Right heart failure is very misunderstood and often ignored. I am hoping to simplify right heart failure to its base hemodynamics. This should make understanding the management easier. The main takeaway from all of this should be that we should respect it more and stop teaching people to give fluids for right heart failure.
Breaking down cardiac output in terms of the right heart
I have separated out cardiac output before, but I did it referencing the hemodynamics of left heart failure. Here, I will break down the right heart into its four core components (Figure 1).
Figure 1:
Heart rate is the first of the 4 core components. It is not unique to the right heart. If the patient is inappropriately bradycardic, it can lead to a low cardiac output. Since it is not unique to the right heart, I will not discuss it in greater detail in this post. The other extreme can lead to heart failure with significant tachycardia, like SVT, but that is due to a loss of stroke volume more than an increase in heart rate leading to a drop in cardiac output. But, the issues do come from the increased heart rate, so it is a gray area.
This leaves the 3 core components for right heart failure: too much preload, not enough contractility, and too much afterload. Each one of these will be a post and then a final post discussing the overall management.
1. Preload
Definition: the stretch of the cardiomyocytes at the end of diastole. It is often referred to as ventricular filling or the volume in the right ventricle at the end of diastole (RVEDV).
Disease physiology: The right ventricle handles preload significantly better than the left ventricle. It is thin and can stretch much easier than the LV which is thicker. This is one of the reasons for the misguided belief of fluid being the treatment for right ventricular failure. As shown in figure 2, volume was added and the increase in right and left atrial pressure was graphed against the increase in work of the ventricles. The left ventricle has a significant increase in work compared to the right ventricle.
Figure 2: RV vs LV work increase in response to increased preload (1)
When there is too much preload it overstretches the cardiomyocytes and will move the patient to the descending limb of the Starling curve. The right ventricle does have a Starling curve just like the LV (Figure 3).
Figure 3:
Additionally, increased preload stretches the ventricle which separates the tricuspid valves and since they cannot stretch with the ventricular dilation this causes tricuspid regurgitation. The tricuspid regurgitation leads to the reversal of flow back into the venous system. The pulsatile reverse flow causes renal and hepatic congestion and leads to organ dysfunction.
There are preload problems that occur in the right ventricle that do not occur in the left ventricle. These problems are septal flattening and pressure-related ischemia. The septum is usually bowed to the right ventricle since it is part of the left ventricle. The left ventricle usually has more pressure and therefore it remains rounded, whereas the right ventricle is a thin wall attached to the LV and does not push the septum except during certain disease states. This has been referred to as pericardial compartment syndrome, but basically, if the right ventricular volume is excessive, during diastole it can flatten the ventricular septum. This will cause a decrease in LV preload since it cannot fill as well. It is known as the “D” sign on echo since it resembles a D in the parasternal short view (Figure 4).
Figure 4: Right ventricle during diastole
Another unique complication to the right heart is an increased risk for ischemia related to pressure. The right ventricular wall is thin, when it gets overdistended it can cause a collapse of the small arterioles and capillaries and increase ischemia. RV failure due to increased preload only is not common and is typically only seen with atrial or ventricular septal defects in children (1).
Too little preload would also lead to less stroke volume but decreased preload would be due to hypovolemia more so than diastolic dysfunction leading to worse preload.
Measuring Preload:
Being able to determine if a patient has too much preload is the most important part. You can know the physiology and treatment, but if you cannot identify that a patient has too much preload it will not make a difference.
CVP:
Central venous pressure has never been shown to be reliable in determining volume status in a patient. Potentially it could be helpful at the extremes, but it is difficult to use it consistently and it is invasive. Let us explore how CVP could represent preload.
CVP is a surrogate for
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RAP, which is a surrogate for
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RVEDP, which is a surrogate for
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RVEDV
The end answer is that we are trying to make a pressure represent a volume. In order for a pressure to represent a volume, there would have to be a linear relationship (Figure 5).
Figure 5: Incorrect assumption for pressure and volume
This is not an accurate representation of the pressure versus volume relationship. The actual relationship can be seen on the pressure-volume loop of the RV. The pressure-volume loop of the RV is different from the LV because there is no isovolumetric contraction or relaxation. The bottom of the loop is the pressure change with adding volume during diastole with the end-diastolic volume in the bottom right (Figure 6).
