This lesson is a follow up to the Hemodynamics lesson. If you haven’t watched it yet, we highly recommend you watch that before you watch this one! In this lesson we are going to delve deeper into the world of Preload and Afterload, as well as touch on Contractility.

If you remember from the Hemodynamics lesson, Cardiac Output = Stroke Volume x Heart Rate. And the three factors that help determine Stroke Volume are Preload, Afterload, and Contractility. So let’s zoom in on these three one at a time and then we’ll bring it back together again at the end.

Let’s start with Preload. There are a lot of ways that people use to understand preload. The best way to understand it is as stretch. It’s the amount that the heart stretches because of how much it is filled. So it’s the blood returning to the heart that impacts preload. Think Pre = before, so it’s about the volume just before it returns to the heart. During diastole, the heart is filling up with blood. It’s completely full at the end of diastole - just before the ventricles contract. So one of the ways we measure Preload is with something called End Diastolic Volume. In clinical practice, though, it requires an echocardiogram to get that measurement. Instead, we are able to use a central line inserted into the superior vena cava to measure pressures in the right atrium - remember this is where blood returns from the body. That pressure is called Central Venous Pressure, or CVP. The normal CVP for a healthy person is around 2-6 mmHg. Because preload is defined as the stretch on the muscle, it’s not exactly a volume or a pressure, but those measurements give us a good idea of how much the heart is stretching.

As we begin to understand preload better, I want you to think about a balloon. The preload is how much you blow it up. How much air are you putting into the balloon? How much is it stretching?

So...what kinds of things can cause a change in preload? Anything that decreases the return of blood to the heart. Hemorrhage...dehydration...or even massive peripheral vasodilation. If all the blood is pooling in the body, it’s not making it back to the heart, right? So how can we improve someone’s preload if it’s too low? Well we should always treat the cause. Usually that means giving fluids or blood products. But what if their preload is too high? Maybe they’re volume overloaded because of heart failure or kidney failure? In this case we can give diuretics or ACE inhibitors, or we could even give vasodilators to relieve the filling pressure on the heart.

To better understand the impact of preload, we have to understand something called Frank Starling’s law. What this law says is that the more the heart muscle stretches the stronger it will contract and therefore the higher the stroke volume. So, ultimately, more stretch, more force. What you see is that as the preload increases, so does the stroke volume. However, this effect is limited. At a certain point, this curve will begin to level off, meaning that more preload won’t actually lead to an increased Stroke Volume. Remember your balloon - the more you fill it with air, the more it stretches, the more forcefully it will push that air out when you let it go, right? BUT, at a certain point, putting more air into the balloon will no longer cause more stretch and force...what happens? The balloon pops! Now, the heart itself doesn’t pop, but it does stop responding to preload at a certain point.

So why is this important? A few reasons. First, the curve itself explains why low blood volume or dehydration can make such a difference in the patient’s cardiac output! It’s decreasing their preload and therefore their stroke volume. We also need to understand that at a certain point just giving fluids won’t be enough and we will have to address something else. Finally, it’s important to realize that everyone’s Frank-Starling Curve looks different. One person might require much more preload to get any change in their stroke volume, while another might respond really well to just a little bit of preload. Ultimately, we need to see how well the patient responds and address each patient’s needs individually.

So let’s talk about afterload. When the heart contracts during systole, it has to contract strong enough to overcome the pressure on the other side of the aortic and pulmonic valves, right? It would be like someone trying to hold your door shut - you have to push harder to get the door open! The force that the heart has to overcome is called Afterload. Think about it this way. Afterload is what the heart has to pump Against. The higher the afterload, the harder the heart has to work against it to eject the blood. In other words, it’s the resistance in the vessels that the heart has to overcome. So there are two measurements of afterload, one for the right side of the heart, called Pulmonary Vascular Resistance, or PVR, and one for the left side of the heart, called Systemic Vascular Resistance, or SVR. SVR is the most common measurement we use for Afterload. Normal SVR is 800-1400. It’s important to note that an increased SVR is closely correlated with an increase in blood pressure.

Things that cause an increased afterload are hypertension, blood clots blocking the vessels, and vasoconstriction. Remember it’s the resistance in the vessels. Decreasing afterload can help to decrease blood pressure and also decrease the workload on the heart - we can do that with vasodilators and antihypertensives - or by getting rid of any clots. Things that cause afterload to be too low would be things like massive peripheral vasodilation, or low blood pressure caused by other issues. So first we always want to treat the cause, but we can also give vasoconstrictors or vasopressors like norepinephrine, epinephrine, neosynephrine, and vasopressin. This will increase their afterload and therefore their blood pressure.

So, I’ve mentioned massive peripheral vasodilation twice now - it affects both preload and afterload and can cause major cardiac output issues - we see this the most in distributive shocks like septic and anaphylactic shock - so be sure to check out that lesson later in this course!

The final component to stroke volume is contractility. This is the strength or force of contraction. If we find that the heart is working too hard and we want to decrease the force of contraction, we would give negative inotropes - something like a beta blocker or calcium channel blocker. If we find that it isn’t beating strong enough, we would give a positive inotrope - this could be cardiac glycosides like digoxin or sympathomimetics like epinephrine.

Ultimately, though, if my preload and afterload aren’t optimal, the force of contraction or contractility won’t be enough to provide sufficient cardiac output - we have to optimize all three to get a good stroke volume.

So let’s recap - cardiac output equals heart rate times stroke volume, and there are three factors affecting Stroke Volume - Preload, Afterload, and Contractility. Preload is the stretch of the heart muscle when it fills during diastole. The more stretch, the higher the stroke volume - but only to a certain extent because of Frank Starling’s Law. Afterload is the resistance that the heart has to pump against in order to eject blood out of the ventricles during systole. Contractility is the strength or force of contraction of the heart muscles during systole. And finally don’t forget about the balloon analogy. The more you fill it, the stronger you squeeze it, and the tighter you hold the opening will all determine how much air comes out at a time. This is a great way to understand how to improve cardiac output. Does it need to be filled up? Am I not squeezing it hard enough? Or am I holding the opening too tight?

We really hope this has helped you to understand these hemodynamics and how they affect our cardiac output. As you progress through the Cardiac Course and learn more about various disease processes, you will see how these things factor into their assessment, therapeutic management and nursing care.

Now, go out and be your best self today. And, as always, happy nursing!