Continuing on with right heart failure with part 2 of the 4-part series. The next core component to discuss is contractility.
Breaking down cardiac output in terms of the right heart.
Let’s relook at the breakdown of cardiac output into its four core components (Figure 1). I have added in the preload component that was filled out in part 1.
Figure 1: Cardiac output breakdown
2. Contractility
Definition:
Now it is time to define the contractility of the right ventricle and already this is a controversial topic. Right ventricular contractility is defined as the performance of the ventricle at a given filling volume and systolic pressure. This is the definition we use when referring to the Frank-Starling curve and how changes in RVEDV will improve contractility on the ascending limb (Figure 2) (1).
Figure 2: Starling Curve
Whereas, myocardial contractility is the intrinsic ability of the myocyte to contract independent of preload or afterload conditions. Myocardial contractility is the force of the contraction of the myocyte. This force depends on the degree of binding between actin and myosin. To improve this interaction the actin-myosin bridge needs calcium. The more calcium available the better the connection is between the actin and myosin and the greater the force of contraction. Beta-1 agonists and phosphodiesterase inhibitors increase the amount of available calcium.
Disease physiology:
Primary contractility right heart failure is usually due to a right-sided myocardial infarction. The infarct leads to decreased contractility, which leads to less stroke volume through the lungs to the left heart. The decrease in ejected volume causes an increase in both the end-diastolic and end-systolic volumes. The increased volume causes RV dilation and tricuspid valve separation leading to tricuspid regurgitation. The increased volume at end-diastole mixed with the decreased inotropy will put the RV on a new Starling curve for myocardial dysfunction, as demonstrated in Figure 2, which makes it more likely to overdistend and decrease cardiac output. The increasing volume, worsening tricuspid regurgitation, and worsening cardiac output cause RV ischemic due to the increased pressure on the free wall from the volume, organ failure due to venous congestion, and decreased perfusion due to the decreased cardiac output. These all further worsen RV function and a spiral is created leading to death if it is not intervened upon.
The incidence of RV dysfunction being due to pure contractility issues is low in the ICU. The most common cause of RV dysfunction in the ICU is due to increased afterload. However, it is the right-sided MI with RV dysfunction management that is most often taught in medical school and residency. In patients with RV dysfunction due to MI, the patient is more dependent on preload than a patient without decreased contractility. The teaching is to avoid nitrates in patients with concerns for right-sided MI because it will venodilate, drop preload, and make them hypotensive. We have taken this point and over-compensated the other direction and said that right heart failure patients need fluid. This is not the case. If they are volume replete they should not get extra volume because they have RV dysfunction. If they have a primary contractility issue then just make sure they are not hypovolemic. The other component to this myth that gets passed along is due to the decrease in lusitropy. The ischemia will also cause a decrease in lusitropy which will cause diastolic dysfunction and an increase in pressure on the pressure-volume curve. This increase means that there will be a higher RVEDP for the same RV volume. This increase, which is measured with CVP, has led providers to say that RV failure patients need higher CVPs, which people equate to more volume. In my previous blog, I discussed why CVP measurements were unreliable, and trying to use CVP in an ischemic RV failure patient is even more unreliable. This thought path will lead to volume overload and worse outcomes.
Measuring Contractility:
TAPSE:
This is the simplest and least invasive method used to measure contractility. TAPSE stands for tricuspid annular plane systolic excursion. The right ventricle is primarily just a thin wall attached to the LV. The RV does not constrict inwardly like the LV, it shortens on the vertical plane. The more it shortens the better the function. TAPSE is done in the apical 4 view of a transthoracic echo with M-mode over the tricuspid annulus (Figure 3) and measures how much the free wall shortens during systole.
Figure 3:
Stroke work index:
The force of the contraction over a distance equates to work. The stroke work of the right ventricle is a great marker for contractility and is frequently used. The stroke work is the area within the pressure-volume loop of the cardiac cycle. In figure 4 the LV stroke work is shaded in red whereas the RV stroke work is shaded in blue. The RV requires less work and has no isovolumetric contraction or relaxation unless there is RV hypertrophy or dysfunction. The right ventricular stroke work is shown in Figure 5.
Figure 4: Ventricular Cardiac Loops (3)
Figure 5: Right ventricular pressure-volume loop
As mentioned above, ventricular contractility varies with different preload and afterload conditions. When stroke work is graphed against diastolic pressure the graph matches the Starling curve, showing that RVSW is a good measure of contractility. The RVSW is divided by BSA to get RVSWI, which is better than RVSW because it standardizes the range.
To calculate the stroke work index the pressure after the ventricle is subtracted from the pressure before the ventricle and then multiplied by the stroke volume and a constant.
RVSWI = [(mPAP – RAP) x SV x 0.0136]/BSA
PAPi:
Pulmonary artery pulsatility index or PAPi has been used for RV function for a long time but has gained more popularity recently. The formula for PAPi is the difference in pulmonary artery pressures divided by the right atrial pressure or central venous pressure.
