00:01 Let's summarize a number of the changes that happen on the Frank-Starling curve. 00:07 This will allow us to bring concepts together because we know they’re hard. 00:12 But if we review them again, we’ll be able to gain better insight into them. 00:16 And as you see them change in close proximity, you’ll be able to comprehend all the different changes that happen because, remember, nothing ever changes in isolation. 00:27 So, let's go through those. 00:29 And increase in preload, you travel along the same curve, but just two upward points. 00:37 A decrease preload, use the same curve again. 00:41 But now, you're going down in the curve, which means you're at a lower left ventricular end-diastolic pressure. 00:50 If you have an increase in inotropy or a decrease in afterload, you shift the whole curve to the left and upwards a little bit. 01:00 That means per amount of left ventricular end-diastolic pressure you’re going to get a greater stroke volume. 01:09 If you have an increase in afterload or a decrease in inotropy you get a shift in which the curve moves downward and to the right. 01:18 This means that at any given left ventricular end-diastolic pressure you’re going to have a lower stroke volume. 01:26 Now, let's really dive in to these interrelationships because there are certain times that the body is going to change multiple things at the same time. 01:38 So, let's take a good example that is a fight or flight response. 01:42 This is something where your body is going to have to respond to something and runaway. 01:47 To be able to do that, you're going to have to increase your cardiac output. 01:51 So how are you going to do it? Well, there are a couple of mechanisms that you can start with. 01:56 The first mechanism that you’re going to go through here is you're going to increase the left ventricular end-diastolic volume. 02:06 You're also then going to increase the end-systolic pressure-volume relationship. 02:12 So, both of these effects are going to occur almost at the same time. 02:18 Now the change in left ventricular end-systolic pressure-volume relationship, that is a change in inotropy. 02:25 The change in the increase in left ventricular end-diastolic volume, that is a change in preload. 02:31 So, that is our inotropic change and our preload change. 02:37 Interestingly, what that allows then to happen is for greater stroke volume than would've occurred with either one of them independently. 02:47 So, this sympathetic stimulation utilizes multiple mechanisms /to make that curve as wide as possible and that wide curve gives you a bigger stroke volume. 02:59 If you have a large stroke volume, then all you need to do is beat more frequently and you’ll have a higher cardiac output. 03:07 The top part of the heart also responds to a number of changes in preload, in afterload, in inotropy. 03:16 And these changes will occur and help to facilitate the amount of venous return, or sometimes, we’ll just refer to that as preload. 03:27 If you have an increase in venous return, you will have a greater contraction of the left and right atria. 03:34 That should fill the left ventricles to a greater degree. 03:40 However, if you have too much flow in those areas, you can lead to things like regurgitation of the valve; and sometimes if there are stenotic valves, you can also get some buildup of fluid within the ventricles. 03:56 A lot of stimulation with nerves also affect the atrium's ability to contract. 04:02 There, a sympathetic nervous stimulation will give an increase force of contraction, and vagal stimulation typically allows for greater amount of failing to occur, but does not change ionotropy.
The lecture Frank-Starling Curve and Atrial Dynamics – Cardiac Mechanics by Thad Wilson, PhD is from the course Cardiac Physiology.
Which of the following cardiac changes will increase stroke volume?
Which of the following physiological conditions causes a greater atrial contraction?
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I enjoyed the breakdown of each intricate part of the system. I feel that I understand pharmacology better, especially digoxin and its effect on the heart.