Figure 6: Right ventricular pressure-volume loop (2)
This shows that there is a large volume increase before seeing any significant change in pressure. An elevated CVP is often a late finding of too much preload. When you consider that diastolic dysfunction makes a whole new pressure-volume curve, which is higher up than the original, then CVP becomes even more unreliable (Figure 7).
Figure 7: Diastolic dysfunction and pressure-volume loop
The end result is that CVP is unreliable on a physiological level. It may be helpful in trends. If the patient’s CVP was 15 mmHg and now it is 6 mmHg, that probably means a decrease in volume.
RV dilation/Tricuspid regurgitation/pulsatile flow:
As mentioned above, when the RV gets overdistended, the tricuspid valve separates and there is tricuspid regurgitation that worsens as the overdistention worsens. This regurgitation causes reversal of flow and the venous blood goes back into the liver and kidneys. Tricuspid regurgitation can be organic, as in endocarditis, but most often in the ICU is functional due to volume overload and right heart dysfunction.
All of this can be seen on bedside echo and can help guide volume status. VExUS is a great way to look at the venous system and assess for congestion (Figure 8). If there is congestion this means there is too much volume for the current hemodynamic state.
Figure 8: VExUS Protocol
There is a caveat to this which will make more sense when we go over increased afterload, but increased afterload can lead to the same dilated RV with TR and a “relative” increased preload since the blood cannot go right to left, even if the body is overall euvolemic or hypovolemic. When the afterload is corrected the RV dilation and tricuspid regurgitation improves.
RVEDVI:
Directly measuring RVEDV is not commonly done but has been studied. RVEDV divided by body surface area (BSA) is the right ventricular end-diastolic volume index (RVEDVI). RVEDVI has been shown to be a better indicator of preload. It is calculated with both ultrasound and a pulmonary artery catheter. It has also been shown to correlate well with left ventricular preload. The stroke volume of the LV and RV should match, so it fits that the preload should be reliable (3). Calculating RVEDVI with echo is done with area x length x constant. This can be done in the apical 4 view (Figure 9). It can also be done with the Simpson biplane method.
Figure 9: Area x length method of RVEDV (4,5)
The RVEDV/RVEDVI can also be assessed with a volume-based pulmonary artery catheter. It is specialized and uses an algorithm to calculate the RVEDV and RVEDVI.
D-sign:
Extremely elevated preload can lead to a D-sign in diastole as mentioned above. This is seen in parasternal short, and if it is during systole it is a pressure problem, discussed in part 3. Since a diastolic D-sign occurs when severe volume overload and is seen late and therefore less helpful for diagnosing early.
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For a deeper dive:
GEDV:
The global end-diastolic volume measures the volume in all 4 chambers. This can be calculated using the transpulmonary thermodilution catheter. This is also divided by BSA for a global end-diastolic index (GEDI), normal 680-900mL/m2. This requires specialized equipment so I will not go into more detail here.
Stroke volume variation:
This is not an actual measure of preload and more of an evaluation of fluid responsiveness during resuscitation. If there is no volume responsiveness seen, you may be able to say the there is normal or too much preload. This can be evaluated using the arterial line, or more in-depth using a device that measures the actual percentage of stroke volume variation (SVV). The Vigileo-FloTrac is a version of this where the is no SVV when the change is <13% (Figure 11). It is used more for resuscitation and not preload evaluation.
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Summary:
Increased preload can lead to significant RV dysfunction and heart failure. It is important to evaluate for too much preload and treat if found. I use venous pulsatility and VExUS as my main method and will try to make sure that I have optimized afterload. By optimizing afterload I hope to make sure it is not related to high pressure and just increased preload.
Figure 12: RV Preload
References:
1. Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. doi:10.1513/AnnalsATS.201312-446FR
2. Bellofiore A, Chesler NC. Methods for measuring right ventricular function and hemodynamic coupling with the pulmonary vasculature. Ann Biomed Eng. 2013;41(7):1384-1398. doi:10.1007/s10439-013-0752-3
3. Durham R, Neunaber K, Vogler G, Shapiro M, Mazuski J. Right ventricular end-diastolic volume as a measure of preload. J Trauma. 1995 Aug;39(2):218-23; discussion 223-4. doi: 10.1097/00005373-199508000-00006. PMID: 7674388.
4. Partington SL, Kilner PJ. How to Image the Dilated Right Ventricle. Circ Cardiovasc Imaging. 2017;10(5):e004688. doi:10.1161/CIRCIMAGING.116.004688
5. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):685-788. doi:10.1016/j.echo.2010.05.010
Nice article!