Today, I'm going to be talking about some important aspects of right heart function. Hello, this is Cliff Grayson. I'm an associate professor of medicine at the University of Colorado School of Medicine and a staff cardiologist at the Rocky Mountain Regional VA Medical Center in Aurora, Colorado. I have, regrettably, no disclosures. Specifically, I'm going to focus on how the RV's shape, structure, and blood supply affect its normal function and its response to stress. Way back in 1943, Starr and colleagues anesthetized dogs, opened their chests, then destroyed the RV free wall with, as they said, a red-hot soldering iron. Surprisingly, they found minimal impact on systemic hemodynamics, and they specifically noted that there were no increments of venous pressure, what we might observe as an increase in jugular venous distension. Maybe they speculated the RV served no purpose other than as a conduit for venous return. Well, of course, we know that's not really true, at least in children. Indeed, in newborns, the RV generates nearly systemic pressures. But as you can see from this graph, RV pressure declines rapidly and reaches adult pressures over the first several days of life. It's worth reviewing normal hemodynamics in the RV and LV in adults. Remember that normal left ventricular diastolic pressure is actually quite low in healthy spontaneously breathing adults, usually less than 12 millimeters of mercury. And right atrial, or central venous pressure, is even lower, typically less than 5 millimeters of mercury at rest. Transpulmonary vascular resistance is only a fraction of systemic resistance, so low in fact that normal transpulmonary flow can continue even without a functioning RV free wall, as was seen by Starr and colleagues. That's a good thing because the RV is strikingly weak compared with the LV. This shows changes in stroke volume as a fraction of control in the RV compared with the LV as RV or LV pressure load is increased. As the load on the RV rises from 15 millimeters of mercury to only about 30 millimeters of mercury, stroke volume generated by the RV declines dramatically. The LV, in comparison, generates much higher pressures at baseline, of course, and maintains stroke volume over a much larger increment in pressure. So is the right ventricle just for kids? It does seem that RV function isn't very important in healthy adults. In this investigation, Brooks and colleagues showed that RV contractile function doesn't seem to be important for overall hemodynamics at all. This is a tracing that shows LV pressure and RV pressure after RV function is reduced by occluding the right coronary artery. Even though RV free wall function plummets, seen in the lowest tracing here, systemic hemodynamics remain essentially normal. Notice that RV diastolic pressure remains well under 5 millimeters of mercury. Under normal conditions, pulmonary vascular resistance is so low that even ablating RV function by interrupting right coronary artery flow, which provides essentially all the nutrient flow to the RV free wall, doesn't affect overall hemodynamics in any measurable way. But under conditions that are common in our business, the RV becomes critically important. This is from that same investigation by Brooks. After obtaining the hemodynamic tracings I showed you just a moment ago, they then constricted the main pulmonary artery to modestly raise RV pressure to about 40 millimeters of mercury. At first, it didn't seem to make much difference. And you can see here that the RV diastolic pressure remained under 5 millimeters of mercury. In other words, there was no evidence of right heart failure. But once they constricted the right coronary artery, everything went south with progressive declines in both aortic pressure and flow. So with modestly elevated RV pressure, contractile function of the RV free wall does become necessary to maintain systemic pressure. So Starr was wrong. The RV isn't just for kids. While it's true that under normal baseline conditions, the RV doesn't need to work very hard to support high flow at low pressure, during conditions that are common in both disease states, such as respiratory failure, and under healthy stress states, such as intense exercise, the RV needs to kick in and support higher pressures, at least for short periods of time. But it turns out that one of the RV's critical functions under normal hemodynamic conditions is to buffer blood return from the venous circulation and to accommodate the variation in venous return without changing stroke volume. It's this function where some of the differences from the LV are most dramatic. Consider, because of changes in intrathoracic pressure, it turns out that respiration causes enormous breath-to-breath variability in venous return without any corresponding need for a change in LV stroke volume or systemic pressure. And of course, ordinary changes in posture lead to dramatically conflicting hemodynamic responses. Specifically, when you go from an upright to a supine position, you increase venous return, but you decrease demand on the LV. You've all studied cardiac physiology and are intimately familiar with the Frank-Starling relation. This figure shows how, with increasing diastolic volume, we get increasing stroke volume and increasing developed pressure. With large breath-to-breath variation in venous return, you would expect RV stroke volume and RV pressure generation would vary wildly with every breath. Of course, we actually don't want that to happen. Under normal conditions, we don't want the RV to follow the Frank-Starling relation and we don't want the RV to generate higher pressure during ordinary changes in venous return. We do want the RV to be able to accommodate increases in demand. This figure, from a report by Santamore and Amore, modeling different components of the circulatory system, illustrates how the normally large breath-to-breath variation in venous return, seen in the leftmost trace, is buffered by downstream vascular structures. A large amount of buffering occurs in the RV, allowing LV stroke volume to remain fairly constant. So how does the RV accommodate normal breath-to-breath variability in venous return without changing pressure or stroke volume and yet still support higher