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Heart Failure: Etiology and Compensatory Measures (Nursing)

by Rhonda Lawes, PhD, RN

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    00:01 Let's look at the etiology of heart failure.

    00:03 Something bad had to happen to the heart.

    00:06 It all starts with a cardiac insult, right? And you have this cardiac insult, which leads to decreased cardiac output. Tada.

    00:16 But wait a minute, we've talked about a lot of other things, right.

    00:19 But what I want you to keep in mind that cardiac insult is all those things we've talked about, what could it be? An MI of alveolar disease, ischemic disease, core, all those things that can cause the heart to be insulted or harmed, which lead to a decreased cardiac output.

    00:41 That means not enough blood or volume is going to be pumped around to my tissues to meet my metabolic needs, and to keep fluid where it's supposed to be kept, right, and it's appropriate space.

    00:52 So there's some insult to the heart.

    00:55 We've talked about all the things that can insult the heart, that leads to a decreased cardiac output.

    01:00 Here's how the body responds.

    01:02 That's what a compensatory measure is.

    01:05 So, heart is damaged, decreasing cardiac output.

    01:09 Here's how the body tries to compensate.

    01:12 You've got the RAAS, which you remember from blood pressure, SNS stimulation. Remember? That's my fight or flight system where you're going to really come, everything goes faster.

    01:22 heartbeats faster, things move faster, and myocardial adaptations.

    01:27 Well, it means that tissue is actually going to get bigger.

    01:31 Sometimes you'll hear it called myocardial remodeling.

    01:34 So, you take a hit cardiac insult.

    01:37 Cardiac output to the point where cardiac output is lowered three main ways the body is going to compensate or try to respond.

    01:46 So, let's break these down a little bit more.

    01:48 Now, I know, you remember the RAAS, the Renin-angiotensin -aldosterone System, right? This is the one that helps raise your blood pressure because when the body senses, "Whoa, whoa, whoa, whoa, that's not an adequate blood pressure for us," that the kidneys, they squirt out renin.

    02:07 Well, they're going to connect up with the livers angiotensinogen and that's going to give you angiotensin I.

    02:14 Now, angiotensin I connects with ACE, Angiotensin Converting Enzyme, then you come up with a bad [unintelligible], you got angiotensin II.

    02:27 This causes really intense vasoconstriction and ends up hanging on to sodium and you hang on to water, so you end up with more volume, because aldosterone tells your body to hang on to sodium.

    02:43 Wherever sodium goes, water follows.

    02:46 When I have more water on board, I have more volume on board.

    02:50 So there are two ways this system that starts with a body recognising blood pressure's not adequate to perfuse all my tissues.

    02:58 Renin + angiotensinogen = angiotensin I + ACE = angiotensin II.

    03:05 When angiotensin II is available in the body, it causes potent vasoconstriction and fluid reabsorption.

    03:14 So, that's the way it raises blood pressure.

    03:19 Now, remember, the RAAS what is meant to keep us safe, but if your heart isn't functioning well, this could be a real problem.

    03:28 Now the second compensatory measure is SNS stimulation.

    03:33 Keep in mind, the heart has taken a hit cardiac insult the decreased cardiac output is the result.

    03:40 One way you respond is the RAAS, we just talked about it.

    03:43 The second way is SNS, sympathetic nervous system stimulation.

    03:48 Now, when this happens, all these neurotransmitters that are released cause increased heart rate in contractility.

    03:56 Okay, so what would that feel like to you? If your heart rate was pumping faster and harder? Would that increase your workload or decrease it? Well, clearly, this would increase the workload of the heart.

    04:10 Faster heart rate, pumping harder, that's what contractility is how hard it pumps.

    04:16 This is going to be really challenging for a struggling heart.

    04:19 In fact, it can be a recipe for disaster.

    04:22 Because all of this is happening in an already exhausted heart.

    04:27 We've got more fluid on board, and we've got the vessels constricted, because of the RAAS.

    04:34 We've got the heart beating faster and harder because of the SNS.

    04:39 And the third one is myocardial adaptations.

    04:43 So, here's a healthy heart.

    04:45 We've got a real close up picture of the wall there.

    04:48 I love that where they show you the cardiac cells there.

    04:51 You've got blood moving through that star arrow that shows us, "Wow, that looks pretty good." Pretty good systemic output there, right, stroke volume.

    04:59 Now, let's look at what happens when the heart muscle seems to be impacted by the workload.

    05:05 Look at that left ventricular wall, what's changed? See how thick it's become? It can't compress and relax as much.

    05:14 Look how much smaller the left ventricle is now than it used to be in the previous picture.

    05:20 And look what the artist has left for you in that arrow.

    05:23 See how it is much smaller in this picture? Yeah, that's to let you know when the body starts making these adaptations in the heart because it's been working so hard initially, it got bigger to try to help, but now it's just way too big and thick and floppy.

    05:39 It's not effective in pushing out the amount of blood volume your body needs.

    05:44 So, let's look at all three of these together.

    05:47 I know we've walked through them, but think about what are the things that could be considered a cardiac insult? Can you write a quick list of them on your slides? Now, when all of those things happen to the point that you have a decreased cardiac output, that's when these compensatory measures kick in.

    06:06 A decreased cardiac output the equals a lower blood pressure.

    06:11 When it's too low, the RAAS kicks in.

    06:16 And that's when you have vasoconstriction and extra volume on board.

    06:19 In addition, the sympathetic nervous system is stimulated and your heart rate will be faster and harder.

    06:27 The last one does not help.

    06:30 Myocardial adaptation means the myocardium becomes hypertrophied.

    06:35 Big and not effective.

    06:37 Remember, each one of these three compensatory measures can be happening in a heart that's already struggling and that's when it becomes especially problematic.


    About the Lecture

    The lecture Heart Failure: Etiology and Compensatory Measures (Nursing) by Rhonda Lawes, PhD, RN is from the course Heart Failure (Nursing).


    Included Quiz Questions

    1. Increased heart rate
    2. Increased contractility of the heart
    3. Vasodilation
    4. Fluid reabsorption
    5. Thickening of the left ventricular wall
    1. Vasoconstriction
    2. Reabsorption of NaCl
    3. Reabsorption of H2O
    4. Hypotension
    5. Increased contractility of the heart
    1. A cardiac insult
    2. Decreased cardiac output
    3. Increased cardiac output
    4. Cardiac wall damage

    Author of lecture Heart Failure: Etiology and Compensatory Measures (Nursing)

     Rhonda Lawes, PhD, RN

    Rhonda Lawes, PhD, RN


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