rate to try to maintain blood pressure, because that's not affected.

    02:52 So in hypovolemic shock, you'll see a fast heart rate.

    02:56 Now, will it try to increase your SVR and your vasoconstriction? Yes, it'll vasoconstrict so it'll increase your systemic vascular resistance to try to maintain a blood pressure.

    03:08 That's how in hypovolemic shock, the body tries to compensate.

    03:13 So let's move on to sepsis.

    03:14 There's two parts of septic shock, the hyperdynamic state of septic shock, and the hypodynamic state of septic shock.

    03:23 In the hyperdynamic state of septic shock, basically your vasculature is vasodilating like crazy.

    03:29 So your SVR drops, which then in turn drops your mean arterial pressure.

    03:34 Now, how does your body try to compensate to that? Can it pull more fluid into that bigger tank that vasodilation of the arteries? No, not quickly.

    03:45 Well can it increase heart rate and contractility quickly? Yes.

    03:49 So you'll see your cardiac output and your heart rate start to increase dramatically, because just trying to compensate for that low blood pressure because your SVR is really low plus there's no afterload it gets to the left ventricle.

    04:02 So your cardiac output is going to come out really, really easy, because there's no resistance against it.

    04:08 Your CVP and your PAD are going to stay about the same.

    04:12 If you've got a lot of vasodilation, you may see your CVP start to drop.

    04:16 Now, with hypodynamic state, which is the last stage of septic shock, you'll see again more extreme decrease in systemic vascular resistance, which is probably going to cause your CVP to decrease unless you've given a lot of fluid and it's going to cause your PAD or your wedge pressure to decrease.

    04:35 But what's more important is now the heart is starting to get affected.

    04:38 So you'll still see a fast heart rate because that's the last compensatory mechanism that the body has to try to maintain a map but your cardiac output is decreasing because the contractility is just not able to contract hard enough in the last stage of sepsis.

    04:53 So now that we know the four parts of blood pressure, we know how they relate with one another and we know how they are affected during shock.

    05:00 We need to start learning what can we do about it.

    05:02 What intervention can we do that will start affecting these four parts of blood pressure and allow them to compensate so that we can increase our main arterial pressure.

    05:14 So starting with our heart rate.

    05:16 If our heart rate is too low, that's decreasing our mean arterial pressure, what can we do to increase it? Well, the first thing that we can do is atropine.

    05:27 Atropine basically increases the heart rate because it works on the parasympathetic nervous system.

    05:32 It doesn't really actually increase the heart rate, what it does is it prevents the body's parasympathetic nervous system from decreasing the heart rate.

    05:41 So it really allows that SA node to start beating a lot faster.

    05:46 Now, atropine may not work in a complete heart block because there is complete separation from that SA and AV node to the Purkinje fibers of the of the ventricles.

    05:57 So if you're in a complete heart block, and you need to increase heart rate, atropine probably is not going to work.

    06:03 The next thing that we can do for heart rate if we need to increase it to increase blood pressure is a pacemaker, we can transcutaneously pace with patches to increase that heart rate.

    06:15 Also, the patient could be taken to the cath lab to get a temporary pacemaker, and then eventually a permanent pacemaker to increase that heart rate.

    06:23 Now, if the heart rate is too high, and we need to decrease it, what can we do to decrease that heart rate? Well, we can use a beta-blocker, most commonly metoprolol or labetalol, or some of these beta-blockers, which the goal of that is to decrease heart rate.

    06:41 Just know that a beta-blocker will also decrease contractility.

    06:45 So you'll see cardiac output start to drop with that.

    06:49 We can also use a calcium channel blocker that is selective with with the heart, Diltiazem will decrease heart rate because it's selective with the heart.

    06:59 Now, calcium channel blocker like Nicardipine is more selective with smooth muscle, and that causes vasodilation.

    07:06 So you need to use a calcium channel blocker that is selective to the heart to decrease heart rate.

    07:13 Going on to contractility.

    07:15 If we've identified that the reason our blood pressure is low is because we do not have enough contractility.

    07:20 How do we increase contractility? Well, we can increase contractility by an Inotrope.

    07:27 The goal of an inotropic medication is to increase that contractility that squeezed power of the left ventricle.

    07:37 The inotropes that we have are epinephrine, dopamine, dobutamine and milrinone.

    07:43 Now don't worry about these medications, we're going to go over them more in depth later on in the series.

    07:50 So just know if I want to increase my contractility, I need a medication that is an inotrope.

    07:56 But what if our contractility is too high? What if the cardiac output is above 8? Well, remember, that's an hyperdynamic left ventricle, and we need to give fluids to help lower that cardiac output to help just relax that left ventricle, stretch it out a little bit and and bring that hyperdynamic left ventricle back to a normal dynamic state.

    08:20 Alright, moving on to our vascular resistance.

    08:24 What if we noticed that our blood pressure is too low because we're vasodilated? Our SVR is 600 and we are vasodilated causing our map to be too low.

    08:35 Well, we can use medications that vasoconstrict.

    08:38 Those medications we have are Levophed, vasopressin, phenylephrine and angiotensin II.

    08:45 Those medication's jobs, the primary jobs are to vasoconstrict.

    08:50 Well, if our blood pressure is way too high, and we find that our SVR is 2000 that means we're too vasoconstricted.

    09:00 So how do we vasodilate? How do we expand the aorta and the arterioles to decrease our blood pressure? In order to do that, you need vasodilators, you need medications that would vasodilate the aorta and the arterioles.

    09:17 Those medications are nitroglycerin, nicardipine, Cleviprex and hydralazine.

    09:24 Now, our last part is fluid volume status.

    09:26 If we've identified that our blood pressure is too low, because we don't have enough blood volume, our tank is empty.

    09:34 What can we do? We can administer blood products, we can administer albumin and we can administer crystalloids.

    09:42 Crystalloids are normal saline so we can administer those to get more volume.

    09:50 Now, what happens if we're too hypervolemic, we've got too much volume on in our vasculature? We can administer administer diuretics to help us pee out some of that fluid and if that's not working we can go to dialysis to remove some of that fluid.

    About the Lecture

    The lecture Hemodynamic Changes in Shock (Nursing) by Corey Hardin, BSN, RN, CCRN-CMC, CV-BC is from the course Hemodynamic Concepts and Values (Nursing).

    Included Quiz Questions

    1. Decreased cardiac output
    2. Increased systemic vascular resistance
    3. Vasodilation
    4. Decreased central venous pressure
    5. Increased contractility
    1. Increased heart rate.
    2. Decreased central venous pressure.
    3. Decreased pulmonary artery diastolic pressure (PAD).
    4. Increased cardiac index.
    5. Increased systemic vascular resistance.
    1. Cardiac output is increased in the hyperdynamic state and decreased in the hypodynamic state.
    2. Systemic vascular resistance is increased in the hyperdynamic state and decreased in the hypodynamic state.
    3. Central venous pressure is decreased in the hyperdynamic state and normalizes in the hypodynamic state.
    4. Heart rate is decreased in the hyperdynamic state and increased in the hypodynamic state.
    1. Nitroglycerin
    2. Vasopressin
    3. Levophed
    4. Phenylephrine
    1. Metoprolol
    2. Atropine
    3. Epinephrine
    4. Dopamine

    Author of lecture Hemodynamic Changes in Shock (Nursing)

     Corey Hardin, BSN, RN, CCRN-CMC, CV-BC

    Corey Hardin, BSN, RN, CCRN-CMC, CV-BC

    Customer reviews

    5,0 of 5 stars
    5 Stars
    4 Stars
    3 Stars
    2 Stars
    1  Star