PAPi = (PASP – PADP)/RAP
A closer look at this formula really shows why this is now being used in the national cardiogenic shock protocol and many other hospital-specific cardiogenic shock protocols. The difference between PASP and PADP is a sign of pulsatility. Just like with the left ventricle and systemic blood pressure, a narrow pulse pressure is a sign of poor systolic function, so a narrow pulmonary pulse pressure would imply poor systolic function. Dividing by RAP is just as important, the better the contraction and unloading of the RV the less volume in RV, the lower the RVEDV, and therefore the lower the RAP. This equation looks at the RV’s ability to generate a pressure with its force and its ability to unload its volume. The higher the PAPi the better the function and is usually >2, where a value <1.7 is poor. A value of <0.9 is used as a marker for needing mechanical support for the RV (7).
RAP/PAOP:
This is a quick look at RV contractility that is not as accurate but does not require a lot of calculations. Usually, the RAP is <50% of the left atrial pressure (LAP). The LAP is measured with the pulmonary artery occlusion pressure (PAOP) or wedge pressure. The closer the RAP is to the PAOP the worse the RV function. If the RAP is increasing and the PAOP is not, this implies poor forward flow from the RV through the pulmonary artery to the LV. This causes back pressure which is why the RAP increases. In short, the closer the RAP is to the PAOP the worse the function.
EF:
The ejection fraction of the RV seems like an obvious marker for RV contractility since it is looked at so closely on the left side. The problem with this calculation is that the RV shortens and twists and makes it difficult to visualize with a transthoracic echo. It is more commonly mentioned with a transesophageal echo (TEE) with a normal EF of ≥45%.
For a Deeper Look
S’
Looking at the velocity of the tricuspid annulus during systole is another way to objectively measure RV function. The tissue doppler (TDI) of the tricuspid annulus is called s’. It is not often done with a traditional echo but does have a good correlation in a more binomial score. If it is <10 cm/sec then there is RV dysfunction.
RIMP
The right ventricular index of myocardial performance (RIMP) is not looked at in a traditional echo. It is a ratio of the non-ejection time compared to the ejection time during RV systole.
Figure 6: Measuring RIMP
RIMP = (IVCT + IVRT) / ET
As noted before, the RV does not typically have isovolumetric contraction (IVC) or relaxation (IVR) unless there is RV hypertrophy or RV dysfunction. Using this information, the longer the isovolumetric times (IVCT and IVRT) compared to the actual ejection time (ET), the worse the RV function. This is well described along with s’ at https://www.cardioserv.net/rv-function-rimp/.
Potential Pitfalls:
The big caveat to looking at the RV contractility is that it can be falsely low due to increased afterload. The increased afterload may be the primary issue and if it is resolved the RV contractility will improve and will not need intervention. A great example is acute pulmonary embolism. When there is a large acute clot in the pulmonary arteries the pressure increase causes an abrupt backup of volume. This abrupt increase of volume and pressure proximal to the clot overwhelms the RV and it will even stop moving all together. McConnell’s sign is akinesis of the right ventricular free wall due to an acute PE. Afterload issues should always be carefully explored when evaluating RV contractility issues.
Summary:
Decreased contractility is usually not the stand-alone cause for RV dysfunction. If RV contractility issues are seen it is important to look at whether excess preload, excess afterload, or both are causing the decreased contractility before assuming a RV infarct as the cause. The answer is rarely fluid for these patients, except in the rare acute MI with acute RV dysfunction who is hypovolemic or becomes vasoplegic and drops to an abnormally low preload.
I typically look at TAPSE because it is measured in a complete echo, is easy to measure, and is non-invasive. When a patient has a pulmonary artery catheter, I will look at RVSWI, PAPi, and RAP:PAOP ratio, but personally I have not decided on which one I will put ahead of the others if they disagree with each other.
Figure 7:
Figure 8: RV Contractility Measurements
Table 1: Contractility Assessment
References:
1. Davidson, B.P., Giraud, G.D., 2012. Left Ventricular Function and the Systemic Arterial Vasculature: Remembering What We Have Learned. Journal of the American Society of Echocardiography 25, 891–894.. doi:10.1016/j.echo.2012.06.020
2. 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
3. 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
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
6. Jeffers JL, Boyd KL, Parks LJ. Right Ventricular Myocardial Infarction. [Updated 2020 Aug 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431048/
7. Kochav SM, Flores RJ, Truby LK, Topkara VK. Prognostic Impact of Pulmonary Artery Pulsatility Index (PAPi) in Patients With Advanced Heart Failure: Insights From the ESCAPE Trial. J Card Fail. 2018;24(7):453-459. doi:10.1016/j.cardfail.2018.03.008
8. Caballero L, Kou S, Dulgheru R, et al. Echocardiographic reference ranges for normal cardiac Doppler data: results from the NORRE Study. Eur Heart J Cardiovasc Imaging. 2015;16(9):1031-1041. doi:10.1093/ehjci/jev083
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