pressure when it needs to? Well, it turns out much of the magic is in the shape. Let's start with RV anatomy. Here are cross-sections through the heart from apex to base. You can see that the RV shape is dramatically different depending on how you slice it. This complex shape accounts for why it's so difficult to quantitatively measure RV size and function, and why 3D imaging techniques are so important. But the important point here is that the bulk of the RV's volume is encompassed by a thin, flattened, crescentic wall. This shape is both the boon and the bane of RV function. This shows roughly how the RV and the LV eject blood. This is of course highly simplified and neglects any twisting or peristaltic characteristics of ventricular motion, but roughly speaking, the LV can be modeled as a cylinder and its basic shape doesn't change that much during systole. As the LV contracts, the wall thickens, the radius decreases, and the surface area of the LV endocardium and epicardium both decline. In contrast, ejection from the RV is not so much a function of a uniform reduction in RV free wall surface area as it is due to a bellows-like flattening of the RV free wall over the interventricular septum. This difference has a number of important consequences. First, RV ejection fraction under normal loading conditions bears very little relationship to RV free wall surface area changes. In fact, you can get flow into and out of the RV with absolutely no change in RV free wall surface area whatsoever. Second, the radius of curvature of the RV actually increases during contraction rather than decreasing as happens in the LV. According to the Laplace relationship, a smaller radius of curvature has lower wall stress. LV contraction results in a reduction in radius of curvature and this size-dependent reduction of stress during systole facilitates LV ejection. When you let air out of a balloon, that little puff that you hear right at the end is also a consequence of that. Because RV ejection occurs during flattening of the RV free wall, radius of curvature actually rises during ejection of the RV. If anything, this flattening reduces the RV's capacity to generate pressure. So that's how the RV ejects blood. How does the RV fill? Most of us were taught to think of ventricular filling as being due to rising pressure from venous return, that could be systemic or pulmonary venous return, depending on whether you're talking about the right or the left ventricle. In the left ventricle, this rising pressure is due to blood passively moving through the lungs under the pressure differential between the pulmonary artery and the left atrium. In the right ventricle, we think of central venous pressure as driving flow into the right atrium. But in reality, there's a huge contribution to the pressure differential and filling from so-called restoring forces or elastic recoil. This is well known to be an important contributor to LV diastolic filling, but it's actually an even larger contributor to RV diastolic filling. While the panel on the left reflects how most of us typically view right ventricular filling, in reality, the RV spends much of its diastolic life at subatmospheric pressure. This is in small part due to negative intrathoracic pressure during expiration, but it's even more a result of this elastic recoil. Let's talk about how the RV responds to increases in load. Recall that the LV and the RV share the same space, with the pericardium constraining their total combined volume. Since the pericardial space is filled, increments in RV volume cause minimal increments in RV free wall surface area, and further increases in RV volume occur mainly through shifting of the interventricular septum at the expense of the LV. If you don't increase the surface area of the RV free wall, you don't stretch the muscle, and if you don't stretch the muscle, you don't get recruitment of function via the Frank Starling mechanism. Under normal conditions, the crescentic RV flattens insistently, leading to a large volume change with minimal change in RV free wall area. As we just discussed, under normal conditions, the RV fills mainly at an unstressed volume and doesn't depend on the Frank Starling mechanism at all. Under conditions of mild RV pressure and volume overload, small increases in RV free wall area enhance RV function via the Frank Starling mechanism. During moderate RV pressure and volume overload, the interventricular septum begins to shift. At that point, RV end-diastolic volume begins to increase with less change in end-diastolic RV free wall area and a decrease in left ventricular end-diastolic volume. In part, this is due to pericardial constraint, which limits the total volume of the heart. As RV volume increases further, there may be no further recruitment of RV function via the Frank Starling mechanism at all, while at the same time, there can be a loss of function in the left ventricle from the Frank Starling mechanism. But notice that the RV is taking on a more circular appearance. This leads to a reduction in the change in stroke volume for any given change in RV free wall surface area, equivalent to shifting into a lower gear on a bicycle. In essence, the RV is switching from a volume pump to a pressure pump. During severe RV pressure overload, the septum shifts even further, at which point the paradoxical motion of the septum can actually enhance RV output but will worsen LV output. Between the shape of the RV and the normally low or sub-atmospheric diastolic pressure, preload for the RV is a completely different matter compared with the LV. Under normal conditions, RV preload is unrelated to RA pressure. Shape change, not stretch or strain, accounts for most RV volume change under normal conditions. Under normal conditions, the RV at end-diastole is unstressed, in contrast with the LV, which is usually stressed at end-diastole. Unlike the LV, the RV rarely uses the Frank-Starling relation to augment stroke volume, at least under normal conditions. When the RV needs to use the Frank-Starling relation, it can, but only to a limited extent. These differences have major consequences for clinical management in the intensive care unit. The first thing most intensivists try when a patient is hypotensive is volume loading, but volume loading is maladaptive in right heart failure for a number of reasons. As we just discussed, pericardial constraint causes enhanced interventricular interaction in LV-SSH, which is exacerbated by volume loading. SSH can actually lead to higher left atrial pressure, which was already raised to some extent by the volume loading. High LATP increases the load on the RV, directly of course, through back transmission of pressure through the pulmonary circulation, but also indirectly because high LATP decreases compliance of the pulmonary vasculature, which increases RV pulse pressure. Together, these further impair RV free-wall function, leading to further septal shift and a vicious cycle ensues. For this reason, and in part because of differences in the RV energy supply that we'll discuss in a moment, vasoconstrictors rather than volume loading should probably be your first go-to in hypotension from RV failure. While it's common to think of ventricular interaction as occurring only under abnormal conditions, in fact, under normal conditions, the LV may contribute up to 40% of RV function via the septum and shared fibers. In this experimental study, Damiano and colleagues electrically isolated the LV and the RV from each other, then measured RV and LV pressure when the two chambers were individually electrically paced. The lower right panel shows the RV pressure generated by RV pacing alone, while the upper right panel shows RV pressure generated by LV pacing alone. Even without any RV free-wall contraction, there is a significant pressure signal provided by the LV and its shared structures. Not surprisingly, the RV doesn't normally add that much to the LV, as seen in the lower left panel. This shared structure issue partly explains why disrupting blood supply to the RV free-wall doesn't necessarily result in significant hemodynamic abnormalities. Conversely, unloading the LV using support devices or medications can reduce its contribution to RV function, which is one of the main reasons that LVADs can abruptly worsen right heart failure. A moment ago, I alluded to differences in RV and LV energy supply. As everyone knows, coronary perfusion to the LV is heavily dependent on the pressure differential between the aortic root, where the coronary ostea live, and the myocardial venous system. This perfusion occurs almost exclusively during diastole, as seen in the right panel here. This is because during systole, LV tissue pressure rises to equal aortic root pressure and effectively stops coronary perfusion. In the RV, in contrast, unless RV systolic pressure exceeds aortic root pressure, coronary perfusion continues through the cardiac cycle and, in fact, is often or even generally higher during systole than during diastole, as seen in the left panel. Systemic hypertension can cause left ventricular subendocardial ischemia due to increased demand, but left ventricular coronary flow doesn't normally decline during systemic hypertension. Conversely, as RV pressure begins to approach aortic pressure, RV perfusion can fall dramatically, as seen in the right panel, where right coronary flow declines to near zero during systole with an overall reduction in flow compared with normal conditions, as seen in the left panel. An appropriate choice of a vasoconstrictor agent can increase aortic pressure without worsening pulmonary hypertension and thereby reverse RV ischemia, interrupting a vicious cycle of right heart failure. Recall the key differences in the response to vasoactive stimuli between the pulmonary and systemic circulations. Pulmonary arteries constrict in response to hypoxia. Systemic arteries dilate. That makes physiologic sense. You want comparatively less flow to underventilated parts of the lung, but you want more flow to go to ischemic tissue. In general, response of pulmonary vessels to extrinsic vasoconstrictors is weak. That's good, because by the time circulating catecholamines are rising, you're probably already dealing with pulmonary hypertension and an additional load on the RV is undesirable. It may be clinically relevant that the response of pulmonary vessels to vasopressin is much lower than their response to alpha agents like phenylephrine. This may have practical application when thinking about what agent to use to maintain blood pressure in the setting of right heart failure from RV pressure overload, as we just discussed. At least in theory, vasopressin may be a better choice than phenylephrine or norepinephrine, although I can't point to any clinical studies to prove it. Finally, I have to say something about the tricuspid valve, which has been overlooked for decades. Over the past few years, there's been an increasing appreciation for its importance. I show this video to emphasize the delicacy of the tricuspid valve. Also, I think it's a really cool website from the University of Minnesota. Similar to how we can see functional mitral regurgitation as the mitral valve annulus dilates, as the right atrium and right ventricle dilate, the tricuspid annulus stretches and flattens and coaptation of the tricuspid leaflets begins to suffer. This can lead to progressive tricuspid regurgitation and worse volume overload of the RV, creating a vicious cycle just as we see in severe mitral regurgitation. This is another reason to avoid volume loading in the setting of right heart failure, and in fact, one of the reasons that diuretic therapy can be so helpful, just as it is in mitral valve disease. So to sum up, the RV may be wimpy, but it's not a wimpy left ventricle. The RV gains strength through its wimpiness. The ability to dilate without stretching is the key to the RV's function. The effect of the LV on the RV is different from the effect of the RV on the LV. This is a consequence of having two very different types of hearts in one package. The LV makes a major contribution to RV systolic function via the interventricular septum and shared fibers. The RV makes a contribution to LV diastolic function when the RV is stressed by impairing LV filling. The RV can find strength when it needs to by acting more like the LV, but only to a point. Thanks.

right heart function

shape of right ventricle

blood supply

RV and LV filling

clinical management

tricuspid valve